Benign Focal Epilepsy of Childhood

Lerman, Pinchas

doi:10.1001/archneur.1975.00490460077010

Cited by 197 publications

(32 citation statements)

References 8 publications

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“…This is eight to ten times higher than normal [4]. An increased incidence of febrile convulsions in children with rolandic epilepsy has been reported several times [13,21]. Some of the children had complex psychomental retardation or partial developmental deficits even before onset of seizures.…”

Section: Discussionmentioning

confidence: 97%

Symptomatology in children with focal sharp waves of genetic origin

Doose

1989

Eur J Pediatr

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The purpose of the study was to identify the clinical symptomatology of children with focal sharp waves of genetic nature. Genetic determination was assumed if the EEG of at least one sib revealed typical focal sharp waves. Forty-one probands (27 boys, 14 girls) and their 44 sibs showed a broad spectrum of different seizure types of focal origin including so-called atypical benign partial epilepsy (pseudo-Lennox-syndrome) and febrile convulsions. Numerous cases showed psychomental retardation or selective deficits of development. The classical syndrome of rolandic seizures with normal psychomental development and normal neurological findings was present in only a few cases. Similarly, EEG findings were quite variable. Rolandic sharp wave foci alone were found in only 22% of the probands. The remainder had foci in other regions (17%), or multiple foci (61%). Depending on age at first seizure, 42%-79% of the seizure-affected probands and 50% of the affected sibs showed generalized heritable EEG traits such as 4-7/s rhythms, generalized irregular spikes and waves, and/or photoparoxysmal response. Three pairs of monozygotic twins were concordant for the special type of EEG findings, two of them also for clinical symptoms.

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Section: Discussionmentioning

confidence: 97%

Symptomatology in children with focal sharp waves of genetic origin

Doose

1989

Eur J Pediatr

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“…The discharges are often activated by sleep (Lerman and Kivity , 1975). Topographical spike analysis has indicated dipole formation across the rolandic region (Gregory and Wong, 1984).…”

Section: Benign Epilepsy Of Childhood With Centrotemporal Spikes (Bect)mentioning

confidence: 99%

“…Ictal recordings have shown low-voltage fast activity maximal over the temporal and centroparietal regions, spreading to involve the anterior and midline regions (Dalla Bernardina and Tassinari, 1975). The rolandic spike discharges reduce in time, and the EEG usually normalizes in 6 months to 6 years (Lerman and Kivity , 1975), paralleling clinical resolution (Blom and Hejbel, 1982).…”

Section: Benign Epilepsy Of Childhood With Centrotemporal Spikes (Bect)mentioning

confidence: 99%

Parietal and Occipital Lobe Epilepsy: A Review

1993

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There has been considerable recent interest in frontal lobe epileptic syndromes, and less attention paid to occipital and parietal epilepsies. The occipital and parietal lobes have arbitrary anatomical borders. The prinicpal seizure symptomatology includes somatosensory (paresthetic, painful, thermal, sexual, apraxia, disturbances of body image); visual (amaurotic, elementary and complex hallucinations, illusions) and other phenomena (anosognosia, apraxia, acalculia, alexia, aphemia, confusional states, gustatory, vertiginous, adversive, oculoclonic and eyelid flutter). The seizure symptoms are of varying localizing and lateralizing value and seizure discharges may spread rapidly and perceived symptoms may reflect secondary spread rather than the primary site of seizure onset. Recognized parietal and occipital epilepsy syndromes include benign epilepsy of childhood with centrotemporal spikes, benign epilepsy of childhood with parietal evoked spikes, benign occipital epilepsy of childhood, migraine/epilepsy syndromes, and epilepsy with bilateral occipital calcification. In addition, occipital and parietal epilepsy may be on the basis of any underlying structural lesion. There is frequently a poor correlation between clinical and EEG features. MRI and functional imaging often reveals underlying pathology. There have been no specific trials of different antiepileptic drugs for occipital and parietal seizures. Surgical treatment has its place, with attention to the risk of causing a fixed neurological deficit.

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“…Puberty might therefore be a time during which epilepsy is more likely to arise and preexisting seizure disorders worsen (Dickerson, 194 1 ;Gastaut and Broughton, 1972). Certain epileptic syndromes, such as photosensitivity epilepsy (Jeavons et al, 1986) and juvenile myoclonic epilepsy (Janz and Christian, 1957), characteristically develop around the onset of puberty, whereas childhood absence (Sato et al, 1976) and benign rolandic epilepsy with centrotemporal spikes frequently remit (Lerman and Kivity, 1975). However, most seizure disorders are not altered with puberty.…”

Section: Pubertymentioning

confidence: 99%

Hormones and Epilepsy Through the Lifetime

Morrell

1992

Epilepsia

106

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Hormones influence brain function from gestation throughout life and may affect the seizure threshold by altering neuronal excitability. Estrogen enhances and progesterone diminishes neuronal excitability experimentally, whereas testosterone and corticosteroids have less consistent effects. Hormonal effects in the C N S also depend on the region of brain in which the hormone acts. Sites of action for most steroid hormones include the hypothalamus and limbic cortex, providing a mechanism for modulating behavior and endocrine function. Seizure patterns may change at certain life stages, perhaps as a result of alterations in hormones. At puberty, epilepsy and benign rolandic epilepsy often remit, while juvenile myoclonic and photosensitive epilepsy may arise. Other types of epilepsy do not respond predictably to events in the reproductive life or to advancing age. In some women, fluctuations in hormones over the menstrual cycle appear to increase seizure vulnerability, probably reflecting changes in relative amounts of estrogen and progesterone. Seizure patterns can be altered, for better or worse, during pregnancy. Whether this reflects the effects of hormones or changes in levels of antiepileptic drugs is not resolved. More information is needed about changes in established epilepsy at menopause and in the elderly. Better understanding of endocrine e 5 m on seizures over a lifetime should lead to more effective epilepsy therapies.

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Benign Focal Epilepsy of Childhood

Cited by 197 publications

References 8 publications

Symptomatology in children with focal sharp waves of genetic origin

Symptomatology in children with focal sharp waves of genetic origin

Parietal and Occipital Lobe Epilepsy: A Review

Hormones and Epilepsy Through the Lifetime

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