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Seizures Early (seizures + early)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Effects of early seizures on later behavior and epileptogenicity

DEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 2 2004
Gregory L. Holmes
Abstract Both clinical and laboratory studies demonstrate that seizures early in life can result in permanent behavioral abnormalities and enhance epileptogenicity. Understanding the critical periods of vulnerability of the developing nervous system to seizure-induced changes may provide insights into parallel or divergent processes in the development of autism. In experimental rodent models, the consequences of seizures are dependent on age, etiology, seizure duration, and frequency. Recurring seizures in immature rats result in long-term adverse effects on learning and memory. These behavioral changes are paralleled by changes in brain connectivity, changes in excitatory neurotransmitter receptor distribution, and decreased neurogenesis. These changes occur in the absence of cell loss. Although impaired cognitive function and brain changes have been well-documented following early-onset seizures, the mechanisms of seizure-induced dysfunction remain unclear. MRDD Research Reviews 2004;10:101,105. © 2004 Wiley-Liss, Inc. [source]

Seizures in the Developing Brain Cause Adverse Long-term Effects on Spatial Learning and Anxiety

EPILEPSIA, Issue 12 2004
Umit Sayin
Summary:,Purpose: Seizures in the developing brain cause less macroscopic structural damage than do seizures in adulthood, but accumulating evidence shows that seizures early in life can be associated with persistent behavioral and cognitive impairments. We previously showed that long-term spatial memory in the eight-arm radial-arm maze was impaired in rats that experienced a single episode of kainic acid (KA)-induced status epilepticus during early development (postnatal days (P) 1,14). Here we extend those findings by using a set of behavioral paradigms that are sensitive to additional aspects of learning and behavior. Methods: On P1, P7, P14, or P24, rats underwent status epilepticus induced by intraperitoneal injections of age-specific doses of KA. In adulthood (P90,P100), the behavioral performance of these rats was compared with that of control rats that did not receive KA. A modified version of the radial-arm maze was used to assess short-term spatial memory; the Morris water maze was used to evaluate long-term spatial memory and retrieval; and the elevated plus maze was used to determine anxiety. Results: Compared with controls, rats with KA seizures at each tested age had impaired short-term spatial memory in the radial-arm maze (longer latency to criterion and more reference errors), deficient long-term spatial learning and retrieval in the water maze (longer escape latencies and memory for platform location), and a greater degree of anxiety in the elevated plus maze (greater time spent in open arms). Conclusions: These findings provide additional support for the concept that seizures early in life may be followed by life-long impairment of certain cognitive and behavioral functions. These results may have clinical implications, favoring early and aggressive control of seizures during development. [source]

Clinical and genetic features of human prion diseases in Catalonia: 1993,2002

EUROPEAN JOURNAL OF NEUROLOGY, Issue 10 2004
R. Sanchez-Valle
We describe the clinical and genetic characteristics of the 85 definite or probable human prion diseases cases died between January 1993 and December 2002 in Catalonia (an autonomous community of Spain, 6 million population). Seventy-three (86%) cases were sporadic Creutzfeld-Jakob diseases (sCJD) (49 definite, 24 probable), with a median age at onset of 66 years. The clinical presentation was dementia in 29 cases, ataxia in 14 and visual symptoms in five. The median survival was 3 months. The 14-3-3 assay was positive in 93% cases, 62% presented periodic sharp wave complexes (PSWC) in EEG but only 18% the typical signs on MRI. Forty-eight sCJD were studied for codon 129 PRNP polymorphism: 69% were methionine/methionine (M/M), 14.5% valine/valine (V/V) and 16.5% M/V. Six out of seven V/V cases did not present PSWC and in two survival was longer than 20 months. Eleven cases (13%) were genetic: five familial fatal insomnia and six familial CJD (fCJD). Up to four (67%) fCJD lacked family history of disease, two presented seizures early at onset and one neurosensorial deafness. The only iatrogenic case was related to a dura mater graft. No case of variant CJD was registered. The study confirms in our population the consistent pattern reported worldwide on human prion diseases. Atypical features were seen more frequently in sporadic 129 V/V CJD and fCJD cases. [source]

Seizures, enhanced excitation, and increased vesicle number in Lis1 mutant mice,

ANNALS OF NEUROLOGY, Issue 5 2009
Joel S.F. Greenwood PhD
Objective In humans, abnormal neuronal migration and severe neuronal disorganization resulting from Lis1 (lissencephaly) haploinsufficiency contributes to cognitive impairment and seizures early in life. In Lis1 heterozygotic mice, severe hippocampal disorganization and cognitive impairment have also been reported. Using this mouse model, we examined the functional impact of LIS1 deficiency with particular focus on excitatory glutamate-mediated synaptic transmission. Methods We used visualized patch-clamp recordings in acute hippocampal slices. We recorded spontaneous, miniature and stimulation-evoked excitatory postsynaptic current (EPSC). Additional mice were processed for immunohistochemistry, electron microscopy (EM), or video-electroencephalographic (EEG) monitoring. Results Video-EEG confirmed the presence of spontaneous electrographic seizures in Lis1 mutant mice. In disorganized hippocampal slices from Lis1+/, mice, we noted a nearly two-fold significant increase in the frequency of spontaneous and miniature EPSC; no significant change in amplitude or decay was noted. Synaptic function assessed using brief repetitive or paired-pulse stimulation protocols, also revealed significant enhancement of glutamate-mediated excitation. Low concentrations of cadmium, a nonspecific blocker of voltage-dependent calcium channels mediating vesicle release, effectively restored paired-pulse facilitation deficits back to control levels. Analysis of synapse ultrastructure at the EM level identified a large increase in synaptic vesicle number. Interpretation Seizure activity, possibly associated with increased glutamate-mediated excitation and an increased pool of vesicles at the presynaptic site, was demonstrated in a mouse model of type I lissencephaly. Ann Neurol 2009;66:644,653 [source]