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)

Memory impairment in a 63-year-old man was the most prominent expression of partial epileptic seizures from the temporal lobe, probably resulting from a head injury. Treatment with antiepileptic drugs resulted in complete recovery. This case illustrates that epilepsy should be considered in the differential diagnosis in elderly patients with an isolated memory disorder. The diagnosis is made by clinical methods and may be confirmed by electroencephalography.
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PMID:[Reversible memory disorders in an older patient caused by epilepsy]. 1074 49

We describe 21 affected individuals from a kindred with early-onset autosomal dominant familial Alzheimer's disease caused by an intronic presenilin-1 mutation (in intron 4). Mean age at onset of symptoms was 37.4 years [95% confidence interval (CI): 36.6-38.2 years], mean age at death was 44.7 years (95% CI: 43.1-46.3 years) and mean duration of illness was 7.3 years (95% CI: 5.9-8.7 years). Myoclonus and seizures were prominent features of this pedigree. In the four cases for whom neuropsychometric data were available, verbal memory impairment preceded visual memory deficits; naming was relatively preserved until late in the disease. One of these four cases underwent serial volumetric MRI scans demonstrating in vivo brain tissue loss of 3.9% (38.9 ml, annualized rate of atrophy: 1. 7%) over 22 months of follow-up. The four individuals who had necropsies demonstrated the neuropathological hallmarks of Alzheimer's disease. Apolipoprotein E (APOE) status was assessed in five individuals: the case with the youngest age at onset at 33 years of age was found to be homozygous epsilon4/epsilon4, > 1 SD below the mean age of onset for those of known APOE genotype (36.4 +/- 2.3 years, mean +/- SD), and > 2 SDs below the mean age of onset for the pedigree as a whole (37.4 +/- 1.7 years, mean +/- SD). APOE genotype may therefore modulate age at onset in this pedigree.
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PMID:Alzheimer's disease due to an intronic presenilin-1 (PSEN1 intron 4) mutation: A clinicopathological study. 1077 35

Cyclosporine (CSP) is the most frequently used immunosuppressive agent for prevention of graft versus host disease (GVHD) in allogeneic bone marrow transplantation (BMT). Some adverse effects such as hepatic and renal toxicity have been frequently encountered, but central nervous system (CNS) toxicity caused by CSP is rare. We report an adult male patient with acute myeloid leukemia who developed CSP-induced encephalopathy under treatment for allogeneic BMT from an unrelated donor. Methotrexate and CSP were used for GVHD prophylaxis. Leukocyte and platelet engraftment were successfully achieved on days 21 and 24 after BMT, respectively. Abrupt onset of mental confusion and disorientation occurred on day 25, followed by a generalized tonic clonic seizure and consciousness disturbance. The whole blood CSP level was 160.65 ng/mL. Magnetic resonance (MR) imaging revealed high signal intensities in the bilateral occipital lobes with predominant involvement of the cortical areas. The patient recovered from the CNS toxicity, but with slight memory impairment, 6 days after CSP was discontinued. When patients receiving CSP treatment for allogeneic BMT develop mental confusion, consciousness disturbance, or seizure, CSP-induced CNS toxicity should be taken into consideration.
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PMID:Cyclosporine-induced encephalopathy in a patient with relapsed acute myeloid leukemia treated with unrelated allogeneic bone marrow transplantation. 1082 Sep 59

The aim of this study was to evaluate the influence of 7-acetyl-5-(4-aminophenyl)-8,9-dihydro-8-methyl-7H-1,3-dioxolo(4,5 H)-2,3-benzodiazepine (LY 300164), a selective non-competitive antagonist at alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate receptors, on the protection provided by diazepam against electrically- and chemically-evoked seizures in rodents. LY 300164 (2 mg/kg) was devoid of any significant action upon each seizure parameter in kindled rats (seizure severity, seizure duration, after-discharge duration). LY 300164 (5 mg/kg) exerted a significant anticonvulsive effect as regards seizure and after-discharge durations. Combined treatment with LY 300164 (2 mg/kg) and diazepam (0.3125-1.25 mg/kg) resulted in the clear-cut anticonvulsive activity. It is noteworthy that the antiseizure potency of the combined treatment (diazepam 1.25 mg/kg plus LY 300164 2 mg/kg) was comparable to that of diazepam (10-20 mg/kg) alone. The combination of diazepam (1.25 mg/kg) with LY 300164 (2 mg/kg) did not induce any significant motor impairment in the rotorod test or memory deficit in the passive-avoidance task. In contrast, diazepam alone (10-20 mg/kg) had pronounced adverse effects in kindled animals. LY 300164 (up to 2 mg/kg) did not influence the threshold for electro- and pentylenetetrazol-induced convulsions but potentiated the anticonvulsive action of diazepam in the maximal electroshock and pentylenetetrazol test in mice, the ED50s of the benzodiazepine being reduced from 13 to 8.7 and from 0.29 to 0.049 mg/kg, respectively. As shown in the passive-avoidance task, combination of LY 300164 (2 mg/kg) with diazepam (8.7 mg/ kg) produced significant motor and long-term memory impairment. Diazepam alone (at the dose equal to its ED50 against maximal electroshock) also caused motor and memory deficits in mice. Interaction at the pharmacokinetic level, at least in plasma, can be excluded, because LY 300164 (2 mg/kg) did not affect the free plasma diazepam concentration. In conclusion, LY 300164 potentiates the protective action of diazepam in some animal models of seizures. This profitable interaction may create a new approach for the treatment of drug resistant epilepsy or status epilepticus.
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PMID:The AMPA/kainate receptor antagonist, LY 300164, increases the anticonvulsant effects of diazepam. 1088 38

The nature of remote memory impairment in patients with medial temporal lobe damage is the subject of some debate. While some investigators have found that retrograde amnesia in such patients is temporally graded, with relative sparing of remote memories (Squire and Alvarez, 1995), others contend that impairment is of very long duration and that remote memories are not necessarily spared (Sanders and Warrington, 1971; Nadel and Moscovitch, 1997). In this study, remote memory was assessed in 25 patients with unilateral temporal lobe epilepsy and 22 non-neurologically impaired controls using the Autobiographical Memory Interview (Kopelman et al., 1989). Results indicate that patients have impaired personal episodic memory but intact personal semantic memory. The impairment extends even to the most remote time periods in early childhood, long before seizure onset in many patients. As well, patients awaiting temporal lobectomy for control of seizures perform as poorly as those who have already undergone resective surgery. These results support the hypothesis that temporal lobe damage or dysfunction, caused by recurrent seizures or surgical excision, results in extensive retrograde amnesia for personal episodic memories. Interestingly, patients with radiological evidence of hippocampal sclerosis were not significantly more impaired than those without obvious sclerosis. These results indicate that even minimal damage to medial temporal lobes results in significant impairment to autobiographical episodic memory. These findings are more compatible with a memory loss or retrieval deficit rather than a consolidation account of remote memory impairment.
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PMID:Remote episodic memory deficits in patients with unilateral temporal lobe epilepsy and excisions. 1090 28

Little is known about the differential long-term outcome from surgical and nonsurgical therapy in patients with chronic epilepsy. In the present study, 161 surgically or nonsurgically treated patients with drug-resistant temporal lobe epilepsy (TLE) were re-evaluated according to a detailed clinical, neuropsychological, and psychosocial protocol with a mean follow-up interval of 58 months. Freedom from seizures was achieved in 64% of the surgical group; yet 23% of the nonsurgical patients became seizure-free as a result of modifications in drug therapy. Generally, socioeconomic development was poorer in nonsurgical than in surgical patients. Freedom from seizures, employment, and the absence of depression were significant determinants of better quality of life. As for neuropsychological outcome, verbal memory impairment was common after left-sided temporal resection; however, there was no evidence of a marked progression of cognitive impairment after the first postoperative year. In nonsurgical patients, too, cognitive capacities were surprisingly stable over time, although persisting seizures and good baseline performance predicted a poorer neuropsychological outcome.
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PMID:[Temporal lobe epilepsy: longitudinal clinical, neuropsychological and psychosocial follow-up of surgically and conservatively managed patients]. 1099 13

We present a 35-year-old male patient with intractable temporal lobe epilepsy in whom spitting automatism was documented by ictal recordings during seizures. Spitting is an uncommon automatism and occurs mainly with right-sided, nondominant, temporal focus. However, our patient had left mesial temporal sclerosis with nonverbal memory impairment, but intracarotid amobarbital test demonstrated language and memory dominance on the right hemisphere. The authors feel that this case supports the hypothesis of a nondominant, temporal lobe origin for the spitting automatism.
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PMID:Ictal spitting during a left emporal lobe-originated complex partial seizure: a case report. 1131 24

This study compares the acute cognitive effects of short nonconvulsive seizures with the effects of interictal epileptiform electroencephalographic (EEG) discharges in children. The study is a prospective, standardized, nonrandomized, and open clinical comparative study. Eligible patients were included when they had (a) unclear seizures and fluctuations in cognitive performance and (b) frequent epileptiform EEG discharges in a recent EEG. All children were assessed with EEG/video (Brainlab) simultaneously with computerized neuropsychologic testing (FePsy) assessing motor speed/alertness, mental speed/attention, and memory function. Eleven patients with short nonconvulsive seizures during cognitive testing were included and compared with 11 matched patients with interictal epileptiform EEG discharges during cognitive testing but without seizures. Patients included in both groups had a reconfirmed diagnosis of epilepsy. Cognitive performance for both groups was compared. Statistical analysis showed significant correlations between the number of seizures (during cognitive testing) and impaired alertness and between the duration of the ictal period and memory impairment. Interictal epileptiform EEG discharges do not have an additional independent effect on cognitive function. The results demonstrate the accumulating cognitive effect of seizures and illustrate that frequent seizures, even when these are short in duration and with subtle symptomatology, can have a substantial impact on daily life and can lead to state-dependent learning impairment. Alertness and short-term memory appeared to be the functions that are most vulnerable for the acute effects of seizures.
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PMID:Acute cognitive effects of nonconvulsive difficult-to-detect epileptic seizures and epileptiform electroencephalographic discharges. 1129 17

The concept of the neuromatrix assumes that all behaviours are associated with complex spatiotemporal electromagnetic fields within the brain. The same complex magnetic field can be supported potentially by different mosaics of neuronal associations and result in the same behaviours. In the present study the accuracy of long-term and short-term spatial memory for rats that had been treated with 100 mg/kg of ketamine immediately after the induction of seizures by lithium and pilocarpine did not differ from normal rats despite the conspicuous multifocal neuronal loss. A 30-min. delay of treatment with ketamine resulted in significant memory impairment. Whereas deficits in short-term memory were significantly correlated with cell loss within the CA field of the hippocampus, deficits in long-term memory were related to cell loss within specific thalamic-amygdaloid structures. Implications for the concept of the neuromatrix, if valid, are discussed.
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PMID:Normalization of spatial learning despite brain damage in rats receiving ketamine after seizure-induction: evidence for the neuromatrix. 1129 16

Animal models are crucial for understanding human pathophysiological processes and for understanding how connections are injured, lost, or even regenerated and/or repaired. When animal models are used in conjunction with theoretical computational models, an ideal combination is achieved that potentially yields insight and encourages the formation of new theories concerning connectionism, cognitive functioning, and synaptic mechanisms. Mechanisms regulating glutamate receptor activation and intracellular calcium levels are important for normal synaptic transmission. These mechanisms (and others) are also critical during and after brain injury when the potential exists for these mechanisms to function pathologically. Interestingly enough, the regulation of glutamate receptor activation and intracellular calcium levels is also involved in normal processes of neuronal and synaptic plasticity. In addition, studies have shown that neurotrophins and cytokines, which are released after brain injury, can be neuroprotective and may also be important in synaptic plasticity. Furthermore, synaptic plasticity is a phenomenon thought by many to be necessary for memory encoding. If this is the case, then research described in this review has significant scientific merit concerning plasticity and memory and clinical benefit for understanding pathophysiologic processes associated with brain injury and memory impairment. This paper reviews the application of experimental animal models of brain injury for simulating conditions of stroke, trauma, and epilepsy (and/or seizure generation) and the associated cellular mechanisms of brain injury. The paper also briefly addresses the advantage of using computational models in combination with experimental models for hypothesis building and for aiding in the interpretation of empirical data. Finally, it reviews studies concerning brain injury and synaptic plasticity.
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PMID:Models of brain injury and alterations in synaptic plasticity. 1149 62


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