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.
Aquaporin 4 is the major water-selective channel in the CENTRAL NERVOUS SYSTEM of mammals.
Inflammation of a transverse portion of the spinal cord characterized by acute or subacute segmental demyelination or necrosis. The condition may occur sporadically, follow an infection or vaccination, or present as a paraneoplastic syndrome (see also ENCEPHALOMYELITIS, ACUTE DISSEMINATED). Clinical manifestations include motor weakness, sensory loss, and incontinence. (Adams et al., Principles of Neurology, 6th ed, pp1242-6)
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
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)
Inflammation of the optic nerve. Commonly associated conditions include autoimmune disorders such as MULTIPLE SCLEROSIS, infections, and granulomatous diseases. Clinical features include retro-orbital pain that is aggravated by eye movement, loss of color vision, and contrast sensitivity that may progress to severe visual loss, an afferent pupillary defect (Marcus-Gunn pupil), and in some instances optic disc hyperemia and swelling. Inflammation may occur in the portion of the nerve within the globe (neuropapillitis or anterior optic neuritis) or the portion behind the globe (retrobulbar neuritis or posterior optic neuritis).
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
The 2nd cranial nerve which conveys visual information from the RETINA to the brain. The nerve carries the axons of the RETINAL GANGLION CELLS which sort at the OPTIC CHIASM and continue via the OPTIC TRACTS to the brain. The largest projection is to the lateral geniculate nuclei; other targets include the SUPERIOR COLLICULI and the SUPRACHIASMATIC NUCLEI. Though known as the second cranial nerve, it is considered part of the CENTRAL NERVOUS SYSTEM.
A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.
Multiple protein bands serving as markers of specific ANTIBODIES and detected by ELECTROPHORESIS of CEREBROSPINAL FLUID or serum. The bands are most often seen during inflammatory or immune processes and are found in most patients with MULTIPLE SCLEROSIS.
A small, rounded eminence on each side of the FOURTH VENTRICLE, which receives nerve fibers from the SOLITARY NUCLEUS; SPINAL CORD; and adjacent areas of the MEDULLA OBLONGATA. The area postrema lies outside the BLOOD-BRAIN BARRIER and its functions include acting as an emetic chemoreceptor.
A PREDNISOLONE derivative with similar anti-inflammatory action.
Degenerative or inflammatory conditions affecting the central or peripheral nervous system that develop in association with a systemic neoplasm without direct invasion by tumor. They may be associated with circulating antibodies that react with the affected neural tissue. (Intern Med 1996 Dec;35(12):925-9)
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.
Ocular manifestations secondary to various NEOPLASMS in which antibodies to antigens of the primary tumor cross-react with ocular antigens. This autoimmune response often leads to visual loss and other ocular dysfunctions.
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
A 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.
The return of a sign, symptom, or disease after a remission.
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
A motor neuron disease marked by progressive weakness of the muscles innervated by cranial nerves of the lower brain stem. Clinical manifestations include dysarthria, dysphagia, facial weakness, tongue weakness, and fasciculations of the tongue and facial muscles. The adult form of the disease is marked initially by bulbar weakness which progresses to involve motor neurons throughout the neuroaxis. Eventually this condition may become indistinguishable from AMYOTROPHIC LATERAL SCLEROSIS. Fazio-Londe syndrome is an inherited form of this illness which occurs in children and young adults. (Adams et al., Principles of Neurology, 6th ed, p1091; Brain 1992 Dec;115(Pt 6):1889-1900)
The practice of sending a patient to another program or practitioner for services or advice which the referring source is not prepared to provide.
The inhabitants of peripheral or adjacent areas of a city or town.

Hyperprolactinemia in optico-spinal multiple sclerosis. (1/195)

OBJECTIVE: To clarify the clinical features of MS patients with hyperprolactinemia. SUBJECTS AND METHODS: The serum prolactin level was measured in 67 Japanese patients (19 men and 48 women) with multiple sclerosis (MS) and in 16 patients (4 men and 12 women) with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) using a two-site immunoradiometric assay. RESULTS: In the MS patients, 32 were classified as having Asian type MS showing a selective involvement of the optic nerves and spinal cord, while the other 35 were classified as having Western type MS which displayed disseminated central nervous system involvement. In women, the serum prolactin level was found to be significantly higher only in Asian type MS (mean=23.1 ng/ml, n=25) than in HAM/TSP (mean=6.9 ng/ml, n=12) (p=0.0297), while it did not differ significantly in men among the three groups. Hyperprolactinemia was significantly associated with acute relapse involving the optic nerves. All MS patients with hyperprolactinemia (7 women with Asian type MS and 2 women with Western type MS) showed recurrent opticomyelitis either throughout or in the early course of the disease, and also had a higher age of onset, a higher Expanded Disability Status Scale score, a greater visual impairment, and higher cell counts and protein contents in the cerebrospinal fluid than did the normoprolactinemic patients. CONCLUSION: Hyperprolactinemia may be one of the characteristic features of Asian patients with MS who preferentially show the optic nerve involvement.  (+info)

Matrix metalloproteinases and tissue inhibitors of metalloproteinases in cerebrospinal fluid differ in multiple sclerosis and Devic's neuromyelitis optica. (2/195)

Matrix metalloproteinases (MMPs) are increased in the CSF of patients with multiple sclerosis. Devic's neuromyelitis optica (DNO) is a demyelinating syndrome that involves the optic nerve and cervical cord but differs pathologically from multiple sclerosis. Therefore, we hypothesized that the type of inflammatory reaction that causes MMPs to be elevated in multiple sclerosis would be absent in patients with DNO. CSF was collected from 23 patients with relapsing-remitting or secondary progressive multiple sclerosis, all of whom were experiencing acute symptoms, from seven patients with DNO, and from seven normal volunteers. Diagnoses were made according to current criteria on the basis of clinical manifestations, imaging results and CSF studies. IgG synthesis was increased in the CSF of multiple sclerosis patients but not in that of DNO patients. Zymography, reverse zymography and ELISA (enzyme-linked immunosorbent assay) were used to measure gelatinase A (MMP-2), gelatinase B (MMP-9) and tissue inhibitors of metalloproteinases (TIMPs). Zymograms showed that multiple sclerosis patients had elevated MMP-9 compared with DNO patients and controls (P: < 0.05). TIMP-1 and TIMP-2 levels were similar in all three groups. We conclude that multiple sclerosis patients have higher MMP-9 levels in the CSF than patients with DNO, which supports the different pathological mechanisms of these diseases.  (+info)

A role for humoral mechanisms in the pathogenesis of Devic's neuromyelitis optica. (3/195)

Devic's disease [neuromyelitis optica (NMO)] is an idiopathic inflammatory demyelinating disease of the CNS, characterized by attacks of optic neuritis and myelitis. The mechanisms that result in selective localization of inflammatory demyelinating lesions to the optic nerves and spinal cord are unknown. Serological and clinical evidence of B cell autoimmunity has been observed in a high proportion of patients with NMO. The purpose of this study was to investigate the importance of humoral mechanisms, including complement activation, in producing the necrotizing demyelination seen in the spinal cord and optic nerves. Eighty-two lesions were examined from nine autopsy cases of clinically confirmed Devic's disease. Demyelinating activity in the lesions was immunocytochemically classified as early active (21 lesions), late active (18 lesions), inactive (35 lesions) or remyelinating (eight lesions) by examining the antigenic profile of myelin degradation products within macrophages. The pathology of the lesions was analysed using a broad spectrum of immunological and neurobiological markers, and lesions were defined on the basis of myelin protein loss, the geography and extension of plaques, the patterns of oligodendrocyte destruction and the immunopathological evidence of complement activation. The pathology was identical in all nine patients. Extensive demyelination was present across multiple spinal cord levels, associated with cavitation, necrosis and acute axonal pathology (spheroids), in both grey and white matter. There was a pronounced loss of oligodendrocytes within the lesions. The inflammatory infiltrates in active lesions were characterized by extensive macrophage infiltration associated with large numbers of perivascular granulocytes and eosinophils and rare CD3(+) and CD8(+) T cells. There was a pronounced perivascular deposition of immunoglobulins (mainly IgM) and complement C9neo antigen in active lesions associated with prominent vascular fibrosis and hyalinization in both active and inactive lesions. The extent of complement activation, eosinophilic infiltration and vascular fibrosis observed in the Devic NMO cases is more prominent compared with that in prototypic multiple sclerosis, and supports a role for humoral immunity in the pathogenesis of NMO. Based on this study, future therapeutic strategies designed to limit the deleterious effects of complement activation, eosinophil degranulation and neutrophil/macrophage/microglial activation are worthy of further investigation.  (+info)

Optic neuromyelitis syndrome in Brazilian patients. (4/195)

OBJECTIVES: To report the clinical features and outcome of 24 Brazilian patients with optic neuromyelitis syndrome (ONM); discuss the underlying pathological events associated with the ONM syndrome; review the nosological situation of ONM in the group of inflammatory and demyelinating diseases of the central nervous system. PATIENTS AND METHODS: Patients with ONM treated at the Hospital da Lagoa, Rio de Janeiro were studied. Demographic, clinical, magnetic resonance imaging, cerebrospinal fluid, and pathological data were analysed. RESULTS: The study consisted of 20 women, four men of whom 10 were white and 14 Afro-Brazilians. Clinical course was recurrent in 22 cases and monophasic in two. Neurological manifestations at inclusion were: sensory impairment (66%), bilateral (41.6%) or unilateral blindness (20.8%), paraplegia or quadriplegia (37.5%). The EDSS was moderate/severe in 70.8%. The underlying pathological events were respectively pulmonary tuberculosis and upper respiratory infection in the two monophasic cases; in the 22 recurrent ONM patients: pulmonary tuberculosis (3), neurocysticercosis (1), polyarteritis nodosa (1), antinuclear antibody and rheumatoid factor (1), antiphospholipid antibody primary syndrome (1), diabetes mellitus (1), hypothyroidism (1), and amenorrhea-galactorrhea (4). Normal cerebrospinal fluid was found in 52% and an inflammatory profile in 48%. Only four recurrent ONM white patients had brain and spinal cord magnetic resonance imaging and cerebrospinal fluid findings compatible with the diagnosis of multiple sclerosis. Large lesions were seen in 62% of spinal magnetic resonance images. Six of 12 recurrent ONM Afro-Brazilian died. There were no statistical differences in the demographic data of the two ethnic groups. Afro-Brazilians were significantly more severely impaired and had a higher mortality rate than the white patients. CONCLUSION: These cases were classified as follows: two monophasic acute disseminated encephalomyelitis; one recurrent disseminated encephalomyelitis; three recurrent ONM associated with Hughes syndrome, autoantibodies and polyarteritis nodosa; six recurrent ONM with endocrinopathies; and finally, four multiple sclerosis cases. The remaining cases were not associated with any other condition. It would seem clear that ONM is a syndrome rather than a single disease.  (+info)

Devic's neuromyelitis optica and Schilder's myelinoclastic diffuse sclerosis. (5/195)

An adult patient developed both Devic's neuromyelitis optica and Schilder's myelinoclastic diffuse sclerosis, suggesting that these entities represent rare topographical and aggressive variants within the spectrum of multiple sclerosis.  (+info)

Recurrent neuromyelitis optica with diffuse central nervous system involvement: case report. (6/195)

Several demyelinating disorders can affect children. The differential diagnosis between these diseases is usually an arduous task. Diagnostic criteria have been proposed for some of these disorders, however most of them have not yet been clinically and prospectively validated. Here we present a case of a ten year-old boy with recurrent bilateral optic neuritis and spinal cord involvement. Clinical and cerebrospinal fluid data have fulfilled diagnostic criteria for Devic's neuromyelitis optica (NMO). The differential diagnosis with multiple sclerosis (MS) has become troublesome since not only optic nerves and spinal cord were involved. In one of the relapses a left hemiparesis with facial involvement was registered. Magnetic resonance imaging was also compatible with MS. This case illustrates that CNS demyelinating disorders can fulfill diagnostic criteria for more than one demyelinating disease, making the clinical judgment an important tool in the management of these patients.  (+info)

Clinicopathological study of a myelin oligodendrocyte glycoprotein-induced demyelinating disease in LEW.1AV1 rats. (7/195)

Although multiple sclerosis is considered to be an autoimmune disease in the CNS, the immune responses that take place in the CNS and lymphoid organs remain to be elucidated. Here, we have successfully induced various subtypes of experimental autoimmune encephalitis (EAE) in LEW.1AV1 rats carrying RT1(av1) on the Lewis background genes by immunization with recombinant rat myelin oligodendrocyte glycoprotein (MOG) in various solutions with adjuvants. The purpose of the present study was to analyse in more detail the clinical and immunopathological features of MOG-induced EAE in LEW.1AV1 rats. Immunization with high doses of soluble MOG with pertussis toxin induced acute, frequently fatal EAE, whereas medium doses of partially aggregated MOG without pertussis toxin produced relapsing and remitting EAE. Secondary progressive EAE was induced in some rats by immunization with the immunization protocol having an intermediate nature between the above two. The optic nerve (approximately 60% of the immunized rats) and spinal cord (100%) were frequently involved and detectable both clinically and pathologically, while there was no lesion in the cerebrum. Histological examination revealed that, despite variety in the clinical subtypes, progression of the pathological processes was strikingly uniform, i.e. initial inflammation with minimal demyelination followed by predominant demyelination with minimal lymphocyte infiltration. These findings suggest that the lesion during the later stage is maintained by humoral factors. Taken together, this experimental system can serve as a model of neuromyelitis optica. Further analysis will provide useful information to elucidate the pathogenesis and to develop immunotherapy for neuromyelitis optica and multiple sclerosis.  (+info)

Intrathecal activation of the IL-17/IL-8 axis in opticospinal multiple sclerosis. (8/195)

There are two distinct subtypes of multiple sclerosis in Asians, opticospinal (OS-multiple sclerosis) and conventional (C-multiple sclerosis). In OS-multiple sclerosis, selective and severe involvement of the optic nerves and spinal cord is characteristic, though its mechanisms are unknown. The present study aimed to find out possible differences in the cytokine/chemokine profiles in CSF between OS-multiple sclerosis and C-multiple sclerosis and to delineate the relationships between these profiles and neuroimaging and pathological features. Sixteen cytokines/chemokines, namely interleukin (IL)-1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12 (p70), IL-13, IL-17, interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha, granulocyte colony-stimulating factor (G-CSF), monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1beta (MIP-1beta), were measured simultaneously in CSF supernatants from 40 patients with relapsing-remitting multiple sclerosis (20 OS-multiple sclerosis and 20 C-multiple sclerosis) at relapse and 19 control patients with spinocerebellar degeneration (SCD), together with intracellular production of IFN-gamma and IL-4 in CSF CD4+ T cells. In CSF supernatants relative to controls, IL-17, MIP-1beta, IL-1beta and IL-13 were only significantly increased in OS-multiple sclerosis patients, while TNF-alpha was only significantly increased in C-multiple sclerosis patients, using a cut-off level of 1 pg/ml. IL-8 was significantly elevated in both OS-multiple sclerosis and C-multiple sclerosis patients. MCP-1 was significantly decreased in both OS-multiple sclerosis and C-multiple sclerosis patients, while IL-7 was only significantly decreased in C-multiple sclerosis patients. IL-17, IL-8 and IL-5 were significantly higher in OS-multiple sclerosis patients than in C-multiple sclerosis patients. The increases in IL-17 and IL-8 in OS-multiple sclerosis were still significant even after exclusion of the patients undergoing various immunomodulatory therapies. Assays of intracellular cytokine production revealed that both the IFN-gamma+IL-4- T-cell percentage and intracellular IFN-gamma/IL-4 ratio in CSF cells were significantly greater in C-multiple sclerosis patients than in controls. Contrarily, OS-multiple sclerosis patients showed not only a significantly greater percentage of IFN-gamma+IL-4- T cells than controls but also a significantly higher percentage of IFN-gamma-IL-4+ T cells than C-multiple sclerosis patients. Among the cytokines elevated in multiple sclerosis, only IL-8 showed a significant positive correlation with the Expanded Disability Status Scale of Kurtzke score. Both the length of the spinal cord lesions on MRI and the CSF/serum albumin ratio had a significant positive correlation with IL-8 and IL-17 in multiple sclerosis, in which the spinal cord lesions were significantly longer in OS-multiple sclerosis than in C-multiple sclerosis. Three of six spinal cord specimens from autopsied OS-multiple sclerosis cases demonstrated numerous myeloperoxidase-positive neutrophils infiltrating necrotic lesions. These findings strongly suggest that in OS-multiple sclerosis, in addition to the Th1 cell upregulation seen in C-multiple sclerosis, intrathecal activation of the IL-17/IL-8 axis inducing heavy neutrophil infiltration contributes to extensive spinal cord lesion formation.  (+info)

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.

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.

Transverse Myelitis is a neurological disorder that involves inflammation of the spinal cord, leading to damage in both sides of the cord. This results in varying degrees of motor, sensory, and autonomic dysfunction, typically defined by the level of the spine that's affected. Symptoms may include a sudden onset of lower back pain, muscle weakness, paraesthesia or loss of sensation, and bowel/bladder dysfunction. The exact cause is often unknown but can be associated with infections, autoimmune disorders, or other underlying conditions.

Autoantibodies are defined as antibodies that are produced by the immune system and target the body's own cells, tissues, or organs. These antibodies mistakenly identify certain proteins or molecules in the body as foreign invaders and attack them, leading to an autoimmune response. Autoantibodies can be found in various autoimmune diseases such as rheumatoid arthritis, lupus, and thyroiditis. The presence of autoantibodies can also be used as a diagnostic marker for certain conditions.

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.

Optic neuritis is a medical condition characterized by inflammation and damage to the optic nerve, which transmits visual information from the eye to the brain. This condition can result in various symptoms such as vision loss, pain with eye movement, color vision disturbances, and pupillary abnormalities. Optic neuritis may occur in isolation or be associated with other underlying medical conditions, including multiple sclerosis, neuromyelitis optica, and autoimmune disorders. The diagnosis typically involves a comprehensive eye examination, including visual acuity testing, dilated funduscopic examination, and possibly imaging studies like MRI to evaluate the optic nerve and brain. Treatment options may include corticosteroids or other immunomodulatory therapies to reduce inflammation and prevent further damage to the optic nerve.

Immunoglobulin G (IgG) is a type of antibody, which is a protective protein produced by the immune system in response to foreign substances like bacteria or viruses. IgG is the most abundant type of antibody in human blood, making up about 75-80% of all antibodies. It is found in all body fluids and plays a crucial role in fighting infections caused by bacteria, viruses, and toxins.

IgG has several important functions:

1. Neutralization: IgG can bind to the surface of bacteria or viruses, preventing them from attaching to and infecting human cells.
2. Opsonization: IgG coats the surface of pathogens, making them more recognizable and easier for immune cells like neutrophils and macrophages to phagocytose (engulf and destroy) them.
3. Complement activation: IgG can activate the complement system, a group of proteins that work together to help eliminate pathogens from the body. Activation of the complement system leads to the formation of the membrane attack complex, which creates holes in the cell membranes of bacteria, leading to their lysis (destruction).
4. Antibody-dependent cellular cytotoxicity (ADCC): IgG can bind to immune cells like natural killer (NK) cells and trigger them to release substances that cause target cells (such as virus-infected or cancerous cells) to undergo apoptosis (programmed cell death).
5. Immune complex formation: IgG can form immune complexes with antigens, which can then be removed from the body through various mechanisms, such as phagocytosis by immune cells or excretion in urine.

IgG is a critical component of adaptive immunity and provides long-lasting protection against reinfection with many pathogens. It has four subclasses (IgG1, IgG2, IgG3, and IgG4) that differ in their structure, function, and distribution in the body.

The optic nerve, also known as the second cranial nerve, is the nerve that transmits visual information from the retina to the brain. It is composed of approximately one million nerve fibers that carry signals related to vision, such as light intensity and color, from the eye's photoreceptor cells (rods and cones) to the visual cortex in the brain. The optic nerve is responsible for carrying this visual information so that it can be processed and interpreted by the brain, allowing us to see and perceive our surroundings. Damage to the optic nerve can result in vision loss or impairment.

The spinal cord is a major part of the nervous system, extending from the brainstem and continuing down to the lower back. It is a slender, tubular bundle of nerve fibers (axons) and support cells (glial cells) that carries signals between the brain and the rest of the body. The spinal cord primarily serves as a conduit for motor information, which travels from the brain to the muscles, and sensory information, which travels from the body to the brain. It also contains neurons that can independently process and respond to information within the spinal cord without direct input from the brain.

The spinal cord is protected by the bony vertebral column (spine) and is divided into 31 segments: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal. Each segment corresponds to a specific region of the body and gives rise to pairs of spinal nerves that exit through the intervertebral foramina at each level.

The spinal cord is responsible for several vital functions, including:

1. Reflexes: Simple reflex actions, such as the withdrawal reflex when touching a hot surface, are mediated by the spinal cord without involving the brain.
2. Muscle control: The spinal cord carries motor signals from the brain to the muscles, enabling voluntary movement and muscle tone regulation.
3. Sensory perception: The spinal cord transmits sensory information, such as touch, temperature, pain, and vibration, from the body to the brain for processing and awareness.
4. Autonomic functions: The sympathetic and parasympathetic divisions of the autonomic nervous system originate in the thoracolumbar and sacral regions of the spinal cord, respectively, controlling involuntary physiological responses like heart rate, blood pressure, digestion, and respiration.

Damage to the spinal cord can result in various degrees of paralysis or loss of sensation below the level of injury, depending on the severity and location of the damage.

Oligoclonal bands (OB) are a pattern of immunoglobulin (antibody) proteins found in the cerebrospinal fluid (CSF) when it is analyzed using a technique called electrophoresis. This pattern shows a limited number (oligo) of distinct protein bands, which are clonally expanded (clonal), indicating the presence of an intr Theatreaterathecal immunoglobulin synthesis, typically in response to some sort of central nervous system (CNS) antigenic stimulation or immune response.

The detection of oligoclonal bands is often associated with inflammatory conditions affecting the CNS, such as multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), and other infectious or autoimmune diseases. However, it's important to note that their presence alone does not confirm a specific diagnosis, but rather serves as a supportive finding in conjunction with other clinical and diagnostic data.

The area postrema is a small, chemoreceptive region located in the caudal part (the back) of the fourth ventricle in the brainstem. It is part of the vomiting center and is sensitive to various stimuli such as chemical substances, emotions, and vestibular signals that can trigger nausea and vomiting. The area postrema is not protected by the blood-brain barrier, allowing it to directly detect toxins and other harmful substances in the bloodstream. This region plays a crucial role in maintaining homeostasis by regulating fluid balance, electrolyte levels, and the elimination of potentially toxic substances from the body.

Methylprednisolone is a synthetic glucocorticoid drug, which is a class of hormones that naturally occur in the body and are produced by the adrenal gland. It is often used to treat various medical conditions such as inflammation, allergies, and autoimmune disorders. Methylprednisolone works by reducing the activity of the immune system, which helps to reduce symptoms such as swelling, pain, and redness.

Methylprednisolone is available in several forms, including tablets, oral suspension, and injectable solutions. It may be used for short-term or long-term treatment, depending on the condition being treated. Common side effects of methylprednisolone include increased appetite, weight gain, insomnia, mood changes, and increased susceptibility to infections. Long-term use of methylprednisolone can lead to more serious side effects such as osteoporosis, cataracts, and adrenal suppression.

It is important to note that methylprednisolone should be used under the close supervision of a healthcare provider, as it can cause serious side effects if not used properly. The dosage and duration of treatment will depend on various factors such as the patient's age, weight, medical history, and the condition being treated.

Paraneoplastic syndromes of the nervous system are a group of rare disorders that occur in some individuals with cancer. These syndromes are caused by an immune system response to the cancer tumor, which can lead to the damage or destruction of nerve cells. The immune system produces antibodies and/or activated immune cells that attack the neural tissue, leading to neurological symptoms.

Paraneoplastic syndromes can affect any part of the nervous system, including the brain, spinal cord, peripheral nerves, and muscles. Symptoms vary depending on the specific syndrome and the location of the affected nerve tissue. Some common neurological symptoms include muscle weakness, numbness or tingling, seizures, memory loss, confusion, difficulty speaking or swallowing, visual disturbances, and coordination problems.

Paraneoplastic syndromes are often associated with specific types of cancer, such as small cell lung cancer, breast cancer, ovarian cancer, and lymphoma. Diagnosis can be challenging because the symptoms may precede the discovery of the underlying cancer. A combination of clinical evaluation, imaging studies, laboratory tests, and sometimes a brain biopsy may be necessary to confirm the diagnosis.

Treatment typically involves addressing the underlying cancer with surgery, chemotherapy, or radiation therapy. Immunosuppressive therapies may also be used to manage the immune response that is causing the neurological symptoms. While treatment can help alleviate symptoms and improve quality of life, paraneoplastic syndromes are often difficult to cure completely.

Myelitis is a medical term that refers to inflammation of the spinal cord. This inflammation can cause damage to the myelin sheath, which is the protective covering of nerve fibers in the spinal cord. As a result, the transmission of nerve impulses along the spinal cord may be disrupted, leading to various neurological symptoms.

Myelitis can affect any part of the spinal cord and can have many different causes, including infections (such as viral or bacterial infections), autoimmune disorders (such as multiple sclerosis), and other conditions (such as spinal cord injuries or tumors). The specific symptoms of myelitis depend on the location and severity of the inflammation. They may include muscle weakness, numbness or tingling sensations, pain, bladder or bowel dysfunction, and difficulty with coordination and balance.

Myelitis can be a serious condition that requires prompt medical attention and treatment. Treatment typically focuses on addressing the underlying cause of the inflammation, as well as managing symptoms and supporting recovery.

Paraneoplastic syndromes are a group of rare disorders that occur in some individuals with cancer. These syndromes are caused by substances produced by the tumor or the body's immune response to the tumor, which can affect distant organs and cause various symptoms.

Ocular paraneoplastic syndromes refer to a subset of these disorders that specifically affect the eyes. They are caused by an abnormal immune response directed against antigens shared by both the tumor and the nervous tissue of the eye. This results in damage to the nerve cells and can lead to various visual symptoms, such as:

1. Visual loss or blurring
2. Double vision (diplopia)
3. Light sensitivity (photophobia)
4. Abnormalities in pupil size or reactivity
5. Jerky eye movements (nystagmus)
6. Loss of peripheral vision (visual field defects)
7. Impaired color vision
8. Deterioration of the optic nerve (optic neuropathy)

Some examples of ocular paraneoplastic syndromes include:

1. Paraneoplastic retinopathy: A condition characterized by damage to the light-sensitive cells in the retina, leading to visual loss and other visual disturbances.
2. Paraneoplastic optic neuropathy: Damage to the optic nerve that can result in visual loss and visual field defects.
3. Cancer-associated retinopathy (CAR): A condition characterized by progressive vision loss, night blindness, and abnormalities in the electroretinogram (ERG), a test used to assess retinal function.
4. Melanoma-associated retinopathy (MAR): Similar to CAR but specifically associated with melanoma, this condition can cause visual loss, night blindness, and abnormal ERG results.
5. Opsoclonus-myoclonus syndrome: A rare disorder characterized by rapid, involuntary eye movements (opsoclonus) and muscle jerks (myoclonus), which can be associated with various types of cancer, including breast, lung, and ovarian cancer.

It is important to note that these conditions are relatively rare but can significantly impact a patient's quality of life. Early diagnosis and treatment of the underlying cancer can help improve outcomes for patients with ocular paraneoplastic syndromes.

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.

Astrocytes are a type of star-shaped glial cell found in the central nervous system (CNS), including the brain and spinal cord. They play crucial roles in supporting and maintaining the health and function of neurons, which are the primary cells responsible for transmitting information in the CNS.

Some of the essential functions of astrocytes include:

1. Supporting neuronal structure and function: Astrocytes provide structural support to neurons by ensheathing them and maintaining the integrity of the blood-brain barrier, which helps regulate the entry and exit of substances into the CNS.
2. Regulating neurotransmitter levels: Astrocytes help control the levels of neurotransmitters in the synaptic cleft (the space between two neurons) by taking up excess neurotransmitters and breaking them down, thus preventing excessive or prolonged activation of neuronal receptors.
3. Providing nutrients to neurons: Astrocytes help supply energy metabolites, such as lactate, to neurons, which are essential for their survival and function.
4. Modulating synaptic activity: Through the release of various signaling molecules, astrocytes can modulate synaptic strength and plasticity, contributing to learning and memory processes.
5. Participating in immune responses: Astrocytes can respond to CNS injuries or infections by releasing pro-inflammatory cytokines and chemokines, which help recruit immune cells to the site of injury or infection.
6. Promoting neuronal survival and repair: In response to injury or disease, astrocytes can become reactive and undergo morphological changes that aid in forming a glial scar, which helps contain damage and promote tissue repair. Additionally, they release growth factors and other molecules that support the survival and regeneration of injured neurons.

Dysfunction or damage to astrocytes has been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

Recurrence, in a medical context, refers to the return of symptoms or signs of a disease after a period of improvement or remission. It indicates that the condition has not been fully eradicated and may require further treatment. Recurrence is often used to describe situations where a disease such as cancer comes back after initial treatment, but it can also apply to other medical conditions. The likelihood of recurrence varies depending on the type of disease and individual patient factors.

The complement system is a group of proteins found in the blood and on the surface of cells that when activated, work together to help eliminate pathogens such as bacteria, viruses, and fungi from the body. The proteins are normally inactive in the bloodstream. When they encounter an invading microorganism or foreign substance, a series of reactions take place leading to the activation of the complement system. Activation results in the production of effector molecules that can punch holes in the cell membranes of pathogens, recruit and activate immune cells, and help remove debris and dead cells from the body.

There are three main pathways that can lead to complement activation: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteins that work together in a cascade-like manner to amplify the response and generate effector molecules. The three main effector molecules produced by the complement system are C3b, C4b, and C5b. These molecules can bind to the surface of pathogens, marking them for destruction by other immune cells.

Complement proteins also play a role in the regulation of the immune response. They help to prevent excessive activation of the complement system, which could damage host tissues. Dysregulation of the complement system has been implicated in a number of diseases, including autoimmune disorders and inflammatory conditions.

In summary, Complement System Proteins are a group of proteins that play a crucial role in the immune response by helping to eliminate pathogens and regulate the immune response. They can be activated through three different pathways, leading to the production of effector molecules that mark pathogens for destruction. Dysregulation of the complement system has been linked to various diseases.

Progressive bulbar palsy (PBP) is a form of motor neuron disease (MND), also known as Amyotrophic Lateral Sclerosis (ALS). It is characterized by the progressive degeneration of the motor neurons in the brainstem, which control vital functions such as swallowing, speaking, chewing, and breathing.

In PBP, these symptoms gradually worsen over time, often resulting in severe disability and ultimately death due to respiratory failure. The progression of the disease can vary from person to person, but it typically advances more slowly than other forms of ALS. There is currently no cure for PBP or any other form of MND, and treatment is focused on managing symptoms and maintaining quality of life.

**Referral:**
A referral in the medical context is the process where a healthcare professional (such as a general practitioner or primary care physician) sends or refers a patient to another healthcare professional who has specialized knowledge and skills to address the patient's specific health condition or concern. This could be a specialist, a consultant, or a facility that provides specialized care. The referral may involve transferring the patient's care entirely to the other professional or may simply be for a consultation and advice.

**Consultation:**
A consultation in healthcare is a process where a healthcare professional seeks the opinion or advice of another professional regarding a patient's medical condition. This can be done in various ways, such as face-to-face meetings, phone calls, or written correspondence. The consulting professional provides their expert opinion to assist in the diagnosis, treatment plan, or management of the patient's condition. The ultimate decision and responsibility for the patient's care typically remain with the referring or primary healthcare provider.

I'm sorry for any confusion, but "Suburban Population" is not a medical term. It refers to the people living in suburban areas, which are typically residential districts or communities that lie outside a city center. They are often characterized by single-family homes and less population density than in urban areas. If you have any questions related to medical terminology, I would be happy to help with those!

... s (NMOSD), including neuromyelitis optica (NMO), are autoimmune diseases characterized by ... "Treatment of neuromyelitis optica and neuromyelitis optica spectrum disorders with rituximab using a maintenance treatment ... Neuromyelitis optica 2020; https://www.mayoclinic.org/diseases-conditions/neuromyelitis-optica/symptoms-causes/syc-20375652. ... "Neuromyelitis optica - Diagnosis and treatment - Mayo Clinic". www.mayoclinic.org. Retrieved 2020-08-03. Kowarik, Markus C.; ...
Jarius S, Paul F, Weinshenker BG, Levy M, Kim HJ, Wildemann B (October 2020). "Neuromyelitis optica". Nature Reviews. Disease ... March 2015). "Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype". Journal of ... Oshiro A, Nakamura S, Tamashiro K, Fujihara K (May 2016). "[Anti-MOG + neuromyelitis optica spectrum disorders treated with ... December 2011). "Complement activating antibodies to myelin oligodendrocyte glycoprotein in neuromyelitis optica and related ...
"Treatment of neuromyelitis optica and neuromyelitis optica spectrum disorders with rituximab using a maintenance treatment ... Iorio R, Rindi G, Erra C, Damato V, Ferilli M, Sabatelli M (May 2015). "Neuromyelitis optica spectrum disorder as a ... The collection of these condition has been named "anti-AQP4 disease" and "neuromyelitis optica spectrum disorders" (NMSD) and ... Morgan SM, Zantek ND, Carpenter AF (June 2014). "Therapeutic plasma exchange in neuromyelitis optica: a case series". Journal ...
Chang KH, Ro LS, Lyu RK, Chen CM (February 2015). "Biomarkers for neuromyelitis optica". Clinica Chimica Acta; International ... Neuromyelitis optica (NMO) (Devic's disease) In humans the gene for CCL17 is located on chromosome 16 along with other ...
For example, neuromyelitis optica was previously considered MS and currently is not, even if it appears that the MS definition ... March 2015). "Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype". Journal of ... Wingerchuk D (2006). "Neuromyelitis Optica (Devic's Syndrome)" (PDF). 2006 Rare Neuroimmunologic Disorders Symposium. Archived ... See Anti-AQP4 diseases Originally found in neuromyelitis optica, this autoantibody has been associated with other conditions. ...
Today this disorder is referred to as Devic's disease or neuromyelitis optica (NMO). Miyazawa I, Fujihara K, Itoyama Y (March ... Jarius S, Wildemann B (Jan 2013). "The history of neuromyelitis optica". J. Neuroinflammation. 10 (1): 8. doi:10.1186/1742-2094 ...
Misu T, Fujihara K, Itoyama Y (May 2008). "[Neuromyelitis optica and anti-aquaporin 4 antibody--an overview]". Brain and Nerve ... The condition known as neuromyelitis optica, NMO, is a rare demyelinating, inflammatory disorder of the CNS that primarily ... Jarius S, Wildemann B (November 2013). "Aquaporin-4 antibodies (NMO-IgG) as a serological marker of neuromyelitis optica: a ... Aquaporin-4 is the predominant autoimmune target in 2/3 neuromyelitis optica and higher AQP4 autoantibody levels are associated ...
... as Monotherapy to Treat Participants With Neuromyelitis Optica (NMO) and Neuromyelitis Optica Spectrum Disorder (NMOSD)" at ... Duchow A, Paul F, Bellmann-Strobl J (September 2020). "Current and emerging biologics for the treatment of neuromyelitis optica ... Satralizumab is indicated for the treatment of neuromyelitis optica spectrum disorder (NMOSD) in adults with a particular ... The effectiveness and safety of satralizumab for the treatment of neuromyelitis optica spectrum disorder (NMOSD) were ...
This is most commonly MS, but it may also occur with neuromyelitis optica spectrum disorder or Guillain-Barre Syndrome. It ... Park, Kwiyoung; Tanaka, Keiko; Tanaka, Masami (2014). "Uhthoff's Phenomenon in Multiple Sclerosis and Neuromyelitis Optica". ...
Anti-AQP4 autoantibodies were found in neuromyelitis optica (NMO), which was previously considered a MS variant. A spectrum of ... Intractable vomiting, severe optic neuritis, or bilateral optic neuritis raises suspicion for neuromyelitis optica spectrum ... Fujihara K (June 2019). "Neuromyelitis optica spectrum disorders: still evolving and broadening". Current Opinion in Neurology ... Misu T, Fujihara K (February 2019). "Neuromyelitis optica spectrum and myelin oligodendrocyte glycoprotein antibody‐related ...
"An epidemiological study of neuromyelitis optica in Cuba". Journal of Neurology. 256 (1): 35-44. doi:10.1007/s00415-009-0009-0 ...
In a study conducted to identify rare genetic variants contributing to Neuromyelitis optica in Finland, Four missense variants ... December 2015). "Exome and regulatory element sequencing of neuromyelitis optica patients". Journal of Neuroimmunology. 289: ...
Brück W, Popescu B, Lucchinetti CF, Markovic-Plese S, Gold R, Thal DR, Metz I (Sep 2012). "Neuromyelitis optica lesions may ... October 2009). "Humoral pattern II multiple sclerosis pathology not associated with neuromyelitis Optica IgG". Arch Neurol. 66 ... 2015). "Imaging Surrogates of Disease Activity in Neuromyelitis Optica Allow Distinction from Multiple Sclerosis". PLOS ONE. 10 ... studies that found a relatively high rate of false diagnoses of MS among patients with AQP4-IgG-positive neuromyelitis optica ...
First of all, anti-AQP4 autoantibodies were found in neuromyelitis optica (NMO), which was previously considered a MS variant. ... Mar 2015). "Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype". Journal of ... Misu, Tatsuro; Fujihara, Kazuo (2019). "Neuromyelitis optica spectrum and myelin oligodendrocyte glycoprotein antibody‐related ... 2008). "Brain magnetic resonance imaging abnormalities in neuromyelitis optica". Acta Neurologica Scandinavica. 118 (4): 218-25 ...
Brück W, Popescu B, Lucchinetti CF, Markovic-Plese S, Gold R, Thal DR, Metz I (Sep 2012). "Neuromyelitis optica lesions may ... Devic's disease and neuromyelitis optica (NMO) (sometimes previously called optic-spinal MS) Acute disseminated ... October 2009). "Humoral pattern II multiple sclerosis pathology not associated with neuromyelitis Optica IgG". Arch. Neurol. 66 ... from Neuromyelitis Optica Spectrum Disorders (NMOSD) and MOG Antibody Disorder (MOGAD)? (2399) Jasmin Patel, Antonio Pires, ...
Neuromyelitis optica: NF auto antibodies can also appear in NMO cases. These antibodies are more related to the peripheral ... "Anti-neurofascin-155 antibody-positive neuromyelitis optica spectrum disorders". Journal of the Neurological Sciences. 398: 16- ...
Brück W, Popescu B, Lucchinetti CF, Markovic-Plese S, Gold R, Thal DR, Metz I (Sep 2012). "Neuromyelitis optica lesions may ... This measure can be used to predict disease activity and to establish a differential diagnosis from Neuromyelitis optica About ... October 2009). "Humoral pattern II multiple sclerosis pathology not associated with neuromyelitis Optica IgG". Arch Neurol. 66 ... Balo concentric sclerosis lesions have been classified as pattern III (distal oligodendrogliopathy). Neuromyelitis optica was ...
"Common CYP7A1 promoter polymorphism associated with risk of neuromyelitis optica". Neurobiology of Disease. 37 (2): 349-55. doi ...
"Anti-MOG antibodies are present in a subgroup of patients with a neuromyelitis optica phenotype". Journal of Neuroinflammation ... "Myelin-oligodendrocyte glycoprotein antibodies in adults with a neuromyelitis optica phenotype". Neurology. 79 (12): 1273-7. ... autoantibodies has been associated with the following conditions Most cases of aquaporin-4-seronegative neuromyelitis optica: ...
In neuromyelitis optica higher AQP4 autoantibody levels are associated with the occurrence of optic neuritis. Less common ... Clinical relevance of serum aquaporin-4 antibody levels in neuromyelitis optica. Neurochem Res. 2013;38(5):997-1001. doi: ... it has been found to be associated to anti-MOG and AQP4-negative neuromyelitis optica. When an inflammatory recurrent optic ... neuromyelitis optica), methanol poisoning, vitamin B12 deficiency, beriberi, dysautonomia (i.e. autonomic nervous system ...
2011). "Comparative brain stem lesions on MRI of acute disseminated encephalomyelitis, neuromyelitis optica, and multiple ... Misu T, Fujihara K (February 2019). "Neuromyelitis optica spectrum and myelin oligodendrocyte glycoprotein antibody‐related ... neuromyelitis optica, and multiple sclerosis". Current Opinion in Neurology. 20 (3): 343-50. doi:10.1097/WCO.0b013e3280be58d8. ...
Pittock SJ, Weinshenker BG, Lucchinetti CF, Wingerchuk DM, Corboy JR, Lennon VA (2006). "Neuromyelitis optica brain lesions ...
Patients should be carefully worked up to rule out Neuromyelitis optica (Devic's disease) due to the distinctive ... Pittock SJ, Weinshenker BG, Lucchinetti CF, Wingerchuk DM, Corboy JR, Lennon VA (2006). "Neuromyelitis optica brain lesions ...
2018 (2018). "A whole-genome sequence study identifies genetic risk factors for neuromyelitis optica". Nature Communications. 9 ...
Neuromyelitis optica, once considered a subtype of multiple sclerosis, is characterized by neuromyelitis optica IgG antibodies ... Multiple sclerosis and Neuromyelitis optica are autoimmune diseases which both frequently present with optic neuritis, an ... May 2007). "Pattern-specific loss of aquaporin-4 immunoreactivity distinguishes neuromyelitis optica from multiple sclerosis". ...
Most patients are seronegative for NMO-IgG and GFAP, biomarkers for neuromyelitis optica. ANA, indicative of autoimmune optic ... and neuromyelitis optica) and systemic disease (diabetic, toxic, nutritional, and infectious causes). Corticosteroid responsive ...
"Purified human C1-esterase inhibitor is safe in acute relapses of neuromyelitis optica". Neurology: Neuroimmunology & ...
Anti-glutamate receptor antibodies Neuromyelitis optica spectrum disorder Kayser MS, Dalmau J (September 2016). "Anti-NMDA ...
... neuromyelitis optica spectrum disorder (NMOSD), diabetes, atherosclerosis, depression, Alzheimer's disease, systemic lupus ... "Increased frequency of IL-6-producing non-classical monocytes in neuromyelitis optica spectrum disorder". Journal of ...
9 December 2013). "Neuromyelitis optica spectrum disorder complicated with Sjogren syndrome successfully treated with ... March 2013). "Interleukin 6 receptor blockade in patients with neuromyelitis optica nonresponsive to anti-CD20 therapy". JAMA ... March 2013). "Disease amelioration with tocilizumab in a treatment-resistant patient with neuromyelitis optica: implication for ... "Clinical improvement in a patient with neuromyelitis optica following therapy with the anti-IL-6 receptor monoclonal antibody ...
Neuromyelitis optica spectrum disorders (NMOSD), including neuromyelitis optica (NMO), are autoimmune diseases characterized by ... "Treatment of neuromyelitis optica and neuromyelitis optica spectrum disorders with rituximab using a maintenance treatment ... Neuromyelitis optica 2020; https://www.mayoclinic.org/diseases-conditions/neuromyelitis-optica/symptoms-causes/syc-20375652. ... "Neuromyelitis optica - Diagnosis and treatment - Mayo Clinic". www.mayoclinic.org. Retrieved 2020-08-03. Kowarik, Markus C.; ...
... Arch Neurol. 2006 Mar;63(3):390-6. doi: 10.1001/archneur.63.3.390. ... Neuromyelitis optica-IgG was detected in 41 patients (68%). Brain MRI lesions were detected in 36 patients (60%). Most were ... Background: Neuromyelitis optica (NMO) is a severe demyelinating disease defined principally by its tendency to selectively ...
Vaccines Tied to Relapses in Neuromyelitis Optica. - Retrospective review finds protective factor in immunotherapy. by Kristina ... Source Reference: Mealy M, et al "Vaccines increase the risk of relapses in neuromyelitis optica spectrum disorder among ... PARIS - Vaccines may trigger relapses in patients with neuromyelitis optica spectrum disorder (NMOSD), but that risk is ...
Neuromyelitis optica spectrum disorder (NMOSD) is the one. Todays article will throw light on the Neuromyelitis optica ... NMOSD is also known as Devics disease or Neuromyelitis optica (NMO).. TYPES OF NMOSD. There are two types of NMOSD. *RELAPSING ... Neuromyelitis optica spectrum disorder (NMOSD) is a disorder of the central nervous system that majorly affects the nerves of ... Ayurveda system has some natural herbs which are very helpful in getting rid from Neuromyelitis optica syndrome disorder. ...
... Mult Scler. 2010 Dec;16(12):1443-52. doi ... Background: Neuromyelitis optica (NMO) is assumed to be immunologically distinct from multiple sclerosis (MS). Adequate studies ...
NINDS Neuromyelitis Optica Information Page, 2015, http://www.ninds.nih.gov/disorders/neuromyelitis_optica/neuromyelitis_optica ... "Update on the diagnosis and treatment of neuromyelitis optica: recommendations of the Neuromyelitis Optica Study Group (NEMOS ... A Case Study of Intractable Vomiting with Final Diagnosis of Neuromyelitis Optica. Rachel Bramson. 1,2and Angela Hairrell1 ... Neuromyelitis optica (NMO) is an uncommon disease syndrome of the central nervous system (CNS) that affects the optic nerves ...
Please note that NORD provides this information for the benefit of the rare disease community. NORD is not a medical provider or health care facility and thus can neither diagnose any disease or disorder nor endorse or recommend any specific medical treatments. Patients must rely on the personal and individualized medical advice of their qualified health care professionals before seeking any information related to their particular diagnosis, cure or treatment of a condition or disorder.. ...
Please note that NORD provides this information for the benefit of the rare disease community. NORD is not a medical provider or health care facility and thus can neither diagnose any disease or disorder nor endorse or recommend any specific medical treatments. Patients must rely on the personal and individualized medical advice of their qualified health care professionals before seeking any information related to their particular diagnosis, cure or treatment of a condition or disorder.. ...
... antibody positive neuromyelitis optica spectrum disorder (NMOSD) in adults ... for Neuromyelitis Optica Spectrum Disorder Eculizumab (Soliris) for Neuromyelitis Optica Spectrum Disorder ... Eculizumab (Soliris) for Neuromyelitis Optica Spectrum Disorder * The Role of Physical Exercise in Managing Multiple Sclerosis ... Q. What did the clinical trials of eculizumab in neuromyelitis optica show?. Eculizumab was first studied in 14 AQP4 antibody ...
The PAN Foundation opened a new financial assistance program for people living with neuromyelitis optica spectrum disorder. ... Neuromyelitis optica spectrum disorder, also known as Devics disease and neuromyelitis optica, is a rare autoimmune disease ... To get financial assistance for neuromyelitis optica spectrum disorder, patients must: *Be getting treatment for neuromyelitis ... New neuromyelitis optica spectrum disorder fund opens Share this page * Share on Facebook ...
RNA profiles to distinguish multiple sclerosis and neuromyelitis optica in peripheral whole blood at the American Academny of ... Oral presentation: RNA profiles to distinguish multiple sclerosis and neuromyelitis optica in peripheral whole blood ... RNA profiles to distinguish multiple sclerosis and neuromyelitis optica in peripheral whole blood ... RNA profiles to distinguish multiple sclerosis and neuromyelitis optica in peripheral whole blood ...
Neuromyelitis Optica. Melissa Parks, MSN, NP-C. May 19, 2023. Melissa Parks, MSN, NP-C, is an advanced practice provider at ...
... for the treatment of neuromyelitis optica spectrum disorder. Developed by MedImmune, inebilizumab is currently in Phase IIb ... Astrazenecas Inebilizumab Gains EU Orphan Designation in Neuromyelitis Optica Spectrum Disorder. April 12, 2017 ... Home » Astrazenecas Inebilizumab Gains EU Orphan Designation in Neuromyelitis Optica Spectrum Disorder ... for the treatment of neuromyelitis optica spectrum disorder. Developed by MedImmune, inebilizumab is currently in Phase IIb ...
Neuromyelitis optica (NMO) is an inflammatory disorder that can cause pain, paralysis, and even death. In most cases, NMO is ... Study identifies antibody that alleviates symptoms in neuromyelitis optica in rats. Jan 18, 2018 ... Study shows drug reduces risk of relapse with neuromyelitis optica. May 3, 2019 ... FDA OKs second treatment for neuromyelitis optica spectrum disorder. Jun 15, 2020 ...
About NMONeuromyelitis optica (NMO) and neuromyelitis optica spectrum disorder (NMOSD) occur when the immune system mistakes ... A review of cases of neuromyelitis optica. Tags: approved, circulating, clinical, met, multiple, observed, relapse, response, ... ResearchBrowse through the results of over $70 million donated to basic and clinical research to solve neuromyelitis optica. ... DiagnosisThe release of new diagnostic criteria for NMO by the International Panel for Neuromyelitis Optica Diagnosis (IPND). ...
Keywords: Neuromyelitis optica, NMO-IgG, anti-aquaporin-4 antibody, early diagnosis, antibody titration ... Neuromyelitis optica (NMO) is a devastating neurologic disease characterized by severe optic neuritis and transverse myelitis. ...
Aquaporin 4-positive neuromyelitis optica spectrum disorder with meningoencephalitis-like onset: A case report. ... Neuromyelitis optica spectrum disease (NMOSD) is a debilitating autoimmune inflammatory demyelinating disease of the central ...
A mathematical model of cellular swelling in Neuromyelitis optica Laranjeira S., Symmonds M., Palace J., Payne SJ., Orlowski P. ...
Neuromyelitis Optica Spectrum Disorder Market Dynamics: Neuromyelitis Optica Spectrum Disorder market drivers and Neuromyelitis ... 6. Neuromyelitis Optica Spectrum Disorder Late Stage Products (Phase II/III). 7. Neuromyelitis Optica Spectrum Disorder Mid ... Neuromyelitis Optica Spectrum Disorder By Stage and Product Type. *Neuromyelitis Optica Spectrum Disorder Assessment by Route ... Download the Neuromyelitis Optica Spectrum Disorder pipeline report to learn more about the emerging Neuromyelitis Optica ...
The evolving clinical spectrum of neuromyelitis optica Viegas SD., Weir A., Esiri M., Hart Y., Newsom-Davis J., Vincent A., ...
The life expectancy of the patient suffering from neuromyelitis optica depends upon various factors. ... What Leads To Neuromyelitis Optica & Can It Be Cured?. *How Long Will It Take To Recover From Neuromyelitis Optica & How Long ... Life Expectancy Of Someone With Neuromyelitis Optica. The life expectancy of the patient suffering from neuromyelitis optica ... It the in two forms known as monophasic neuromyelitis optica and relapsing neuromyelitis optica. In the monophasic form, the ...
Neuromyelitis Optica (NMO) is a severe form of demyelinating disease, characterized by involvement of the optic nerve and ...
... ask questions in our neuromyelitis optica discussion forums, covering topics like treatment, unusual symptoms, coping, ... Neuromyelitis-Optica.net does not provide medical advice, diagnosis or treatment. Use of the site is conditional upon your ... Neuromyelitis-Optica.net is a Health Union community. Health Union reaches millions of people through condition-specific online ... Read conversations, start a discussion, and connect with others about neuromyelitis optica. ...
The Neuromyelitis-Optica.net team does not recommend or endorse any products or treatments discussed herein. Learn more about ... Neuromyelitis-Optica.net does not provide medical advice, diagnosis or treatment. Use of the site is conditional upon your ... Neuromyelitis-Optica.net is a Health Union community. Health Union reaches millions of people through condition-specific online ... Is your doctor considering a new treatment? - Jada (neuromyelitis-optica.net team member),/p, ...
Neuromyelitis Optica Spectrum Disorder (NMOSD), Multiple Sclerosis (MS), and Alzheimers Disease ... Once thought to be a type of Multiple Sclerosis (MS), Neuromyelitis Optica Spectrum Disorder (NMOSD) is a distinct and rare ... ENDECE is developing NDC-1308 to stop progression, reverse damage, and improve function in patients with Neuromyelitis Optica ... of action that may reduce inflammation and induce remyelination in neurodegenerative diseases such as Neuromyelitis Optica ...
Neuromyelitis Optica. The signs fall into two categories: optic neuritis and transverse myelitis. Optic neuritis is ... Symptoms and signs for children who have neuromyelitis optica include confusion, seizures, or ...
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Dive into the research topics of Neuromyelitis optica spectrum disorders. Together they form a unique fingerprint. ...
... View File(s). Totonis_PST148_93508.pdf ... Neuromyelitis optica spectrum disorder is a rare CNS autoimmune disease, resulting in lesions throughout the optic nerves and ...

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