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

Diffuse cerebral atrophy (CA), a frequent computed tomography (CT) finding in late-onset epilepsy, is sometimes of unknown origin or cryptogenous (CCA). From a series of 228 patients with late-onset epilepsy with diffuse CA, we excluded patients with a presumed etiology. The remaining 73 (36.8%) patients were studied for a mean of 7.2 years; 15.1% had a family history of epilepsy. CCA was cortical in 50.7%, subcortical in 6.8%, and corticosubcortical in 42.5%. Seizures, generalized in 71.2%, and focal in 28.8% were generally of low occurrence with good therapeutic response. Background EEG activity was normal in most patients. During follow-up, the clinical and EEG features remained unchanged. In a control series of 92 nonepileptic subjects with diffuse CA, CCA was noted in only 4 (4.3%). No variation in grade or distribution of CCA was noted in repeated CT scans of the two groups, except in 2 epileptic patients. Psychometric tests demonstrated no cognitive impairment during evolution. The results appear to confirm the hypothesis that late-onset epilepsy associated with CCA constitutes a syndrome that is related to the characteristics of the atrophy.
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PMID:Late-onset epilepsy and diffuse cryptogenous cerebral atrophy. 139 23

The postconcussion syndrome refers to a large number of symptoms and signs that may occur alone or in combination following usually mild head injury. The most common complaints are headaches, dizziness, fatigue, irritability, anxiety, insomnia, loss of consciousness and memory, and noise sensitivity. Mild head injury is a major public health concern because the annual incidence is about 150 per 100,000 population, accounting for 75% or more of all head injuries. The postconcussion syndrome has been recognized for at least the last few hundred years and has been the subject of intense controversy for more than 100 years. The Hollywood head injury myth has been an important contributor to persisting skepticism and might be countered by educational efforts and counter-examples from boxing. The organicity of the postconcussion syndrome has now become well documented. Abnormalities following mild head injury have been reported in neuropathologic, neurophysiologic, neuroimaging, and neuropsychologic studies. There are multiple sequelae of mild head injury, including headaches of multiple types, cranial nerve symptoms and signs, psychologic and somatic complaints, and cognitive impairment. Rare sequelae include hematomas, seizures, transient global amnesia, tremor, and dystonia. Neuroimaging and physiologic and psychologic testing should be used judiciously based on the problems of the particular patient rather than in a cookbook fashion. Prognostic studies clearly substantiate the existence of a postconcussion syndrome. Manifestations of the postconcussion syndrome are common, with resolution in most patients by 3 to 6 months after the injury. Persistent symptoms and cognitive deficits are present in a distinct minority of patients for additional months or years. Risk factors for persisting sequelae include age over 40 years; lower educational, intellectual, and socioeconomic level; female gender; alcohol abuse; prior head injury; and multiple trauma. Although a small minority are malingerers, frauds, or have compensation neurosis, most patients have genuine complaints. Contrary to a popular perception, most patients with litigation or compensation claims are not cured by a verdict. Treatment is individualized depending on the specific complaints of the patient. Although a variety of medication and psychologic treatments are currently available, ongoing basic and clinical research of all aspects of mild head injury are crucial to provide more efficacious treatment in the future.
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PMID:The postconcussion syndrome and the sequelae of mild head injury. 143 59

This is a descriptive study of 50 randomly selected male patients retained in a maximum-security state hospital for mentally disordered offenders. Data regarding the prevalence of several indicators of potential organic brain dysfunction are presented, including: (1) a diagnosis of any organic brain disorder, (2) a history of severe head injury with loss of consciousness, (3) a history of seizure activity, (4) evidence of cognitive impairment, (5) abnormal neurological findings, and (6) other relevant neurodiagnostic or historical findings. Results show that multiple indicators of potential brain dysfunction were present in 64% of the cases. At least one indicator of potential brain dysfunction was present for 84% of the subjects. Subjects with a diagnosis or history suggesting brain dysfunction were significantly more likely to have been indicted for violent criminal charges (p = 0.01). Implications of these findings for clinical treatment and forensic science decision-making are discussed.
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PMID:Estimating the prevalence of organic brain dysfunction in maximum-security forensic psychiatric patients. 162 82

Extensive electrical stimulation of the perforant pathway input to the hippocampus results in a characteristic pattern of neuronal death, which is accompanied by an impairment of cognitive functions similar to that seen in human temporal lobe epilepsy. The excitotoxic hypothesis of epileptic cell death [Olney, J. W. (1978) in Kainic Acid as a Tool in Neurobiology, eds. McGeer, E., Olney, J. W. & McGeer, P. (Raven, New York), pp. 95-121; Olney, J. W. (1983) in Excitotoxins, eds. Fuxe, K., Roberts, P. J. & Schwartch, R. (Wenner-Gren International Symposium Series, Macmillan, London), Vol. 39, pp. 82-96; and Rothman, S. M. & Olney, J. W. (1986) Ann. Neurol. 19, 105-111] predicts an imbalance between excitation and inhibition, which occurs probably as a result of hyperactivity in afferent pathways or impaired inhibition. In the present study, we investigated whether the enhancement of gamma-aminobutyric acid (GABA)-mediated (GABAergic) inhibition of neurotransmission by blocking the GABA-metabolizing enzyme, GABA transaminase, could influence the histopathological and/or the behavioral outcome in this epilepsy model. We demonstrate that the loss of pyramidal cells and hilar somatostatin-containing neurons can be abolished by enhancing the level of synaptically released GABA, and that the preservation of hippocampal structure is accompanied by a significant sparing of spatial memory as compared with placebo-treated controls. These results suggest that enhanced GABAergic inhibition can effectively block the pathophysiological processes that lead to excitotoxic cell death and, as a result, protect the brain from seizure-induced cognitive impairment.
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PMID:Enhanced GABAergic inhibition preserves hippocampal structure and function in a model of epilepsy. 165 57

A wide cavum septum pellucidum defined as a separation of greater than 1 cm of the leaves occurs uncommonly. Nine children with wide cavum septum pellucidum were studied; 8 were abnormal. Observed abnormalities included cognitive impairment (8), seizures (4), hypoplasia of the corpus callosum (4), optic nerve hypoplasia (2), and growth failure (4). The incidence of intellectual dysfunction, the association with midline anomalies of the brain, and growth failure all suggest that wide cavum septum pellucidum may represent part of a spectrum of midline brain anomalies.
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PMID:Wide cavum septum pellucidum: a marker of disturbed brain development. 170

Children with epilepsy are at significant risk for cognitive impairment and behavioral abnormalities. In most children with epilepsy, the likely reason for cognitive impairment is the underlying pathology responsible for the seizures. However, there is considerable controversy about whether seizures per se can cause brain damage or increase subsequent susceptibility to seizure. Although some longitudinal studies have related a decline in intellectual abilities to continued seizures, other studies indicate that treatment with antiepileptic drugs or progression of the encephalopathic process is responsible for the decline. Both clinical and animal studies have focused on the long-term effects of seizures on the developing brain. Whereas prolonged seizures may cause permanent neurologic sequelae in the mature animal, the immature brain may be more resistant to the long-term sequelae of seizures.
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PMID:Do seizures cause brain damage? 174 67

The long-term effects of seizures on the developing brain is a difficult clinical problem to study since cognitive impairment and behavioral abnormalities may be related to the etiological agent responsible for the seizures, age at time of onset of seizures, the type, frequency, or duration of the seizures, or the antiepileptic drugs used to treat the seizures. Many of these variables can be eliminated by using animal models of epilepsy. Work in our laboratory using the kainic acid (KA) model has demonstrated that status epilepticus in prepubescent and mature rats leads to significant deficits in memory, learning and behavior as adults when compared to control littermates without seizures. These rats also had a high incidence of spontaneous recurrent seizures (SRS) and an increased susceptibility to seizures using kindling and flurothyl. However, younger animals (less than or equal to 20 day old) with KA-induced seizures of similar severity were not associated with later neurological deficits. The immature animals also had a low rate of SRS and did not differ from controls in susceptibility to kindling or flurothyl. Studies using the continuous hippocampal stimulation model of epilepsy have also demonstrated that prolonged seizures in the developing brain are less severe than those in the mature animal. The pathophysiological mechanisms that "protect" the young brain from long-term detrimental effects of prolonged seizures are unknown.
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PMID:The long-term effects of seizures on the developing brain: clinical and laboratory issues. 181 Jan 53

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

Nineteen cases are described, including 12 cases from three different families and 7 nonfamilial cases, in which multisystem neurological disease was associated with acanthocytosis in peripheral blood and normal plasma lipoproteins. Mild acanthocytosis can easily be overlooked, and scanning electron microscopy may be helpful. Some neurologically asymptomatic relatives with significant acanthocytosis were identified during family screening, including some who were clinically affected. The mean age of onset was 32 (range 8-62) yrs and the clinical course was usually progressive but there was marked phenotypic variation. Cognitive impairment, psychiatric features and organic personality change occurred in over half the cases, and more than one-third had seizures. Orofaciolingual involuntary movements and pseudobulbar disturbance commonly caused dysphagia and dysarthria that was sometimes severe, but biting of the lips or tongue was rarely seen. Chorea was seen in almost all symptomatic cases but dystonia, tics, involuntary vocalizations and akinetic-rigid features also occurred. Two cases had no movement disorder at all. Computerized tomography often demonstrated cerebral atrophy. Caudate atrophy was seen less commonly, and nonspecific focal and symmetric signal abnormalities from the caudate or lentiform nuclei were seen by magnetic resonance imaging in 3 out of 4 cases. Depression or absence of tendon reflexes was noted in 13 cases and neurophysiological abnormalities often indicated an axonal neuropathy. Sural nerve biopsies from 3 cases showed evidence of a chronic axonal neuropathy with prominent regenerative activity, predominantly affecting the large diameter myelinated fibres. Serum creatine kinase activity was increased in 11 cases but without clinical evidence of a myopathy. Postmortem neuropathological examination in 1 case revealed extensive neuronal loss and gliosis affecting the corpus striatum, pallidum, and the substantia nigra, especially the pars reticulata. The cerebral cortex appeared spared and the spinal cord showed no evidence of anterior horn cell loss. Two examples of the McLeod phenotype, an X-linked abnormality of expression of Kell blood group antigens, were identified in a single family and included 1 female. The genetics of neuroacanthocytosis are unclear and probably heterogeneous, but the available pedigree data and the association with the McLeod phenotype suggest that there may be a locus for this disorder on the short arm of the X chromosome.
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PMID:Neuroacanthocytosis. A clinical, haematological and pathological study of 19 cases. 199 79

Specific cognitive abilities and motor function were investigated at 5.5 years in 104 children with epileptic mothers and in 105 control children, all with normal general intelligence. The majority (89 per cent) of the children of epileptic mothers had been exposed to anti-epileptic drugs during pregnancy, most commonly phenytoin (69 per cent). Maternal seizures had occurred during pregnancy in 52 per cent. A significant difference, with poorer performance in the study group, was found in block design (WPPSI) and auditory closure (ITPA). Significantly more study than control children had some type of specific cognitive dysfunction. Within the study group, increased risk was associated with maternal partial seizures, with seizures occurring during pregnancy, and with low paternal education, but not with exposure to anti-epileptic drugs. Three possible mechanisms of this effect are suggested: subtle brain-damage associated with fetal asphyxia during the mothers' generalized convulsions; genetically transmitted brain abnormalities; and psychosocial disadvantage limiting partner choice.
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PMID:Specific cognitive dysfunction in children with epileptic mothers. 211 15


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