Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This report describes vaccine-induced canine distemper virus (CDV) infection in four European mink (Mustela lutreola) induced by the administration of a multivalent, avian-origin vaccine. Clinical signs consisting of seizures, ataxia, facial twitching, oculonasal discharge, hyperkeratosis of footpads, and anorexia developed 16-20 days postvaccination. Conjunctival smears from one animal were positive for CDV antigen by direct fluorescent antibody testing, confirming the clinical diagnosis. The four mink died 16-26 days postvaccination. Gross and microscopic lesions that were diagnostic for CDV infection included interstitial pneumonia, lymphoid depletion, nonsuppurative encephalitis, and dermatitis. Vaccine-strain virus was isolated from tissues of three animals. Cases of vaccine-induced distemper in mustelids using avian-origin vaccine have seldom been reported.
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PMID:Vaccine-induced canine distemper in European mink, Mustela lutreola. 936 45

Mice infected with the LP-BM5 murine leukemia virus (MuLV) develop an immune deficiency syndrome together with an encephalopathy characterized by impairments in spatial learning and memory. These cognitive deficits are evident before the appearance of neuron loss and lymphoid cell invasion of the brain. Nonetheless, a prominent gliosis and a variety of neurochemical changes precede the development of cognitive deficits. The neurochemical abnormalities include significant decreases in striatal Met-enkephalin and substance P (but not somatostatin), increases in concentrations of quinolinic acid and platelet-activating factor, and alterations in brain fyn kinase. At this stage of the infection, some of these neurochemical changes can be reversed by glutamate receptor antagonists, cytokine inhibitors, and anti-retroviral agents. In later stages of the infection, however, the infected mice develop irreversible neuronal loss, invasion of hematopoietic cells, and increased viral burden in the CNS. In addition, motor-neuron dysfunction (hindlimb paralysis, weakness, and ataxia) and seizures are sometimes observed during the late stages of infection. Thus, the LP-BM5 MuLV-infected mouse is a useful model for studying the chronology of neurodegenerative changes, ranging from reversible neuron dysfunction to irreversible neuron loss, that are associated with retrovirus-induced immunodeficiency.
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PMID:The encephalopathy associated with murine acquired immunodeficiency syndrome. 962 8

Primary central nervous system lymphomas (PCNSL) represent only 1% of all non-Hodgkin's lymphomas (NHLs). A 66 year-old woman was hospitalized due to multiple episodes of syncope and seizures which occurred the week before admission to the hospital. A computerized tomography (CT) scan of the brain showed a right parietal lesion suggesting a subdural effusion. The patient was operated and a dural lesion extending to the epidural space and cerebral cortex was excised. Histologic findings suggested diagnosis of a low-grade lymphoma of the mucosa associated lymphoid tissue (MALT) type. The patient was treated with radiation therapy and has now completely recovered 12 months after surgery.
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PMID:Primary low grade B-cell lymphoma of the dura in an immunocompetent patient. 1096 27

Plasma cell granulomas (PCGs) are benign, inflammatory masses of unknown etiology composed of polyclonal mature plasma and lymphoid cells. The lung is their most common location, and occurrence within the cranial cavity is extremely rare. We report the case of an 11-year-old girl who presented with seizures and was diagnosed as having a dural-based right frontal tumor that extended toward the sagittal sinus and the falx. The lesion was totally excised, together with the abnormal dura. A limited cortical excision was also performed using electrocorticographic guidance. Histopathologic diagnosis of intracranial plasma cell granuloma was reached after extensive immunohistochemical tests and electron microscopy. This is the third case of PCG with description of changes in the neighboring cerebral tissue. Although PCGs are well-circumscribed lesions, lymphoplasmocytic inflammation, neuronal loss, and reactive gliosis occur within the adjacent cortex. Disturbed cortical lamination, as we have observed, appears to be a histological finding that has not been described previously.
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PMID:Intracranial plasma cell granuloma. 1131 Sep 25

We report the case of a meningeal inflammatory pseudotumour occurring in a 23-year-old male presenting with focal seizures and headaches. Brain imaging techniques showed a 3.5 cm left parietal meningeal tumour. Histology of the surgical specimen showed a dense lymphoid infiltrate permeating the dura mater and leptomeninges, consisting of a predominant polyclonal B cell population as confirmed by immunophenotyping and genotyping. Cultures of serum, CSF, and surgical specimen were negative and there was no serological evidence of a systemic dysimmune disease. The postoperative course was complicated by an episode of brain oedema resolving under steroid therapy. The patient, free from all medication, is asymptomatic at 3 years of follow-up. We discuss previously published cases and the nosology of intracranial inflammatory pseudotumours.
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PMID:Meningeal inflammatory pseudotumour: a case report. 1148 58

The effects of phenytoin sodium on lymphoid tissue have been known for some time. However, its effect on the lymphoid tissue of Waldeyer's ring is unreported in the otolaryngology literature. We present the case of a 78-year-old woman who was treated with phenytoin for generalized tonic-clonic seizures for 4 months and who subsequently developed lingual hyperplasia that caused laryngeal obstruction eventually requiring a tracheotomy. Of note, no history of airway compromise or difficulty with intubation from a prior operation 20 years ago was reported; these findings suggest that the lingual tonsillar hyperplasia was a consequence of phenytoin therapy and not a preexisting condition. The findings of histopathologic evaluation were consistent with lymphoid hyperplasia without evidence of malignancy. We also report our operative management and follow-up of this rare condition.
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PMID:Phenytoin-induced lingual tonsil hyperplasia causing laryngeal obstruction. 1151 Jul 40

ICA69 (islet cell Ag 69 kDa) is a diabetes-associated autoantigen with high expression levels in beta cells and brain. Its function is unknown, but knockout of its Caenorhabditis elegans homologue, ric-19, compromised neurotransmission. We disrupted the murine gene, ica-1, in 129-strain mice. These animals aged normally, but speed-congenic ICA69(null) nonobese diabetic (NOD) mice developed mid-life lethality, reminiscent of NOD-specific, late lethal seizures in glutamic acid decarboxylase 65-deficient mice. In contrast to wild-type and heterozygous animals, ICA69(null) NOD congenics fail to generate, even after immunization, cross-reactive T cells that recognize the dominant Tep69 epitope in ICA69, and its environmental mimicry Ag, the ABBOS epitope in BSA. This antigenic mimicry is thus driven by the endogenous self Ag, and not initiated by the environmental mimic. Insulitis, spontaneous, and adoptively transferred diabetes develop normally in ICA69(null) NOD congenics. Like glutamic acid decarboxylase 65, ICA69 is not an obligate autoantigen in diabetes. Unexpectedly, ICA69(null) NOD mice were resistant to cyclophosphamide (CY)-accelerated diabetes. Transplantation experiments with hemopoietic and islet tissue linked CY resistance to ICA69 deficiency in islets. CY-accelerated diabetes involves not only ablation of lymphoid cells, but ICA69-dependent drug toxicity in beta cells that boosts autoreactivity in the regenerating lymphoid system.
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PMID:ICA69(null) nonobese diabetic mice develop diabetes, but resist disease acceleration by cyclophosphamide. 1175 95

We retrospectively reviewed the clinicopathologic features and immunohistochemical profiles of 7 patients with Rasmussen encephalitis (age range, 3.5-15 years at surgery). All had medically intractable seizures (6 months' to 7 years' duration); all but 1 developed unilateral hemiparesis. Histologically, all cases were characterized by leptomeningeal and parenchymal perivascular chronic inflammation consisting primarily of T lymphocytes (CD3+, CD5+, CD7+). In all but 1 case, a predominance of CD8+ T-cytotoxic/suppressor lymphoid cells over CD4+ cells was observed. All cases had rare B lymphocytes (CD79a+, CD20+). Rare CD10+ and no CD56+ cells were noted. All cases were marked by diffuse proliferation of microglial cells, highlighted on CD68 immunostaining. Focal microglial nodule formations were observed in 4 cases and focal cortical atrophy in 5 cases. Viral inclusions were not noted. There was no evidence of Epstein-Barr virus by LMP-1 antibody immunostaining. The histologic findings of Rasmussen encephalitis resemble those of viral meningoencephalitis. The pathologicfindings may be only focally present, and missed, if diagnosis is made or confirmed with biopsy alone. Most lymphoid cells have a T-cell immunophenotype, with a predominance of CD8+ cells in most cases.
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PMID:Rasmussen encephalitis: a clinicopathologic and immunohistochemical study of seven patients. 1209 Apr 28

L-asparaginase is frequently used in combination therapy for the treatment of lymphoid malignancies. We report 5 children aged between 8 and 14 years with neurologic complications presenting with headache and seizures during the first three weeks of L-asparaginase treatment. Three patients had venous thrombosis, one presented a parenchymal hemorrhage, and one showed a peculiar encephalopathy with extended cortical and subcortical lesions suggesting a neurotoxic reaction. Decreased fibrinogen and antithrombin III levels were found. Early MRI is critical even in cases with mild neurologic symptoms. Diagnosis should be followed by early cessation of l-asparaginase application.
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PMID:Cerebrovascular complications of L-asparaginase in the therapy of acute lymphoblastic leukemia. 1279 28

The January Case of the Month (COM). A 56 year-old female presented with a 5-month history of dizziness, focal motor seizures and progressive immobility. CT scan showed a large frontal tumor with a meningioma-like pattern. The patient underwent right frontal craniotomy and complete resection of the tumor. Biopsy showed lymphoid infiltrates consisting predominantly of centrocyte-like cells admixed with plasma cells and lymphoid follicles. Immunohistochemistry revealed CD20-positive cells and light chain restriction with reactive T cells. These appearances are characteristic of the MALT-type lymphomas. There was no evidence of systemic lymphoma. The patient is symptom-free 18 months after complete resection. MALT lymphoma is rare but recognized subtype of primary meningeal lymphoma. MALT lymphoma of dura tends to be relatively indolent, with excellent prognosis. It is suggested that meningeal MALT-type lymphoma may follow on from a pre-existing inflammatory process.
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PMID:January 2003: 56-year-old female with right frontal tumor of the dura. 1294 31


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