Bulbo spinal atrophy x linked. Medical search

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.

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

Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).

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.

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)

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 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)

Introduction of therapeutic agents into the spinal region using a needle and syringe.

Pathologic conditions which feature SPINAL CORD damage or dysfunction, including disorders involving the meninges and perimeningeal spaces surrounding the spinal cord. Traumatic injuries, vascular diseases, infections, and inflammatory/autoimmune processes may affect the spinal cord.

The 31 paired peripheral nerves formed by the union of the dorsal and ventral spinal roots from each spinal cord segment. The spinal nerve plexuses and the spinal roots are also included.

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)

Procedure in which an anesthetic is injected directly into the spinal cord.

Paired bundles of NERVE FIBERS entering and leaving the SPINAL CORD at each segment. The dorsal and ventral nerve roots join to form the mixed segmental spinal nerves. The dorsal roots are generally afferent, formed by the central projections of the spinal (dorsal root) ganglia sensory cells, and the ventral roots are efferent, comprising the axons of spinal motor and PREGANGLIONIC AUTONOMIC FIBERS.

Benign and malignant neoplasms which occur within the substance of the spinal cord (intramedullary neoplasms) or in the space between the dura and spinal cord (intradural extramedullary neoplasms). The majority of intramedullary spinal tumors are primary CNS neoplasms including ASTROCYTOMA; EPENDYMOMA; and LIPOMA. Intramedullary neoplasms are often associated with SYRINGOMYELIA. The most frequent histologic types of intradural-extramedullary tumors are MENINGIOMA and NEUROFIBROMA.

The cavity within the SPINAL COLUMN through which the SPINAL CORD passes.

Acute and chronic conditions characterized by external mechanical compression of the SPINAL CORD due to extramedullary neoplasm; EPIDURAL ABSCESS; SPINAL FRACTURES; bony deformities of the vertebral bodies; and other conditions. Clinical manifestations vary with the anatomic site of the lesion and may include localized pain, weakness, sensory loss, incontinence, and impotence.

Narrowing of the spinal canal.

Operative immobilization or ankylosis of two or more vertebrae by fusion of the vertebral bodies with a short bone graft or often with diskectomy or laminectomy. (From Blauvelt & Nelson, A Manual of Orthopaedic Terminology, 5th ed, p236; Dorland, 28th ed)

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)

Injuries involving the vertebral column.

Progressive, autosomal recessive, diffuse atrophy of the choroid, pigment epithelium, and sensory retina that begins in childhood.

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.

Neurons which activate MUSCLE CELLS.

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.

Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.

Reduced blood flow to the spinal cord which is supplied by the anterior spinal artery and the paired posterior spinal arteries. This condition may be associated with ARTERIOSCLEROSIS, trauma, emboli, diseases of the aorta, and other disorders. Prolonged ischemia may lead to INFARCTION of spinal cord tissue.

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 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.

Severe or complete loss of motor function in the lower extremities and lower portions of the trunk. This condition is most often associated with SPINAL CORD DISEASES, although BRAIN DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; and MUSCULAR DISEASES may also cause bilateral leg weakness.

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).

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.

The spinal or vertebral column.

A group of twelve VERTEBRAE connected to the ribs that support the upper trunk region.

Osteitis or caries of the vertebrae, usually occurring as a complication of tuberculosis of the lungs.

A surgical procedure that entails removing all (laminectomy) or part (laminotomy) of selected vertebral lamina to relieve pressure on the SPINAL CORD and/or SPINAL NERVE ROOTS. Vertebral lamina is the thin flattened posterior wall of vertebral arch that forms the vertebral foramen through which pass the spinal cord and nerve roots.

Deformities of the SPINE characterized by abnormal bending or flexure in the vertebral column. They may be bending forward (KYPHOSIS), backward (LORDOSIS), or sideway (SCOLIOSIS).

The first seven VERTEBRAE of the SPINAL COLUMN, which correspond to the VERTEBRAE of the NECK.

A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.

A rare epidural hematoma in the spinal epidural space, usually due to a vascular malformation (CENTRAL NERVOUS SYSTEM VASCULAR MALFORMATIONS) or TRAUMA. Spontaneous spinal epidural hematoma is a neurologic emergency due to a rapidly evolving compressive MYELOPATHY.

Neurons in the SPINAL CORD DORSAL HORN whose cell bodies and processes are confined entirely to the CENTRAL NERVOUS SYSTEM. They receive collateral or direct terminations of dorsal root fibers. They send their axons either directly to ANTERIOR HORN CELLS or to the WHITE MATTER ascending and descending longitudinal fibers.

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 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.

Region of the back including the LUMBAR VERTEBRAE, SACRUM, and nearby structures.

MOTOR NEURONS in the anterior (ventral) horn of the SPINAL CORD which project to SKELETAL MUSCLES.

VERTEBRAE in the region of the lower BACK below the THORACIC VERTEBRAE and above the SACRAL VERTEBRAE.

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.

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.

The female sex chromosome, being the differential sex chromosome carried by half the male gametes and all female gametes in human and other male-heterogametic species.

Broken bones in the vertebral column.

An X-linked recessive form of spinal muscular atrophy. It is due to a mutation of the gene encoding the ANDROGEN RECEPTOR.

Repair of the damaged neuron function after SPINAL CORD INJURY or SPINAL CORD DISEASES.

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.

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

Severe or complete loss of motor function in all four limbs which may result from BRAIN DISEASES; SPINAL CORD DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; or rarely MUSCULAR DISEASES. The locked-in syndrome is characterized by quadriplegia in combination with cranial muscle paralysis. Consciousness is spared and the only retained voluntary motor activity may be limited eye movements. This condition is usually caused by a lesion in the upper BRAIN STEM which injures the descending cortico-spinal and cortico-bulbar tracts.

An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.

Nucleus of the spinal tract of the trigeminal nerve. It is divided cytoarchitectonically into three parts: oralis, caudalis (TRIGEMINAL CAUDAL NUCLEUS), and interpolaris.

An increased sensation of pain or discomfort produced by mimimally noxious stimuli due to damage to soft tissue containing NOCICEPTORS or injury to a peripheral nerve.

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

Movement or the ability to move from one place or another. It can refer to humans, vertebrate or invertebrate animals, and microorganisms.

A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.

X-ray visualization of the spinal cord following injection of contrast medium into the spinal arachnoid space.

Adjustment and manipulation of the vertebral column.

Recording of the changes in electric potential of muscle by means of surface or needle electrodes.

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

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.

Renewal or physiological repair of damaged nerve tissue.

Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.

A general term most often used to describe severe or complete loss of muscle strength due to motor system disease from the level of the cerebral cortex to the muscle fiber. This term may also occasionally refer to a loss of sensory function. (From Adams et al., Principles of Neurology, 6th ed, p45)

Space between the dura mater and the walls of the vertebral canal.

Scales, questionnaires, tests, and other methods used to assess pain severity and duration in patients or experimental animals to aid in diagnosis, therapy, and physiological studies.

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.

Any operation on the spinal cord. (Stedman, 26th ed)

Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)

Tapping fluid from the subarachnoid space in the lumbar region, usually between the third and fourth lumbar vertebrae.

Inflammation of the spinal cord. Relatively common etiologies include infections; AUTOIMMUNE DISEASES; SPINAL CORD; and ischemia (see also SPINAL CORD VASCULAR DISEASES). Clinical features generally include weakness, sensory loss, localized pain, incontinence, and other signs of autonomic dysfunction.

Use of electric potential or currents to elicit biological responses.

An appreciable lateral deviation in the normally straight vertical line of the spine. (Dorland, 27th ed)

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).

Peripheral AFFERENT NEURONS which are sensitive to injuries or pain, usually caused by extreme thermal exposures, mechanical forces, or other noxious stimuli. Their cell bodies reside in the DORSAL ROOT GANGLIA. Their peripheral terminals (NERVE ENDINGS) innervate target tissues and transduce noxious stimuli via axons to the CENTRAL NERVOUS SYSTEM.

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)

An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord.

Nerve structures through which impulses are conducted from a peripheral part toward a nerve center.

Application of electric current to the spine for treatment of a variety of conditions involving innervation from the spinal cord.

A surgical operation for the relief of pressure in a body compartment or on a body part. (From Dorland, 28th ed)

The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)

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)

The part of the brain that connects the CEREBRAL HEMISPHERES with the SPINAL CORD. It consists of the MESENCEPHALON; PONS; and MEDULLA OBLONGATA.

The measurement of an organ in volume, mass, or heaviness.

Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.

Congenital defects of closure of one or more vertebral arches, which may be associated with malformations of the spinal cord, nerve roots, congenital fibrous bands, lipomas, and congenital cysts. These malformations range from mild (e.g., SPINA BIFIDA OCCULTA) to severe, including rachischisis where there is complete failure of neural tube and spinal cord fusion, resulting in exposure of the spinal cord at the surface. Spinal dysraphism includes all forms of spina bifida. The open form is called SPINA BIFIDA CYSTICA and the closed form is SPINA BIFIDA OCCULTA. (From Joynt, Clinical Neurology, 1992, Ch55, p34)

Act of eliciting a response from a person or organism through physical contact.

Subdural hematoma of the SPINAL CANAL.

Diseases of the uvea.

Application of electric current in treatment without the generation of perceptible heat. It includes electric stimulation of nerves or muscles, passage of current into the body, or use of interrupted current of low intensity to raise the threshold of the skin to pain.

The physical activity of a human or an animal as a behavioral phenomenon.

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.

A nerve which originates in the lumbar and sacral spinal cord (L4 to S3) and supplies motor and sensory innervation to the lower extremity. The sciatic nerve, which is the main continuation of the sacral plexus, is the largest nerve in the body. It has two major branches, the TIBIAL NERVE and the PERONEAL NERVE.

Outgrowth of immature bony processes or bone spurs (OSTEOPHYTE) from the VERTEBRAE, reflecting the presence of degenerative disease and calcification. It commonly occurs in cervical and lumbar SPONDYLOSIS.

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.

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

A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.

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 worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.

The 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 protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.

The resection or removal of the innervation of a muscle or muscle tissue.

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.

Fibers that arise from cells within the cerebral cortex, pass through the medullary pyramid, and descend in the spinal cord. Many authorities say the pyramidal tracts include both the corticospinal and corticobulbar tracts.

Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

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)

Most generally any NEURONS which are not motor or sensory. Interneurons may also refer to neurons whose AXONS remain within a particular brain region in contrast to projection neurons, which have axons projecting to other brain regions.

Deformities of the SPINE characterized by an exaggerated convexity of the vertebral column. The forward bending of the thoracic region usually is more than 40 degrees. This deformity sometimes is called round back or hunchback.

The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.

The outermost of the three MENINGES, a fibrous membrane of connective tissue that covers the brain and the spinal cord.

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.

Compounds capable of relieving pain without the loss of CONSCIOUSNESS.

The lower part of the SPINAL CORD consisting of the lumbar, sacral, and coccygeal nerve roots.

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.

Five fused VERTEBRAE forming a triangle-shaped structure at the back of the PELVIS. It articulates superiorly with the LUMBAR VERTEBRAE, inferiorly with the COCCYX, and anteriorly with the ILIUM of the PELVIS. The sacrum strengthens and stabilizes the PELVIS.

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

A class of nerve fibers as defined by their structure, specifically the nerve sheath arrangement. The AXONS of the myelinated nerve fibers are completely encased in a MYELIN SHEATH. They are fibers of relatively large and varied diameters. Their NEURAL CONDUCTION rates are faster than those of the unmyelinated nerve fibers (NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.

A 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.

Tomography using x-ray transmission and a computer algorithm to reconstruct the image.

A form of muscle hypertonia associated with upper MOTOR NEURON DISEASE. Resistance to passive stretch of a spastic muscle results in minimal initial resistance (a "free interval") followed by an incremental increase in muscle tone. Tone increases in proportion to the velocity of stretch. Spasticity is usually accompanied by HYPERREFLEXIA and variable degrees of MUSCLE WEAKNESS. (From Adams et al., Principles of Neurology, 6th ed, p54)

The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.

Dysfunction of the URINARY BLADDER due to disease of the central or peripheral nervous system pathways involved in the control of URINATION. This is often associated with SPINAL CORD DISEASES, but may also be caused by BRAIN DISEASES or PERIPHERAL NERVE DISEASES.

A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.

Common name for the only family (Petromyzontidae) of eellike fish in the order Petromyzontiformes. They are jawless but have a sucking mouth with horny teeth.

A class of nerve fibers as defined by their nerve sheath arrangement. The AXONS of the unmyelinated nerve fibers are small in diameter and usually several are surrounded by a single MYELIN SHEATH. They conduct low-velocity impulses, and represent the majority of peripheral sensory and autonomic fibers, but are also found in the BRAIN and SPINAL CORD.

Pathological processes involving any of the BLOOD VESSELS feeding the SPINAL CORD, such as the anterior and paired posterior spinal arteries or their many branches. Disease processes may include ATHEROSCLEROSIS; EMBOLISM; and ARTERIOVENOUS MALFORMATIONS leading to ISCHEMIA or HEMORRHAGE into the spinal cord (hematomyelia).

The space between the arachnoid membrane and PIA MATER, filled with CEREBROSPINAL FLUID. It contains large blood vessels that supply the BRAIN and SPINAL CORD.

Assessment of sensory and motor responses and reflexes that is used to determine impairment of the nervous system.

A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)

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)

Slender processes of NEURONS, including the AXONS and their glial envelopes (MYELIN SHEATH). Nerve fibers conduct nerve impulses to and from the CENTRAL NERVOUS SYSTEM.

Mild to moderate loss of bilateral lower extremity motor function, which may be a manifestation of SPINAL CORD DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; MUSCULAR DISEASES; INTRACRANIAL HYPERTENSION; parasagittal brain lesions; and other conditions.

A condition characterized by abnormal posturing of the limbs that is associated with injury to the brainstem. This may occur as a clinical manifestation or induced experimentally in animals. The extensor reflexes are exaggerated leading to rigid extension of the limbs accompanied by hyperreflexia and opisthotonus. This condition is usually caused by lesions which occur in the region of the brainstem that lies between the red nuclei and the vestibular nuclei. In contrast, decorticate rigidity is characterized by flexion of the elbows and wrists with extension of the legs and feet. The causative lesion for this condition is located above the red nuclei and usually consists of diffuse cerebral damage. (From Adams et al., Principles of Neurology, 6th ed, p358)

The observable response an animal makes to any situation.

Disturbances in mental processes related to learning, thinking, reasoning, and judgment.

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.

Storage-stable glycoprotein blood coagulation factor that can be activated to factor Xa by both the intrinsic and extrinsic pathways. A deficiency of factor X, sometimes called Stuart-Prower factor deficiency, may lead to a systemic coagulation disorder.

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

The relationship between the dose of an administered drug and the response of the organism to the drug.

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)

Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.

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.

Amount of stimulation required before the sensation of pain is experienced.

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

The principal alkaloid in opium and the prototype opiate analgesic and narcotic. Morphine has widespread effects in the central nervous system and on smooth muscle.

The electric response evoked in the CEREBRAL CORTEX by stimulation along AFFERENT PATHWAYS from PERIPHERAL NERVES to CEREBRUM.

Neural tracts connecting one part of the nervous system with another.

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.

Circumscribed collections of suppurative material occurring in the spinal or intracranial EPIDURAL SPACE. The majority of epidural abscesses occur in the spinal canal and are associated with OSTEOMYELITIS of a vertebral body; ANALGESIA, EPIDURAL; and other conditions. Clinical manifestations include local and radicular pain, weakness, sensory loss, URINARY INCONTINENCE, and FECAL INCONTINENCE. Cranial epidural abscesses are usually associated with OSTEOMYELITIS of a cranial bone, SINUSITIS, or OTITIS MEDIA. (From Adams et al., Principles of Neurology, 6th ed, p710 and pp1240-1; J Neurol Neurosurg Psychiatry 1998 Aug;65(2):209-12)

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.

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

The 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 syndrome associated with damage to the spinal cord above the mid thoracic level (see SPINAL CORD INJURIES) characterized by a marked increase in the sympathetic response to minor stimuli such as bladder or rectal distention. Manifestations include HYPERTENSION; TACHYCARDIA (or reflex bradycardia); FEVER; FLUSHING; and HYPERHIDROSIS. Extreme hypertension may be associated with a STROKE. (From Adams et al., Principles of Neurology, 6th ed, pp538 and 1232; J Spinal Cord Med 1997;20(3):355-60)

An abnormal response to a stimulus applied to the sensory components of the nervous system. This may take the form of increased, decreased, or absent reflexes.

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

A variety of anesthetic methods such as EPIDURAL ANESTHESIA used to control the pain of childbirth.

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

A general term encompassing lower MOTOR NEURON DISEASE; PERIPHERAL NERVOUS SYSTEM DISEASES; and certain MUSCULAR DISEASES. Manifestations include MUSCLE WEAKNESS; FASCICULATION; muscle ATROPHY; SPASM; MYOKYMIA; MUSCLE HYPERTONIA, myalgias, and MUSCLE HYPOTONIA.

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

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

An alkaloid found in the seeds of STRYCHNOS NUX-VOMICA. It is a competitive antagonist at glycine receptors and thus a convulsant. It has been used as an analeptic, in the treatment of nonketotic hyperglycinemia and sleep apnea, and as a rat poison.

Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.

Proteins that bind to RNA molecules. Included here are RIBONUCLEOPROTEINS and other proteins whose function is to bind specifically to RNA.

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

Injuries to the PERIPHERAL NERVES.

Behavioral manifestations of cerebral dominance in which there is preferential use and superior functioning of either the left or the right side, as in the preferred use of the right hand or right foot.

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.

Nerve structures through which impulses are conducted from a nerve center toward a peripheral site. Such impulses are conducted via efferent neurons (NEURONS, EFFERENT), such as MOTOR NEURONS, autonomic neurons, and hypophyseal neurons.

Drugs that block nerve conduction when applied locally to nerve tissue in appropriate concentrations. They act on any part of the nervous system and on every type of nerve fiber. In contact with a nerve trunk, these anesthetics can cause both sensory and motor paralysis in the innervated area. Their action is completely reversible. (From Gilman AG, et. al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed) Nearly all local anesthetics act by reducing the tendency of voltage-dependent sodium channels to activate.

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.

The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.

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

Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.

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

Diseases that affect the structure or function of the cerebellum. Cardinal manifestations of cerebellar dysfunction include dysmetria, GAIT ATAXIA, and MUSCLE HYPOTONIA.

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

Contractile tissue that produces movement in animals.

Longitudinal cavities in the spinal cord, most often in the cervical region, which may extend for multiple spinal levels. The cavities are lined by dense, gliogenous tissue and may be associated with SPINAL CORD NEOPLASMS; spinal cord traumatic injuries; and vascular malformations. Syringomyelia is marked clinically by pain and PARESTHESIA, muscular atrophy of the hands, and analgesia with thermoanesthesia of the hands and arms, but with the tactile sense preserved (sensory dissociation). Lower extremity spasticity and incontinence may also develop. (From Adams et al., Principles of Neurology, 6th ed, p1269)

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.

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.

Increased sensitivity to cutaneous stimulation due to a diminished threshold or an increased response to stimuli.

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.

The three membranes that cover the BRAIN and the SPINAL CORD. They are the dura mater, the arachnoid, and the pia mater.

Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.

A reflex in which the AFFERENT NEURONS synapse directly on the EFFERENT NEURONS, without any INTERCALATED NEURONS. (Lockard, Desk Reference for Neuroscience, 2nd ed.)

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

Electrical responses recorded from nerve, muscle, SENSORY RECEPTOR, or area of the CENTRAL NERVOUS SYSTEM following stimulation. They range from less than a microvolt to several microvolts. The evoked potential can be auditory (EVOKED POTENTIALS, AUDITORY), somatosensory (EVOKED POTENTIALS, SOMATOSENSORY), visual (EVOKED POTENTIALS, VISUAL), or motor (EVOKED POTENTIALS, MOTOR), or other modalities that have been reported.

A widely used local anesthetic agent.

The medial terminal branch of the sciatic nerve. The tibial nerve fibers originate in lumbar and sacral spinal segments (L4 to S2). They supply motor and sensory innervation to parts of the calf and foot.

Neoplasms located in the space between the vertebral PERIOSTEUM and DURA MATER surrounding the SPINAL CORD. Tumors in this location are most often metastatic in origin and may cause neurologic deficits by mass effect on the spinal cord or nerve roots or by interfering with blood supply to the spinal cord.

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.

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.

Combined 3T diffusion tensor tractography and 1H-MR spectroscopy in motor neuron disease. (1/23)

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Spinal and bulbar muscular atrophy: a motoneuron or muscle disease? (2/23)

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Mitochondrial abnormalities in spinal and bulbar muscular atrophy. (3/23)

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Altered RNA splicing contributes to skeletal muscle pathology in Kennedy disease knock-in mice. (4/23)

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Autophagy and access: understanding the role of androgen receptor subcellular localization in SBMA. (5/23)

Ridding neurons of toxic misfolded proteins is a critical feature of many neurodegenerative diseases. We have recently reported that lack of access of nuclear polyglutamine-expanded androgen receptor (AR) to the autophagic degradation pathway is a critical point in pathogenesis. When mutant AR is contained within the cytoplasm, it can be degraded by autophagy, resulting in amelioration of its toxic effects, as has been observed in other polyglutamine expansion diseases involving cytoplasmic mutant proteins. However, we have also found that pharmacological induction of autophagy protects SBMA motor neurons from the toxic effects of even nuclear localized mutant AR, albeit without affecting mutant nuclear AR levels. Thus, we have further investigated the mechanism by which autophagy elicits therapeutic benefit in cell culture. We found that endogenous autophagy only slightly alters nuclear mutant AR aggregation compared to substantial effects on cytoplasmic AR aggregation. Interestingly, pharmacological activation of mTOR-dependent autophagy did not significantly alter nuclear AR aggregation, whereas we observed that it protects SBMA motor neurons. Our findings indicate that therapeutic intervention to induce autophagy represents a potential potent benefit for SBMA, and that it likely does so by protecting SBMA motor neurons independent of a direct effect on mutant AR. (+info)

Clinical features of spinal and bulbar muscular atrophy. (6/23)

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B2 attenuates polyglutamine-expanded androgen receptor toxicity in cell and fly models of spinal and bulbar muscular atrophy. (7/23)

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Prenatal flutamide enhances survival in a myogenic mouse model of spinal bulbar muscular atrophy. (8/23)

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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 different types of spinal cord injuries that can occur, depending on the location and severity of the damage. These include:

1. Complete spinal cord injuries: In these cases, the spinal cord is completely severed, resulting in a loss of all sensation and function below the level of the injury.
2. Incomplete spinal cord injuries: In these cases, the spinal cord is only partially damaged, resulting in some remaining sensation and function below the level of the injury.
3. Brown-Sequard syndrome: This is a specific type of incomplete spinal cord injury that affects one side of the spinal cord, resulting in weakness or paralysis on one side of the body.
4. Conus medullaris syndrome: This is a type of incomplete spinal cord injury that affects the lower part of the spinal cord, resulting in weakness or paralysis in the legs and bladder dysfunction.

The symptoms of spinal cord injuries can vary depending on the location and severity of the injury. They may include:

* Loss of sensation in the arms, legs, or other parts of the body
* Weakness or paralysis in the arms, legs, or other parts of the body
* Difficulty walking or standing
* Difficulty with bowel and bladder function
* Numbness or tingling sensations
* Pain or pressure in the neck or back

Treatment for spinal cord injuries typically involves a combination of medical and rehabilitative therapies. Medical treatments may include:

* Immobilization of the spine to prevent further injury
* Medications to manage pain and inflammation
* Surgery to relieve compression or stabilize the spine

Rehabilitative therapies may include:

* Physical therapy to improve strength and mobility
* Occupational therapy to learn new ways of performing daily activities
* Speech therapy to improve communication skills
* Psychological counseling to cope with the emotional effects of the injury.

Overall, the prognosis for spinal cord injuries depends on the severity and location of the injury, as well as the age and overall health of the individual. While some individuals may experience significant recovery, others may experience long-term or permanent impairment. It is important to seek medical attention immediately if symptoms of a spinal cord injury are present.

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.

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.

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 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.

Some common examples of spinal cord diseases include:

1. Spinal muscular atrophy: This is a genetic disorder that affects the nerve cells responsible for controlling voluntary muscle movement. It can cause muscle weakness and wasting, as well as other symptoms such as respiratory problems and difficulty swallowing.
2. Multiple sclerosis: This is an autoimmune disease that causes inflammation and damage to the protective covering of nerve fibers in the spinal cord. Symptoms can include vision problems, muscle weakness, balance and coordination difficulties, and cognitive impairment.
3. Spinal cord injuries: These can occur as a result of trauma, such as a car accident or a fall, and can cause a range of symptoms including paralysis, numbness, and loss of sensation below the level of the injury.
4. Spinal stenosis: This is a condition in which the spinal canal narrows, putting pressure on the spinal cord and nerve roots. Symptoms can include back pain, leg pain, and difficulty walking or standing for long periods.
5. Tumors: Benign or malignant tumors can grow in the spinal cord, causing a range of symptoms including pain, weakness, and numbness or tingling in the limbs.
6. Infections: Bacterial, viral, or fungal infections can cause inflammation and damage to the spinal cord, leading to symptoms such as fever, headache, and muscle weakness.
7. Degenerative diseases: Conditions such as amyotrophic lateral sclerosis (ALS) and primary lateral sclerosis (PLS) can cause progressive degeneration of the spinal cord nerve cells, leading to muscle weakness, twitching, and wasting.
8. Trauma: Traumatic injuries, such as those caused by sports injuries or physical assault, can damage the spinal cord and result in a range of symptoms including pain, numbness, and weakness.
9. Ischemia: Reduced blood flow to the spinal cord can cause tissue damage and lead to symptoms such as weakness, numbness, and paralysis.
10. Spinal cord infarction: A blockage in the blood vessels that supply the spinal cord can cause tissue damage and lead to symptoms similar to those of ischemia.

It's important to note that some of these conditions can be caused by a combination of factors, such as genetics, age, lifestyle, and environmental factors. It's also worth noting that some of these conditions can have a significant impact on quality of life, and in some cases, may be fatal.

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.

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

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

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

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

Some common types of spinal diseases include:

1. Degenerative disc disease: This is a condition where the discs between the vertebrae in the spine wear down over time, leading to pain and stiffness in the back.
2. Herniated discs: This occurs when the gel-like center of a disc bulges out through a tear in the outer layer, putting pressure on nearby nerves and causing pain.
3. Spinal stenosis: This is a narrowing of the spinal canal, which can put pressure on the spinal cord and nerve roots, causing pain, numbness, and weakness in the legs.
4. Spondylolisthesis: This is a condition where a vertebra slips out of place, either forward or backward, and can cause pressure on nearby nerves and muscles.
5. Scoliosis: This is a curvature of the spine that can be caused by a variety of factors, including genetics, injury, or disease.
6. Spinal infections: These are infections that can affect any part of the spine, including the discs, vertebrae, and soft tissues.
7. Spinal tumors: These are abnormal growths that can occur in the spine, either primary ( originating in the spine) or metastatic (originating elsewhere in the body).
8. Osteoporotic fractures: These are fractures that occur in the spine as a result of weakened bones due to osteoporosis.
9. Spinal cysts: These are fluid-filled sacs that can form in the spine, either as a result of injury or as a congenital condition.
10. Spinal degeneration: This is a general term for any type of wear and tear on the spine, such as arthritis or disc degeneration.

If you are experiencing any of these conditions, it is important to seek medical attention to receive an accurate diagnosis and appropriate treatment.

There are several types of spinal cord compression, including:

1. Central canal stenosis: This occurs when the central canal of the spine narrows, compressing the spinal cord.
2. Foraminal stenosis: This occurs when the openings on either side of the spine (foramina) narrow, compressing the nerves exiting the spinal cord.
3. Spondylolisthesis: This occurs when a vertebra slips out of place, compressing the spinal cord.
4. Herniated discs: This occurs when the gel-like center of a disc bulges out and presses on the spinal cord.
5. Bone spurs: This occurs when bone growths develop on the vertebrae, compressing the spinal cord.
6. Tumors: This can be either primary or metastatic tumors that grow in the spine and compress the spinal cord.
7. Trauma: This occurs when there is a direct blow to the spine, causing compression of the spinal cord.

Symptoms of spinal cord compression may include:

* Pain, numbness, weakness, or tingling in the arms and legs
* Difficulty walking or maintaining balance
* Muscle wasting or loss of muscle mass
* Decreased reflexes
* Loss of bladder or bowel control
* Weakness in the muscles of the face, arms, or legs
* Difficulty with fine motor skills such as buttoning a shirt or typing

Diagnosis of spinal cord compression is typically made through a combination of physical examination, medical history, and imaging tests such as X-rays, CT scans, or MRI scans. Treatment options for spinal cord compression depend on the underlying cause and may include medication, surgery, or a combination of both.

In conclusion, spinal cord compression is a serious medical condition that can have significant impacts on quality of life, mobility, and overall health. It is important to be aware of the causes and symptoms of spinal cord compression in order to seek medical attention if they occur. With proper diagnosis and treatment, many cases of spinal cord compression can be effectively managed and improved.

Types of Spinal Neoplasms:

1. Benign tumors: Meningiomas, schwannomas, and osteochondromas are common types of benign spinal neoplasms. These tumors usually grow slowly and do not spread to other parts of the body.
2. Malignant tumors: Primary bone cancers (chordoma, chondrosarcoma, and osteosarcoma) and metastatic cancers (cancers that have spread to the spine from another part of the body) are types of malignant spinal neoplasms. These tumors can grow rapidly and spread to other parts of the body.

Causes and Risk Factors:

1. Genetic mutations: Some genetic disorders, such as neurofibromatosis type 1 and tuberous sclerosis complex, increase the risk of developing spinal neoplasms.
2. Previous radiation exposure: People who have undergone radiation therapy in the past may have an increased risk of developing a spinal tumor.
3. Family history: A family history of spinal neoplasms can increase an individual's risk.
4. Age and gender: Spinal neoplasms are more common in older adults, and males are more likely to be affected than females.

Symptoms:

1. Back pain: Pain is the most common symptom of spinal neoplasms, which can range from mild to severe and may be accompanied by other symptoms such as numbness, weakness, or tingling in the arms or legs.
2. Neurological deficits: Depending on the location and size of the tumor, patients may experience neurological deficits such as paralysis, loss of sensation, or difficulty with balance and coordination.
3. Difficulty with urination or bowel movements: Patients may experience changes in their bladder or bowel habits due to the tumor pressing on the spinal cord or nerve roots.
4. Weakness or numbness: Patients may experience weakness or numbness in their arms or legs due to compression of the spinal cord or nerve roots by the tumor.
5. Fractures: Spinal neoplasms can cause fractures in the spine, which can lead to a loss of height, an abnormal curvature of the spine, or difficulty with movement and balance.

Diagnosis:

1. Medical history and physical examination: A thorough medical history and physical examination can help identify the presence of symptoms and determine the likelihood of a spinal neoplasm.
2. Imaging studies: X-rays, CT scans, MRI scans, or PET scans may be ordered to visualize the spine and detect any abnormalities.
3. Biopsy: A biopsy may be performed to confirm the diagnosis and determine the type of tumor present.
4. Laboratory tests: Blood tests may be ordered to assess liver function, electrolyte levels, or other parameters that can help evaluate the patient's overall health.

Treatment:

1. Surgery: Surgical intervention is often necessary to remove the tumor and relieve pressure on the spinal cord or nerve roots.
2. Radiation therapy: Radiation therapy may be used before or after surgery to kill any remaining cancer cells.
3. Chemotherapy: Chemotherapy may be used in combination with radiation therapy or as a standalone treatment for patients who are not candidates for surgery.
4. Supportive care: Patients may require supportive care, such as physical therapy, pain management, and rehabilitation, to help them recover from the effects of the tumor and any treatment-related complications.

Prognosis:

The prognosis for patients with spinal neoplasms depends on several factors, including the type and location of the tumor, the extent of the disease, and the patient's overall health. In general, the prognosis is better for patients with slow-growing tumors that are confined to a specific area of the spine, as compared to those with more aggressive tumors that have spread to other parts of the body.

Survival rates:

The survival rates for patients with spinal neoplasms vary depending on the type of tumor and other factors. According to the American Cancer Society, the 5-year survival rate for primary spinal cord tumors is about 60%. However, this rate can be as high as 90% for patients with slow-growing tumors that are confined to a specific area of the spine.

Lifestyle modifications:

There are no specific lifestyle modifications that can cure spinal neoplasms, but certain changes may help improve the patient's quality of life and overall health. These may include:

1. Exercise: Gentle exercise, such as yoga or swimming, can help improve mobility and strength.
2. Diet: A balanced diet that includes plenty of fruits, vegetables, whole grains, and lean protein can help support overall health.
3. Rest: Getting enough rest and avoiding strenuous activities can help the patient recover from treatment-related fatigue.
4. Managing stress: Stress management techniques, such as meditation or deep breathing exercises, can help reduce anxiety and improve overall well-being.
5. Follow-up care: Regular follow-up appointments with the healthcare provider are crucial to monitor the patient's condition and make any necessary adjustments to their treatment plan.

In conclusion, spinal neoplasms are rare tumors that can develop in the spine and can have a significant impact on the patient's quality of life. Early diagnosis is essential for effective treatment, and survival rates vary depending on the type of tumor and other factors. While there are no specific lifestyle modifications that can cure spinal neoplasms, certain changes may help improve the patient's overall health and well-being. It is important for patients to work closely with their healthcare provider to develop a personalized treatment plan and follow-up care to ensure the best possible outcome.

Symptoms of spinal stenosis may include:

* Pain in the neck, back, or legs that worsens with walking or standing
* Numbness, tingling, or weakness in the arms or legs
* Difficulty controlling bladder or bowel functions
* Muscle weakness in the legs

Treatment for spinal stenosis may include:

* Pain medications
* Physical therapy to improve mobility and strength
* Injections of steroids or pain relievers
* Surgery to remove bone spurs or decompress the spinal cord

It is important to seek medical attention if symptoms of spinal stenosis worsen over time, as untreated condition can lead to permanent nerve damage and disability.

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.

Symptoms of spinal injuries may include:

* Loss of sensation below the level of the injury
* Weakness or paralysis below the level of the injury
* Pain or numbness in the back, arms, or legs
* Difficulty breathing or controlling bladder and bowel functions
* Changes in reflexes or sensation below the level of the injury.

Spinal injuries can be diagnosed using a variety of tests, including:

* X-rays or CT scans to assess the alignment of the spine and detect any fractures or dislocations
* MRI scans to assess the soft tissues of the spine and detect any damage to the spinal cord
* Electromyography (EMG) tests to assess the function of muscles and nerves below the level of the injury.

Treatment for spinal injuries depends on the severity and location of the injury, and may include:

* Immobilization using a brace or cast to keep the spine stable
* Medications to manage pain, inflammation, and other symptoms
* Rehabilitation therapies such as physical therapy, occupational therapy, and recreational therapy to help restore function and mobility.

In summary, spinal injuries can be classified into two categories: complete and incomplete, and can be caused by a variety of factors. Symptoms may include loss of sensation, weakness or paralysis, pain, difficulty breathing, and changes in reflexes or sensation. Diagnosis is typically made using X-rays, MRI scans, and EMG tests, and treatment may involve immobilization, medications, and rehabilitation therapies.

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.

Symptoms of Spinal Cord Ischemia may include weakness, paralysis, loss of sensation, and loss of reflexes in the affected area. Diagnosis is typically made through a combination of physical examination, imaging studies such as MRI or CT scans, and laboratory tests.

Treatment for Spinal Cord Ischemia depends on the underlying cause and may include medications to dissolve blood clots, surgery to repair arterial damage, or supportive care to manage symptoms and prevent further damage. In severe cases, Spinal Cord Ischemia can lead to permanent neurological damage or death.

Spinal Cord Ischemia is a serious medical condition that requires prompt diagnosis and treatment to prevent long-term neurological damage or death.

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.

Paraplegia is classified into two main types:

1. Complete paraplegia: Total loss of motor function in both legs and pelvis.
2. Incomplete paraplegia: Some degree of motor function remains in the affected limbs.

Symptoms of paraplegia can include weakness, paralysis, numbness, or tingling sensations below the level of the spinal cord injury. Loss of bladder and bowel control, sexual dysfunction, and changes in sensation (such as decreased sensitivity to touch and temperature) are also common.

Diagnosis typically involves a physical examination, medical history, neurological tests such as reflexes and muscle strength, and imaging studies like X-rays or MRIs to determine the underlying cause of paraplegia. Treatment depends on the specific cause of the condition and may include medications, rehabilitation therapy, and assistive devices such as braces, canes, or wheelchairs.

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.

Symptoms of spinal tuberculosis may include:

* Back pain
* Weakness or numbness in the arms or legs
* Difficulty walking or maintaining balance
* Fever, fatigue, and weight loss
* Loss of bladder or bowel control

If left untreated, spinal tuberculosis can lead to severe complications such as paralysis, nerve damage, and infection of the bloodstream. Treatment typically involves a combination of antibiotics and surgery to remove infected tissue.

Spinal TB is a rare form of TB, but it is becoming more common due to the increasing number of people living with HIV/AIDS, which weakens the immune system and makes them more susceptible to TB infections. Spinal TB can be difficult to diagnose as it may present like other conditions such as cancer or herniated discs.

The prognosis for spinal tuberculosis is generally good if treated early, but the condition can be challenging to treat and may require long-term management.

Kyphosis is an exaggerated forward curvature of the spine, also known as "roundback" or "hunchback". This type of curvature can be caused by a variety of factors such as osteoporosis, degenerative disc disease, and Scheuermann's disease.

Lordosis is an excessive inward curvature of the spine, also known as "swayback". This type of curvature can be caused by factors such as pregnancy, obesity, and spinal injuries.

Scoliosis is a sideways curvature of the spine, which can be caused by a variety of factors such as genetics, injury, or birth defects. Scoliosis can be classified into two main types: Cervical (neck) scoliosis and Thoracic (chest) scoliosis.

All three types of curvatures can cause discomfort, pain and decreased mobility if left untreated. Treatment options vary depending on the severity of the curvature and may include physical therapy, bracing, or surgery.

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.

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 spinal fractures, including:

1. Vertebral compression fractures: These occur when the vertebrae collapses due to pressure, often caused by osteoporosis or trauma.
2. Fracture-dislocations: This type of fracture occurs when the vertebra is both broken and displaced from its normal position.
3. Spondylolysis: This is a type of fracture that occurs in the spine, often due to repetitive stress or overuse.
4. Spondylolisthesis: This is a type of fracture where a vertebra slips out of its normal position and into the one below it.
5. Fracture-subluxation: This type of fracture occurs when the vertebra is both broken and partially dislocated from its normal position.

The diagnosis of spinal fractures typically involves imaging tests such as X-rays, CT scans, or MRI to confirm the presence of a fracture and determine its severity and location. Treatment options for spinal fractures depend on the severity of the injury and may include pain management, bracing, physical therapy, or surgery to stabilize the spine and promote healing. In some cases, surgical intervention may be necessary to realign the vertebrae and prevent further damage.

Overall, spinal fractures can have a significant impact on an individual's quality of life, and it is important to seek medical attention if symptoms persist or worsen over time.

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.

Quadriplegia can be classified into two types:

1. Complete quadriplegia: This is when all four limbs are paralyzed and there is no movement or sensation below the level of the injury.
2. Incomplete quadriplegia: This is when some movement or sensation remains below the level of the injury, but not in all four limbs.

The symptoms of quadriplegia can vary depending on the underlying cause and severity of the condition. They may include:

* Loss of movement in the arms and legs
* Weakness or paralysis of the muscles in the arms and legs
* Decreased or absent sensation in the arms and legs
* Difficulty with balance and coordination
* Difficulty with walking, standing, or sitting
* Difficulty with performing daily activities such as dressing, grooming, and feeding oneself

The diagnosis of quadriplegia is typically made through a combination of physical examination, medical history, and imaging studies such as X-rays or MRIs. Treatment for quadriplegia depends on the underlying cause and may include:

* Physical therapy to improve strength and mobility
* Occupational therapy to learn new ways of performing daily activities
* Assistive devices such as braces, walkers, or wheelchairs
* Medications to manage pain, spasticity, or other symptoms
* Surgery to repair or stabilize the spinal cord or other affected areas.

Overall, quadriplegia is a severe condition that can significantly impact a person's quality of life. However, with appropriate treatment and support, many people with quadriplegia are able to lead active and fulfilling lives.

There are several different types of pain, including:

1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.

The medical field uses a range of methods to assess and manage pain, including:

1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.

It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.

Hyperalgesia is often seen in people with chronic pain conditions, such as fibromyalgia, and it can also be a side effect of certain medications or medical procedures. Treatment options for hyperalgesia depend on the underlying cause of the condition, but may include pain management techniques, physical therapy, and medication adjustments.

In clinical settings, hyperalgesia is often assessed using a pinprick test or other pain tolerance tests to determine the patient's sensitivity to different types of stimuli. The goal of treatment is to reduce the patient's pain and improve their quality of life.

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.

Neuralgia is often difficult to diagnose and treat, as the underlying cause can be challenging to identify. However, various medications and therapies can help manage the pain and other symptoms associated with this condition. These may include pain relievers, anticonvulsants, antidepressants, and muscle relaxants, as well as alternative therapies such as acupuncture or physical therapy.

Some common forms of neuralgia include:

1. Trigeminal neuralgia: This is a condition that affects the trigeminal nerve, which carries sensation from the face to the brain. It is characterized by sudden, intense pain in the face, typically on one side.
2. Postherpetic neuralgia (PHN): This is a condition that occurs after a shingles infection, and is characterized by persistent pain in the affected area.
3. Occipital neuralgia: This is a condition that affects the nerves in the back of the head and neck, and can cause pain in the back of the head, neck, and face.
4. Geniculate neuralgia: This is a rare condition that affects the nerves in the jaw and ear, and can cause pain in the jaw, face, and ear.

Overall, neuralgia is a complex and debilitating condition that can significantly impact an individual's quality of life. It is important for individuals experiencing symptoms of neuralgia to seek medical attention to determine the underlying cause and develop an appropriate treatment plan.

1. Complete paralysis: When there is no movement or sensation in a particular area of the body.
2. Incomplete paralysis: When there is some movement or sensation in a particular area of the body.
3. Localized paralysis: When paralysis affects only a specific part of the body, such as a limb or a facial muscle.
4. Generalized paralysis: When paralysis affects multiple parts of the body.
5. Flaccid paralysis: When there is a loss of muscle tone and the affected limbs feel floppy.
6. Spastic paralysis: When there is an increase in muscle tone and the affected limbs feel stiff and rigid.
7. Paralysis due to nerve damage: This can be caused by injuries, diseases such as multiple sclerosis, or birth defects such as spina bifida.
8. Paralysis due to muscle damage: This can be caused by injuries, such as muscular dystrophy, or diseases such as muscular sarcopenia.
9. Paralysis due to brain damage: This can be caused by head injuries, stroke, or other conditions that affect the brain such as cerebral palsy.
10. Paralysis due to spinal cord injury: This can be caused by trauma, such as a car accident, or diseases such as polio.

Paralysis can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, work, and participate in social and recreational activities. Treatment options for paralysis depend on the underlying cause and may include physical therapy, medications, surgery, or assistive technologies such as wheelchairs or prosthetic devices.

* Thoracic scoliosis: affects the upper back (thoracic spine)
* Cervical scoliosis: affects the neck (cervical spine)
* Lumbar scoliosis: affects the lower back (lumbar spine)

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

* Genetics: inherited conditions that affect the development of the spine
* Birth defects: conditions that are present at birth and affect the spine
* Infections: infections that affect the spine, such as meningitis or tuberculosis
* Injuries: injuries to the spine, such as those caused by car accidents or falls
* Degenerative diseases: conditions that affect the spine over time, such as osteoporosis or arthritis

Symptoms of scoliosis can include:

* An uneven appearance of the shoulders or hips
* A difference in the height of the shoulders or hips
* Pain or discomfort in the back or legs
* Difficulty standing up straight or maintaining balance

Scoliosis can be diagnosed through a variety of tests, including:

* X-rays: images of the spine that show the curvature
* Magnetic resonance imaging (MRI): images of the spine and surrounding tissues
* Computed tomography (CT) scans: detailed images of the spine and surrounding tissues

Treatment for scoliosis depends on the severity of the condition and can include:

* Observation: monitoring the condition regularly to see if it progresses
* Bracing: wearing a brace to support the spine and help straighten it
* Surgery: surgical procedures to correct the curvature, such as fusing vertebrae together or implanting a metal rod.

It is important for individuals with scoliosis to receive regular monitoring and treatment to prevent complications and maintain proper spinal alignment.

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 several types of spinal dysraphism, including:

1. Spina bifida: This is the most common type of spinal dysraphism, and it occurs when the spine fails to close properly during fetal development. As a result, the spinal cord and meninges (the protective covering of the spinal cord) are exposed and can be damaged.
2. Myelomeningocele: This is a type of spina bifida that occurs when the spinal cord protrudes through an opening in the spine. It is often associated with hydrocephalus (a buildup of fluid in the brain).
3. Meningomyelocele: This is a type of spinal dysraphism that occurs when the meninges protrude through an opening in the spine, but the spinal cord remains within the spine.
4. Diastematomyelia: This is a rare type of spinal dysraphism that occurs when there is a separation or division of the spinal cord.
5. Hemicord syndrome: This is a rare type of spinal dysraphism that occurs when one half of the spinal cord is underdeveloped or absent.

The symptoms of spinal dysraphism can vary depending on the severity and location of the disorder. They may include:

* Muscle weakness or paralysis
* Loss of sensation in the affected limbs
* Bladder and bowel dysfunction
* Hydrocephalus (a buildup of fluid in the brain)
* Neurological problems such as seizures, learning disabilities, and developmental delays.

Treatment for spinal dysraphism depends on the severity of the disorder and may include:

* Surgery to repair or close the opening in the spine
* Shunting procedures to drain excess fluid from the brain
* Physical therapy to improve muscle strength and mobility
* Occupational therapy to help with daily activities and developmental delays.

The long-term outlook for individuals with spinal dysraphism varies depending on the severity of the disorder and the effectiveness of treatment. Some individuals may experience significant improvement with surgery and other treatments, while others may have ongoing neurological problems and developmental delays. It is important for individuals with spinal dysraphism to receive regular medical care and follow-up to monitor their condition and address any complications that may arise.

Surgery is often required to treat hematoma, subdural spinal, as prompt intervention is necessary to prevent long-term neurological damage. The prognosis for this condition is generally good if treated early and effectively, but can be poor if left untreated or if there are complications such as infection or hydrocephalus (fluid accumulation in the brain).

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 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.

The condition can occur anywhere along the spine, but it is most common in the neck (cervical spine) and lower back (lumbar spine). Spinal osteophytosis can put pressure on surrounding nerves and the spinal cord, leading to pain, numbness, or weakness in the arms or legs.

There are several risk factors for developing spinal osteophytosis, including:

* Age (as wear and tear on the spine increases with age)
* Genetics (some people may be more prone to developing bone spurs due to their genetic makeup)
* Injury or trauma (a sudden injury can cause bone growths to form in response)
* Degenerative conditions (such as osteoarthritis or rheumatoid arthritis)

Symptoms of spinal osteophytosis can include:

* Back pain that worsens with activity and improves with rest
* Pain, numbness, or weakness in the arms or legs
* Limited range of motion in the neck or lower back
* Difficulty walking or maintaining balance

Treatment for spinal osteophytosis depends on the severity of the condition and can include:

* Medications (such as pain relievers or anti-inflammatory drugs)
* Physical therapy (to improve flexibility and strength)
* Injections (such as steroids or pain medication)
* Surgery (in severe cases, to remove the bone growths or to fuse vertebrae together)

It is important to seek medical attention if symptoms persist or worsen over time, as untreated spinal osteophytosis can lead to chronic pain and limited mobility.

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.

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.

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.

There are several types of kyphosis, including:

1. Postural kyphosis: This type of kyphosis is caused by poor posture and is often seen in teenagers.
2. Scheuermann's kyphosis: This type of kyphosis is caused by a structural deformity of the spine and is most common during adolescence.
3. Degenerative kyphosis: This type of kyphosis is caused by degenerative changes in the spine, such as osteoporosis or degenerative disc disease.
4. Neuromuscular kyphosis: This type of kyphosis is caused by neuromuscular disorders such as cerebral palsy or muscular dystrophy.

Symptoms of kyphosis can include:

* An abnormal curvature of the spine
* Back pain
* Difficulty breathing
* Difficulty maintaining posture
* Loss of height
* Tiredness or fatigue

Kyphosis can be diagnosed through a physical examination, X-rays, and other imaging tests. Treatment options for kyphosis depend on the type and severity of the condition and can include:

* Physical therapy
* Bracing
* Medication
* Surgery

It is important to seek medical attention if you or your child is experiencing any symptoms of kyphosis, as early diagnosis and treatment can help prevent further progression of the condition and improve quality of life.

Anatomy59

Organisms8

Diseases87

Chemicals and Drugs23

Analytical, Diagnostic and Therapeutic Techniques and Equipment41

Psychiatry and Psychology12

Phenomena and Processes35

Disciplines and Occupations2

Information Science2

Health Care8

Combined 3T diffusion tensor tractography and 1H-MR spectroscopy in motor neuron disease. (1/23)

Spinal and bulbar muscular atrophy: a motoneuron or muscle disease? (2/23)

Mitochondrial abnormalities in spinal and bulbar muscular atrophy. (3/23)

Altered RNA splicing contributes to skeletal muscle pathology in Kennedy disease knock-in mice. (4/23)

Autophagy and access: understanding the role of androgen receptor subcellular localization in SBMA. (5/23)

Clinical features of spinal and bulbar muscular atrophy. (6/23)

B2 attenuates polyglutamine-expanded androgen receptor toxicity in cell and fly models of spinal and bulbar muscular atrophy. (7/23)

Prenatal flutamide enhances survival in a myogenic mouse model of spinal bulbar muscular atrophy. (8/23)

Atrophy

Spinal Cord

Spinal Cord Injuries

Muscular Atrophy

Muscular Atrophy, Spinal

Optic Atrophy

Spinal Muscular Atrophies of Childhood

Injections, Spinal

Spinal Cord Diseases

Spinal Nerves

Multiple System Atrophy

Anesthesia, Spinal

Spinal Nerve Roots

Spinal Cord Neoplasms

Spinal Canal

Spinal Diseases

Spinal Cord Compression

Spinal Neoplasms

Spinal Stenosis

Spinal Fusion

Olivopontocerebellar Atrophies

Spinal Injuries

Gyrate Atrophy

Survival of Motor Neuron 1 Protein

Motor Neurons

Magnetic Resonance Imaging

Ganglia, Spinal

Spinal Cord Ischemia

SMN Complex Proteins

Geographic Atrophy

Paraplegia

Muscular Disorders, Atrophic

Survival of Motor Neuron 2 Protein

Spine

Thoracic Vertebrae

Tuberculosis, Spinal

Laminectomy

Spinal Curvatures

Cervical Vertebrae

Rats, Sprague-Dawley

Hematoma, Epidural, Spinal

Posterior Horn Cells

Optic Atrophy, Autosomal Dominant

Muscle, Skeletal

Lumbosacral Region

Anterior Horn Cells

Lumbar Vertebrae

Brain

Disease Models, Animal

X Chromosome

Spinal Fractures

Bulbo-Spinal Atrophy, X-Linked

Spinal Cord Regeneration

Hindlimb Suspension

Axons

Quadriplegia

Pain

Trigeminal Nucleus, Spinal

Hyperalgesia

Time Factors

Locomotion

Recovery of Function

Myelography

Manipulation, Spinal

Electromyography

Neurons

Gastritis, Atrophic

Nerve Regeneration

Neuralgia

Paralysis

Nerve Tissue Proteins

Epidural Space

Pain Measurement

SKP Cullin F-Box Protein Ligases

Cordotomy

Hindlimb

Spinal Puncture

Myelitis

Electric Stimulation

Scoliosis