Thalamocortical Relationships in Generalized Epilepsy with Bilaterally Synchronous Spike-and-Wave Discharge

Gloor, P.; Avoli, Massimo; Kostopoulos, George

doi:10.1007/978-1-4684-6767-3_14

Cited by 118 publications

(100 citation statements)

References 49 publications

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“…In some of these infants, obvious cortical abnormalities had been disclosed by neuroimaging, but in others neither examination nor neuroimaging suggested the presence of any lesions. On the basis of other parameters, surgery was performed and a focal dysplastic area was detected in the ablated specimen; postoperatively, both the generalized electrical discharges and the spasms disappeared, as did the partial seizures (41). In rare instances during the present investigation, just before a generalized symmetrical discharge of S / W , with a documented absence, a few focal discharges preceded the generalized burst (Fig.…”

Section: Discussionmentioning

confidence: 61%

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Consistent EEG Focalities Detected in Subjects with Primary Generalized Epilepsies Monitored for Two Decades

Lombroso

1997

Epilepsia

135

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Summary:Purpose: To describe the evolution of interictal findings in serial EEGs from patients with primary generalized epilepsy.Methods: A cohort of 89 subjects with various primary generalized epilepsies were reviewed. Thirty-one did not meet a priori criteria. Of the 58 patients analyzed, 12 had only absence seizures, 28 had absence seizures followed by one or more generalized tonic-clonic seizures, 9 had generalized tonicclonic seizures followed by absence and/or myoclonic seizures, and 9 had juvenile myoclonic epilepsy. Patients were followed for a mean of 16 years. An average of 39 EEGs were obtained on each patient.Results: Thirty-two patients (56%) had focal features present in up to 65% of the EEGs in each of the patients. Accepted focalities were only those that were consistent in lateralization, location and, often, morphology across the span of the study. Focal findings were most often temporal or frontal.Conclusions: Patients with typical primary generalized epilepsies show a high incidence of focal EEG features that cannot be explainea on the basis of structural lesions, coincidental factors, or to artifacts of the selection criteria. Although the data do not allow a definitive explanation, possible mechanisms include associated focal cortical pathology such as microdysgenesis, and development over time of localized, self-sustaining hyperexcitability in low-threshold cortical structures subjected to repeated generalized spike-wave activity. Either hypothesis implies the participation and interaction of genetic, ontogenic, and environmental factors. Key Words: Focal electroencephalograms-Idiopathic generalized epilepsy-Longterm follow-up.The classification of epilepsies and epileptic syndromes proposed in 1989 (1) defines the idiopathic (primary) generalized epilepsies (ICE) as those whose seizure phenotypes indicate the involvement of -both hemispheres from the onset, both clinically and electrographically. By definition, the IGE show no evidence of structural brain lesions, in contrast to the secondarily generalized group of epilepsies, and no known or suspected etiology other than the contributions of polygenic factors. Their EEG expression (ictally or interictally) consists of initially generalized, bilaterally symmetrical discharges, whereas the background patterns are normal for age.Despite many efforts made in the past half century by both clinicians and neuroscientists, the pathophysiology of IGE remains unsettled. Among still-controversial issues are the predicated complete lack of structural brain lesions and the precise role played by the cortex.A long-term follow-up in a population of subjects with ICE shows that their EEGs often contain focal abnormalities that are persistent and consistent in location-an

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Section: Discussionmentioning

confidence: 61%

“…If this were so, could these cortical aberrant foci be the triggers that, with the necessary participation of subcortical systems (40,41) and under the influence of genetic, ontogenic, and environmental factors, would then lead to the electrical and clinical expressions of the various phenotypic phenomenologies of IGE?…”

Section: Discussionmentioning

confidence: 99%

Consistent EEG Focalities Detected in Subjects with Primary Generalized Epilepsies Monitored for Two Decades

Lombroso

1997

Epilepsia

135

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“…The transition from spindles to SWD was just what was observed in the particular FGPE model (awake cats under fentanyl and curare successively injected with pentobarbital and penicillin [97]) and gave major support to the hypothesis that SWDs develop from the same TC circuits as spindles. Further more it was these experiments in FGPE, which first argued in favor of above (b -not compromised GABA inhibition) and (cprimacy of cortical mechanisms) [9,69,91,92,93,99,100]. One of the first robust observations, pivotal to the suggestion of this hypothesis, but not adequately followed up since, is that the spectral frequencies of spindles and SWD model co-varied in different cats displaying an impressively accurate for EEG almost 2:1 or 3:1 relationship [98] and most importantly that the transition from one to the other in FGPE was not continuous but step-like.…”

Section: Spindles and Epilepsymentioning

confidence: 92%

“…Gloor in 1978 [91] proposed that the same TC circuit producing sleep spindles would generate SWDs in states of cortical hyperexcitability [91]. The hypothesis was based in experiments in the animal model of feline generalized epilepsy with penicillin (FGPE) and developed further on the basis of in vitro and in vivo experiments, especially using rodent genetic models of absence seizures [92][93][94][95].…”

Section: Spindles and Epilepsymentioning

confidence: 99%

“…This slower cortical rhythm was proposed to be transferred to the thalamus to gradually grow as a corticothalamo-cortical SWD rhythm. The experiments in the FGPE model that followed and supported this hypothesis have been reviewed [92][93]100]. Further testing of this hypothesis was made possible when in vivo and in vitro studies revealed the exact mechanism of spindles generation in thalamus [44] (see chapter 2.1) and when this knowledge was applied to experiments on rodent genetic models of absence seizures [94][95].…”

Section: Spindles and Epilepsymentioning

confidence: 99%

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