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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sparganosis is a rare infection caused by a tapeworm larva from the genus Spirometra. A 21-year-old Indian man presented with an 18-month history of episodic confusion followed by a grand mal seizure. Computed tomography and magnetic resonance imaging of the brain confirmed the presence of a lesion of the left occipital lobe. Subsequent stereotactic biopsy revealed a plerocercoid larva or sparganum. Surgical resection resulted in cure. This case prompted a review of the literature on central nervous system sparganosis. Altogether, 17 other cases of primary cerebral sparganosis have been reported previously. Seizures, headache, and focal neurologic signs are common at presentation. Neuroradiologic imaging is sensitive but not specific for the identification of lesions. Enzyme-linked immunosorbent assay of cerebrospinal fluid or serum may be diagnostically helpful. However, the diagnosis is generally made after surgical resection, which is usually curative.
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PMID:Cerebral sparganosis: case report and review. 201 16

Within the last four years, we have observed five patients with epidemiological, clinical, and serological features that were consistent with Q fever meningoencephalitis. Attempts to isolate Coxiella burnetii from the cerebrospinal fluid of two patients were unsuccessful. Neurological features ranged from coma, general seizures, confusion, to palsy and meningitis. All patients were febrile. These patients were neuroradiologicaly investigated. Since 1984, four other cases have been reported in the literature. Antibiotics with good penetration into the cerebrospinal fluid, such as new quinolones, may be useful for treatment of confirmed cases. Q fever should be considered as a possible etiology of meningitis in endemic areas, and diagnosis should be confirmed by serology.
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PMID:Q fever meningoencephalitis in five patients. 204 9

Ifosfamide-associated central nervous system toxicity has been reported in 5% to 30% of patients treated with ifosfamide. Its pattern is characterized by metabolic encephalopathy with confusion, blurred vision, mutism, auditory or visual paranoid hallucinations, seizures, and rarely coma. The biochemical cause of the neurotoxicity is not understood completely, but it is thought to result from an accumulation of drug metabolites with direct central nervous system effects. A case of ifosfamide neurotoxicity is reported that had unusual extrapyramidal features in a patient treated with a 5-day course of infused ifosfamide. Although usually spontaneously reversible with cessation of drug administration, ifosfamide neurotoxicity occasionally has been associated with prolonged psychopathologic sequelae. Death from irreversible encephalopathy has also been reported rarely. The authors believe that classic extrapyramidal symptoms should be considered to be a part of the neurotoxic profile of ifosfamide.
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PMID:Ifosfamide extrapyramidal neurotoxicity. 142 8

Severe complications involving the central nervous system occurred in 7 of 36 children (19%) after renal transplantation. The children, aged 1.6-13.1 years at transplantation were treated with ciclosporin and prednisolone. Six of them had azathioprine as well. The neurological symptoms consisted of seizures, drowsiness, confusion, hallucinations, visual disturbances, and mental changes. In all cases electroencephalograms were severely pathological, showing diffuse abnormalities with or without focal abnormalities and epileptic activity. In all but one case the ciclosporin trough blood levels were within the therapeutic range. Blood glucose and electrolytes were normal. Several factors might contribute to the central nervous system complications: ciclosporin, corticosteroids, hypertension, rejection, and as yet unknown ones.
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PMID:Central nervous system complications in children treated with ciclosporin after renal transplantation. 208 97

Two patients developed clinical and laboratory evidence of systemic lupus erythematosus (SLE) during treatment with valproate (VPA) preparations. The first patient, a 47-year-old man, had fever, malaise, and thrombocytopenia 1 month after VPA was added to phenytoin (PHT) and primidone (PRM). He developed high titers of antinuclear antibodies (ANA) and anti-DNA antibodies, and hypocomplementemia. After discontinuation of PHT and VPA, steroid and immunoglobulin treatment was required for 4 weeks before his condition improved. The second patient, a 28-year-old woman, had been followed for idiopathic leukopenia for 3 years and had previously experienced fever and lymphadenopathy from PHT. After 4 months of divalproex therapy, she developed confusion, joint pain, and a dramatic increase in seizure frequency. She also developed high titers of ANA and anti-DNA antibodies and hypocomplementemia, along with a further decrease in white blood cell (WBC) count. These responded to steroid therapy and withdrawal of divalproex. Three months later, reintroduction of divalproex was followed by a return of ANA in low titer, which resolved after discontinuation. We believe that VPA may have caused true SLE in these patients, one of whom was probably predisposed.
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PMID:Possible induction of systemic lupus erythematosus by valproate. 211 70

Nosological confusion within the epilepsies with myoclonic manifestations occurring in early life has led several epileptologists to separate more rigorously true myoclonic seizures from pseudomyoclonic ones and to identify clusters of homogeneous parameters that may lead to the formulation of syndromatic groupings. In recent years, four neonatal, infantile, and early myoclonic syndromes have been proposed: early myoclonic encephalopathy (EME), early infantile epileptic encephalopathy (EIEE), benign infantile myoclonic epilepsy (BIME), and severe infantile myoclonic epilepsy (SIME). These are reviewed critically, historically, and in the context of personal observations. The author's conclusions are that there is some justification to support, provisionally, a nosological place for the EME syndrome, that a nosologically separate position for the EIEE syndrome appears less firm, and that it seems safer to consider it at this time as an early variant of the West syndrome. From personal observations it appears that BIME and SIME, while justifiably constituting recognizable entities, may best be combined into a single syndrome of "infantile myoclonic epilepsy following febrile convulsions," with variable clinical outcomes.
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PMID:Early myoclonic encephalopathy, early infantile epileptic encephalopathy, and benign and severe infantile myoclonic epilepsies: a critical review and personal contributions. 212 Feb 81

It has been suggested from studies of patients with progressive myoclonus epilepsy that the term Ramsay Hunt syndrome should be abandoned, as its use has led to nosologic confusion, and because, in the light of modern diagnostic techniques, the majority of cases can be allocated to specific disease categories, chiefly, Unverricht-Lundborg disease (Baltic myoclonus) and mitochondrial encephalomyopathy. Review of 30 cases of this syndrome, defined as progressive ataxia and myoclonus and infrequent seizures in the absence of dementia, showed that a clinical or biochemically supported diagnosis could not be made in 43%. This low diagnostic yield probably reflects differences in ascertainment of patients; those described here were referred with a syndrome of progressive myoclonic ataxia (the Ramsay Hunt syndrome) rather than progressive myoclonus epilepsy. These two syndromes share common causes, but a smaller proportion of patients with progressive myoclonic ataxia can currently be diagnosed precisely during life.
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PMID:Progressive myoclonic ataxia (the Ramsay Hunt syndrome). 212 Nov 21

The Lennox-Gastaut syndrome (LGS), although described earlier, was first accepted in 1966 as a form of severe childhood epileptic encephalopathy, characterized by refractory epileptic seizures of diverse types, typical EEG abnormalities and slow mental development. This condition, however, is surrounded by controversy as the clinical criteria used by various authors to define it are quite different. It is very likely that this eponym has been used to harbour distinct epileptic conditions, all of which have in common a slow spike and wave complex in their EEG recording. Despite the fact that one of the hallmarks of LGS is an onset in early childhood, to add to the confusion, some cases of a LGS-like condition with onset in adulthood have been described. We report here one such case: a 28 year old man whose LGS-like condition started after severe head trauma at the age of 20. In addition we briefly review the difficulties in making this diagnosis, using this case to illustrate these aspects.
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PMID:[Lennox-Gastaut syndrome of late onset? Report of a case]. 212 96

An acute psychosis characterized by auditory hallucinations and paranoid delusions developed in a 19-year-old man with temporal lobe epilepsy after he had a cluster of seizures when antiepileptic drugs (AEDs) had been gradually discontinued. Continuous sterotactic depth and epidural EEG recordings confirmed that this was a postictal rather than an ictal event. Acute postictal psychosis is a self-limited condition phenomenologically distinct from ictal or postictal confusion.
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PMID:Acute postictal psychosis: a stereo EEG study. 218 Jun 91

A 15-year-old boy with non-T ALL in early 2nd remission was autografted using a regimen with busulphan 4 mg/kg/day, po, from day -9 to -6, and cyclophosphamide 50 mg/kg/day, iv, from day -5 to -2. During busulphan administration he experienced a few generalized seizures, and starting on day 25 post ABMT he developed a progressively severe neurological symptomatology characterized by nystagmus, right VIth cranial nerve palsy, truncal ataxia and, finally, confusion and coma. MRI showed lesions in the periaqueductal gray matter, thalamus, mammillary bodies and putamen. Within 24 hours of treatment with thiamine he improved dramatically, but during the following weeks permanent neurologic damage with memory deficit, truncal ataxia and nystagmus became evident. To our knowledge this is the first case of Wernicke's encephalopathy reported after BMT. We suspect in this case a contribution of busulphan to the development of the syndrome.
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PMID:Wernicke-like encephalopathy after autologous bone marrow transplantation. 222 27


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