A slowly progressive autoimmune demyelinating disease of peripheral nerves and nerve roots. Clinical manifestations include weakness and sensory loss in the extremities and enlargement of peripheral nerves. The course may be relapsing-remitting or demonstrate a step-wise progression. Protein is usually elevated in the spinal fluid and cranial nerves are typically spared. GUILLAIN-BARRE SYNDROME features a relatively rapid progression of disease which distinguishes it from this condition. (Adams et al., Principles of Neurology, 6th ed, p1337)
Diseases characterized by injury or dysfunction involving multiple peripheral nerves and nerve roots. The process may primarily affect myelin or nerve axons. Two of the more common demyelinating forms are acute inflammatory polyradiculopathy (GUILLAIN-BARRE SYNDROME) and POLYRADICULONEUROPATHY, CHRONIC INFLAMMATORY DEMYELINATING. Polyradiculoneuritis refers to inflammation of multiple peripheral nerves and spinal nerve roots.
Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.
An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur. (From Adams et al., Principles of Neurology, 6th ed, pp1312-1314)
Diseases of multiple peripheral nerves simultaneously. Polyneuropathies usually are characterized by symmetrical, bilateral distal motor and sensory impairment with a graded increase in severity distally. The pathological processes affecting peripheral nerves include degeneration of the axon, myelin or both. The various forms of polyneuropathy are categorized by the type of nerve affected (e.g., sensory, motor, or autonomic), by the distribution of nerve injury (e.g., distal vs. proximal), by nerve component primarily affected (e.g., demyelinating vs. axonal), by etiology, or by pattern of inheritance.
A branch of the tibial nerve which supplies sensory innervation to parts of the lower leg and foot.
Immunoglobulin preparations used in intravenous infusion, containing primarily IMMUNOGLOBULIN G. They are used to treat a variety of diseases associated with decreased or abnormal immunoglobulin levels including pediatric AIDS; primary HYPERGAMMAGLOBULINEMIA; SCID; CYTOMEGALOVIRUS infections in transplant recipients, LYMPHOCYTIC LEUKEMIA, CHRONIC; Kawasaki syndrome, infection in neonates, and IDIOPATHIC THROMBOCYTOPENIC PURPURA.
Removal of plasma and replacement with various fluids, e.g., fresh frozen plasma, plasma protein fractions (PPF), albumin preparations, dextran solutions, saline. Used in treatment of autoimmune diseases, immune complex diseases, diseases of excess plasma factors, and other conditions.
Air that is reduced in volume by pressure.
The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.
Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.
Disease or injury involving multiple SPINAL NERVE ROOTS. Polyradiculitis refers to inflammation of multiple spinal nerve roots.
Conditions characterized by loss or dysfunction of myelin (see MYELIN SHEATH) in the brain, spinal cord, or optic nerves secondary to autoimmune mediated processes. This may take the form of a humoral or cellular immune response directed toward myelin or OLIGODENDROGLIA associated autoantigens.
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)
Proteins in the cerebrospinal fluid, normally albumin and globulin present in the ratio of 8 to 1. Increases in protein levels are of diagnostic value in neurological diseases. (Brain and Bannister's Clinical Neurology, 7th ed, p221)
The 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.
Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use.
A protein that accounts for more than half of the peripheral nervous system myelin protein. The extracellular domain of this protein is believed to engage in adhesive interactions and thus hold the myelin membrane compact. It can behave as a homophilic adhesion molecule through interactions with its extracellular domains. (From J Cell Biol 1994;126(4):1089-97)
A syndrome characterized by acute OPTIC NEURITIS; MYELITIS, TRANSVERSE; demyelinating and/or necrotizing lesions in the OPTIC NERVES and SPINAL CORD; and presence of specific autoantibodies to AQUAPORIN 4.
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)
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.
The most common clinical variant of MULTIPLE SCLEROSIS, characterized by recurrent acute exacerbations of neurologic dysfunction followed by partial or complete recovery. Common clinical manifestations include loss of visual (see OPTIC NEURITIS), motor, sensory, or bladder function. Acute episodes of demyelination may occur at any site in the central nervous system, and commonly involve the optic nerves, spinal cord, brain stem, and cerebellum. (Adams et al., Principles of Neurology, 6th ed, pp903-914)
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care. (Dictionary of Health Services Management, 2d ed)
An acute or subacute inflammatory process of the CENTRAL NERVOUS SYSTEM characterized histologically by multiple foci of perivascular demyelination. Symptom onset usually occurs several days after an acute viral infection or immunization, but it may coincide with the onset of infection or rarely no antecedent event can be identified. Clinical manifestations include CONFUSION, somnolence, FEVER, nuchal rigidity, and involuntary movements. The illness may progress to COMA and eventually be fatal. (Adams et al., Principles of Neurology, 6th ed, p921)
An experimental animal model for the demyelinating disease of GUILLAINE-BARRE SYNDROME. In the most frequently used protocol, animals are injected with a peripheral nerve tissue protein homogenate. After approximately 2 weeks the animals develop a neuropathy secondary to a T cell-mediated autoimmune response directed towards the MYELIN P2 PROTEIN in peripheral nerves. Pathologic findings include a perivascular accumulation of macrophages and T lymphocytes in the peripheral nervous system, similar to that seen in the Guillaine-Barre syndrome. (From Adams et al., Principles of Neurology, 6th ed, p1314; J Neuroimmunol 1998 Apr 1;84(1):40-52)
Aquaporin 4 is the major water-selective channel in the CENTRAL NERVOUS SYSTEM of mammals.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
Substances that reduce or suppress INFLAMMATION.
An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5)
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 species of CARDIOVIRUS which contains three strains: Theiler's murine encephalomyelitis virus, Vilyuisk human encephalomyelitis virus, and Rat encephalomyelitis virus.
Diagnosis of disease states by recording the spontaneous electrical activity of tissues or organs or by the response to stimulation of electrically excitable tissue.
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.
MYELIN-specific proteins that play a structural or regulatory role in the genesis and maintenance of the lamellar MYELIN SHEATH structure.

The sera from GM1 ganglioside antibody positive patients with Guillain-Barre syndrome or chronic inflammatory demyelinating polyneuropathy blocks Na+ currents in rat single myelinated nerve fibers. (1/44)

OBJECTIVE: To determine the possible role of anti-GM1 ganglioside antisera from patients with Gullain-Barr*e syndrome (GBS) or chronic inflammatory demyelinating polyneuropathy (CIDP) in the development of nerve dysfunction. METHODS: The effect of the anti-GM1 antibody positive antisera obtained from 4 GBS patients and 1 CIDP patient on membrane potential and ionic currents in rat single myelinated nerve fibers was investigated using the voltage clamp technique and compared with that of the anti-GM1 negative antisera obtained from 3 healthy controls and 2 GBS patients. RESULTS: In the presence of active complement, anti-GM1 positive antisera from 5 patients including 4 GBS patients and 1 CIDP patient significantly suppressed Na+ current more than anti-GM1 negative antisera. CONCLUSION: This study supports the notion that anti-GM1 antibody is one of the causative factors of conduction abnormality in GBS patients.  (+info)

Differential expression of NK T cell V alpha 24J alpha Q invariant TCR chain in the lesions of multiple sclerosis and chronic inflammatory demyelinating polyneuropathy. (2/44)

Human V alpha 24+ NK T cells are a unique subset of lymphocytes expressing the V alpha 24J alpha Q invariant TCR chain. Because they can rapidly produce large amounts of regulatory cytokines, a reduction of NK T cells may lead to the development of certain autoimmune diseases. Using a single-strand conformation polymorphism method, we demonstrate that a great reduction of V alpha 24J alpha Q NK T cells in the peripheral blood is an immunological hallmark of multiple sclerosis, whereas it is not appreciable in other autoimmune/inflammatory diseases such as chronic inflammatory demyelinating polyneuropathy. The chronic inflammatory demyelinating polyneuropathy lesions were often found to be infiltrated with V alpha 24J alpha Q NK T cells, but multiple sclerosis lesions only rarely expressed the V alpha 24J alpha Q TCR. It is therefore possible that the extent of NK T cell alteration may be a critical factor which would define the clinical and pathological features of autoimmune disease. Although the mechanism underlying the NK T cell deletion remains largely unclear, a remarkable contrast between the CNS and peripheral nervous system diseases allows us to speculate a role of tissue-specific elements such as the level of CD1d expression or differences in the CD1d-bound glycolipid.  (+info)

Clinicopathologic analysis of 124 biopsy-proven peripheral nerve diseases. (3/44)

We reviewed dinical, histological and ultrastructural findings of 124 cases of sural nerve biopsy specimens to delineate the trends of peripheral nerve diseases in our institute. Eighty-one were men and 43 were women. We categorized them into five groups: specific diagnosis (66 cases, 53.2%), axonal degeneration type (47 cases, 37.9%), demyelinating type (4 cases, 3.2%), mixed axonal degeneration-demyelinating type (6 cases, 4.8%) and normal (1 case, 0.9%). Cases with specific diagnosis included 21 inflammatory demyelinating polyneuropathy (15 chronic inflammatory demyelinating polyradiculoneuropathy, 6 Guillain-Barre disease), 13 hereditary motor and sensory neuropathy (7 Charcot-Marie-Tooth type I, 6 Charcot-Marie-Tooth type II), 10 vasculitis, 6 toxic neuropathy, 4 leprosy, 3 diabetic neuropathy, 2 alcoholic neuropathy, 1 Fabry's disease and other specific diseases (5 cases). In our cases, the proportion of specific diagnoses was higher, while the proportion of demyelinating peripheral neuropathies and normal were lower than those of Western series. The results of this study indicate that 1) a dose clinicopathologic correlation is important to make a precise diagnosis of peripheral nerve biopsy, 2) Biopsy under strict indication may reduce unnecessary histologic examination, 3) There is no difference in disease pattern of peripheral neuropathy between Western people and Koreans.  (+info)

Expression of the co-stimulatory molecule BB-1, the ligands CTLA-4 and CD28 and their mRNAs in chronic inflammatory demyelinating polyneuropathy. (4/44)

To examine whether the Schwann cells in patients with autoimmune neuropathies have the potential to behave as professional antigen-presenting cells, we investigated the expression of the co-stimulatory molecules BB-1, B7-1 (CD80) B7-2 (CD86) and their counter-receptors CD28 or CTLA-4 (CD152) at the protein and mRNA levels in sural nerve biopsies of patients with chronic inflammatory demyelinating polyneuropathy (CIDP), CIDP associated with human immunodeficiency virus infection (HIV-CIDP), IgM paraproteinaemic neuropathy and normal or non-immune axonal neuropathy. In single- and double-labelling experiments, we used the S-100 antigen as a pan-Schwann cell marker, myelin-associated glycoprotein as a marker for myelinating Schwann cells and the fibrillary acidic protein as a marker for unmyelinating Schwann cells. The expression of the B7 family of molecules was limited to BB-1 and was observed only on the Schwann cells. There was constitutive expression of BB-1 on unmyelinating Schwann cells in all nerves studied. However, in CIDP and HIV-CIDP, but not the other diseases, there was prominent upregulation of BB-1 on the myelinating Schwann cells. The endoneurial T cells in the proximity of BB-1-positive Schwann cells expressed the CD28 or CTLA-4 counter-receptors. Reverse transcription-polymerase chain reaction confirmed that these ligands were upregulated only in CIDP. Because the myelinating BB-1-positive Schwann cells expressed HLA-DR antigen, the findings indicate that, in CIDP, Schwann cells possess the necessary markers to function as antigen-presenting cells.  (+info)

Expression of accessory molecules for T-cell activation in peripheral nerve of patients with CIDP and vasculitic neuropathy. (5/44)

Vasculitic neuropathy and chronic inflammatory demyelinating polyneuropathy (CIDP) are neuropathies characterized by a T-lymphocyte infiltrate in the peripheral nerves. The microenvironment in which these T cells become activated, and the molecules and cells that play a role in this process are incompletely understood. Using immunohistochemical analysis, we studied the effect of the presence of adhesion, costimulatory and antigen-presenting molecules on different cell types as a precondition for local T-cell activation in human sural nerve biopsies of seven patients with CIDP, three patients with vasculitic neuropathy and three healthy controls. In biopsies from CIDP and vasculitic neuropathy patients, but not in those from healthy controls, Schwann cells expressed the adhesion/T-cell stimulatory molecule CD58 (LFA-3). The CD58 molecule was also present on endothelial cells of all vasculitic neuropathy patients and one CIDP patient. In biopsies from normal controls and patients, CD54 (ICAM-1) expression was detectable on microvascular endothelial cells. In addition, expression of the costimulatory molecule CD86 was detected on vascular tissue in patients with vasculitic neuropathy. Although macrophages were always present in all subjects, expression of the major histocompatibility complex (MHC)-like molecule CD1a by macrophages was restricted to biopsies from two CIDP patients and one vasculitic neuropathy patient. Unexpectedly, Schwann cells of a single vasculitis patient strongly expressed CD1b, a molecule involved in the presentation of self-glycolipids to T cells. Schwann cells in biopsies from patients and normal controls expressed high levels of the invariant chain, CD74, a molecule involved in the intracellular sorting of MHC class II molecules. There was no evidence for the presence of dendritic cells in sural nerve biopsies. These findings support a model in which T-cell activation can be initiated and/or perpetuated locally in sural nerve biopsies of patients with CIDP and vasculitic neuropathy, and predict an important role for Schwann cells and endothelial cells.  (+info)

Inflammatory demyelinating polyneuropathy: a complication of immunotherapy in malignant melanoma. (6/44)

Paraneoplastic syndromes (PNS) involving the central nervous system are a rare manifestation of malignant disease. As they commonly precede the diagnosis of malignancy their acute manifestations do not often present themselves to oncologists in the first instance. It is currently believed that most, if not all, neurological PNS are autoimmune in nature. Proteins expressed ectopically on the surface of tumour cells generate an immune response which cross-reacts with the same, or similar, proteins in the nervous system resulting in damage. This can involve a single cell type of the nervous system whilst in other cases the impairment is more widespread. The following report is of a case of chronic inflammatory demyelinating polyneuropathy (CIDP) occurring in metastatic malignant melanoma, following treatment with interferon-alpha. We review the current literature on this rare association and speculate on its pathogenesis, and the implications for future therapeutic strategies in melanoma targeting tumour antigens.  (+info)

Diagnostic value of sural nerve demyelination in chronic inflammatory demyelinating polyneuropathy. (7/44)

The objective of the study was to determine the diagnostic value of features of demyelination and inflammation in sural nerve biopsy specimens of patients with chronic inflammatory demyelinating polyneuropathy (CIDP). The features of (i) demyelination, (ii) axonal de- and regeneration and (iii) inflammation were investigated by measuring the number of onion bulbs, g ratio (axon diameter/total nerve fibre diameter), myelinated nerve fibre density, number of clusters and endoneurial area in 21 patients with CIDP, as well as in 13 patients with chronic idiopathic axonal polyneuropathy (CIAP) and six autopsy controls. In addition, teased fibres were classified and lengths of internodes measured. We found no difference in demyelinating features between patients with CIDP and CIAP, as the percentage of fibres with segmental de- and remyelination and the number of onion bulbs were similar in both polyneuropathy groups. The g ratio, expected to be higher in a demyelinating disease due to thinner myelin sheaths, was significantly lower in CIDP than CIAP. Evidence for axonal degeneration was found in both CIDP and CIAP, as both showed a decrease in myelinated nerve fibre density. There was no evidence of endoneurial oedema in CIDP, as the endoneurial area did not differ between CIDP, CIAP and the autopsy controls. Although significant differences of features of demyelination, axonal degeneration and inflammation were found in sural nerve biopsy specimens, there was a considerable overlap between abnormalities in CIDP and CIAP patients. In the majority of patients, quantitative analysis of light microscopical abnormalities in sural nerves was similar in CIDP and CIAP. Therefore, a sural nerve biopsy is of limited diagnostic value in CIDP.  (+info)

Motor dominant neuropathy in Sjogren's syndrome: report of two cases. (8/44)

Most of the peripheral neuropathies in Sjogren's syndrome (SS) are sensory- or autonomic-dominant. In this report, we present two cases of a rare type of neuropathy, motor dominant neuropathy, in SS. One showed signs similar to those of Guillain-Barre syndrome, and the other showed signs characteristic of chronic inflammatory demyelinating polyradiculoneuropathy. These patients received i.v. immunoglobulin therapy. To our knowledge, this is the first report indicating that i.v. immunoglobulin has beneficial effects on motor dominant neuropathy in SS.  (+info)

Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) is a rare neurological disorder characterized by progressive and persistent inflammation of the peripheral nerves' myelin sheaths, leading to significant damage and impaired nerve function. Myelin is the fatty insulation that surrounds and protects nerve fibers, enabling efficient electrical conduction and communication between the brain, spinal cord, and muscles.

In CIDP, the immune system mistakenly attacks the myelin sheath, causing its gradual deterioration (demyelination) and subsequent impairment of nerve function. This results in symptoms such as progressive muscle weakness, numbness, tingling, or sensory loss affecting both sides of the body. The onset of CIDP can be either acute or insidious, with symptoms developing slowly over several months.

CIDP is typically classified into two categories based on the distribution of nerve involvement:

1. Distal acquired demyelinating symmetric (DADS) neuropathy: This form of CIDP affects the longest nerves first, leading to symmetrical sensory and motor disturbances in the feet and hands.
2. Asymmetric or multifocal acquired demyelinating sensory and motor neuropathy: In this form, the damage is more localized and asymmetrical, affecting various parts of the peripheral nervous system.

The diagnosis of CIDP relies on a combination of clinical presentation, electrodiagnostic studies (nerve conduction studies and electromyography), and supportive findings from cerebrospinal fluid analysis and nerve biopsy. Treatment usually involves immunosuppressive therapies to control the immune response and promote nerve recovery, such as corticosteroids, intravenous immunoglobulins, or plasma exchange. Early diagnosis and treatment can significantly improve outcomes and prevent long-term disability in patients with CIDP.

Polyradiculoneuropathy is a medical term that refers to a condition affecting multiple nerve roots and peripheral nerves. It's a type of neuropathy, which is damage or disease affecting the peripheral nerves, and it involves damage to the nerve roots as they exit the spinal cord.

The term "poly" means many, "radiculo" refers to the nerve root, and "neuropathy" indicates a disorder of the nerves. Therefore, polyradiculoneuropathy implies that multiple nerve roots and peripheral nerves are affected.

This condition can result from various causes, such as infections (like Guillain-Barre syndrome), autoimmune disorders (such as lupus or rheumatoid arthritis), diabetes, cancer, or exposure to toxins. Symptoms may include weakness, numbness, tingling, or pain in the limbs, which can progress and become severe over time. Proper diagnosis and management are crucial for improving outcomes and preventing further nerve damage.

Demyelinating diseases are a group of disorders that are characterized by damage to the myelin sheath, which is the protective covering surrounding nerve fibers in the brain, optic nerves, and spinal cord. Myelin is essential for the rapid transmission of nerve impulses, and its damage results in disrupted communication between the brain and other parts of the body.

The most common demyelinating disease is multiple sclerosis (MS), where the immune system mistakenly attacks the myelin sheath. Other demyelinating diseases include:

1. Acute Disseminated Encephalomyelitis (ADEM): An autoimmune disorder that typically follows a viral infection or vaccination, causing widespread inflammation and demyelination in the brain and spinal cord.
2. Neuromyelitis Optica (NMO) or Devic's Disease: A rare autoimmune disorder that primarily affects the optic nerves and spinal cord, leading to severe vision loss and motor disability.
3. Transverse Myelitis: Inflammation of the spinal cord causing damage to both sides of one level (segment) of the spinal cord, resulting in various neurological symptoms such as muscle weakness, numbness, or pain, depending on which part of the spinal cord is affected.
4. Guillain-Barré Syndrome: An autoimmune disorder that causes rapid-onset muscle weakness, often beginning in the legs and spreading to the upper body, including the face and breathing muscles. It occurs when the immune system attacks the peripheral nerves' myelin sheath.
5. Central Pontine Myelinolysis (CPM): A rare neurological disorder caused by rapid shifts in sodium levels in the blood, leading to damage to the myelin sheath in a specific area of the brainstem called the pons.

These diseases can result in various symptoms, such as muscle weakness, numbness, vision loss, difficulty with balance and coordination, and cognitive impairment, depending on the location and extent of the demyelination. Treatment typically focuses on managing symptoms, modifying the immune system's response, and promoting nerve regeneration and remyelination when possible.

Guillain-Barré syndrome (GBS) is a rare autoimmune disorder in which the body's immune system mistakenly attacks the peripheral nervous system, leading to muscle weakness, tingling sensations, and sometimes paralysis. The peripheral nervous system includes the nerves that control our movements and transmit signals from our skin, muscles, and joints to our brain.

The onset of GBS usually occurs after a viral or bacterial infection, such as respiratory or gastrointestinal infections, or following surgery, vaccinations, or other immune system triggers. The exact cause of the immune response that leads to GBS is not fully understood.

GBS typically progresses rapidly over days or weeks, with symptoms reaching their peak within 2-4 weeks after onset. Most people with GBS experience muscle weakness that starts in the lower limbs and spreads upward to the upper body, arms, and face. In severe cases, the diaphragm and chest muscles may become weakened, leading to difficulty breathing and requiring mechanical ventilation.

The diagnosis of GBS is based on clinical symptoms, nerve conduction studies, and sometimes cerebrospinal fluid analysis. Treatment typically involves supportive care, such as pain management, physical therapy, and respiratory support if necessary. In addition, plasma exchange (plasmapheresis) or intravenous immunoglobulin (IVIG) may be used to reduce the severity of symptoms and speed up recovery.

While most people with GBS recover completely or with minimal residual symptoms, some may experience long-term disability or require ongoing medical care. The prognosis for GBS varies depending on the severity of the illness and the individual's age and overall health.

Polyneuropathy is a medical condition that refers to the damage or dysfunction of peripheral nerves (nerves outside the brain and spinal cord) in multiple areas of the body. These nerves are responsible for transmitting sensory, motor, and autonomic signals between the central nervous system and the rest of the body.

In polyneuropathies, this communication is disrupted, leading to various symptoms depending on the type and extent of nerve damage. Commonly reported symptoms include:

1. Numbness or tingling in the hands and feet
2. Muscle weakness and cramps
3. Loss of reflexes
4. Burning or stabbing pain
5. Balance and coordination issues
6. Increased sensitivity to touch
7. Autonomic dysfunction, such as bowel, bladder, or digestive problems, and changes in blood pressure

Polyneuropathies can be caused by various factors, including diabetes, alcohol abuse, nutritional deficiencies, autoimmune disorders, infections, toxins, inherited genetic conditions, or idiopathic (unknown) causes. The treatment for polyneuropathy depends on the underlying cause and may involve managing underlying medical conditions, physical therapy, pain management, and lifestyle modifications.

The sural nerve is a purely sensory peripheral nerve in the lower leg and foot. It provides sensation to the outer ( lateral) aspect of the little toe and the adjacent side of the fourth toe, as well as a small portion of the skin on the back of the leg between the ankle and knee joints.

The sural nerve is formed by the union of branches from the tibial and common fibular nerves (branches of the sciatic nerve) in the lower leg. It runs down the calf, behind the lateral malleolus (the bony prominence on the outside of the ankle), and into the foot.

The sural nerve is often used as a donor nerve during nerve grafting procedures due to its consistent anatomy and relatively low risk for morbidity at the donor site.

Intravenous Immunoglobulins (IVIG) are a preparation of antibodies, specifically immunoglobulins, that are derived from the plasma of healthy donors. They are administered intravenously to provide passive immunity and help boost the immune system's response in individuals with weakened or compromised immune systems. IVIG can be used for various medical conditions such as primary immunodeficiency disorders, secondary immunodeficiencies, autoimmune diseases, and some infectious diseases. The administration of IVIG can help prevent infections, reduce the severity and frequency of infections, and manage the symptoms of certain autoimmune disorders. It is important to note that while IVIG provides temporary immunity, it does not replace a person's own immune system.

Plasma exchange, also known as plasmapheresis, is a medical procedure where the liquid portion of the blood (plasma) is separated from the blood cells. The plasma, which may contain harmful substances such as antibodies, clotting factors, or toxins, is then removed and replaced with fresh plasma or a plasma substitute. This process helps to remove the harmful substances from the blood and allows the body to replenish its own plasma with normal components. Plasma exchange is used in the treatment of various medical conditions including autoimmune diseases, poisonings, and certain types of kidney diseases.

Compressed air is defined in a medical context as air that has been pressurized and forced into a smaller space or volume. It is often used in medical devices and treatments, such as in the case of aerosolized medications or in certain surgical procedures. Compressed air can also be used to power medical equipment, such as drills and saws.

It's important to note that the use of compressed air in medical settings must follow strict guidelines and regulations to ensure the safety and effectiveness of the treatment. For example, the air must be clean and free from contaminants, and the pressure must be carefully controlled to avoid causing harm to patients or healthcare providers.

Neural conduction is the process by which electrical signals, known as action potentials, are transmitted along the axon of a neuron (nerve cell) to transmit information between different parts of the nervous system. This electrical impulse is generated by the movement of ions across the neuronal membrane, and it propagates down the length of the axon until it reaches the synapse, where it can then stimulate the release of neurotransmitters to communicate with other neurons or target cells. The speed of neural conduction can vary depending on factors such as the diameter of the axon, the presence of myelin sheaths (which act as insulation and allow for faster conduction), and the temperature of the environment.

Peripheral Nervous System (PNS) diseases, also known as Peripheral Neuropathies, refer to conditions that affect the functioning of the peripheral nervous system, which includes all the nerves outside the brain and spinal cord. These nerves transmit signals between the central nervous system (CNS) and the rest of the body, controlling sensations, movements, and automatic functions such as heart rate and digestion.

PNS diseases can be caused by various factors, including genetics, infections, toxins, metabolic disorders, trauma, or autoimmune conditions. The symptoms of PNS diseases depend on the type and extent of nerve damage but often include:

1. Numbness, tingling, or pain in the hands and feet
2. Muscle weakness or cramps
3. Loss of reflexes
4. Decreased sensation to touch, temperature, or vibration
5. Coordination problems and difficulty with balance
6. Sexual dysfunction
7. Digestive issues, such as constipation or diarrhea
8. Dizziness or fainting due to changes in blood pressure

Examples of PNS diseases include Guillain-Barre syndrome, Charcot-Marie-Tooth disease, diabetic neuropathy, and peripheral nerve injuries. Treatment for these conditions varies depending on the underlying cause but may involve medications, physical therapy, lifestyle changes, or surgery.

Polyradiculopathy is a medical term that refers to a condition affecting multiple nerve roots. It's a type of neurological disorder where there is damage or injury to the nerve roots, which are the beginning portions of nerves as they exit the spinal cord. This damage can result in various symptoms such as weakness, numbness, tingling, and pain in the affected areas of the body, depending on the specific nerves involved.

Polyradiculopathy can be caused by a variety of factors, including trauma, infection, inflammation, compression, or degenerative changes in the spine. Some common causes include spinal cord tumors, herniated discs, spinal stenosis, and autoimmune disorders such as Guillain-Barre syndrome.

Diagnosing polyradiculopathy typically involves a thorough neurological examination, imaging studies such as MRI or CT scans, and sometimes nerve conduction studies or electromyography (EMG) to assess the function of the affected nerves. Treatment for polyradiculopathy depends on the underlying cause but may include medications, physical therapy, surgery, or a combination of these approaches.

Demyelinating autoimmune diseases of the central nervous system (CNS) are a group of disorders characterized by inflammation and damage to the myelin sheath, which is the protective covering that surrounds nerve fibers in the brain and spinal cord. This damage can result in various neurological symptoms, including muscle weakness, sensory loss, vision problems, and cognitive impairment.

The most common demyelinating autoimmune disease of the CNS is multiple sclerosis (MS), which affects approximately 2.3 million people worldwide. Other examples include neuromyelitis optica spectrum disorder (NMOSD), acute disseminated encephalomyelitis (ADEM), and transverse myelitis.

These conditions are thought to arise when the immune system mistakenly attacks the myelin sheath, leading to inflammation, damage, and scarring (sclerosis) in the CNS. The exact cause of this autoimmune response is not fully understood, but it is believed to involve a complex interplay between genetic, environmental, and immunological factors.

Treatment for demyelinating autoimmune diseases of the CNS typically involves a combination of medications to manage symptoms, reduce inflammation, and modify the course of the disease. These may include corticosteroids, immunosuppressive drugs, and disease-modifying therapies (DMTs) that target specific components of the immune system.

Multiple Sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS), which includes the brain, spinal cord, and optic nerves. In MS, the immune system mistakenly attacks the protective covering of nerve fibers, called myelin, leading to damage and scarring (sclerosis). This results in disrupted communication between the brain and the rest of the body, causing a variety of neurological symptoms that can vary widely from person to person.

The term "multiple" refers to the numerous areas of scarring that occur throughout the CNS in this condition. The progression, severity, and specific symptoms of MS are unpredictable and may include vision problems, muscle weakness, numbness or tingling, difficulty with balance and coordination, cognitive impairment, and mood changes. There is currently no cure for MS, but various treatments can help manage symptoms, modify the course of the disease, and improve quality of life for those affected.

Cerebrospinal fluid (CSF) proteins refer to the proteins present in the cerebrospinal fluid, which is a clear, colorless fluid that surrounds and protects the brain and spinal cord. The protein concentration in the CSF is much lower than that in the blood, and it contains a specific set of proteins that are produced by the brain, spinal cord, and associated tissues.

The normal range for CSF protein levels is typically between 15-45 mg/dL, although this can vary slightly depending on the laboratory's reference range. An elevation in CSF protein levels may indicate the presence of neurological disorders such as meningitis, encephalitis, multiple sclerosis, or Guillain-Barre syndrome. Additionally, certain conditions such as spinal cord injury, brain tumors, or neurodegenerative diseases can also cause an increase in CSF protein levels.

Therefore, measuring CSF protein levels is an important diagnostic tool for neurologists to evaluate various neurological disorders and monitor disease progression. However, it's essential to interpret the results of CSF protein tests in conjunction with other clinical findings and laboratory test results to make an accurate diagnosis.

Peripheral nerves are nerve fibers that transmit signals between the central nervous system (CNS, consisting of the brain and spinal cord) and the rest of the body. These nerves convey motor, sensory, and autonomic information, enabling us to move, feel, and respond to changes in our environment. They form a complex network that extends from the CNS to muscles, glands, skin, and internal organs, allowing for coordinated responses and functions throughout the body. Damage or injury to peripheral nerves can result in various neurological symptoms, such as numbness, weakness, or pain, depending on the type and severity of the damage.

Plasmapheresis is a medical procedure where the liquid portion of the blood (plasma) is separated from the blood cells. The plasma, which may contain harmful substances such as antibodies or toxins, is then removed and replaced with fresh plasma or a plasma substitute. The remaining blood cells are mixed with the new plasma and returned to the body. This process is also known as therapeutic plasma exchange (TPE). It's used to treat various medical conditions including certain autoimmune diseases, poisonings, and neurological disorders.

Myelin P0 protein, also known as P0 or MPZ (myelin protein zero), is a major structural component of the myelin sheath in the peripheral nervous system. The myelin sheath is a multilayered membrane that surrounds and insulates nerve fibers to increase the speed of electrical impulse transmission.

P0 protein is a transmembrane glycoprotein, which means it spans the lipid bilayer of the myelin membrane and has sugar molecules (glycans) attached to it. It plays a crucial role in maintaining the compact structure of the myelin sheath by forming homodimers that interact with each other through their extracellular domains, creating tight junctions between the apposing layers of the myelin membrane.

P0 protein also contributes to the stability and integrity of the myelin sheath by interacting with other myelin proteins, such as connexin 32 and peripheral myelin protein 22 (PMP22). Mutations in the MPZ gene can lead to various peripheral neuropathies, including Charcot-Marie-Tooth disease type 1B and Dejerine-Sottas syndrome.

Neuromyelitis optica (NMO), also known as Devic's disease, is an autoimmune disorder that affects the central nervous system (CNS). It primarily causes inflammation and damage to the optic nerves (which transmit visual signals from the eye to the brain) and the spinal cord. This results in optic neuritis (inflammation of the optic nerve, causing vision loss) and myelitis (inflammation of the spinal cord, leading to motor, sensory, and autonomic dysfunction).

A key feature of NMO is the presence of autoantibodies against aquaporin-4 (AQP4-IgG), a water channel protein found in astrocytes (a type of glial cell) in the CNS. These antibodies play a crucial role in the development of the disease, as they target and damage the AQP4 proteins, leading to inflammation, demyelination (loss of the protective myelin sheath around nerve fibers), and subsequent neurological dysfunction.

NMO is distinct from multiple sclerosis (MS), another autoimmune disorder affecting the CNS, as it has different clinical features, radiological findings, and treatment responses. However, NMO can sometimes be misdiagnosed as MS due to overlapping symptoms in some cases. Accurate diagnosis of NMO is essential for appropriate management and treatment, which often includes immunosuppressive therapies to control the autoimmune response and prevent further damage to the nervous system.

Motor Neuron Disease (MND) is a progressive neurodegenerative disorder that affects the motor neurons, which are nerve cells in the brain and spinal cord responsible for controlling voluntary muscles involved in movement, speaking, breathing, and swallowing. As the motor neurons degenerate and die, they stop sending signals to the muscles, causing them to weaken, waste away (atrophy), and eventually lead to paralysis.

There are several types of MND, including:

1. Amyotrophic Lateral Sclerosis (ALS): Also known as Lou Gehrig's disease, this is the most common form of MND. It affects both upper and lower motor neurons, causing muscle weakness, stiffness, twitching, and atrophy throughout the body.
2. Progressive Bulbar Palsy (PBP): This type primarily affects the bulbar muscles in the brainstem, which control speech, swallowing, and chewing. Patients with PBP experience difficulties with speaking, slurred speech, and problems swallowing and may also have weak facial muscles and limb weakness.
3. Primary Lateral Sclerosis (PLS): This form of MND affects only the upper motor neurons, causing muscle stiffness, spasticity, and weakness, primarily in the legs. PLS progresses more slowly than ALS, and patients usually maintain their ability to speak and swallow for a longer period.
4. Progressive Muscular Atrophy (PMA): This type of MND affects only the lower motor neurons, causing muscle wasting, weakness, and fasciculations (muscle twitches). PMA progresses more slowly than ALS but can still be severely disabling over time.
5. Spinal Muscular Atrophy (SMA): This is a genetic form of MND that typically presents in infancy or childhood, although adult-onset forms exist. SMA affects the lower motor neurons in the spinal cord, causing muscle weakness and atrophy, primarily in the legs and trunk.

The exact cause of Motor Neuron Disease is not fully understood, but it is believed to involve a combination of genetic, environmental, and lifestyle factors. There is currently no cure for MND, and treatment focuses on managing symptoms, maintaining quality of life, and slowing disease progression through various therapies and medications.

Spinal nerve roots are the initial parts of spinal nerves that emerge from the spinal cord through the intervertebral foramen, which are small openings between each vertebra in the spine. These nerve roots carry motor, sensory, and autonomic fibers to and from specific regions of the body. There are 31 pairs of spinal nerve roots in total, with 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal pair. Each root has a dorsal (posterior) and ventral (anterior) ramus that branch off to form the peripheral nervous system. Irritation or compression of these nerve roots can result in pain, numbness, weakness, or loss of reflexes in the affected area.

Relapsing-remitting multiple sclerosis (RRMS) is a type of multiple sclerosis (MS), which is a chronic autoimmune disease that affects the central nervous system (CNS). In RRMS, the immune system attacks the protective covering of nerve fibers (myelin sheath) in the CNS, leading to the formation of lesions or scars (scleroses). These attacks result in episodes of new or worsening symptoms, known as relapses or exacerbations.

The distinguishing feature of RRMS is that these relapses are followed by periods of partial or complete recovery (remissions), during which symptoms may improve, stabilize, or even disappear temporarily. The duration and severity of relapses and remissions can vary significantly among individuals with RRMS. Over time, the accumulation of damage to the nervous system can lead to progressive disability.

Approximately 85% of people with MS are initially diagnosed with the relapsing-remitting form. With appropriate treatment and management, many people with RRMS can effectively manage their symptoms and maintain a good quality of life for several years.

A chronic disease is a long-term medical condition that often progresses slowly over a period of years and requires ongoing management and care. These diseases are typically not fully curable, but symptoms can be managed to improve quality of life. Common chronic diseases include heart disease, stroke, cancer, diabetes, arthritis, and COPD (chronic obstructive pulmonary disease). They are often associated with advanced age, although they can also affect children and younger adults. Chronic diseases can have significant impacts on individuals' physical, emotional, and social well-being, as well as on healthcare systems and society at large.

Acute disseminated encephalomyelitis (ADEM) is a rare inflammatory demyelinating disease of the central nervous system, characterized by a sudden onset of widespread inflammation and damage to the brain and spinal cord. It typically follows a viral infection or, less commonly, vaccination and is more prevalent in children than adults.

The condition involves the rapid development of multiple inflammatory lesions throughout the white matter of the brain and spinal cord. These lesions lead to demyelination, which means the loss of the protective myelin sheath surrounding nerve fibers, disrupting communication between neurons. This results in various neurological symptoms such as:

1. Encephalopathy (changes in consciousness, behavior, or mental status)
2. Weakness or paralysis of limbs
3. Visual disturbances
4. Speech and language problems
5. Seizures
6. Ataxia (loss of coordination and balance)
7. Sensory changes
8. Autonomic nervous system dysfunction (e.g., temperature regulation, blood pressure, heart rate)

The diagnosis of ADEM is based on clinical presentation, radiological findings, and laboratory tests to exclude other possible causes. Magnetic resonance imaging (MRI) typically shows multiple, large, bilateral lesions in the white matter of the brain and spinal cord. Cerebrospinal fluid analysis may reveal an elevated white blood cell count and increased protein levels.

Treatment for ADEM generally includes high-dose corticosteroids to reduce inflammation and improve outcomes. Intravenous immunoglobulin (IVIG) or plasma exchange (plasmapheresis) may be used if there is no response to steroid therapy. Most patients with ADEM recover completely or have significant improvement within several months, although some may experience residual neurological deficits.

I'm sorry for any confusion, but "Autoimmune Experimental Neuritis" is not a widely recognized medical term or diagnosis. It seems that this term might be referring to a specific experimental model used in research to study autoimmune neuritis.

Neuritis generally refers to inflammation of a nerve or nerves, which can cause symptoms such as pain, tingling, numbness, or weakness. Autoimmune neuritis is a condition where the immune system mistakenly attacks the peripheral nerves, leading to these symptoms.

In research settings, an "experimental" model refers to a controlled study in a laboratory setting, often using animals, to investigate a particular medical condition or test new treatments. Therefore, "Autoimmune Experimental Neuritis" might refer to a specific animal model used to study the mechanisms and potential treatments of autoimmune neuritis.

However, without more context, it's difficult to provide a precise definition. If you have more information about where you encountered this term or its intended meaning, I would be happy to help further!

Aquaporin 4 (AQP4) is a water channel protein that is primarily found in the membranes of astrocytes, which are a type of glial cell in the central nervous system. AQP4 plays a crucial role in the regulation of water homeostasis and the clearance of excess fluid from the brain and spinal cord. It also facilitates the rapid movement of water across the blood-brain barrier and between astrocytes, which is important for maintaining proper neuronal function and protecting the brain from edema or swelling.

Mutations in the AQP4 gene can lead to various neurological disorders, such as neurodegenerative diseases and neuromyelitis optica spectrum disorder (NMOSD), a severe autoimmune condition that affects the optic nerves and spinal cord. In NMOSD, the immune system mistakenly attacks AQP4 proteins, causing inflammation, demyelination, and damage to the nervous tissue.

A biopsy is a medical procedure in which a small sample of tissue is taken from the body to be examined under a microscope for the presence of disease. This can help doctors diagnose and monitor various medical conditions, such as cancer, infections, or autoimmune disorders. The type of biopsy performed will depend on the location and nature of the suspected condition. Some common types of biopsies include:

1. Incisional biopsy: In this procedure, a surgeon removes a piece of tissue from an abnormal area using a scalpel or other surgical instrument. This type of biopsy is often used when the lesion is too large to be removed entirely during the initial biopsy.

2. Excisional biopsy: An excisional biopsy involves removing the entire abnormal area, along with a margin of healthy tissue surrounding it. This technique is typically employed for smaller lesions or when cancer is suspected.

3. Needle biopsy: A needle biopsy uses a thin, hollow needle to extract cells or fluid from the body. There are two main types of needle biopsies: fine-needle aspiration (FNA) and core needle biopsy. FNA extracts loose cells, while a core needle biopsy removes a small piece of tissue.

4. Punch biopsy: In a punch biopsy, a round, sharp tool is used to remove a small cylindrical sample of skin tissue. This type of biopsy is often used for evaluating rashes or other skin abnormalities.

5. Shave biopsy: During a shave biopsy, a thin slice of tissue is removed from the surface of the skin using a sharp razor-like instrument. This technique is typically used for superficial lesions or growths on the skin.

After the biopsy sample has been collected, it is sent to a laboratory where a pathologist will examine the tissue under a microscope and provide a diagnosis based on their findings. The results of the biopsy can help guide further treatment decisions and determine the best course of action for managing the patient's condition.

Anti-inflammatory agents are a class of drugs or substances that reduce inflammation in the body. They work by inhibiting the production of inflammatory mediators, such as prostaglandins and leukotrienes, which are released during an immune response and contribute to symptoms like pain, swelling, redness, and warmth.

There are two main types of anti-inflammatory agents: steroidal and nonsteroidal. Steroidal anti-inflammatory drugs (SAIDs) include corticosteroids, which mimic the effects of hormones produced by the adrenal gland. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a larger group that includes both prescription and over-the-counter medications, such as aspirin, ibuprofen, naproxen, and celecoxib.

While both types of anti-inflammatory agents can be effective in reducing inflammation and relieving symptoms, they differ in their mechanisms of action, side effects, and potential risks. Long-term use of NSAIDs, for example, can increase the risk of gastrointestinal bleeding, kidney damage, and cardiovascular events. Corticosteroids can have significant side effects as well, particularly with long-term use, including weight gain, mood changes, and increased susceptibility to infections.

It's important to use anti-inflammatory agents only as directed by a healthcare provider, and to be aware of potential risks and interactions with other medications or health conditions.

Autoimmune encephalomyelitis (EAE) is a model of inflammatory demyelinating disease used in medical research to study the mechanisms of multiple sclerosis (MS) and develop new therapies. It is experimentally induced in laboratory animals, typically mice or rats, through immunization with myelin antigens or T-cell transfer. The resulting immune response leads to inflammation, demyelination, and neurological dysfunction in the central nervous system (CNS), mimicking certain aspects of MS.

EAE is a valuable tool for understanding the pathogenesis of MS and testing potential treatments. However, it is essential to recognize that EAE is an experimental model and may not fully recapitulate all features of human autoimmune encephalomyelitis.

The myelin sheath is a multilayered, fatty substance that surrounds and insulates many nerve fibers in the nervous system. It is essential for the rapid transmission of electrical signals, or nerve impulses, along these nerve fibers, allowing for efficient communication between different parts of the body. The myelin sheath is produced by specialized cells called oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS). Damage to the myelin sheath, as seen in conditions like multiple sclerosis, can significantly impair nerve function and result in various neurological symptoms.

Theilovirus is not typically considered a separate virus in modern virology. Instead, it is now classified as a genotype (genotype 3) of the human parechovirus (HPeV), which belongs to the family Picornaviridae. HPeVs are small, non-enveloped, single-stranded RNA viruses that can cause various clinical manifestations, ranging from mild respiratory or gastrointestinal symptoms to severe neurological diseases in infants and young children.

Historically, Theilovirus was first identified as a separate virus in 1958 by H. Theil and K. Maassab, isolated from the feces of healthy children. It was initially classified as a member of the Enterovirus genus but was later reclassified as a distinct genus, Theilovirus, in 1999. However, subsequent genetic analysis revealed that Theilovirus is closely related to HPeVs, and it is now considered a genotype within the HPeV species.

In summary, Theilovirus is not a separate medical term or virus but rather a historical name for what is now classified as human parechovirus genotype 3 (HPeV3).

Electrodiagnosis, also known as electromyography (EMG), is a medical diagnostic procedure that evaluates the health and function of muscles and nerves. It measures the electrical activity of skeletal muscles at rest and during contraction, as well as the conduction of electrical signals along nerves.

The test involves inserting a thin needle electrode into the muscle to record its electrical activity. The physician will ask the patient to contract and relax the muscle while the electrical activity is recorded. The resulting data can help diagnose various neuromuscular disorders, such as nerve damage or muscle diseases, by identifying abnormalities in the electrical signals.

Electrodiagnosis can be used to diagnose conditions such as carpal tunnel syndrome, peripheral neuropathy, muscular dystrophy, and amyotrophic lateral sclerosis (ALS), among others. It is a valuable tool in the diagnosis and management of neuromuscular disorders, helping physicians to develop appropriate treatment plans for their patients.

Medical Definition:

Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.

Myelin proteins are proteins that are found in the myelin sheath, which is a fatty (lipid-rich) substance that surrounds and insulates nerve fibers (axons) in the nervous system. The myelin sheath enables the rapid transmission of electrical signals (nerve impulses) along the axons, allowing for efficient communication between different parts of the nervous system.

There are several types of myelin proteins, including:

1. Proteolipid protein (PLP): This is the most abundant protein in the myelin sheath and plays a crucial role in maintaining the structure and function of the myelin sheath.
2. Myelin basic protein (MBP): This protein is also found in the myelin sheath and helps to stabilize the compact structure of the myelin sheath.
3. Myelin-associated glycoprotein (MAG): This protein is involved in the adhesion of the myelin sheath to the axon and helps to maintain the integrity of the myelin sheath.
4. 2'3'-cyclic nucleotide 3' phosphodiesterase (CNP): This protein is found in oligodendrocytes, which are the cells that produce the myelin sheath in the central nervous system. CNP plays a role in maintaining the structure and function of the oligodendrocytes.

Damage to myelin proteins can lead to demyelination, which is a characteristic feature of several neurological disorders, including multiple sclerosis (MS), Guillain-Barré syndrome, and Charcot-Marie-Tooth disease.

Kissel JT (2003). "The treatment of chronic inflammatory demyelinating polyradiculoneuropathy". Seminars in Neurology. 23 (2): ... The disorder is sometimes called chronic relapsing polyneuropathy (CRP) or chronic inflammatory demyelinating ... "Prednisone improves chronic inflammatory demyelinating polyradiculoneuropathy more than no treatment". Annals of Neurology. 11 ... "Fatigue as the main presenting symptom of chronic inflammatory demyelinating polyradiculoneuropathy: a study of 11 cases". ...
"Treatments for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): an overview of systematic reviews". The ... Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) is an inflammatory neuropathy, which while pathophysiologically ... Immune dysfunction over the course of infection may also result in chronic inflammatory demyelinating polyneuropathy or ... Lewis RA (October 2017). "Chronic inflammatory demyelinating polyneuropathy". Current Opinion in Neurology. 30 (5): 508-512. ...
"Orphanet: Acute inflammatory demyelinating polyradiculoneuropathy". www.orpha.net. Retrieved 2016-08-26. "Chronic Inflammatory ... Chronic inflammatory demyelinating polyneuropathy, for instance, is an autoimmune disease: T cells involvement has been ... Lopate, Glenn; Pestronk, Alan; Al-Lozi, Muhammad (1 February 2005). "Treatment of Chronic Inflammatory Demyelinating ... Dimachkie, Mazen M.; Barohn, Richard J. (7 April 2013). "Chronic Inflammatory Demyelinating Polyneuropathy". Current Treatment ...
... such as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Friedreich's ataxia Ménière's disease Romberg's test ...
Also anti-GM1 IgG has been identified in Guillain-Barré syndrome or chronic inflammatory demyelinating polyradiculoneuropathy. ... Multifocal motor neuropathy (MMN) with conduction block is closely related to CIDP (chronic inflammatory demyelinating ... 1989). "Total, anti-viral, and anti-myelin IgG subclass reactivity in inflammatory diseases of the central nervous system". J. ... 1999). "Anti-GD1a antibody is associated with axonal but not demyelinating forms of Guillain-Barré syndrome". Ann. Neurol. 45 ( ...
In 2006, Bruce was hospitalized due to the effects of chronic inflammatory demyelinating polyradiculoneuropathy, which he had ...
Polyneuropathies And Chronic Inflammatory Demyelinating Polyradiculoneuropathy In Multiple Sclerosis, Neurology April 6, 2015 ... Ayrignac, X., Rigau, V., Lhermitte, B. et al., Pathologic and MRI analysis in acute atypical inflammatory demyelinating lesions ... These glial scars are the remnants of previous demyelinating inflammatory lesions (encephalomyelitis disseminata) which are ... "inflammatory demyelinating lesions consistent with MS": hematoxylin and eosin stain (demonstrates tissue and cell morphology) ...
Other differential diagnoses to consider are Chronic Inflammatory Demyelinating Polyradiculoneuropathy, neoplastic lumbosacral ... In general terms, such nerve damage may present in stages, earlier as demyelination and later as complications of chronic ...
... polyradiculoneuropathy, chronic inflammatory demyelinating MeSH C20.111.258.850 - stiff-person syndrome MeSH C20.111.258.925 - ... demyelinating autoimmune diseases, cns MeSH C20.111.258.250.175 - diffuse cerebral sclerosis of schilder MeSH C20.111.258.250. ... chronic MeSH C20.673.774.600 - Job's syndrome MeSH C20.683.460.640 - monoclonal gammopathies, benign MeSH C20.683.515.250 - ... chronic progressive MeSH C20.111.258.250.500.600 - multiple sclerosis, relapsing-remitting MeSH C20.111.258.250.500.650 - ...
... polyradiculoneuropathy, chronic inflammatory demyelinating MeSH C10.114.875.175 - aids arteritis, central nervous system MeSH ... polyradiculoneuropathy, chronic inflammatory demyelinating MeSH C10.314.750.450 - guillain-barre syndrome MeSH C10.314.750.450. ... polyradiculoneuropathy, chronic inflammatory demyelinating MeSH C10.668.829.800.750.700 - polyradiculopathy MeSH C10.668. ... chronic MeSH C10.228.140.140.127 - brain injury, chronic MeSH C10.228.140.140.254 - cerebral palsy MeSH C10.228.140.140.627 - ...
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They looked at chronic inflammatory demyelinating polyneuropathy which is characterized by progressive weakness and sensory ... Tracy, Jennifer A.; Dyck, P. James B. (1 June 2011). "Auto-immune polyradiculoneuropathy and a novel IgG biomarker in workers ... Progressive inflammatory neuropathy is a disease that was identified in a report, released on January 31, 2008, by the Centers ... It is expected that there will be no new cases of progressive inflammatory neuropathy since the process of aerosolizing the pig ...
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Nerve ultrasound has been proven to be an accurate tool in diagnosing chronic inflammatory demyelinating polyradiculoneuropathy ... Nerve ultrasound has been proven to be an accurate tool in diagnosing chronic inflammatory demyelinating polyradiculoneuropathy ... Nerve ultrasound may help predicting response to immune treatment in chronic inflammatory demyelinating polyradiculoneuropathy ... Chronic inflammatory demyelinating polyradiculoneuropathy: from pathology to phenotype. J Neurol Neurosurg Psychiatry 86:973- ...
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Chronic inflammatory demyelinating polyradiculoneuropathy is presumed to occur because of immunologic antibody-mediated ... reaction along with interstitial and perivascular infiltration of the endoneurium with inflammatory T cells and macrophages. ... Chronic Inflammatory Demyelinating Polyradiculoneuropathy) and Chronic Inflammatory Demyelinating Polyradiculoneuropathy What ... Chronic inflammatory demyelinating polyradiculoneuropathy most commonly has an insidious onset and either chronic progressive ...
Chronic inflammatory demyelinating polyradiculoneuropathy is presumed to occur because of immunologic antibody-mediated ... reaction along with interstitial and perivascular infiltration of the endoneurium with inflammatory T cells and macrophages. ... Chronic Inflammatory Demyelinating Polyradiculoneuropathy) and Chronic Inflammatory Demyelinating Polyradiculoneuropathy What ... Chronic Inflammatory Demyelinating Polyradiculoneuropathy Clinical Presentation. Updated: Apr 03, 2014 * Author: Richard A ...
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Chronic inflammatory demyelinating polyradiculoneuropathy-Diagnostic pitfalls and treatment approach FREE MEMBER CME! Chronic ... Journal Review: Chronic inflammatory demyelinating polyradiculoneuropathy-Diagnostic pitfalls and treatment approach Course ... inflammatory demyelinating polyradiculoneuropathy (CIDP) is characterized by progressive weakness and sensory loss, often ... and the demonstra-tion of demyelinating changes on electrodiagnostic (EDx) testing and nerve pathology. As a result, patients ...
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Frequency of diabetes and other comorbidities in chronic inflammatory demyelinating polyradiculoneuropathy and their impact on ... Objectives: To determine the prevalence of different comorbidities in chronic inflammatory demyelinating polyradiculoneuropathy ... Objectives: To determine the prevalence of different comorbidities in chronic inflammatory demyelinating polyradiculoneuropathy ...
Ten patients with Charcot-Marie-Tooth disease type 1A (CMT1A) and nine patients with chronic inflammatory demyelinating ...
Chronic Inflammatory Demyelinating Polyradiculoneuropathy: Applying the New Guidelines 0.25 CME Credits Clinical Case ... Chronic osteomyelitis. In chronic osteomyelitis, the patients temperature is usually less than 102°F. Discharge is commonly ... Chronic diabetic ulceration with underlying osteomyelitis. Plain film radiograph exhibiting cortical disruption at the medial ... Chronic diabetic ulceration with underlying osteomyelitis. Plain film radiograph exhibiting cortical disruption at the medial ...
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Chronic Inflammatory Demyelinating Polyradiculoneuropathy, CIDP por MohamadAlhes. Chronic Inflammatory Demyelinating ... Medical shockwaves for chronic low back pain - a case series por Medical shockwaves for chronic low back pain - a case series ...
Medical condition: Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) Disease: Version. SOC Term. Classification ... and Tolerability of Rozanolixizumab in Subjects with Chronic .... ...
A case of chronic inflammatory demyelinating polyradiculoneuropathy presenting recurrent attacks associated with pregnancies ... At 37 years of age, the patient initially presented with symptoms of chronic inflammatory demyelinating polyradiculoneuropathy ... A case of chronic progressive neuro-Behcets disease with cerebellar ataxia and bulbar palsy preceding mucocutaneo-ocular ... Blood examinations showed various elevated inflammatory values and positive for HLA-B51. Cerebrospinal fluid (CSF) revealed ...
Investigators identified 3 records comparing IVIG and TPE efficacy in chronic inflammatory demyelinating polyradiculoneuropathy ...
Treatments for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): an overview of systematic reviews. Cochrane ... History, diagnosis, and management of chronic inflammatory demyelinating polyradiculoneuropathy. Mayo Clin Proc. 2018;93:777- ... Long-term immunoglobulin therapy for chronic inflammatory demyelinating polyradiculoneuropathy. Muscle Nerve. 2015;51:657-661. ... Randomized controlled trial of IVIg in untreated chronic inflammatory demyelinating polyradiculoneuropathy. Neurology. 2001;56: ...
Clinical Relevance of Distinguishing Autoimmune Nodopathies From Chronic Inflammatory Demyelinating Polyradiculoneuropathy * ... Clinical Relevance of Distinguishing Autoimmune Nodopathies From Chronic Inflammatory Demyelinating Polyradiculoneuropathy J. ...
... intravenous steroids according to our protocol to patients with chronic inflammatory demyelinating polyradiculoneuropathies( ...
  • Clinical trials with similar autoimmune inflammatory diseases such as Guillain-Barré syndrome, multiple sclerosis and Crohn's disease may also provide some guidance in treatment options for those suffering from CIDP. (medscape.com)
  • [ 38 , 39 ] Currently a clinical trial is underway to observe whether alpha lipoic acid, an antioxidant with anti-inflammatory properties may prove effective to treat CIDP symptoms (ClinicalTrials.gov Identifier: NCT00962429). (medscape.com)
  • Oaklander AL, Lunn MP, Hughes RA, van Schaik IN, Frost C, Chalk CH. Treatments for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): an overview of systematic reviews. (medscape.com)
  • As reliable biomarkers of disease activity are lacking, monitoring of therapeutic response in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) remains a challenge. (springer.com)
  • In CIDP patients (fulfilling EFNS/PNS criteria), we performed high-resolution nerve ultrasound to determine ultrasound pattern sum scores (UPSS) and predominant echotexture nerve conduction study scores (NCSS) as well as Medical Research Council sum scores (MRCSS) and inflammatory neuropathy cause and treatment disability scores (INCAT) at baseline and after 12 months of standard treatment. (springer.com)
  • Chronic inflammatory demyelinating polyradiculoneuropathies (CIDP) is a type of acquired immune-mediated disorder that affects the peripheral nervous system. (nih.gov)
  • The time course of 8 weeks and the duration to reach nadir help distinguish CIDP from Guillain-Barre syndrome (GBS) or other acute inflammatory demyelinating polyneuropathies (AIDP). (nih.gov)
  • The term chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) has been used to identify patients with a chronically progressive or relapsing symmetric sensorimotor disorder with cytoalbuminologic dissociation and interstitial and perivascular endoneurial infiltration by lymphocytes and macrophages. (medscape.com)
  • Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an autoimmune disorder of the peripheral nerves with clinical and immunological heterogeneity. (nih.gov)
  • Diagnoses of Morvan syndrome and chronic inflammatory demyelinating polyradiculopathy (CIDP) were made. (bmj.com)
  • Chronic inflammatory demyelinating polyneuropathy (CIDP) is a disorder that involves nerve swelling and irritation (inflammation) that leads to a loss of strength or sensation. (medlineplus.gov)
  • Health care providers also consider CIDP as the chronic form of Guillain-Barré syndrome. (medlineplus.gov)
  • Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired autoimmune disease of the peripheral nervous system characterized by progressive weakness and impaired sensory function in the legs and arms. (wikipedia.org)
  • CIDP is closely related to Guillain-Barré syndrome and it is considered the chronic counterpart of that acute disease. (wikipedia.org)
  • Specially important are: An asymmetrical variant of CIDP is known as Lewis-Sumner Syndrome or MADSAM (multifocal acquired demyelinating sensory and motor neuropathy). (wikipedia.org)
  • Autoantibodies to components of the Ranvier nodes, specially autoantibodies the Contactin-associated protein 1 (CASPR), cause a form of CIDP with an acute "Guillain-Barre-like" phase, followed by a chronic phase with progressive symptoms. (wikipedia.org)
  • Abstract Background and purpose: The aim was to identify the clinical and diagnostic investigations that may help to support a diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) in patients not fulfilling the European Federation of Neurological Societies and Peripheral Nerve Society (EFNS/PNS) electrodiagnostic criteria. (openaire.eu)
  • Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is the most common chronic immune-mediated inflammatory polyneuropathy. (medscape.com)
  • Intravenous immunoglobulins (IVIg) represent an established cornerstone for the immunotherapy of chronic inflammatory demyelinating polyneuropathy (CIDP). (uni-regensburg.de)
  • Octagam® 10% also is indicated for primary immunodeficiency, secondary immunodeficiencies and Guillain Barré syndrome in the EU and Canada, and adult dermatomyositis in the EU and U.S., and for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), multifocal motor neuropathy (MMN), and Kawasaki disease in the EU. (octapharma.com)
  • Intravenous immunoglobulin (IVIg) is an effective treatment in chronic inflammatory demyelinating polyneuropathy (CIDP). (biomedcentral.com)
  • Chronic inflammatory demyelinating polyneuropathy (CIDP) belongs to the most common immune-mediated chronic disorders of the peripheral nervous system. (biomedcentral.com)
  • Objective: To investigate the frequency and clinical correlates of anti-nerve autoantibodies in an unselected series of Italian patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) METHODS: Sera from 276 CIDP patients fulfilling the EFNS/PNS criteria and included in the Italian CIDP database were examined for the presence of anti-nerve autoantibodies. (hunimed.eu)
  • Background Approximately two-thirds of patients with chronic inflammatory demyelinating polyneuropathy (CIDP) need long-term intravenous immunoglobulin. (houstonmethodist.org)
  • 3. Treatments for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP): an overview of systematic reviews . (neuropathycommons.org)
  • Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) is a neurological disorder characterized by progressive weakness and impaired sensory function in the arms and legs. (polyneuroexchange.com)
  • He has a particular interest in acquired inflammatory neuropathies, and recently successfully speared an effort to have the University of Minnesota named as a certified Center of Excellence by the GBS/CIDP International Foundation. (polyneuroexchange.com)
  • Moreover, antibodies to NF155 have been reported consistently, although with low frequency, in patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP),5,-7 thus questioning their specificity and pathogenicity in CCDP. (unipv.it)
  • Have you, or a family member been diagnosed with Guillain-Barre Syndrome, (GBS) or perhaps Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)? (gbs-cidp-nsw.org.au)
  • Epidemiologic variability of chronic inflammatory demyelinating polyneuropathy with different diagnostic criteria: study of a UK population. (medscape.com)
  • Chronic inflammatory demyelinating polyneuropathy disease activity status: recommendations for clinical research standards and use in clinical practice. (medscape.com)
  • Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy. (medscape.com)
  • Clinicopathologic findings and prognosis of chronic inflammatory demyelinating polyneuropathy. (medscape.com)
  • Comparison of electrodiagnostic criteria for primary demyelination in chronic polyneuropathy. (medscape.com)
  • The disorder is sometimes called chronic relapsing polyneuropathy (CRP) or chronic inflammatory demyelinating polyradiculoneuropathy (because it involves the nerve roots). (wikipedia.org)
  • citation needed] Dendrite Soma Axon Nucleus Node of Ranvier Axon terminal Schwann cell Myelin sheath Chronic inflammatory demyelinating polyneuropathy (or polyradiculoneuropathy) is considered an autoimmune disorder destroying myelin, the protective covering of the nerves. (wikipedia.org)
  • 17. Chronic inflammatory demyelinating polyneuropathy mimicking diabetic neuropathy in a young female with type 2 diabetes mellitus. (nih.gov)
  • Longer-term effects of intravenous immunoglobulin treatment in chronic inflammatory demyelinating polyneuropathy: Who benefits? (uni-regensburg.de)
  • A rare chronic immune-mediated demyelinating polyneuropathy. (cdc.gov)
  • Rogue immune cells sometimes attack peripheral nerves, leading to autoimmune nerve conditions such as Guillain-Barré syndrome , chronic inflammatory demyelinating polyneuropathy , and multifocal motor neuropathy . (neuropathycommons.org)
  • It can be considered the chronic equivalent of acute inflammatory demyelinating polyradiculoneuropathy, the most common form of Guillain-Barré syndrome. (medscape.com)
  • A controlled study of intravenous immunoglobulin in demyelinating neuropathy with IgM gammopathy. (medscape.com)
  • inflammatory neuropathy cause and treatment disability scores INCAT r 2 = 0.053, p = 0.048). (springer.com)
  • Diagnosis and guidance of anti-inflammatory therapy are challenging aspects of immune-mediated neuropathy, mainly because reliable biomarkers for disease activity and treatment response are lacking [ 1 ]. (springer.com)
  • This activity reviews the evaluation, diagnosis, and treatment of neuropathy, demyelinating polyradiculoneuropathy, chronic, and inflammatory, and highlights the role of the interprofessional team in evaluating and treating patients with this condition. (nih.gov)
  • Its symptoms are also similar to progressive inflammatory neuropathy. (wikipedia.org)
  • The de novo patients all had a post-polio syndrome, whereas the remaining patients received maintenance therapy for the neuromuscular disorders chronic inflammatory demyelinating polyradiculoneuropathy and multifocal motor neuropathy. (nih.gov)
  • 7. Demyelinating neuropathy in diabetes mellitus. (nih.gov)
  • Neurophysiology revealed homogenous slowing of motor nerve conduction velocities (24 m/s in right median nerve), with absence of temporal dispersion, conduction block, and of accentuated proximal and distal slowing, consistent with an inherited demyelinating neuropathy. (bmj.com)
  • Autoimmune disorders like Sjögren's Syndrome, lupus, rheumatoid arthritis, fibromyalgia, Guillain-Barré Syndrome and chronic inflammatory demyelinating polyradiculoneuropathy cause inflammation that can damage nerves and lead to neuropathy. (hartfordhealthcare.org)
  • The clinical picture comprises a chronic neuropathy with marked sensory ataxia and areflexia, and with relatively preserved motor function in the limbs. (cdc.gov)
  • In 2014 he moved to the University of Minnesota, but still holds an adjunct appointment at Northwestern and continues to see patients with inflammatory neuropathy in Chicago on a limited basis. (polyneuroexchange.com)
  • Dr. AllenÔÇÖs research efforts have focused on improving the diagnosis and treatment of patients with inflammatory neuropathy. (polyneuroexchange.com)
  • Functional health status of patients with chronic inflammatory neuropathies. (medscape.com)
  • Inflammatory neuropathies. (nih.gov)
  • These variants comprise a subgroup of inflammatory neuropathies with IgG4 autoantibodies against the paranodal proteins neurofascin-155, contactin-1 and caspr-1. (wikipedia.org)
  • 18. Inflammatory neuropathies. (nih.gov)
  • In several case reports, treatment with tumor necrosis factor-alpha inhibitors has been associated with the subsequent development of chronic demyelinating neuropathies. (checkorphan.org)
  • Steroids for chronic inflammatory demyelinating polyradiculoneuropathy: evidence base and clinical practice. (medscape.com)
  • 3. [The clinical analysis of diabetic patients with chronic inflammatory demyelinating polyradiculoneuropathy]. (nih.gov)
  • Clinical potential of harnessing dead cell clearance It is well established that aberrant clearance of dying cells can trigger inflammatory disease. (p38-mapk-inhibitors.com)
  • A clinical syndrome characterized by development, usually in infancy or childhood, of a chronic, often widespread candidiasis of skin, nails, and mucous membranes. (nih.gov)
  • Intravenous immune globulin (10% caprylate-chromatography purified) for the treatment of chronic inflammatory demyelinating polyradiculoneuropathy (ICE study): a randomised placebo-controlled trial. (medscape.com)
  • Octagam® 10% [Immune Globulin Intravenous (Human)] is an immune globulin intravenous (human) liquid preparation indicated for chronic idiopathic thrombocytopenic purpura in the U.S., European Union and Canada. (octapharma.com)
  • Dataset related to article "Chronic inflammatory demyelinating polyradiculoneuropathy: can a diagnosis be made in patients not fulfilling electrodiagnostic criteria? (openaire.eu)
  • This diagnosis fulfilled the EFNS/PNS criteria in 468 patients (87.2%) (definite in 430, probable in 33, possible in three, while two had chronic immune sensory polyradiculopathy). (openaire.eu)
  • Describe the pathophysiology, of chronic inflammatory demyelinating polyradiculoneuropathy. (nih.gov)
  • However, it has variants associated with a neoplastic process (e.g., osteosclerotic myeloma, Waldenstrom macroglobulinemia, lymphoma, monoclonal gammopathy of undetermined significance), HIV infections, and chronic history of diabetes mellitus type II. (nih.gov)
  • 11. Chronic inflammatory demyelinating polyradiculoneuropathy in diabetes mellitus. (nih.gov)
  • A plasma exchange versus immune globulin infusion trial in chronic inflammatory demyelinating polyradiculoneuropathy. (medscape.com)
  • IgG3 Caspr autoantibodies were found during the acute GBS-like phase, while IgG4 Caspr autoantibodies were present during the chronic phase of disease. (wikipedia.org)
  • A slowly progressive autoimmune demyelinating disease of peripheral nerves and nerve roots. (nih.gov)
  • European Federation of Neurological Societies/Peripheral Nerve Society Guideline on management of chronic inflammatory demyelinating polyradiculoneuropathy. (medscape.com)
  • Chronic inflammatory demyelinating polyradiculoneuropathy can be caused by multiple diseases, from infectious as well as immunology diseases. (nih.gov)
  • Dr. Berger's research has focused on control of inflammatory responses and on antigen-antibody and complement interactions, particularly in primary immune deficiency diseases and cystic fibrosis. (polyneuroexchange.com)
  • Patients commonly suffer from severe rashes, chronic muscle inflammation and progressive muscle weakness, usually affecting adults in their late 40s to early 60s and children between the ages of 5 and 15. (octapharma.com)
  • Chronic inflammatory demyelinating polyradiculoneuropathy: new views and guidelines. (medscape.com)
  • Chronic inflammatory demyelinating polyradiculoneuropathy is presumed to occur because of immunologic antibody-mediated reaction along with interstitial and perivascular infiltration of the endoneurium with inflammatory T cells and macrophages. (medscape.com)
  • Summarize the management options available for chronic inflammatory demyelinating polyradiculoneuropathy. (nih.gov)
  • Impact of respiratory virus infections on persons with chronic underlying conditions. (cdc.gov)
  • No article was found for Polyradiculoneuropathy, Chronic Inflammatory Demyelinating and SH2D2A[original query] . (cdc.gov)
  • Symptom development beyond a month suggests an subacute inflammatory demyelinating polyradiculoneuropathy and if development continues beyond eight weeks chronic inflammatory demyelinating polyradiculoneuropathy can be a consideration. (arqueologiamendoza.com)