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)
The most common clinical variant of MULTIPLE SCLEROSIS, characterized by recurrent acute exacerbations of neurologic dysfunction followed by partial or complete recovery. Common clinical manifestations include loss of visual (see OPTIC NEURITIS), motor, sensory, or bladder function. Acute episodes of demyelination may occur at any site in the central nervous system, and commonly involve the optic nerves, spinal cord, brain stem, and cerebellum. (Adams et al., Principles of Neurology, 6th ed, pp903-914)
A form of multiple sclerosis characterized by a progressive deterioration in neurologic function which is in contrast to the more typical relapsing remitting form. If the clinical course is free of distinct remissions, it is referred to as primary progressive multiple sclerosis. When the progressive decline is punctuated by acute exacerbations, it is referred to as progressive relapsing multiple sclerosis. The term secondary progressive multiple sclerosis is used when relapsing remitting multiple sclerosis evolves into the chronic progressive form. (From Ann Neurol 1994;36 Suppl:S73-S79; Adams et al., Principles of Neurology, 6th ed, pp903-914)
A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve.
A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)
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)
Autosomal dominant neurocutaneous syndrome classically characterized by MENTAL RETARDATION; EPILEPSY; and skin lesions (e.g., adenoma sebaceum and hypomelanotic macules). There is, however, considerable heterogeneity in the neurologic manifestations. It is also associated with cortical tuber and HAMARTOMAS formation throughout the body, especially the heart, kidneys, and eyes. Mutations in two loci TSC1 and TSC2 that encode hamartin and tuberin, respectively, are associated with the disease.
Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.
Inflammation of the optic nerve. Commonly associated conditions include autoimmune disorders such as MULTIPLE SCLEROSIS, infections, and granulomatous diseases. Clinical features include retro-orbital pain that is aggravated by eye movement, loss of color vision, and contrast sensitivity that may progress to severe visual loss, an afferent pupillary defect (Marcus-Gunn pupil), and in some instances optic disc hyperemia and swelling. Inflammation may occur in the portion of the nerve within the globe (neuropapillitis or anterior optic neuritis) or the portion behind the globe (retrobulbar neuritis or posterior optic neuritis).
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.
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
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.
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.
Multiple protein bands serving as markers of specific ANTIBODIES and detected by ELECTROPHORESIS of CEREBROSPINAL FLUID or serum. The bands are most often seen during inflammatory or immune processes and are found in most patients with MULTIPLE SCLEROSIS.
One of the type I interferons produced by fibroblasts in response to stimulation by live or inactivated virus or by double-stranded RNA. It is a cytokine with antiviral, antiproliferative, and immunomodulating activity.
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.
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.
A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.
Determination of the degree of a physical, mental, or emotional handicap. The diagnosis is applied to legal qualification for benefits and income under disability insurance and to eligibility for Social Security and workmen's compensation benefits.
MYELIN-specific proteins that play a structural or regulatory role in the genesis and maintenance of the lamellar MYELIN SHEATH structure.
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.
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 syndrome characterized by acute OPTIC NEURITIS; MYELITIS, TRANSVERSE; demyelinating and/or necrotizing lesions in the OPTIC NERVES and SPINAL CORD; and presence of specific autoantibodies to AQUAPORIN 4.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.
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)
Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.
Biologically active substances whose activities affect or play a role in the functioning of the immune system.
A broad specificity HLA-DR antigen that is associated with HLA-DRB1 CHAINS encoded by DRB1*01:15 and DRB1*01:16 alleles.
An acute or subacute inflammatory process of the CENTRAL NERVOUS SYSTEM characterized histologically by multiple foci of perivascular demyelination. Symptom onset usually occurs several days after an acute viral infection or immunization, but it may coincide with the onset of infection or rarely no antecedent event can be identified. Clinical manifestations include CONFUSION, somnolence, FEVER, nuchal rigidity, and involuntary movements. The illness may progress to COMA and eventually be fatal. (Adams et al., Principles of Neurology, 6th ed, p921)
Copper chelator that inhibits monoamine oxidase and causes liver and brain damage.
A class of nerve fibers as defined by their structure, specifically the nerve sheath arrangement. The AXONS of the myelinated nerve fibers are completely encased in a MYELIN SHEATH. They are fibers of relatively large and varied diameters. Their NEURAL CONDUCTION rates are faster than those of the unmyelinated nerve fibers (NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.
A rare central nervous system demyelinating condition affecting children and young adults. Pathologic findings include a large, sharply defined, asymmetric focus of myelin destruction that may involve an entire lobe or cerebral hemisphere. The clinical course tends to be progressive and includes dementia, cortical blindness, cortical deafness, spastic hemiplegia, and pseudobulbar palsy. Concentric sclerosis of Balo is differentiated from diffuse cerebral sclerosis of Schilder by the pathologic finding of alternating bands of destruction and preservation of myelin in concentric rings. Alpers' Syndrome refers to a heterogeneous group of diseases that feature progressive cerebral deterioration and liver disease. (From Adams et al., Principles of Neurology, 6th ed, p914; Dev Neurosci 1991;13(4-5):267-73)
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.
Derivatives of propylene glycol (1,2-propanediol). They are used as humectants and solvents in pharmaceutical preparations.
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.
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 species of CARDIOVIRUS which contains three strains: Theiler's murine encephalomyelitis virus, Vilyuisk human encephalomyelitis virus, and Rat encephalomyelitis virus.
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.
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.
The return of a sign, symptom, or disease after a remission.
The age, developmental stage, or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual.
A watery fluid that is continuously produced in the CHOROID PLEXUS and circulates around the surface of the BRAIN; SPINAL CORD; and in the CEREBRAL VENTRICLES.
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.
A subtype of HLA-DRB beta chains that includes over one hundred allele variants. The HLA-DRB1 subtype is associated with several of the HLA-DR SEROLOGICAL SUBTYPES.
Proteins in the cerebrospinal fluid, normally albumin and globulin present in the ratio of 8 to 1. Increases in protein levels are of diagnostic value in neurological diseases. (Brain and Bannister's Clinical Neurology, 7th ed, p221)
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 2nd cranial nerve which conveys visual information from the RETINA to the brain. The nerve carries the axons of the RETINAL GANGLION CELLS which sort at the OPTIC CHIASM and continue via the OPTIC TRACTS to the brain. The largest projection is to the lateral geniculate nuclei; other targets include the SUPERIOR COLLICULI and the SUPRACHIASMATIC NUCLEI. Though known as the second cranial nerve, it is considered part of the CENTRAL NERVOUS SYSTEM.
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
Infections caused by viruses of the genus CARDIOVIRUS, family PICORNAVIRIDAE.
Assessment of sensory and motor responses and reflexes that is used to determine impairment of the nervous system.
A spontaneous diminution or abatement of a disease over time, without formal treatment.
The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.
Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.
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.
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.
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 PREDNISOLONE derivative with similar anti-inflammatory action.
The electric response evoked in the cerebral cortex by visual stimulation or stimulation of the visual pathways.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
A rapid onset form of SYSTEMIC SCLERODERMA with progressive widespread SKIN thickening over the arms, the legs and the trunk, resulting in stiffness and disability.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
A subclass of HLA-D antigens that consist of alpha and beta chains. The inheritance of HLA-DR antigens differs from that of the HLA-DQ ANTIGENS and HLA-DP ANTIGENS.
Elements of limited time intervals, contributing to particular results or situations.
A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
Gadolinium. An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors.
A general term indicating inflammation of a peripheral or cranial nerve. Clinical manifestation may include PAIN; PARESTHESIAS; PARESIS; or HYPESTHESIA.
Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
Inflammation of a transverse portion of the spinal cord characterized by acute or subacute segmental demyelination or necrosis. The condition may occur sporadically, follow an infection or vaccination, or present as a paraneoplastic syndrome (see also ENCEPHALOMYELITIS, ACUTE DISSEMINATED). Clinical manifestations include motor weakness, sensory loss, and incontinence. (Adams et al., Principles of Neurology, 6th ed, pp1242-6)
Improvement of the quality of a picture by various techniques, including computer processing, digital filtering, echocardiographic techniques, light and ultrastructural MICROSCOPY, fluorescence spectrometry and microscopy, scintigraphy, and in vitro image processing at the molecular level.
Persons with physical or mental disabilities that affect or limit their activities of daily living and that may require special accommodations.
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.
Diseases of any component of the brain (including the cerebral hemispheres, diencephalon, brain stem, and cerebellum) or the spinal cord.
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.
The statistical reproducibility of measurements (often in a clinical context), including the testing of instrumentation or techniques to obtain reproducible results. The concept includes reproducibility of physiological measurements, which may be used to develop rules to assess probability or prognosis, or response to a stimulus; reproducibility of occurrence of a condition; and reproducibility of experimental results.
A class of statistical methods applicable to a large set of probability distributions used to test for correlation, location, independence, etc. In most nonparametric statistical tests, the original scores or observations are replaced by another variable containing less information. An important class of nonparametric tests employs the ordinal properties of the data. Another class of tests uses information about whether an observation is above or below some fixed value such as the median, and a third class is based on the frequency of the occurrence of runs in the data. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1284; Corsini, Concise Encyclopedia of Psychology, 1987, p764-5)
Broad plate of dense myelinated fibers that reciprocally interconnect regions of the cortex in all lobes with corresponding regions of the opposite hemisphere. The corpus callosum is located deep in the longitudinal fissure.
Substances that augment, stimulate, activate, potentiate, or modulate the immune response at either the cellular or humoral level. The classical agents (Freund's adjuvant, BCG, Corynebacterium parvum, et al.) contain bacterial antigens. Some are endogenous (e.g., histamine, interferon, transfer factor, tuftsin, interleukin-1). Their mode of action is either non-specific, resulting in increased immune responsiveness to a wide variety of antigens, or antigen-specific, i.e., affecting a restricted type of immune response to a narrow group of antigens. The therapeutic efficacy of many biological response modifiers is related to their antigen-specific immunoadjuvanticity.
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.
Pathologic conditions which feature SPINAL CORD damage or dysfunction, including disorders involving the meninges and perimeningeal spaces surrounding the spinal cord. Traumatic injuries, vascular diseases, infections, and inflammatory/autoimmune processes may affect the spinal cord.
Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.
Diseases characterized by a selective degeneration of the motor neurons of the spinal cord, brainstem, or motor cortex. Clinical subtypes are distinguished by the major site of degeneration. In AMYOTROPHIC LATERAL SCLEROSIS there is involvement of upper, lower, and brainstem motor neurons. In progressive muscular atrophy and related syndromes (see MUSCULAR ATROPHY, SPINAL) the motor neurons in the spinal cord are primarily affected. With progressive bulbar palsy (BULBAR PALSY, PROGRESSIVE), the initial degeneration occurs in the brainstem. In primary lateral sclerosis, the cortical neurons are affected in isolation. (Adams et al., Principles of Neurology, 6th ed, p1089)
The least progressive form of SYSTEMIC SCLERODERMA with skin thickening restricted to the face, neck and areas distal to the elbows and/or knees, sparing the trunk. The CREST SYNDROME is a form of limited scleroderma.
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.
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.
A rare, slowly progressive encephalitis caused by chronic infection with the MEASLES VIRUS. The condition occurs primarily in children and young adults, approximately 2-8 years after the initial infection. A gradual decline in intellectual abilities and behavioral alterations are followed by progressive MYOCLONUS; MUSCLE SPASTICITY; SEIZURES; DEMENTIA; autonomic dysfunction; and ATAXIA. DEATH usually occurs 1-3 years after disease onset. Pathologic features include perivascular cuffing, eosinophilic cytoplasmic inclusions, neurophagia, and fibrous gliosis. It is caused by the SSPE virus, which is a defective variant of MEASLES VIRUS. (From Adams et al., Principles of Neurology, 6th ed, pp767-8)
A technique of inputting two-dimensional images into a computer and then enhancing or analyzing the imagery into a form that is more useful to the human observer.
Type III intermediate filament proteins that assemble into neurofilaments, the major cytoskeletal element in nerve axons and dendrites. They consist of three distinct polypeptides, the neurofilament triplet. Types I, II, and IV intermediate filament proteins form other cytoskeletal elements such as keratins and lamins. It appears that the metabolism of neurofilaments is disturbed in Alzheimer's disease, as indicated by the presence of neurofilament epitopes in the neurofibrillary tangles, as well as by the severe reduction of the expression of the gene for the light neurofilament subunit of the neurofilament triplet in brains of Alzheimer's patients. (Can J Neurol Sci 1990 Aug;17(3):302)
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.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
The three membranes that cover the BRAIN and the SPINAL CORD. They are the dura mater, the arachnoid, and the pia mater.
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.
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.
Disturbances in mental processes related to learning, thinking, reasoning, and judgment.
Inflammation of the BRAIN due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see ENCEPHALITIS, VIRAL) are a relatively frequent cause of this condition.
An opportunistic viral infection of the central nervous system associated with conditions that impair cell-mediated immunity (e.g., ACQUIRED IMMUNODEFICIENCY SYNDROME and other IMMUNOLOGIC DEFICIENCY SYNDROMES; HEMATOLOGIC NEOPLASMS; IMMUNOSUPPRESSION; and COLLAGEN DISEASES). The causative organism is JC Polyomavirus (JC VIRUS) which primarily affects oligodendrocytes, resulting in multiple areas of demyelination. Clinical manifestations include DEMENTIA; ATAXIA; visual disturbances; and other focal neurologic deficits, generally progressing to a vegetative state within 6 months. (From Joynt, Clinical Neurology, 1996, Ch26, pp36-7)
Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)
Diseases of viral origin, characterized by incubation periods of months to years, insidious onset of clinical manifestations, and protracted clinical course. Though the disease process is protracted, viral multiplication may not be unusually slow. Conventional viruses produce slow virus diseases such as SUBACUTE SCLEROSING PANENCEPHALITIS, progressive multifocal leukoencephalopathy (LEUKOENCEPHALOPATHY, PROGRESSIVE MULTIFOCAL), and AIDS. Diseases produced by unconventional agents were originally considered part of this group. They are now called PRION DISEASES.
The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.
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.
The part of the brain that connects the CEREBRAL HEMISPHERES with the SPINAL CORD. It consists of the MESENCEPHALON; PONS; and MEDULLA OBLONGATA.
A form of muscle hypertonia associated with upper MOTOR NEURON DISEASE. Resistance to passive stretch of a spastic muscle results in minimal initial resistance (a "free interval") followed by an incremental increase in muscle tone. Tone increases in proportion to the velocity of stretch. Spasticity is usually accompanied by HYPERREFLEXIA and variable degrees of MUSCLE WEAKNESS. (From Adams et al., Principles of Neurology, 6th ed, p54)

Mental change as an early feature of multiple sclerosis. (1/4431)

Five patients with mental change as a prominent and early feature of an illness which appeared to be multiple sclerosis are reported. All the patients had in addition clinical signs of predominant brain stem involvement and the cerebrospinal fluid findings were similar. It is emphasised that mental change may be an early feature of multiple sclerosis even in those patients in whom the onset of the disease is insidious.  (+info)

Activated human T cells, B cells, and monocytes produce brain-derived neurotrophic factor in vitro and in inflammatory brain lesions: a neuroprotective role of inflammation? (2/4431)

Brain-derived neurotrophic factor (BDNF) has potent effects on neuronal survival and plasticity during development and after injury. In the nervous system, neurons are considered the major cellular source of BDNF. We demonstrate here that in addition, activated human T cells, B cells, and monocytes secrete bioactive BDNF in vitro. Notably, in T helper (Th)1- and Th2-type CD4(+) T cell lines specific for myelin autoantigens such as myelin basic protein or myelin oligodendrocyte glycoprotein, BDNF production is increased upon antigen stimulation. The BDNF secreted by immune cells is bioactive, as it supports neuronal survival in vitro. Using anti-BDNF monoclonal antibody and polyclonal antiserum, BDNF immunoreactivity is demonstrable in inflammatory infiltrates in the brain of patients with acute disseminated encephalitis and multiple sclerosis. The results raise the possibility that in the nervous system, inflammatory infiltrates have a neuroprotective effect, which may limit the success of nonselective immunotherapies.  (+info)

Cortical lesions in multiple sclerosis. (3/4431)

Although previous studies have shown that the lesions of multiple sclerosis may involve the cerebral cortex, there is little published research on the prevalence and distribution of such lesions. Using neuropathological techniques and MRI, a series of studies has been undertaken in order to assess this, in particular to identify their relationship to cortical veins. A serial MRI study showed that the use of gadolinium proffered an increase in cortical lesion detection of 140% and showed that 26% of active lesions arose within or adjacent to the cortex. In a post-mortem study, MRI under-reported lesions subsequently analysed neuropathologically, particularly those arising within the cortex. In a further 12 cases examined, 478 cortical lesions were identified, of which 372 also involved the subcortical white matter. Seven different lesion types were identified; the majority arose within the territory of the principal cortical veins, whilst the remaining quarter arose within the territory of the small branch or superficial veins. Small cortical lesions are common in multiple sclerosis and are under-reported by MRI. Investigation of the cortical venous supply shows how such lesions may arise, and why the majority also involve the underlying white matter.  (+info)

The psychometric properties of clinical rating scales used in multiple sclerosis. (4/4431)

OullII;l y Many clinical rating scales have been proposed to assess the impact of multiple sclerosis on patients, but only few have been evaluated formally for reliability, validity and responsiveness. We assessed the psychometric properties of five commonly used scales in multiple sclerosis, the Expanded Disability Status Scale (EDSS), the Scripps Neurological Rating Scale (SNRS), the Functional Independence Measure (FIM), the Ambulation Index (AI) and the Cambridge Multiple Sclerosis Basic Score (CAMBS). The score frequency distributions of all five scales were either bimodal (EDSS and AI) or severely skewed (SNRS, FIM and CAMBS). The reliability of each scale depended on the definition of 'agreement'. Inter-and intra-rater reliabilities were high when 'agreement' was considered to exist despite a difference of up to 1.0 EDSS point (two 0.5 steps), 13 SNRS points, 9 FIM points, 1 AI point and 1 point on the various CAMBS domains. The FIM, AI, and the relapse and progression domains of the CAMBS were sensitive to clinical change, but the EDSS and the SNRS were unresponsive. The validity of these scales as impairment (SNRS and EDSS) and disability (EDSS, FIM, AI and the disability domain of the CAMBS) measures was established. All scales correlated closely with other measures of handicap and quality of life. None of these scales satisfied the psychometric requirements of outcome measures completely, but each had some desirable properties. The SNRS and the EDSS were reliable and valid measures of impairment and disability, but they were unresponsive. The FIM was a reliable, valid and responsive measure of disability, but it is cumbersome to administer and has a limited content validity. The AI was a reliable and valid ambulation-related disability scale, but it was weakly responsive. The CAMBS was a reliable (all four domains) and responsive (relapse and progression domains) outcome measure, but had a limited validity (handicap domain). These psychometric properties should be considered when designing further clinical trials in multiple sclerosis.  (+info)

Respiratory muscle involvement in multiple sclerosis. (5/4431)

Respiratory complications are common in the terminal stages of multiple sclerosis and contribute to mortality in these patients. When respiratory motor pathways are involved, respiratory muscle weakness frequently occurs. Although it is well established that weakness of the respiratory muscles produces a restrictive ventilatory defect, the degree of muscle weakness and pulmonary function are poorly related. Respiratory muscle weakness was observed in patients with normal or near normal pulmonary function. Expiratory muscle weakness is more prominent than inspiratory muscle weakness and may impair performance of coughing. Subsequently, in addition to bulbar dysfunction, respiratory muscle weakness may contribute to ineffective coughing, pneumonia, and sometimes even acute ventilatory failure may ensue. Respiratory muscle weakness may also occur early in the course of the disease. Recent studies suggest that the respiratory muscles can be trained for both strength and endurance in multiple sclerosis patients. Whether respiratory muscle training delays the development of respiratory dysfunction and subsequently improves exercise capacity and cough efficacy, prevents pulmonary complications or prolongs survival in the long-term remains to be determined.  (+info)

Non-coding plasmid DNA induces IFN-gamma in vivo and suppresses autoimmune encephalomyelitis. (6/4431)

Regulatory sequences used in plasmids for naked DNA vaccination can modulate cytokine production in vivo. We demonstrate here that injection of plasmid DNA can suppress the prototypic T cell-mediated autoimmune disease, experimental autoimmune encephalomyelitis, by inducing IFN-gamma.  (+info)

Serum gelatinase B, TIMP-1 and TIMP-2 levels in multiple sclerosis. A longitudinal clinical and MRI study. (7/4431)

Metalloproteinases have been implicated in the pathogenesis of multiple sclerosis. We report longitudinal serum levels of gelatinase B and of the tissue inhibitors of matrix metalloproteinases (TIMP), TIMP-1 and TIMP-2, in 21 patients with relapsing multiple sclerosis. Patients had monthly clinical and gadolinium-enhanced MRI follow-up for 10 months. Longitudinal samples in nine healthy controls and cross-sectional samples from 12 patients with inflammatory CNS disease and 15 patients with other neurological diseases were used for comparison. Average serum gelatinase B, TIMP-1 and TIMP-2 levels were significantly higher in multiple sclerosis patients and those with other neurological diseases than in healthy controls. In the patients with multiple sclerosis, gelatinase B levels were significantly higher during clinical relapse compared with periods of clinical stability. Multiple sclerosis patients with high mean serum gelatinase B levels had significantly more T1-weighted gadolinium-enhancing MRI lesions than those with mean levels within the control range. TIMP-1 levels were not different during relapse and between relapses. There was a trend for TIMP-2 levels to be lower during relapse compared with non-relapse periods. For similar levels of serum gelatinase B, associated TIMP-1 levels were significantly lower and TIMP-2 levels significantly higher in multiple sclerosis patients compared with the inflammatory CNS control group. We propose that an abnormality in the inhibitory response to metalloproteinases may play an aetiological role in the chronicity of multiple sclerosis.  (+info)

A clinical study of motor evoked potentials using a triple stimulation technique. (8/4431)

Amplitudes of motor evoked potentials (MEPs) are usually much smaller than those of motor responses to maximal peripheral nerve stimulation, and show marked variation between normal subjects and from one stimulus to another. Consequently, amplitude measurements have low sensitivity to detect central motor conduction failures due to the broad range of normal values. Since these characteristics are mostly due to varying desynchronization of the descending action potentials, causing different degrees of phase cancellation, we applied the recently developed triple stimulation technique (TST) to study corticospinal conduction to 489 abductor digiti minimi muscles of 271 unselected patients referred for possible corticospinal dysfunction. The TST allows resynchronization of the MEP, and thereby a quantification of the proportion of motor units activated by the transcranial stimulus. TST results were compared with those of conventional MEPs. In 212 of 489 sides, abnormal TST responses suggested conduction failure of various degrees. By contrast, conventional MEPs detected conduction failures in only 77 of 489 sides. The TST was therefore 2.75 times more sensitive than conventional MEPs in disclosing corticospinal conduction failures. When the results of the TST and conventional MEPs were combined, 225 sides were abnormal: 145 sides showed central conduction failure, 13 sides central conduction slowing and 67 sides both conduction failure and slowing. It is concluded that the TST is a valuable addition to the study of MEPs, since it improves detection and gives quantitative information on central conduction failure, an abnormality which appears to be much more frequent than conduction slowing. This new technique will be useful in following the natural course and the benefit of treatments in disorders affecting central motor conduction.  (+info)

Fingolimod is the much anticipated oral disease modifying treatment for patients with highly active Multiple sclerosis. A total of 42 patients were commenced on Fingolimod from December 2012 to June 2014 in Leeds Hospitals NHS Trust.. Four patients discontinued treatment due to patient choice, consecutive severe relapses and hepatotoxicity. No other severe side effects were noted in these 42 patients. A total of ten relapses were seen in nine patients. Of which eight out of ten relapses occurred within the first two months. Of the nine patients who experienced relapses, five (55%) were previously treated with Natalizumab, as opposed to four on injectable Disease Modifying Treatments (45%).. The five patients previously treated with Natalizumab all underwent a three month wash out period prior to commencing Fingolimod. The relapses all took place within the first two months following initiation of Fingolimod.. Early relapses in a patient group with highly active disease would suggest that a ...
Imaging studies in multiple sclerosis have shown that spinal cord atrophy correlates with clinical disability. The pathological substrate of atrophy has not as yet been investigated adequately. In order to determine the cause of spinal cord atrophy in multiple sclerosis, five different sections of the spinal cord were examined histopathologically in 33 controls and 55 multiple sclerosis cases. In the multiple sclerosis cases in each section the total lesion load and the cross-sectional area of the cord were measured. Multiple regression models were estimated, controlling for sex, age, duration of the disease and location of the cord sections. The multiple sclerosis cords were found to be significantly smaller than the controls. The duration of the disease played the most important role in determining cord atrophy. The degree of atrophy varied in different parts of the cord. Individual lesions played a minor role in local atrophy. Our findings suggest that axonal degeneration, possibly caused by the
Background: Several diagnostic imaging criteria are being described and examined in pediatric multiple sclerosis (MS). Compared to adults, children are more likely to experience acute or relapsing demyelinating episodes of various etiologies which show similar clinical and magnetic resonance imaging (MRI) findings. Aim: To investigate the fulfillment of MRI diagnostic criteria at initial episode in pediatric MS. Methods: We reviewed our series of children and adolescents with the final diagnosis of clinically definite MS and applied the McDonald dissemination in space (DIS) and KIDMUS criteria to their initial MRI scans. Results: Thirty patients (17 girls, 13 boys), most with brainstem dysfunction and polysymptomatic presentation, were included in the study. Twenty-five (83.3%) patients fulfilled both McDonald and KIDMUS criteria. Patients who did not meet any McDonald DIS criteria did not meet KIDMUS criteria either. Only one patient met the McDonald criteria but not the KIDMUS criteria because ...
Mira Ay en nsal. Trial of Fingolimod Versus Interferon Beta-1a in Pediatric Multiple Sclerosis. Turk J Neurol. 2019; 25(1): 50- ...
PubMedID: 26280173 | A Longitudinal Study of Disability, Cognition and Gray Matter Atrophy in Early Multiple Sclerosis Patients According to Evidence of Disease Activity. | PloS one | 8/17/2015
Benign multiple sclerosis (BMS) occurs in about 15% of patients with relapsing-remitting multiple sclerosis (RRMS) that over time do not develop significant neurological disability. The molecular events associated with BMS are not clearly understood. This study sought to underlie the biological mechanisms associated with BMS. Blood samples obtained from a cohort of 31 patients with BMS and 36 patients with RRMS were applied for gene expression microarray analysis using HG-U133A-2 array (Affymetrix). Data were analyzed by Partek and pathway reconstruction was performed by Ingenuity for the most informative genes (MIGs). We identified a differing gene expression signature of 406 MIGs between BMS patients, mean±SE age 44.5±1.5 years, 24 females, 7 males, EDSS 1.9±0.2, disease duration 17.0±1.3 years, and RRMS patients, age 40.3±1.8 years, 24 females, 12 males, EDSS 3.5±0.2, disease duration 10.9±1.4 years. The signature was enriched by genes related RNA polymerase I (POL-1) transcription, general
Researchers from the University of Nottingham and Nottingham University Hospitals found a new way of using MRI scans to help detect the signs of multiple sclerosis in the brain. Multiple sclerosis can be difficult to diagnose as many do not experience symptoms for quite some time and symptoms may overlap with other conditions as well. MRI scans can be helpful in diagnosing multiple sclerosis at they can detect white matter lesions in the brain, but unfortunately these lesions do not always indicate multiple sclerosis.. The researchers found a way to use MRI scans to distinguish between lesions and other white spots in the brain which can be found in multiple sclerosis. The clinical MRI scanners can conduct a specific type of scan known as T2-weighted imaging, which can detect lesions in the brains white matter centered on a vein - a known indicator of multiple sclerosis.. Study lead Dr. Nikos Evangelou said, We already knew that large research MRI scanners could detect the proportion of ...
Multiple sclerosis (MS) is an immune-mediated, chronic inflammatory, and demyelinating disease of the central nervous system (CNS). Several cytokines are thought to be involved in the regulation of MS pathogenesis. We recently identified interleukin (IL)-9 as a cytokine reducing inflammation and protecting from neurodegeneration in relapsing-remitting MS patients. However, the expression of IL-9 in CNS, and the mechanisms underlying the effect of IL-9 on CNS infiltrating immune cells have never been investigated. To address this question, we first analyzed the expression levels of IL-9 in post-mortem cerebrospinal fluid of MS patients and the in situ expression of IL-9 in post-mortem MS brain samples by immunohistochemistry. A complementary investigation focused on identifying which immune cells express IL-9 receptor (IL-9R) by flow cytometry, western blot, and immunohistochemistry. Finally, we explored the effect of IL-9 on IL-9-responsive cells, analyzing the induced signaling pathways and functional
Sleep disorders and epileptic seizures are of higher prevalence in those with multiple sclerosis. Multiple sclerosis is a chronic disease that affects the nervous system. Multiple studies have shown higher prevalence of other co-morbid disorders in those with multiple sclerosis, including sleep disorders and epileptic seizures.. One study conducted a large scale review of other research in regards to multiple sclerosis, sleep disorders and epileptic seizures. They evaluated 32 studies regarding seizures and 18 studies involving sleep disorders. Prevalence of seizures in multiple sclerosis patients was 2.28 percent and sleep disorders was 1.6 percent for narcolepsy, 14.5 - 57.5 percent for restless leg syndrome, 2.22 - 3.2 percent for REM behavior disorder and 7.14 - 58.1 percent for obstructive sleep apnea.. The review of the literature revealed that there are higher occurrences of sleep disorders and seizures in those with multiple sclerosis. The review acknowledged gaps in the research and ...
First multiple sclerosis (MS) therapy to achieve positive NICE recommendation in the shortest possible timeframe Mavenclad has shown sustained
1. Havrdová E. Roztroušená skleróza mozkomíšní. In: Havrdová E (ed). Neuroimunologie. 3rd ed. Praha: Maxdorf 2001: 231. 2. Benedict RH. Integrating cognitive function screening and assessment into the routine care of multiple sclerosis patients. CNS Spectr 2005; 10(5): 384-391. 3. Rao SM, Leo GJ, Bernardin L, Unverzang F. Cognitive dysfunction in multiple sclerosis. Frequency, patterns and prediction. Neurology 1991; 41(5): 685-691. 4. Jennekens-Schinkel A, Sanders EA. Decline of cognition in multiple sclerosis: dissociable deficits. J Neurol Neurosurg Psychiatry 1986; 49(12): 1354-1360. 5. Peyser JM, Edwards KR, Poser CM, Filskov SB. Cognitive function in patients with multiple sclerosis. Arch Neurol 1980; 37(9): 577-579. 6. Rao SM. Multiple sclerosis. In: Cummings JL (ed). Subcortical demention. New York: Oxford University Press 1990: 164-180. 7. Feldman RG, Albert ML, Willis AL. The subcortical dementia of progressive supranuclear palsy. J Neurol Neurosurg Psychiatry 1974; 37(2): ...
Multiple sclerosis is a disease of the central nervous system, brain, optic nerve, and spinal cord. In multiple sclerosis, the protective covering known as myelin that protects the nerves becomes damaged. Damaged myelin and damaged nerves disrupt the smooth flow of nerve impulses within the brain and between the brain, spinal cord, and body, causing the symptoms of multiple sclerosis. The areas of inflammation or damage that occur in the central nervous system are known as lesions or plaques.. Approximately 400,000 individuals have multiple sclerosis in the United States and 2.5 million worldwide. Most people are diagnosed with multiple sclerosis between the ages of 15 and 50. Women are more likely than men to develop the relapsing form of multiple sclerosis. Caucasians have a higher incidence of multiple sclerosis than those of African heritage. African Americans may experience more problems with vision and mobility. People living further from the Equator have a higher risk of multiple ...
1. Esparza ML, Sasaki S, Kesteloot H. Nutrition, latitude, and multiple sclerosis mortality: an ecologic study. Am J Epidemiol. 1995;142:733-737. 2. Lauer K. The risk of multiple sclerosis in the U.S.A. in relation to sociogeographic features: a factor-analytic study. J Clin Epidemiol. 1994;47:43-48. 3. Alter M, Yamoor M, Harshe M. Multiple sclerosis and nutrition. Arch Neurol. 1974;31:267-272. 4. Esparza ML, Sasaki S, Kesteloot H. Nutrition, latitude, and multiple sclerosis mortality: an ecologic study. Am J Epidemiol. 1995;142:733-737. 5. Swank RL. Multiple sclerosis: twenty years on low fat diet. Arch Neurol. 1970;23:460-474. 6. Swank RL, Dugan BB. Effect of low saturated fat diet in early and late cases of multiple sclerosis. Lancet.1990;336:37-39. 7. Millar JH, Zilkha KJ, Langman MJ, et al. Double-blind trial of linoleate supplementation of the diet in multiple sclerosis. Br Med J. 1973;1:765-768. 8. Bates D, Fawcett PR, Shaw DA, et al. Polyunsaturated fatty acids in treatment of acute ...
0007]The following references identify the numbers indicated above. [0008]1. Platten, M., and L. Steinman. 2005. Multiple sclerosis: trapped in deadly glue. Nature Medicine 11:252-253. [0009]2. Oksenberg, J. R., S. E. Baranzini, L. F. Barcellos, and S. L. Hauser. 2001. Multiple sclerosis: genomic rewards. Journal of neuroimmunology 113:171-184. [0010]3. 1993. Interferon beta-1b is effective in relapsing-remitting multiple sclerosis. I. Clinical results of a multicenter, randomized, double-blind, placebo-controlled trial. The IFNB Multiple Sclerosis Study Group. Neurology 43:655-661. [0011]4. 1998. Randomised double-blind placebo-controlled study of interferon beta-1a in relapsing/remitting multiple sclerosis. PRISMS (Prevention of Relapses and Disability by Interferon beta-1a Subcutaneously in Multiple Sclerosis) Study Group. Lancet 352:1498-1504. [0012]5. Johnson, K. P., B. R. Brooks, J. A. Cohen, C. C. Ford, J. Goldstein, R. P. Lisak, L. W. Myers, H. S. Panitch, J. W. Rose, and R. B. Schiffer. ...
Im sure you know a lot of people with diabetes. I can bet you have relatives diagnosed with hypertension. However, the chances are that you dont know anyone with multiple sclerosis.. After all, multiple sclerosis (MS) is thought to be relatively rare in the Philippines and in other tropical countries. Literally meaning numerous scars, it is an immunologic disorder of the central nervous system, characterized by the demyelination of axons and formation of plaques.. We cant let misconceptions about multiple sclerosis contribute to diagnostic and therapeutic difficulties! Its time to do a little myth-busting.. Myth #1: If someone in your family has it, youll have it, too. Having a family history of multiple sclerosis does not guarantee that one will get diagnosed with it later on.. Yes, the expert consensus on multiple sclerosis is that it comes with a genetic risk. Once exposed to the environmental triggers, someone genetically susceptible to MS may develop the disease.. Take note, ...
libro multiple sclerosis : The most trusted book on multiple sclerosis, updated and revised with the latest research in combating the disease.Once known as the crippler of young adults, now more than 75 percent of MS patients will never need a wheelchair. In Multiple Sclerosis, Dr. Louis J. Rosner and Shelley Ross explain that there genuinely is new hope, more than ever before, both for controlling the disease today and curing it tomorrow. Updated with the latest research and terminology, this revised edition gets to the bottom of every treatment option from the tried-and-true to todays cutting-edge and experimental therapies. Its trusted advice covers every step of living with MS, what you need to know, and what you need to ask. Dr. Louis Rosner and Shelley Ross explain what the disease is, who gets it and why, and what people with MS can do to continue living happy and healthy lives. Whether you or your loved one has just been diagnosed with MS or has lived with it for a while, Multiple Sclerosis
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1. Tullman MJ. Overview of the epidemiology, diagnosis, and disease progression associated with multiple scleoris. Am J Manage Care. 2013;19(2 Suppl): S15-20.. 2. Alonso A, Hernan MA. Temporal trends in the incidence of multiple sclerosis: a systematic review. Neurology. 2008;71(2): 129-135.. 3. Compston A, Coles A. Multiple sclerosis. The Lancet Neurology. 2008;372(9648): 1502-1517.. 4. Weiner HL. Multiple sclerosis is an inflammatory t-cell mediated autoimmune disease. Arch Neurol. 2004;61(10): 1613-1615.. 5. Bermel RA, Badshi R. The measurement and clinical relevance of brain atrophy in multiple sclerosis. The Lancet Neurology. 2006;5(2): 158-170. 6. Resolution of Lhermittes sign in multiple sclerosis by treatment with weak electromagnetic fields. Int J Neurosci. 1995;81(3-4): 215-224. 7. Multiple sclerosis: Hope through research. National Institute of Neurological Disorders and Stoke. Available at: http://www.ninds.nih.gov/disorders/multiple_sclerosis/detail_multiple_sclerosis.htm. Accessed ...
The following article presents the very latest information on Multiple Sclerosis. If you have a particular interest in Multiple Sclerosis, then this informative article is required reading.. What the physicians think. Doctors at Liverpool have discovered a drug that can be considered as a miracle treatment for multiple sclerosis, a debilitating and muscle-wasting disease. The scientists held their research and tests at the Walton Neurological Centre and they claim that they have just heralded a breakthrough for the eighty-five thousand multiple sclerotic people in the United Kingdom.. Those who had multiple sclerosis, otherwise known as MS, who suffered from blindness, immobility and paralysis, have described the moments when they have eventually regained their ability to see and to walk again.. What the doctors used for treating such patients were a combination of mitoxantrone, which is a drug for chemotherapy, and copaxone, which is an anti-relapse medication of multiple sclerosis.. The ...
The women who already have at least one child have a thirty-four percent less of the possibility of having a progressive state of multiple sclerosis. According to studies, those women who do not have children yet are more likely to reach a stage of MS where they would need assistance in walking with a brace or a cane.. Having a child before or after the symptoms of multiple sclerosis started to appear is of great help. On the other hand, those women who had children even after the onset of their disease?s symptoms were much better off. Either way, it seems that pregnancy helps in cases of multiple sclerosis. What the experts say. In fact, according to an expert from the Department of Neurology at the National MS Centrum which is located in Mesbroek, Belgium, named Marie D?hooghe, women who have multiple sclerosis and children tend to have a benign type of MS. This finding is in comparison to those women who have not yet given birth.. Research on multiple sclerosis indicates that eighty-five ...
Evidence for the efficacy of interferon beta-1b in delaying the onset of clinically definite multiple sclerosis in individuals with clinically isolated syndrome. - Mark S Freedman
Benign multiple sclerosis (BMS) includes a triad of criteria: medium disability with the duration of the disease for |10 years while maintaining working - Медичний часопис
Relief is when you and the right researcher find each other Finding the right clinical trial for Multiple sclerosis susceptibility can be challenging. However, with TrialsFinder (which uses the Reg4ALL database and privacy controls by Private Access), you can permit researchers to let you know opportunities to consider - all without revealing your identity. ...
Improved management of multiple sclerosis (MS) would result from understanding of MS pathogenesis, risk factors, immune abnormalities, and mechanism of action of MS treatments, including understanding of complications that can result from those treatments. Faculty will discuss new understanding in MS pathogenesis and how immune interventions can alter disease pathogenesis for an improved clinical outcome, and the mechanism of action of current MS therapies. This program complements C201: Multiple Sclerosis Overview: Clinical Pearls and C214: Multiple Sclerosis Overview: Clinical Advances, but covers independent topics ...
The clinical and pathological manifestations of multiple sclerosis are due to areas of demyelination which occur throughout the white matter of the central nervous system. MRI of the brain frequently shows abnormalities in the hemispheric subcortical white matter; these are demonstrable in the majority of patients and support the clinical diagnosis of multiple sclerosis. Our studies have shown that while MRI identifies such cerebral lesions in nearly all clinically definite multiple sclerosis patients with illness of duration greater than 10 years, these areas of abnormal T2 signal are present less often in the brains of patients studied within 3 years of disease onset. However, symptoms referable to the long tracts of the spinal cord are prominent in many of these patients. Imaging of the spinal cord has presented technical problems because of the small size of the cord, patient body, heart and respiratory movements, and limitations of surface coil technology. The spinal cord of 77 patients ...
In this study, we analyzed the equilibrium between histone acetylation, mediated by HATs, and histone deacetylation, mediated by HDACs, in the NAWM of chronic MS brains. Similar to what was reported for the old rodent brain, also in the NAWM of human brains from aged individuals and chronic MS patients we detected a shift toward acetylation. This shift toward acetylation detected in a subset of female patients correlated with the consistent and reproducible increase of several histone acetyltransferase family members, including CBP, P300, MYST3, and MYST4. It is worth noting that, although we also detected increased levels of HDAC11 in this subpopulation, the increased of the acetyltransferases was much greater and likely determined the shift in favor of increased acetylation. These differences were most prominent in a subset of female MS patients and were associated with high levels of developmentally regulated genes (i.e., TCF7L2, SOX2, ID2) compared with controls. Several other genes (i.e., ...
OBJECTIVE: To examine whether past high sun exposure is associated with a reduced risk of multiple sclerosis. DESIGN: Population based case-control study. SETTING: Tasmania, latitudes 41-3 degrees S. PARTICIPANTS: 136 cases with multiple sclerosis and 272 controls randomly drawn from the community and matched on sex and year of birth. MAIN OUTCOME MEASURE: Multiple sclerosis defined by both clinical and magnetic resonance imaging criteria. RESULTS: Higher sun exposure when aged 6-15 years (average 2-3 hours or more a day in summer during weekends and holidays) was associated with a decreased risk of multiple sclerosis (adjusted odds ratio 0.31, 95% confidence interval 0.16 to 0.59). Higher exposure in winter seemed more important than higher exposure in summer. Greater actinic damage was also independently associated with a decreased risk of multiple sclerosis (0.32, 0.11 to 0.88 for grades 4-6 disease). A dose-response relation was observed between multiple sclerosis and decreasing sun exposure when
Acknowledgements. None.. Financial support and sponsorship. The research of I.K.S. is supported by the National Multiple Sclerosis Society, the United States Department of Defense, and the Guthy Jackson Charitable Foundation.. REFERENCES AND RECOMMENDED READING. Papers of particular interest, published within the annual period of review, have been highlighted as: * of special interest. ** of outstanding interest 1. Belbasis L, Bellou V, Evangelou E, et al. Environmental risk factors and multiple sclerosis: An umbrella review of systematic reviews and metaanalyses. Lancet Neurol 2015; 14:263-273.. 2. Sawcer S, Franklin RJ, Ban M. Multiple sclerosis genetics. Lancet Neurol 2014; 13:700-709.. 3. Lublin FD, Reingold SC. Defining the clinical course of multiple sclerosis: results of an international survey. National Multiple Sclerosis Society (USA) Advisory Committee on clinical trials of new agents in multiple sclerosis. Neurology 1996; 46:907-911. 4. Kuceyeski AF, Vargas W, Dayan M, et al. Modeling ...
Results: Significant differences were detected in the genotype and allele distribution of 26-bp Ins/Del polymorphisms of VAMP2 between patients with multiple sclerosis and control subjects; Del/Del genotype and Del allele of VAMP2 were more frequent in patients with multiple sclerosis (p=0.011 and p=0.004, respectively). Similarly, Ddel polymorphism of SNAP-25 gene C/C genotype (p=0.059), syntaxin 1A T/C and C/C genotypes (p=0.005), and synaptotagmin XI gene C allele (p=0.001) were observed more frequently in patients with multiple sclerosis. CC, syntaxin rs1569061 1A gene for 33-bp promoter region TC haplotypes, and synaptotagmin XI gene were found to be associated with an increased risk for multiple sclerosis (p=0.012). Similarly, GC haplotype for rs3746544 of SNAP-25 gene and rs1051312 of SNAP-25 gene were associated with an increased risk for multiple sclerosis (p=0.022 ...
TY - JOUR. T1 - Lower Extremity Motor Evoked Potentials in Multiple Sclerosis. AU - Jones, Seth M.. AU - Streletz, Leopold. AU - Raab, Vicki E.. AU - Knobler, Robert L.. AU - Lublin, Fred D.. PY - 1991. Y1 - 1991. N2 - Transcranial magnetic stimulation was performed on 25 patients with definite multiple sclerosis. Motor evoked potentials were recorded from the anterior tibial muscle. Central motor conduction time was calculated using the equation (F + M-1)/2 by stimulation of the common peroneal nerve. Motor evoked potentials were capable of detecting subclinical pyramidal tract lesions in multiple sclerosis. In patients with multiple sclerosis, the incidence of abnormality of motor and somatosensory evoked potentials was similar. Central motor conduction time was correlated with overall and pyramidal tract subscores on the Kurtzke Disability Status Scale and the Scripps Neurological Rating Scale. Central motor conduction time abnormalities correlated best with the presence of a Babinskis sign ...
The study is a 24 months randomized, double-blind, Placebo-controlled, multi-center clinical trial with an optional 12 months open label extension.. The primary objective of the study is to evaluate the effect of fetal bovine serum [FBS]-free/human serum albumin [HSA]-free formulation of Interferon [IFN] beta-1a (RNF) 44 microgram (three times weekly and once weekly) versus placebo on the time to conversion to McDonald multiple sclerosis (MS) criteria (2005) in subjects with a first clinical demyelinating event at high risk of converting to MS.. The main secondary objective of study is to evaluate the effect of RNF 44 microgram (three times weekly and once weekly) versus placebo on the Time to conversion to clinically definite MS (CDMS) in subjects with a first clinical demyelinating event at high risk of converting to MS.. At the end of 24 month double-blind core REFLEX trial, subjects who will not convert to CDMS and decide to receive open-label (OL) treatment will be enrolled into an ...
TY - JOUR. T1 - Can glatiramer acetate reduce brain atrophy development in multiple sclerosis?. AU - Rovaris, Marco. AU - Comi, Giancarlo. AU - Filippi, Massimo. PY - 2005/6/15. Y1 - 2005/6/15. N2 - The assessment of brain volume changes on serial magnetic resonance imaging (MRI) scans can provide an objective measure of progressive atrophy reflecting the neurodegenerative aspects of multiple sclerosis (MS) pathology. The present article reviews the results of studies assessing the effect of glatiramer acetate (GA) treatment in preventing MS-related, MRI-measurable brain volume decrease. Whilst data from the extended, open-label follow-up of the US trial seem to indicate that long-term treatment with GA might prevent the loss of brain parenchyma in relapsing-remitting MS patients, longitudinal data from the European/Canadian MRI trial suggest that, over a short-term period of treatment, GA does not have a clear-cut impact on the decrease of brain volume. The effect of GA on MS-related brain ...
An SAE was defined as any untoward medical occurrence that at any dose: results in death; in the view of the Investigator, places the subject at immediate risk of death (a life-threatening event; however, this does not include an event that, had it occurred in a more severe form, might have caused death); requires inpatient hospitalization or prolongation of existing hospitalization; results in persistent or significant disability/incapacity; or results in a congenital anomaly/birth defect. An SAE may also have been any other medically important event that, in the opinion of the Investigator, may jeopardize the subject or may require intervention to prevent one of the other outcomes listed in the definition above. See Adverse Events section below for further details ...
2) Infection. It has been theorized that multiple sclerosis can be caused by viral or bacterial infections. Over 90% of multiple sclerosis sufferers have bands of antibodies called immunoglobulins in the brain and spine fluid. These usually indicate the presence of an infectious agent to which the immune system has responded. These findings appear to indicate that an unknown or known, but unidentified virus or bacteria may trigger the onset of the disease. The theory is supported by the ability of some viruses to cause demyelination, or damage to the protective fatty myelin layer covering the tail of nerve cells.. 3) Geographical causes. Research shows an increase in multiple sclerosis cases in people living further from the equator, although exceptions exist. Northern Europeans, for example, appear to have a higher incidence of multiple sclerosis. Moreover, the disease appears to have an earlier onset in sufferers living in countries with little sunshine and cooler climates. The main ...
Allegretta M, Nicklas JA, Sriram S, Albertini RJ (1990) T cells responsive to myelin basic protein in patients with multiple sclerosis. Science 247:718721 10. Wucherpfennig KW, Newcombe J, Li H, Keddy C, Cuzner ML, Hafler DA (1992) yo T cell receptor in acute multiple sclerosis lesions. Proc Nat! Acad Sci USA 89:4588-4592 11. Triebel F, Hercend T (1989) Subpopulations of human peripheral yo T lymphocytes. Immunol Today 10:186-188 12. Selmaj K, Brosnan CF, Raine CS (1991) Co-localization of lymphocytes bearing yo T cell receptor and heat shock protein hsp65+ oligodendrocytes in multiple sclerosis. Recent data indicate that glutamate released by electrically active neurons was indirectly involved in this inhibitory process and prevented MHC class II induction on microglia [13]. In our laboratory, glutamate (at lower concentrations, 20 flM) was found to reduce MHC class II inducibility of microglia in cultured brain tissue [13]. However, no direct effect of glutamate on isolated microglial cells ...
Objective: To investigate accidental falls and near fall incidents in people with multiple sclerosis with respect to clinical variables and the predictive values of four tests. Design: A longitudinal, multi-centred cohort study with prospectively collected falls. Procedures: Self-reported incidents during the three months following a standardized test procedure. Subjects: Seventy-six people with multiple sclerosis and an Expanded Disability Status Scale score between 3.5 and 6.0. Main outcome measures: Berg Balance Scale, Timed Up and Go cognitive, Four Square Step Test (FSST) and 12-item Multiple Sclerosis Walking Scale. Results: Forty-eight people (63%) registered 270 falls. Most falls occurred indoors during activities of daily life. We found a correlation of r(s) = 0.57 between near falls and falls, and of r(s) = 0.82 between registered and retrospectively recalled falls. Fallers and non-fallers differed significantly regarding Expanded Disability Status Score (odds ratio (OR) 1.99, 95% ...
Lack of Association between Antimyelin Antibodies and Progression to Multiple Sclerosis. Kuhle, Jens; Pohl, Christoph; Mehling, Matthias; Edan, Gilles; Freedman, Mark S.; Hartung, Hans-Peter; Polman, Chris H.; Miller, David H.; Montalban, Xavier; Barkhof, Frederik; Bauer, Lars; Dahms, Susanne; Lindberg, Raija; Kappos, Ludwig; Sandbrink, Rupert // New England Journal of Medicine;1/25/2007, Vol. 356 Issue 4, p371 Background: Patients with a single episode of neurologic dysfunction and brain magnetic resonance imaging (MRI) scans suggestive of multiple sclerosis are at high risk for clinically definite multiple sclerosis, but the outcome for individual patients is unpredictable. An increased risk of... ...
Treatment of Multiple sclerosis (MS) is a chronic, potentially debilitating disease that affects your central nervous system, which is made up of your brain and spinal cord. Multiple sclerosis is widely believed to be an autoimmune disease, a condition in which your immune system attacks components of your body as if theyre foreign, In multiple sclerosis, the body mistakenly directs antibodies and white blood cells against proteins in the myelin sheath, a fatty substance that insulates nerve fibers in your brain and spinal cord. This results in inflammation and injury to the sheath and ultimately to the nerves that it surrounds. The result may be multiple areas of scarring (sclerosis). Eventually, this damage can slow or block the nerve signals that control muscle coordination, strength, sensation and vision, Multiple sclerosis affects an estimated 300,000 people in the United States and probably more than 1 million people around the world - including twice as many women as men. Most people experience
According to the results of a new clinical trial, stem cell transplants are likely to induce remission of multiple sclerosis in the long run. The trial indicates that high-dose immunosuppressive therapy and transplantation of an individuals own stem cells may stimulate sustained reduction of relapsing-remitting multiple sclerosis. After five years of receiving high-dose immunosupprresive therapy treatment and autologous hematopoietic cell transplant, 69 percent of the participants did not experience continued disability. Additionally, they did not suffer from progression of MS symptoms or a relapse. Noteworthy, after obtaining HDIT/HCT, participants did not take any medication. Some studies have noted that the success rates of the present MS drugs are lower.. The National Institute of Allergy and Infectious Diseases (NIAID) were the sponsors of the trial dubbed HALT-MS. Immune Tolerance Network, which is funded by NIAID, conducted the research. The researchers published both the initial ...
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Multiple Sclerosis is a type of demyelinating disease, a disease in which the nervous system is damaged by the deterioration of the outer layer of the neurons, called myelin. This phenomenon affects the transmission of the nerve impulses between neurons, which results in a variety of symptoms of multiple sclerosis, which may impair the sufferer to a certain degree. These symptoms may vary from physical, psychiatric and even mental issues. Specific symptoms of multiple sclerosis include double vision, weak muscles, and blindness in one or both eyes, difficulties with coordination or difficulties with sensations. Patients with multiple sclerosis usually experience one or more symptoms, in some cases these episodes being isolated. Between these episodes, the symptoms usually disappear completely. Nevertheless, the condition continues to develop, leaving permanent neurological damage, as the nerves continue to deteriorate. Up until the present time, the exact cause of multiple sclerosis remains ...
TY - JOUR. T1 - Gene-microarray analysis of multiple sclerosis lesions yields new targets validated in autoimmune encephalomyelitis. AU - Lock, Christopher. AU - Hermans, Guy. AU - Pedotti, Rosetta. AU - Brendolan, Andrea. AU - Schadt, Eric. AU - Garren, Hideki. AU - Langer-Gould, Annette. AU - Strober, Samuel. AU - Cannella, Barbara. AU - Allard, John. AU - Klonowski, Paul. AU - Austin, Angela. AU - Lad, Nagin. AU - Kaminski, Naftali. AU - Galli, Stephen J.. AU - Kaminski, Naftali. AU - Raine, Cedric S.. AU - Heller, Renu. AU - Steinman, Lawrence. PY - 2002/1/1. Y1 - 2002/1/1. N2 - Microarray analysis of multiple sclerosis (MS) lesions obtained at autopsy revealed increased transcripts of genes encoding inflammatory cytokines, particularly interleukin-6 and - 17, interferon-γ and associated downstream pathways. Comparison of two poles of MS pathologyacute lesions with inflammation versus silent lesions without inflammation-revealed differentially transcribed genes. Some products of these ...
Objective: We are evaluating the therapeutic roles of high-dose immunosuppressive therapy (HDIT) rescued with autologous stem cell transplantation (SCT) in the management of patients with severe, nonresponsive multiple sclerosis (MS). Our hypothesis was that by ablating the immunoactive cells in a patient with MS and replacing them with nonconditional naïve cells, the disease process could be stopped. Design/Methods: We enrolled 26 patients with severe MS, including primary progressive MS (n = 7), secondary progressive MS (n = 18) and relapsing remitting MS (n = 1). Their median age was 41 years (range, 27-60). The median expanded disability status scale (EDSS) at HDIT was 7.0 (5.0-8.0). Eligibility requirements included an EDSS from 5.0 to 8.0 and deterioration of 1 or more points over the previous year. Twent-one patients had previous therapy with interferon-beta fail, and 15 had multiple therapies including Copaxone, prednisone, and methotrexate fail. The median follow-up was 12 months ...
We performed Affymetrix gene arrays (HU133, ~38,500 genes) using RNA from the in vitro activated PBMCs from patients with clinically isolated syndrome suggestive of multiple sclerosis (CIS) (n=15) and matched healthy controls (HC) (n=8). Results were confirmed and further supported by RT-PCR and RayBio Cytokine Arrays. Affymetrix data revealed that IFNB-1a induced significant (p,0.05) up-regulation of 711, and down-regulation of 587 genes in CIS patients, and 446 and 543 in HC, respectively. CXCL11 and CXCL10, the ligands of CXCR3 were significantly increased in CIS patients and HC, whereas proinflammatory chemokines CXCL2, CXCL3 and CXCL5 were decreased in CIS patients. CCL18 and CCL19 were increased in CIS, while CCL22 and CCL17 were decreased in CIS and HC. Those chemokine gene changes reflect the complex effects of IFNB-1a that likely affect differentiation/ maturation and chemotaxis of DCs and other cells bridging the innate and adaptive immune response. The anti-inflammatory cytokine IL-10 ...
Multiple sclerosis is an inflammatory neurological disease that can generate a wide range of physical and psychological symptoms. Multiple sclerosis involves the deterioration of myelin, a substance that surrounds the bodys nervous cells. Myelin has a very important role in the transmission of nervous impulses, and if this substance is affected, the entire activity of the nervous system is seriously compromised. Although the actual causes of multiple sclerosis remain unknown, there are several hypotheses that present genetic abnormalities as the main factors responsible for causing the disease. Medical scientists believe that multiple sclerosis occurs on the background of inherited genetic predispositions, and environmental factors are suspected to be triggers of the disease. Some hypotheses also introduce viral infections in this scenario, although infections with viruses dont seem to contribute to the development of the disease. Multiple sclerosis can affect the body on different levels. The ...
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DelveInsight has launched a new report on Primary Progressive Multiple Sclerosis Epidemiology. Primary-progressive multiple sclerosis (PPMS) is a neurodegenerative disease that interferes with the brains ability to control the body. There are four main types of MS: relapsing-remitting MS (RRMS), primary-progressive MS (PPMS), secondary-progressive MS (SPMS), and progressive-relapsing MS. Each type might be mild, moderate, or severe.. Request for free sample copy- https://www.delveinsight.com/sample-request/primary-progressive-multiple-sclerosis-ppms-epidemiology-forecast Primary Progressive Multiple Sclerosis Epidemiology historical as well as forecasted Primary Progressive Multiple Sclerosis Epidemiology in the 7MM, covering the United States, EU5 (Germany, France, Italy, Spain and the United Kingdom), and Japan from 2018-2030. Primary Progressive Multiple Sclerosis Epidemiology PPMS can be further characterized at different points in time as either active (with an occasional relapse and/or ...
Clinical trial for Dermatite Atopique modérée ou grave | Chronic progressive multiple sclerosis | Multiple Sclerosis | Radiologically Isolated Syndrome , Primary Progressive Multiple Sclerosis (PPMS) Study of Brutons Tyrosine Kinase (BTK) Inhibitor Tolebrutinib (SAR442168)
Title: Chronic Cerebrospinal Venous Insufficiency (CCSVI) and Multiple Sclerosis (MS): A Critical Review. VOLUME: 10 ISSUE: 6. Author(s):Chiara Zecca and Claudio Gobbi. Affiliation:Servizio di Neurologia e Neuroradiologia, Neurocentro della Svizzera Italiana, Ospedale Regionale di Lugano, via esserete 46, 6903 Lugano, Switzerland.. Keywords:Chronic cerebrospinal venous insufficiency, MRI, Multiple Sclerosis, Pathogenesis, CCSVI, ECD, TCCD, MRI Venography, CCSVI Theory, Doppler sonography. Abstract: Multiple sclerosis (MS) is a chronic disease of the central nervous system with not yet completely understood pathogenesis. The so called chronic cerebrospinal venous insufficiency (CCSVI) theory has recently emerged, supporting the concept of a cerebrospinal venous drainage impairment as the cause of MS. Since the first publication on this topic with a claimed 100% specificity and sensitivity of the condition for MS diagnosis, CCSVI theory has generated a scientific and mass media debate with a ...
VÉCSEI László. [Recent data suggest that long-term worsening is common in relapsing-remitting multiple sclerosis patients and is largely independent of relapses or new lesion formation on brain MRI. The current definition of secunder progressive multiple sclerosis is worsening of disability independent of relapses over at least 6-month interval. Early focal inflammatory disease activity and spinal cord lesion are predictors of very-long term disease outcomes in relapse - onset multiple sclerosis. The potential of PET imaging to visualize hidden inflammation in MS brain in vivo is an important contribution for better understanding the progression of the disease. Therefore, PET imaging is a promising tool in detecting the conversion from relapsing remitting multiple sclerosis to secunder progressive form of multiple sclerosis. Furthermore, neuro-axonal damage is the pathological substrate of permanent disability in different neurological disorders including multiple sclerosis. The neurofilament ...
Additional evidence comes from a group of researchers and clinicians from the United Kingdom who treated MS patients in the study, Autologous Mesenchymal Stem Cells for the Treatment of Secondary Progressive Multiple Sclerosis: An Open-Label Phase 2a Proof-of-Concept Study.. Research findings show that intravenous administration of autologous mesenchymal stem cells to patients with secondary progressive multiple sclerosis is feasible and safe and suggests structural, functional, and physiological improvement in patients after receiving treatment with autologous mesenchymal stem cells which is consistent with remyelination. In addition, patients experienced enhanced visual acuity.. Dr. Andre Lallande, Medical Director of StemGenex Medical Group and Principal Investigator of the observational study Outcomes Data of Adipose Stem Cells to Treat Multiple Sclerosis, evaluates the quality of life changes measured by the Multiple Sclerosis Quality of Life Inventory (MSQLI) in individuals following ...
The subject invention provides a method of treating a subject afflicted with a form of multiple sclerosis comprising periodically administering to the subject an amount of glatiramer acetate and an amount of mitoxantrone, wherein the amounts when taken together are effective to alleviate a symptom of the form of multiple sclerosis in the subject so as to thereby treat the subject. The subject invention also provides a package comprising glatiramer acetate, mitoxantrone and instructions for use of the together to alleviate a symptom of a form of multiple sclerosis in a subject. Additionally, the subject invention provides a pharmaceutical composition comprising an amount of glatiramer acetate and an amount of mitoxantrone, wherein the amounts when taken together are effective to alleviate a symptom of a form of multiple sclerosis in a subject. The subject invention further provides a pharmaceutical combination comprising separate dosage forms of an amount of glatiramer acetate and an amount of ...
TY - JOUR. T1 - Physiotherapy rehabilitation for people with progressive Multiple Sclerosis: a systematic review. AU - Campbell, Evan. AU - Coulter, Elaine. AU - Mattison, Paul G.. AU - Miller, Linda. AU - McFadyen, Angus. AU - Paul, Lorna. PY - 2016/1. Y1 - 2016/1. N2 - ObjectiveTo assess the efficacy of physiotherapy interventions, including exercise therapy, for the rehabilitation of people with progressive multiple sclerosis.Data SourcesFive databases (Cochrane Library, Physiotherapy Evidence Database [PEDro], Web of Science Core Collections, MEDLINE, Embase) and reference lists of relevant articles were searched.Study SelectionRandomized experimental trials, including participants with progressive multiple sclerosis and investigating a physiotherapy intervention or an intervention containing a physiotherapy element, were included.Data ExtractionData were independently extracted using a standardized form, and methodologic quality was assessed using the PEDro scaleData SynthesisThirteen ...
TY - JOUR. T1 - Longitudinal changes in social functioning in mildly disabled patients with relapsing-remitting multiple sclerosis receiving subcutaneous interferon β-1a. T2 - Results from the COGIMUS (COGnitive Impairment in MUltiple Sclerosis) study (II). AU - Patti, Francesco. AU - Amato, Maria Pia. AU - Trojano, Maria. AU - Bastianello, Stefano. AU - Tola, Maria Rosalia. AU - Picconi, Orietta. AU - Cilia, Sabina. AU - Cottone, Salvatore. AU - Grimaldi, Luigi M E. PY - 2012/9. Y1 - 2012/9. N2 - Purpose To report longitudinal changes in and explore the influence of cognition on social functioning in mildly disabled patients with relapsing-remitting multiple sclerosis (RRMS). Methods Italian patients (18-50 years) with RRMS and Expanded Disability Status Scale (EDSS) score ≤4.0 were assigned to interferon β-1a, 44 or 22 μg subcutaneously three times weekly, and underwent annual assessments for social functioning (Environmental Status Scale [ESS]) over 3 years. Results Baseline total ESS ...
Lorscheider, Johannes, Buzzard, Katherine, Jokubaitis, Vilija, Spelman, Tim, Havrdova, Eva, Horakova, Dana, Trojano, Maria, Izquierdo, Guillermo, Girard, Marc, Duquette, Pierre, Prat, Alexandre, Lugaresi, Alessandra, GrandMaison, Francois, Grammond, Pierre, Hupperts, Raymond, Alroughani, Raed, Sola, Patrizia, Boz, Cavit, Shaw, Cameron and Barnett, Michael H. 2016, Defining secondary progressive multiple sclerosis, Brain a journal of neurology, vol. 139, no. 9, pp. 2395-2405, doi: 10.1093/brain/aww173. ...
Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology / Owain, Howell ...
PubMed journal article TNFRSF1A polymorphisms and their role in multiple sclerosis susceptibility and severity in the Slovak populatio were found in PRIME PubMed. Download Prime PubMed App to iPhone or iPad.
SUMMARY Evidence of damage to cerebral vein walls was sought in 70 cases of multiple sclerosis. Seventy control cases were also examined. The multiple sclerosis cases showed venous intramural fibrinoid deposition (7 %), recent haemorrhages (17%), old haemorrhages revealed by haemosiderin deposition (30%), thrombosis (6%) and thickened veins (19%). In all, 41% of all multiple sclerosis cases showed some evidence of vein damage. Occasional control cases showed haemosiderin deposition in the brain but, unlike the multiple sclerosis cases, these were diffuse and almost entirely related to coexistent cardiovascular or cerebrovascular disease. Haemosiderin deposition was common in the substantia nigra and other pigmented nuclei in all cases. It is concluded that the cerebral vein wall in multiple sclerosis is subject to chronic inflammatory damage, which promotes haemorrhage and increased permeability, and constitutes a form of vasculitis ...
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According to a report from Scientific American, just this past September, pharmaceutical company Hoffmann-La Roche announced they achieved positive results from three large clinical trials of a drug called Ocrelizumab,. It is an injectable antibody medication that targets the bodys B cells, and works for both relapsing and progressive multiple sclerosis.. Up until this point, most patients have received the best results with a drug called interferon beta-1a. Ocrelizumab is believed to be even more effective. Even better, it also slowed the advance of symptoms in patients with progressive multiple sclerosis.. Dr. Stephen Hauser is a neurologist at the University of California, San Francisco. He was involved in the trials.. The drug has dramatic effects on relapsing MS, and we finally have our foot in the door with the progressive form, he says.. Scientists working on the root causes of multiple sclerosis are excited about the may Ocrelizumab works on those with the disease. ...
According to a report from Scientific American, just this past September, pharmaceutical company Hoffmann-La Roche announced they achieved positive results from three large clinical trials of a drug called Ocrelizumab,. It is an injectable antibody medication that targets the bodys B cells, and works for both relapsing and progressive multiple sclerosis.. Up until this point, most patients have received the best results with a drug called interferon beta-1a. Ocrelizumab is believed to be even more effective. Even better, it also slowed the advance of symptoms in patients with progressive multiple sclerosis.. Dr. Stephen Hauser is a neurologist at the University of California, San Francisco. He was involved in the trials.. The drug has dramatic effects on relapsing MS, and we finally have our foot in the door with the progressive form, he says.. Scientists working on the root causes of multiple sclerosis are excited about the may Ocrelizumab works on those with the disease.. ...
OBJECTIVE: We tested whether it is possible to differentiate relapsing-remitting (RR) from secondary progressive (SP) disease stages in patients with multiple sclerosis (MS) using a combination of nuclear magnetic resonance (NMR) metabolomics and partial least squares discriminant analysis (PLS-DA) of biofluids, which makes no assumptions on the underlying mechanisms of disease. METHODS: Serum samples were obtained from patients with primary progressive MS (PPMS), SPMS, and RRMS; patients with other neurodegenerative conditions; and age-matched controls. Samples were analyzed by NMR and PLS-DA models were derived to separate disease groups. RESULTS: The PLS-DA models for serum samples from patients with MS enabled reliable differentiation between RRMS and SPMS. This approach also identified significant differences between the metabolite profiles of each of the MS groups (PP, SP, and RR) and the healthy controls, as well as predicting disease group membership with high specificity and sensitivity.
A 54 year old female patient, born in 1959, was diagnosed suffering from primary progressive multiple sclerosis more than 10 years ago, and retrospectively symptoms started already in 1992. She underwent various operations (3 times) to correct a fixed kyphosis and 2 years ago started to suffer from increasing pains and muscle spasms. She was…
Digital Download Price: $20 [purchase_link id=696 style=button color=blue text=Download Immediately price=0 direct=true] Intensive Directed Nutrition And Neuromuscular Electrical Stimulation In The Setting Of Secondary Progressive Multiple Sclerosis - Allied Health Professionals Version Dr. Terry Wahls has secondary progressive multiple sclerosis and spent nearly four years dependent upon a tilt-recline wheelchair. An accomplished internal medicine physician, […]
Hackensack Meridian Health Hackensack University Medical Center announced a newly approved U.S. Food and Drug Administration drug is now available to treat adult patients with relapsing forms of multiple sclerosis (MS) and primary progressive multiple sclerosis (PPMS). The drug, Ocrevus, which received FDA approval on March 28th, is the first and only medicine for both relapsing and primary progressive forms of multiple sclerosis.. Click here to view the full article on njbmagazine.com. ...
Multiple sclerosis is a condition characterized by areas of damage (lesions) on the brain and spinal cord. These lesions are associated with destruction of the covering that protects nerves and promotes the efficient transmission of nerve impulses (the myelin sheath) and damage to nerve cells. Multiple sclerosis is considered an autoimmune disorder; autoimmune disorders occur when the immune system malfunctions and attacks the bodys own tissues and organs, in this case tissues of the nervous system.. Multiple sclerosis usually begins in early adulthood, between ages 20 and 40. The symptoms vary widely, and affected individuals can experience one or more effects of nervous system damage. Multiple sclerosis often causes sensory disturbances in the limbs, including a prickling or tingling sensation (paresthesia), numbness, pain, and itching. Some people experience Lhermitte sign, which is an electrical shock-like sensation that runs down the back and into the limbs. This sensation usually occurs ...
Introduction Multiple Sclerosis is a demyelization disorder of the central nervous system and the spinal cord; which leads to patches of plaques in the regions of the brain and spinal cord. (Stedmans Medical Dictionary, 2000) There are many types of multiple sclerosis, however the severity and type of multiple
The contribution of genetic factors to the age at onset in multiple sclerosis is poorly understood. Our objective was to investigate the disease modifying effects of HLA-DRB1 alleles and allele interactions on age at onset of multiple sclerosis. High-resolution four-digit HLA-DRB1 genotyping was performed in a cohort of 461 multiple sclerosis patients from the Perth Demyelinating Diseases Database. Carriage of the HLA-DRB1*1501 risk allele was not significantly associated with age at onset but HLA-DRB1*0801 was associated with a later onset of the disease. The HLA-DRB1*0401 allele was associated with a reduced age at onset when combined with DRB1*1501 but may delay age at onset when combined with DRB1*0801. These findings indicate that epistatic interactions at the HLA-DRB1 locus have significant modifying effects on age at onset of multiple sclerosis and demonstrate the value of high-resolution genotyping in detecting such associations.. ...
Delaying disability progression is a critical goal of MS treatment, and historically, patients with advancing disease have had very few options to help them, said Fabrice Chouraqui, President, Novartis Pharmaceuticals Corporation. Weve had a longstanding mission to enhance the understanding of MS and help reimagine treatment options, and were excited to expand on our legacy with Mayzent for patients with relapsing forms of MS, including SPMS with active disease.. Most patients transition from RRMS to SPMS over time1. Therefore, starting therapy early is critical for patients to help slow the rate of disability progression. Disability progression most frequently includes - but is not limited to - an impact on ambulation, which could lead to patients needing a walking aid or a wheelchair5.. We are grateful that there is a new treatment option for adults with active secondary progressive MS, said Bruce Bebo, PhD, Executive Vice President, Research, National MS Society. We are hopeful this ...
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of Myelin and Maintenance of Axonal Conduction in the MOG-induced EAE Mouse Model (Poster Session I -- P1.220; April 28; 3:00 p.m. EDT) -- Anti-murine CD52 Antibody Treatment Does Not Adversely Affect the Migratory Ability of Immune Cells (Poster Session I -- P1.222; April 28; 3:00 p.m. EDT) -- Successful Detection and Management of Immune Thrombocytopenia in Alemtuzumab-Treated Patients with Active Relapsing-Remitting Multiple Sclerosis (Poster Session II -- P2.198; April 29; 7:30 a.m. EDT) -- Thyroid Autoimmune Adverse Events in Patients Treated with Alemtuzumab for Relapsing-remitting Multiple Sclerosis: Four-year Follow-up of the CARE-MS Studies (Poster Session II -- P2.199; April 29; 7:30 a.m. EDT) -- Safety of Using Disease-modifying Therapy Post-alemtuzumab Treatment in Patients With Relapsing-remitting Multiple Sclerosis in the Core and Extension Phases of CAMMS223, CARE-MS I, and CARE-MS II Studies (Poster Session II -- P2.201; April 29; 7:30 a.m. EDT) -- Alemtuzumab Has Similar ...
Background: To develop more effective treatments for multiple sclerosis (MS), researchers require a better understanding of the biological processes that lead to susceptibility and progression, as well as animal models that emulate human disease. Unlike relapsing-remitting MS, progressive MS is not managed with current therapies, and the development of effective treatments is hindered due to the lack of animal models that resemble human disease.. Overview: To address this gap, this team of researchers developed the first mouse model of MS based on a human mutation (Nr1h3 gene) to understand the mechanisms involved in disease progression. The Nr1h3 gene mutation is known to cause severe and rapidly progressive MS in families. Preliminary analysis of this model has already revealed parallels with the human disease. Dr. Jacqueline Quandt and team will conduct a comprehensive characterization of this new animal model to identify the underlying biological pathways and mechanisms responsible for the ...
The Phase 3 ASCEND study investigating natalizumab in the treatment of secondary progressive multiple sclerosis (SPMS) did not achieve its primary and secondary endpoints, Biogen (NASDAQ: BIIB) reported today. During the study, natalizumab was generally well tolerated and adverse events were consistent with its known safety profile. ASCEND evaluated the efficacy and safety of natalizumab to slow the accumulation of disability progression unrelated to relapse in SPMS patients, an unmet medical need. The majority of study participants had EDSS scores of 6.0 to 6.5 (walking aid required) and were non-relapsing for two years prior to enrollment in the study. The studys composite primary endpoint evaluated the percentage of patients whose disability had progressed on one or more of three disability measurements comprising the composite endpoint. Natalizumab demonstrated a
Previous research has found that multiple sclerosis (MS) patients may have a specific microbial signature in their gut microbiota that could impact disease pathogenesis. However, it is not known to what extent structural and functional changes in the gut microbiota are primary contributors to MS pathogenesis and which underlying mechanisms are involved.. A new study, led by Dr. Sergio Baranzini from the Department of Neurology at the University of California San Francisco (USA), has found that specific gut bacteria from multiple sclerosis patients regulate immune responses and exacerbate MS-like symptoms in mice.. The researchers used 16S ribosomal ribonucleic acid (rRNA) gene sequencing of stool samples from 71 untreated relapsing-remitting MS patients and 71 healthy controls.. Although they did not find shifts in the gut microbiota structure, specific bacterial taxa were significantly associated with MS. Both Akkermansia muciniphila and Acinetobacter calcoaceticus were increased in MS ...
Eighteen patients with acquired demyelinating syndromes and multiple sclerosis were included, the total annual incidence being 1.15/100,000 (acquired demyelinating syndromes 1.02 and multiple sclerosis 0.45/100,000). The median age at diagnosis was 14.25 years (range 1.25-17.5 years). Thirteen patients were initially diagnosed with clinically isolated syndrome, two had acute disseminated encephalomyelitis, two had multiple sclerosis, and one had neuromyelitis optica. Seven children were diagnosed with multiple sclerosis; three patients with clinically isolated syndrome developed multiple sclerosis after the age of 18 and were not included in the multiple sclerosis group. The gender ratio was equal. Of the nine girls, seven were diagnosed with clinically isolated syndrome. Most patients (11 of 18) were diagnosed during the period January through March. Oligoclonal bands in cerebrospinal fluid were exclusively found in patients with multiple sclerosis and clinically isolated syndrome and 13 of 14 ...
The major intermediate cytoskeletal protein of astrocytes, glial fibrillary acidic protein (GFAP), and that of axons, neurofilament light protein (NFL), may both be released into the cerebrospinal fluid (CSF) during pathological processes in the central nervous system (CNS). We investigated GFAP and NFL levels in CSF as possible biomarkers for progression in multiple sclerosis (MS). Patients with relapsing-remitting MS (RRMS, n = 15) or secondary progressive MS (SPMS, n = 10) and healthy control subjects (n = 28) were examined twice with an interval of 8-10 years apart. Neurological deficits were scored with the Expanded Disability Status Scale (EDSS). GFAP and NFL levels were determined in CSF by enzyme-linked immunosorbent assay (ELISA). GFAP levels and NFL levels correlated with age (r and r (s) = 0.50, p = 0.006). Adjusting for age, MS patients had increased GFAP levels compared with controls (p = 0.03) and GFAP levels correlated with neurological disability (EDSS, r = 0.51, p | 0.05) and disease
This is an updated Cochrane review of the previous version published (Cochrane Database of Systematic Reviews 2004 , Issue 1 . Art. No.: CD004678. DOI: 10.1002/14651858.CD004678). Treatment with glatiramer acetate (Copaxone ®) of patients with Relapsing-Remitting (RRMS) and with Progressive Multiple Sclerosis (PMS) seems to have few beneficial effects in RRMS, while the drug is not effective in PMS patients. Previous studies indicate that glatiramer acetate, a synthetic drug, is effective in animal models of MS, and shows some benefits in MS patients. The objective of this review was to assess the efficacy of glatiramer acetate in RRMS and PMS patients.. Among the pertinent medical literature six studies met the criteria of the methodological quality necessary for their inclusion in this review. 540 RRMS patients and 1049 PMS patients contributed to this analysis. The data showed no beneficial effects on disease progression in both MS forms, a slight beneficial effect in the reduction of risk ...
The cause of MS is unknown. MS is more common in temperate than tropical areas, and moving between geographic regions at certain ages can affect the risk developing the disorder. Theories as to cause have considered a virus, brain trauma, or a problem in the immune system, but these are little more than speculation. Close relatives of people with multiple sclerosis have a higher incidence of the disorder, and this supports the possibility of a genetic contribution.. Genes on multiple chromosomes are suspected of playing some role in MS. People with multiple sclerosis are more likely to have abnormalities in human leukocyte antigens (HLA), proteins coded from chromosome 6 and important in the functioning of the immune system. If there is a genetic contribution to the development of MS, the path of cause and effect is not yet understood. There is no genetic test for multiple sclerosis, and even if there is a genetic contribution to cause, unknown environmental factors (such as a particular ...
Multiple sclerosis is a disease of the central nervous system, resulting in the demyelination of neurons, causing mild to severe symptoms. Several anti-inflammatory treatments now play a significant role in ameliorating the disease. Glatiramer acetate (GA) is a formulation of random polypeptide copolymers for the treatment of relapsing-remitting MS by limiting the frequency of attacks. While evidence suggests the influence of GA on inflammatory responses, the targeted molecular mechanisms remain poorly understood. Here, we review the multiple pharmacological modes-of-actions of glatiramer acetate in treatment of multiple sclerosis. We discuss in particular a newly discovered interaction between the leukocyte-expressed integrin αMβ2 (also called Mac-1, complement receptor 3, or CD11b/CD18) and perspectives on the GA co-polymers as an influence on the function of the innate immune system.
Dan and Jennifer Digmann, authors of the book Despite MS to Spite MS, share how they set goals and prioritize what matters to them. Jennifer lives with secondary progressive MS and Dan lives with relapsing-remitting MS.
By Joe Elia A phase 2 study shows a slowing of brain atrophy with a high-dose statin in patients with secondary progressive multiple sclerosis.According to a Lancet study, 140 patients were … (Source: Physicians First Watch current issue)
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This Is MS Multiple Sclerosis Knowledge & Support Community. Welcome to This is MS, the leading forum for Multiple Sclerosis ... Re: Multiple Sclerosis drug R… by iKat View the latest post Mon Mar 17, 2014 12:43 pm ... If its on your mind and it has to do with multiple sclerosis in any way, post it here. Topics: 9785 ... A forum for parents with multiple sclerosis, and how to cope with family life when a parent has MS. Topics: 19 ...
This Is MS Multiple Sclerosis Knowledge & Support Community. Welcome to This is MS, the leading forum for Multiple Sclerosis ... Does the venous pressure theory of multiple sclerosis pathophysiology deserve a second chance? Summary The theory that multiple ... Does the venous pressure theory of multiple sclerosis pathophysiology deserve a second chance? Last post by frodo « Fri Sep 17 ...
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This Is MS Multiple Sclerosis Knowledge & Support Community. Welcome to This is MS, the leading forum for Multiple Sclerosis ... Iron Heterogeneity in Early Active Multiple Sclerosis Lesions Abstract Objective Multiple sclerosis (MS) is a heterogeneous ... Diagnosis of multiple sclerosis using multifocal erg data feature fusion Abstract. The purpose of this paper is to implement a ... Classification of multiple sclerosis based on patterns of CNS regional atrophy covariance Abstract There is evidence that ...
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This Is MS Multiple Sclerosis Knowledge & Support Community. Welcome to This is MS, the leading forum for Multiple Sclerosis ... This Is MS Multiple Sclerosis Knowledge & Support Community - Registration. By accessing "This Is MS Multiple Sclerosis ... You agree that "This Is MS Multiple Sclerosis Knowledge & Support Community" have the right to remove, edit, move or close any ... While this information will not be disclosed to any third party without your consent, neither "This Is MS Multiple Sclerosis ...
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