摘要:

Summary:Previous studies showed that brainstem sei zures can still be evoked after transections that separate forebrain from brainstem. We sought to determine wheth er forebrain‐evoked electrographic seizures require brain stem connections for initiation and generalization. Male Sprague‐Dawley rats weighing 295–320 g implanted with epidural electrodes had brain transections placed at the pre‐, mid‐, or postcollicular level. In experiment 1, the transections were limited to severing the brainstem, spar ing the telencephalon laterally; these are referred to as “core” transections. In experiment 2, the transections severed the brainstem and also cut through the lateral telencephalon. These “extended” transections were ei ther (a) bilateral, (b) unilateral (i.e., a hemitransection confined to one hemisphere), or (c) partial (sparing path ways ventral to the pretectal nuclei). All transections were performed under ether anesthesia, and seizures were initiated 3 h later by focal infusion of bicuculline (BIC) into the area tempestas (AT) through a previously implanted guide cannula. In experiment 1, bilateral fore brain electrographic seizures occurred in the complete absence of connections between forebrain and brainstem, showing that the brainstem is not required for forebrain evoked seizures. In experiment 2, forebrain seizures evoked by BIC in AT were suppressed by bilateral ex tended transections which interrupted connections be tween AT and the caudal lateral telencephalon. Under these circumstances, application of carbachol with BIC reinstated the forebrain seizure response. These results indicate that carbachol application served to compensate for loss of an excitatory influence on AT resulting from the severing of connections with the caudal telencepha lon. The demonstration of direct projections from ento rhinal cortex to AT using Fluoro‐Gold tracing together with the finding that extended brain transections caudal to the telencephalon do not suppress focally evoked fore brain seizures provided further support for the notion that AT afferents from the caudal telencephalon regulate the sensitivity of AT to BIC. The present findings provide further evidence that seizure substrates in the forebrain and brainstem are separa

ISSN:0013-9580    

DOI:10.1111/j.1528-1157.1993.tb02579.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0013-9580    

DOI:10.1111/j.1528-1157.1993.tb02580.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Summary:The relation between kindling and susceptibil ity to ethanol withdrawal seizures was investigated using withdrawal seizure‐prone (WSP) and withdrawal seizure resistant (WSR) mice. These lines were developed by se lective breeding to be prone and resistant, respectively, to handling‐induced convulsions after chronic exposure to ethanol. Development of kindled seizures in response to electrical stimulation of the olfactory bulb was inves tigated in mice aged 2 and 8 months with no exposure to ethanol. Older WSP mice kindled more slowly than older WSR mice, requiring significantly more stimulations to reach the first stage 3 and the first stage 5 seizures. In younger mice, there was no significant difference be tween the two lines in the rate of kindling. The lower kindling rate in mature WSP mice is in contrast to their higher sensitivity to handling‐induced convulsions on withdrawal from ethanol and other agents. This finding suggests that separate genetic factors underlie these two models of mouse sei

ISSN:0013-9580    

DOI:10.1111/j.1528-1157.1993.tb02581.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:0013-9580    

DOI:10.1111/j.1528-1157.1993.tb02582.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Summary:Dopamine (DA) and norepinephrine (NE) brain levels and turnover rate were examined in the spontaneously epileptic rat (SER:zi/zi, tm/tm), a double mutant rat obtained by mating tremor heterozygotes (tml +) with zitter homozygotes associated with epileptic seizures composed of spontaneously occurring tonic convulsion and absence‐like seizure. DA and NE levels were also determined in age‐matched male zitter, tremor and Kyo:Wistar rats. DA levels in caudate nucleus were significantly lower in adult age (10–12 weeks) SER, which showed epileptic seizures, and zitter rats than in adultKyo:Wistar and tremor rats. DA levels in other areas such as thalamus‐hypothalamus, midbrain, and ponsmedulla were not different among SER, zitter, tremor, and Kyo:Wistar rats at age 10–12 weeks. Except in cerebral cortex and hippocampus, there were no differences in brain DA levels between young seizure‐free SER (age 5 weeks) and young Kyo:Wistar rats. Furthermore, the turnover rate of DA was significantly lower in caudate nucleus of adult SER than of Kyo:Wistar rat, whereas in pons‐medulla there was no difference between the two strains. In contrast, NE levels in the thalamushypothalamus, midbrain, cerebellum and pons‐medulla were higher in SER and zitter rats at age 10–12 weeks than in age‐matched tremor and Kyo:Wistar rats. Higher NE levels were also observed in midbrain, cerebellum, and pons‐medulla of young SER as compared with young Kyo:Wistar rats. Turnover rates of NE were significantly lower in pons‐medulla and cerebellum of the adult SER than in those of Kyo:Wistar rat. In genetic studies using backcross mating of zitter and BN rats, decreased DA was also observed in caudate nucleus of backcrossed zitter rats as compared with BN, F1, and zitter wild‐type rats. Increased NE contents were observed in the thalamus‐hypothalamus, midbrain, and pons‐medulla of zitter rats as compared with other rats, although the increase was also observed in the thalamus‐hypothalamus and midbrain of zitter wild‐type rats. Results suggest that a decrease in DA in caudate nucleus and an increase in NE in midbrain and pons‐medulla are due to the homozygous zi gene, and together with previous findings, suggest that the decrease in DA, although probably not the only cause, facilitates appearance of tonic and absence‐like seizures by lowering t

ISSN:0013-9580    

DOI:10.1111/j.1528-1157.1993.tb02583.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Summary:Low blood manganese (Mn2+) concentration is associated with epilepsy in humans and rats. The low Mn2+concentration is attributed by some investigators to the seizure activity associated with the epilepsy, whereas others propose that the low Mn2+concentration may be secondary to genetic mechanisms underlying the epilepsy. To begin to differentiate between these possibilities, Mn2+‐binding enzymes of liver and brain (i.e., arginase and glutamine synthetase, respectively) were assayed in rats exposed to chronically induced seizures and in genetically epilepsy‐prone rats (GEPRs). Chronic seizures caused a decrease in whole blood Mn2+levels but did not affect brain Mn2+concentrations. Arginase activity was increased in livers of rats with chronic seizure as compared with controls, but this difference was eliminated when Mn2+was added to the assay. Brain glutamine synthetase activity was unaffected by chronic seizures, but the activity of this enzyme was significantly lower in GEPR brain than in control brain. Liver arginase activity tended to be lower in GEPRs, although the difference was not statistically significant. These data indicate that seizures affect liver arginase activity through changes in liver Mn2+concentration, but GEPRs show abnormalities in Mn2+‐dependent enzymes apparently independent of seizure act

ISSN:0013-9580    

DOI:10.1111/j.1528-1157.1993.tb02584.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Summary:Hyperthermia induces seizures in both humans and rodents, but the underlying mechanism remains unknown. The present study showed that hyperthermia, causing rapid increase in body temperature, increases the concentration of glutamate (Glu) released into a cortical perfusate before onset of seizures in rats and that this increase in Glu concentration correlated with a decrease in seizure threshold temperature. These results indicate that increased cortical extracellular Glu induced by hyperthermia contributes to onset of seizures. The same mechanism may be involved in clinical seizures induced by fever in patients with febrile convulsions or epilepsy.

ISSN:0013-9580    

DOI:10.1111/j.1528-1157.1993.tb02585.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Summary:The incidence of epilepsy and of all unprovoked seizures was determined for residents of Rochester, Minnesota U.S.A. from 1935 through 1984. Ageadjusted incidence of epilepsy was 44 per 100,000 personyears. Incidence in males was significantly higher than in females and was high in the first year of life but highest in persons aged ≥75years. Sixty percent of new cases had epilepsy manifested by partial seizures, and two thirds had no clearly identified antecedent. Cerebrovascular disease was the most commonly identified antecedent, accounting for 11% of cases. Neurologic deficits from birth, mental retardation and/or cerebral palsy, observed in 8% of cases, was the next most frequently identified preexisting condition. The cumulative incidence of epilepsy through age 74 years was 3.1%. The age‐adjusted incidence of all unprovoked seizures was 61 per 100,000 person‐years. Age‐and gender‐specific incidence trends were similar to those of epilepsy, but a higher proportion of cases was of unknown etiology and was characterized by generalized onset seizures. The cumulative incidence of all unprovoked seizures was 4.1% through age 74 years. With time, the incidence of epilepsy and of unprovoked seizures decreased in children and increased in th

ISSN:0013-9580    

DOI:10.1111/j.1528-1157.1993.tb02586.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Summary:Accurate family histories of seizure disorders are important for both clinical practice and genetic research. This study evaluated validity of seizure histories of parents and siblings, obtained by interviewing 1,957 adults with epilepsy (probands). Probands were asked two questions to screen for occurrence of seizures in each relative; the first asked about epilepsy specifically, the second asked about “other seizures.” For each relative who screened positive for seizures, a detailed clinical description was obtained. The final diagnosis was based on a review of all assembled information. Whenever possible, the proband's mother was interviewed independently about the family history, as were eligible relatives reported to have had seizures. Sensitivity, or the proportion of affected relatives who screened positive for seizures, was higher for epilepsy than for other seizures (87% vs. 32% assuming the mother's report to be correct, and 93% vs. 18% assuming self‐report to be correct). For epilepsy, estimates of risk in siblings based on the final diagnoses were similar to previously reported findings in Rochester, Minnesota. For both isolated unprovoked seizures and acute symptomatic seizures, however, risk estimates were lower than in Rochester. These findings suggest that adults with epilepsy can report reasonably accurately about epilepsy in their parents and siblings, but isolated unprovoked seizures and acute symptomatic seizures are underrep

ISSN:0013-9580    

DOI:10.1111/j.1528-1157.1993.tb02587.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Summary:Twenty‐one cases (12 males, 9 females) of Lafora's disease in 16 families were studied at the National Institute of Mental Health and Neuro Sciences (NIMHANS), Bangalore, India, from 1982 to 1990. Mean age of onset was 13.5 years (range 9.5–18 years). First symptom was generalized tonic‐clonic seizure (17), myoclonus (3), or dementia (1). All patients eventually developed the classical triad, except 1 who has had only myoclonus. Seven had occipital seizures. Other signs included behavioral changes (9), brisk tendon reflexes (11), cerebellar signs (8), and visual impairment (4). Patients from 14 of the 16 families (85%) were products of consanguineous marriage. More than 1 sibling was affected in 6 families. Scalp EEGs showed diffuse background slowing with epileptiform discharges in all and progressive slowing as the disease progressed in 3. Photosensitivity occurred in 4 of the 17 cases studied (23.5%). EEC abnormalities were documented in the presymptomatic stage in 2 cases 6 months and 6 years before clinical symptom onset. Visual evoked responses were abnormal in 4 of the 6 cases studied. Giant somatosensory evoked potentials (SSEP) were observed in all 8 cases studied. Lafora bodies were demonstrated in axillary skin in 14 of 17 (82.4%), in liver in 4 of 10 (40%), and in both brain biopsy specimens. In 2 cases, liver biopsy was positive while axillary skin biopsy was negative. In the brain, inclusions were evident in glial and capillary endothelial cells in addition to neurons. Although our cases were similar to those described earlier, the relative rarity of visual phenomena is emphasized. The clinical pattern was consistent with autosomal recessive inheritance. The high frequency of consanguinity in the South Indian population may be responsible for the many cases observed at our c

ISSN:0013-9580    

DOI:10.1111/j.1528-1157.1993.tb02588.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY