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)

Focal and generalized seizures occurred in 4 patients with acute lymphoblastic leukemia and non-Hodgkin-lymphoma. The etiology of the neurological complications could be established by cranial computerized tomography (CT): i.e., 1. localized metastasis with calcification and 2. acute intracerebral hemorrhage during induction therapy in two patients with malignant lymphomas; 3. diffuse cerebral infiltration with blast cells and 4. cerebral atrophy in two children with acute lymphoblastic leukemia who were in relapse. Accurate diagnosis of cerebral complications in hemoblastoses is essential for appropriate therapy and CT may lead to more effective treatment in patients with lymphoid malignancy and seizures.
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PMID:Cranial computerized tomography in children with lymphoid malignancy and seizures. 27 69

Carbamazepine is an important drug used in the management of seizures, trigeminal neuralgia, and chronic pain syndromes. It has been associated with a variety of adverse skin reactions including urticaria, lichenoid eruptions, erythroderma, erythema multiforme, Stevens-Johnson syndrome, and toxic epidermal necrolysis. A 39-year-old white male had been started on carbamazepine for intractable pain which resulted from a right foot crush injury. Approximately 3 months after the start of therapy, the patient had developed a generalized skin eruption following an entire day of sun exposure. Skin biopsies revealed an atypical lymphoid infiltrate in the dermis with collections of the atypical lymphocytes within spongiotic vesicles in the epidermis, suggestive of mycosis fungoides. The patient was treated with systemic prednisone. Subsequent biopsies failed to reveal atypical lymphocytes. Previous reports have described spongiotic eruptions with foci of atypical lymphocytes in contact dermatitis and in patients treated with phenytoin. To the best of our knowledge, this is the first reported case of a carbamazepine-induced eruption simulating mycosis fungoides histologically.
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PMID:Carbamazepine-induced eruption histologically mimicking mycosis fungoides. 214 Jan 16

We describe 2 brothers with a malformation syndrome consisting of agenesis of the corpus callosum, cutaneous hypopigmentation, bilateral cataract, cleft lip and palate, and combined immunodeficiency. The clinical history of both patients was characterized by severe psychomotor retardation, seizures, recurrent severe respiratory infections, and chronic mucocutaneous candidiasis. The children died of bronchopneumonia at age 2 and 3 years, respectively. Immunological investigations showed, in one sib studied, skin anergy to recall antigens, profound depletion of T4+ lymphocytes, and serum IgG2 deficiency. Necropsy showed agenesis of the corpus callosum, hypoplasia of the cerebellar vermis, and profound hypoplasia of the thymus and of the peripheral lymphoid tissue. The distinctive features of these sibs appear to define a previously undescribed hereditary MCA/MR syndrome. The clinical and pathological findings seem to indicate, as a pathogenetic mechanism, a defect involving the embryonic organization of the central nervous system and of the immune system.
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PMID:Agenesis of the corpus callosum, combined immunodeficiency, bilateral cataract, and hypopigmentation in two brothers. 334 62

A case of phenytoin-induced hepatitis with mononucleosis is reported, and syndromes associated with phenytoin hypersensitivity reactions are discussed. A 23-year-old black woman with a two-month history of seizure disorder was admitted to a hospital with nausea, vomiting, fever, lymphadenopathy, diffuse maculopapular rash, left-upper-quadrant tenderness, and hepatomegaly. She was receiving phenytoin sodium 300 mg/day; carbamazepine 200 mg four times daily had been discontinued four days before admission because of leukopenia. Phenytoin was discontinued after admission; however, phenytoin 1 g i.v. was given for a tonic-clonic seizure two days after admission, after which swelling of the face and legs and pruritus developed. Over the next few days, signs and symptoms of hepatotoxicity progressed, and she became comatose. Seizures were treated with diazepam. She began to recover after 10 days of supportive therapy and was discharged several weeks later on primidone therapy. Serious phenytoin hypersensitivity reactions may appear as dermatologic, lymphoid, or hepatic syndromes. Fever, rash, and lymphadenopathy often accompany hepatic injury. Encephalopathy and death may occur. Proposed mechanisms for phenytoin hypersensitivity include antigen-antibody reactions, alteration of lymphocyte function, and an enzyme abnormality causing the production of toxic metabolites. Treatment is supportive; phenobarbital and carbamazepine may be used with caution as alternate anticonvulsant therapy. The possibility of phenytoin hypersensitivity reactions should be considered when patients receiving phenytoin have unusual symptoms, particularly fever, rash, and lymphadenopathy.
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PMID:Phenytoin-induced hypersensitivity reactions. 367 71

Central nervous system lymphosarcoma was diagnosed in 8 dogs with seizures and clinical signs compatible with multifocal central nervous system involvement. Cerebrospinal fluid analysis showed high white cell counts with abnormal lymphoid cells in all dogs, and high protein concentration in 5 dogs. Two dogs were given systemic anticancer chemotherapy, and 4 dogs were given a combination of systemic chemotherapy, intrathecal cytosine arabinoside, and craniospinal irradiation, resulting in marked improvement of the clinical signs.
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PMID:Central nervous system lymphosarcoma in the dog. 654 26

The authors report the brain findings in six cases of familial erythrophagocytic lymphohistiocytosis (FEL) and review the literature, focusing primarily on the neurologic and neuropathologic aspects. Clinically, the most common neurologic abnormalities in the six patients were stupor or coma and seizures, with hemiplegia and cranial nerve palsies. Neuropathologic changes were characterized by infiltration of the meninges by lymphocytes and histiocytes and perivascular lymphocytic cuffing and diffuse proliferation of histiocytes in the brain parenchyma. The severity of the brain involvement was variable. In the mildest case there was only meningeal involvement. More severely involved cases showed meningeal and perivascular infiltration of lymphoid cells in the brain. In the most severely involved cases, there was, in addition, diffuse cerebral infiltration by histiocytes accompanied by multifocal necrosis. Some cases showed disproportionately greater involvement of the brain than of the visceral organs. The authors conclude that "meningoencephalitis," histiocytic invasion, and necrotizing brain lesions are characteristic of FEL, although the mechanism of their production is not known. Frequent seizures and disseminated intravascular coagulopathy may be contributory.
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PMID:Neuropathology of familial erythrophagocytic lymphohistiocytosis: six cases and review of the literature. 669 35

A 34-year-old man had polar extremes of B cell dysfunction: systemic lupus erythematosus evolving into common variable hypogammaglobulinemia. He presented in 1974 with seizures and six other criteria for systemic lupus erythematosus; his antinuclear antibody titer was 1:1024 and IgG level, 2870 mg/dL. After 5 months of immunosuppressive treatment, a 79% decrease in serum IgG and 95% decrease in IgA levels occurred and manifestations of systemic lupus erythematosus disappeared. Six years later, he developed panhypogammaglobulinemia, had recurrent sinopulmonary infections, and showed nodular lymphoid hyperplasia on rectal biopsy. For comparison, serum immunoglobulin concentrations were measured serially in 13 other patients with systemic lupus erythematosus. Three developed severe depressions of these levels, two with IgG levels less than 300 mg/dL and one with an IgA level of 8 mg/dL. These decreases were transient, related to treatment, and not associated with infections. Daily high-dose prednisone therapy (60 mg/d) rather than treatment with cytotoxic drugs correlated with decreased immunoglobulin concentrations.
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PMID:Transition from systemic lupus erythematosus to common variable hypogammaglobulinemia. 685 20

Toxicity of single-dose spirogermanium was evaluated after iv and im administration to CDF1 mice and beagle dogs. The im LD50 in mice was approximately threefold greater than the iv LD50. The lethal dose in dogs was the same for both routes of administration, but death was delayed after im injection. Convulsive seizures occurred only after the im doses that were lethal, but they were observed after administration of iv doses that were nonlethal. Microscopic evidence of drug toxicity (necrosis and degeneration) was found in mitotically active tissues: intestinal tract, lymphoid tissue, and bone marrow. Necrosis, hemorrhage, edema, and granulation tissue were observed in the muscle injection site.
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PMID:Toxicity of spirogermanium in mice and dogs after iv or im administration. 747 Nov 12

Graves' disease, which is an organ-specific autoimmune disorder, is the most frequent cause of thyrotoxicosis. Females are more often affected than males. The clinical pattern varies, however, and nearly every organ system may be involved. This case study describes a formerly healthy young woman with Graves' disease who was admitted to the hospital with cardiac failure, convulsions and generalized lymphoid hyperplasia. A reversible thyrotoxic cardiomyopathia combined with hyperdynamic circulation may result in cardiac failure even in younger patients, and the cardiac function normalizes in the euthyroid state. Seizures may occur in association with hyperthyroidism. High doses of propranolol may precipitate the condition by lowering the threshold for seizures.
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PMID:[Heart failure and convulsions in thyrotoxicosis. A young woman with Graves' disease]. 797 5

Patients receiving phenytoin (PHT) may develop pseudolymphoma or, rare ly, malignant lymphoma. Previously, distinguishing the two diseases based solely on histopathology has been difficult. The recent introduction of molecular biologic techniques has provided a powerful tool to reassess this problem. A 17-year-old girl developed systemic lymphadenopathy after receiving PHT for 1 year for generalized tonic-clonic seizures (GTCS). Biopsy of a cervical lymph node showed diffuse proliferation of large lymphoid cells mimicking a large cell lymphoma. Immunophenotypic, immunoglobulin gene rearrangement, and cytogenic studies, however, showed polyclonal B-cell proliferation, consistent with PHT-induced pseudolymphoma. After PHT discontinuation, lymphadenopathy resolved in 1 month and no recurrence developed in the subsequent 10 months. Obtaining a history of drug use is crucial to recognizing this group of patients. Molecular biology and chromosome studies have become the definitive basis differentiating pseudolymphoma from malignant lymphoma in patients receiving chronic PHT therapy.
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PMID:Phenytoin-induced pseudolymphoma: reevaluation using modern molecular biology techniques. 860 15


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