Cases reported "Multiple Sclerosis"

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1/126. Chronic steadily progressive central and peripheral predominantly motor demyelination, involving the cranial nerves, responsive to immunoglobulins.

    The association of central and peripheral demyelination was reported previously. Most of the cases refer to central chronic relapsing demyelination with clinical criteria for multiple sclerosis associated with later signs of peripheral nerve involvement. Other authors, described central lesions in patients with chronic inflammatory demyelinating polyneuropathy and in guillain-barre syndrome, as a seldom occurrence. We report a patient in which a chronic steadily progressive central and peripheral predominantly motor nervous system demyelination, involving the cranial nerves, was identified. The patient improved after intravenous immunoglobulin suggesting an immune-mediated mechanism. To our knowledge this presentation was not described before.
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2/126. Cranial polyneuropathies in multiple sclerosis: case report and literature review.

    Although cranial neuropathies are common disorders in multiple sclerosis patients, multiple cranial nerve involvement is an unusual occurrence. Correlation of clinical symptoms with magnetic resonance imaging evidence of demyelinating central nervous system lesions can confirm the diagnosis. The authors report on the case of a 43-year-old woman who initially was thought to have suffered a brainstem infarct but, in fact, had developed multiple cranial nerve functional deficits. Treatment of multiple sclerosis remains primarily supportive in nature, with corticosteroids used for acute exacerbations and chronic progression.
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3/126. tissue plasminogen activator gene expression in multiple sclerosis brain tissue.

    Recent studies have implicated tissue-type plasminogen activator (tPA) in neurodegeneration. We studied multiple sclerosis (MS) brain tissue for tPA gene and protein expression in comparison with reference tissue, by in situ hybridisation and immunohistochemistry. MS is characterised by demyelination in the central nervous system. In this study, neuronal cell bodies in MS brain showed high expression of tPA mRNA and protein, while in reference brains, staining for protein and mRNA expression were very low in neurons and mostly restricted to blood vessel walls. In MS, there was an additional staining of mononuclear cells within perivascular cuffs and foamy macrophages within demyelinating plaques. In view of evidence that the final process of demyelination in MS is thought to be enzyme-mediated, our work suggests the involvement of tPA and by inference plasmin, in the demyelinating process. Blocking tPA or plasmin activity may be a potentially beneficial therapeutic approach in MS.
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4/126. Demyelination in primate autoimmune encephalomyelitis and acute multiple sclerosis lesions: a case for antigen-specific antibody mediation.

    Neuropathological and ultrastructural features of central nervous system demyelination were compared in marmoset experimental autoimmune encephalomyelitis (EAE) induced with myelin/oligodendrocyte glycoprotein (MOG), and in 3 cases of multiple sclerosis (MS) displaying recent lesions. At the edges of EAE and MS lesions, a zone of myelin vacuolation was common, whereas in the lesion proper, myelin sheaths were consistently transformed into vesiculated membranous networks. These networks became dissociated from axons by cell processes from macrophages. Oligodendrocytes were remarkably spared and evidence of myelin repair was present but not prominent. Axonal pathology was more common in the MS material than in marmoset EAE. Immunocytochemistry, using gold-labeled encephalitogenic peptides of MOG and silver enhancement to detect MOG autoantibodies, revealed the presence of MOG-specific autoantibodies over vesiculated myelin networks. gold-labeled antibody to IgG also gave a positive reaction. gold-labeled peptide of myelin basic protein did not react with MOG/EAE tissue, but the same conjugate gave positive staining in MS (and in marmoset EAE induced by whole white matter), perhaps indicating broader spectrum immunoreactivity or sensitization to myelin antigens. Thus, vesicular disruption of myelin was a constant feature in these evolving, highly active lesions in primate EAE and MS and appeared causally related to the deposition of antigen-specific autoantibodies.
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5/126. Syndrome of inappropriate antidiuresis associated with multiple sclerosis.

    Even though many disorders of the nervous system have been reported to be associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), the association of this syndrome with multiple sclerosis is extremely rare. We describe a patient with multiple sclerosis who developed SIADH and hyponatremia.
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6/126. Primary sjogren's syndrome manifested as multiple sclerosis and cutaneous erythematous lesions: a case report.

    sjogren's syndrome is a chronic autoimmune disorder characterized by lymphocytic infiltration of the lacrimal and salivary glands, leading to dryness of eyes (kerato-conjunctivitis sicca) and mouth (xerostomia). The skin lesions in sjogren's syndrome are usually manifested as xeroderma, but sometimes appear as annular erythema or vasculitis. central nervous system symptoms may be presented as one of extraglandular manifestations, though rare in incidence, and need differential diagnosis from multiple sclerosis. We report a case of a 45-year-old woman diagnosed as multiple sclerosis at first but later as neurologic manifestation of primary sjogren's syndrome, showing signs of multiple sclerosis and cutaneous erythematous lesions.
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7/126. cerebrospinal fluid oligoclonal IgG bands in patients with spinal arteriovenous malformation and structural central nervous system lesions.

    OBJECTIVE: To investigate the incidence and characteristics of patients with structural central nervous system (CNS) lesions and cerebrospinal fluid oligoclonal IgG bands. DESIGN: A retrospective study. METHOD: The medical records of patients with cerebrospinal fluid oligoclonal IgG bands were evaluated for the presence of structural CNS lesions, their location and cause, and for clinical characteristics. SETTING: cerebrospinal fluid oligoclonal IgG bands were examined in the Neuroimmunology Laboratory, Hadassah University Hospital, Jerusalem, israel. patients: Two hundred seventy of 570 patients with positive cerebrospinal fluid oligoclonal IgG bands were available for analysis. Twenty patients had structural CNS lesions. RESULTS: Twenty (7.5%) of the 270 patients had structural CNS lesions: 3 patients had spinal arteriovenous malformation; 5 patients had tumors; 9 patients had compressive cervical myelopathy. Traumatic leukomalacia, arnold-chiari malformation type 1, and CNS hemosiderosis were present in 1 patient each. In 2 patients (1 patient with recurrent meningioma and 1 patient with posttraumatic encephalomalacia) the presence of a structural CNS lesion was followed by the development of multiple sclerosis. In all 3 patients with spinal arteriovenous malformation, oligoclonal IgG identification prolonged the time to diagnosis and therapy, which varied from a few weeks to 3 years. CONCLUSIONS: Structural CNS lesions, responsible for the neurological disorder, were present in 20 patients (7.5%) with cerebrospinal fluid oligoclonal IgG bands. The mechanism underlying oligoclonal IgG presence in spinal arteriovenous malformation and the coexistence of multiple sclerosis and structural CNS lesions is unknown, but may be related to recurrent tissue damage with repeated presentation of CNS antigens to the immune system.
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8/126. neurology. 4: multiple sclerosis.

    multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) and a common cause of disability in young adults; it is most likely an autoimmune disease. Typically, MS initially follows a relapsing-remitting course, but most patients eventually develop secondary progressive MS, where there is progressive deterioration without relapses or remissions; in some patients, MS has a primary progressive course. The diagnosis of MS requires evidence of CNS lesions disseminated in time and place, as well as the exclusion of other likely causes of these lesions; the clinical history, neurological examination and investigations, such as magnetic resonance imaging of the brain and spinal cord, all have key roles in the diagnosis. education and counselling of the patient and family members are essential for good patient management. Moderate to severe attacks of MS are best treated with intravenous infusions of high-dose methylprednisolone. Interferon beta reduces the frequency of attacks and the progression of disability in relapsing-remitting MS. Symptomatic therapy is important in the management of spasticity, pain, urinary problems and the other symptoms or complications of MS.
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9/126. Asymmetric sweating in a child with multiple sclerosis.

    A 10-year-old male with multiple sclerosis complained of excessive sweating on the right side of the forehead and shoulder on relapse 3 months after the onset of multiple sclerosis. Because the neurologic evaluation revealed no abnormalities in the sudomotor function, it is likely that the hyperhidrosis resulted from a lesion in the central or preganglionic sympathetic nervous system. magnetic resonance imaging demonstrated a high-intensity lesion involving the left hypothalamus on T(2)-weighted imaging. Thus hypothalamic involvement might be the reason for the hyperhidrosis in this patient.
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10/126. Diagnostic challenges in combined multiple sclerosis and centronuclear myopathy.

    The first case of combined centronuclear myopathy and multiple sclerosis is reported. The difficulties of diagnosing multiple sclerosis in patients with muscular disorders associated with the central nervous system involvement are discussed.
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