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)

Five patients received overdoses of vincristine ranging from 3.5 to 32 mg. Neurotoxicity accounted for most of the complications observed. Peripheral neuropathies, cranial nerve palsies, paralytic ileus, atony of the bladder, hypertension, hypotension, seizures, inappropriate ADH secretion, and severe bone marrow depression were all encountered. Two patients died within 72 hours of the overdose. Another patient died of sepsis 22 days after the overdose. Two patients recovered and were discharged. The three patients who survived longer than a few days showed improvement in the vincristine-induced neuropathy, and the two long-term survivors had essentially complete recovery. It appears that if a patient can be supported through the critical period following an overdose, he can be expected to recover normal neurologic function.
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PMID:Overdosage with vincristine. 18 48

Institutionalized epileptic patients on long-term anticonvulsant diphenylhydantoin (DPH) therapy were examined clinically. DPH plasma levels were unexpectedly high in 54% despite rather poor seizure control. No patient was free from side effects, which included gingival hypertrophy (90% of patients), increased alkaline phosphatase activity (55%), suggestion of a sensory peripheral neuropathy (34%), central nervous system (CNS) intoxication (22%), coarsened facial features (19%), tendency to bleed excessively (15%), hirsutism (12%), and mild megalocytic anemia (5%). CNS intoxication correlated with high plasma DPH levels, reports of deteriorating behavioral and motor performance, and the findings of nystagmus on vertical gaze or truncal ataxia, though not all patients with high plasma levels were clinically intoxicated. Alarming were the often disfiguring changes of gums and facial structures and the tendency to develop signs of vitamin D deficiency secondary to therapy. Hirsutism was rare in black patients. Plasma DPH level determinations are recommended as part of the management of mentally retarded epileptic patients but do not replace clinical acumen and skill.
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PMID:Effects of diphenylhydantoin in 41 epileptics institutionalized since childhood. 19 Jul 7

Dysesthesia and sensory and reflex loss in the legs developed in a patient treated for seizures with phenytoin (diphenylhydantoin) for one year. Her serum drug levels had been in the therapeutic range, and no other clinical toxic reactions had been noted. The peripheral neuropathy resolved when phenytoin therapy was discontinued.
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PMID:Reversible subacute peripheral neuropathy induced by phenytoin. 19 Sep 87

Sudden permanent blindness of cerebral origin, in addition to severe abdominal pain, hypertension, convulsions, and peripheral neuropathy developed in a 21-year-old woman, a victim of acute intermittent porphyria. Findings of the pathological examination of the brain showed extensive infarction in both occipital lobes. The pathological changes were consistent with anoxia. We discuss and review the literature of the possibility of "vasospasm" of both posterior cerebral arteries. Follow-up studies with serial EEG showed either focal epileptogenic activity or diffuse slow waves. The most consistent epileptic discharges were found in the occipital regions. The favorable response to the treatment of seizures with carbamazepine in this patient might encourage further clinical trials.
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PMID:Blindness of cerebral origin in acute intermittent porphyria. Report of a case and postmortem examination. 19 74

A 27-year-old man had limb weakness, short stature, neurosensory hearing loss, seizures, mild peripheral neuropathy, neurogenic bladder, elevated cerebrospinal fluid (CSF) protein content, primary lactic acidemia, and basal ganglia calcification. Muscle biopsy revealed numerous ragged-red fibers. On electronmicroscopy there were mitochondrial alterations, including many intramitochondrial inclusions. The mother of the patient had Vogt-Koyanagi-Harada syndrome, a combination of rare disorders in the same family that has not been previously described.
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PMID:Lactic acidemia, mitochondrial myopathy, and basal ganglia calcification. 22 42

The responsibility of the folate deficiency in some neuropsychiatric disorders is recent knowledge. The role of the folate on the nervous system is not yet well definite, but the action on the metabolism of the amino-acids, on the purine and the pyrimidine synthesis and on the metabolism of the catecholamins are certainly essential. The neuropsychiatric diseases secondary to the folate deficiency are numerous: dementia, schizophrenia like syndromes, insomnia, irritability, forgetfulness, endogenous depression, organic psychosis, pueperal psychosis, peripheral neuropathy, myelopathy (spinal cord syndrome and/or pyramidal tract damage), restless legs syndrome. Clinically the diagnosis may be difficult with sub acute combined degenration secondary to the pernicious anaemia, and the dosage of the folate (in serum, in red-cells and in cerebrospinal fluid) is necessary. The congenital defects in the uptake or utilization of the folate are associated with neuropsychiatric disturbances. The treatment is easy and safe if the vitamin B12 deficiency is eliminated and if employed with caution in epileptic patients because folate can induced seizures.
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PMID:[Folate and the nervous system (author's transl)]. 22 16

1. Among patients with SLE, 71 (51%) had significant neuropsychiatric problems during the course of the disease. In 52 (37%), the nervous system manifestations were secondary to SLE. 2. The most frequent manifestations were psychiatric dysfunction, seizures, long tract signs, cranial neuropathy, and peripheral neuropathy. 3. Psychiatric abnormalities secondary to SLE were characterized by organic features (present in 22 of 24) and by the association of neurologic lesions which were often diffuse or multifocal. 4. An abnormal cerebrospinal fluid was found in 32% of neuropsychiatric episodes in which specimens were obtained. The most frequently abnormal study was the electroencephalogram (71%), and the least frequent was the brain scan (8%). These studies did not correlate with specific clinical patterns. 5. In 63% of the patients, NP manifestations preceded the diagnosis of SLE or occurred within the first year of diagnosed disease, and in most episodes were associated with evidence of clinical and/or serologic activity of the underlying illness. 6. Only two clinical features showed significant and striking correlations with neuropsychiatric involvement, namely vasculitis and thrombocytopenia. The possible pathogenic implications have been discussed. 7. Only 2 of the 140 patients were felt to have steroid-induced psychoses. In approximately one-half of the NP episodes secondary to SLE, patients were receiving no corticosteriods on presentation. Of those developing while patients were on steroids, the majority occurred on low doses or after tapering from higher levels. 8. The immediate prognosis for improvement in neuropsychiatric function was good with 84% of episodes showing complete or partial resolution. Corticosteroids appeared to be of benefit in a substantial number of patients although their precise role is difficult to quantitate. 9. Five and 10 years survivals for the overall population were 94% and 82%, respectively. There were no significant differences in survival for patients with or without nervous system involvement.
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PMID:Neuropsychiatric manifestations of systemic lupus erythematosus: diagnosis, clinical spectrum, and relationship to other features of the disease. 78 66

Serum levels of IgE, other immunoglobulins and C'3 were measured in 36 MS patients, and the results compared with those of 40 age- and sex-matched patients hospitalized on Neurology Service. Diagnoses among controls included cerebral infarction, cervical spondylosis, nonmigrainous headache, seizure disorders and peripheral neuropathy. Six patients in the MS group and seven in the non-MS group had a past history of allergy to food, drugs, dust or other substances. IgE levels were measured by double-antibody radioimmunoassay. Other immunoglobulins (G, M, D and A) and C'3 were quantitated by Mancini's method. Results indicate that the median IgE and C'3 levels of MS patients were slightly lower than those for non-MS subjects. Concentrations of other immunoglobulins were similar for the two groups. CSF samples from 12 MS and five non-MS patients were studied and none of these contained measureable (greater than 7.5 U/ml) IgE. In view of: 1) recent reports describing mast cells in MS plaques, 2) the suggested role of biogenic amines in the pathogenesis of demyelinating diseases, and 3) because IgE exists in free and cell bound state, it is suggested that tissue surveys of MS plaques for IgE deposits similar to those seen in glomeruli in nephrotic syndromes may provide a clue to the pathogenesis of MS.
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PMID:Circulating IgE, allergy and multiple sclerosis. Serum levels of IgE, other immunoglobulins and complement (C's) in patients with multiple sclerosis in exacerbation and other neurologic diseases. 125 79

Fourteen patients with advanced ovarian cancer received a 72 hour infusion of a new DNA intercalator, crisnatol mesylate, administered intravenously. There was no evidence of antitumor efficacy. A syndrome of nausea and vomiting associated with vertigo, dizziness and ataxia was observed in nearly all patients. Two of the patients developed severe CNS toxicity manifested in one by a grand-mal seizure and in the other by peripheral neuropathy. Further explorations into the potential efficacy of crisnatol mesylate administered intraperitoneally are underway.
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PMID:A phase II study of crisnatol mesylate in patients with ovarian carcinoma. 150 Feb 64

In a retrospective study we investigated the antiviral effect of alpha-interferon in 100 patients with chronic hepatitis B who were treated in controlled trials conducted in Rotterdam (1985-1990). The aim of the treatment was to induce viral latency as indicated by HBeAg seroconversion. Alpha-interferon was administered in a dose of 5 mega-units per day subcutaneously. Sixty-two patients received alpha-interferon for 16 weeks combined with a second antiviral agent (acyclovir or descyclovir) while the other 38 patients were treated with alpha-interferon monotherapy during 20 to 34 weeks. Follow-up continued until 1 year after the start of therapy. Thirty-eight per cent of the patients exhibited an HBeAg seroconversion and 9% exhibited an HBsAg seroconversion indicating a complete eradication of the virus. After 1 year transaminase levels were normalised in 70% of the patients with HBeAg seroconversion compared with 22% in those without seroconversion (p less than 0.05). The combination therapy for 16 weeks and the alpha-interferon monotherapy of longer duration resulted in HBeAg seroconversion rates of 29% and 53%, respectively (p less than 0.05). The predominant adverse effects were fatigue, flue-like illness and leukopenia. Serious side effects such as seizures, psychosis and peripheral neuropathy occurred in seven patients. Side effects led to a dose reduction in 26% of the patients. Alpha-interferon is effective in terminating the virus replication in chronic hepatitis B. However, both the common mild and the uncommon major side effects necessitate intensive patient monitoring during alpha-interferon treatment.
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PMID:[Alpha-interferon antiviral treatment in 100 patients with chronic hepatitis B]. 152 28


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