Autoimmune diseases of the nervous system. Medical search

Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.

The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.

The entire nerve apparatus, composed of a central part, the brain and spinal cord, and a peripheral part, the cranial and spinal nerves, autonomic ganglia, and plexuses. (Stedman, 26th ed)

Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.

Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.

A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.

Diseases of any component of the brain (including the cerebral hemispheres, diencephalon, brain stem, and cerebellum) or the spinal cord.

The nervous system outside of the brain and spinal cord. The peripheral nervous system has autonomic and somatic divisions. The autonomic nervous system includes the enteric, parasympathetic, and sympathetic subdivisions. The somatic nervous system includes the cranial and spinal nerves and their ganglia and the peripheral sensory receptors.

An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5)

Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.

Disorders caused by cellular or humoral immune responses primarily directed towards nervous system autoantigens. The immune response may be directed towards specific tissue components (e.g., myelin) and may be limited to the central nervous system (e.g., MULTIPLE SCLEROSIS) or the peripheral nervous system (e.g., GUILLAIN-BARRE SYNDROME).

Two ganglionated neural plexuses in the gut wall which form one of the three major divisions of the autonomic nervous system. The enteric nervous system innervates the gastrointestinal tract, the pancreas, and the gallbladder. It contains sensory neurons, interneurons, and motor neurons. Thus the circuitry can autonomously sense the tension and the chemical environment in the gut and regulate blood vessel tone, motility, secretions, and fluid transport. The system is itself governed by the central nervous system and receives both parasympathetic and sympathetic innervation. (From Kandel, Schwartz, and Jessel, Principles of Neural Science, 3d ed, p766)

Benign and malignant neoplastic processes that arise from or secondarily involve the brain, spinal cord, or meninges.

Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.

An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)

Chronic inflammatory and autoimmune disease in which the salivary and lacrimal glands undergo progressive destruction by lymphocytes and plasma cells resulting in decreased production of saliva and tears. The primary form, often called sicca syndrome, involves both KERATOCONJUNCTIVITIS SICCA and XEROSTOMIA. The secondary form includes, in addition, the presence of a connective tissue disease, usually rheumatoid arthritis.

Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.

The ENTERIC NERVOUS SYSTEM; PARASYMPATHETIC NERVOUS SYSTEM; and SYMPATHETIC NERVOUS SYSTEM taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the CENTRAL NERVOUS SYSTEM, especially the HYPOTHALAMUS and the SOLITARY NUCLEUS, which receive information relayed from VISCERAL AFFERENTS.

The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.

The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system.

A mouse substrain that is genetically predisposed to the development of systemic lupus erythematosus-like syndrome, which has been found to be clinically similar to the human disease. It has been determined that this mouse strain carries a mutation in the fas gene. Also, the MRL/lpr is a useful model to study behavioral and cognitive deficits found in autoimmune diseases and the efficacy of immunosuppressive agents.

Characteristic properties and processes of the NERVOUS SYSTEM as a whole or with reference to the peripheral or the CENTRAL NERVOUS SYSTEM.

Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.

A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.

Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.

A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.

CD4-positive T cells that inhibit immunopathology or autoimmune disease in vivo. They inhibit the immune response by influencing the activity of other cell types. Regulatory T-cells include naturally occurring CD4+CD25+ cells, IL-10 secreting Tr1 cells, and Th3 cells.

Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.

Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.

Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.

Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.

Pathogenic infections of the brain, spinal cord, and meninges. DNA VIRUS INFECTIONS; RNA VIRUS INFECTIONS; BACTERIAL INFECTIONS; MYCOPLASMA INFECTIONS; SPIROCHAETALES INFECTIONS; fungal infections; PROTOZOAN INFECTIONS; HELMINTHIASIS; and PRION DISEASES may involve the central nervous system as a primary or secondary process.

The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc.

The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.

An abundant cytosolic protein that plays a critical role in the structure of multilamellar myelin. Myelin basic protein binds to the cytosolic sides of myelin cell membranes and causes a tight adhesion between opposing cell membranes.

Inflammatory disease of the THYROID GLAND due to autoimmune responses leading to lymphocytic infiltration of the gland. It is characterized by the presence of circulating thyroid antigen-specific T-CELLS and thyroid AUTOANTIBODIES. The clinical signs can range from HYPOTHYROIDISM to THYROTOXICOSIS depending on the type of autoimmune thyroiditis.

Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

Inflammation of the OVARY, generally caused by an ascending infection of organisms from the endocervix.

Benign and malignant neoplastic processes arising from or involving components of the central, peripheral, and autonomic nervous systems, cranial nerves, and meninges. Included in this category are primary and metastatic nervous system neoplasms.

The normal lack of the ability to produce an immunological response to autologous (self) antigens. A breakdown of self tolerance leads to autoimmune diseases. The ability to recognize the difference between self and non-self is the prime function of the immune system.

A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.

A strain of non-obese diabetic mice developed in Japan that has been widely studied as a model for T-cell-dependent autoimmune insulin-dependent diabetes mellitus in which insulitis is a major histopathologic feature, and in which genetic susceptibility is strongly MHC-linked.

A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached.

A proinflammatory cytokine produced primarily by T-LYMPHOCYTES or their precursors. Several subtypes of interleukin-17 have been identified, each of which is a product of a unique gene.

The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.

A transmembrane protein present in the MYELIN SHEATH of the CENTRAL NERVOUS SYSTEM. It is one of the main autoantigens implicated in the pathogenesis of MULTIPLE SCLEROSIS.

Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.

Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.

A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.

Experimental animal models for human AUTOIMMUNE DISEASES OF THE NERVOUS SYSTEM. They include GUILLAIN-BARRE SYNDROME (see NEURITIS, AUTOIMMUNE, EXPERIMENTAL); MYASTHENIA GRAVIS (see MYASTHENIA GRAVIS, AUTOIMMUNE, EXPERIMENTAL); and MULTIPLE SCLEROSIS (see ENCEPHALOMYELITIS, AUTOIMMUNE, EXPERIMENTAL).

Subset of helper-effector T-lymphocytes which synthesize and secrete IL-17, IL-17F, and IL-22. These cytokines are involved in host defenses and tissue inflammation in autoimmune diseases.

Conditions characterized by loss or dysfunction of myelin (see MYELIN SHEATH) in the brain, spinal cord, or optic nerves secondary to autoimmune mediated processes. This may take the form of a humoral or cellular immune response directed toward myelin or OLIGODENDROGLIA associated autoantigens.

A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.

Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.

The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.

The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.

A chronic multi-system disorder of CONNECTIVE TISSUE. It is characterized by SCLEROSIS in the SKIN, the LUNGS, the HEART, the GASTROINTESTINAL TRACT, the KIDNEYS, and the MUSCULOSKELETAL SYSTEM. Other important features include diseased small BLOOD VESSELS and AUTOANTIBODIES. The disorder is named for its most prominent feature (hard skin), and classified into subsets by the extent of skin thickening: LIMITED SCLERODERMA and DIFFUSE SCLERODERMA.

Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement.

MYELIN-specific proteins that play a structural or regulatory role in the genesis and maintenance of the lamellar MYELIN SHEATH structure.

An encapsulated lymphatic organ through which venous blood filters.

A classification of T-lymphocytes, especially into helper/inducer, suppressor/effector, and cytotoxic subsets, based on structurally or functionally different populations of cells.

Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.

Viral infections of the brain, spinal cord, meninges, or perimeningeal spaces.

Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (IMMUNOTHERAPY, ADOPTIVE).

A subtype of non-receptor protein tyrosine phosphatases that is characterized by the presence of an N-terminal catalytic domain and a C-terminal PROLINE-rich domain. The phosphatase subtype is predominantly expressed in LYMPHOCYTES and plays a key role in the inhibition of downstream T-LYMPHOCYTE activation. Polymorphisms in the gene that encodes this phosphatase subtype are associated with a variety of AUTOIMMUNE DISEASES.

Subset of helper-inducer T-lymphocytes which synthesize and secrete interleukin-2, gamma-interferon, and interleukin-12. Due to their ability to kill antigen-presenting cells and their lymphokine-mediated effector activity, Th1 cells are associated with vigorous delayed-type hypersensitivity reactions.

A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.

The structure of one molecule that imitates or simulates the structure of a different molecule.

A myelin protein found in the periaxonal membrane of both the central and peripheral nervous systems myelin sheaths. It binds to cells surface receptors found on AXONS and may regulate cellular interactions between MYELIN and AXONS.

A myelin protein that is the major component of the organic solvent extractable lipoprotein complexes of whole brain. It has been the subject of much study because of its unusual physical properties. It remains soluble in chloroform even after essentially all of its bound lipids have been removed. (From Siegel et al., Basic Neurochemistry, 4th ed, p122)

ARTHRITIS that is induced in experimental animals. Immunological methods and infectious agents can be used to develop experimental arthritis models. These methods include injections of stimulators of the immune response, such as an adjuvant (ADJUVANTS, IMMUNOLOGIC) or COLLAGEN.

A disorder of neuromuscular transmission characterized by weakness of cranial and skeletal muscles. Autoantibodies directed against acetylcholine receptors damage the motor endplate portion of the NEUROMUSCULAR JUNCTION, impairing the transmission of impulses to skeletal muscles. Clinical manifestations may include diplopia, ptosis, and weakness of facial, bulbar, respiratory, and proximal limb muscles. The disease may remain limited to the ocular muscles. THYMOMA is commonly associated with this condition. (Adams et al., Principles of Neurology, 6th ed, p1459)

Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.

Chronic autoimmune thyroiditis, characterized by the presence of high serum thyroid AUTOANTIBODIES; GOITER; and HYPOTHYROIDISM.

The major interferon produced by mitogenically or antigenically stimulated LYMPHOCYTES. It is structurally different from TYPE I INTERFERON and its major activity is immunoregulation. It has been implicated in the expression of CLASS II HISTOCOMPATIBILITY ANTIGENS in cells that do not normally produce them, leading to AUTOIMMUNE DISEASES.

Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.

The lipid-rich sheath surrounding AXONS in both the CENTRAL NERVOUS SYSTEMS and PERIPHERAL NERVOUS SYSTEM. The myelin sheath is an electrical insulator and allows faster and more energetically efficient conduction of impulses. The sheath is formed by the cell membranes of glial cells (SCHWANN CELLS in the peripheral and OLIGODENDROGLIA in the central nervous system). Deterioration of the sheath in DEMYELINATING DISEASES is a serious clinical problem.

Antibodies produced by a single clone of cells.

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

Mercury chloride (HgCl2). A highly toxic compound that volatizes slightly at ordinary temperature and appreciably at 100 degrees C. It is corrosive to mucous membranes and used as a topical antiseptic and disinfectant.

Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).

A subclass of winged helix DNA-binding proteins that share homology with their founding member fork head protein, Drosophila.

Inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (sclera and cornea, and the retina). (Dorland, 27th ed)

Inflammation of blood vessels within the central nervous system. Primary vasculitis is usually caused by autoimmune or idiopathic factors, while secondary vasculitis is caused by existing disease process. Clinical manifestations are highly variable but include HEADACHE; SEIZURES; behavioral alterations; INTRACRANIAL HEMORRHAGES; TRANSIENT ISCHEMIC ATTACK; and BRAIN INFARCTION. (From Adams et al., Principles of Neurology, 6th ed, pp856-61)

Group of chronic blistering diseases characterized histologically by ACANTHOLYSIS and blister formation within the EPIDERMIS.

Theoretical representations that simulate the behavior or activity of immune system, processes, or phenomena. They include the use of mathematical equations, computers, and other electrical equipment.

A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the NASAL MUCOSA; BUCCAL MUCOSA; and conjunctival mucosa.

Loss of scalp and body hair involving microscopically inflammatory patchy areas.

An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.

Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.

The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.

Mice bearing mutant genes which are phenotypically expressed in the animals.

The body's defense mechanism against foreign organisms or substances and deviant native cells. It includes the humoral immune response and the cell-mediated response and consists of a complex of interrelated cellular, molecular, and genetic components.

Structural abnormalities of the central or peripheral nervous system resulting primarily from defects of embryogenesis.

Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).

RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.

Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.

Surgical removal of the thymus gland. (Dorland, 28th ed)

Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.

A common form of hyperthyroidism with a diffuse hyperplastic GOITER. It is an autoimmune disorder that produces antibodies against the THYROID STIMULATING HORMONE RECEPTOR. These autoantibodies activate the TSH receptor, thereby stimulating the THYROID GLAND and hypersecretion of THYROID HORMONES. These autoantibodies can also affect the eyes (GRAVES OPHTHALMOPATHY) and the skin (Graves dermopathy).

A class of drugs producing both physiological and psychological effects through a variety of mechanisms. They can be divided into "specific" agents, e.g., affecting an identifiable molecular mechanism unique to target cells bearing receptors for that agent, and "nonspecific" agents, those producing effects on different target cells and acting by diverse molecular mechanisms. Those with nonspecific mechanisms are generally further classed according to whether they produce behavioral depression or stimulation. Those with specific mechanisms are classed by locus of action or specific therapeutic use. (From Gilman AG, et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p252)

Molecules on the surface of T-lymphocytes that recognize and combine with antigens. The receptors are non-covalently associated with a complex of several polypeptides collectively called CD3 antigens (ANTIGENS, CD3). Recognition of foreign antigen and the major histocompatibility complex is accomplished by a single heterodimeric antigen-receptor structure, composed of either alpha-beta (RECEPTORS, ANTIGEN, T-CELL, ALPHA-BETA) or gamma-delta (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA) chains.

An inhibitory T CELL receptor that is closely related to CD28 ANTIGEN. It has specificity for CD80 ANTIGEN and CD86 ANTIGEN and acts as a negative regulator of peripheral T cell function. CTLA-4 antigen is believed to play role in inducing PERIPHERAL TOLERANCE.

Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.

The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.

The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.

A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases.

Subpopulation of CD4+ lymphocytes that cooperate with other lymphocytes (either T or B) to initiate a variety of immune functions. For example, helper-inducer T-cells cooperate with B-cells to produce antibodies to thymus-dependent antigens and with other subpopulations of T-cells to initiate a variety of cell-mediated immune functions.

FIBROSIS of the hepatic parenchyma due to obstruction of BILE flow (CHOLESTASIS) in the intrahepatic or extrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC; BILE DUCTS, EXTRAHEPATIC). Primary biliary cirrhosis involves the destruction of small intra-hepatic bile ducts and bile secretion. Secondary biliary cirrhosis is produced by prolonged obstruction of large intrahepatic or extrahepatic bile ducts from a variety of causes.

Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.

Traumatic injuries to the brain, cranial nerves, spinal cord, autonomic nervous system, or neuromuscular system, including iatrogenic injuries induced by surgical procedures.

Elements of limited time intervals, contributing to particular results or situations.

The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.

Biologically active substances whose activities affect or play a role in the functioning of the immune system.

A single, unpaired primary lymphoid organ situated in the MEDIASTINUM, extending superiorly into the neck to the lower edge of the THYROID GLAND and inferiorly to the fourth costal cartilage. It is necessary for normal development of immunologic function early in life. By puberty, it begins to involute and much of the tissue is replaced by fat.

Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.

Autoimmune diseases affecting multiple endocrine organs. Type I is characterized by childhood onset and chronic mucocutaneous candidiasis (CANDIDIASIS, CHRONIC MUCOCUTANEOUS), while type II exhibits any combination of adrenal insufficiency (ADDISON'S DISEASE), lymphocytic thyroiditis (THYROIDITIS, AUTOIMMUNE;), HYPOPARATHYROIDISM; and gonadal failure. In both types organ-specific ANTIBODIES against a variety of ENDOCRINE GLANDS have been detected. The type II syndrome differs from type I in that it is associated with HLA-A1 and B8 haplotypes, onset is usually in adulthood, and candidiasis is not present.

Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.

A general term indicating inflammation of the BRAIN and SPINAL CORD, often used to indicate an infectious process, but also applicable to a variety of autoimmune and toxic-metabolic conditions. There is significant overlap regarding the usage of this term and ENCEPHALITIS in the literature.

One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.

MYCOSES of the brain, spinal cord, and meninges which may result in ENCEPHALITIS; MENINGITIS, FUNGAL; MYELITIS; BRAIN ABSCESS; and EPIDURAL ABSCESS. Certain types of fungi may produce disease in immunologically normal hosts, while others are classified as opportunistic pathogens, causing illness primarily in immunocompromised individuals (e.g., ACQUIRED IMMUNODEFICIENCY SYNDROME).

A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes.

Substances that are recognized by the immune system and induce an immune reaction.

Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.

Diseases of the parasympathetic or sympathetic divisions of the AUTONOMIC NERVOUS SYSTEM; which has components located in the CENTRAL NERVOUS SYSTEM and PERIPHERAL NERVOUS SYSTEM. Autonomic dysfunction may be associated with HYPOTHALAMIC DISEASES; BRAIN STEM disorders; SPINAL CORD DISEASES; and PERIPHERAL NERVOUS SYSTEM DISEASES. Manifestations include impairments of vegetative functions including the maintenance of BLOOD PRESSURE; HEART RATE; pupil function; SWEATING; REPRODUCTIVE AND URINARY PHYSIOLOGY; and DIGESTION.

The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium.

A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.

A cytokine produced by a variety of cell types, including T-LYMPHOCYTES; MONOCYTES; DENDRITIC CELLS; and EPITHELIAL CELLS that exerts a variety of effects on immunoregulation and INFLAMMATION. Interleukin-10 combines with itself to form a homodimeric molecule that is the biologically active form of the protein.

The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.

A low affinity interleukin-2 receptor subunit that combines with the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN to form a high affinity receptor for INTERLEUKIN-2.

Characteristic restricted to a particular organ of the body, such as a cell type, metabolic response or expression of a particular protein or antigen.

All of the processes involved in increasing CELL NUMBER including CELL DIVISION.

Subset of helper-inducer T-lymphocytes which synthesize and secrete the interleukins IL-4, IL-5, IL-6, and IL-10. These cytokines influence B-cell development and antibody production as well as augmenting humoral responses.

Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.

Manipulation of the host's immune system in treatment of disease. It includes both active and passive immunization as well as immunosuppressive therapy to prevent graft rejection.

Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.

Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.

Established cell cultures that have the potential to propagate indefinitely.

Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).

Sites on an antigen that interact with specific antibodies.

A tumor necrosis factor superfamily member that plays a role in the regulation of B-LYMPHOCYTE survival. It occurs as a membrane-bound protein that is cleaved to release an biologically active soluble form with specificity to TRANSMEMBRANE ACTIVATOR AND CAML INTERACTOR PROTEIN; B-CELL ACTIVATION FACTOR RECEPTOR; and B-CELL MATURATION ANTIGEN.

A heterogeneous group of immunocompetent cells that mediate the cellular immune response by processing and presenting antigens to the T-cells. Traditional antigen-presenting cells include MACROPHAGES; DENDRITIC CELLS; LANGERHANS CELLS; and B-LYMPHOCYTES. FOLLICULAR DENDRITIC CELLS are not traditional antigen-presenting cells, but because they hold antigen on their cell surface in the form of IMMUNE COMPLEXES for B-cell recognition they are considered so by some authors.

The craniosacral division of the autonomic nervous system. The cell bodies of the parasympathetic preganglionic fibers are in brain stem nuclei and in the sacral spinal cord. They synapse in cranial autonomic ganglia or in terminal ganglia near target organs. The parasympathetic nervous system generally acts to conserve resources and restore homeostasis, often with effects reciprocal to the sympathetic nervous system.

A class of large neuroglial (macroglial) cells in the central nervous system. Oligodendroglia may be called interfascicular, perivascular, or perineuronal (not the same as SATELLITE CELLS, PERINEURONAL of GANGLIA) according to their location. They form the insulating MYELIN SHEATH of axons in the central nervous system.

Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.

Glycoproteins found on the membrane or surface of cells.

They are oval or bean shaped bodies (1 - 30 mm in diameter) located along the lymphatic system.

The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.

Disorders caused by abnormal or absent immunologic mechanisms, whether humoral, cell-mediated, or both.

Refers to animals in the period of time just after birth.

Immunoglobulin preparations used in intravenous infusion, containing primarily IMMUNOGLOBULIN G. They are used to treat a variety of diseases associated with decreased or abnormal immunoglobulin levels including pediatric AIDS; primary HYPERGAMMAGLOBULINEMIA; SCID; CYTOMEGALOVIRUS infections in transplant recipients, LYMPHOCYTIC LEUKEMIA, CHRONIC; Kawasaki syndrome, infection in neonates, and IDIOPATHIC THROMBOCYTOPENIC PURPURA.

Bacterial infections of the brain, spinal cord, and meninges, including infections involving the perimeningeal spaces.

Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.

Immunosuppression by reduction of circulating lymphocytes or by T-cell depletion of bone marrow. The former may be accomplished in vivo by thoracic duct drainage or administration of antilymphocyte serum. The latter is performed ex vivo on bone marrow before its transplantation.

A critical subpopulation of regulatory T-lymphocytes involved in MHC Class I-restricted interactions. They include both cytotoxic T-lymphocytes (T-LYMPHOCYTES, CYTOTOXIC) and CD8+ suppressor T-lymphocytes.

Soluble factors which stimulate growth-related activities of leukocytes as well as other cell types. They enhance cell proliferation and differentiation, DNA synthesis, secretion of other biologically active molecules and responses to immune and inflammatory stimuli.

Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.

Specific molecular sites on the surface of various cells, including B-lymphocytes and macrophages, that combine with IMMUNOGLOBULIN Gs. Three subclasses exist: Fc gamma RI (the CD64 antigen, a low affinity receptor), Fc gamma RII (the CD32 antigen, a high affinity receptor), and Fc gamma RIII (the CD16 antigen, a low affinity receptor).

Receptors present on activated T-LYMPHOCYTES and B-LYMPHOCYTES that are specific for INTERLEUKIN-2 and play an important role in LYMPHOCYTE ACTIVATION. They are heterotrimeric proteins consisting of the INTERLEUKIN-2 RECEPTOR ALPHA SUBUNIT, the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT, and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN.

A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.

An acquired disease of unknown etiology, chronic course, and tendency to recur. It is characterized by inflammation and degeneration of cartilage and can result in deformities such as floppy ear and saddle nose. Loss of cartilage in the respiratory tract can lead to respiratory obstruction.

A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.

Deliberate prevention or diminution of the host's immune response. It may be nonspecific as in the administration of immunosuppressive agents (drugs or radiation) or by lymphocyte depletion or may be specific as in desensitization or the simultaneous administration of antigen and immunosuppressive drugs.

A classification of B-lymphocytes based on structurally or functionally different populations of cells.

A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES. It has specificity for FAS LIGAND and plays a role in regulation of peripheral immune responses and APOPTOSIS. Multiple isoforms of the protein exist due to multiple ALTERNATIVE SPLICING. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.

The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.

The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.

Alteration of the immune system or of an immune response by agents that activate or suppress its function. This can include IMMUNIZATION or administration of immunomodulatory drugs. Immunomodulation can also encompass non-therapeutic alteration of the immune system effected by endogenous or exogenous substances.

A soluble substance elaborated by antigen- or mitogen-stimulated T-LYMPHOCYTES which induces DNA synthesis in naive lymphocytes.

A subacute or chronic inflammatory disease of muscle and skin, marked by proximal muscle weakness and a characteristic skin rash. The illness occurs with approximately equal frequency in children and adults. The skin lesions usually take the form of a purplish rash (or less often an exfoliative dermatitis) involving the nose, cheeks, forehead, upper trunk, and arms. The disease is associated with a complement mediated intramuscular microangiopathy, leading to loss of capillaries, muscle ischemia, muscle-fiber necrosis, and perifascicular atrophy. The childhood form of this disease tends to evolve into a systemic vasculitis. Dermatomyositis may occur in association with malignant neoplasms. (From Adams et al., Principles of Neurology, 6th ed, pp1405-6)

A soluble factor produced by activated T-LYMPHOCYTES that induces the expression of MHC CLASS II GENES and FC RECEPTORS on B-LYMPHOCYTES and causes their proliferation and differentiation. It also acts on T-lymphocytes, MAST CELLS, and several other hematopoietic lineage cells.

An experimental animal model for the demyelinating disease of GUILLAINE-BARRE SYNDROME. In the most frequently used protocol, animals are injected with a peripheral nerve tissue protein homogenate. After approximately 2 weeks the animals develop a neuropathy secondary to a T cell-mediated autoimmune response directed towards the MYELIN P2 PROTEIN in peripheral nerves. Pathologic findings include a perivascular accumulation of macrophages and T lymphocytes in the peripheral nervous system, similar to that seen in the Guillaine-Barre syndrome. (From Adams et al., Principles of Neurology, 6th ed, p1314; J Neuroimmunol 1998 Apr 1;84(1):40-52)

INFLAMMATION of salivary tissue (SALIVARY GLANDS), usually due to INFECTION or injuries.

The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.

The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.

The biochemical and electrophysiological interactions between the NERVOUS SYSTEM and IMMUNE SYSTEM.

A delayed rectifier subtype of shaker potassium channels that is the predominant VOLTAGE-GATED POTASSIUM CHANNEL of T-LYMPHOCYTES.

Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.

An adrenal disease characterized by the progressive destruction of the ADRENAL CORTEX, resulting in insufficient production of ALDOSTERONE and HYDROCORTISONE. Clinical symptoms include ANOREXIA; NAUSEA; WEIGHT LOSS; MUSCLE WEAKNESS; and HYPERPIGMENTATION of the SKIN due to increase in circulating levels of ACTH precursor hormone which stimulates MELANOCYTES.

Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.

White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.

Deliberate stimulation of the host's immune response. ACTIVE IMMUNIZATION involves administration of ANTIGENS or IMMUNOLOGIC ADJUVANTS. PASSIVE IMMUNIZATION involves administration of IMMUNE SERA or LYMPHOCYTES or their extracts (e.g., transfer factor, immune RNA) or transplantation of immunocompetent cell producing tissue (thymus or bone marrow).

Large, transmembrane, non-covalently linked glycoproteins (alpha and beta). Both chains can be polymorphic although there is more structural variation in the beta chains. The class II antigens in humans are called HLA-D ANTIGENS and are coded by a gene on chromosome 6. In mice, two genes named IA and IE on chromosome 17 code for the H-2 antigens. The antigens are found on B-lymphocytes, macrophages, epidermal cells, and sperm and are thought to mediate the competence of and cellular cooperation in the immune response. The term IA antigens used to refer only to the proteins encoded by the IA genes in the mouse, but is now used as a generic term for any class II histocompatibility antigen.

Deliberate breeding of two different individuals that results in offspring that carry part of the genetic material of each parent. The parent organisms must be genetically compatible and may be from different varieties or closely related species.

A chronic self-perpetuating hepatocellular INFLAMMATION of unknown cause, usually with HYPERGAMMAGLOBULINEMIA and serum AUTOANTIBODIES.

55-kDa antigens found on HELPER-INDUCER T-LYMPHOCYTES and on a variety of other immune cell types. CD4 antigens are members of the immunoglobulin supergene family and are implicated as associative recognition elements in MAJOR HISTOCOMPATIBILITY COMPLEX class II-restricted immune responses. On T-lymphocytes they define the helper/inducer subset. CD4 antigens also serve as INTERLEUKIN-15 receptors and bind to the HIV receptors, binding directly to the HIV ENVELOPE PROTEIN GP120.

Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.

Protection from an infectious disease agent that is mediated by B- and T- LYMPHOCYTES following exposure to specific antigen, and characterized by IMMUNOLOGIC MEMORY. It can result from either previous infection with that agent or vaccination (IMMUNITY, ACTIVE), or transfer of antibody or lymphocytes from an immune donor (IMMUNIZATION, PASSIVE).

Central nervous system vasculitis that is associated with SYSTEMIC LUPUS ERYTHEMATOSUS. Clinical manifestations may include DEMENTIA; SEIZURES; CRANIAL NERVE DISEASES; HEMIPARESIS; BLINDNESS; DYSPHASIA; and other neurological disorders.

Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.

An orphan nuclear receptor found in the THYMUS where it plays a role in regulating the development and maturation of thymocytes. An isoform of this protein, referred to as RORgammaT, is produced by an alternatively transcribed mRNA.

Pathologic conditions affecting the BRAIN, which is composed of the intracranial components of the CENTRAL NERVOUS SYSTEM. This includes (but is not limited to) the CEREBRAL CORTEX; intracranial white matter; BASAL GANGLIA; THALAMUS; HYPOTHALAMUS; BRAIN STEM; and CEREBELLUM.

Tuberculosis of the brain, spinal cord, or meninges (TUBERCULOSIS, MENINGEAL), most often caused by MYCOBACTERIUM TUBERCULOSIS and rarely by MYCOBACTERIUM BOVIS. The infection may be limited to the nervous system or coexist in other organs (e.g., TUBERCULOSIS, PULMONARY). The organism tends to seed the meninges causing a diffuse meningitis and leads to the formation of TUBERCULOMA, which may occur within the brain, spinal cord, or perimeningeal spaces. Tuberculous involvement of the vertebral column (TUBERCULOSIS, SPINAL) may result in nerve root or spinal cord compression. (From Adams et al., Principles of Neurology, 6th ed, pp717-20)

Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.

Inflammation of the lacrimal sac. (Dorland, 27th ed)

The heat-stable antigen determines pathogenicity of self-reactive T cells in experimental autoimmune encephalomyelitis. (1/107)

Induction of myelin-specific CD4 T cells is a pivotal event in the development of experimental autoimmune encephalomyelitis (EAE). Other checkpoints in EAE pathogenesis have not been clearly defined, although multiple genetic loci are known to influence EAE development. We report here that targeted mutation of the heat-stable antigen (HSA) abrogates development of EAE despite a complete lack of effect on induction of autoimmune T cells. To test whether T-cell expression of HSA is sufficient, we created transgenic mice in which HSA is expressed exclusively in the T-cell lineage. We found that these mice remain resistant to EAE induction. Adoptive transfer studies demonstrate that both T cells and non-T cells must express HSA in order for the pathogenic T cells to execute their effector function. Moreover, HSAIg, a fusion protein consisting of the extracellular domain of the HSA and the Fc portion of immunoglobulin, drastically ameliorates the clinical sign of EAE even when administrated after self-reactive T cells had been expanded. Thus, identification of HSA as a novel checkpoint, even after activation and expansion of self-reactive T cells, provides a novel approach for immunotherapy of autoimmune neurologic diseases, such as multiple sclerosis. (+info)

Oligoclonal T cell repertoire in cerebrospinal fluid of patients with inflammatory diseases of the nervous system. (2/107)

OBJECTIVE: To evaluate the T cell receptor beta chain variable region (TCRBV) gene usage ex vivo in CSF cells and peripheral blood mononuclear cells (PBMCs) collected from patients with autoimmune and inflammatory diseases of the nervous system. METHODS: A novel sensitive seminestedpolymerase chain reaction coupled with heteroduplex analysis was developed. RESULTS: Under these experimental conditions, the minimal number of cells required for the analysis of the whole T cell repertoire was established at 2.5x10(4)-sufficient to evaluate most of the samples collected during diagnostic lumbar punctures. In the 21 patients examined, restrictions in TCRBV gene family usage were not seen. However, using heteroduplex analysis, oligoclonal T cell expansions were found in the CSF of 13 patients and monoclonal expansions in five patients. The T cell abnormalities found did not correlate with intrathecal IgG production or with any clinical variable considered. CONCLUSION: T cell clonal expansions, useful for further characterisation of pathogenetic T cells, can be found during the course of nervous system inflammations, but this abnormality is probably not disease specific. (+info)

Paraneoplastic peripheral neuropathy associated with anti-Hu antibodies. A clinical and electrophysiological study of 20 patients. (3/107)

Although paraneoplastic subacute sensory neuronopathy is the most frequent presentation of peripheral neuropathy in patients with anti-Hu antibodies, other neuropathies have been reported. In order to investigate the clinical and electrophysiological manifestations of neuropathies associated with anti-Hu antibodies, we conducted a retrospective study of 20 patients. For the electrophysiological study, each nerve was classified as normal, demyelinating, axonal/neuronal or axonal/demyelinating. Peripheral neuropathy was the presenting symptom in 95% of patients. CNS and autonomic neuropathy were present in 40% and 30% of patients, respectively. The course of the neuropathy was acute, mimicking Guillain-Barre syndrome in one patient (5%), and subacute (55%) or progressive (40%) in the others. Clinically, the neuropathy was sensory (70%), sensorimotor (25%) or motor (5%). At onset, symptoms were symmetrical (65%), asymmetrical (25%) or multifocal (10%). Pain was a predominant manifestation (80%). Amyotrophia and fasciculations were rare. The median Rankin's score was 2, three patients having an indolent form. Electrophysiology showed the axonal/neuronal pattern to be the most frequent (46.9% of studied nerves); an axonal/demyelinating or demyelinating pattern being seen in 18.3% and 4.9% of nerves, respectively. The axonal/neuronal pattern was more frequent in sensory nerves and the mixed axonal/demyelinating pattern more frequent in motor nerves (P < 0.01). A higher proportion of abnormal nerves correlated with a progressive course (P < 0.05) or a Rankin's score between 3 and 5 (P < 0.01). In patients with sensory neuropathy, 88.5% of sensory nerves were abnormal, mostly with an axonal/neuronal pattern. In addition, 47% of motor nerves were abnormal so that only four out of 14 patients with a clinically pure sensory neuropathy (28.6%) had an electrophysiological pattern typical of sensory neuronopathy. In patients with a sensorimotor neuropathy, 96.6% of sensory and 71% of motor nerves were abnormal. The only statistical difference between sensory and sensorimotor neuropathies was that patients with sensorimotor neuropathy had more frequent motor nerve involvement (P < 0.05) without differences concerning the distribution of the abnormal patterns. Needle neuromyography showed only limited evidence of motor neurone degeneration in both sensory and sensorimotor neuropathy. The present work shows that the typical clinical and electrophysiological pattern of subacute sensory neuronopathy is rarely encountered in patients with anti-Hu antibody and that motor nerve involvement is frequently seen, even in the absence of a motor deficit. In addition to their potential pathophysiological involvement in the mechanism of the paraneoplastic neuropathy, these findings have practical consequences for the diagnosis of the disorder. (+info)

Myelin protein P0-specific IgM producing monoclonal B cell lines were established from polyneuropathy patients with monoclonal gammopathy of undetermined significance (MGUS). (4/107)

Monoclonal expansion of B cells and plasma cells, producing antibodies against 'self' molecules, can be found not only in different autoimmune diseases, such as peripheral neuropathy (PN), but also in malignancies, such as Waldenstrom's macroglobulinaemia and B-type of chronic lymphocytic leukaemia (B-CLL), as well as in precancerous conditions including monoclonal gammopathy of undetermined significance (MGUS). About 50% of patients with PN-MGUS have serum antibodies against peripheral nerve myelin, but the specific role of these antibodies remains uncertain. The aims of the study were to establish, and characterize, myelin-specific B cell clones from peripheral blood of patients with PN-MGUS, by selection of cells bearing specific membrane Ig-receptors for myelin protein P0, using beads coated with P0. P0-coated magnetic beads were used for selection of cells, which subsequently were transformed by Epstein--Barr virus. The specificity of secreted antibodies was tested by ELISA. Two of the clones producing anti-P0 antibodies were selected and expanded. The magnetic selection procedure was repeated and new clones established. The cells were CD5+ positive, although the expression declined in vitro over time. The anti-P0 antibodies were of IgM-lambda type. The antibodies belonged to the VH3 gene family with presence of somatic mutations. The IgM reacted with P0 and myelin-associated glycoprotein (MAG), and showed no evidence for polyreactivity, in contrast to other IgM CD5+ clones included in the study as controls. The expanded clones expressed CD80 and HLA-DR, which is compatible with properties of antigen-presenting cells. The immunomagnetic selection technique was successfully used for isolation of antimyelin protein P0-specific clones. The cell lines may provide useful tools in studies of monoclonal gammopathies, leukaemia, and autoimmune diseases, including aspects of antigen-presentation by these cells followed by T cell activation. (+info)

Autoimmunity and the basal ganglia: new insights into old diseases. (5/107)

Sydenham's chorea (SC) occurs weeks or months after Group A streptococcal infection, and is characterized by involuntary, purposeless movements of the limbs, in addition to behavioural alteration. There is a body of evidence which suggests that SC is an immune-mediated brain disorder with regional localization to the basal ganglia. Recent reports have suggested that the spectrum of post-streptococcal CNS disease is broader than chorea alone, and includes other hyperkinetic movement disorders (tics, dystonia and myoclonus). In addition, there are high rates of behavioural sequelae, particularly emotional disorders such as obsessive-compulsive disorder, anxiety and depression. These findings have lead to the hypothesis that similar immune-mediated basal ganglia processes may be operating in common neuropsychiatric disease such as tic disorders, Tourette syndrome and obsessive-compulsive disorder. This review analyses the historical aspects of post-streptococcal CNS disease, and the recent immunological studies which have addressed the hypothesis that common neuropsychiatric disorders may be secondary to basal ganglia autoimmunity. (+info)

Immunization with neuronal nicotinic acetylcholine receptor induces neurological autoimmune disease. (6/107)

Neuronal nicotinic AChRs (nAChRs) are implicated in the pathogenesis of diverse neurological disorders and in the regulation of small-cell lung carcinoma growth. Twelve subunits have been identified in vertebrates, and mutations of one are recognized in a rare form of human epilepsy. Mice with genetically manipulated neuronal nAChR subunits exhibit behavioral or autonomic phenotypes. Here, we report the first model of an acquired neuronal nAChR disorder and evidence for its pertinence to paraneoplastic neurological autoimmunity. Rabbits immunized once with recombinant alpha3 subunit (residues 1-205) develop profound gastrointestinal hypomotility, dilated pupils with impaired light response, and grossly distended bladders. As in patients with idiopathic and paraneoplastic autoimmune autonomic neuropathy, the severity parallels serum levels of ganglionic nAChR autoantibody. Failure of neurotransmission through abdominal sympathetic ganglia, with retention of neuronal viability, confirms that the disorder is a postsynaptic channelopathy. In addition, we found ganglionic nAChR protein in small-cell carcinoma lines, identifying this cancer as a potential initiator of ganglionic nAChR autoimmunity. The data support our hypothesis that immune responses driven by distinct neuronal nAChR subtypes expressed in small-cell carcinomas account for several lung cancer-related paraneoplastic disorders affecting cholinergic systems, including autoimmune autonomic neuropathy, seizures, dementia, and movement disorders. (+info)

Thyrotoxic autoimmune encephalopathy: a repeat positron emission tomography study. (7/107)

Thyroid related autoantibodies have been related to the development of encephalopathy, known as Hashimoto's encephalopathy. However, their relation with the encephalopathy occurring in patients with Graves' disease has not been well established. The case is reported of a 51 year old woman presenting with subacute progressive dementia with evidence of hyperthyroidism. She had Graves' disease associated with high titres of thyroid related autoantibodies. Her encephalopathy was not improved by antithyroid drugs, but promptly responded to corticosteroid treatment, and stabilised with a gradual reduction of thyroid related autoantibody titres. Brain positron emission tomography initially showed a diffuse and multifocal cerebral hypometabolism with subsequent normalisation on her clinical recovery, which was consistent with the acute and reversible cerebral inflammation probably mediated by autoimmune mechanisms. (+info)

Tourette's syndrome: a cross sectional study to examine the PANDAS hypothesis. (8/107)

BACKGROUND: The classical neurological disorder after group A beta haemolytic streptococcal infection is Sydenham's chorea. Recently a tic disorder occurring after group A streptococcal infection has been described and termed PANDAS (paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection). It is proposed that antibodies induced after group A streptococcal infection react with basal ganglia neurones in Sydenham's chorea and PANDAS. Anti-basal ganglia antibodies (ABGA) are present in most cases of acute Sydenham's chorea, but rarely in controls. OBJECTIVE: To investigate the hypothesis that Tourette's syndrome may be associated with group A streptococcal infection and ABGA. METHODS: 100 patients with Tourette's syndrome (DSM-IV-TR) were enrolled in a cross sectional study. Children with neurological disease (n = 50) and recent uncomplicated streptococcal infection (n = 40), adults with neurological disease (n = 50), and healthy adults (n = 50) were studied as controls. Recent group A streptococcal infection was defined using antistreptolysin O titre (ASOT). ABGA were detected using western immunoblotting and indirect immunofluorescence. RESULTS: ASOT was raised in 64% of children with Tourette's syndrome compared with 15% of paediatric neurological disease controls (p < 0.0001), and in 68% of adults with Tourette's syndrome compared with 12% of adult neurological controls and 8% of adult healthy controls (p < 0.05). Western immunoblotting showed positive binding in 20% of children and 27% of adults with Tourette's syndrome, compared with 2-4% of control groups (p < 0.05). The most common basal ganglia binding was to a 60 kDa antigen, similar to the proposed antigen in Sydenham's chorea. Indirect immunofluorescence revealed autoantibody binding to basal ganglia neurones. Serological evidence of recent group A streptococcal infection, assessed by a raised ASOT, was detected in 91% (21/23) of Tourette's syndrome patients with positive ABGA compared with 57% (44/77) with negative ABGA (p < 0.01). CONCLUSIONS: The results support a role of group A streptococcal infection and basal ganglia autoimmunity in a subgroup of patients with Tourette's syndrome and suggest a pathogenic similarity between Sydenham's chorea and some patients with Tourette's syndrome. (+info)

Examples of autoimmune diseases include:

1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.

The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.

The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.

There are several subtypes of LES, including:

1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.

There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.

It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.

1. Neurodegenerative diseases: These are diseases that cause progressive loss of brain cells, leading to cognitive decline and motor dysfunction. Examples include Alzheimer's disease, Parkinson's disease, and Huntington's disease.
2. Stroke: A stroke occurs when blood flow to the brain is interrupted, leading to cell death and potential long-term disability.
3. Traumatic brain injury: This type of injury occurs when the brain is subjected to a sudden and forceful impact, such as in a car accident or fall.
4. Infections: Bacterial, viral, and fungal infections can all cause CNS diseases, such as meningitis and encephalitis.
5. Autoimmune disorders: These are conditions in which the immune system mistakenly attacks healthy cells in the brain, leading to inflammation and damage. Examples include multiple sclerosis and lupus.
6. Brain tumors: Tumors can occur in any part of the brain and can be benign or malignant.
7. Cerebrovascular diseases: These are conditions that affect the blood vessels in the brain, such as aneurysms and arteriovenous malformations (AVMs).
8. Neurodevelopmental disorders: These are conditions that affect the development of the brain and nervous system, such as autism spectrum disorder and attention deficit hyperactivity disorder (ADHD).

CNS diseases can have a significant impact on quality of life, and some can be fatal. Treatment options vary depending on the specific diagnosis and severity of the disease. Some CNS diseases can be managed with medication, while others may require surgery or other interventions.

The disease is typically induced in laboratory animals such as mice or rats by immunizing them with myelin proteins, such as myelin basic protein (MBP) or proteolipid protein (PLP), emulsified in adjuvants. The resulting immune response leads to the production of autoantibodies and activated T cells that cross the blood-brain barrier and attack the CNS.

EAE is used as a model for MS because it shares many similarities with the human disease, including:

1. Demyelination: EAE induces demyelination of nerve fibers in the CNS, which is also a hallmark of MS.
2. Autoimmune response: The immune response in EAE is triggered by autoantigens, similar to MS.
3. Chronic course: EAE is a chronic disease with recurrent relapses, similar to MS.
4. Lesion distribution: EAE lesions are distributed throughout the CNS, including the cerebral cortex, cerebellum, brainstem, and spinal cord, which is also true for MS.

EAE has been used extensively in the study of MS to investigate the immunopathogenesis of the disease, to develop new diagnostic markers and treatments, and to test the efficacy of potential therapeutic agents.

Some common autoimmune diseases of the nervous system include:

1. Multiple sclerosis (MS): A chronic condition that affects the brain, spinal cord, and optic nerves, causing a range of symptoms including numbness, weakness, and vision problems.
2. Neuromyelitis optica (NMO): A rare condition that causes inflammation in the optic nerves and spinal cord, leading to vision loss and muscle weakness.
3. Guillain-Barré syndrome: A rare autoimmune disorder that causes muscle weakness and paralysis, often after a viral infection.
4. Chronic inflammatory demyelinating polyneuropathy (CIDP): A chronic condition that affects the peripheral nerves, causing numbness, weakness, and pain in the hands and feet.
5. Acute disseminated encephalomyelitis (ADEM): A rare condition that causes inflammation in the brain and spinal cord, leading to a range of symptoms including fever, headache, and muscle weakness.

The exact cause of autoimmune diseases of the nervous system is not fully understood, but they are believed to be triggered by a combination of genetic and environmental factors. Treatment options vary depending on the specific condition, but may include medications to reduce inflammation and modulate the immune system, as well as physical therapy and lifestyle modifications.

Benign CNS neoplasms include:

1. Meningiomas: These are the most common type of benign CNS tumor, arising from the meninges (the membranes covering the brain and spinal cord).
2. Acoustic neuromas: These tumors arise from the nerve cells that connect the inner ear to the brain.
3. Pineal gland tumors: These are rare tumors that occur in the pineal gland, a small gland located in the brain.
4. Craniopharyngiomas: These are rare tumors that arise from the remnants of the embryonic pituitary gland and can cause a variety of symptoms including headaches, vision loss, and hormonal imbalances.

Malignant CNS neoplasms include:

1. Gliomas: These are the most common type of malignant CNS tumor and arise from the supporting cells of the brain called glial cells. Examples of gliomas include astrocytomas, oligodendrogliomas, and medulloblastomas.
2. Lymphomas: These are cancers of the immune system that can occur in the CNS.
3. Melanomas: These are rare tumors that arise from the pigment-producing cells of the skin and can spread to other parts of the body, including the CNS.
4. Metastatic tumors: These are tumors that have spread to the CNS from other parts of the body, such as the breast, lung, or colon.

The diagnosis and treatment of central nervous system neoplasms depend on the type, size, location, and severity of the tumor, as well as the patient's overall health and medical history. Treatment options can include surgery, radiation therapy, chemotherapy, targeted therapy, and immunotherapy.

The prognosis for CNS neoplasms varies depending on the type of tumor and the effectiveness of treatment. In general, gliomas have a poorer prognosis than other types of CNS tumors, with five-year survival rates ranging from 30% to 60%. Lymphomas and melanomas have better prognoses, with five-year survival rates of up to 80%. Metastatic tumors have a more guarded prognosis, with five-year survival rates depending on the primary site of the cancer.

In summary, central nervous system neoplasms are abnormal growths of tissue in the brain and spinal cord that can cause a variety of symptoms and can be benign or malignant. The diagnosis and treatment of these tumors depend on the type, size, location, and severity of the tumor, as well as the patient's overall health and medical history. The prognosis for CNS neoplasms varies depending on the type of tumor and the effectiveness of treatment, but in general, gliomas have a poorer prognosis than other types of CNS tumors.

The symptoms of MS can vary widely depending on the location and severity of the damage to the CNS. Common symptoms include:

* Weakness, numbness, or tingling in the limbs
* Fatigue
* Vision problems, such as blurred vision, double vision, or loss of vision
* Difficulty with balance and coordination
* Tremors or spasticity
* Memory and concentration problems
* Mood changes, such as depression or mood swings
* Bladder and bowel problems

There is no cure for MS, but various treatments can help manage the symptoms and slow the progression of the disease. These treatments include:

* Disease-modifying therapies (DMTs) - These medications are designed to reduce the frequency and severity of relapses, and they can also slow the progression of disability. Examples of DMTs include interferons, glatiramer acetate, natalizumab, fingolimod, dimethyl fumarate, teriflunomide, and alemtuzumab.
* Steroids - Corticosteroids can help reduce inflammation during relapses, but they are not a long-term solution.
* Pain management medications - Pain relievers, such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs), can help manage pain caused by MS.
* Muscle relaxants - These medications can help reduce spasticity and tremors.
* Physical therapy - Physical therapy can help improve mobility, balance, and strength.
* Occupational therapy - Occupational therapy can help with daily activities and assistive devices.
* Speech therapy - Speech therapy can help improve communication and swallowing difficulties.
* Psychological counseling - Counseling can help manage the emotional and psychological aspects of MS.

It's important to note that each person with MS is unique, and the best treatment plan will depend on the individual's specific symptoms, needs, and preferences. It's essential to work closely with a healthcare provider to find the most effective treatment plan.

Sjögren's syndrome can affect people of all ages, but it most commonly occurs in women between the ages of 40 and 60. The exact cause of the disorder is not known, but it is believed to be an autoimmune response, meaning that the immune system mistakenly attacks the glands as if they were foreign substances.

Symptoms of Sjögren's syndrome can vary in severity and may include:

* Dry mouth (xerostomia)
* Dry eyes (dry eye syndrome)
* Fatigue
* Joint pain
* Swollen lymph nodes
* Rash
* Sores on the skin
* Numbness or tingling in the hands and feet
* Sexual dysfunction

There is no cure for Sjögren's syndrome, but various treatments can help manage the symptoms. These may include:

* Medications to stimulate saliva production
* Eye drops to moisturize the eyes
* Mouthwashes to stimulate saliva production
* Pain relief medication for joint pain
* Anti-inflammatory medication to reduce swelling
* Immunosuppressive medication to suppress the immune system
* Hormone replacement therapy (HRT) to treat hormonal imbalances.

Sjögren's syndrome can also increase the risk of developing other autoimmune disorders, such as rheumatoid arthritis or lupus. It is important for people with Sjögren's syndrome to work closely with their healthcare provider to manage their symptoms and monitor their condition over time.

There are several symptoms of RA, including:

1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)

RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.

There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

Symptoms of type 1 diabetes can include increased thirst and urination, blurred vision, fatigue, weight loss, and skin infections. If left untreated, type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, and blindness.

Type 1 diabetes is diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood glucose measurements and autoantibody tests. Treatment typically involves insulin therapy, which can be administered via injections or an insulin pump, as well as regular monitoring of blood glucose levels and appropriate lifestyle modifications such as a healthy diet and regular exercise.

Examples of Nervous System Diseases include:

1. Alzheimer's disease: A progressive neurological disorder that affects memory and cognitive function.
2. Parkinson's disease: A degenerative disorder that affects movement, balance and coordination.
3. Multiple sclerosis: An autoimmune disease that affects the protective covering of nerve fibers.
4. Stroke: A condition where blood flow to the brain is interrupted, leading to brain cell death.
5. Brain tumors: Abnormal growth of tissue in the brain.
6. Neuropathy: Damage to peripheral nerves that can cause pain, numbness and weakness in hands and feet.
7. Epilepsy: A disorder characterized by recurrent seizures.
8. Motor neuron disease: Diseases that affect the nerve cells responsible for controlling voluntary muscle movement.
9. Chronic pain syndrome: Persistent pain that lasts more than 3 months.
10. Neurodevelopmental disorders: Conditions such as autism, ADHD and learning disabilities that affect the development of the brain and nervous system.

These diseases can be caused by a variety of factors such as genetics, infections, injuries, toxins and ageing. Treatment options for Nervous System Diseases range from medications, surgery, rehabilitation therapy to lifestyle changes.

The most common types of CNS infections include:

1. Meningitis: Inflammation of the protective membranes (meninges) that cover the brain and spinal cord, often caused by bacteria or viruses.
2. Encephalitis: Inflammation of the brain tissue itself, usually caused by a virus.
3. Abscesses: Pockets of pus that form in the brain or spinal cord, typically caused by bacterial infections.
4. Cryptococcal infections: Caused by a fungus called Cryptococcus neoformans, often affecting people with weakened immune systems.
5. Toxoplasmosis: A parasitic infection caused by the Toxoplasma gondii parasite, which can affect the CNS in people with compromised immune systems.

Symptoms of CNS infections can vary depending on the specific type and severity of the infection, but may include fever, headache, confusion, seizures, weakness, and stiff neck. Diagnosis is typically made through a combination of physical examination, laboratory tests, and imaging studies such as CT or MRI scans.

Treatment of CNS infections depends on the underlying cause, but may involve antibiotics, antiviral medications, or antifungal drugs. In severe cases, hospitalization and supportive care such as intravenous fluids, oxygen therapy, and respiratory support may be necessary.

Prevention of CNS infections includes good hygiene practices such as frequent handwashing, avoiding close contact with people who are sick, and getting vaccinated against certain viruses that can cause CNS infections. Early diagnosis and prompt treatment are critical to preventing long-term complications of CNS infections and improving outcomes for patients.

Symptoms of oophoritis may include:

* Pelvic pain or discomfort
* Fever
* Abdominal tenderness
* Vaginal discharge
* Painful urination
* Nausea and vomiting

To diagnose oophoritis, a healthcare provider may perform a physical exam, take a medical history, and order diagnostic tests such as a pelvic exam, ultrasound, or blood tests to check for infection markers.

Treatment of oophoritis depends on the underlying cause and may include antibiotics, pain management medication, and other supportive care. In severe cases, hospitalization may be necessary. It's important to seek medical attention if symptoms persist or worsen over time, as untreated oophoritis can lead to complications such as infertility or chronic pelvic pain.

Some common types of nervous system neoplasms include:

1. Brain tumors: These are abnormal growths that develop in the brain, including gliomas (such as glioblastoma), meningiomas, and acoustic neuromas.
2. Spinal cord tumors: These are abnormal growths that develop in the spinal cord, including astrocytomas, oligodendrogliomas, and metastatic tumors.
3. Nerve sheath tumors: These are abnormal growths that develop in the covering of nerves, such as neurofibromas and schwannomas.
4. Pineal gland tumors: These are abnormal growths that develop in the pineal gland, a small endocrine gland located in the brain.

Symptoms of nervous system neoplasms can vary depending on their location and size, but may include headaches, seizures, weakness or numbness in the arms or legs, and changes in vision, speech, or balance. Diagnosis is typically made through a combination of imaging studies (such as MRI or CT scans) and tissue biopsy. Treatment options vary depending on the type and location of the tumor, but may include surgery, radiation therapy, and chemotherapy.

In summary, nervous system neoplasms are abnormal growths that can develop in the brain, spinal cord, and nerves, and can have a significant impact on the body. Diagnosis and treatment require a comprehensive approach, involving a team of medical professionals with expertise in neurology, neurosurgery, radiation oncology, and other related specialties.

The exact cause of vitiligo is still unknown, but it is believed to involve a combination of genetic and environmental factors. In people with vitiligo, the immune system mistakenly attacks and destroys melanocytes, leading to a loss of skin pigmentation. The disease can also be triggered by physical or emotional stress, sun exposure, and certain medications.

The symptoms of vitiligo can vary in severity and progression. They may include:

1. White patches on the skin, which can appear suddenly or gradually over time.
2. Loss of skin pigmentation in specific areas, such as the face, hands, or limbs.
3. Thinning or loss of hair on affected areas.
4. Premature whitening or graying of the hair.
5. Itching, pain, or sensitivity in the affected areas.
6. Emotional distress and reduced quality of life due to the visible appearance of the disease.

There is no cure for vitiligo, but various treatments can help manage the symptoms and slow down its progression. These may include:

1. Topical corticosteroids to reduce inflammation and suppress the immune system.
2. Topical immunomodulators to suppress the immune system and promote skin repigmentation.
3. Narrowband ultraviolet B (UVB) phototherapy to slow down the progression of the disease and improve skin appearance.
4. Psoralen photochemotherapy to promote skin repigmentation and reduce inflammation.
5. Surgical skin grafting or blister grafting to cover small areas of depigmentation.
6. Camouflage makeup to cover the affected areas and improve self-esteem.

In addition to these treatments, it is essential for patients with vitiligo to protect their skin from the sun by using broad-spectrum sunscreens, wearing protective clothing, and seeking shade when the sun is strongest.

Early diagnosis and appropriate treatment can help improve the quality of life for patients with vitiligo. However, the emotional and psychological impact of the disease should not be underestimated, and patients may require long-term support and counseling to cope with the challenges of living with this condition.

Nervous System Autoimmune Disease, Experimental: A condition in which the immune system mistakenly attacks the body's own nerve tissue, leading to damage and disruption of normal nerve function. This type of condition is often referred to as an autoimmune disease because the body's immune system is attacking its own tissues rather than foreign substances.

The term 'experimental' is used to indicate that this is a research-based definition, and not all of the information may be fully established or widely accepted by the medical community at this time. It is important to note that an experimental condition is one that has not yet been proven through rigorous scientific study, and more research is needed to determine its validity and potential clinical applications.

Examples of Nervous System Autoimmune Diseases include:

* Multiple Sclerosis (MS): A chronic autoimmune disease affecting the central nervous system (CNS), including the brain, spinal cord, and optic nerves. The immune system attacks the protective covering of nerve fibers, leading to communication problems between the brain and the rest of the body.
* Guillain-Barre Syndrome (GBS): A rare autoimmune disorder that causes damage to the nerves outside of the brain and spinal cord, often resulting in muscle weakness, paralysis, and other symptoms. GBS is thought to be triggered by a viral or bacterial infection that stimulates an immune response.
* Peripheral Neuropathy: A condition affecting the nerves outside of the brain and spinal cord, often resulting in numbness, tingling, weakness, or pain in the hands and feet. Peripheral neuropathy can be caused by a variety of factors, including diabetes, autoimmune disorders, infections, and certain medications.
* Myasthenia Gravis (MG): An autoimmune disorder that affects the nerve-muscle connection, leading to muscle weakness and fatigue. MG can cause a variety of symptoms, including double vision, drooping eyelids, difficulty swallowing, and weakness in the arms and legs.
* Neuromyelitis Optica (NMO): A rare autoimmune disease that affects the optic nerves and spinal cord, leading to vision loss, pain, and muscle weakness. NMO is often misdiagnosed as multiple sclerosis, but it has a distinct set of symptoms and requires different treatment approaches.

These are just a few examples of nervous system autoimmune diseases, and there are many others that can affect the body in different ways. It's important to note that each condition has its unique set of symptoms and diagnostic criteria, and treatment options may vary depending on the specific diagnosis and severity of the disease. If you suspect that you or a loved one may have an autoimmune disease affecting the nervous system, it's essential to consult with a healthcare professional for proper evaluation and care.

The most common demyelinating autoimmune diseases affecting the CNS are:

1. Multiple sclerosis (MS): A chronic and often disabling disease that affects the brain, spinal cord, and optic nerves. MS is caused by an abnormal response of the immune system, leading to inflammation and damage to the myelin sheath.
2. Neuromyelitis optica (NMO): A rare autoimmune disorder that affects the optic nerves and spinal cord, causing inflammation and demyelination. NMO is often associated with a specific type of antibody in the blood.
3. Acute disseminated encephalomyelitis (ADEM): A rare autoimmune disease that affects the brain and spinal cord, causing widespread inflammation and demyelination. ADEM is often triggered by a viral infection.
4. Chronic inflammatory demyelinating polyneuropathy (CIDP): A rare autoimmune disorder that affects the peripheral nerves, causing weakness, numbness, and pain. CIDP is characterized by inflammation and demyelination of the nerve fibers.

The symptoms of demyelinating autoimmune diseases affecting the CNS can vary depending on the specific disease and the severity of the condition. Common symptoms include:

* Weakness, numbness, or tingling sensations in the limbs
* Vision problems, such as blurred vision or loss of vision
* Difficulty with coordination and balance
* Fatigue, fever, and general malaise
* Cognitive impairment and memory loss

The diagnosis of demyelinating autoimmune diseases affecting the CNS is based on a combination of clinical evaluation, laboratory tests, and imaging studies. Laboratory tests may include:

1. Blood tests to rule out other conditions and measure the levels of specific antibodies and immune cells.
2. Cerebrospinal fluid (CSF) analysis to detect inflammatory markers and specific antibodies.
3. Imaging studies, such as magnetic resonance imaging (MRI) or computed tomography (CT) scans, to visualize the lesions and assess the extent of the damage.
4. Evoked potentials testing to evaluate the function of the nerves.

Treatment for demyelinating autoimmune diseases affecting the CNS depends on the specific disease and the severity of the condition. Common treatments include:

1. Corticosteroids to reduce inflammation and modulate the immune response.
2. Immunoglobulins to block the activity of harmful antibodies.
3. Plasmapheresis to remove harmful antibodies from the blood.
4. Disease-modifying therapies, such as interferons or glatiramer acetate, to reduce the frequency and severity of relapses.
5. Physical therapy and rehabilitation to help restore lost function and improve quality of life.

In conclusion, demyelinating autoimmune diseases affecting the CNS can be challenging to diagnose and treat, but with a comprehensive approach that includes clinical evaluation, laboratory tests, and imaging studies, it is possible to identify the underlying cause and develop an effective treatment plan.

Explanation: Genetic predisposition to disease is influenced by multiple factors, including the presence of inherited genetic mutations or variations, environmental factors, and lifestyle choices. The likelihood of developing a particular disease can be increased by inherited genetic mutations that affect the functioning of specific genes or biological pathways. For example, inherited mutations in the BRCA1 and BRCA2 genes increase the risk of developing breast and ovarian cancer.

The expression of genetic predisposition to disease can vary widely, and not all individuals with a genetic predisposition will develop the disease. Additionally, many factors can influence the likelihood of developing a particular disease, such as environmental exposures, lifestyle choices, and other health conditions.

Inheritance patterns: Genetic predisposition to disease can be inherited in an autosomal dominant, autosomal recessive, or multifactorial pattern, depending on the specific disease and the genetic mutations involved. Autosomal dominant inheritance means that a single copy of the mutated gene is enough to cause the disease, while autosomal recessive inheritance requires two copies of the mutated gene. Multifactorial inheritance involves multiple genes and environmental factors contributing to the development of the disease.

Examples of diseases with a known genetic predisposition:

1. Huntington's disease: An autosomal dominant disorder caused by an expansion of a CAG repeat in the Huntingtin gene, leading to progressive neurodegeneration and cognitive decline.
2. Cystic fibrosis: An autosomal recessive disorder caused by mutations in the CFTR gene, leading to respiratory and digestive problems.
3. BRCA1/2-related breast and ovarian cancer: An inherited increased risk of developing breast and ovarian cancer due to mutations in the BRCA1 or BRCA2 genes.
4. Sickle cell anemia: An autosomal recessive disorder caused by a point mutation in the HBB gene, leading to defective hemoglobin production and red blood cell sickling.
5. Type 1 diabetes: An autoimmune disease caused by a combination of genetic and environmental factors, including multiple genes in the HLA complex.

Understanding the genetic basis of disease can help with early detection, prevention, and treatment. For example, genetic testing can identify individuals who are at risk for certain diseases, allowing for earlier intervention and preventive measures. Additionally, understanding the genetic basis of a disease can inform the development of targeted therapies and personalized medicine."

There are two main types of systemic scleroderma: diffuse cutaneous systemic sclerosis (DCSS) and limited cutaneous systemic sclerosis (LCSS). DCSS is characterized by skin thickening and scar formation over the trunk, arms, and legs, while LCSS is characterized by skin tightening and patches of scaly skin on the hands and face.

The symptoms of systemic scleroderma can include:

* Skin hardening and tightening
* Fatigue
* Joint pain and stiffness
* Muscle weakness
* Swallowing difficulties
* Heartburn and acid reflux
* Shortness of breath
* Raynaud's phenomenon (pale or blue-colored fingers and toes in response to cold temperatures or stress)

The exact cause of systemic scleroderma is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment options for systemic scleroderma include medications to manage symptoms such as pain, stiffness, and swallowing difficulties, as well as physical therapy and lifestyle modifications to improve quality of life.

In summary, systemic scleroderma is a chronic autoimmune disease that affects multiple systems in the body, causing skin hardening and thickening, fatigue, joint pain, and other symptoms. While there is no cure for systemic scleroderma, treatment options are available to manage symptoms and improve quality of life.

1. Rheumatoid arthritis (RA): An autoimmune disease that causes inflammation in the joints, leading to pain, stiffness, and swelling.
2. Osteoarthritis (OA): A degenerative condition that occurs when the cartilage in the joints wears down over time, causing pain and stiffness.
3. Psoriatic arthritis (PsA): An inflammatory disease that affects both the skin and joints, often occurring in people with psoriasis.
4. Ankylosing spondylitis (AS): A condition that causes inflammation in the spine and peripheral joints, leading to stiffness and pain.
5. Lupus: An autoimmune disease that can affect multiple systems in the body, including the joints, skin, and kidneys.
6. Juvenile idiopathic arthritis (JIA): A condition that affects children under the age of 16, causing inflammation in the joints and potentially leading to long-term complications.
7. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dryness in the eyes and mouth.
8. Fibromyalgia: A condition characterized by widespread pain, fatigue, and sleep disturbances.
9. Gout: A type of inflammatory arthritis caused by excessive levels of uric acid in the blood, leading to sudden and severe attacks of joint pain.
10. Osteoporosis: A condition characterized by brittle bones and an increased risk of fractures, often occurring in older adults.

Rheumatic diseases can be challenging to diagnose and treat, as they often involve complex symptoms and a range of possible causes. However, with the help of rheumatology specialists and advanced diagnostic tools, it is possible to manage these conditions effectively and improve quality of life for patients.

Some common examples of CNSVD include:

1. Herpes simplex virus (HSV) encephalitis: This is an inflammation of the brain caused by the herpes simplex virus. It can cause fever, headache, confusion, and seizures.
2. West Nile virus (WNV) encephalitis: This is an infection of the brain caused by the West Nile virus, which is transmitted through the bite of an infected mosquito. Symptoms can include fever, headache, muscle weakness, and confusion.
3. Japanese encephalitis (JE): This is a viral infection that affects the brain and is transmitted through the bite of an infected mosquito. Symptoms can include fever, headache, seizures, and changes in behavior or cognitive function.
4. Rabies: This is a viral infection that affects the brain and is transmitted through the bite of an infected animal, usually a dog, bat, or raccoon. Symptoms can include fever, headache, agitation, and changes in behavior or cognitive function.
5. Enteroviral encephalitis: This is an infection of the brain caused by enteroviruses, which are common viruses that affect the gastrointestinal tract. Symptoms can include fever, vomiting, diarrhea, and changes in behavior or cognitive function.

The diagnosis of CNSVD typically involves a combination of physical examination, laboratory tests (such as blood tests or lumbar puncture), and imaging studies (such as CT or MRI scans). Treatment options vary depending on the specific disease and may include antiviral medications, supportive care, and rehabilitation.

Prevention of CNSVD includes avoiding exposure to mosquitoes and other vectors that can transmit disease, maintaining good hygiene practices (such as washing hands frequently), and getting vaccinated against diseases such as rabies and measles. In addition, taking steps to prevent head trauma and using protective equipment when engaging in activities that involve risk of head injury can help reduce the risk of CNSVD.

Overall, while central nervous system viral diseases can be serious and potentially life-threatening, early diagnosis and treatment can improve outcomes and prevent long-term complications. It is important to seek medical attention promptly if symptoms persist or worsen over time.

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

These animal models allow researchers to study the underlying causes of arthritis, test new treatments and therapies, and evaluate their effectiveness in a controlled environment before moving to human clinical trials. Experimental arthritis models are used to investigate various aspects of the disease, including its pathophysiology, immunogenicity, and potential therapeutic targets.

Some common experimental arthritis models include:

1. Collagen-induced arthritis (CIA): This model is induced in mice by immunizing them with type II collagen, which leads to an autoimmune response and inflammation in the joints.
2. Rheumatoid arthritis (RA) models: These models are developed by transferring cells from RA patients into immunodeficient mice, which then develop arthritis-like symptoms.
3. Osteoarthritis (OA) models: These models are induced in animals by subjecting them to joint injury or overuse, which leads to degenerative changes in the joints and bone.
4. Psoriatic arthritis (PsA) models: These models are developed by inducing psoriasis in mice, which then develop arthritis-like symptoms.

Experimental arthritis models have contributed significantly to our understanding of the disease and have helped to identify potential therapeutic targets for the treatment of arthritis. However, it is important to note that these models are not perfect representations of human arthritis and should be used as tools to complement, rather than replace, human clinical trials.

The symptoms of myasthenia gravis can vary in severity and may include:

* Weakness in the arms and legs
* Fatigue and muscle tiredness
* Difficulty swallowing (dysphagia)
* Difficulty speaking or slurred speech (dysarthria)
* Drooping eyelids (ptosis)
* Double vision (diplopia)
* Weakness in the muscles of the face, arms, and legs

The exact cause of myasthenia gravis is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissues. It can also be caused by other medical conditions such as thyroid disease, vitamin deficiencies, or infections.

There is no cure for myasthenia gravis, but there are various treatments available to manage the symptoms and improve quality of life. These include:

* Medications such as corticosteroids, immunosuppressants, and cholinesterase inhibitors
* Plasmapheresis, a procedure that removes harmful antibodies from the blood
* Intravenous immunoglobulin (IVIG), which contains antibodies that can help block the immune system's attack on the nerve-muscle junction
* Surgery to remove the thymus gland, which is believed to play a role in the development of myasthenia gravis

It is important for individuals with myasthenia gravis to work closely with their healthcare provider to manage their symptoms and prevent complications. With proper treatment and self-care, many people with myasthenia gravis are able to lead active and fulfilling lives.

The disease is named after Hakama Hashimoto, a Japanese physician who first described it in 1912. It is characterized by the presence of inflammatory cells in the thyroid gland, which can lead to damage to the gland and disrupt its ability to produce thyroid hormones.

The symptoms of Hashimoto's disease are similar to those of hypothyroidism and can include fatigue, weight gain, cold intolerance, dry skin, constipation, and depression. The disease is more common in women than men and typically affects people between the ages of 30 and 50.

Hashimoto's disease is diagnosed based on a combination of symptoms, physical examination findings, and laboratory tests, such as blood tests to measure thyroid hormone levels and an ultrasound or biopsy to examine the thyroid gland. Treatment typically involves replacing missing thyroid hormones with synthetic hormones, but in some cases, surgery may be necessary to remove part or all of the thyroid gland.

While Hashimoto's disease is a chronic condition and cannot be cured, it can be effectively managed with appropriate treatment. With early diagnosis and proper management, most people with Hashimoto's disease can lead normal, healthy lives.

There are several types of lupus nephritis, each with its own unique characteristics and symptoms. The most common forms include:

* Class I (mesangial proliferative glomerulonephritis): This type is characterized by the growth of abnormal cells in the glomeruli (blood-filtering units of the kidneys).
* Class II (active lupus nephritis): This type is characterized by widespread inflammation and damage to the kidneys, with or without the presence of antibodies.
* Class III (focal lupus nephritis): This type is characterized by localized inflammation in certain areas of the kidneys.
* Class IV (lupus nephritis with crescentic glomerulonephritis): This type is characterized by widespread inflammation and damage to the kidneys, with crescent-shaped tissue growth in the glomeruli.
* Class V (lupus nephritis with sclerotic changes): This type is characterized by hardening and shrinkage of the glomeruli due to scarring.

Lupus Nephritis can cause a range of symptoms, including:

* Proteinuria (excess protein in the urine)
* Hematuria (blood in the urine)
* Reduced kidney function
* Swelling (edema)
* Fatigue
* Fever
* Joint pain

Lupus Nephritis can be diagnosed through a combination of physical examination, medical history, laboratory tests, and kidney biopsy. Treatment options for lupus nephritis include medications to suppress the immune system, control inflammation, and prevent further damage to the kidneys. In severe cases, dialysis or a kidney transplant may be necessary.

There are several different types of uveitis, including:

1. Anterior uveitis: This type affects the front part of the eye and is the most common form of uveitis. It is often caused by an infection or injury.
2. Posterior uveitis: This type affects the back part of the eye and can be caused by a systemic disease such as sarcoidosis or juvenile idiopathic arthritis.
3. Intermediate uveitis: This type affects the middle layer of the eye and is often caused by an autoimmune disorder.
4. Panuveitis: This type affects the entire uvea and can be caused by a systemic disease such as vasculitis or Behçet's disease.

Symptoms of uveitis may include:

* Eye pain
* Redness and swelling in the eye
* Blurred vision
* Sensitivity to light
* Floaters (specks or cobwebs in your vision)
* Flashes of light

If you experience any of these symptoms, it is important to see an eye doctor as soon as possible. Uveitis can be diagnosed with a comprehensive eye exam, which may include imaging tests such as ultrasound or MRI. Treatment for uveitis depends on the cause and severity of the condition, but may include medication to reduce inflammation, antibiotics for infections, or surgery to remove any diseased tissue.

Early diagnosis and treatment are important to prevent complications such as cataracts, glaucoma, and blindness. If you have uveitis, it is important to follow your doctor's recommendations for treatment and monitoring to protect your vision.

The exact cause of CNS vasculitis is not fully understood, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissues in the CNS. The condition can occur at any age, but it most commonly affects adults between the ages of 40 and 60.

Symptoms of CNS vasculitis can vary depending on the location and severity of the inflammation, but may include:

* Headaches
* Confusion
* Memory loss
* Seizures
* Weakness or numbness in the limbs
* Vision problems
* Speech difficulties

Diagnosis of CNS vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as MRI or CT scans, lumbar puncture, and blood tests. Treatment options for CNS vasculitis vary depending on the severity of the condition and may include corticosteroids, immunosuppressive drugs, and plasmapheresis. In severe cases, surgery may be necessary to relieve pressure on the brain or spinal cord.

Overall, CNS vasculitis is a serious condition that can have significant neurological consequences if left untreated. Early diagnosis and aggressive treatment are critical to prevent long-term damage and improve outcomes for patients with this condition.

There are several types of pemphigus, including:

1. Pemphigus vulgaris: This is the most common form of the disease and is characterized by the formation of large, painful blisters on the skin and mucous membranes.
2. Pemphigus foliaceus: This type of pemphigus is characterized by the formation of smaller, crusting sores on the skin.
3. Pemphigus erythematosus: This type of pemphigus is characterized by the formation of flat, red sores on the skin.
4. Bullous pemphigoid: This is a rare form of pemphigus that is characterized by the formation of large, fluid-filled blisters on the skin.

Treatment for pemphigus typically involves the use of corticosteroids and immunosuppressive drugs to reduce inflammation and suppress the immune system. In severe cases, hospitalization may be necessary to manage complications such as infection and fluid loss.

Prevention of pemphigus is difficult, but avoiding exposure to known triggers such as certain medications and taking steps to maintain good skin care can help reduce the risk of developing the disease. Early diagnosis and treatment are important to prevent complications and improve outcomes for patients with pemphigus.

The symptoms of lupus vulgaris typically include:

* Rough, scaly patches on the skin that may be dark red or purple in color
* Itching or burning sensation on the skin
* Skin thickening or hardening
* Painless ulcers or sores on the skin
* Swollen lymph nodes
* Fever
* Headache
* Joint pain or swelling

The diagnosis of lupus vulgaris is based on a combination of clinical findings and laboratory tests. A physical examination of the skin and mucous membranes can reveal characteristic signs of the condition, such as scaly patches or ulcers. Laboratory tests, such as blood tests or biopsies, may be performed to confirm the diagnosis and rule out other conditions.

Treatment of lupus vulgaris typically involves antibiotics, which can help to clear the infection and reduce symptoms. In severe cases, surgical debridement or laser therapy may be necessary to remove damaged tissue and promote healing. In addition, patients with lupus vulgaris may require supportive care to manage symptoms such as pain, itching, and swelling.

Overall, lupus vulgaris is a chronic skin condition that can cause significant discomfort and disfigurement if left untreated. It is important for individuals in regions where the condition is common to be aware of the signs and symptoms and seek medical attention if they suspect they may have the condition. With proper diagnosis and treatment, however, most patients with lupus vulgaris can experience significant improvement in their symptoms and quality of life.

There are several types of alopecia areata, including:

1. Alopecia areata patchy - This is the most common form of the disease, where hair loss occurs in patches on the scalp or other parts of the body.
2. Alopecia totalis - Hair loss occurs over the entire scalp.
3. Alopecia universalis - Hair loss occurs over the entire body, including the scalp, eyebrows, and eyelashes.
4. Alopecia areata barbae - Hair loss occurs in the beard area.
5. Alopecia areata traction - Hair loss occurs due to pulling or tension on the hair shaft, often seen in children who pull their own hair.

The symptoms of alopecia areata may include:

1. Patchy hair loss
2. Thinning of hair
3. Redness and scalp inflammation
4. Itching or burning sensation on the scalp
5. Nail changes such as ridging, thinning, or pitting

Alopecia areata can be diagnosed through a physical examination and medical history. A skin scraping or biopsy may be performed to confirm the diagnosis.

Treatment for alopecia areata depends on the severity and location of hair loss, as well as the individual's overall health. Options may include:

1. Topical corticosteroids - Medicated creams or ointments applied directly to the affected area to reduce inflammation and promote hair growth.
2. Oral corticosteroids - Medications taken by mouth to reduce inflammation and suppress the immune system.
3. Anthralin - A medication that is applied to the skin to reduce inflammation and promote hair growth.
4. Immunotherapy - Injections or tablets that stimulate the immune system to attack cancer cells, but also can cause hair loss.
5. Wigs, hats, or other hairpieces - Used to cover up patchy hair loss.
6. Counseling or therapy - To help cope with the emotional impact of hair loss.
7. Hair transplantation - A surgical procedure that involves moving healthy hair follicles from one part of the scalp to another.

It is important to note that these treatments may not work for everyone and may have side effects. It's important to talk to a doctor or dermatologist to determine the best course of treatment for alopecia areata.

In addition to medical treatment, there are also some natural remedies that can help with alopecia areata such as:

1. Diet and nutrition - Eating a balanced diet rich in vitamins and minerals can promote hair growth.
2. Stress management - High stress levels have been linked to alopecia areata, so finding ways to manage stress, such as through exercise or meditation, may help.
3. Saw palmetto - A herb that has been shown to promote hair growth and slow down hair loss.
4. Fish oil - Omega-3 fatty acids found in fish oil have been shown to promote hair growth.
5. Coconut oil - Applying coconut oil to the scalp may help to stimulate hair growth.
6. Henna - A natural dye that can be used to color and strengthen hair, and may also help to promote hair growth.
7. Rosemary essential oil - May help to promote hair growth by increasing blood flow to the scalp.
8. Lavender essential oil - May help to reduce stress and promote relaxation, which can help with alopecia areata.

Some examples of nervous system malformations include:

1. Neural tube defects: These are among the most common types of nervous system malformations and occur when the neural tube, which forms the brain and spinal cord, fails to close properly during fetal development. Examples include anencephaly (absence of a major portion of the brain), spina bifida (incomplete closure of the spine), and encephalocele (protrusion of the brain or meninges through a skull defect).
2. Cerebral palsy: This is a group of disorders that affect movement, balance, and posture, often resulting from brain damage during fetal development or early childhood. The exact cause may not be known, but it can be related to genetic mutations, infections, or other factors.
3. Hydrocephalus: This is a condition in which there is an abnormal accumulation of cerebrospinal fluid (CSF) in the brain, leading to increased pressure and enlargement of the head. It can be caused by a variety of factors, including genetic mutations, infections, or blockages in the CSF circulatory system.
4. Moyamoya disease: This is a rare condition caused by narrowing or blockage of the internal carotid artery and its branches, leading to reduced blood flow to the brain. It can result in stroke-like episodes, seizures, and cognitive impairment.
5. Spinal muscular atrophy: This is a genetic disorder that affects the nerve cells responsible for controlling voluntary muscle movement, leading to progressive muscle weakness and wasting. It can be diagnosed through blood tests or genetic analysis.
6. Neurofibromatosis: This is a genetic disorder that causes non-cancerous tumors to grow on nerve tissue, leading to symptoms such as skin changes, learning disabilities, and eye problems. It can be diagnosed through clinical evaluation and genetic testing.
7. Tuberous sclerosis: This is a rare genetic disorder that causes non-cancerous tumors to grow in the brain and other organs, leading to symptoms such as seizures, developmental delays, and skin changes. It can be diagnosed through clinical evaluation, imaging studies, and genetic testing.
8. Cerebral palsy: This is a group of disorders that affect movement, posture, and muscle tone, often resulting from brain damage sustained during fetal development or early childhood. It can be caused by a variety of factors, including premature birth, infections, and genetic mutations.
9. Down syndrome: This is a genetic disorder caused by an extra copy of chromosome 21, leading to intellectual disability, developmental delays, and physical characteristics such as a flat face and short stature. It can be diagnosed through blood tests or genetic analysis.
10. William syndrome: This is a rare genetic disorder caused by a deletion of genetic material on chromosome 7, leading to symptoms such as cardiovascular problems, growth delays, and learning disabilities. It can be diagnosed through clinical evaluation and genetic testing.

It's important to note that these are just a few examples of developmental disorders, and there are many other conditions that can affect cognitive and physical development in children. If you suspect your child may have a developmental disorder, it's important to speak with a qualified healthcare professional for an accurate diagnosis and appropriate treatment.

Grave's disease is the most common cause of hyperthyroidism and affects about 1 in 200 people. It can occur at any age but is more common in women and tends to run in families. The exact cause of Grave's disease is not known, but it may be related to a combination of genetic and environmental factors.

Symptoms of Grave's disease can vary from person to person, but common signs include:

* Weight loss
* Nervousness or anxiety
* Irregular heartbeat (palpitations)
* Increased sweating
* Heat intolerance
* Fatigue
* Changes in menstrual cycle in women
* Enlargement of the thyroid gland, known as a goiter
* Bulging eyes (exophthalmos)

Grave's disease can be diagnosed through blood tests and scans. Treatment options include medication to reduce the production of thyroxine, radioactive iodine therapy to destroy part of the thyroid gland, and surgery to remove part or all of the thyroid gland.

It is important to seek medical attention if you experience any symptoms of Grave's disease, as untreated hyperthyroidism can lead to complications such as heart problems, osteoporosis, and eye problems. With proper treatment, most people with Grave's disease can manage their symptoms and lead a normal life.

The most common demyelinating diseases include:

1. Multiple sclerosis (MS): An autoimmune disease that affects the CNS, including the brain, spinal cord, and optic nerves. MS causes inflammation and damage to the myelin sheath, leading to a range of symptoms such as muscle weakness, vision problems, and cognitive difficulties.
2. Acute demyelination: A sudden, severe loss of myelin that can be caused by infections, autoimmune disorders, or other factors. This condition can result in temporary or permanent nerve damage.
3. Chronic inflammatory demyelination (CIDP): A rare autoimmune disorder that causes progressive damage to the myelin sheath over time. CIDP can affect the CNS and the peripheral nervous system (PNS).
4. Moore's disease: A rare genetic disorder that results in progressive demyelination of the CNS, leading to a range of neurological symptoms including muscle weakness, seizures, and cognitive difficulties.
5. Leukodystrophies: A group of genetic disorders that affect the development or function of myelin-producing cells in the CNS. These conditions can cause progressive loss of myelin and result in a range of neurological symptoms.

Demyelinating diseases can be challenging to diagnose, as the symptoms can be similar to other conditions and the disease progression can be unpredictable. Treatment options vary depending on the specific condition and its severity, and may include medications to reduce inflammation and modulate the immune system, as well as rehabilitation therapies to help manage symptoms and improve quality of life.

There are several types of disease susceptibility, including:

1. Genetic predisposition: This refers to the inherent tendency of an individual to develop a particular disease due to their genetic makeup. For example, some families may have a higher risk of developing certain diseases such as cancer or heart disease due to inherited genetic mutations.
2. Environmental susceptibility: This refers to the increased risk of developing a disease due to exposure to environmental factors such as pollutants, toxins, or infectious agents. For example, someone who lives in an area with high levels of air pollution may be more susceptible to developing respiratory problems.
3. Lifestyle susceptibility: This refers to the increased risk of developing a disease due to unhealthy lifestyle choices such as smoking, lack of exercise, or poor diet. For example, someone who smokes and is overweight may be more susceptible to developing heart disease or lung cancer.
4. Immune system susceptibility: This refers to the increased risk of developing a disease due to an impaired immune system. For example, people with autoimmune disorders such as HIV/AIDS or rheumatoid arthritis may be more susceptible to opportunistic infections.

Understanding disease susceptibility can help healthcare providers identify individuals who are at risk of developing certain diseases and provide preventive measures or early intervention to reduce the risk of disease progression. Additionally, genetic testing can help identify individuals with a high risk of developing certain diseases, allowing for earlier diagnosis and treatment.

In summary, disease susceptibility refers to the predisposition of an individual to develop a particular disease or condition due to various factors such as genetics, environment, lifestyle choices, and immune system function. Understanding disease susceptibility can help healthcare providers identify individuals at risk and provide appropriate preventive measures or early intervention to reduce the risk of disease progression.

The condition is often caused by gallstones or other blockages that prevent the normal flow of bile from the liver to the small intestine. Over time, the scarring can lead to the formation of cirrhosis, which is characterized by the replacement of healthy liver tissue with scar tissue.

Symptoms of liver cirrhosis, biliary may include:

* Jaundice (yellowing of the skin and eyes)
* Itching
* Fatigue
* Abdominal pain
* Dark urine
* Pale stools

The diagnosis of liver cirrhosis, biliary is typically made through a combination of physical examination, medical history, and diagnostic tests such as ultrasound, CT scans, and blood tests.

Treatment for liver cirrhosis, biliary depends on the underlying cause of the condition. In some cases, surgery may be necessary to remove gallstones or repair damaged bile ducts. Medications such as antioxidants and anti-inflammatory drugs may also be prescribed to help manage symptoms and slow the progression of the disease. In severe cases, a liver transplant may be necessary.

Prognosis for liver cirrhosis, biliary is generally poor, as the condition can lead to complications such as liver failure, infection, and cancer. However, with early diagnosis and appropriate treatment, it is possible to manage the symptoms and slow the progression of the disease.

Trauma to the nervous system can have a profound impact on an individual's quality of life, and can lead to a range of symptoms including:

* Headaches
* Dizziness and vertigo
* Memory loss and difficulty concentrating
* Mood changes such as anxiety, depression, or irritability
* Sleep disturbances
* Changes in sensation, such as numbness or tingling
* Weakness or paralysis of certain muscle groups

Trauma to the nervous system can also have long-lasting effects, and may lead to chronic conditions such as post-traumatic stress disorder (PTSD), chronic pain, and fibromyalgia.

Treatment for trauma to the nervous system will depend on the specific nature of the injury and the severity of the symptoms. Some common treatments include:

* Medication to manage symptoms such as pain, anxiety, or depression
* Physical therapy to help regain strength and mobility
* Occupational therapy to help with daily activities and improve function
* Cognitive-behavioral therapy (CBT) to address any emotional or psychological issues
* Alternative therapies such as acupuncture, massage, or meditation to help manage symptoms and promote relaxation.

It's important to seek medical attention if you experience any symptoms of trauma to the nervous system, as prompt treatment can help reduce the risk of long-term complications and improve outcomes.

The term "polyendocrinopathy" refers to the involvement of multiple endocrine glands, while "autoimmune" indicates that the disorder is caused by an abnormal immune response against the body's own tissues.

Examples of polyendocrinopathies, autoimmune include:

1. Type 1 diabetes with thyroiditis and adrenal insufficiency
2. Hashimoto's thyroiditis with hypophyseal and adrenal involvement
3. Addison's disease with hypothyroidism and hemolytic anemia
4. Autoimmune polyglandular syndrome type 1 (APS-1) with autoantibodies against multiple endocrine glands
5. Autoimmune polyglandular syndrome type 2 (APS-2) with autoantibodies against thyroid, adrenal, and gonadal glands.

The exact cause of polyendocrinopathies, autoimmune is not fully understood, but it is thought to involve a combination of genetic and environmental factors that trigger an abnormal immune response against endocrine tissues. Treatment varies depending on the specific disorder and may include hormone replacement therapy, immunosuppressive medications, and management of associated symptoms.

The symptoms of encephalomyelitis can vary depending on the cause and severity of the condition. Common symptoms include fever, headache, neck stiffness, muscle weakness, confusion, seizures, and loss of sensation or paralysis in parts of the body. In severe cases, encephalomyelitis can lead to life-threatening complications such as brain damage, stroke, and respiratory failure.

The diagnosis of encephalomyelitis is based on a combination of clinical features, laboratory tests, and imaging studies. Laboratory tests may include blood tests to detect the presence of inflammatory markers or antibodies against specific infectious agents. Imaging studies such as CT or MRI scans can help to identify inflammation in the brain and spinal cord.

Treatment of encephalomyelitis depends on the underlying cause of the condition. In some cases, antiviral medications may be used to treat infections such as herpes simplex or West Nile virus. In other cases, corticosteroids may be prescribed to reduce inflammation and prevent further damage. Supportive care such as intravenous fluids, oxygen therapy, and physical therapy may also be necessary to manage symptoms and promote recovery.

In conclusion, encephalomyelitis is a serious condition that can cause significant morbidity and mortality. Early diagnosis and prompt treatment are essential to prevent complications and improve outcomes for patients with this condition.

The most common types of CNS fungal infections include:

1. Meningitis: An inflammation of the membranes that cover the brain and spinal cord, caused by fungi such as Candida, Aspergillus, or Cryptococcus.
2. Encephalitis: An inflammation of the brain tissue itself, caused by fungi such as Histoplasma or Coccidioides.
3. Abscesses: Pocket of pus that form in the brain or spinal cord, caused by bacteria or fungi.
4. Opportunistic infections: Infections that occur in people with compromised immune systems, such as HIV/AIDS patients or those taking immunosuppressive drugs after an organ transplant.

CNS fungal infections can cause a wide range of symptoms, including headache, fever, confusion, seizures, and loss of coordination. They are typically diagnosed through a combination of physical examination, laboratory tests, and imaging studies such as CT or MRI scans.

Treatment of CNS fungal infections usually involves the use of antifungal medications, which can be administered intravenously or orally. The choice of treatment depends on the severity and location of the infection, as well as the patient's overall health status. In some cases, surgery may be necessary to drain abscesses or relieve pressure on the brain.

Prevention of CNS fungal infections is important for individuals at risk, such as those with compromised immune systems or underlying medical conditions. This includes taking antifungal medications prophylactically, avoiding exposure to fungal spores, and practicing good hygiene.

Overall, CNS fungal infections are serious and potentially life-threatening conditions that require prompt diagnosis and treatment. With appropriate management, many patients can recover fully, but delays in diagnosis and treatment can lead to poor outcomes.

There are many different types of ANS diseases, including:

1. Dysautonomia: a general term that refers to dysfunction of the autonomic nervous system.
2. Postural orthostatic tachycardia syndrome (POTS): a condition characterized by rapid heart rate and other symptoms that occur upon standing.
3. Neurocardiogenic syncope: a form of fainting caused by a sudden drop in blood pressure.
4. Multiple system atrophy (MSA): a progressive neurodegenerative disorder that affects the autonomic nervous system and other parts of the brain.
5. Parkinson's disease: a neurodegenerative disorder that can cause autonomic dysfunction, including constipation, urinary incontinence, and erectile dysfunction.
6. Dopamine deficiency: a condition characterized by low levels of the neurotransmitter dopamine, which can affect the ANS and other body systems.
7. Autonomic nervous system disorders associated with autoimmune diseases, such as Guillain-Barré syndrome and lupus.
8. Trauma: physical or emotional trauma can sometimes cause dysfunction of the autonomic nervous system.
9. Infections: certain infections, such as Lyme disease, can affect the autonomic nervous system.
10. Genetic mutations: some genetic mutations can affect the functioning of the autonomic nervous system.

Treatment for ANS diseases depends on the specific condition and its underlying cause. In some cases, medication may be prescribed to regulate heart rate, blood pressure, or other bodily functions. Lifestyle changes, such as regular exercise and stress management techniques, can also be helpful in managing symptoms. In severe cases, surgery may be necessary to correct anatomical abnormalities or repair damaged nerves.

Osteoarthritis (OA) is a degenerative condition that occurs when the cartilage that cushions the joints breaks down over time, causing the bones to rub together. It is the most common form of arthritis and typically affects older adults.

Rheumatoid arthritis (RA) is an autoimmune condition that occurs when the body's immune system attacks the lining of the joints, leading to inflammation and pain. It can affect anyone, regardless of age, and is typically seen in women.

Other types of arthritis include psoriatic arthritis, gouty arthritis, and lupus-related arthritis. Treatment for arthritis depends on the type and severity of the condition, but can include medications such as pain relievers, anti-inflammatory drugs, and disease-modifying anti-rheumatic drugs (DMARDs). Physical therapy and lifestyle changes, such as exercise and weight loss, can also be helpful. In severe cases, surgery may be necessary to repair or replace damaged joints.

Arthritis is a leading cause of disability worldwide, affecting over 50 million adults in the United States alone. It can have a significant impact on a person's quality of life, making everyday activities such as walking, dressing, and grooming difficult and painful. Early diagnosis and treatment are important to help manage symptoms and slow the progression of the disease.

Peripheral Nervous System Diseases can result from a variety of causes, including:

1. Trauma or injury
2. Infections such as Lyme disease or HIV
3. Autoimmune disorders such as Guillain-Barré syndrome
4. Genetic mutations
5. Tumors or cysts
6. Toxins or poisoning
7. Vitamin deficiencies
8. Chronic diseases such as diabetes or alcoholism

Some common Peripheral Nervous System Diseases include:

1. Neuropathy - damage to the nerves that can cause pain, numbness, and weakness in the affected areas.
2. Multiple Sclerosis (MS) - an autoimmune disease that affects the CNS and PNS, causing a range of symptoms including numbness, weakness, and vision problems.
3. Peripheral Neuropathy - damage to the nerves that can cause pain, numbness, and weakness in the affected areas.
4. Guillain-Barré syndrome - an autoimmune disorder that causes muscle weakness and paralysis.
5. Charcot-Marie-Tooth disease - a group of inherited disorders that affect the nerves in the feet and legs, leading to muscle weakness and wasting.
6. Friedreich's ataxia - an inherited disorder that affects the nerves in the spine and limbs, leading to coordination problems and muscle weakness.
7. Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) - an autoimmune disorder that causes inflammation of the nerves, leading to pain, numbness, and weakness in the affected areas.
8. Amyotrophic Lateral Sclerosis (ALS) - a progressive neurological disease that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness, atrophy, and paralysis.
9. Spinal Muscular Atrophy - an inherited disorder that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness and wasting.
10. Muscular Dystrophy - a group of inherited disorders that affect the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness and wasting.

It's important to note that this is not an exhaustive list and there may be other causes of muscle weakness. If you are experiencing persistent or severe muscle weakness, it is important to see a healthcare professional for proper evaluation and diagnosis.

There are several types of vasculitis, each with its own set of symptoms and characteristics. Some common forms of vasculitis include:

1. Giant cell arteritis: This is the most common form of vasculitis, and it affects the large arteries in the head, neck, and arms. Symptoms include fever, fatigue, muscle aches, and loss of appetite.
2. Takayasu arteritis: This type of vasculitis affects the aorta and its major branches, leading to inflammation in the blood vessels that supply the heart, brain, and other vital organs. Symptoms include fever, fatigue, chest pain, and shortness of breath.
3. Polymyalgia rheumatica: This is an inflammatory condition that affects the muscles and joints, as well as the blood vessels. It often occurs in people over the age of 50 and is frequently associated with giant cell arteritis. Symptoms include pain and stiffness in the shoulders, hips, and other joints, as well as fatigue and fever.
4. Kawasaki disease: This is a rare condition that affects children under the age of 5, causing inflammation in the blood vessels that supply the heart and other organs. Symptoms include high fever, rash, swollen lymph nodes, and irritability.

The exact cause of vasculitis is not fully understood, but it is thought to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks its own blood vessels. Genetic factors may also play a role in some cases.

Diagnosis of vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies (e.g., MRI or CT scans), and biopsies. Treatment options vary depending on the specific type of vasculitis and its severity, but may include medications to reduce inflammation and suppress the immune system, as well as lifestyle modifications such as exercise and stress management techniques. In severe cases, surgery or organ transplantation may be necessary.

In addition to these specific types of vasculitis, there are other conditions that can cause similar symptoms and may be included in the differential diagnosis, such as:

1. Rheumatoid arthritis (RA): This is a chronic autoimmune disorder that affects the joints and can cause inflammation in blood vessels.
2. Systemic lupus erythematosus (SLE): This is another autoimmune disorder that can affect multiple systems, including the skin, joints, and blood vessels.
3. Polyarteritis nodosa: This is a condition that causes inflammation of the blood vessels, often in association with hepatitis B or C infection.
4. Takayasu arteritis: This is a rare condition that affects the aorta and its branches, causing inflammation and narrowing of the blood vessels.
5. Giant cell arteritis: This is a condition that causes inflammation of the large and medium-sized blood vessels, often in association with polymyalgia rheumatica (PMR).
6. Kawasaki disease: This is a rare condition that affects children, causing inflammation of the blood vessels and potential heart complications.
7. Henoch-Schönlein purpura: This is a rare condition that causes inflammation of the blood vessels in the skin, joints, and gastrointestinal tract.
8. IgG4-related disease: This is a condition that can affect various organs, including the pancreas, bile ducts, and blood vessels, causing inflammation and potentially leading to fibrosis or tumor formation.

It is important to note that these conditions may have similar symptoms and signs as vasculitis, but they are distinct entities with different causes and treatment approaches. A thorough diagnostic evaluation, including laboratory tests and imaging studies, is essential to determine the specific diagnosis and develop an appropriate treatment plan.

Autoimmune hemolytic anemia (AIHA) is a specific type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells. This can happen due to various underlying causes such as infections, certain medications, and some types of cancer.

In autoimmune hemolytic anemia, the immune system produces antibodies that coat the surface of red blood cells and mark them for destruction by other immune cells called complement proteins. This leads to the premature destruction of red blood cells in the spleen, liver, and other organs.

Symptoms of autoimmune hemolytic anemia can include fatigue, weakness, shortness of breath, jaundice (yellowing of the skin and eyes), dark urine, and a pale or yellowish complexion. Treatment options for AIHA depend on the underlying cause of the disorder, but may include medications to suppress the immune system, plasmapheresis to remove antibodies from the blood, and in severe cases, splenectomy (removal of the spleen) or bone marrow transplantation.

In summary, autoimmune hemolytic anemia is a type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells, leading to premature destruction of red blood cells and various symptoms such as fatigue, weakness, and jaundice. Treatment options depend on the underlying cause of the disorder and may include medications, plasmapheresis, and in severe cases, splenectomy or bone marrow transplantation.

1. Autoimmune diseases: These occur when the immune system mistakenly attacks healthy cells and tissues in the body. Examples include rheumatoid arthritis, lupus, multiple sclerosis, and type 1 diabetes.
2. Allergies: An allergic reaction occurs when the immune system overreacts to a harmless substance, such as pollen, dust mites, or certain foods. Symptoms can range from mild hives to life-threatening anaphylaxis.
3. Immunodeficiency disorders: These are conditions that impair the immune system's ability to fight infections. Examples include HIV/AIDS and primary immunodeficiency diseases.
4. Infectious diseases: Certain infections, such as tuberculosis or bacterial meningitis, can cause immune system dysfunction.
5. Cancer: Some types of cancer, such as lymphoma, affect the immune system's ability to fight disease.
6. Immune thrombocytopenic purpura (ITP): This is a rare autoimmune disorder that causes the immune system to attack and destroy platelets, leading to bleeding and bruising.
7. Guillain-Barré syndrome: This is a rare autoimmune disorder that occurs when the immune system attacks the nerves, leading to muscle weakness and paralysis.
8. Chronic fatigue syndrome (CFS): This is a condition characterized by persistent fatigue, muscle pain, and joint pain, which is thought to be related to an immune system imbalance.
9. Fibromyalgia: This is a chronic condition characterized by widespread muscle pain, fatigue, and sleep disturbances, which may be linked to immune system dysfunction.
10. Autoimmune hepatitis: This is a condition in which the immune system attacks the liver, leading to inflammation and damage to the liver cells.

It's important to note that a weakened immune system can increase the risk of infections and other health problems, so it's important to work with your healthcare provider to identify any underlying causes and develop an appropriate treatment plan.

CNS bacterial infections can cause a wide range of symptoms, including fever, headache, confusion, seizures, and loss of consciousness. In severe cases, these infections can lead to meningitis, encephalitis, or abscesses in the brain or spinal cord.

The diagnosis of CNS bacterial infections is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests may include blood cultures, cerebrospinal fluid (CSF) cultures, and polymerase chain reaction (PCR) tests to identify the causative bacteria. Imaging studies, such as computed tomography (CT) or magnetic resonance imaging (MRI), may be used to visualize the extent of the infection.

Treatment of CNS bacterial infections typically involves the use of antibiotics, which can help to clear the infection and prevent further complications. In some cases, surgical intervention may be necessary to drain abscesses or relieve pressure on the brain or spinal cord.

Preventive measures for CNS bacterial infections include vaccination against certain types of bacteria, such as Streptococcus pneumoniae and Haemophilus influenzae, good hygiene practices, and appropriate use of antibiotics. Early diagnosis and treatment are critical to preventing long-term neurological damage or death.

In conclusion, CNS bacterial infections can be serious and potentially life-threatening conditions that require prompt diagnosis and treatment. Understanding the causes, symptoms, diagnosis, treatment, and prevention of these infections is essential for effective management and optimal outcomes for patients affected by them.

The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:

* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure

Glomerulonephritis can be caused by a variety of factors, including:

* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia

The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.

Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:

* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases

The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.

A rare autoimmune disorder characterized by inflammation and damage to cartilage and connective tissue throughout the body, often leading to arthritis, skin rashes, and other symptoms. The condition is often triggered by infections or exposure to certain medications, and can be difficult to diagnose due to its diverse range of symptoms. Treatment typically involves immunosuppressive medications and surgery to repair damaged tissue.

Polychondritis, relapsing: A rare autoimmune disorder affecting cartilage and connective tissue throughout the body, often causing arthritis and skin rashes. The condition is difficult to diagnose due to its diverse range of symptoms, but treatment involves immunosuppressive medications and surgery to repair damaged tissue.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body. The condition can cause a wide range of symptoms, including arthritis, skin rashes, and inflammation in various organs and joints. It is often triggered by infections or exposure to certain medications, and can be difficult to diagnose due to its diverse range of symptoms. Treatment typically involves immunosuppressive medications and surgery to repair damaged tissue.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, causing arthritis, skin rashes, and other symptoms. Treatment involves immunosuppressive medications and surgery to repair damaged tissue.

Polychondritis, relapsing is a rare autoimmune disorder characterized by inflammation and damage to cartilage and connective tissue throughout the body, often leading to arthritis, skin rashes, and other symptoms. Treatment typically involves immunosuppressive medications and surgery to repair damaged tissue.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, causing arthritis, skin rashes, and other symptoms. Treatment involves immunosuppressive medications and surgery to repair damaged tissue.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment typically involves immunosuppressive medications and surgery to repair damaged tissue.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment often involves immunosuppressive medications and surgery to repair damaged tissue.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment typically involves immunosuppressive medications and surgery to repair damaged tissue. In some cases, bone marrow transplantation may be necessary.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment usually involves immunosuppressive medications and surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment typically involves immunosuppressive medications and surgery to repair damaged tissue. In some cases, bone marrow transplantation may be necessary to treat severe cases of the disorder.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment often involves a combination of medications and surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to treat the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment typically involves a combination of medications and surgery to repair damaged tissue. In some cases, bone marrow transplantation may be necessary to treat severe cases of the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment often involves a combination of medications and surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to treat the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment typically involves a combination of medications and surgery to repair damaged tissue. In some cases, bone marrow transplantation may be necessary to treat severe cases of the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment often involves a combination of medications and surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to treat the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment typically involves a combination of medications and surgery to repair damaged tissue. In some cases, bone marrow transplantation may be necessary to treat severe cases of the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment often involves a combination of medications and surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to treat the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment typically involves a combination of medications and surgery to repair damaged tissue. In some cases, bone marrow transplantation may be necessary to treat severe cases of the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment often involves a combination of medications and surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to treat the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment often involves a combination of medications and surgery to repair damaged tissue. In some cases, bone marrow transplantation may be necessary to treat severe cases of the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment often involves a combination of medications and surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to treat the disorder effectively.

Polychondritis, relapsing is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to arthritis, skin rashes, and other symptoms. Treatment often involves a combination of medications and surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to treat the disorder effectively.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis and skin rashes. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that affects cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

Polychondritis is a rare autoimmune disorder that can cause inflammation in cartilage and connective tissue throughout the body, leading to symptoms such as arthritis, skin rashes, and other symptoms. Treatment typically involves medications to reduce inflammation and suppress the immune system, as well as surgery to repair damaged tissue. In severe cases, bone marrow transplantation may be necessary to effectively treat the disorder.

The symptoms of dermatomyositis can vary in severity and may include:

* Rashes and lesions on the skin, particularly on the face, neck, and hands
* Muscle weakness and fatigue
* Joint pain and stiffness
* Swelling and redness in the affected areas
* Fever
* Headaches
* Fatigue

Dermatomyositis is often associated with other autoimmune disorders, such as polymyositis, and can be triggered by certain medications or infections. There is no cure for dermatomyositis, but treatment options are available to manage the symptoms and prevent complications. Treatment may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy to maintain muscle strength and flexibility.

The term "dermatomyositis" is derived from the Greek words "derma," meaning skin, "myo," meaning muscle, and "-itis," indicating inflammation. The condition was first described in the medical literature in the early 20th century, and since then has been studied extensively to better understand its causes and develop effective treatments.

In summary, dermatomyositis is a rare autoimmune disease that affects both the skin and muscles, causing inflammation and various symptoms such as rashes, weakness, and joint pain. While there is no cure for the condition, treatment options are available to manage the symptoms and prevent complications.

In NAE, the immune system mistakenly attacks the nerves, leading to inflammation and damage. This can cause a range of symptoms, including pain, numbness, tingling, and weakness in the affected area. The condition is often triggered by exposure to certain environmental factors or by a genetic predisposition.

Some of the key features of NAE include:

* Inflammation of the nerves: The immune system releases chemicals that cause inflammation in the nerves, leading to damage and disruption of normal nerve function.
* Nerve damage: The inflammation can cause damage to the nerves, leading to a loss of function and potentially permanent damage.
* Pain: One of the most common symptoms of NAE is pain in the affected area. This can range from mild to severe and can be persistent or intermittent.
* Numbness and tingling: The inflammation can also cause numbness and tingling sensations in the affected area.
* Weakness: In some cases, NAE can cause weakness or paralysis of the muscles in the affected area.

There is currently no cure for NAE, but various treatments are being studied to manage its symptoms and slow its progression. These include medications to reduce inflammation and modulate the immune response, as well as physical therapy and lifestyle modifications.

Symptoms of sialadenitis may include:

* Swelling and tenderness of the salivary gland
* Pain in the jaw, cheek, or neck
* Difficulty swallowing
* Fever
* Redness and warmth of the affected area

The diagnosis of sialadenitis is based on a combination of physical examination, medical history, and imaging studies such as ultrasound or CT scan. Treatment depends on the underlying cause, but may include antibiotics for bacterial infections, anti-inflammatory medications, or drainage of the abscess if present.

Sialadenitis can lead to complications such as abscess formation, cellulitis, and permanent damage to the salivary gland if left untreated. Therefore, it is important to seek medical attention if symptoms persist or worsen over time.

There are two main types of Addison's disease: primary and secondary. Primary Addison's disease is caused by an autoimmune disorder that destroys the adrenal glands, while secondary Addison's disease is caused by a problem with the pituitary gland, which regulates the adrenal glands.

Symptoms of Addison's disease can include fatigue, weakness, weight loss, dehydration, and changes in skin color. Treatment involves replacing the missing hormones with medication and managing symptoms. If left untreated, Addison's disease can be life-threatening.

Specialists who may be involved in treating Addison's disease include endocrinologists, primary care physicians, and surgeons. Treatment options can include medication, hydration therapy, and in some cases, surgery to remove the affected adrenal gland(s).

It is important for individuals with Addison's disease to work closely with their healthcare team to manage their condition and avoid complications. With proper treatment and self-management, most people with Addison's disease can lead active and fulfilling lives.

The exact cause of autoimmune hepatitis is not fully understood, but it is believed to involve a combination of genetic and environmental factors. The condition can occur in people of all ages, although it is most common in women between the ages of 20 and 40.

Symptoms of autoimmune hepatitis may include fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, pale stools, and yellowing of the skin and eyes (jaundice). If left untreated, the condition can lead to liver failure and even death.

Treatment for autoimmune hepatitis typically involves medications to suppress the immune system and reduce inflammation in the liver. In severe cases, a liver transplant may be necessary. Early diagnosis and treatment can improve the chances of a successful outcome.

Symptoms of CNS lupus vasculitis can include headaches, seizures, confusion, weakness or paralysis, vision problems, and changes in personality or behavior. The condition can be difficult to diagnose, as it may mimic other conditions such as stroke, infection, or tumors.

Treatment of CNS lupus vasculitis typically involves high doses of corticosteroids to reduce inflammation and prevent further damage. In severe cases, intravenous immunoglobulin (IVIG) or plasmapheresis may be used to remove harmful antibodies from the blood. Anticoagulation therapy may also be prescribed to prevent blood clots.

While CNS lupus vasculitis can be a life-threatening condition, early diagnosis and aggressive treatment can improve outcomes. However, long-term follow-up is essential to monitor for recurrences of the disease and manage any ongoing neurological symptoms.

Some common types of brain diseases include:

1. Neurodegenerative diseases: These are progressive conditions that damage or kill brain cells over time, leading to memory loss, cognitive decline, and movement disorders. Examples include Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis (ALS).
2. Stroke: This occurs when blood flow to the brain is interrupted, leading to cell death and potential long-term disability.
3. Traumatic brain injury (TBI): This refers to any type of head injury that causes damage to the brain, such as concussions, contusions, or penetrating wounds.
4. Infections: Viral, bacterial, and fungal infections can all affect the brain, leading to a range of symptoms including fever, seizures, and meningitis.
5. Tumors: Brain tumors can be benign or malignant and can cause a variety of symptoms depending on their location and size.
6. Cerebrovascular diseases: These conditions affect the blood vessels of the brain, leading to conditions such as aneurysms, arteriovenous malformations (AVMs), and Moyamoya disease.
7. Neurodevelopmental disorders: These are conditions that affect the development of the brain and nervous system, such as autism spectrum disorder, ADHD, and intellectual disability.
8. Sleep disorders: Conditions such as insomnia, narcolepsy, and sleep apnea can all have a significant impact on brain function.
9. Psychiatric disorders: Mental health conditions such as depression, anxiety, and schizophrenia can affect the brain and its functioning.
10. Neurodegenerative with brain iron accumulation: Conditions such as Parkinson's disease, Alzheimer's disease, and Huntington's disease are characterized by the accumulation of abnormal proteins and other substances in the brain, leading to progressive loss of brain function over time.

It is important to note that this is not an exhaustive list and there may be other conditions or factors that can affect the brain and its functioning. Additionally, many of these conditions can have a significant impact on a person's quality of life, and it is important to seek medical attention if symptoms persist or worsen over time.

The symptoms of TB CNS can vary depending on the location and severity of the infection, but may include:

* Headache
* Fever
* Nausea and vomiting
* Weakness or paralysis of the face, arm, or leg
* Confusion, seizures, or coma
* Vision loss or double vision
* Hearing loss or ringing in the ears
* Meningitis (inflammation of the protective membranes covering the brain and spinal cord)

TB CNS can be difficult to diagnose because the symptoms are often non-specific and can resemble other conditions, such as a stroke or a brain tumor. A diagnosis is typically made through a combination of physical examination, imaging tests (such as CT or MRI scans), and laboratory tests (such as lumbar puncture and culture).

TB CNS is treated with antibiotics, usually for a period of at least 6-12 months. In some cases, surgery may be necessary to remove abscesses or repair damaged tissue. Treatment outcomes are generally good if the diagnosis is made early and the infection is contained within the central nervous system. However, delays in diagnosis and treatment can lead to serious complications, such as permanent neurological damage or death.

Prevention of TB CNS involves identifying and treating cases of active TB infection, as well as taking measures to prevent the spread of the disease. This includes screening for TB in high-risk individuals, such as those with weakened immune systems or living in areas with a high prevalence of TB. Vaccination against TB is also recommended in some cases.

In summary, TB CNS is a rare and potentially life-threatening form of tuberculosis that can cause severe neurological symptoms and complications. Early diagnosis and treatment are critical to preventing serious outcomes and ensuring effective management of the disease.

Symptoms of dacryocystitis may include:

* Pain and swelling in the affected eye
* Redness and tearing of the eye
* Discharge or pus from the eye
* Swollen eyelids
* Fever

If left untreated, dacryocystitis can lead to complications such as abscesses or cellulitis, which can be serious. Treatment usually involves antibiotics and/or surgical drainage of the lacrimal sac.

1. Lymphedema: This is a condition in which the lymph vessels are unable to properly drain fluid from the body, leading to swelling in the affected limb.
2. Lymphangitis: This is an inflammation of the lymph vessels that can cause pain, redness, and swelling.
3. Lymphadenitis: This is an infection of the lymph nodes that can cause swelling, pain, and difficulty breathing.
4. Primary lymphedema: This is a rare genetic condition in which the lymph vessels are missing or do not develop properly.
5. Secondary lymphedema: This is a condition that develops as a result of another condition or injury, such as surgery, radiation therapy, or infection.
6. Lymphatic malformations: These are abnormalities in the development of the lymph vessels and nodes that can cause swelling, pain, and difficulty breathing.
7. Lymphocystis: This is a rare condition in which small cysts form in the lymph vessels and nodes.
8. Lymphangioleiomyomatosis (LAM): This is a rare condition that causes cysts to form in the lungs and can also affect the lymph vessels and nodes.
9. Lipedema: This is a condition in which there is an abnormal accumulation of fat in the legs, thighs, and buttocks, which can cause swelling and pain.
10. Pemphigus: This is a group of rare autoimmune disorders that affect the skin and mucous membranes, leading to blistering and scarring.

Treatment for lymphatic diseases depends on the specific condition and may include compression garments, exercises, and manual lymph drainage therapy. In some cases, medications such as antibiotics or anti-inflammatory drugs may be prescribed to help manage symptoms. Surgery may also be necessary in some cases to remove blockages or repair damaged vessels.

It is important to seek medical attention if you experience any persistent swelling or pain, as these can be signs of a lymphatic disease. Early diagnosis and treatment can help to manage symptoms and improve quality of life.

Experimental myasthenia gravis refers to a type of myasthenia gravis that is caused by experimental or artificial means, such as through the use of drugs or other substances that mimic or trigger an immune response. This type of myasthenia gravis is often used in research settings to study the underlying mechanisms of the disease and to test new treatments.

Autoimmune myasthenia gravis, on the other hand, refers to a type of myasthenia gravis that is caused by an abnormal immune response, where the immune system mistakenly attacks the acetylcholine receptors at the neuromuscular junction. This type of myasthenia gravis is more common than experimental myasthenia gravis and can be caused by a variety of factors, such as genetic predisposition, infections, or environmental triggers.

Overall, myasthenia gravis, autoimmune, and experimental refer to different aspects of the disease, with each term having its own specific meaning and application in the medical field.

Encephalitis can cause a range of symptoms, including fever, headache, confusion, seizures, and loss of consciousness. In severe cases, encephalitis can lead to brain damage, coma, and even death.

The diagnosis of encephalitis is based on a combination of clinical signs, laboratory tests, and imaging studies. Laboratory tests may include blood tests to detect the presence of antibodies or antigens specific to the causative agent, as well as cerebrospinal fluid (CSF) analysis to look for inflammatory markers and/or bacteria or viruses in the CSF. Imaging studies, such as CT or MRI scans, may be used to visualize the brain and identify any areas of damage or inflammation.

Treatment of encephalitis typically involves supportive care, such as intravenous fluids, oxygen therapy, and medication to manage fever and pain. Antiviral or antibacterial drugs may be used to target the specific causative agent, if identified. In severe cases, hospitalization in an intensive care unit (ICU) may be necessary to monitor and manage the patient's condition.

Prevention of encephalitis includes vaccination against certain viruses that can cause the condition, such as herpes simplex virus and Japanese encephalitis virus. Additionally, avoiding exposure to mosquitoes and other insects that can transmit viruses or bacteria that cause encephalitis, as well as practicing good hygiene and sanitation, can help reduce the risk of infection.

Overall, encephalitis is a serious and potentially life-threatening condition that requires prompt medical attention for proper diagnosis and treatment. With appropriate care, many patients with encephalitis can recover fully or partially, but some may experience long-term neurological complications or disability.

1. Common cold: A viral infection that affects the upper respiratory tract and causes symptoms such as sneezing, running nose, coughing, and mild fever.
2. Influenza (flu): A viral infection that can cause severe respiratory illness, including pneumonia, bronchitis, and sinus and ear infections.
3. Measles: A highly contagious viral infection that causes fever, rashes, coughing, and redness of the eyes.
4. Rubella (German measles): A mild viral infection that can cause fever, rashes, headache, and swollen lymph nodes.
5. Chickenpox: A highly contagious viral infection that causes fever, itching, and a characteristic rash of small blisters on the skin.
6. Herpes simplex virus (HSV): A viral infection that can cause genital herpes, cold sores, or other skin lesions.
7. Human immunodeficiency virus (HIV): A viral infection that attacks the immune system and can lead to acquired immunodeficiency syndrome (AIDS).
8. Hepatitis B: A viral infection that affects the liver, causing inflammation and damage to liver cells.
9. Hepatitis C: Another viral infection that affects the liver, often leading to chronic liver disease and liver cancer.
10. Ebola: A deadly viral infection that causes fever, vomiting, diarrhea, and internal bleeding.
11. SARS (severe acute respiratory syndrome): A viral infection that can cause severe respiratory illness, including pneumonia and respiratory failure.
12. West Nile virus: A viral infection that can cause fever, headache, and muscle pain, as well as more severe symptoms such as meningitis or encephalitis.

Viral infections can be spread through contact with an infected person or contaminated surfaces, objects, or insects such as mosquitoes. Prevention strategies include:

1. Practicing good hygiene, such as washing hands frequently and thoroughly.
2. Avoiding close contact with people who are sick.
3. Covering the mouth and nose when coughing or sneezing.
4. Avoiding sharing personal items such as towels or utensils.
5. Using condoms or other barrier methods during sexual activity.
6. Getting vaccinated against certain viral infections, such as HPV and hepatitis B.
7. Using insect repellents to prevent mosquito bites.
8. Screening blood products and organs for certain viruses before transfusion or transplantation.

Treatment for viral infections depends on the specific virus and the severity of the illness. Antiviral medications may be used to reduce the replication of the virus and alleviate symptoms. In severe cases, hospitalization may be necessary to provide supportive care such as intravenous fluids, oxygen therapy, or mechanical ventilation.

Prevention is key in avoiding viral infections, so taking the necessary precautions and practicing good hygiene can go a long way in protecting oneself and others from these common and potentially debilitating illnesses.

The main symptoms of PTI include:

* Purple spots or bruises (purpura) on the skin, which may be caused by minor trauma or injury.
* Thrombocytopenia (low platelet count), typically less than 50,000 platelets/mm3.
* Mild anemia and reticulocytosis (increased immature red blood cells).
* Elevated levels of autoantibodies against platelet membrane glycoproteins (GP) and other platelet proteins.
* No evidence of other causes of thrombocytopenia, such as bone marrow disorders or infections.

The exact cause of PTI is unknown, but it is believed to involve an immune-mediated response triggered by a genetic predisposition. Treatment options for PTI include corticosteroids, intravenous immunoglobulin (IVIG), and splenectomy in severe cases. The prognosis for PTI is generally good, with most patients experiencing resolution of symptoms and normalization of platelet counts within a few months to a year after treatment. However, some individuals may experience recurrent episodes of thrombocytopenia and purpura throughout their lives.

Psoriasis can affect any part of the body, including the scalp, elbows, knees, and lower back. The symptoms of psoriasis can vary in severity, and the condition can have a significant impact on quality of life. In addition to physical discomfort, psoriasis can also cause emotional distress and stigma.

There is no cure for psoriasis, but there are several treatment options available, including topical creams and ointments, light therapy, and systemic medications such as biologic drugs. With proper treatment, many people with psoriasis are able to manage their symptoms and improve their quality of life.

Psoriasis is relatively common, affecting approximately 2-3% of the global population, with a higher prevalence in Caucasians than in other races. It can occur at any age, but typically starts in the late teenage years or early adulthood. Psoriasis is often associated with other health conditions, such as diabetes, heart disease, and depression.

Overall, psoriasis is a complex and multifactorial condition that requires a comprehensive approach to management, including both physical and emotional support. With appropriate treatment and self-care, people with psoriasis can lead full and active lives.

There are several possible causes of lymphopenia, including:

1. Viral infections: Many viral infections can cause lymphopenia, such as HIV/AIDS, hepatitis B and C, and influenza.
2. Bacterial infections: Some bacterial infections, such as tuberculosis and leprosy, can also cause lymphopenia.
3. Cancer: Certain types of cancer, such as Hodgkin's disease and non-Hodgkin's lymphoma, can cause lymphopenia by destroying lymphocytes.
4. Autoimmune disorders: Autoimmune disorders, such as rheumatoid arthritis and lupus, can cause lymphopenia by attacking the body's own tissues, including lymphocytes.
5. Radiation therapy: Radiation therapy can destroy lymphocytes and cause lymphopenia.
6. Medications: Certain medications, such as chemotherapy drugs and antibiotics, can cause lymphopenia as a side effect.
7. Genetic disorders: Some genetic disorders, such as X-linked lymphoproliferative disease, can cause lymphopenia by affecting the development or function of lymphocytes.

Symptoms of lymphopenia can include recurring infections, fatigue, and swollen lymph nodes. Treatment of lymphopenia depends on the underlying cause and may involve antibiotics, antiviral medications, or immunoglobulin replacement therapy. In some cases, a bone marrow transplant may be necessary.

Overall, lymphopenia is a condition that can have a significant impact on quality of life, and it is important to seek medical attention if symptoms persist or worsen over time. With proper diagnosis and treatment, many people with lymphopenia can experience improved health outcomes and a better quality of life.

The primary symptoms of celiac disease include diarrhea, abdominal pain, fatigue, weight loss, and bloating. However, some people may not experience any symptoms at all, but can still develop complications if the disease is left untreated. These complications can include malnutrition, anemia, osteoporosis, and increased risk of other autoimmune disorders.

The exact cause of celiac disease is unknown, but it is believed to be triggered by a combination of genetic and environmental factors. The disease is more common in people with a family history of celiac disease or other autoimmune disorders. Diagnosis is typically made through a combination of blood tests and intestinal biopsy, and treatment involves a strict gluten-free diet.

Dietary management of celiac disease involves avoiding all sources of gluten, including wheat, barley, rye, and some processed foods that may contain hidden sources of these grains. In some cases, nutritional supplements may be necessary to ensure adequate intake of certain vitamins and minerals.

While there is no known cure for celiac disease, adherence to a strict gluten-free diet can effectively manage the condition and prevent long-term complications. With proper management, people with celiac disease can lead normal, healthy lives.

Types of Infection:

1. Bacterial Infections: These are caused by the presence of harmful bacteria in the body. Examples include pneumonia, urinary tract infections, and skin infections.
2. Viral Infections: These are caused by the presence of harmful viruses in the body. Examples include the common cold, flu, and HIV/AIDS.
3. Fungal Infections: These are caused by the presence of fungi in the body. Examples include athlete's foot, ringworm, and candidiasis.
4. Parasitic Infections: These are caused by the presence of parasites in the body. Examples include malaria, giardiasis, and toxoplasmosis.

Symptoms of Infection:

1. Fever
2. Fatigue
3. Headache
4. Muscle aches
5. Skin rashes or lesions
6. Swollen lymph nodes
7. Sore throat
8. Coughing
9. Diarrhea
10. Vomiting

Treatment of Infection:

1. Antibiotics: These are used to treat bacterial infections and work by killing or stopping the growth of bacteria.
2. Antiviral medications: These are used to treat viral infections and work by interfering with the replication of viruses.
3. Fungicides: These are used to treat fungal infections and work by killing or stopping the growth of fungi.
4. Anti-parasitic medications: These are used to treat parasitic infections and work by killing or stopping the growth of parasites.
5. Supportive care: This includes fluids, nutritional supplements, and pain management to help the body recover from the infection.

Prevention of Infection:

1. Hand washing: Regular hand washing is one of the most effective ways to prevent the spread of infection.
2. Vaccination: Getting vaccinated against specific infections can help prevent them.
3. Safe sex practices: Using condoms and other safe sex practices can help prevent the spread of sexually transmitted infections.
4. Food safety: Properly storing and preparing food can help prevent the spread of foodborne illnesses.
5. Infection control measures: Healthcare providers use infection control measures such as wearing gloves, masks, and gowns to prevent the spread of infections in healthcare settings.

1. Polymyositis: This is an inflammatory disease that affects the muscles and can cause muscle weakness, pain, and stiffness.
2. Dercum's disease: This is a rare condition that causes fatty degeneration of the muscles, leading to muscle pain, weakness, and wasting.
3. Inflammatory myopathy: This is a group of conditions that cause inflammation in the muscles, leading to muscle weakness and pain.
4. Dermatomyositis: This is an inflammatory condition that affects both the skin and the muscles, causing skin rashes and muscle weakness.
5. Juvenile myositis: This is a rare condition that affects children and can cause muscle weakness, pain, and stiffness.

The symptoms of myositis can vary depending on the type of condition and its severity. Common symptoms include muscle weakness, muscle pain, stiffness, and fatigue. Other symptoms may include skin rashes, fever, and joint pain.

The diagnosis of myositis typically involves a combination of physical examination, medical history, and laboratory tests such as blood tests and muscle biopsies. Treatment for myositis depends on the underlying cause and may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy. In some cases, surgery may be necessary to remove affected muscle tissue.

1. Hypothyroidism: This is a condition where the thyroid gland does not produce enough thyroid hormones. Symptoms can include fatigue, weight gain, dry skin, constipation, and depression.
2. Hyperthyroidism: This is a condition where the thyroid gland produces too much thyroid hormone. Symptoms can include weight loss, anxiety, tremors, and an irregular heartbeat.
3. Thyroid nodules: These are abnormal growths on the thyroid gland that can be benign or cancerous.
4. Thyroid cancer: This is a type of cancer that affects the thyroid gland. There are several types of thyroid cancer, including papillary, follicular, and medullary thyroid cancer.
5. Goiter: This is an enlargement of the thyroid gland that can be caused by a variety of factors, including hypothyroidism, hyperthyroidism, and thyroid nodules.
6. Thyrotoxicosis: This is a condition where the thyroid gland produces too much thyroid hormone, leading to symptoms such as weight loss, anxiety, tremors, and an irregular heartbeat.
7. Thyroiditis: This is an inflammation of the thyroid gland that can cause symptoms such as pain, swelling, and difficulty swallowing.
8. Congenital hypothyroidism: This is a condition where a baby is born without a functioning thyroid gland or with a gland that does not produce enough thyroid hormones.
9. Thyroid cancer in children: This is a type of cancer that affects children and teenagers, usually in the form of papillary or follicular thyroid cancer.
10. Thyroid storm: This is a life-threatening condition where the thyroid gland produces an excessive amount of thyroid hormones, leading to symptoms such as fever, rapid heartbeat, and cardiac arrest.

These are just a few examples of the many conditions that can affect the thyroid gland. It's important to be aware of these conditions and seek medical attention if you experience any symptoms or concerns related to your thyroid health.

Brain neoplasms can arise from various types of cells in the brain, including glial cells (such as astrocytes and oligodendrocytes), neurons, and vascular tissues. The symptoms of brain neoplasms vary depending on their size, location, and type, but may include headaches, seizures, weakness or numbness in the limbs, and changes in personality or cognitive function.

There are several different types of brain neoplasms, including:

1. Meningiomas: These are benign tumors that arise from the meninges, the thin layers of tissue that cover the brain and spinal cord.
2. Gliomas: These are malignant tumors that arise from glial cells in the brain. The most common type of glioma is a glioblastoma, which is aggressive and hard to treat.
3. Pineal parenchymal tumors: These are rare tumors that arise in the pineal gland, a small endocrine gland in the brain.
4. Craniopharyngiomas: These are benign tumors that arise from the epithelial cells of the pituitary gland and the hypothalamus.
5. Medulloblastomas: These are malignant tumors that arise in the cerebellum, specifically in the medulla oblongata. They are most common in children.
6. Acoustic neurinomas: These are benign tumors that arise on the nerve that connects the inner ear to the brain.
7. Oligodendrogliomas: These are malignant tumors that arise from oligodendrocytes, the cells that produce the fatty substance called myelin that insulates nerve fibers.
8. Lymphomas: These are cancers of the immune system that can arise in the brain and spinal cord. The most common type of lymphoma in the CNS is primary central nervous system (CNS) lymphoma, which is usually a type of B-cell non-Hodgkin lymphoma.
9. Metastatic tumors: These are tumors that have spread to the brain from another part of the body. The most common types of metastatic tumors in the CNS are breast cancer, lung cancer, and melanoma.

These are just a few examples of the many types of brain and spinal cord tumors that can occur. Each type of tumor has its own unique characteristics, such as its location, size, growth rate, and biological behavior. These factors can help doctors determine the best course of treatment for each patient.

The exact cause of MCTD is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissues in the body. The disease is more common in women than men and typically affects people between the ages of 20 and 50.

Symptoms of MCTD can vary widely and may include:

* Skin rashes or lesions
* Joint pain and stiffness
* Fatigue
* Fever
* Raynaud's phenomenon (digits turn white or blue in response to cold or stress)
* Swollen lymph nodes
* Shortness of breath
* Chest pain
* Abdominal pain
* Weakness and wasting of muscles

There is no cure for MCTD, but treatment focuses on managing symptoms and preventing complications. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive drugs may be used to reduce inflammation and suppress the immune system. Physical therapy and exercise may also be helpful in maintaining joint mobility and strength.

The prognosis for MCTD varies depending on the severity of the disease and the presence of certain complications, such as lung or heart involvement. Some people with MCTD may experience a gradual worsening of symptoms over time, while others may experience periods of remission. With appropriate treatment, many people with MCTD are able to manage their symptoms and lead active lives.

There are several types of lymphoproliferative disorders, including:

1. Lymphoma: This is a type of cancer that affects the immune system and can arise from either B cells or T cells. There are several subtypes of lymphoma, including Hodgkin lymphoma and non-Hodgkin lymphoma.
2. Leukemia: This is a type of cancer that affects the blood and bone marrow. It occurs when there is an abnormal proliferation of white blood cells, which can lead to an overproduction of immature or malignant cells.
3. Myelodysplastic syndrome (MDS): This is a group of disorders that affect the bone marrow and can lead to an abnormal production of blood cells. MDS can progress to acute myeloid leukemia (AML).
4. Chronic lymphocytic leukemia (CLL): This is a type of cancer that affects the blood and bone marrow, characterized by the accumulation of mature-looking but dysfunctional B cells in the blood.
5. Marginal zone lymphoma: This is a type of cancer that arises from the marginal zone of the spleen, which is the area where the white pulp and red pulp of the spleen meet.
6. Mantle cell lymphoma: This is a type of cancer that affects the lymph nodes and other lymphoid tissues, characterized by the accumulation of malignant B cells in the mantle zone of the lymph node.
7. Primary central nervous system lymphoma (PCNSL): This is a rare type of cancer that affects the brain and spinal cord, characterized by the accumulation of malignant B cells in the central nervous system.
8. Hairy cell leukemia: This is a rare type of cancer that affects the blood and bone marrow, characterized by the accumulation of abnormal B cells with a "hairy" appearance in the blood and bone marrow.
9. Lymphoplasmacytic lymphoma: This is a type of cancer that affects the lymph nodes and other lymphoid tissues, characterized by the accumulation of malignant B cells in the lymph nodes and other lymphoid tissues.
10. AIDS-related lymphoma: This is a type of cancer that affects people with HIV/AIDS, characterized by the accumulation of malignant B cells in the lymph nodes and other lymphoid tissues.

It's important to note that these are just some examples of B-cell non-Hodgkin lymphomas, and there are many other subtypes and variants of this disease. Each type of lymphoma has its own unique characteristics and may require different treatment approaches.

There are several types of retinitis, including:

1. Retinitis pigmentosa: This is a group of inherited conditions that cause progressive vision loss due to degeneration of the retina.
2. Cytomegalovirus (CMV) retinitis: This is a type of retinitis caused by the CMV virus, which is common in people with weakened immune systems, such as those with HIV/AIDS.
3. Toxoplasma retinitis: This is a type of retinitis caused by the Toxoplasma gondii parasite, which can cause vision loss if left untreated.
4. Syphilitic retinitis: This is a type of retinitis caused by the bacteria Treponema pallidum, which can cause vision loss if left untreated.
5. Uveitis-related retinitis: This is a type of retinitis that occurs as a complication of uveitis, an inflammation of the uvea, the middle layer of the eye.

Symptoms of retinitis can include vision loss, blurred vision, sensitivity to light, and floaters (specks or cobwebs in your vision). If you experience any of these symptoms, it is important to seek medical attention as soon as possible.

Retinitis is typically diagnosed through a combination of physical examination, imaging tests such as optical coherence tomography (OCT), and laboratory tests to identify the underlying cause. Treatment for retinitis depends on the underlying cause and may include antiviral or antibacterial medications, immunosuppressive drugs, or surgery. In some cases, vision loss may be permanent, but early diagnosis and treatment can help prevent further damage and improve outcomes.

The symptoms of Behcet syndrome can vary widely, but may include:

* Skin lesions, such as ulcers or rashes
* Eye inflammation (uveitis)
* Joint pain and swelling
* Digestive problems such as diarrhea and abdominal pain
* Nervous system problems such as seizures and headaches
* Inflammation of the blood vessels, which can lead to aneurysms or blood clots

The exact cause of Behcet syndrome is not known, but it is believed to be related to a combination of genetic and environmental factors. There is no cure for the disease, but various treatments are available to manage the symptoms and prevent complications. These may include medications such as corticosteroids, immunosuppressive drugs, and antibiotics, as well as lifestyle modifications such as avoiding triggers like spicy foods or stress.

Behcet syndrome is rare in the United States, but it is more common in certain parts of the world, including Turkey, Japan, and other countries with high prevalence of autoimmune disorders. It affects both men and women equally, and typically begins during adulthood, although it can sometimes begin in childhood or adolescence.

Overall, Behcet syndrome is a complex and multifaceted disease that requires careful management by a healthcare team to prevent complications and improve quality of life for patients.

Causes: Thyroiditis can be caused by a viral or bacterial infection, autoimmune disorders, or radiation exposure.

Symptoms: Symptoms of thyroiditis may include pain and swelling in the neck, difficulty swallowing, hoarseness, fatigue, weight gain, muscle weakness, and depression.

Types: There are several types of thyroiditis, including subacute thyroiditis, silent thyroiditis, and postpartum thyroiditis.

Diagnosis: Thyroiditis is typically diagnosed through a combination of physical examination, blood tests, and imaging studies such as ultrasound or CT scans.

Treatment: Treatment for thyroiditis usually involves antibiotics to treat any underlying infection, pain relief medication to manage neck swelling and discomfort, and hormone replacement therapy to address hormonal imbalances. In some cases, surgery may be necessary to remove part or all of the affected thyroid gland.

Complications: Untreated thyroiditis can lead to complications such as hypothyroidism (underactive thyroid), hyperthyroidism (overactive thyroid), and thyroid nodules or cancer.

Prevention: Preventing thyroiditis is challenging, but maintaining good overall health, avoiding exposure to radiation, and managing any underlying autoimmune disorders can help reduce the risk of developing the condition.

Prognosis: With proper treatment, most people with thyroiditis experience a full recovery and normalization of thyroid function. However, in some cases, long-term hormone replacement therapy may be necessary to manage persistent hypothyroidism or hyperthyroidism.

A group of autoimmune blistering diseases that are characterized by the formation of large, tense bullae on the skin and mucous membranes. These diseases are caused by abnormal immunological responses to certain antigens, which lead to the production of autoantibodies that attack the basement membrane zone of the skin and mucous membranes, causing damage and blister formation.

There are several types of pemphigoid, bullous diseases, including:

* Pemphigoid, benign chronic
* Pemphigoid, severe
* Bullous pemphigoid
* Epidermolysis bullosa acquisita

Symptoms of pemphigoid, bullous diseases may include:

* Blisters on the skin and mucous membranes
* Redness and swelling around the blisters
* Itching or pain
* Fever

Diagnosis of pemphigoid, bullous diseases is based on a combination of clinical findings, laboratory tests, and biopsy. Treatment involves the use of corticosteroids, immunosuppressive drugs, and antibiotics to manage symptoms and prevent complications.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.

Conclusion

Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

Polymyositis can affect people of all ages, but it most commonly occurs in adults between the ages of 30 and 60. It is more common in women than men, and the symptoms can vary in severity. The disease may be acute or chronic, and it can affect one or more muscle groups.

The symptoms of polymyositis include:

* Muscle weakness and fatigue
* Pain in the affected muscles
* Wasting of the affected muscles
* Difficulty swallowing (in severe cases)
* Shortness of breath (in severe cases)

The diagnosis of polymyositis is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests may include blood tests to check for muscle enzymes and inflammatory markers, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Imaging studies, such as magnetic resonance imaging (MRI), can help to confirm the diagnosis and assess the extent of the disease.

There is no cure for polymyositis, but treatment can help to manage the symptoms and slow the progression of the disease. Treatment options may include:

* Corticosteroids to reduce inflammation
* Immunosuppressive drugs to suppress the immune system
* Physical therapy to maintain muscle strength and function
* Pain management with analgesics and other medications
* Plasmapheresis to remove antibodies from the blood

The prognosis for polymyositis varies, depending on the severity of the disease and the response to treatment. In general, the prognosis is better for patients who have a mild form of the disease and who respond well to treatment. However, in severe cases, the disease can be life-threatening, and mortality rates are estimated to be as high as 20% to 30%.

Disease progression can be classified into several types based on the pattern of worsening:

1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.

Disease progression can be influenced by various factors, including:

1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.

Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.

The symptoms of myocarditis can vary depending on the severity of the inflammation and the location of the affected areas of the heart muscle. Common symptoms include chest pain, shortness of breath, fatigue, and swelling in the legs and feet.

Myocarditis can be difficult to diagnose, as its symptoms are similar to those of other conditions such as coronary artery disease or heart failure. Diagnosis is typically made through a combination of physical examination, medical history, and results of diagnostic tests such as electrocardiogram (ECG), echocardiogram, and blood tests.

Treatment of myocarditis depends on the underlying cause and severity of the condition. Mild cases may require only rest and over-the-counter pain medication, while more severe cases may require hospitalization and intravenous medications to manage inflammation and cardiac function. In some cases, surgery may be necessary to repair or replace damaged heart tissue.

Prevention of myocarditis is important, as it can lead to serious complications such as heart failure and arrhythmias if left untreated. Prevention strategies include avoiding exposure to viruses and other infections, managing underlying medical conditions such as diabetes and high blood pressure, and getting regular check-ups with a healthcare provider to monitor cardiac function.

In summary, myocarditis is an inflammatory condition that affects the heart muscle, causing symptoms such as chest pain, shortness of breath, and fatigue. Diagnosis can be challenging, but treatment options range from rest and medication to hospitalization and surgery. Prevention is key to avoiding serious complications and maintaining good cardiac health.

A type of encephalitis caused by a virus that inflames the brain and spinal cord, leading to fever, headache, confusion, seizures, and in severe cases, coma or death. Viral encephalitis is usually transmitted through the bite of an infected mosquito or tick, but can also be spread through contact with infected blood or organs. Diagnosis is made through a combination of physical examination, laboratory tests, and imaging studies. Treatment typically involves supportive care, such as intravenous fluids, oxygen therapy, and medication to manage fever and seizures, as well as antiviral medications in severe cases.

Synonyms: viral encephalitis

Antonyms: bacterial encephalitis

Similar term: meningitis

There are several types of JA, including:

1. Systemic juvenile idiopathic arthritis (SJIA): A severe form of JA that affects the entire body, causing fever, rash, and swollen lymph nodes in addition to joint inflammation.
2. Polyarticular juvenile idiopathic arthritis (PJIA): A common form of JA that affects multiple joints, especially in the hands and feet.
3. Oligoarticular juvenile idiopathic arthritis (OJIA): A mild form of JA that affects only a few joints.
4. Juvenile psoriatic arthritis (JPsA): A type of JA that is associated with psoriasis, a skin condition characterized by red, scaly patches.
5. Enthesitis-related juvenile idiopathic arthritis (ER-JIA): A rare form of JA that affects the areas where tendons and ligaments attach to bones.
6. Undifferentiated arthritis: A type of JA that does not fit into any of the other categories.

The symptoms of JA can vary depending on the specific type and severity of the condition, but may include:

* Joint pain and stiffness
* Swelling and redness in the affected joints
* Fatigue and fever
* Loss of mobility and range of motion
* Difficulty walking or standing

The exact cause of JA is not known, but it is believed to involve a combination of genetic and environmental factors. There is no cure for JA, but treatment options are available to help manage symptoms and prevent long-term joint damage. These may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and disease-modifying anti-rheumatic drugs (DMARDs), as well as physical therapy and lifestyle modifications.

The symptoms of meningoencephalitis can vary depending on the cause, but common signs include fever, headache, stiff neck, confusion, seizures, and loss of consciousness. The disease can progress rapidly and can be fatal if not treated promptly.

Diagnosis is typically made through a combination of physical examination, laboratory tests (such as blood cultures and PCR), and imaging studies (such as CT or MRI scans). Treatment options depend on the underlying cause, but may include antibiotics, antiviral medications, and supportive care to manage symptoms and prevent complications.

Prognosis for meningoencephalitis depends on the severity of the disease and the promptness and effectiveness of treatment. In general, the prognosis is better for patients who receive prompt medical attention and have a mild form of the disease. However, the disease can be severe and potentially life-threatening, especially in young children, older adults, and those with weakened immune systems.

There are three main types of CLE:

1. Discoid lupus erythematosus (DLE): Characterized by the presence of discrete, flat, round lesions with a scaly border. These lesions can scar and leave behind pale or dark patches on the skin.
2. Subacute cutaneous lupus erythematosus (SCLE): Characterized by the sudden appearance of red, painful, tender lesions that may resemble hives or folliculitis. These lesions can resolve on their own within weeks to months but can leave behind scarring.
3. Chronic cutaneous lupus erythematosus (CCLE): Characterized by the presence of widespread, thickened, darkened skin that can resemble leather or violet-colored plaques. This type is less common than DLE and SCLE.

CLE can be caused by a combination of genetic and environmental factors, including exposure to sunlight, hormonal changes, and certain medications. The disease is more common in women, especially those of childbearing age, and in people with a family history of autoimmune disorders.

The diagnosis of CLE is based on the presence of characteristic skin lesions and can be confirmed by a skin biopsy. Treatment options for CLE include topical corticosteroids, antimalarials, and immunosuppressive medications. In severe cases, phototherapy or systemic corticosteroids may be necessary. Prognosis is generally good, but the disease can be challenging to treat and recurrences are common.

There are several causes of hypergammaglobulinemia, including:

1. Chronic infections: Prolonged infections can cause an increase in the production of immunoglobulins to fight off the infection.
2. Autoimmune disorders: Conditions such as rheumatoid arthritis, lupus, and multiple sclerosis can cause the immune system to produce excessive amounts of antibodies.
3. Cancer: Some types of cancer, such as Hodgkin's disease and non-Hodgkin's lymphoma, can cause an increase in immunoglobulin production.
4. Genetic disorders: Certain genetic conditions, such as X-linked agammaglobulinemia, can lead to a deficiency or excess of immunoglobulins.
5. Medications: Certain medications, such as corticosteroids and chemotherapy drugs, can suppress the immune system and reduce the production of immunoglobulins.

Symptoms of hypergammaglobulinemia can include:

1. Infections: Recurring infections are a common symptom of hypergammaglobulinemia, as the excessive amount of antibodies can make it difficult for the body to fight off infections effectively.
2. Fatigue: Chronic infections and inflammation can cause fatigue and weakness.
3. Weight loss: Recurring infections and chronic inflammation can lead to weight loss and malnutrition.
4. Swollen lymph nodes: Enlarged lymph nodes are a common symptom of hypergammaglobulinemia, as the body tries to fight off infections.
5. Fever: Recurring fevers can be a symptom of hypergammaglobulinemia, as the body tries to fight off infections.
6. Night sweats: Excessive sweating at night can be a symptom of hypergammaglobulinemia.
7. Skin rashes: Certain types of skin rashes can be a symptom of hypergammaglobulinemia, such as a rash caused by allergic reactions to medications or infections.
8. Joint pain: Pain and stiffness in the joints can be a symptom of hypergammaglobulinemia, particularly if the excessive amount of antibodies is causing inflammation in the joints.
9. Headaches: Chronic headaches can be a symptom of hypergammaglobulinemia, particularly if the excessive amount of antibodies is causing inflammation in the brain or other parts of the body.
10. Swollen liver and spleen: Enlarged liver and spleen can be a symptom of hypergammaglobulinemia, as the body tries to filter out excess antibodies and fight off infections.

It is important to note that these symptoms can also be caused by other medical conditions, so it is essential to consult a healthcare professional for proper diagnosis and treatment. A healthcare professional may perform blood tests and other diagnostic procedures to determine the underlying cause of the symptoms and develop an appropriate treatment plan. Treatment for hypergammaglobulinemia typically involves addressing the underlying cause of the condition, such as infections, allergies, or autoimmune disorders, and may include medications to reduce inflammation and suppress the immune system.

Some common types of skin diseases include:

1. Acne: a condition characterized by oil clogged pores, pimples, and other blemishes on the skin.
2. Eczema: a chronic inflammatory skin condition that causes dry, itchy, and scaly patches on the skin.
3. Psoriasis: a chronic autoimmune skin condition characterized by red, scaly patches on the skin.
4. Dermatitis: a term used to describe inflammation of the skin, often caused by allergies or irritants.
5. Skin cancer: a type of cancer that affects the skin cells, often caused by exposure to UV radiation from the sun or tanning beds.
6. Melanoma: the most serious type of skin cancer, characterized by a mole that changes in size, shape, or color.
7. Vitiligo: a condition in which white patches develop on the skin due to the loss of pigment-producing cells.
8. Alopecia: a condition characterized by hair loss, often caused by autoimmune disorders or genetics.
9. Nail diseases: conditions that affect the nails, such as fungal infections, brittleness, and thickening.
10. Mucous membrane diseases: conditions that affect the mucous membranes, such as ulcers, inflammation, and cancer.

Skin diseases can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as biopsies or blood tests. Treatment options vary depending on the specific condition and may include topical creams or ointments, oral medications, light therapy, or surgery.

Preventive measures to reduce the risk of skin diseases include protecting the skin from UV radiation, using sunscreen, wearing protective clothing, and avoiding exposure to known allergens or irritants. Early detection and treatment can help prevent complications and improve outcomes for many skin conditions.

Symptoms of orchitis may include:

* Scrotal pain
* Swelling of the scrotum
* Redness and tenderness of the scrotum
* Fever
* Chills
* Abdominal pain
* Nausea and vomiting

Treatment for orchitis typically involves antibiotics to clear up any bacterial infections, as well as supportive care such as rest, ice packs, and over-the-counter pain medication. In severe cases, hospitalization may be necessary to monitor and treat the condition.

Prevention of orchitis includes avoiding close contact with people who have the infection, practicing safe sex, and maintaining good hygiene. Vaccination against certain types of bacteria that can cause orchitis, such as the H. influenzae type b (Hib) vaccine, can also help prevent the condition.

It is important to seek medical attention if symptoms of orchitis are present, as early treatment can help prevent complications and improve outcomes.

There are several types of lymphoma, including:

1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.

The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:

* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching

Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.

Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.

Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.

Types of Neoplasms

There are many different types of neoplasms, including:

1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.

Causes and Risk Factors of Neoplasms

The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:

1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.

Signs and Symptoms of Neoplasms

The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:

1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.

Diagnosis and Treatment of Neoplasms

The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.

The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:

1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.

Prevention of Neoplasms

While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:

1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.

It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.

Blisters are caused by friction or rubbing against a surface, which causes the top layer of skin to separate from the underlying layer. This separation creates a space that fills with fluid, forming a blister. Blisters can also be caused by burns, chemical exposure, or other types of injury.

There are different types of blisters, including:

1. Friction blisters: These are the most common type of blister and are caused by friction or rubbing against a surface. They are often seen on the hands, feet, and buttocks.
2. Burn blisters: These are caused by burns and can be more severe than friction blisters.
3. Chemical blisters: These are caused by exposure to chemicals and can be very painful.
4. Blisters caused by medical conditions: Certain medical conditions, such as epidermolysis bullosa (a genetic disorder that affects the skin), can cause blisters to form easily.

Blisters can be treated in several ways, depending on their size and location. Small blisters may not require treatment and can heal on their own within a few days. Larger blisters may need to be drained and covered with a bandage to prevent infection. In severe cases, surgical intervention may be necessary.

Preventing blisters is key to avoiding the discomfort and pain they can cause. To prevent blisters, it is important to:

1. Wear properly fitting shoes and clothing to reduce friction.
2. Use lubricating creams or powders to reduce friction.
3. Take regular breaks to rest and allow the skin to recover.
4. Avoid using harsh chemicals or detergents that can cause irritation.
5. Keep the affected area clean and dry to prevent infection.

In conclusion, blisters are a common and uncomfortable condition that can be caused by a variety of factors. While they can be treated and managed, prevention is key to avoiding the discomfort and pain they can cause. By taking steps to prevent blisters and seeking medical attention if they do occur, individuals can reduce their risk of developing this uncomfortable condition.

The hallmark of Wegener Granulomatosis is the formation of granulomas, which are clusters of immune cells that form in response to infection or inflammation. In this condition, however, the granulomas are not caused by an infectious agent but rather by the body's own immune system attacking its own tissues.

The symptoms of Wegener Granulomatosis can vary depending on the organs affected and can include:

* Fever
* Joint pain
* Fatigue
* Weight loss
* Shortness of breath
* Chest pain
* Coughing up blood
* Abdominal pain
* Blood in urine or stool
* Headache

The exact cause of Wegener Granulomatosis is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment typically involves the use of corticosteroids and other immunosuppressive medications to reduce inflammation and prevent further damage to the body. In some cases, plasmapheresis (plasma exchange) may also be used to remove harmful antibodies from the blood.

Wegener Granulomatosis is a relatively rare condition, affecting approximately 2-4 people per million each year. It can occur at any age but is most commonly diagnosed in adults between the ages of 40 and 60. With early diagnosis and proper treatment, many people with Wegener Granulomatosis can experience a good outcome and improved quality of life. However, if left untreated, the condition can be fatal.

Examples of syndromes include:

1. Down syndrome: A genetic disorder caused by an extra copy of chromosome 21 that affects intellectual and physical development.
2. Turner syndrome: A genetic disorder caused by a missing or partially deleted X chromosome that affects physical growth and development in females.
3. Marfan syndrome: A genetic disorder affecting the body's connective tissue, causing tall stature, long limbs, and cardiovascular problems.
4. Alzheimer's disease: A neurodegenerative disorder characterized by memory loss, confusion, and changes in personality and behavior.
5. Parkinson's disease: A neurological disorder characterized by tremors, rigidity, and difficulty with movement.
6. Klinefelter syndrome: A genetic disorder caused by an extra X chromosome in males, leading to infertility and other physical characteristics.
7. Williams syndrome: A rare genetic disorder caused by a deletion of genetic material on chromosome 7, characterized by cardiovascular problems, developmental delays, and a distinctive facial appearance.
8. Fragile X syndrome: The most common form of inherited intellectual disability, caused by an expansion of a specific gene on the X chromosome.
9. Prader-Willi syndrome: A genetic disorder caused by a defect in the hypothalamus, leading to problems with appetite regulation and obesity.
10. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dry eyes and mouth.

Syndromes can be diagnosed through a combination of physical examination, medical history, laboratory tests, and imaging studies. Treatment for a syndrome depends on the underlying cause and the specific symptoms and signs presented by the patient.

During relapses, new symptoms may appear or existing ones may worsen, such as vision problems, muscle weakness, coordination and balance difficulties, and cognitive impairment. The immune system mistakenly attacks the protective covering of nerve fibers, leading to communication problems between the brain and the rest of the body.

During remissions, the inflammation and symptoms may subside, but the disease is still active, and some residual disability may persist. RRMS is the most common form of MS, accounting for approximately 85% of all cases.

The syndrome is typically diagnosed based on the presence of anticardiolipin antibodies (aCL) or lupus anticoagulant in the blood. Treatment for antiphospholipid syndrome may involve medications to prevent blood clots, such as heparin or warfarin, and aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce pain and inflammation. In some cases, intravenous immunoglobulin (IVIG) may be given to reduce the levels of antibodies in the blood. Plasmapheresis, a process that removes antibodies from the blood, may also be used in some cases.

Antiphospholipid syndrome is associated with other autoimmune disorders, such as systemic lupus erythematosus (SLE), and may be triggered by certain medications or infections. It is important for individuals with antiphospholipid syndrome to work closely with their healthcare provider to manage their condition and reduce the risk of complications.

The term splenomegaly is used to describe any condition that results in an increase in the size of the spleen, regardless of the underlying cause. This can be caused by a variety of factors, such as infection, inflammation, cancer, or genetic disorders.

Splenomegaly can be diagnosed through a physical examination, where the doctor may feel the enlarged spleen during an abdominal palpation. Imaging tests, such as ultrasound, computed tomography (CT) scans, or magnetic resonance imaging (MRI), may also be used to confirm the diagnosis and evaluate the extent of the splenomegaly.

Treatment for splenomegaly depends on the underlying cause. For example, infections such as malaria or mononucleosis are treated with antibiotics, while cancerous conditions may require surgical intervention or chemotherapy. In some cases, the spleen may need to be removed, a procedure known as splenectomy.

In conclusion, splenomegaly is an abnormal enlargement of the spleen that can be caused by various factors and requires prompt medical attention for proper diagnosis and treatment.

Examples of delayed hypersensitivity reactions include contact dermatitis (a skin reaction to an allergic substance), tuberculin reactivity (a reaction to the bacteria that cause tuberculosis), and sarcoidosis (a condition characterized by inflammation in various organs, including the lungs and lymph nodes).

Delayed hypersensitivity reactions are important in the diagnosis and management of allergic disorders and other immune-related conditions. They can be detected through a variety of tests, including skin prick testing, patch testing, and blood tests. Treatment for delayed hypersensitivity reactions depends on the underlying cause and may involve medications such as antihistamines, corticosteroids, or immunosuppressants.

There are many different types of nerve degeneration that can occur in various parts of the body, including:

1. Alzheimer's disease: A progressive neurological disorder that affects memory and cognitive function, leading to degeneration of brain cells.
2. Parkinson's disease: A neurodegenerative disorder that affects movement and balance, caused by the loss of dopamine-producing neurons in the brain.
3. Amyotrophic lateral sclerosis (ALS): A progressive neurological disease that affects nerve cells in the brain and spinal cord, leading to muscle weakness, paralysis, and eventually death.
4. Multiple sclerosis: An autoimmune disease that affects the central nervous system, causing inflammation and damage to nerve fibers.
5. Diabetic neuropathy: A complication of diabetes that can cause damage to nerves in the hands and feet, leading to pain, numbness, and weakness.
6. Guillain-Barré syndrome: An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and paralysis.
7. Chronic inflammatory demyelinating polyneuropathy (CIDP): An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and numbness.

The causes of nerve degeneration are not always known or fully understood, but some possible causes include:

1. Genetics: Some types of nerve degeneration may be inherited from one's parents.
2. Aging: As we age, our nerve cells can become damaged or degenerate, leading to a decline in cognitive and physical function.
3. Injury or trauma: Physical injury or trauma to the nervous system can cause nerve damage and degeneration.
4. Infections: Certain infections, such as viral or bacterial infections, can cause nerve damage and degeneration.
5. Autoimmune disorders: Conditions such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) are caused by the immune system attacking and damaging nerve cells.
6. Toxins: Exposure to certain toxins, such as heavy metals or pesticides, can damage and degenerate nerve cells.
7. Poor nutrition: A diet that is deficient in essential nutrients, such as vitamin B12 or other B vitamins, can lead to nerve damage and degeneration.
8. Alcoholism: Long-term alcohol abuse can cause nerve damage and degeneration due to the toxic effects of alcohol on nerve cells.
9. Drug use: Certain drugs, such as chemotherapy drugs and antiviral medications, can damage and degenerate nerve cells.
10. Aging: As we age, our nerve cells can deteriorate and become less functional, leading to a range of cognitive and motor symptoms.

It's important to note that in some cases, nerve damage and degeneration may be irreversible, but there are often strategies that can help manage symptoms and improve quality of life. If you suspect you have nerve damage or degeneration, it's important to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment.

Cardiovirus infections are a type of viral infection that affects the heart muscle, leading to cardiomyopathy and potentially heart failure. The most common cause of cardiovirus infections is the adenovirus, which is a common virus that can infect people of all ages.

Symptoms of Cardiovirus Infections:

The symptoms of cardiovirus infections can vary depending on the severity of the infection and the individual's overall health. Common symptoms include:

* Chest pain or discomfort
* Shortness of breath
* Fatigue
* Swelling of the legs, ankles, and feet
* Fast or irregular heartbeat
* Low blood pressure

Diagnosis of Cardiovirus Infections:

To diagnose a cardiovirus infection, a healthcare provider will typically perform a physical examination and ask about the individual's symptoms. They may also order one or more diagnostic tests, such as:

* Electrocardiogram (ECG) to measure the heart's electrical activity
* Echocardiogram to visualize the heart and its function
* Blood tests to look for signs of inflammation or cardiac damage

Treatment of Cardiovirus Infections:

There is no specific treatment for cardiovirus infections, but the following treatments may be recommended to manage symptoms and prevent complications:

* Rest and avoiding strenuous activities
* Medications to control heart rate and rhythm
* Diuretics to reduce fluid buildup in the body
* Oxygen therapy to improve oxygen levels in the blood

Prevention of Cardiovirus Infections:

Preventing cardiovirus infections is challenging, but taking steps to avoid exposure can help reduce the risk. These steps include:

* Practicing good hygiene, such as washing hands frequently and avoiding close contact with people who are sick
* Avoiding sharing food, drinks, or personal items with people who are sick
* Covering the mouth and nose when coughing or sneezing
* Staying home from work or school if experiencing symptoms

It is important to note that cardiovirus infections can be severe and potentially life-threatening, especially for certain populations such as older adults, young children, and people with underlying heart conditions. If you suspect you or someone else may have a cardiovirus infection, it is essential to seek medical attention right away.

1. Ovarian cysts: These are fluid-filled sacs that form on the ovaries. They can be benign (non-cancerous) or malignant (cancerous). Common symptoms include pelvic pain, bloating, and irregular periods.
2. Polycystic ovary syndrome (PCOS): This is a hormonal disorder that affects ovulation and can cause cysts on the ovaries. Symptoms include irregular periods, acne, and excess hair growth.
3. Endometriosis: This is a condition in which tissue similar to the lining of the uterus grows outside the uterus, often on the ovaries. Symptoms include pelvic pain, heavy bleeding, and infertility.
4. Ovarian cancer: This is a type of cancer that affects the ovaries. It is rare, but can be aggressive and difficult to treat. Symptoms include abdominal pain, bloating, and vaginal bleeding.
5. Premature ovarian failure (POF): This is a condition in which the ovaries stop functioning before the age of 40. Symptoms include hot flashes, vaginal dryness, and infertility.
6. Ovarian torsion: This is a condition in which the ovary becomes twisted, cutting off blood flow. Symptoms include severe pelvic pain, nausea, and vomiting.
7. Ovarian abscess: This is an infection that forms on the ovaries. Symptoms include fever, abdominal pain, and vaginal discharge.
8. Ectopic pregnancy: This is a condition in which a fertilized egg implants outside the uterus, often on the ovaries. Symptoms include severe pelvic pain, bleeding, and fainting.
9. Ovarian cysts: These are fluid-filled sacs that form on the ovaries. They can be benign or cancerous. Symptoms include abdominal pain, bloating, and irregular periods.
10. Polycystic ovary syndrome (PCOS): This is a hormonal disorder that affects the ovaries, causing symptoms such as irregular periods, cysts on the ovaries, and excess hair growth.

It's important to note that these are just a few examples of the many possible conditions that can affect the ovaries. If you experience any persistent or severe symptoms in your pelvic area, it is important to seek medical attention to determine the cause and receive proper treatment.

The most common symptoms of enterovirus infections include:

* Diarrhea
* Vomiting
* Fever
* Abdominal pain
* Headache
* Fatigue

In some cases, enterovirus infections can lead to more severe complications, such as:

* Hand, foot, and mouth disease (HFMD)
* Aseptic meningitis
* Encephalitis
* Myocarditis

Enteroviruses are highly contagious and can be spread through:

* Close contact with an infected person
* Contaminated food and water
* Insect vectors

There is no specific treatment for enterovirus infections, but symptoms can be managed with supportive care, such as hydration, rest, and pain relief. Antiviral medications may be used in severe cases.

Prevention measures include:

* Good hygiene practices, such as frequent handwashing
* Avoiding close contact with people who are sick
* Properly preparing and storing food and water
* Avoiding sharing items that come into contact with the mouth, such as utensils and drinking glasses.

Some common examples of neurodegenerative diseases include:

1. Alzheimer's disease: A progressive loss of cognitive function, memory, and thinking skills that is the most common form of dementia.
2. Parkinson's disease: A disorder that affects movement, balance, and coordination, causing tremors, rigidity, and difficulty with walking.
3. Huntington's disease: An inherited condition that causes progressive loss of cognitive, motor, and psychiatric functions.
4. Amyotrophic lateral sclerosis (ALS): A disease that affects the nerve cells responsible for controlling voluntary muscle movement, leading to muscle weakness, paralysis, and eventually death.
5. Prion diseases: A group of rare and fatal disorders caused by misfolded proteins in the brain, leading to neurodegeneration and death.
6. Creutzfeldt-Jakob disease: A rare, degenerative, and fatal brain disorder caused by an abnormal form of a protein called a prion.
7. Frontotemporal dementia: A group of diseases that affect the front and temporal lobes of the brain, leading to changes in personality, behavior, and language.

Neurodegenerative diseases can be caused by a variety of factors, including genetics, age, lifestyle, and environmental factors. They are typically diagnosed through a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment options for neurodegenerative diseases vary depending on the specific condition and its underlying causes, but may include medications, therapy, and lifestyle changes.

Preventing or slowing the progression of neurodegenerative diseases is a major focus of current research, with various potential therapeutic strategies being explored, such as:

1. Stem cell therapies: Using stem cells to replace damaged neurons and restore brain function.
2. Gene therapies: Replacing or editing genes that are linked to neurodegenerative diseases.
3. Small molecule therapies: Developing small molecules that can slow or prevent the progression of neurodegenerative diseases.
4. Immunotherapies: Harnessing the immune system to combat neurodegenerative diseases.
5. Lifestyle interventions: Promoting healthy lifestyle choices, such as regular exercise and a balanced diet, to reduce the risk of developing neurodegenerative diseases.

In conclusion, neurodegenerative diseases are a complex and diverse group of disorders that can have a profound impact on individuals and society. While there is currently no cure for these conditions, research is providing new insights into their causes and potential treatments. By continuing to invest in research and developing innovative therapeutic strategies, we can work towards improving the lives of those affected by neurodegenerative diseases and ultimately finding a cure.

There are several types of salivary gland diseases, including:

1. Parotid gland disease: This type of disease affects the parotid gland, which is located in the jaw and produces saliva to aid in digestion.
2. Sublingual gland disease: This type of disease affects the sublingual gland, which is located under the tongue and produces saliva to keep the mouth moist.
3. Submandibular gland disease: This type of disease affects the submandibular gland, which is located below the jaw and produces saliva to aid in digestion.
4. Mucocele: This is a benign tumor that occurs in the salivary glands and can cause swelling and pain.
5. Mucoceles: These are benign tumors that occur in the salivary glands and can cause swelling and pain.
6. Salivary gland stones: This is a condition where small stones form in the salivary glands and can cause pain and swelling.
7. Salivary gland cancer: This is a type of cancer that affects the salivary glands and can be treated with surgery, radiation therapy, or chemotherapy.
8. Sialadenitis: This is an inflammation of the salivary glands that can cause pain, swelling, and difficulty swallowing.
9. Sialosis: This is a condition where the salivary glands become blocked and cannot produce saliva.
10. Salivary gland cysts: These are fluid-filled sacs that occur in the salivary glands and can cause pain, swelling, and difficulty swallowing.

Salivary gland diseases can be diagnosed through a variety of tests, including imaging studies, biopsies, and blood tests. Treatment for these conditions depends on the specific type of disease and may include medications, surgery, or radiation therapy.

Some common types of connective tissue diseases include:

1. Rheumatoid arthritis (RA): A chronic autoimmune disorder that causes inflammation and joint damage.
2. Systemic lupus erythematosus (SLE): An autoimmune disorder that can affect multiple systems in the body, including the skin, joints, and kidneys.
3. Sjogren's syndrome: An autoimmune disorder that causes dry eyes and mouth, as well as joint pain and swelling.
4. Fibromyalgia: A chronic condition characterized by widespread muscle pain and fatigue.
5. Myositis: Inflammatory diseases that affect the muscles, such as dermatomyositis and polymyositis.
6. Giant cell arteritis: A condition that causes inflammation of the blood vessels, particularly in the head and neck.
7. Takayasu arteritis: A condition that causes inflammation of the blood vessels in the aorta and its branches.
8. Polyarteritis nodosa: A condition that causes inflammation of the blood vessels, particularly in the hands and feet.
9. IgG4-related disease: A condition characterized by inflammation and damage to various organs, including the pancreas, salivary glands, and liver.

Connective tissue diseases can cause a wide range of symptoms, including joint pain and stiffness, fatigue, skin rashes, fever, and weight loss. Treatment options vary depending on the specific disease and its severity, but may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs). In some cases, surgery or physical therapy may also be necessary.

Proteinuria is usually diagnosed by a urine protein-to-creatinine ratio (P/C ratio) or a 24-hour urine protein collection. The amount and duration of proteinuria can help distinguish between different underlying causes and predict prognosis.

Proteinuria can have significant clinical implications, as it is associated with increased risk of cardiovascular disease, kidney damage, and malnutrition. Treatment of the underlying cause can help reduce or eliminate proteinuria.

The term "immune complex disease" was first used in the 1960s to describe a group of conditions that were thought to be caused by the formation of immune complexes. These diseases include:

1. Systemic lupus erythematosus (SLE): an autoimmune disorder that can affect multiple organ systems and is characterized by the presence of anti-nuclear antibodies.
2. Rheumatoid arthritis (RA): an autoimmune disease that causes inflammation in the joints and can lead to joint damage.
3. Type III hypersensitivity reaction: a condition in which immune complexes are deposited in tissues, leading to inflammation and tissue damage.
4. Pemphigus: a group of autoimmune diseases that affect the skin and mucous membranes, characterized by the presence of autoantibodies against desmosomal antigens.
5. Bullous pemphigoid: an autoimmune disease that affects the skin and is characterized by the formation of large blisters.
6. Myasthenia gravis: an autoimmune disorder that affects the nervous system, causing muscle weakness and fatigue.
7. Goodpasture's syndrome: a rare autoimmune disease that affects the kidneys and lungs, characterized by the presence of immune complexes in the glomeruli of the kidneys.
8. Hemolytic uremic syndrome (HUS): a condition in which red blood cells are destroyed and waste products accumulate in the kidneys, leading to kidney failure.

Immune complex diseases can be caused by various factors, including genetic predisposition, environmental triggers, and exposure to certain drugs or toxins. Treatment options for these diseases include medications that suppress the immune system, such as corticosteroids and immunosuppressive drugs, and plasmapheresis, which is a process that removes harmful antibodies from the blood. In some cases, organ transplantation may be necessary.

In conclusion, immune complex diseases are a group of disorders that occur when the body's immune system mistakenly attacks its own tissues and organs, leading to inflammation and damage. These diseases can affect various parts of the body, including the skin, kidneys, lungs, and nervous system. Treatment options vary depending on the specific disease and its severity, but may include medications that suppress the immune system and plasmapheresis.

Recurrence can also refer to the re-emergence of symptoms in a previously treated condition, such as a chronic pain condition that returns after a period of remission.

In medical research, recurrence is often studied to understand the underlying causes of disease progression and to develop new treatments and interventions to prevent or delay its return.

The symptoms of GBS can range from mild to severe and may include:

* Weakness or tingling sensations in the legs, arms, or face
* Muscle weakness that progresses to paralysis
* Loss of reflexes
* Difficulty swallowing or speaking
* Numbness or pain in the hands and feet
* Fatigue and fever

The diagnosis of GBS is based on a combination of symptoms, physical examination findings, and laboratory tests. There is no cure for GBS, but treatment can help manage symptoms and prevent complications. Plasmapheresis, immunoglobulin therapy, and corticosteroids are common treatments used to reduce inflammation and slow the progression of the disease.

GBS is a rare condition that affects about one in 100,000 people per year in the United States. It can affect anyone, but it is more common in children and young adults. The prognosis for GBS varies depending on the severity of the disease, but most people recover fully within a few weeks or months with proper treatment.

In conclusion, Guillain-Barré Syndrome is a rare autoimmune disorder that can cause muscle weakness and paralysis. While there is no cure for GBS, early diagnosis and treatment can help manage symptoms and prevent complications. With proper care, most people with GBS can recover fully within a few weeks or months.

Benign spinal cord neoplasms are typically slow-growing and may not cause any symptoms in the early stages. However, as they grow, they can compress or damage the surrounding healthy tissue, leading to a range of symptoms such as pain, numbness, weakness, or paralysis.

Malignant spinal cord neoplasms are more aggressive and can grow rapidly, invading surrounding tissues and spreading to other parts of the body. They can cause similar symptoms to benign tumors, as well as other symptoms such as fever, nausea, and weight loss.

The diagnosis of spinal cord neoplasms is based on a combination of clinical findings, imaging studies (such as MRI or CT scans), and biopsy. Treatment options vary depending on the type and location of the tumor, but may include surgery, radiation therapy, and chemotherapy.

The prognosis for spinal cord neoplasms depends on the type and location of the tumor, as well as the patient's overall health. In general, benign tumors have a better prognosis than malignant tumors, and early diagnosis and treatment can improve outcomes. However, even with successful treatment, some patients may experience long-term neurological deficits or other complications.

The symptoms of PAN can vary depending on the location and severity of the inflammation, but may include:

* Fever
* Headache
* Joint pain and swelling
* Skin rash or lesions
* Abdominal pain
* Weight loss
* Fatigue
* Numbness or weakness in the limbs

The exact cause of PAN is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissues. It can occur at any age, but is more common in adults between the ages of 40 and 60.

There is no cure for PAN, but treatment options include:

* Corticosteroids to reduce inflammation
* Immunosuppressive drugs to suppress the immune system
* Plasmapheresis to remove harmful antibodies from the blood
* Biologics to target specific proteins involved in the disease process

The prognosis for PAN varies depending on the severity and location of the inflammation, as well as the promptness and effectiveness of treatment. In general, the condition can be challenging to diagnose and treat, and the long-term outcome is often uncertain.

There are several types of hypersensitivity reactions, including:

1. Type I hypersensitivity: This is also known as immediate hypersensitivity and occurs within minutes to hours after exposure to the allergen. It is characterized by the release of histamine and other chemical mediators from immune cells, leading to symptoms such as hives, itching, swelling, and difficulty breathing. Examples of Type I hypersensitivity reactions include allergies to pollen, dust mites, or certain foods.
2. Type II hypersensitivity: This is also known as cytotoxic hypersensitivity and occurs within days to weeks after exposure to the allergen. It is characterized by the immune system producing antibodies against specific proteins on the surface of cells, leading to their destruction. Examples of Type II hypersensitivity reactions include blood transfusion reactions and serum sickness.
3. Type III hypersensitivity: This is also known as immune complex hypersensitivity and occurs when antigens bind to immune complexes, leading to the formation of deposits in tissues. Examples of Type III hypersensitivity reactions include rheumatoid arthritis and systemic lupus erythematosus.
4. Type IV hypersensitivity: This is also known as delayed-type hypersensitivity and occurs within weeks to months after exposure to the allergen. It is characterized by the activation of T cells, leading to inflammation and tissue damage. Examples of Type IV hypersensitivity reactions include contact dermatitis and toxic epidermal necrolysis.

The diagnosis of hypersensitivity often involves a combination of medical history, physical examination, laboratory tests, and elimination diets or challenges. Treatment depends on the specific type of hypersensitivity reaction and may include avoidance of the allergen, medications such as antihistamines or corticosteroids, and immunomodulatory therapy.

The endocrine system is a network of glands and hormones that regulate various bodily functions, such as growth, development, metabolism, and reproductive processes. Endocrine system diseases refer to disorders or abnormalities that affect one or more of the endocrine glands or the hormones they produce.

Types of Endocrine System Diseases:

1. Diabetes Mellitus (DM): A group of metabolic disorders characterized by high blood sugar levels due to insulin deficiency or insulin resistance.
2. Hypothyroidism: A condition where the thyroid gland does not produce enough thyroid hormones, leading to symptoms such as fatigue, weight gain, and cold intolerance.
3. Hyperthyroidism: A condition where the thyroid gland produces too much thyroid hormone, leading to symptoms such as anxiety, weight loss, and heart palpitations.
4. Cushing's Syndrome: A rare disorder caused by excessive levels of cortisol hormone in the body, leading to symptoms such as weight gain, high blood pressure, and mood changes.
5. Addison's Disease: A rare disorder caused by a deficiency of cortisol and aldosterone hormones in the body, leading to symptoms such as fatigue, weight loss, and dehydration.
6. Pituitary Gland Disorders: Tumors or cysts in the pituitary gland can affect the production of hormones that regulate other endocrine glands.
7. Adrenal Insufficiency: A condition where the adrenal glands do not produce enough cortisol and aldosterone hormones, leading to symptoms such as fatigue, weight loss, and dehydration.
8. Polycystic Ovary Syndrome (PCOS): A hormonal disorder that affects women of reproductive age, characterized by irregular menstrual cycles, cysts on the ovaries, and insulin resistance.
9. Graves' Disease: An autoimmune disorder that causes hyperthyroidism (an overactive thyroid gland), leading to symptoms such as rapid weight loss, nervousness, and heart palpitations.
10. Hashimoto's Thyroiditis: An autoimmune disorder that causes hypothyroidism (an underactive thyroid gland), leading to symptoms such as fatigue, weight gain, and depression.

These are just a few examples of endocrine disorders, and there are many more that can affect different parts of the endocrine system. It's important to be aware of the signs and symptoms of these disorders so that you can seek medical attention if you experience any unusual changes in your body.

The main features of scleroderma, limited, include:

1. Skin thickening and hardening on the hands and face, which can be painful and limit movement.
2. Swelling and inflammation in the fingers (called "hand pitting").
3. Thickening and tightening of the skin on the face, which can cause facial distortion.
4. Inflammation of the digestive tract, leading to abdominal pain, diarrhea, and constipation.
5. Increased risk of kidney problems and high blood pressure.
6. Muscle weakness and fatigue.
7. Joint pain and stiffness.
8. Raynaud's phenomenon (a condition that causes discoloration and pain in the fingers and toes when exposed to cold or stress).

Scleroderma, limited, is a chronic disease, and there is no cure. Treatment focuses on managing symptoms and preventing complications. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive drugs may be prescribed to reduce inflammation and slow disease progression. Physical therapy and lifestyle modifications, such as regular exercise and stress management techniques, can also help manage symptoms and improve quality of life.

There are several subtypes of localized scleroderma, including:

* Linear morphea: This is the most common form of localized scleroderma and appears as a linear or polylinear band of hardened skin on the arms, legs, or torso.
* Plaque morphea: This type of scleroderma causes flat, disk-shaped patches of thickened skin that can be red, purple, or brown.
* Guttate morphea: This form of localized scleroderma is characterized by numerous small, drop-like lesions on the arms, legs, or torso.

The exact cause of localized scleroderma is not known, but it is believed to be an autoimmune disorder that triggers the immune system to attack healthy tissue in the skin. The condition can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as biopsies or imaging studies.

Treatment for localized scleroderma typically involves topical medications, such as corticosteroids or immunosuppressants, to reduce inflammation and slow the progression of the disease. In some cases, phototherapy or physical therapy may also be recommended to improve symptoms and prevent complications.

While there is no cure for localized scleroderma, early diagnosis and appropriate treatment can help manage the condition and improve quality of life for those affected.

Anatomy45

Organisms14

Diseases72

Chemicals and Drugs66

Analytical, Diagnostic and Therapeutic Techniques and Equipment28

Phenomena and Processes36

Disciplines and Occupations1

Information Science3

Health Care2

The heat-stable antigen determines pathogenicity of self-reactive T cells in experimental autoimmune encephalomyelitis. (1/107)

Oligoclonal T cell repertoire in cerebrospinal fluid of patients with inflammatory diseases of the nervous system. (2/107)

Paraneoplastic peripheral neuropathy associated with anti-Hu antibodies. A clinical and electrophysiological study of 20 patients. (3/107)

Myelin protein P0-specific IgM producing monoclonal B cell lines were established from polyneuropathy patients with monoclonal gammopathy of undetermined significance (MGUS). (4/107)

Autoimmunity and the basal ganglia: new insights into old diseases. (5/107)

Immunization with neuronal nicotinic acetylcholine receptor induces neurological autoimmune disease. (6/107)

Thyrotoxic autoimmune encephalopathy: a repeat positron emission tomography study. (7/107)

Tourette's syndrome: a cross sectional study to examine the PANDAS hypothesis. (8/107)

Autoimmune Diseases

Central Nervous System

Nervous System

Autoimmunity

Autoantibodies

Lupus Erythematosus, Systemic

Central Nervous System Diseases

Peripheral Nervous System

Encephalomyelitis, Autoimmune, Experimental

Autoantigens

Autoimmune Diseases of the Nervous System

Enteric Nervous System

Central Nervous System Neoplasms

T-Lymphocytes

Mice, Inbred C57BL

Multiple Sclerosis

Sjogren's Syndrome

Antibodies, Antinuclear

Autonomic Nervous System

Brain

Sympathetic Nervous System

Mice, Inbred MRL lpr

Nervous System Physiological Phenomena

Lymphocyte Activation

Arthritis, Rheumatoid

Disease Models, Animal

Diabetes Mellitus, Type 1

T-Lymphocytes, Regulatory

Nervous System Diseases

Mice, Transgenic

B-Lymphocytes

Mice, Knockout

Central Nervous System Infections

Immune Tolerance

Neurons

Myelin Basic Protein

Thyroiditis, Autoimmune

Molecular Sequence Data

Oophoritis

Nervous System Neoplasms

Mice, Inbred NZB

Self Tolerance

CD4-Positive T-Lymphocytes

Mice, Inbred NOD

Vitiligo

Interleukin-17

Immunoglobulin G

Myelin-Oligodendrocyte Glycoprotein

Cells, Cultured

Cytokines

Spinal Cord

Nervous System Autoimmune Disease, Experimental

Th17 Cells

Demyelinating Autoimmune Diseases, CNS

Genetic Predisposition to Disease

Mice, Inbred Strains

Signal Transduction

Amino Acid Sequence

Scleroderma, Systemic

Rats, Inbred Lew

Rheumatic Diseases

Myelin Proteins

Mice, Inbred BALB C

Spleen

T-Lymphocyte Subsets

Cell Differentiation

Central Nervous System Viral Diseases

Adoptive Transfer

Protein Tyrosine Phosphatase, Non-Receptor Type 22

Th1 Cells

Inflammation

Molecular Mimicry

Myelin-Associated Glycoprotein

Myelin Proteolipid Protein

Arthritis, Experimental

Myasthenia Gravis

Immunosuppressive Agents

Hashimoto Disease

Interferon-gamma

Flow Cytometry