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)

Six patients with Hashimoto thyroiditis (HT) and associated encephalopathy (HE) are described and compared with 14 well-documented cases retrieved from the literature. HE typically affects patients when they are euthyroid and, in an appropriate clinical situation, antithyroid autoantibodies are the main indicators of HE. Since clinical features of HE are unspecific, other aetiologies such as infectious, metabolic, toxic, vascular, neoplastic, and paraneoplastic causes have to be excluded. Our own six cases and those from the literature show that two types of initial clinical presentation can be differentiated: a vasculitic type with stroke-like episodes and mild cognitive impairment in nine patients, and a diffuse progressive type with dementia, seizures, psychotic episodes or altered consciousness in 11 patients. These types may overlap, particularly in the long-term course without treatment. Response to steroids was usually excellent with complete remission in 80%. Eighteen of the 20 patients were women. Characteristic, though unspecific, findings were abnormal EEG (90%) and CSF (80%). Together with quantitative neuropsychological testing, these proved sensitive for monitoring the efficacy of therapy. Conversely, antithyroid autoantibody titres did not correlate with the severity or type of clinical presentation. The link between HE and HT is not clear. A pathogenetic role for antithyroid autoantibodies in the central nervous system seems unlikely.
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PMID:Encephalopathy associated with Hashimoto thyroiditis: diagnosis and treatment. 886 25

A patient presenting with a severe subacute encephalopathy was shown to be infected with a stealth virus. Although the patient partially recovered, he remained lethargic with cognitive impairment and worsening headaches. Ten months after the onset of his illness, his clinical condition further deteriorated with seizures, coma and death. A brain biopsy revealed vacuolated degenerate neural cells consistent with a stealth viral encephalopathy. Focal perivascular lymphocytic inflammation was present within the leptomeninges and to a lesser extent within the parenchyma of the brain. Vasculitis may occasionally contribute to the complex symptomatology of stealth viral encephalopathy.
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PMID:Stealth viral encephalopathy: report of a fatal case complicated by cerebral vasculitis. 888 69

Seizures and epilepsy in the elderly are an important and increasingly common clinical problem. Major known causes include cerebrovascular disease, brain tumor, degenerative disorders such as Alzheimer disease and cerebral amyloid angiopathy, and toxic-metabolic syndromes such as nonketotic hyperglycemia, postcardiac arrest, and drug-induced seizures. Recognition of seizures may be complicated by relatively unique clinical presentations and differential diagnosis. Nonconvulsive status epilepticus may present as recurrent episodes of confusion. The electroencephalogram is less useful than in the pediatric age group, but has a role in the evaluation of a first seizure and may rarely show characteristic patterns, such as poststroke periodic lateralized epileptiform discharges. Convulsive status, especially that associated with drug toxicity, is associated with increased mortality in the elderly. Pharmacological treatment is complicated by age-related changes in pharmacokinetics and pharmacodynamics and drug-drug and drug-disease interactions. Some of the new antiepileptic drugs may offer advantages for use in the elderly. Oxcarbazepine has fewer drug interactions than carbamazepine, and gabapentin has one, a reduction of felbamate renal elimination. Vigabatrin causes little cognitive dysfunction, while drugs that reduce excitatory amino acid neurotransmission, such as lamotrigine and felbamate, have potentially protective effects in patients with ischemic cerebrovascular disease. The use of barbiturates, primidone, the benzodiazepine clobazam, and the calcium blockers flunarizine and cinnarizine should preferably be avoided in the elderly.
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PMID:Seizures and epilepsy in the elderly. 943 89

Several relationships have been obtained between cognitive impairment and epilepsy-related or treatment-related factors. One of these factors is treatment-related: the central cognitive side effects of the antiepileptic drugs (AEDs). The second and third factors are disease-related factors, i.e., the effect of the seizures and underlying epileptiform discharges in the brain and the localization of the epileptogenic focus in specific areas of the brain. Although most cognitive problems have a multifactorial origin and often several factors combined are responsible for the "make-up" of a cognitive problem, we have attempted to isolate one factor: the effect of seizures and epileptiform EEG discharges on cognitive function. Several studies show the impact of ictal activity, but special attention is required for the postictal and interictal effects of epilepsy on cognitive functions. This may explain substantial cognitive impairments in children with subclinical epileptiform discharges or with infrequent subtle seizures.
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PMID:Effect of seizures and epileptiform discharges on cognitive function. 909 61

While disorders of neuronal migration are associated with as much as 25% of recurrent childhood seizures, few of the genes required to establish neuronal position in cerebral cortex are known. Subcortical band heterotopia (SBH) and lissencephaly (LIS), two distinct neuronal migration disorders producing epilepsy and variable cognitive impairment, can be inherited alone or together in a single pedigree. Here we report a new genetic locus, XLIS, mapped by linkage analysis of five families and physical mapping of a balanced X;2 translocation in a girl with LIS. Linkage places the critical region in Xq21-q24, containing the breakpoint that maps to Xq22.3-q23 by high-resolution chromosome analysis. Markers used for somatic cell hybrid and fluorescence in situ hybridization analyses place the XLIS region within a 1 cM interval. These data suggest that SBH and X-linked lissencephaly are caused by mutation of a single gene, XLIS, that the milder SBH phenotype in females results from random X-inactivation (Lyonization), and that cloning of genes from the breakpoint region on X will yield XLIS.
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PMID:Linkage and physical mapping of X-linked lissencephaly/SBH (XLIS): a gene causing neuronal migration defects in human brain. 909 58

To study the cognitive effects of diphenylhydantoin (PTH), 17 patients of simple partial or generalised tonic clonic seizure, who were on PTH monotherapy for at least 6 months were included. None of them had a seizure in last one month and their CT scans were normal. Serum PTH levels of these patients were in the therapeutic range (10.2-17.7 micrograms/ml). The clinical signs of PTH toxicity in the form of gingival hyperplasia and cerebellar ataxia were present in 1 patient only. In 3 patients memory quotient (MQ) and Benton visual retention test (BVRT) scores were marginally abnormal but the group difference in the clinical psychometric tests were not significant. P3 latency was also normal in all the patients. In the therapeutic range, PTH does not seem to produce significant cognitive dysfunction.
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PMID:Clinical psychometry and P3 in patients on phenytoin monotherapy. 909 77

To clarify the relationship between cognitive function and clinical seizures, auditory event-related potentials (P300) were examined in 72 patients (185 trials) with partial epilepsy. Twenty-six patients (67 trials) had idiopathic partial epilepsies (IPE), and 46 (118 trials) symptomatic or cryptogenic partial epilepsies (SPE). In this study, to rule out the effects of epileptogenesis and other factors, we only examined patients with partial epilepsies undergoing carbamazepine (CBZ) monotherapy at doses of less than 16 mg/kg/day. The results were: 1) the mean age-corrected P300 latency in the patients with SPE (394 +/- 38 msec) was significantly prolonged compared with that in the patients with IPE (378 +/- 28). 2) The prolongation of the P300 latency had no relationship to the seizure frequency, seizure type or seizure duration. 3) In both epileptic groups, there was no significant correlation between the seizure-free period and the age-corrected P300 latency. Our results suggest that the effect of clinical seizures on the cognitive function may be relatively little, and that the cognitive dysfunction in partial epilepsies may mainly originate from epileptogenesis or other factors.
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PMID:Epileptic seizures and event-related potentials (P300) in childhood partial epilepsies. 913 74

A number of treatment options are currently available for the medical management of epilepsy. Conventional antiepileptic drugs (AEDs) include phenytoin, carbamazepine, valproic acid, ethosuximide, barbiturates, and benzodiazepines. Although these drugs control seizures, they may also cause blood dyscrasias, sedation, and cognitive impairment. Felbamate, gabapentin, lamotrigine, and vigabatrin are new AEDs believed to cause fewer side effects than conventional medications. Felbamate, however, has been linked with substantially increased incidence of aplastic anemia, and the other new AEDs have been studied for relatively short periods of time. Ketogenic diets, comprised of foods high in fat and low in protein and carbohydrate content, have been reported to improve seizure control. However, these diets are widely acknowledged to be unpalatable, making sustained compliance with dietary restrictions difficult. To promote long-term control of seizures, physicians must consider the side effects of therapeutic interventions for epilepsy, as well as their anticonvulsant efficacy.
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PMID:Pharmacologic and dietary therapies in epilepsy: conventional treatments and recent advances. 916 61

While many children with recurrent seizures have a good prognosis, a small percentage of children with intractable epilepsy have a more ominous course with a gradual decline in cognitive abilities over time. While the reasons for this cognitive decline may be multifactorial, there is evidence both from human and animal studies that recurrent seizures may lead to gradual cognitive impairment in some children. Laboratory studies have also demonstrated that recurrent seizures can lead to deficits in learning and memory as well as structural changes in the brain. It is important for the clinical to be aware of gradual declines in intelligence that may occur over time.
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PMID:[Consequences of recurrent seizures during development]. 920 3

The Neurotoxicity Scale was devised as a patient-based report scale to assess the adverse effects of antiepileptic drugs on cognitive function. In a previous report we reported the clinical validity of the scale, tested in a double-blind randomized study, using a benzodiazepine in normal volunteers. In the present study, the clinical sensitivity, construct validity and reliability of the scale was tested in patients with epilepsy. Patients (n = 189), selected from both participating centres, representative for the patients with chronic epilepsy were included in the study. Reliability was tested with Cronbachs alpha and yields an almost maximal score (.95). Clinical sensitivity was compared with the previous normal volunteer study and was evaluated as satisfactory. Construct validity showed a five-factor structure, explaining 66.5% of the variance, with 'fatigue and slowing' as the dominant factor. In line with the assumptions for this scale and with the results obtained in normal volunteers, the scale appears to be unsuitable for differential assessment of type or severity of drug-induced impairment. The most valid primary outcome measure is the overall score that renders a global ('all or nothing') evaluation indicating that a subject experiences cognitive impairment and associates this with the antiepileptic treatment. Other factors that may impair cognitive function, such as seizure frequency do not influence this score. The scale has therefore maximal applicability as a screening instrument in outpatient practice and in early (phase II, IIIa) drug trials.
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PMID:The Neurotoxicity Scale--II. Results of a patient-based scale assessing neurotoxicity in patients with epilepsy. 923 50


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