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)

Cognitive function of patients on monotherapy specific for their epileptic syndrome has been studied infrequently. We evaluated 7 patients with symptomatic localised epilepsies (SEL) on phenytoin aged 30 +/- 12 (mean +/- standard deviation) years, 8 with idiopathic generalised epilepsies on sodium valproate aged 18 +/- 4 years, 16 with SEL on carbamazepine aged 28 +/- 11 years, and 35 healthy controls aged 27 +/- 11 years. All subjects were of normal intelligence, educated appropriately to age, and led productive lives in the community. Two of the patients on carbamazepine and one on valproate had less than five partial, absence or myoclonic seizures monthly, the remaining were controlled. Carbamazepine serum concentrations were 12 +/- 5 micrograms/ml, phenytoin were 23 +/- 7, and valproate were 62 +/- 23 (mean +/- sd). Tests included immediate recall and recognition for pictures, Stroop test, delayed recall and recognition of pictures. Patients on phenytoin and valproate performed significantly worse than controls on immediate recall, and patients on carbamazepine performed significantly worse than controls in Stroop test (p < 0.01). The results indicate relatively minor effects of the epileptic syndromes and of phenytoin, carbamazepine and valproate on cognition of patients with controlled epilepsy leading productive lives in the community. We conclude that the cognitive deficit found in chronic epileptic patients on poly-therapeutic drug regimen must be multifactorial, and that future studies need to control for all possible variables in order to achieve meaningful results.
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PMID:Cognitive functions, epileptic syndromes and antiepileptic drugs. 130 74

This study examined the early and late outcome in head injury patients with focal or multifocal (unilateral or bilateral) brain contusions revealed by computerized tomography (CT) scanning. The outcome was also evaluated in patients hospitalized due to brain concussion. Three months after the injury (the early outcome) 43% of the 86 cases with multifocal contusions on the CT scan were dead. As evaluated by the Glasgow Outcome Scale, all the 57 patients with a focal brain contusion, as well as the 117 cases with brain concussion, made a good recovery or were moderately disabled. The late outcome (1 to 5 years after injury) was evaluated in 78 cases with brain contusion and in 85 cases with brain concussion, and revealed that complaints and impaired adaptive functioning were frequent in both the contusion and concussion group. The occurrence of headache, dizziness and sleep problems did not significantly differ among the various head injury groups. However, focal or multifocal brain contusions on the CT scan increased the frequency of impaired memory, impaired concentration, speech problems, weakness in arms or legs and seizures with loss of consciousness. Cognitive deficits and speech problems were particularly common in patients with a focal contusion in the temporal lobe. The late adaptive and social functioning were most markedly impaired in cases with multifocal bilateral contusions.
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PMID:Early and late outcome in head injury patients with radiological evidence of brain damage. 141 31

To determine the IQ profile of children with epilepsy and the influence of various epilepsy-related variables on IQ scores, we studied 50 children with idiopathic generalized epilepsy of > 1-year duration, 25 of their siblings, and 30 healthy controls. IQ assessments were made with Malin's Indian modification of the Wechsler Intelligence Scale for Children. The mean +/- SD IQ scores of children with epilepsy (85.6 +/- 12) and their siblings (93.2 +/- 11) were significantly lower than those of the controls (101.6 +/- 9). The IQ scores of the children with epilepsy were also significantly lower than those of their siblings (p < 0.05). The IQ scores showed a significant correlation with socioeconomic status (SES) score (r = 0.33), a history of status epilepticus (r = -0.38), duration of seizure disorder (r = -0.31), and total number of seizures (r = -0.31). On multiple regression analysis, status epilepticus emerged as the most significant variable, accounting for 14% variance, followed by SES score (9% variance), duration of seizure disorder (6% variance), and sex of the child (5% variance). Genetic or environmental factors that probably lead to cognitive deficit in children with epilepsy and their siblings require further study.
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PMID:Determinants of IQ profile in children with idiopathic generalized epilepsy. 146 72

Quantitative measurements have indicated that heredity, cerebral damage, psycho-social aspects, ictal and inter-ictal phenomena and antiepileptic drugs may interfere in the cognitive dysfunction of epileptic patients. In the present study objective methods included immediate and late recall and recognition of pictures, Stroop test and auditory selection. Twenty patients with symptomatic localized epilepsy aged 17-52 years (27 +/- 10, mean +/- sd) were compared to age and socially matched healthy controls. Patients were on therapeutic serum concentrations (25 +/- 12 mu/ml) of phenobarbitone and had active epilepsy with 1.94 generalized tonic-clonic, 0.85 simple partial and 6.28 complex partial seizures monthly (means). Patients performed worse than controls in all 6 tests (p less than 0.05 to p less than 0.001), indicating a generalized cognitive deficit related to seizures and/or barbiturate therapy. We suggest further studies should be carried out in populations with uniform monotherapeutic regimens and epileptic syndromes in order to isolate factors related to the cognitive dysfunction of epileptic patients.
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PMID:Cognitive functions of epileptic patients on monotherapy with phenobarbitone and healthy controls. 181 Feb 28

Mesial temporal sclerosis (MTS) is probably the most common symptomatic pathologic entity--alone or mixed with other pathologic features--for seizures of temporal lobe origin. The pathophysiology of MTS, including any genetic influence, needs clarification. A characteristic ictal expression for seizures of MTS origin appears not to exist. The majority of patients (78%) with postresection MTS who are seizure-free have tightly localized interictal abnormalities restricted to F7/F8, Sp1/Sp2, T3/T4, and T5/T6 more than 96% of the time. MRI abnormalities may be seen in 55% of patients with MTS if both "hard" and "soft" criteria are used or in 20% when only "hard" criteria are used. The neuropsychologic evaluation of patients with MTS, which includes intracarotid amobarbital test (IAT), may prove to be increasingly useful in identifying patterns of cognitive deficit that correlate with enhancement of both lateralizing and localizing preoperative information.
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PMID:Mesial temporal sclerosis: pathogenesis, diagnosis, and management. 222 72

The cognitive deficit often associated with epilepsy is attributable to the presence and interaction of several factors but whether recurrent subclinical spike-wave discharges interfere with cognitive development is not yet clear. In the present study, the presence of subclinical discharges proved to be significantly associated with lower than average Full-Scale Intelligence Quotient (IQ), Verbal IQ and Performance IQ scores (Wechsler Intelligence Scale for Children) in comparison with patients not presenting EEG abnormalities during test. These findings confirm the adverse effect both of generalized and focal EEG epileptiform abnormalities, even if unaccompanied by overt seizures.
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PMID:Neuropsychological correlates of subclinical paroxysmal EEG activity in children with epilepsy. 1: Qualitative features (generalized and focal abnormalities). 279 57

The clinical spectrum of autism spans a broad range of functions, but the core symptoms remain the same regardless of the intelligence of the child: the autistic type of social deficit that ranges from a lack of inclination to relate to extreme difficulty with the mechanics of social interactions, a global communication deficit that involves both verbal and nonverbal modes, and a severe cognitive deficit involving concept formation (abstraction) that is combined with an exceptional memory for factual information. These symptoms may vary dramatically in severity, but the basic deficits are identifiable regardless of IQ. Under-recognition of autism is a major problem at all IQs, but especially in patients with IQs above 50. No drugs have been found to significantly improve the core deficits in autism. Antipsychotics should be avoided except for short-term use. Antidepressants, anxiolytics, and anticonvulsants are important in the treatment of depression, affective modulation, situation-related stress, and seizures. Intensive social skills training is assuming a prominent role in behavior modification programs, and success with higher-functioning autistic children suggests that outcome can be improved by intensive training. The neurobiology of autism has also undergone dramatic changes. The psychogenic theories of etiology have been completely invalidated. Autism is now considered to be a neurological disorder resulting from an error in brain development. The precise location and nature of this deficit are still being actively debated and investigated. One theory emphasizes a dysfunction of the limbic system that results in an impairment in the acquisition of information. A second theory proposes a primary role for dysfunction of the cortical association network responsible for the processing of information.
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PMID:New perspectives in autism, Part II: The differential diagnosis and neurobiology of autism. 306 39

A 55 year old man developed an acute confusional state with grossly impaired short-term memory accompanied by a Status Petit Mal epilepsy pattern on EEG, one to two weeks after abruptly discontinuing a large amount of oxazepam and a smaller amount of alcohol. Both his mental status and EEG pattern normalized markedly after intravenous diazepam. On 5 year follow-up the patient was seizure-free and medication-free without any significant residual cognitive deficit.
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PMID:Acute confusional state with status petit mal as a withdrawal syndrome--and five year follow-up. 336 42

In a group of 78 children with hydrocephalus in the first months of life, the level and pattern of intelligence were considered in relation to various parameters and symptoms of their condition. These included demography (age, sex, handedness); early developmental status; symptoms (visual, motor, and seizure); formative pathology; type of hydrocephalus; site of CSF obstruction; extent and configuration of cortical thinning; and shunt treatment. The common outcome of early hydrocephalus is an uneven growth of intelligence during childhood, with nonverbal intelligence developing less well than verbal intelligence. The origin of this selective cognitive deficit is in neither the hydrocephalic condition itself nor its treatment, but rather in the developmental brain anomalies and symptoms to which the hydrocephalic child is prone: In children with aqueduct blocks and intraventricular hydrocephalus, a selectively thin vertex and occipital lobe; in any hydrocephalic child, ocular abnormalities, motor deficits, and seizures.
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PMID:The intelligence of hydrocephalic children. 697 94

We present clinical, neuropsychological, and neuropathologic data on a large pedigree including 34 subjects with early-onset progressive dementia. The mean (+/- SD) age at onset was 46 +/- 3.5 years and the mean age at death 52.6 +/- 5.7 years. Twelve patients were clinically diagnosed as having probable Alzheimer's disease (AD) according to the NINCDS-ADRDA criteria. Neuropsychological evaluation, performed at a moderate stage of the disease, was available in six subjects and showed a classic pattern of cognitive deficit. Myoclonus and extrapyramidal signs were common, and seizures were present in all affected subjects. There were neuropathologic changes typical of AD in two brains. A significant lod score of 5.48 was observed at a recombination fraction of theta = 0.0 with the genetic marker D14S43, thereby establishing that the responsible gene was located on chromosome 14q24.3. These results suggest that epilepsy could represent a particular feature in AD families linked to chromosome 14q.
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PMID:A large pedigree with early-onset Alzheimer's disease: clinical, neuropathologic, and genetic characterization. 782 41


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