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.
Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation.
Atrophy of the optic disk which may be congenital or acquired. This condition indicates a deficiency in the number of nerve fibers which arise in the RETINA and converge to form the OPTIC DISK; OPTIC NERVE; OPTIC CHIASM; and optic tracts. GLAUCOMA; ISCHEMIA; inflammation, a chronic elevation of intracranial pressure, toxins, optic nerve compression, and inherited conditions (see OPTIC ATROPHIES, HEREDITARY) are relatively common causes of this condition.
A group of disorders marked by progressive degeneration of motor neurons in the spinal cord resulting in weakness and muscular atrophy, usually without evidence of injury to the corticospinal tracts. Diseases in this category include Werdnig-Hoffmann disease and later onset SPINAL MUSCULAR ATROPHIES OF CHILDHOOD, most of which are hereditary. (Adams et al., Principles of Neurology, 6th ed, p1089)
A syndrome complex composed of three conditions which represent clinical variants of the same disease process: STRIATONIGRAL DEGENERATION; SHY-DRAGER SYNDROME; and the sporadic form of OLIVOPONTOCEREBELLAR ATROPHIES. Clinical features include autonomic, cerebellar, and basal ganglia dysfunction. Pathologic examination reveals atrophy of the basal ganglia, cerebellum, pons, and medulla, with prominent loss of autonomic neurons in the brain stem and spinal cord. (From Adams et al., Principles of Neurology, 6th ed, p1076; Baillieres Clin Neurol 1997 Apr;6(1):187-204; Med Clin North Am 1999 Mar;83(2):381-92)
A group of recessively inherited diseases that feature progressive muscular atrophy and hypotonia. They are classified as type I (Werdnig-Hoffman disease), type II (intermediate form), and type III (Kugelberg-Welander disease). Type I is fatal in infancy, type II has a late infantile onset and is associated with survival into the second or third decade. Type III has its onset in childhood, and is slowly progressive. (J Med Genet 1996 Apr:33(4):281-3)
A group of inherited and sporadic disorders which share progressive ataxia in combination with atrophy of the CEREBELLUM; PONS; and inferior olivary nuclei. Additional clinical features may include MUSCLE RIGIDITY; NYSTAGMUS, PATHOLOGIC; RETINAL DEGENERATION; MUSCLE SPASTICITY; DEMENTIA; URINARY INCONTINENCE; and OPHTHALMOPLEGIA. The familial form has an earlier onset (second decade) and may feature spinal cord atrophy. The sporadic form tends to present in the fifth or sixth decade, and is considered a clinical subtype of MULTIPLE SYSTEM ATROPHY. (From Adams et al., Principles of Neurology, 6th ed, p1085)
Progressive, autosomal recessive, diffuse atrophy of the choroid, pigment epithelium, and sensory retina that begins in childhood.
A form of MACULAR DEGENERATION also known as dry macular degeneration marked by occurrence of a well-defined progressive lesion or atrophy in the central part of the RETINA called the MACULA LUTEA. It is distinguishable from WET MACULAR DEGENERATION in that the latter involves neovascular exudates.
A SMN complex protein that is essential for the function of the SMN protein complex. In humans the protein is encoded by a single gene found near the inversion telomere of a large inverted region of CHROMOSOME 5. Mutations in the gene coding for survival of motor neuron 1 protein may result in SPINAL MUSCULAR ATROPHIES OF CHILDHOOD.
Disorders characterized by an abnormal reduction in muscle volume due to a decrease in the size or number of muscle fibers. Atrophy may result from diseases intrinsic to muscle tissue (e.g., MUSCULAR DYSTROPHY) or secondary to PERIPHERAL NERVOUS SYSTEM DISEASES that impair innervation to muscle tissue (e.g., MUSCULAR ATROPHY, SPINAL).
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.
Dominant optic atrophy is a hereditary optic neuropathy causing decreased visual acuity, color vision deficits, a centrocecal scotoma, and optic nerve pallor (Hum. Genet. 1998; 102: 79-86). Mutations leading to this condition have been mapped to the OPA1 gene at chromosome 3q28-q29. OPA1 codes for a dynamin-related GTPase that localizes to mitochondria.
A complex of proteins that assemble the SNRNP CORE PROTEINS into a core structure that surrounds a highly conserved RNA sequence found in SMALL NUCLEAR RNA. They are found localized in the GEMINI OF COILED BODIES and in the CYTOPLASM. The SMN complex is named after the Survival of Motor Neuron Complex Protein 1, which is a critical component of the complex.
A SMN complex protein that is closely-related to SURVIVAL OF MOTOR NEURON 1 PROTEIN. In humans, the protein is encoded by an often duplicated gene found near the inversion centromere of a large inverted region of CHROMOSOME 5.
Technique for limiting use, activity, or movement by immobilizing or restraining animal by suspending from hindlimbs or tails. This immobilization is used to simulate some effects of reduced gravity and study weightlessness physiology.
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
An X-linked recessive form of spinal muscular atrophy. It is due to a mutation of the gene encoding the ANDROGEN RECEPTOR.
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.
GASTRITIS with atrophy of the GASTRIC MUCOSA, the GASTRIC PARIETAL CELLS, and the mucosal glands leading to ACHLORHYDRIA. Atrophic gastritis usually progresses from chronic gastritis.
A subset of ubiquitin protein ligases that are formed by the association of a SKP DOMAIN PROTEIN, a CULLIN DOMAIN PROTEIN and a F-BOX DOMAIN PROTEIN.
Hereditary conditions that feature progressive visual loss in association with optic atrophy. Relatively common forms include autosomal dominant optic atrophy (OPTIC ATROPHY, AUTOSOMAL DOMINANT) and Leber hereditary optic atrophy (OPTIC ATROPHY, HEREDITARY, LEBER).
Incoordination of voluntary movements that occur as a manifestation of CEREBELLAR DISEASES. Characteristic features include a tendency for limb movements to overshoot or undershoot a target (dysmetria), a tremor that occurs during attempted movements (intention TREMOR), impaired force and rhythm of diadochokinesis (rapidly alternating movements), and GAIT ATAXIA. (From Adams et al., Principles of Neurology, 6th ed, p90)
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)
Diseases of the uvea.
The measurement of an organ in volume, mass, or heaviness.
A degenerative disease of the central nervous system characterized by balance difficulties; OCULAR MOTILITY DISORDERS (supranuclear ophthalmoplegia); DYSARTHRIA; swallowing difficulties; and axial DYSTONIA. Onset is usually in the fifth decade and disease progression occurs over several years. Pathologic findings include neurofibrillary degeneration and neuronal loss in the dorsal MESENCEPHALON; SUBTHALAMIC NUCLEUS; RED NUCLEUS; pallidum; dentate nucleus; and vestibular nuclei. (From Adams et al., Principles of Neurology, 6th ed, pp1076-7)
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
A syndrome characterized by slowly progressive unilateral atrophy of facial subcutaneous fat, muscle tissue, skin, cartilage, and bone. The condition typically progresses over a period of 2-10 years and then stabilizes.
A pyridoxal phosphate enzyme that catalyzes the formation of glutamate gamma-semialdehyde and an L-amino acid from L-ornithine and a 2-keto-acid. EC 2.6.1.13.
A progressive neurodegenerative condition of the central and autonomic nervous systems characterized by atrophy of the preganglionic lateral horn neurons of the thoracic spinal cord. This disease is generally considered a clinical variant of MULTIPLE SYSTEM ATROPHY. Affected individuals present in the fifth or sixth decade with ORTHOSTASIS and bladder dysfunction; and later develop FECAL INCONTINENCE; anhidrosis; ATAXIA; IMPOTENCE; and alterations of tone suggestive of basal ganglia dysfunction. (From Adams et al., Principles of Neurology, 6th ed, p536)
The resection or removal of the innervation of a muscle or muscle tissue.
Large, multinucleate single cells, either cylindrical or prismatic in shape, that form the basic unit of SKELETAL MUSCLE. They consist of MYOFIBRILS enclosed within and attached to the SARCOLEMMA. They are derived from the fusion of skeletal myoblasts (MYOBLASTS, SKELETAL) into a syncytium, followed by differentiation.
Disturbances in mental processes related to learning, thinking, reasoning, and judgment.
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 heterogenous group of degenerative syndromes marked by progressive cerebellar dysfunction either in isolation or combined with other neurologic manifestations. Sporadic and inherited subtypes occur. Inheritance patterns include autosomal dominant, autosomal recessive, and X-linked.
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.
Lower lateral part of the cerebral hemisphere responsible for auditory, olfactory, and semantic processing. It is located inferior to the lateral fissure and anterior to the OCCIPITAL LOBE.
An inhibitor of apoptosis protein that was initially identified during analysis of CHROMOSOME DELETIONS associated with SPINAL MUSCULAR ATROPHY. Naip contains a nucleotide binding oligomerization domain and a carboxy-terminal LEUCINE rich repeat.
This is one of 2 related pepsinogen systems in humans and is also known as pepsinogen. (The other is PEPSINOGEN C.) This includes isozymogens Pg1-Pg5 (pepsinogens 1-5, group I or products of PGA1-PGA5 genes). This is the main pepsinogen found in urine.
A heterogeneous group of primarily familial disorders characterized by myoclonic seizures, tonic-clonic seizures, ataxia, progressive intellectual deterioration, and neuronal degeneration. These include LAFORA DISEASE; MERRF SYNDROME; NEURONAL CEROID-LIPOFUSCINOSIS; sialidosis (see MUCOLIPIDOSES), and UNVERRICHT-LUNDBORG SYNDROME.
An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.
The restriction of the MOVEMENT of whole or part of the body by physical means (RESTRAINT, PHYSICAL) or chemically by ANALGESIA, or the use of TRANQUILIZING AGENTS or NEUROMUSCULAR NONDEPOLARIZING AGENTS. It includes experimental protocols used to evaluate the physiologic effects of immobility.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
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.
Degenerative changes in the RETINA usually of older adults which results in a loss of vision in the center of the visual field (the MACULA LUTEA) because of damage to the retina. It occurs in dry and wet forms.
Neurons which activate MUSCLE CELLS.
The concave interior of the eye, consisting of the retina, the choroid, the sclera, the optic disk, and blood vessels, seen by means of the ophthalmoscope. (Cline et al., Dictionary of Visual Science, 4th ed)
A growth differentiation factor that is a potent inhibitor of SKELETAL MUSCLE growth. It may play a role in the regulation of MYOGENESIS and in muscle maintenance during adulthood.
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.
Diseases that affect the structure or function of the cerebellum. Cardinal manifestations of cerebellar dysfunction include dysmetria, GAIT ATAXIA, and MUSCLE HYPOTONIA.
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.
A protein that has been shown to function as a calcium-regulated transcription factor as well as a substrate for depolarization-activated CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASES. This protein functions to integrate both calcium and cAMP signals.
MOTOR NEURONS in the anterior (ventral) horn of the SPINAL CORD which project to SKELETAL MUSCLES.
Visualization of a vascular system after intravenous injection of a fluorescein solution. The images may be photographed or televised. It is used especially in studying the retinal and uveal vasculature.
A malabsorption syndrome that is precipitated by the ingestion of foods containing GLUTEN, such as wheat, rye, and barley. It is characterized by INFLAMMATION of the SMALL INTESTINE, loss of MICROVILLI structure, failed INTESTINAL ABSORPTION, and MALNUTRITION.
This is one of the 2 related pepsinogen systems in humans. It is found in prostate and seminal fluid whereas PEPSINOGEN A is not.
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.
Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures.
The most common clinical form of FRONTOTEMPORAL LOBAR DEGENERATION, this dementia presents with personality and behavioral changes often associated with disinhibition, apathy, and lack of insight.
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.
The thin, highly vascular membrane covering most of the posterior of the eye between the RETINA and SCLERA.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
A vague complaint of debility, fatigue, or exhaustion attributable to weakness of various muscles. The weakness can be characterized as subacute or chronic, often progressive, and is a manifestation of many muscle and neuromuscular diseases. (From Wyngaarden et al., Cecil Textbook of Medicine, 19th ed, p2251)
The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.
A prodromal phase of cognitive decline that may precede the emergence of ALZHEIMER DISEASE and other dementias. It may include impairment of cognition, such as impairments in language, visuospatial awareness, ATTENTION and MEMORY.
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)
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Four CSF-filled (see CEREBROSPINAL FLUID) cavities within the cerebral hemispheres (LATERAL VENTRICLES), in the midline (THIRD VENTRICLE) and within the PONS and MEDULLA OBLONGATA (FOURTH VENTRICLE).
Proteins that bind to RNA molecules. Included here are RIBONUCLEOPROTEINS and other proteins whose function is to bind specifically to RNA.
A spiral bacterium active as a human gastric pathogen. It is a gram-negative, urease-positive, curved or slightly spiral organism initially isolated in 1982 from patients with lesions of gastritis or peptic ulcers in Western Australia. Helicobacter pylori was originally classified in the genus CAMPYLOBACTER, but RNA sequencing, cellular fatty acid profiles, growth patterns, and other taxonomic characteristics indicate that the micro-organism should be included in the genus HELICOBACTER. It has been officially transferred to Helicobacter gen. nov. (see Int J Syst Bacteriol 1989 Oct;39(4):297-405).
Inflammation of the GASTRIC MUCOSA, a lesion observed in a number of unrelated disorders.
Lining of the STOMACH, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. The surface cells produce MUCUS that protects the stomach from attack by digestive acid and enzymes. When the epithelium invaginates into the LAMINA PROPRIA at various region of the stomach (CARDIA; GASTRIC FUNDUS; and PYLORUS), different tubular gastric glands are formed. These glands consist of cells that secrete mucus, enzymes, HYDROCHLORIC ACID, or hormones.

Indirect evidence for cholinergic inhibition of intestinal bicarbonate absorption in humans. (1/3164)

BACKGROUND: The aim of the study was to test the hypothesis that in the fasting state, proximal intestinal HCO3- absorption, which depends on villus Na+/H+ exchanger activity, is tonically inhibited by a cholinergic atropine sensitive mechanism. SUBJECTS: The experiments were performed in 34 healthy volunteers and in eight patients with intestinal villus atrophy. METHODS: HCO3- absorption was measured with a modified triple lumen perfusion technique in the distal duodenum, the most proximal portion of the small intestine. The study was designed to compensate for the inhibitory effects of atropine on intestinal motor activity. RESULTS: Atropine had three effects on HCO3- transport: it reduced HCO3- concentration at the proximal aspiration site, it displaced the relation between HCO3- concentration and HCO3- absorption to the left, and it induced a significant acidification of the perfusate at the distal aspiration site. The magnitude of the stimulatory effect on HCO3- absorption was similar to the difference between patients with intestinal villus atrophy and healthy controls. CONCLUSION: The data suggest that, in the fasting state, duodenal HCO3- absorption, which depends on villus Na+/H+ exchanger activity, may be tonically inhibited by an atropine sensitive cholinergic mechanism.  (+info)

Proteinuria induces tubular cell turnover: A potential mechanism for tubular atrophy. (2/3164)

BACKGROUND: Proteinuria and tubular atrophy have both been closely linked with progressive renal failure. We hypothesized that apoptosis may be induced by tubular cell exposure to heavy proteinuria, potentially leading to tubular atrophy. Apoptosis was studied in a rat model of "pure" proteinuria, which does not induce renal impairment, namely protein-overload proteinuria. METHODS: Adult female Lewis rats underwent intraperitoneal injection of 2 g of bovine serum albumin (BSA, N = 16) or sham saline injections (controls, N = 8) daily for seven days. Apoptosis was assessed at day 7 in tissue sections using in situ end labeling (ISEL) and electron microscopy. ISEL-positive nuclei (apoptotic particles) were counted in blinded fashion using image analysis with NIH Image. Cell proliferation was assessed by detection of mRNA for histone by in situ hybridization, followed by counting of positive cells using NIH Image. RESULTS: Animals injected with saline showed very low levels of apoptosis on image analysis. BSA-injected rats had heavy proteinuria and showed both cortical and medullary apoptosis on ISEL. This was predominantly seen in the tubules and, to a lesser extent, in the interstitial compartment. Overall, the animals injected with BSA showed a significant 30-fold increase in the number of cortical apoptotic particles. Electron microscopy of tubular cells in a BSA-injected animal showed a progression of ultrastructural changes consistent with tubular cell apoptosis. The BSA-injected animals also displayed a significant increase in proximal tubular cell proliferation. This increased proliferation was less marked than the degree of apoptosis. CONCLUSION: Protein-overload proteinuria in rats induces tubular cell apoptosis. This effect is only partially balanced by proliferation and potentially provides a direct mechanism whereby heavy proteinuria can induce tubular atrophy and progressive renal failure.  (+info)

Computerised tomography and intellectual impairment in the elderly. (3/3164)

Sixty-six elderly subjects (mean age 77 years) whose mental state was assessed clinically and by simple psychometric tests have been studied by computerised tomography. The mean maximum ventricular area in the 17 mentally normal subjects was above the upper limit of normal for younger subjects, and there was a broad relationship between increasing ventricular dilatation and increasing intellectual impairment. No such clear relationship was demonstrable for measures of cortical atrophy.  (+info)

Computerised axial tomography in patients with severe migraine: a preliminary report. (4/3164)

Patients suffering from severe migraine, usually for many years, have been examined by the EMI scanner between attacks. Judged by criteria validated originally by comparison with pneumoencephalography, about half of the patients showed evidence of cerebral atrophy. Perhaps of more significance than generalised atrophy was the frequency of areas of focal atrophy and of evidence of infarction.  (+info)

Increased neurodegeneration during ageing in mice lacking high-affinity nicotine receptors. (5/3164)

We have examined neuroanatomical, biochemical and endocrine parameters and spatial learning in mice lacking the beta2 subunit of the nicotinic acetylcholine receptor (nAChR) during ageing. Aged beta2(-/-) mutant mice showed region-specific alterations in cortical regions, including neocortical hypotrophy, loss of hippocampal pyramidal neurons, astro- and microgliosis and elevation of serum corticosterone levels. Whereas adult mutant and control animals performed well in the Morris maze, 22- to 24-month-old beta2(-/-) mice were significantly impaired in spatial learning. These data show that beta2 subunit-containing nAChRs can contribute to both neuronal survival and maintenance of cognitive performance during ageing. beta2(-/-) mice may thus serve as one possible animal model for some of the cognitive deficits and degenerative processes which take place during physiological ageing and in Alzheimer's disease, particularly those associated with dysfunction of the cholinergic system.  (+info)

Contributory and exacerbating roles of gaseous ammonia and organic dust in the etiology of atrophic rhinitis. (6/3164)

Pigs reared commercially indoors are exposed to air heavily contaminated with particulate and gaseous pollutants. Epidemiological surveys have shown an association between the levels of these pollutants and the severity of lesions associated with the upper respiratory tract disease of swine atrophic rhinitis. This study investigated the role of aerial pollutants in the etiology of atrophic rhinitis induced by Pasteurella multocida. Forty, 1-week-old Large White piglets were weaned and divided into eight groups designated A to H. The groups were housed in Rochester exposure chambers and continuously exposed to the following pollutants: ovalbumin (groups A and B), ammonia (groups C and D), ovalbumin plus ammonia (groups E and F), and unpolluted air (groups G and H). The concentrations of pollutants used were 20 mg m-3 total mass and 5 mg m-3 respirable mass for ovalbumin dust and 50 ppm for ammonia. One week after exposure commenced, the pigs in groups A, C, E, and G were infected with P. multocida type D by intranasal inoculation. After 4 weeks of exposure to pollutants, the pigs were killed and the extent of turbinate atrophy was assessed with a morphometric index (MI). Control pigs kept in clean air and not inoculated with P. multocida (group H) had normal turbinate morphology with a mean MI of 41.12% (standard deviation [SD], +/- 1. 59%). In contrast, exposure to pollutants in the absence of P. multocida (groups B, D, and F) induced mild turbinate atrophy with mean MIs of 49.65% (SD, +/-1.96%), 51.04% (SD, +/-2.06%), and 49.88% (SD, +/-3.51%), respectively. A similar level of atrophy was also evoked by inoculation with P. multocida in the absence of pollutants (group G), giving a mean MI of 50.77% (SD, +/-2.07%). However, when P. multocida inoculation was combined with pollutant exposure (groups A, C, and E) moderate to severe turbinate atrophy occurred with mean MIs of 64.93% (SD, +/-4.64%), 59.18% (SD, +/-2.79%), and 73.30% (SD, +/-3.19%), respectively. The severity of atrophy was greatest in pigs exposed simultaneously to dust and ammonia. At the end of the exposure period, higher numbers of P. multocida bacteria were isolated from the tonsils than from the nasal membrane, per gram of tissue. The severity of turbinate atrophy in inoculated pigs was proportional to the number of P. multocida bacteria isolated from tonsils (r2 = 0.909, P < 0.05) and nasal membrane (r2 = 0.628, P < 0.05). These findings indicate that aerial pollutants contribute to the severity of lesions associated with atrophic rhinitis by facilitating colonization of the pig's upper respiratory tract by P. multocida and also by directly evoking mild atrophy.  (+info)

Quantitative assessment of gastric atrophy using the syntactic structure analysis. (7/3164)

AIM: To assess the topographical relation between gastric glands, using the minimum spanning tree (MST), to derive both a model of neighbourhood and quantitative representation of the tissue's architecture, to assess the characteristic features of gastric atrophy, and to assess the grades of gastric atrophy. METHODS: Haematoxylin and eosin stained sections from corporal and antral biopsy specimens (n = 139) from normal patients and from patients with nonatrophic gastritis and atrophic gastritis of grades 1, 2, and 3 (Sydney system) were assessed by image analysis system (Prodit 5.2) and 11 syntactic structure features were derived. These included both line and connectivity features. RESULTS: Syntactic structure analysis was correlated with the semiquantitative grading system of gastric atrophy. The study showed significant reductions in the number of points and the length of MST in both body and antrum. The standard deviation of the length of MST was significantly increased in all grades of atrophy. The connectivity to two glands was the highest and most affected by the increased grade of atrophy. The reciprocal values of the Wiener, Randic, and Balaban indices showed significant changes in the volume of gland, abnormality in the shape of glands, and changes in irregularity and branching of the glands in both types of gastric mucosa. There was a complete separation in the MST, connectivity, and index values between low grade and high grade gastric atrophy. CONCLUSIONS: (1) Gastric atrophy was characterised by loss of the gland, variation in the volume, reduction in the neighbourhood, irregularity in spacing, and abnormality in the shape of the glands. (2) Syntactic structure analysis significantly differentiated minor changes in gastric gland (low grade atrophy) from high grade atrophy of clinical significance. (3) Syntactic structure analysis is a simple, fast, and highly reproducible technique and appears a promising method for quantitative assessment of atrophy.  (+info)

Infratentorial atrophy on magnetic resonance imaging and disability in multiple sclerosis. (8/3164)

Loss of tissue volume in the central nervous system may provide an index of fixed neurological dysfunction in multiple sclerosis. Recent magnetic resonance studies have shown a modest relationship between clinical disability rating scores and transverse sectional area of the cervical spinal cord. To explore further the relationship between atrophy and disability in multiple sclerosis, we estimated the volumes of infratentorial structures from MRIs in a cross-sectional study of 41 patients, 21 with relapsing-remitting multiple sclerosis and 20 with secondary progressive multiple sclerosis. We used the Cavalieri method of modern design stereology with point counting to estimate the volume of brainstem, cerebellum and upper cervical spinal cord from three-dimensional MRIs acquired with an MPRAGE (Magnetization-prepared Rapid Acquisition Gradient Echo) sequence. The volume of the upper (C1-C3) cervical spinal cord was significantly correlated with a composite spinal cord score derived from the appropriate Functional Scale scores of the Expanded Disability Status Scale (r = -0.50, P < 0.01). The cerebellar (r = 0.49, P < 0.01) and brainstem (r = 0.34, P < 0.05) volumes correlated with the Scripp's Neurological Disability Rating Scale scores. The upper cervical cord volumes (r = -0.39, P < 0.01), but not the brainstem or cerebellar volumes, were significantly associated with disease duration. MRI-estimated structural volumes may provide a simple index of axonal and/or myelin loss, the presumed pathological substrates of irreversible impairment and disability in multiple sclerosis.  (+info)

There are several types of atrophy that can occur in different parts of the body. For example:

1. Muscular atrophy: This occurs when muscles weaken and shrink due to disuse or injury.
2. Neuronal atrophy: This occurs when nerve cells degenerate, leading to a loss of cognitive function and memory.
3. Cardiac atrophy: This occurs when the heart muscle weakens and becomes less efficient, leading to decreased cardiac output.
4. Atrophic gastritis: This is a type of stomach inflammation that can lead to the wasting away of the stomach lining.
5. Atrophy of the testes: This occurs when the testes shrink due to a lack of use or disorder, leading to decreased fertility.

Atrophy can be diagnosed through various medical tests and imaging studies, such as MRI or CT scans. Treatment for atrophy depends on the underlying cause and may involve physical therapy, medication, or surgery. In some cases, atrophy can be prevented or reversed with proper treatment and care.

In summary, atrophy is a degenerative process that can occur in various parts of the body due to injury, disease, or disuse. It can lead to a loss of function and decreased quality of life, but with proper diagnosis and treatment, it may be possible to prevent or reverse some forms of atrophy.

There are several types of muscular atrophy, including:

1. Disuse atrophy: This type of atrophy occurs when a muscle is not used for a long period, leading to its degeneration.
2. Neurogenic atrophy: This type of atrophy occurs due to damage to the nerves that control muscles.
3. Dystrophic atrophy: This type of atrophy occurs due to inherited genetic disorders that affect muscle fibers.
4. Atrophy due to aging: As people age, their muscles can degenerate and lose mass and strength.
5. Atrophy due to disease: Certain diseases such as cancer, HIV/AIDS, and muscular dystrophy can cause muscular atrophy.
6. Atrophy due to infection: Infections such as polio and tetanus can cause muscular atrophy.
7. Atrophy due to trauma: Traumatic injuries can cause muscular atrophy, especially if the injury is severe and leads to prolonged immobilization.

Muscular atrophy can lead to a range of symptoms depending on the type and severity of the condition. Some common symptoms include muscle weakness, loss of motor function, muscle wasting, and difficulty performing everyday activities. Treatment for muscular atrophy depends on the underlying cause and may include physical therapy, medication, and lifestyle changes such as exercise and dietary modifications. In severe cases, surgery may be necessary to restore muscle function.

Optic atrophy is a condition where there is a degeneration or loss of the optic nerve fibers, leading to vision loss. It can be caused by various factors such as trauma, inflammation, tumors, and certain medical conditions like multiple sclerosis.

The symptoms of optic atrophy may include:

1. Blind spots in the visual field
2. Difficulty perceiving colors
3. Difficulty adjusting to bright light
4. Double vision or other abnormalities in binocular vision
5. Eye pain or discomfort
6. Loss of peripheral vision
7. Nausea and vomiting
8. Sensitivity to light
9. Tunnel vision
10. Weakness or numbness in the face or extremities.

The diagnosis of optic atrophy is based on a comprehensive eye exam, which includes a visual acuity test, dilated eye exam, and other specialized tests such as an OCT (optical coherence tomography) scan.

Treatment for optic atrophy depends on the underlying cause and may include medications to manage inflammation or infection, surgery to remove a tumor or repair damaged tissue, or management of associated conditions such as diabetes or multiple sclerosis. In some cases, vision loss due to optic atrophy may be permanent and cannot be reversed, but there are strategies to help improve remaining vision and adapt to any visual impairment.

There are different types of SMA, ranging from mild to severe, with varying degrees of muscle wasting and weakness. The condition typically becomes apparent during infancy or childhood and can progress rapidly or slowly over time. Symptoms may include muscle weakness, spinal curvature (scoliosis), respiratory problems, and difficulty swallowing.

SMA is caused by a defect in the Survival Motor Neuron 1 (SMN1) gene, which is responsible for producing a protein that protects motor neurons from degeneration. The disorder is usually inherited in an autosomal recessive pattern, meaning that a person must inherit two copies of the defective gene - one from each parent - to develop the condition.

There is currently no cure for SMA, but various treatments are available to manage its symptoms and slow its progression. These may include physical therapy, occupational therapy, bracing, and medications to improve muscle strength and function. In some cases, stem cell therapy or gene therapy may be considered as potential treatment options.

Prognosis for SMA varies depending on the type and severity of the condition, but it is generally poor for those with the most severe forms of the disorder. However, with appropriate management and support, many individuals with SMA can lead fulfilling lives and achieve their goals despite physical limitations.

The term "multiple system atrophy" was first used in 1985 to describe this condition, which was previously known as "parkinsonism-dementia." MSA is classified into two main types: cerebellar type (MSA-C) and parkinsonian type (MSA-P). The cerebellar type is characterized by progressive cerebellar ataxia, loss of coordination, and balance problems, while the parkinsonian type is characterized by parkinsonism, rigidity, and bradykinesia.

The exact cause of MSA is not known, but it is believed to be related to abnormal protein accumulation in the brain and mitochondrial dysfunction. There is currently no cure for MSA, and treatment is focused on managing symptoms and improving quality of life. The progression of MSA is variable and can range from several years to several decades.

MSA is a rare disorder, with an estimated prevalence of 5-10 cases per million people worldwide. It affects both men and women equally, and the symptoms typically begin in adulthood, although some cases may present in children or older adults. The diagnosis of MSA is based on a combination of clinical features, imaging studies, and laboratory tests, including dopamine transporter scans and CSF analysis.

There are several prominent features of MSA that distinguish it from other neurodegenerative disorders, such as Parkinson's disease or Alzheimer's disease. These include:

1. Autonomic dysfunction: MSA is characterized by a range of autonomic dysfunctions, including orthostatic hypotension, urinary incontinence, and constipation.
2. Cerebellar ataxia: MSA is often associated with progressive cerebellar ataxia, which can lead to difficulties with coordination, balance, and gait.
3. Pyramidal signs: MSA can also present with pyramidal signs, such as bradykinesia, rigidity, and tremors, which are similar to those seen in Parkinson's disease.
4. Dysphagia: Many individuals with MSA experience difficulty swallowing, known as dysphagia, which can increase the risk of aspiration pneumonia.
5. Cognitive impairment: Some people with MSA may experience cognitive impairment, including memory loss and confusion.
6. Sleep disorders: MSA can also be associated with sleep disorders, such as rapid eye movement sleep behavior disorder and restless leg syndrome.
7. Emotional changes: MSA can cause significant emotional changes, including depression, anxiety, and apathy.
8. Impaired speech and language: Some individuals with MSA may experience impaired speech and language, including slurred speech and difficulty with word-finding.
9. Dysautonomia: MSA can also cause dysautonomia, which can lead to a range of symptoms, such as orthostatic hypotension, hypertension, and abnormal sweating.
10. Bladder and bowel dysfunction: MSA can cause bladder and bowel dysfunction, including urinary frequency, urgency, and constipation.

It is important to note that not all individuals with MSA will experience all of these symptoms, and the severity of the disease can vary greatly between individuals. If you suspect you or a loved one may be experiencing symptoms of MSA, it is essential to consult with a healthcare professional for proper diagnosis and treatment.

There are several types of spinal muscular atrophies, including:

Type 1 (Werdnig-Hoffmann disease): This is the most severe form of SMA, characterized by complete paralysis and life-threatening respiratory problems. It is usually diagnosed in infancy and children typically die before the age of two.

Type 2 (Dubowitz disease): This type of SMA is less severe than Type 1, but still causes significant muscle weakness and wasting. Children with this condition may be able to sit, stand, and walk with support, but will eventually lose these abilities as the disease progresses.

Type 3 (Kugelberg-Welander disease): This is an adult-onset form of SMA that causes slowly progressive muscle weakness and wasting. It can be mild or severe and may affect individuals in their teens to mid-life.

The symptoms of spinal muscular atrophies vary depending on the type and severity of the disorder, but may include:

* Muscle weakness and wasting, particularly in the limbs and trunk
* Difficulty breathing and swallowing
* Delayed development of motor skills such as sitting, standing, and walking
* Weakness of facial muscles, leading to a "floppy" appearance
* Poor reflexes and decreased muscle tone

The exact cause of spinal muscular atrophies is not fully understood, but genetics play a role. The disorders are caused by mutations in a gene called the survival motor neuron (SMN) gene, which is responsible for producing a protein that helps maintain the health of nerve cells. Without this protein, nerve cells die, leading to muscle weakness and wasting.

There is currently no cure for spinal muscular atrophies, but treatment options are available to help manage symptoms and improve quality of life. These may include:

* Physical therapy to maintain muscle strength and flexibility
* Occupational therapy to develop coping strategies and assist with daily activities
* Medications to manage muscle spasms and other symptoms
* Respiratory support, such as ventilation, for individuals with severe forms of the disorder
* Nutritional support to ensure adequate nutrition and hydration

Overall, spinal muscular atrophies are a group of rare genetic disorders that can cause muscle weakness and wasting, particularly in the limbs and trunk. While there is currently no cure, treatment options are available to help manage symptoms and improve quality of life. With appropriate care and support, individuals with spinal muscular atrophies can lead fulfilling lives.

The main clinical features of olivopontocerebellar atrophies include:

1. Progressive cerebellar ataxia: a loss of coordination, balance, and gait difficulties.
2. Cognitive decline: problems with memory, language, and other cognitive functions.
3. Eye movements abnormalities: difficulty with eye movements, including nystagmus (involuntary eye movements) and oculomotor disorders.
4. Dysarthria: slurred or distorted speech.
5. Pyramidal signs: symptoms such as rigidity, bradykinesia (slowness of movement), and tremors.

The most common form of olivopontocerebellar atrophy is sporadic cerebellar ataxia, which accounts for about 70% of cases. Other forms include familial cerebellar ataxia, which is inherited in an autosomal dominant or recessive pattern, and acquired cerebellar ataxia, which can be caused by various medical conditions such as stroke, tumors, or infections.

There is currently no cure for olivopontocerebellar atrophy, and treatment is primarily focused on managing the symptoms and slowing down disease progression. Physical therapy, occupational therapy, and speech therapy can help improve motor function, balance, and communication skills. Medications such as antioxidants, cholinesterase inhibitors, and dopaminergic agents may also be used to manage symptoms.

In summary, olivopontocerebellar atrophy is a group of progressive neurodegenerative disorders that affect the cerebellum and brainstem, leading to difficulties with movement, coordination, and balance. While there is currently no cure for these conditions, a range of treatments can help manage symptoms and improve quality of life.

The exact cause of gyrate atrophy is not well understood, but it is thought to be inherited in an autosomal recessive manner. The condition typically presents in childhood or adolescence and can progress rapidly, leading to significant vision loss over a short period of time.

Symptoms of gyrate atrophy may include blurred vision, peripheral vision loss, and sensitivity to light. The condition can be diagnosed through a comprehensive eye exam, including imaging tests such as optical coherence tomography (OCT) and fundus autofluorescence (FAF).

There is currently no cure for gyrate atrophy, but various treatments may be used to slow the progression of the condition and manage its symptoms. These may include vitamin supplements, anti-inflammatory medications, and protective eyewear to reduce exposure to bright light. In severe cases, surgical intervention such as retinal implantation or vision restoration therapy may be considered.

Early detection and ongoing monitoring are essential for managing gyrate atrophy and preserving vision as much as possible. With appropriate treatment and support, individuals with this condition can lead active and fulfilling lives despite significant vision loss.

The term "geographic" refers to the characteristic map-like pattern of atrophy that occurs in the retina, with areas of degeneration resembling geographical features such as rivers, lakes, and islands. The progression of GA is typically slower than that of neovascular AMD, but it can still lead to significant vision loss over time.

The exact cause of GA is not fully understood, but it is believed to be related to the aging process and the accumulation of waste material in the retina. Risk factors for developing GA include age, family history, and prior history of AMD. There is currently no cure for GA, but various treatments are being developed to slow its progression and manage symptoms. These may include vitamin supplements, anti-inflammatory medications, and photodynamic therapy. Regular eye exams are important for early detection and monitoring of GA to help preserve vision and quality of life.

Examples of atrophic muscular disorders include:

1. Muscular dystrophy: A group of inherited disorders that cause progressive loss of muscle mass and strength, leading to muscle wasting and weakness.
2. Myotonia congenita: An autosomal dominant disorder characterized by muscle stiffness and spasms, particularly in the neck, shoulder, and limb muscles.
3. Inclusion body myositis: An inflammatory muscle disease that leads to progressive muscle weakness and wasting, with deposits of abnormal protein called inclusion bodies in the muscle fibers.
4. Limb-girdle muscular dystrophy: A group of inherited disorders that cause progressive loss of muscle mass and strength in the arms and legs, leading to muscle wasting and weakness.
5. Facioscapulohumeral muscular dystrophy: An inherited disorder characterized by progressive weakness of the facial, shoulder, and upper arm muscles, with a loss of motor neurons in the spinal cord.

The symptoms of atrophic muscular disorders can vary depending on the specific disorder and its severity, but may include:

1. Muscle weakness and wasting
2. Muscle cramps and spasms
3. Difficulty walking or standing
4. Fatigue and decreased endurance
5. Loss of motor neurons in the spinal cord
6. Cognitive impairment
7. Developmental delays
8. Vision loss
9. Hearing loss
10. Skeletal deformities

Atrophic muscular disorders can be diagnosed through a combination of clinical evaluation, electromyography (EMG), and muscle biopsy. Treatment is focused on managing the symptoms and slowing the progression of the disease, and may include:

1. Physical therapy to maintain muscle strength and function
2. Medications to manage pain and spasms
3. Assistive devices such as braces and walkers
4. Respiratory support in advanced cases
5. Gene therapy is an area of ongoing research, but it is not yet widely available for the treatment of atrophic muscular disorders.

It is important to note that atrophic muscular disorders are a group of rare and complex conditions, and each type has its own unique set of symptoms and characteristics. If you suspect that you or someone you know may be experiencing symptoms of an atrophic muscular disorder, it is important to consult with a healthcare professional for proper evaluation and diagnosis.

The symptoms of optic atrophy, autosomal dominant typically begin in adulthood and may include:

* Gradual loss of vision in one or both eyes
* Blurred vision
* Difficulty with peripheral vision
* Sensitivity to light
* Eye pain
* Abnormal eye movements

The condition is caused by mutations in several genes that are responsible for the structure and function of the optic nerve. The exact cause of the condition can be determined through genetic testing.

There is no cure for optic atrophy, autosomal dominant, but treatment may include:

* Glasses or contact lenses to correct refractive errors
* Prism glasses to improve vision
* Low vision aids such as telescopes or magnifying glasses
* Counseling and support to help cope with the visual loss.

The progression of the condition can vary widely, and some people may experience a rapid decline in vision while others may remain stable for many years. Regular monitoring by an eye care professional is important to monitor for any changes in vision and to adjust treatment as needed.

The symptoms of BSAX usually become apparent during early childhood and may include:

1. Delayed development of motor skills such as sitting, standing, and walking
2. Muscle weakness and wasting in the limbs
3. Poor coordination and balance
4. Impaired speech and swallowing
5. Vision loss or blindness
6. Cognitive decline and intellectual disability

The diagnosis of BSAX is based on a combination of clinical evaluation, imaging studies such as MRI, and genetic testing. There is currently no cure for BSAX, and treatment is focused on managing the symptoms and supporting the patient's quality of life. Physical therapy, occupational therapy, and speech therapy may be helpful in improving muscle strength and coordination.

The progression of BSAX is variable and can be rapid or slow, with some individuals experiencing a more aggressive course than others. The mean age of death is around 20-30 years, but some individuals may live into their 40s or 50s.

BSAX is an X-linked disorder, meaning that the gene mutation is located on the X chromosome and is more common in males who have only one X chromosome. Females can be carriers of the mutation and may exhibit mild symptoms or be asymptomatic.

In summary, Bulbo-spinal atrophy, x-linked (BSAX) is a rare genetic disorder that affects males almost exclusively and is characterized by progressive loss of nerve cells in the spinal cord and cerebellum leading to muscle weakness, atrophy, and loss of coordination. There is currently no cure for BSAX, but therapies such as physical, occupational, and speech therapy may be helpful in improving quality of life. The progression of the disease can vary and is often rapid, with a mean age of death around 20-30 years.

This definition is based on the data provided by the Healthcare Common Procedure Coding System (HCPCS) and the American Medical Association (AMA).

It's important to note that there may be other definitions or meanings of "Gastritis, Atrophic" in the medical field, and this definition is not intended to be an exhaustive or definitive one.

The information provided herein is only for informational purposes, and it should not be relied upon as medical advice or a substitute for professional medical care. If you have any specific questions or concerns about your health, or if you are seeking medical attention, you should consult with a qualified healthcare provider who can provide personalized and appropriate care based on your individual needs.

Causes:

* Genetic mutations or deletions
* Infections such as meningitis or encephalitis
* Stroke or bleeding in the brain
* Traumatic head injury
* Multiple sclerosis or other demyelinating diseases
* Brain tumors
* Cerebellar degeneration due to aging

Symptoms:

* Coordination difficulties, such as stumbling or poor balance
* Tremors or shaky movements
* Slurred speech and difficulty with fine motor skills
* Nystagmus (involuntary eye movements)
* Difficulty with gait and walking
* Fatigue, weakness, and muscle wasting

Diagnosis:

* Physical examination and medical history
* Neurological examination to test coordination, balance, and reflexes
* Imaging studies such as MRI or CT scans to rule out other conditions
* Genetic testing to identify inherited forms of cerebellar ataxia
* Electromyography (EMG) to test muscle activity and nerve function

Treatment:

* Physical therapy to improve balance, coordination, and gait
* Occupational therapy to help with daily activities and fine motor skills
* Speech therapy to address slurred speech and communication difficulties
* Medications to manage symptoms such as tremors or spasticity
* Assistive devices such as canes or walkers to improve mobility

Prognosis:

* The prognosis for cerebellar ataxia varies depending on the underlying cause. In some cases, the condition may be slowly progressive and lead to significant disability over time. In other cases, the condition may remain stable or even improve with treatment.

Living with cerebellar ataxia can be challenging, but there are many resources available to help individuals with the condition manage their symptoms and maintain their quality of life. These resources may include:

* Physical therapy to improve balance and coordination
* Occupational therapy to assist with daily activities
* Speech therapy to address communication difficulties
* Assistive devices such as canes or walkers to improve mobility
* Medications to manage symptoms such as tremors or spasticity
* Support groups for individuals with cerebellar ataxia and their families

Overall, the key to managing cerebellar ataxia is early diagnosis and aggressive treatment. With proper management, individuals with this condition can lead active and fulfilling lives despite the challenges they face.

The symptoms of Alzheimer's disease can vary from person to person and may progress slowly over time. Early symptoms may include memory loss, confusion, and difficulty with problem-solving. As the disease progresses, individuals may experience language difficulties, visual hallucinations, and changes in mood and behavior.

There is currently no cure for Alzheimer's disease, but there are several medications and therapies that can help manage its symptoms and slow its progression. These include cholinesterase inhibitors, memantine, and non-pharmacological interventions such as cognitive training and behavioral therapy.

Alzheimer's disease is a significant public health concern, affecting an estimated 5.8 million Americans in 2020. It is the sixth leading cause of death in the United States, and its prevalence is expected to continue to increase as the population ages.

There is ongoing research into the causes and potential treatments for Alzheimer's disease, including studies into the role of inflammation, oxidative stress, and the immune system. Other areas of research include the development of biomarkers for early detection and the use of advanced imaging techniques to monitor progression of the disease.

Overall, Alzheimer's disease is a complex and multifactorial disorder that poses significant challenges for individuals, families, and healthcare systems. However, with ongoing research and advances in medical technology, there is hope for improving diagnosis and treatment options in the future.

There are many different types of uveal diseases, including:

1. Uveitis: This is inflammation of the uvea, which can be caused by a variety of factors such as infection, injury, or autoimmune disorders.
2. Iridocyclitis: This is inflammation of the iris and ciliary body.
3. Choroiditis: This is inflammation of the choroid layer of the uvea.
4. Retinal vein occlusion: This is a blockage of the veins that carry blood away from the retina, which can cause vision loss.
5. Macular edema: This is swelling of the macula, the part of the retina responsible for central vision.
6. Age-related macular degeneration (AMD): This is a condition that affects the macula and can cause vision loss over time.
7. Diabetic retinopathy: This is a complication of diabetes that can cause damage to the blood vessels in the retina and lead to vision loss.
8. Retinal detachment: This is a condition where the retina becomes separated from the underlying tissue, leading to vision loss.
9. Retinal vein thrombosis: This is a blockage of the veins that carry blood away from the retina, which can cause vision loss.
10. Uveal melanoma: This is a type of cancer that affects the uvea and can be potentially life-threatening.

These are just a few examples of uveal diseases, and there are many other conditions that can affect the uvea as well. Treatment options for uveal diseases vary depending on the specific condition and its cause, but may include medications, laser surgery, or other procedures to treat inflammation, reduce swelling, or remove tumors.

There are two main types of SNP:

1. Steele-Richardson-Olszewski syndrome (SRO): This is the most common form of SNP and is characterized by progressive gait disturbance, rigidity, and dementia.
2. Richardson's syndrome: This type is characterized by a more rapid progression of symptoms, including early cognitive decline and dementia.

The symptoms of SNP can vary from person to person and may include:

* Difficulty walking or maintaining balance
* Rigidity or stiffness in the muscles
* Loss of coordination and equilibrium
* Slurred speech and difficulty with swallowing
* Vision problems, including double vision or difficulty focusing
* Cognitive decline and dementia

There is currently no cure for SNP, but various medications and therapies can help manage the symptoms and slow down the progression of the disease. These may include:

* Medications to control rigidity and tremors
* Physical therapy to maintain mobility and balance
* Speech therapy to improve communication and swallowing difficulties
* Occupational therapy to assist with daily activities
* Cognitive therapy to slow down cognitive decline

It is important for individuals with SNP to receive timely and accurate diagnosis and treatment from a team of specialists, including neurologists, geriatricians, physical therapists, occupational therapists, speech therapists, and social workers. With appropriate care and support, individuals with SNP can improve their quality of life and maintain independence for as long as possible.

The symptoms of Shy-Drager Syndrome can vary widely among individuals and may include:

* Cognitive decline
* Memory loss
* Difficulty with speech and language
* Loss of coordination and balance
* Dysphagia (difficulty swallowing)
* Weakness or paralysis of the limbs
* Bladder and bowel dysfunction
* Sleep disturbances

The exact cause of Shy-Drager Syndrome is not yet fully understood, but it is believed to be related to an autoimmune response, in which the body's immune system mistakenly attacks healthy cells in the brain. Genetic factors may also play a role in the development of the disorder.

There is no cure for Shy-Drager Syndrome, but various medications and therapies can help manage its symptoms. These may include:

* Cholinesterase inhibitors to improve cognitive function and slow the progression of dementia
* Anticholinergic drugs to reduce muscle rigidity and tremors
* Physical therapy to maintain mobility and strength
* Speech and language therapy to improve communication skills
* Occupational therapy to support daily living activities

The prognosis for Shy-Drager Syndrome is generally poor, with a median survival time of around 10-15 years after onset of symptoms. However, the rate of progression can vary widely among individuals, and some may experience a more gradual decline over several decades.

Overall, Shy-Drager Syndrome is a rare and complex disorder that requires careful management by a multidisciplinary team of healthcare professionals. While there is no cure for the condition, various therapies can help manage its symptoms and improve the quality of life for affected individuals.

Types of Cognition Disorders: There are several types of cognitive disorders that affect different aspects of cognitive functioning. Some common types include:

1. Attention Deficit Hyperactivity Disorder (ADHD): Characterized by symptoms of inattention, hyperactivity, and impulsivity.
2. Traumatic Brain Injury (TBI): Caused by a blow or jolt to the head that disrupts brain function, resulting in cognitive, emotional, and behavioral changes.
3. Alzheimer's Disease: A progressive neurodegenerative disorder characterized by memory loss, confusion, and difficulty with communication.
4. Stroke: A condition where blood flow to the brain is interrupted, leading to cognitive impairment and other symptoms.
5. Parkinson's Disease: A neurodegenerative disorder that affects movement, balance, and cognition.
6. Huntington's Disease: An inherited disorder that causes progressive damage to the brain, leading to cognitive decline and other symptoms.
7. Frontotemporal Dementia (FTD): A group of neurodegenerative disorders characterized by changes in personality, behavior, and language.
8. Post-Traumatic Stress Disorder (PTSD): A condition that develops after a traumatic event, characterized by symptoms such as anxiety, avoidance, and hypervigilance.
9. Mild Cognitive Impairment (MCI): A condition characterized by memory loss and other cognitive symptoms that are more severe than normal age-related changes but not severe enough to interfere with daily life.

Causes and Risk Factors: The causes of cognition disorders can vary depending on the specific disorder, but some common risk factors include:

1. Genetics: Many cognitive disorders have a genetic component, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease.
2. Age: As people age, their risk of developing cognitive disorders increases, such as Alzheimer's disease, vascular dementia, and frontotemporal dementia.
3. Lifestyle factors: Factors such as physical inactivity, smoking, and poor diet can increase the risk of cognitive decline and dementia.
4. Traumatic brain injury: A severe blow to the head or a traumatic brain injury can increase the risk of developing cognitive disorders, such as chronic traumatic encephalopathy (CTE).
5. Infections: Certain infections, such as meningitis and encephalitis, can cause cognitive disorders if they damage the brain tissue.
6. Stroke or other cardiovascular conditions: A stroke or other cardiovascular conditions can cause cognitive disorders by damaging the blood vessels in the brain.
7. Chronic substance abuse: Long-term use of drugs or alcohol can damage the brain and increase the risk of cognitive disorders, such as dementia.
8. Sleep disorders: Sleep disorders, such as sleep apnea, can increase the risk of cognitive disorders, such as dementia.
9. Depression and anxiety: Mental health conditions, such as depression and anxiety, can increase the risk of cognitive decline and dementia.
10. Environmental factors: Exposure to certain environmental toxins, such as pesticides and heavy metals, has been linked to an increased risk of cognitive disorders.

It's important to note that not everyone with these risk factors will develop a cognitive disorder, and some people without any known risk factors can still develop a cognitive disorder. If you have concerns about your cognitive health, it's important to speak with a healthcare professional for proper evaluation and diagnosis.

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

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

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

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

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

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

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

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

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

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

There are several types of spinocerebellar degenerations, including:

1. Spinocerebellar ataxia (SCA): This is the most common type of spinocerebellar degeneration, and it is caused by a mutation in one of several genes that code for proteins involved in the function of the cerebellum and spinal cord.
2. Spinocerebellar neurodegeneration with axonal degeneration (SCN1A): This type of spinocerebellar degeneration is caused by a mutation in the SCN1A gene, which codes for a protein that regulates the flow of sodium ions in and out of nerve cells.
3. Spinocerebellar neurodegeneration with Purkinje cell loss (SCN2): This type of spinocerebellar degeneration is caused by a mutation in the SCN2 gene, which codes for a protein that plays a role in the regulation of the cytoskeleton in nerve cells.
4. Spinocerebellar neurodegeneration with optic atrophy (SCN3): This type of spinocerebellar degeneration is caused by a mutation in the SCN3 gene, which codes for a protein that plays a role in the regulation of the cytoskeleton in nerve cells.

The symptoms of spinocerebellar degenerations can vary depending on the specific type of disorder and the age at which they appear. In general, these disorders are characterized by:

1. Progressive loss of motor function: Patients with spinocerebellar degenerations may experience weakness, tremors, and difficulty with coordination and balance.
2. Cognitive decline: Spinocerebellar degenerations can also cause cognitive decline, including memory loss, confusion, and difficulty with language processing.
3. Seizures: Some patients with spinocerebellar degenerations may experience seizures.
4. Vision loss: Spinocerebellar degenerations can cause progressive vision loss, including blindness.
5. Sleep disturbances: Patients with spinocerebellar degenerations may experience sleep disturbances, including insomnia and restlessness.
6. Emotional changes: Spinocerebellar degenerations can also cause emotional changes, such as depression, anxiety, and mood swings.

The diagnosis of spinocerebellar degeneration is based on a combination of clinical examination, imaging studies, and genetic testing. Imaging studies, such as magnetic resonance imaging (MRI) and positron emission tomography (PET), can help to identify the specific type of disorder and the extent of brain damage. Genetic testing can help to confirm the diagnosis by identifying a mutation in one of the genes associated with spinocerebellar degeneration.

There is currently no cure for spinocerebellar degenerations, but there are several treatments available that can help to manage the symptoms and slow the progression of the disease. These include:

1. Physical therapy: Physical therapy can help to improve motor function and balance.
2. Occupational therapy: Occupational therapy can help patients to adapt to their condition and maintain independence.
3. Speech therapy: Speech therapy can help to improve communication and swallowing difficulties.
4. Medications: Various medications, such as anticonvulsants, muscle relaxants, and pain relievers, can be used to manage seizures, muscle spasms, and pain.
5. Deep brain stimulation: Deep brain stimulation is a surgical procedure that involves implanting an electrode in the brain to deliver electrical impulses to specific areas of the brain. This can help to improve motor function and reduce symptoms.
6. Stem cell therapy: Stem cell therapy is a promising area of research for the treatment of spinocerebellar degenerations. Stem cells have the ability to differentiate into different types of cells, including neurons, and may help to replace damaged cells in the brain.
7. Gene therapy: Gene therapy involves using genes to treat or prevent diseases. This can involve replacing a faulty gene with a healthy one or silencing a faulty gene. Gene therapy is still in its infancy for spinocerebellar degenerations, but it is an area of active research.
8. Physical activity: Regular physical activity has been shown to improve motor function and overall health in patients with spinocerebellar degenerations.
9. Cognitive rehabilitation: Cognitive rehabilitation can help to improve cognitive function and independence in daily activities.
10. Supportive care: Supportive care, such as physical therapy, occupational therapy, and speech therapy, can help to improve quality of life and manage symptoms.

It's important to note that the most effective treatment plan for spinocerebellar degenerations will depend on the specific type of disease, the severity of symptoms, and the individual needs of each patient. It is best to work with a healthcare provider to develop a personalized treatment plan.

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

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

Disease progression can be influenced by various factors, including:

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

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

There are several subtypes of myoclonic epilepsies, including:

1. Lafora disease: This is a rare, autosomal recessive disorder caused by mutations in the EPM2A (Laforin) gene. It is characterized by progressive myoclonus, seizures, and cognitive decline.
2. Epilepsy with Myoclonic-Atrophic Rings (EMAR): This is a rare, autosomal recessive disorder caused by mutations in the GRIN1 gene. It is characterized by myoclonus, ataxia, and progressive cognitive decline.
3. Unverricht-Lundborg disease: This is a rare, autosomal recessive disorder caused by mutations in the GABRA1 gene. It is characterized by myoclonus, ataxia, and seizures.
4. Other forms of progressive myoclonic epilepsy: These include rare conditions such as progressive myoclonic epilepsy type 1B (EPM1B), progressive myoclonic epilepsy type 2A (EPM2A), and others.

The symptoms of myoclonic epilepsies, progressive type, can vary depending on the specific subtype and severity of the condition. Common symptoms include:

* Recurrent seizures, including myoclonus (muscle jerks) and other types of seizures
* Muscle stiffness or rigidity
* Ataxia (loss of coordination and balance)
* Cognitive decline and developmental delays
* Vision problems
* Hearing loss
* Autism spectrum disorder

The exact causes of myoclonic epilepsies, progressive type, are not fully understood. However, genetic mutations are thought to play a role in many cases. Some of these conditions are inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. Others may be caused by sporadic mutations or other factors.

There is no cure for myoclonic epilepsies, progressive type, but various treatments can help manage the symptoms. These may include:

* Anticonvulsant medications to control seizures
* Physical therapy to improve coordination and balance
* Occupational therapy to develop daily living skills
* Speech therapy to improve communication
* Assistive devices such as walkers or wheelchairs
* Surgery in some cases to remove the affected area of the brain

The prognosis for myoclonic epilepsies, progressive type, is generally poor, with many individuals experiencing worsening symptoms over time. However, with appropriate treatment and support, some individuals are able to lead relatively active and fulfilling lives despite their condition.

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

* Alzheimer's disease: This is the most common form of dementia, accounting for 50-70% of all cases. It is a progressive disease that causes the death of brain cells, leading to memory loss and cognitive decline.
* Vascular dementia: This type of dementia is caused by problems with blood flow to the brain, often as a result of a stroke or small vessel disease. It can cause difficulty with communication, language, and visual-spatial skills.
* Lewy body dementia: This type of dementia is characterized by the presence of abnormal protein deposits called Lewy bodies in the brain. It can cause a range of symptoms, including memory loss, confusion, hallucinations, and difficulty with movement.
* Frontotemporal dementia: This is a group of diseases that affect the front and temporal lobes of the brain, leading to changes in personality, behavior, and language.

The symptoms of dementia can vary depending on the underlying cause, but common symptoms include:

* Memory loss: Difficulty remembering recent events or learning new information.
* Communication and language difficulties: Struggling to find the right words or understand what others are saying.
* Disorientation: Getting lost in familiar places or having difficulty understanding the time and date.
* Difficulty with problem-solving: Trouble with planning, organizing, and decision-making.
* Mood changes: Depression, anxiety, agitation, or aggression.
* Personality changes: Becoming passive, suspicious, or withdrawn.
* Difficulty with movement: Trouble with coordination, balance, or using utensils.
* Hallucinations: Seeing or hearing things that are not there.
* Sleep disturbances: Having trouble falling asleep or staying asleep.

The symptoms of dementia can be subtle at first and may progress slowly over time. In the early stages, they may be barely noticeable, but as the disease progresses, they can become more pronounced and interfere with daily life. It is important to seek medical advice if you or a loved one is experiencing any of these symptoms, as early diagnosis and treatment can help improve outcomes.

Some common types of brain diseases include:

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

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

There are two main types of MD:

1. Dry Macular Degeneration (DMD): This is the most common form of MD, accounting for about 90% of cases. It is caused by the gradual accumulation of waste material in the macula, which can lead to cell death and vision loss over time.
2. Wet Macular Degeneration (WMD): This type of MD is less common but more aggressive, accounting for about 10% of cases. It occurs when new blood vessels grow underneath the retina, leaking fluid and causing damage to the macula. This can lead to rapid vision loss if left untreated.

The symptoms of MD can vary depending on the severity and type of the condition. Common symptoms include:

* Blurred vision
* Distorted vision (e.g., straight lines appearing wavy)
* Difficulty reading or recognizing faces
* Difficulty adjusting to bright light
* Blind spots in central vision

MD can have a significant impact on daily life, making it difficult to perform everyday tasks such as driving, reading, and recognizing faces.

There is currently no cure for MD, but there are several treatment options available to slow down the progression of the disease and manage its symptoms. These include:

* Anti-vascular endothelial growth factor (VEGF) injections: These medications can help prevent the growth of new blood vessels and reduce inflammation in the macula.
* Photodynamic therapy: This involves the use of a light-sensitive drug and low-intensity laser to damage and shrink the abnormal blood vessels in the macula.
* Vitamin supplements: Certain vitamins, such as vitamin C, E, and beta-carotene, have been shown to slow down the progression of MD.
* Laser surgery: This can be used to reduce the number of abnormal blood vessels in the macula and improve vision.

It is important for individuals with MD to receive regular monitoring and treatment from an eye care professional to manage their condition and prevent complications.

Some common types of cerebellar diseases include:

1. Cerebellar atrophy: This is a condition where the cerebellum shrinks or degenerates, leading to symptoms such as tremors, muscle weakness, and difficulty with movement.
2. Cerebellar degeneration: This is a condition where the cerebellum deteriorates over time, leading to symptoms such as loss of coordination, balance problems, and difficulties with speech and language.
3. Cerebellar tumors: These are abnormal growths that develop in the cerebellum, which can cause a variety of symptoms depending on their size and location.
4. Cerebellar stroke: This is a condition where blood flow to the cerebellum is interrupted, leading to damage to the brain tissue and symptoms such as weakness or paralysis of certain muscle groups.
5. Cerebellar vasculature disorders: These are conditions that affect the blood vessels in the cerebellum, leading to symptoms such as transient ischemic attacks (TIAs) or strokes.
6. Inflammatory diseases: These are conditions that cause inflammation in the cerebellum, leading to symptoms such as tremors, ataxia, and weakness.
7. Infections: Bacterial, viral, or fungal infections can affect the cerebellum and cause a range of symptoms.
8. Trauma: Head injuries or other forms of trauma can damage the cerebellum and lead to symptoms such as loss of coordination, balance problems, and memory loss.
9. Genetic disorders: Certain genetic mutations can affect the development and function of the cerebellum, leading to a range of symptoms.
10. Degenerative diseases: Conditions such as multiple sclerosis, Parkinson's disease, and Huntington's disease can cause degeneration of the cerebellum and lead to symptoms such as tremors, ataxia, and weakness.

It's important to note that this is not an exhaustive list, and there may be other causes of cerebellar symptoms not included here. A healthcare professional can help determine the underlying cause of your symptoms based on a thorough medical history and examination.

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

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

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

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

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

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

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

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

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

Some common examples of neurodegenerative diseases include:

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

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

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

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

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

There are several subtypes of FTD, each with distinct clinical features and rates of progression. The most common subtypes include:

1. Behavioral variant FTD (bvFTD): This subtype is characterized by changes in personality, behavior, and social conduct, such as a lack of empathy, impulsivity, and aggression.
2. Language variant FTD (lvFTD): This subtype is characterized by progressive language decline, including difficulty with word-finding, syntax, and comprehension.
3. Primary progressive agrammatic alexia (PPA): This subtype is characterized by progressive loss of language abilities, including grammar and word retrieval.
4. Progressive supranuclear palsy (PSP): This subtype is characterized by slow movement, rigidity, and dementia, with a higher risk of developing parkinsonism.

The exact cause of FTD is not yet fully understood, but it is believed to be linked to abnormal protein accumulation in the brain, including tau and TDP-43 proteins. There is currently no cure for FTD, but various medications and therapies can help manage its symptoms and slow its progression.

FTD can be challenging to diagnose, as it can resemble other conditions such as Alzheimer's disease or frontal lobe lesions. A definitive diagnosis is typically made through a combination of clinical evaluation, neuroimaging, and pathological analysis of brain tissue after death.

FTD has a significant impact on patients and their families, affecting not only cognitive function but also behavior, mood, and social relationships. It can also place a significant burden on caregivers, who may need to provide around-the-clock support and assistance.

Overall, FTD is a complex and heterogeneous disorder that requires further research to better understand its causes, improve diagnostic accuracy, and develop effective treatments.

There are several causes of muscle weakness, including:

1. Neuromuscular diseases: These are disorders that affect the nerves that control voluntary muscle movement, such as amyotrophic lateral sclerosis (ALS) and polio.
2. Musculoskeletal disorders: These are conditions that affect the muscles, bones, and joints, such as arthritis and fibromyalgia.
3. Metabolic disorders: These are conditions that affect the body's ability to produce energy, such as hypoglycemia and hypothyroidism.
4. Injuries: Muscle weakness can occur due to injuries such as muscle strains and tears.
5. Infections: Certain infections such as botulism and Lyme disease can cause muscle weakness.
6. Nutritional deficiencies: Deficiencies in vitamins and minerals such as vitamin D and B12 can cause muscle weakness.
7. Medications: Certain medications such as steroids and anticonvulsants can cause muscle weakness as a side effect.

The symptoms of muscle weakness can vary depending on the underlying cause, but may include:

1. Fatigue: Feeling tired or weak after performing simple tasks.
2. Lack of strength: Difficulty lifting objects or performing physical activities.
3. Muscle cramps: Spasms or twitches in the muscles.
4. Muscle wasting: Loss of muscle mass and tone.
5. Difficulty speaking or swallowing: In cases where the muscle weakness affects the face, tongue, or throat.
6. Difficulty walking or standing: In cases where the muscle weakness affects the legs or lower back.
7. Droopy facial features: In cases where the muscle weakness affects the facial muscles.

If you are experiencing muscle weakness, it is important to seek medical attention to determine the underlying cause and receive proper treatment. A healthcare professional will perform a physical examination and may order diagnostic tests such as blood tests or imaging studies to help diagnose the cause of the muscle weakness. Treatment will depend on the underlying cause, but may include medication, physical therapy, or lifestyle changes. In some cases, muscle weakness may be a sign of a serious underlying condition that requires prompt medical attention.

The diagnosis of MCI requires a comprehensive medical evaluation, including a thorough history, physical examination, laboratory tests, and cognitive assessments. The goal of the diagnosis is to differentiate MCI from normal aging and other conditions that may cause similar symptoms, such as depression or medication side effects.

There are several subtypes of MCI, including:

1. Amnestic Mild Cognitive Impairment (aMCI): Characterized by memory loss, especially for episodic memory (memory of events and experiences).
2. Non-amnestic Mild Cognitive Impairment (naMCI): Characterized by cognitive impairment without memory loss.
3. Mixed Mild Cognitive Impairment (mMCI): Characterized by a combination of amnestic and non-amnestic symptoms.

The main risk factor for developing MCI is advancing age, but other factors such as family history, genetics, and lifestyle factors may also contribute to the development of the condition. There is currently no cure for MCI, but there are several treatment options available to slow down cognitive decline and improve quality of life. These include:

1. Cognitive training and rehabilitation: To improve memory, attention, and other cognitive functions.
2. Medications: Such as cholinesterase inhibitors, which can improve cognitive function and slow down decline.
3. Lifestyle changes: Such as regular exercise, social engagement, and management of chronic health conditions.
4. Alternative therapies: Such as cognitive training, mindfulness-based interventions, and herbal supplements.

Early detection and treatment of MCI can potentially delay progression to dementia, improve quality of life, and reduce caregiver burden. However, the exact timing and duration of these benefits are not yet fully understood. Further research is needed to understand the mechanisms underlying MCI and to develop more effective treatments for this condition.

In summary, mild cognitive impairment (MCI) is a condition characterized by cognitive decline beyond what is expected for an individual's age and education level, but not severe enough to interfere with daily life. There are three subtypes of MCI, and the main risk factor is advancing age. Treatment options include cognitive training and rehabilitation, medications, lifestyle changes, and alternative therapies. Early detection and treatment may potentially delay progression to dementia and improve quality of life.

MND is often fatal, usually within 2-5 years of diagnosis. There is currently no cure for MND, although various treatments and therapies can help manage the symptoms and slow its progression.

The most common types of MND are amyotrophic lateral sclerosis (ALS) and primary lateral sclerosis (PLS). ALS is characterized by rapid degeneration of motor neurons in the brain and spinal cord, leading to muscle weakness and paralysis. PLS is a slower-progressing form of MND that affects only the lower motor neurons.

MND can be caused by a variety of factors, including genetics, age, and exposure to toxins. It is often diagnosed through a combination of medical history, physical examination, and diagnostic tests such as electromyography (EMG) and magnetic resonance imaging (MRI).

There is ongoing research into the causes and potential treatments for MND, including stem cell therapy, gene therapy, and drugs that target specific molecules involved in the disease process.

Symptoms of gastritis may include abdominal pain, nausea, vomiting, loss of appetite, and difficulty swallowing. In severe cases, bleeding may occur in the stomach and black tarry stools may be present.

Diagnosis of gastritis is typically made through endoscopy, during which a flexible tube with a camera and light on the end is inserted through the mouth to visualize the inside of the stomach. Biopsies may also be taken during this procedure to examine the stomach tissue under a microscope for signs of inflammation or infection.

Treatment of gastritis depends on the underlying cause, but may include antibiotics for bacterial infections, anti-inflammatory medications, and lifestyle modifications such as avoiding alcohol, losing weight, and eating smaller more frequent meals. In severe cases, surgery may be necessary to remove damaged tissue or repair any ulcers that have developed.

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... leads to muscle weakness and causes disability. Disuse causes rapid muscle atrophy and often occurs during ... Atrophy of the throat muscles may cause difficulty swallowing and diaphragm atrophy can cause difficulty breathing. Muscle ... Media related to Muscle atrophy at Wikimedia Commons Muscular atrophy at the US National Library of Medicine Medical Subject ... such as the various spinal muscular atrophies. Muscle atrophy results from an imbalance between protein synthesis and protein ...
Brain atrophy can be classified into two main categories: generalized and focal atrophy. Generalized atrophy occurs across the ... Cerebral atrophy is a common feature of many of the diseases that affect the brain. Atrophy of any tissue means a decrement in ... Besides brain atrophy, aging has also been associated with cerebral microbleeds. Many diseases that cause cerebral atrophy are ... Cerebral atrophy can be hard to distinguish from hydrocephalus because both cerebral atrophy and hydrocephalus involve an ...
... -deafness syndrome "Multiple system atrophy - cerebellar subtype: MedlinePlus Medical Encyclopedia ... Olivopontocerebellar atrophy (OPCA) is the degeneration of neurons in specific areas of the brain - the cerebellum, pons, and ... Olivopontocerebellar atrophy is hereditary, but has an unknown genetic basis. There are two forms: A few non-hereditary ... "NINDS Olivopontocerebellar Atrophy Information Page". Archived from the original on 2012-01-27. Retrieved 7 Feb 2012. synd/1903 ...
... is the normal or spontaneous atrophy or shrinkage of the breasts. Breast atrophy commonly occurs in women during ... breast atrophy may be a desired effect. Examples of treatment options for breast atrophy, depending on the situation/when ...
... (GA), also known as atrophic age-related macular degeneration (AMD) or advanced dry AMD, is an advanced form ... Geographic atrophy is a chronic disease, which leads to visual function loss. This often results in difficulties performing ... Diagnosis of geographic atrophy is made by an ophthalmologist in the clinic. Fundus autofluorescence and optical coherence ... Reading speed is often initially unaffected due to foveal sparing, but worsens progressively as the area of atrophy enlarges. ...
"Atrophy - Might Release New Music This Year". Metal Storm. January 31, 2022. Retrieved January 31, 2022. "Atrophy - From Now On ... "Atrophy - New Music In Progress". metalstorm.net. April 4, 2018. Retrieved April 4, 2018. "ATROPHY Frontman Offers Update On ... "Atrophy - Working On New Music". metalstorm.net. October 24, 2016. Retrieved April 4, 2018. "Thrash Underdogs Atrophy Return ... "Atrophy". sputnikmusic.com. Retrieved November 21, 2013. "Atrophy - Discography - Metal Kingdom". metalkingdom.net. Retrieved ...
Testicular volume measured to be less than 12 mL is a sign of testicular atrophy. In addition, testicular atrophy can be ... Testicular atrophy is a medical condition in which one or both testicles (or "testes") diminish in size and may be accompanied ... Testicular atrophy is not related to the temporary shrinkage of the surrounding scrotum, which might occur in response to cold ... Testicular atrophy is also a side effect of estrogen therapy. COVID-19 can lead to reduced testosterone production and ...
... is the diminished capacity to appreciate new or unfamiliar music or other sensory stimuli. It is typically ... Cizmar, Martin (31 December 2009). "The Scourge of Aesthetic Atrophy, and the Top 50 Albums of the Aughts". Phoenix New Times. ...
... can be explained as cell loss and gliosis or a proliferation of astrocytes in damaged areas of the ... "Multiple system atrophy" at Dorland's Medical Dictionary Peng C, Gathagan RJ, Covell DJ, Medellin C, Stieber A, Robinson JL, et ... Multiple system atrophy is estimated to affect approximately 5 per 100,000 people. At autopsy, many patients diagnosed during ... In MSA-C, a "hot cross bun" sign is sometimes found; it reflects atrophy of the pontocerebellar tracts that give T2 hyper ...
Aran-Duchenne muscular atrophy, and Duchenne-Aran muscular atrophy. The name "spinal muscular atrophy" is ambiguous as it ... Progressive muscular atrophy (PMA), also called Duchenne-Aran disease and Duchenne-Aran muscular atrophy, is a disorder ... The condition has been called progressive muscular atrophy (PMA), spinal muscular atrophy (SMA), Aran-Duchenne disease, ... Instead, a number of other possibilities have to be ruled out, such as multifocal motor neuropathy or spinal muscular atrophy. ...
... since the area of atrophy involves the occipital lobe responsible for visual processing. The atrophy is progressive; early ... Over time, however, atrophy in PCA may spread to regions that are commonly damaged in AD, leading to shared AD symptoms such as ... Posterior cortical atrophy (PCA), also called Benson's syndrome, is a rare form of dementia which is considered a visual ... At this early stage brain atrophy will be shown to be more centrally located in the right posterior lobe and occipital gyrus, ...
2006). "Neuronal Atrophy and Synaptic Alteration in a Mouse Model of Dentatorubral-pallidoluysian Atrophy". Brain. 129 (Pt 9): ... Again, neuronal atrophy was noted, but no neuronal loss (until death). Diffuse accumulation in the nuclei began on post-natal ... Dentatorubral-pallidoluysian atrophy (DRPLA) is an autosomal dominant spinocerebellar degeneration caused by an expansion of a ... 1994). "Dentatorubral-pallidoluysian atrophy and Haw River Syndrome". Lancet. 344 (8938): 1711-2. doi:10.1016/S0140-6736(94) ...
... (PRA) is a group of genetic diseases seen in certain breeds of dogs and, more rarely, cats. Similar ... Central progressive retinal atrophy (CPRA) is a different disease from PRA involving the retinal pigment epithelium (RPE), and ... "Progressive Retinal Atrophy in Dogs". Pet Health Network. Retrieved 2019-12-21. Article on PRA Article on Cataracts (CS1 errors ... The pigmented spots eventually coalesce and fade as the atrophy of the retina increases. It is an inherited condition (in the ...
"Spinal Muscular Atrophy". NORD (National Organization for Rare Disorders). Retrieved 27 May 2019. "Spinal muscular atrophy". ... "Spinal muscular atrophy: MedlinePlus Genetics". medlineplus.gov. Retrieved 24 October 2020. "Spinal Muscular Atrophy (SMA) , ... "Spinal muscular atrophy". Genetics Home Reference. Retrieved 27 May 2019. "Spinal Muscular Atrophy - Conditions , Children's ... Spinal muscular atrophy, Motor neuron diseases, Autosomal recessive disorders, Nucleus diseases, Systemic atrophies primarily ...
... is a rare genetic disorder characterized by olivopontocerebellar atrophy which ... "Olivopontocerebellar atrophy deafness - About the Disease - Genetic and Rare Diseases Information Center". rarediseases.info. ... Pratap-Chand, R.; Gururaj, A. K.; Dilip-Kumar, S. (1995-02-01). "A syndrome of olivopontocerebellar atrophy and deafness with ... "Olivopontocerebellar Atrophy: Background, Pathophysiology, Epidemiology". 2022-03-11. {{cite journal}}: Cite journal requires , ...
ISBN 978-4-263-20140-4. (skin atrophy caused during application of the steroid ointment). "Steroid Atrophy". (CS1: long volume ... Steroid-induced skin atrophy is thinning of the skin as a result of prolonged exposure to steroids. In people with psoriasis ... Skin atrophy can occur with both prescription and over the counter steroids creams. Low doses of prednisone by mouth can also ... Steroid-induced skin atrophy is often permanent, though if caught soon enough and the topical corticosteroid discontinued in ...
June 2012). "Autosomal dominant congenital spinal muscular atrophy: a true form of spinal muscular atrophy caused by early loss ... Congenital distal spinal muscular atrophy is a hereditary condition characterized by muscle wasting (atrophy), particularly of ... The presentation is as follows:[citation needed] Neurogenic muscle weakness Atrophy (of lower and upper limbs) Club foot ... February 2004). "Congenital form of spinal muscular atrophy predominantly affecting the lower limbs: a clinical and muscle MRI ...
"Spinal muscular atrophy, jokela type (Concept Id: C3554398) - MedGen - NCBI". www.ncbi.nlm.nih.gov. Retrieved 5 May 2021. " ... The disease is slowly progressive with adult onset and results in weakness and mild muscle atrophy. The disease does not affect ... Jokela type spinal muscular atrophy (SMAJ), also known as late-onset spinal motor neuronopathy (LOSMoN), is an ultra-rare ... Medicine portal Chromosome 22 Finnish heritage disease Spinal muscular atrophies "Uusi hitaasti etenevä motoneuronitauti ...
"Clinical Features of Spinal and Bulbar Muscular Atrophy". "OMIM Entry - # 313200 - SPINAL AND BULBAR MUSCULAR ATROPHY, X-LINKED ... Spinal muscular atrophies Arvin, Shelley (2013-04-01). "Analysis of inconsistencies in terminology of spinal and bulbar ... In terms of the management of spinal and bulbar muscular atrophy, no cure is known and treatment is supportive. Rehabilitation ... Pennuto, Maria; Rinaldi, Carlo (2018-04-15). "From gene to therapy in spinal and bulbar muscular atrophy: Are we there yet?". ...
Other types of brown atrophy include brown atrophy of neuronia and brown atrophy of the liver.[citation needed] Atrophy ( ... Brown atrophy of the heart is atrophy of the heart muscle (or myocardium) commonly found in the elderly. It is described as ... relating to all tissues, see Muscle atrophy for atrophy in muscle tissue). Xanthosis Roffe, C (Jun 1998). "Ageing of the heart ...
... (DSMA2), also known as Jerash type distal hereditary motor neuropathy (HMNJ), is a very ... Spinal muscular atrophies Distal hereditary motor neuropathies Christodoulou, K; Zamba, E; Tsingis, M; Mubaidin, A; Horani, K; ...
"Keratosis follicularis dwarfism and cerebral atrophy". "Keratosis Follicularis Dwarfism and Cerebral Atrophy". DoveMed. ... "Entry - 308830 - KERATOSIS FOLLICULARIS, DWARFISM, AND CEREBRAL ATROPHY - OMIM". omim.org. Retrieved 2022-09-25. Cantu, J. M.; ... Keratosis follicularis-dwarfism-cerebral atrophy syndrome is a rare, presumably X-linked recessive genetic disorder ... "Keratosis follicularis dwarfism and cerebral atrophy - About the Disease - Genetic and Rare Diseases Information Center". ...
NR2F1 mutations cause optic atrophy with intellectual disability. American Journal of Human Genetics 94: 303-309 Chen CA, Bosch ... "OMIM Entry - # 615722 - Bosch-Boonstra-Schaaf Optic Atrophy Syndrome; BBSOAS". omim.org. Retrieved 19 January 2020. Bosch DGM, ... Bosch-Boonstra-Schaaf optic atrophy syndrome is a rare autosomally inherited condition characterised by developmental delay, ... NR2F1 mutations cause optic atrophy with intellectual disability. American Journal of Human Genetics. 94: 303-309. (Articles ...
... (MARES) This article incorporates public domain material from Muscle Atrophy ... The Muscle Atrophy Research and Exercise System (MARES), part of the Human Research Facility (HRF), was launched on 5 April ... Scientific research on the ISS ESA - MARES "NASA - Muscle Atrophy Research and Exercise System (MARES)". Archived from the ...
... (DSMA1), also known as spinal muscular atrophy with respiratory distress type 1 (SMARD1 ... Distal hereditary motor neuropathies Spinal muscular atrophies Spinal muscular atrophy Messina, M. F.; Messina, S.; Gaeta, M.; ... There is no published practice standard for the care in DSMA1, even though the Spinal Muscular Atrophy Standard of Care ... DSMA1 was identified and classified as a sub-group of spinal muscular atrophies (SMA) in 1974. Currently, various ...
Proximal spinal muscular atrophies, i.e., conditions that affect primarily proximal muscles; Distal spinal muscular atrophies ( ... In all forms of SMA (with an exception of X-linked spinal muscular atrophy type 1), only motor neurons, located at the anterior ... Spinal muscular atrophies (SMAs) are a genetically and clinically heterogeneous group of rare debilitating disorders ... Based on the type of muscles affected, spinal muscular atrophies can be divided into:[citation needed] ...
Spinal muscular atrophies Arthrogryposis Ramser, J.; Ahearn, M. E.; Lenski, C.; Yariz, K. O.; Hellebrand, H.; Von Rhein, M.; ... Symptoms resemble the more severe forms of the more common spinal muscular atrophy (SMA); however, SMAX2 is caused by a ... In infancy it is important to look for the following when considering a X-linked spinal muscular atrophy diagnosis: Congenital ... X-linked spinal muscular atrophy type 2 (SMAX2, XLSMA), also known as arthrogryposis multiplex congenita X-linked type 1 (AMCX1 ...
... (SMA-PME), sometimes called Jankovic-Rivera syndrome, is a very ... "Spinal muscular atrophy with progressive myoclonic epilepsy". Genetics Home Reference. Retrieved 2018-09-24. Zhou, J.; Tawk, M ... Jankovic, J.; Rivera, V. M. (1979). "Hereditary myoclonus and progressive distal muscular atrophy". Annals of Neurology. 6 (3 ... National Institutes of Health (December 2013). "Genetics Home Reference: Spinal muscular atrophy with progressive myoclonic ...
... , sometimes called lower extremity-predominant spinal muscular atrophy ... may refer to: Spinal muscular atrophy with lower extremity predominance 1 Spinal muscular atrophy with lower extremity ... 2B Spinal muscular atrophies This disambiguation page lists articles associated with the title Spinal muscular atrophy with ... predominance 2A Spinal muscular atrophy with lower extremity predominance ...
MSA was formerly known as Shy-Drager syndrome, olivopontocerebellar atrophy (OCPA), or striatonigral degeneration. ... Multiple system atrophy (MSA) is a progressive neurodegenerative disorder characterized by a combination of symptoms that ... What is multiple system atrophy?. Multiple system atrophy (MSA) is a progressive neurodegenerative disorder characterized by a ... How is multiple system atrophy diagnosed and treated?. Diagnosing MSA. Diagnosing MSA can be difficult, particularly in the ...
Find symptoms and other information about Spinal muscular atrophy. ... Spinal muscular atrophy (SMA) is a group of genetic neuromuscular disorders that affect the nerve cells that control voluntary ... About Spinal muscular atrophy. Many rare diseases have limited information. Currently GARD aims to provide the following ... When Do Symptoms of Spinal muscular atrophy Begin?. This section is currently in development. ...
Spinal Muscular Atrophy (SMA) is a genetic disorder that affects approximately 1 out of every 10,000 people. Most cases of SMA ...
... atrophy ) in muscles used for movement (skeletal muscles). Explore symptoms, inheritance, genetics of this condition. ... Spinal muscular atrophy is a genetic disorder characterized by weakness and wasting ( ... Spinal muscular atrophy affects 1 per 8,000 to 10,000 people worldwide. Spinal muscular atrophy type I is the most common type ... Spinal muscular atrophy is a genetic disorder characterized by weakness and wasting (atrophy. ) in muscles used for movement ( ...
Hepatocyte atrophy and glycogen depletion after 90 days of exposure to malonaldehyde. Note paucity of cytoplasm and crowding of ...
... atrophy ) in muscles used for movement (skeletal muscles). Explore symptoms, inheritance, genetics of this condition. ... Spinal muscular atrophy is a genetic disorder characterized by weakness and wasting ( ... Spinal muscular atrophy affects 1 per 8,000 to 10,000 people worldwide. Spinal muscular atrophy type I is the most common type ... Spinal muscular atrophy is a genetic disorder characterized by weakness and wasting (atrophy. ) in muscles used for movement ( ...
Adnexal atrophy is characterized by smaller and reduced numbers of pilosebaceous units (Figure 2 and Figure 3). ... Atrophy" should be used. Whenever present, adnexal atrophy, follicular atrophy, or sebaceous gland atrophy should be diagnosed ... Skin - Atrophy Narrative. Comment:. Adnexal atrophy is characterized by smaller and reduced numbers of pilosebaceous units ( ... Follicular atrophy is characterized by smaller and reduced numbers hair follicles, and sebaceous gland atrophy is characterized ...
A recent study that looked at the rate of atrophy over 18 months in cognitively normal older adults suggests that physical ... Physical activity may help prevent atrophy of the hippocampus, a brain region important for learning and memory that often ... A recent study that looked at the rate of atrophy over 18 months in cognitively normal older adults suggests that physical ... Physical activity may help prevent atrophy of the hippocampus, a brain region important for learning and memory that often ...
Dont get left behind! The modernized ClinicalTrials.gov is coming. Check it out now ...
Wonders of Technology Help Siblings with Spinal Muscular Atrophy Like most kids their age, siblings Emma and Nick Lockwood, ... The siblings have Spinal Muscular Atrophy, an inherited disease that causes loss of motor function. Their family helps run a ...
Data from a phase 1 study of the safety and efficacy of JNJ-1887 in geographic atrophy (GA) indicate that the study met its ... Data from a phase 1 study of the safety and efficacy of JNJ-1887 (Johnson & Johnson) in geographic atrophy (GA) indicate that ...
Multidisciplinary, Specialized Care for Spinal Muscular Atrophy * Fast Five Quiz: Spinal Muscular Atrophy Clinical Presentation ... Spinal muscular atrophy (SMA) refers to a group of hereditary diseases that damage and kill motor neurons in the brain and ... Best Practices in the Care of Adult Patients With Spinal Muscular Atrophy 0.5 CME / CE / ABIM MOC Credits ... Best Practices in the Care of Adult Patients With Spinal Muscular Atrophy ...
... academic and drug industry investigators say they have identified a new biological target for treating spinal muscular atrophy. ... Spinal muscular atrophy, one of the leading genetic killers of infants, arises from not having enough survival motor neuron ( ... One in 40 people carry the defective gene for spinal muscular atrophy, and as many as one in 6,000 babies in the world across ... To see if shutting down the SMN lnc-RNA could increase SMN levels and slow or stop spinal muscular atrophy, the researchers ...
Help support Wordnik (and make this page ad-free) by adopting the word eccentric atrophy. ...
Kidney atrophy means that the kidney is smaller than normal This can happen for two basic reasons. ... What causes kidney atrophy?. Kidney atrophy may be due to:. *Blocked kidney artery (known as renal artery stenosis) - blocks ... How is kidney atrophy treated?. The treatment for kidney atrophy depends on what caused the kidney to become smaller in the ... How is kidney atrophy diagnosed?. Tests for kidney atrophy include imaging tests such as ultrasound, computed tomography (CT or ...
... Posted by Roy in categories: health, life extension. ... "Many of us know from our own experiences that muscle weakness and atrophy are big problems as we become older" ...
... ... Application of DNA-based tests for diagnosis of spinal muscular atrophy in Saudi Arabia. EMHJ - Eastern Mediterranean Health ... genes in patients with spinal muscular atrophy [‎SMA]‎ using polymerase chain reaction followed by restriction site assay ...
Holekamp discuss the need to improve the referral process through educating physicians about geographic atrophy. ... Its OK if its not geographic atrophy. We dont want to miss anybody in the community who could have had access to these ... Although we may be moving toward OCT for clinical trials, its a little more sophisticated to identify the geographic atrophy ... 1, theres still an old mantra among a lot of general ophthalmologists and optometrists that geographic atrophy is a slow ...
Hypothenar atrophy, weak thumb adduction. Normal EMG despite clinically diagnosed atrophy? What could it be? ... I have some shoulder atrophy in both arms. My PT said my shoulders are dropping out of socket. There is no muscle to support ...
Apellis Submits Marketing Authorization Application to the European Medicines Agency for Pegcetacoplan for Geographic Atrophy ... About Geographic Atrophy (GA). Geographic atrophy (GA) is an advanced form of age-related macular degeneration (AMD) and a ... Apellis Submits Marketing Authorization Application to the European Medicines Agency for Pegcetacoplan for Geographic Atrophy. ... About Pegcetacoplan for Geographic Atrophy (GA). Pegcetacoplan is an investigational, targeted C3 therapy designed to regulate ...
Discover causes, natural remedies and treatments for vaginal atrophy and dryness. ... 5 Natural Ways to Treat Vaginal Dryness and Atrophy. Natural treatment options for vaginal dryness and atrophy can also serve ... Vaginal dryness, or atrophy, is when the vaginal lining thins and creates less natural lubrication, due to a decrease in levels ... What Causes Vaginal Dryness and Atrophy?. You may be wondering, why am I dry down there all of a sudden? Estrogen keeps the ...
Patients with posterior cortical atrophy (PCA-AD) show more severe visuospatial and perceptual deficits than those with typical ... Patients with posterior cortical atrophy (PCA-AD) show more severe visuospatial and perceptual deficits than those with typical ... Profound regional spectral, connectivity, and network changes reflect visual deficits in posterior cortical atrophy: an EEG ...
Progress retinal atrophy (PRA) is an encompassing name for a group of canine inherited retinal degenerations that affect many ... Progress retinal atrophy (PRA) is an encompassing name for a group of canine inherited retinal degenerations that affect many ... 00571-A: Identification of Canine Microsatellites Associated with Genes Known to Cause Progressive Retinal Atrophy in Dogs and ... Identification of Canine Microsatellites Associated with Genes Known to Cause Progressive Retinal Atrophy in Dogs and Retinitis ...
Atrophy in the left amygdala was associated with a greater decline in the MMSE scores, while atrophy in both left and right ... Atrophy of the medial and lateral temporal lobe areas is strongly associated with decline in memory, while advanced atrophy of ... Amygdala Atrophy, Plasma EPA and Cognitive Function in Older Adults. Posted by pufa , December 13, 2012 Mental Health and ... MRI-assessed atrophy in medial temporal lobe regions has been used to measure the rate of neurodegeneration in patients with ...
Ge Y, Grossman RJ, Udupa JK, Babb JS, Nyúl LG, Kolson DL. Brain atrophy in relapsing-remitting multiple sclerosis: Fractional ... Brain atrophy in relapsing-remitting multiple sclerosis: Fractional volumetric analysis of gray matter and white matter. ... Címlap » Brain atrophy in relapsing-remitting multiple sclerosis: Fractional volumetric analysis of gray matter and white ...
Bovine spinal muscular atrophy (SMA), an autosomal recessive neurodegenerative disease, has been mapped at moderate resolution ... Bovine spinal muscular atrophy (SMA), an autosomal recessive neurodegenerative disease, has been mapped at moderate resolution ... Fine-mapping and candidate gene analysis of bovine spinal muscular atrophy. Mammalian Genome, 17(1):67-76. ...
Multiple system atrophy- parkinsonian type (MSA-P) is a rare condition that causes symptoms similar to Parkinson disease. ... Multiple system atrophy - parkinsonian type. Shy-Drager syndrome; Neurologic orthostatic hypotension; Shy-McGee-Drager syndrome ... National Organization for Rare Disorders -- rarediseases.org/rare-diseases/multiple-system-atrophy ...
A single nucleotide in the SMN gene regulates splicing and is responsible for spinal muscular atrophy. Proc Natl Acad Sci U S A ... A mouse model for spinal muscular atrophy. Nat Genet. 2000;24(1):66-70.. View this article via: CrossRef PubMed Google Scholar ... Nusinersen versus sham control in infantile-onset spinal muscular atrophy. N Engl J Med. 2017;377(18):1723-1732.. View this ... Systemic peptide-mediated oligonucleotide therapy improves long-term survival in spinal muscular atrophy. Proc Natl Acad Sci U ...
Multiple System Atrophy (MSA) Therapeutics Market. Market Insights on Multiple System Atrophy (MSA) Therapeutics covering sales ... Multiple System Atrophy (MSA) Therapeutics Market by Type, Diagnosis & Region , Forecast 2023 to 2033 ...
Spinal and bulbar muscular atrophy (SBMA) is a currently untreatable adult-onset neuromuscular disease caused by expansion of a ... MiR-298 Counteracts Mutant Androgen Receptor Toxicity in Spinal and Bulbar Muscular Atrophy. Thursday, September 15, 2016. - ...
  • Spinal muscular atrophy type 0 is evident before birth and is the rarest and most severe form of the condition. (medlineplus.gov)
  • Some infants with spinal muscular atrophy type 0 also have heart defects that are present from birth (congenital). (medlineplus.gov)
  • Spinal muscular atrophy type I (also called Werdnig-Hoffmann disease) is the most common form of the condition. (medlineplus.gov)
  • Most children with spinal muscular atrophy type I do not survive past early childhood due to respiratory failure. (medlineplus.gov)
  • Spinal muscular atrophy type II (also called Dubowitz disease) is characterized by muscle weakness that develops in children between ages 6 and 12 months. (medlineplus.gov)
  • Individuals with spinal muscular atrophy type II cannot stand or walk unaided. (medlineplus.gov)
  • The life span of individuals with spinal muscular atrophy type II varies, but many people with this condition live into their twenties or thirties. (medlineplus.gov)
  • Spinal muscular atrophy type III (also called Kugelberg-Welander disease) typically causes muscle weakness after early childhood. (medlineplus.gov)
  • People with spinal muscular atrophy type III typically have a normal life expectancy. (medlineplus.gov)
  • Spinal muscular atrophy type IV is rare and often begins in early adulthood. (medlineplus.gov)
  • Spinal muscular atrophy type I is the most common type, accounting for about half of all cases. (medlineplus.gov)
  • The researchers detected this SMN long noncoding RNA, or lnc-RNA (pronounced 'link RNA') for short, in human embryonic kidney cells, brain cell samples and neurons derived from the stem cells of healthy people and those with spinal muscular atrophy type I and II. (news-medical.net)
  • Progress retinal atrophy (PRA) is an encompassing name for a group of canine inherited retinal degenerations that affect many different breeds of dog and is the phenotypic equivalent of human retinitis pigmentosa (RP). (akcchf.org)
  • WALTHAM, Mass., Dec. 16, 2022 (GLOBE NEWSWIRE) -- Apellis Pharmaceuticals Inc . (Nasdaq: APLS), a global biopharmaceutical company and leader in complement, today announced that the company has submitted a Marketing Authorization Application (MAA) to the European Medicines Agency for intravitreal pegcetacoplan, an investigational, targeted C3 therapy, for the treatment of geographic atrophy (GA) secondary to age-related macular degeneration (AMD). (biospace.com)
  • DERBY (n=621) and OAKS (n=637) are Phase 3, multicenter, randomized, double-masked, sham-controlled studies comparing the efficacy and safety of pegcetacoplan with sham injections across a broad and representative population of patients with geographic atrophy (GA) secondary to age-related macular degeneration (AMD). (biospace.com)
  • Geographic atrophy (GA) is an advanced form of age-related macular degeneration (AMD) and a leading cause of blindness that impacts more than five million people worldwide, including one million people in the United States. (biospace.com)
  • Pegcetacoplan was granted Fast Track designation by the U.S. Food and Drug Administration (FDA) for the treatment of geographic atrophy. (biospace.com)
  • Patients with posterior cortical atrophy (PCA-AD) show more severe visuospatial and perceptual deficits than those with typical AD (tAD). (nih.gov)
  • Posterior cortical atrophy (PCA). (nih.gov)
  • Atrophy of the medial and lateral temporal lobe areas is strongly associated with decline in memory , while advanced atrophy of cortical gray matter is associated with loss of executive function in patients with MCI and Alzheimer's disease. (fatsoflife.com)
  • High resolution 3T MRI showed that participants with LVH had significantly more atrophy of cortical thickness and the cerebral cortex compared to those without LVH at baseline. (thelimbic.com)
  • Brain atrophy was measured using the Scheltens scale for medial temporal atrophy , the posterior cortical atrophy scale for parietal atrophy , and the Pasquier scale for global cortical atrophy . (bvsalud.org)
  • Bovine spinal muscular atrophy (SMA), an autosomal recessive neurodegenerative disease, has been mapped at moderate resolution to the distal part of Chromosome 24. (uzh.ch)
  • Spinal muscular atrophy (SMA) is a recessive, autosomal neuromuscular disease characterized by degeneration of anterior horn spinal cord motor cells and brain stem neurons 1-5 . (bvsalud.org)
  • spinal muscular atrophy patients present muscle weakness, orthopedic problems, nutritional complications and respiratory impairment. (bvsalud.org)
  • Changes in brain structure occur early in the disease, with atrophy of the medial temporal lobe among the first changes. (fatsoflife.com)
  • For distinct regions, higher plasma EPA was associated with less gray matter atrophy of the right amygdala over 4 years, but not with changes in the other medial temporal lobe areas. (fatsoflife.com)
  • The percentage of participants with medial temporal atrophy was 56.3% in the PEX group and 35.4% in the control group . (bvsalud.org)
  • The presence of left ventricular hypertrophy (LVH) is a potential biomarker for cerebral atrophy in patients with type 2 diabetes, Australian researchers have shown. (thelimbic.com)
  • to verify the body composition and chest expansion of type II and III spinal muscular atrophy patients. (bvsalud.org)
  • patients with spinal muscular atrophy presented higher adiposity and lower chest expansion. (bvsalud.org)
  • Therefore, the aim of this study is verify the body composition and chest expansion of type II and III spinal muscular atrophy patients. (bvsalud.org)
  • Abnormal uterine findings were de Recherche et d'Application en identified in 95.8% of patients attending hysteroscopy at GESHRTH. (who.int)
  • The study revealed thymus atrophy in patients with PEM, especially the oedematous type, accompanied by changes in the peripheral lymphocyte subsets. (who.int)
  • Spinal Muscular Atrophy (SMA) is a genetic disorder that affects approximately 1 out of every 10,000 people. (cdc.gov)
  • Spinal muscular atrophy, one of the leading genetic killers of infants, arises from not having enough survival motor neuron (SMN) protein in neurons. (news-medical.net)
  • Te Pātaka Whaioranga - Pharmac has announced the funding of risdiplam (branded as Evrysdi) for people with the rare genetic disorder spinal muscular atrophy, who meet eligibility criteria from 1 May 2023. (pharmac.govt.nz)
  • Spinal muscular atrophy (SMA) is a genetic pediatric condition that affects lower motoneurons leading to their degeneration and muscle weakness. (uni-wuerzburg.de)
  • The Johns Hopkins researchers and their colleagues say the 'boosted' nusinersen therapy, if confirmed by further studies, has the potential to significantly improve the lives of people with spinal muscular atrophy, some with forms of the disease with only weeks or months to live, and others who are unable to sit, stand or walk. (news-medical.net)
  • Higher baseline plasma EPA, but no other PUFA, was significantly associated with less gray matter atrophy in a region comprising 53% right amygdala, 41% right parahippocampus and 6% right hippocampus. (fatsoflife.com)
  • Spinal muscular atrophy affects 1 per 8,000 to 10,000 people worldwide. (medlineplus.gov)
  • The progressive hemifacial atrophy (Parry-Romberg syndrome) is a rare disease of unknown etiology characterized by unilateral facial atrophy that affects skin, subcutaneous tissue, muscle, and rarely osteocartilaginous structures. (bvsalud.org)
  • Fill with grafts of dermal, fat, cartilage or bone, injection of silicone or acrylic prostheses are alternatives suggested to correct the facial atrophy. (bvsalud.org)
  • The siblings have Spinal Muscular Atrophy, an inherited disease that causes loss of motor function. (cincinnatichildrens.org)
  • Multiple system atrophy- parkinsonian type (MSA-P) is a rare condition that causes symptoms similar to Parkinson disease . (adam.com)
  • Pilot Study on Quantitative Cervical Cord and Muscular MRI in Spinal Muscular Atrophy: Promising Biomarkers of Disease Evolution and Treatment? (ucl.ac.uk)
  • Introduction: Nusinersen is a recent promising therapy approved for the treatment of spinal muscular atrophy (SMA), a rare disease characterized by the degeneration of alpha motor neurons (αMN) in the spinal cord (SC) leading to progressive muscle atrophy and dysfunction. (ucl.ac.uk)
  • Association between pseudoexfoliation and Alzheimer's disease-related brain atrophy. (bvsalud.org)
  • Early diagnosis and treatment of kidney atrophy is important to avoid further kidney damage. (kidney.org)
  • Diagnosis and appropriate correction of intrauterine anomalies are considered et d'Application en Chirurgie essential in order to increase chances of conception. (who.int)
  • There are many types of spinal muscular atrophy that are caused by changes in the same genes. (medlineplus.gov)
  • Other forms of spinal muscular atrophy and related motor neuron diseases, such as spinal muscular atrophy with progressive myoclonic epilepsy , spinal muscular atrophy with lower extremity predominance , X-linked infantile spinal muscular atrophy , and spinal muscular atrophy with respiratory distress type 1 are caused by mutations in other genes. (medlineplus.gov)
  • This type of kidney atrophy or small kidney usually does not need any special treatment. (kidney.org)
  • This type of kidney atrophy is due to a lower blood supply to the kidney(s)and/or loss of nephrons, the basic working units of the kidneys. (kidney.org)
  • Dr Patel said the findings suggest type 2 diabetes contributes to accelerated structural brain ageing and brain atrophy which manifests as cerebral atrophy. (thelimbic.com)
  • While the presence of LVH may represent a risk factor for brain atrophy and subsequent cognitive impairment, it was not yet known if LVH contributes to dementia in type 2 diabetes. (thelimbic.com)
  • Some symptoms of kidney atrophy include pain while passing urine, pain in the abdomen (belly) or flank (side and back), blood in urine, urinating more often, feeling tired (fatigue), loss of appetite, itchy skin, general discomfort in the kidney area, muscle cramps and swelling of the hands and feet. (kidney.org)
  • Aging Causes Muscle Weakness And Atrophy, But Can We Treat It? (lifeboat.com)
  • Imagination is a muscle that atrophies but as readers we fill in the blanks and bring just as much to the table as the writer. (wordpress.com)
  • The treatment for kidney atrophy depends on what caused the kidney to become smaller in the first place. (kidney.org)
  • We're pleased to announce that we now have another treatment for people with spinal muscular atrophy," says Pharmac's director of operations Lisa Williams. (pharmac.govt.nz)
  • It's great that young people with spinal muscular atrophy, their families and healthcare practioners will now have another choice for treatment, especially for those people who find it hard to travel to hospitals or prefer to have an oral, at-home solution. (pharmac.govt.nz)
  • Treatment consists of correction of these deformities by replacing tissue that has been lost due to atrophy. (bvsalud.org)
  • This study investigated whether PEX syndrome is associated with AD-related brain atrophy . (bvsalud.org)
  • What are the symptoms of kidney atrophy? (kidney.org)
  • Sometimes kidney atrophy can have no symptoms, especially if the cause is slow and over many years. (kidney.org)
  • Those participants with LVH also had more atrophy in subcortical structures such as the putamen and the cerebellar cortex. (thelimbic.com)
  • The aim of this study is to report a case of progressive hemifacial atrophy treated with dermis-fat graft and demonstrate that this surgical procedure may improve the aesthetic appearance of the patient's face and discuss the therapeutic aspects of this disorder. (bvsalud.org)
  • Johns Hopkins researchers along with academic and drug industry investigators say they have identified a new biological target for treating spinal muscular atrophy. (news-medical.net)
  • In a report on the work, published in Neuron on Dec. 23, the researchers say the combination therapy improved survival time, body weight and motor movements in mice with spinal muscular atrophy, a relatively rare inherited disorder characterized by the loss of motor neurons, or nerve cells that control movement. (news-medical.net)
  • Spinal muscular atrophy (SMA) refers to a group of hereditary diseases that damage and kill motor neurons in the brain and spinal cord. (medscape.com)
  • Both LVH and hypertension appear conflated as risk factors for brain atrophy," she said. (thelimbic.com)
  • PEX deposition shares features with amyloid aggregation in AD, and brain atrophy is a common AD feature, with ß- amyloid accumulation among contributing factors. (bvsalud.org)
  • The main outcome measure was brain atrophy , using a visual rating scale, and AD incidence . (bvsalud.org)
  • PEX is associated with brain atrophy , reflecting the risk of developing AD. (bvsalud.org)
  • One in 40 people carry the defective gene for spinal muscular atrophy, and as many as one in 6,000 babies in the world across all ethnic groups is born with the disorder. (news-medical.net)
  • Alex Muelhaupt, General Manager of Roche Products (New Zealand), says the company is pleased to be helping improve access to medicines for people with spinal muscular atrophy. (pharmac.govt.nz)
  • Since breastfeeding is a naturally low-estrogen state, vaginal dryness and atrophy are common during that postpartum stage. (poise.com)
  • Kidney atrophy means that the kidney is smaller than normal. (kidney.org)
  • Vaginal dryness and atrophy may also lead to pain while urinating, increased urination urgency, incontinence and recurrent urinary tract infections. (poise.com)
  • Tests for kidney atrophy include imaging tests such as ultrasound, computed tomography ( CT or CAT) scan , or magnetic resonance imaging ( MRI ). (kidney.org)
  • Whole-body vibration training in children with Duchenne muscular dystrophy and spinal muscular atrophy. (galileo-training.com)
  • OBJECTIVE: To evaluate safety of whole-body vibration training in ambulatory children with Duchenne muscular dystrophy (DMD) and spinal muscular atrophy (SMA). (galileo-training.com)
  • Help support Wordnik (and make this page ad-free) by adopting the word eccentric atrophy . (wordnik.com)

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