Early Thalamic Injury Associated with Epilepsy and Continuous Spike–Wave during Slow Sleep

Abstract

Summary:Purpose: Mechanisms inducing continuous spikewave during slow sleep (CSWS) in encephalopathy with electrical status epilepticus during sleep are still unclear. Recently, some sporadic cases with early thalamic injury associated with CSWS have been reported. The aim of the study was to investigate in a population of patients with an early thalamic injury the presence of an activation of paroxysmal activities during sleep, their characteristics, and possible relations to neuroimaging and neuropsychological features.Methods: Thirty-two patients with prenatal or perinatal thalamic injuries, mostly due to a vascular mechanisms, were fully examined, including neuroimaging, EEG monitoring, and cognitive follow-up.Results and Conclusions: Twenty-nine of 32 patients showed major sleep EEG activation. Among these 29 patients, two different groups were distinguished: the first included the more or less typical CSWS (12 cases), generally with symmetry of spike and waves (SWs) and often with no spindle at all. The other cases had an usual asymmetry of SWs and presence or reduction of spindles, plus other atypical features concerning synchronism and morphology of SWs. Behavioral disorders were significantly more present in patients with a true CSWS; their improvement (and in one case of the three thoroughly followed the improvement of cognitive competence) paralleled the disappearance of CSWS. The generally predominant injury of the lateral aspect of the thalamus included reticular nucleus and ventral nuclei. An imbalance of γ -aminobutyric acid (GABA) B -versus GABA Amediated receptors may be evoked as a cofactor predisposing to CSWS.Epilepsy with continuous spike-waves (SWs) during slow sleep (CSWS) is an acknowledged epileptic syndrome characterized by a combination of focal epilepsy, neuropsychological impairment, and typical EEG findings with a pattern of diffuse SWs occurring in ≤85% of slow sleep (1). Recently, the possible role of primary early thalamic injury in generating CSWS has been suggested (2), and sporadic cases with similar lesions have been reported (3-8). Morphologic and metabolic thalamic abnormalities have been described in CSWS as well (9). Our study aimed at clarifying (a) the possible presence and eventually the characteristics of an activation of paroxysmal activities during sleep in a population of patients with an early thalamic injury; and (b) their relation to findings from neuroimaging, with thalamic injuries, and with neuropsychological features.Accepted January 23, 2005. Address correspondence and reprint requests to Dr. F. Guzzetta at Division of Child Neurology and Psychiatry, School of Medicine, Catholic University, Largo Gemelli I-00168 Rome, Italy. E-mail: fguzzetta@rm.unicatt.it PATIENTS AND METHODSAll the patients aged between 4 and 12 years (when CSWS usually develops), showing at magnetic resonance imaging (MRI) an early acquired thalamic lesion and consequently admitted to our hospital between 1999 and 2003, were enrolled in the study. Indication for MRI resulted from the cli...

Epilepsy with electrical status epilepticus during slow-wave sleep with a focus on electroencephalographic criteria

“…Раннее органическое поражение таламуса (обычно вследствие дисциркуляторных нарушений в перина-тальном периоде) с резким усилением гиперсинхрони-зации эпилептиформных разрядов во сне может быть одной из причин развития ЭЭСМ [27,44].…”

“…Также важную роль в генезе ПЭМС на ЭЭГ имеет аномальная возбудимость нейрональных сетей в систе-ме кора-таламус-кора [48]. Это подтверждается случа-ями возникновения ЭЭСМ при раннем органическом (перинатальном) повреждении таламуса [27,44].…”

Encephalopathy with Electrical Status Epilepticus in Slow Wave Sleep – a review with an emphasis on regional (perisylvian) aspects

“…Patients with shunted hydrocephalus, represented approximately 30% of cases of reported by Veggiotti et al (1999) and by Caraballo et al (2008). Early thalamic lesions seemed to be also strongly associated with sleep-enhanced epileptiform discharges (Monteiro et al, 2001;Kelemen et al, 2006;Guzzetta et al, 2005;Andrade-Machado et al, 2012;Sánchez Fernán-dez et al, 2012;Loddenkemper et al, 2012;Quigg and Noachtar, 2012). Hegyi et al, (2014) in their study of 33 patients with ESES attending the Bethesda Hospital, Budapest, identified sleep EEGs in 171 records, on average 5/patient and wake recordings in 492 records, on average 15/patient).…”

“…From the etiological point of view there were 15 patients without and 18 patients with structural abnormalities. In the Guzzetta et al (2005) study of the 32 patients identified, all but 3 patients had early thalamic lesion ESES like activation, while in the Bethesda study of the 32 patients with ESES only 4 patients had thalamic lesions (among them an isolated thalamic lesion was present in only one patient).…”

Magnetoencephalography localizing spike sources of atypical benign partial epilepsy

“…The role of MEG remains to be explored in this entity. Kelemen et al [17] reported three patients with CSWS secondary to destructive lesions in the thalamus [14], and CSWS development was often observed in patients with a thalamic lesion, indicative of thalamo-cortical dysfunction with an epileptic 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 Shiraishi et al, page 18 network [15,16]. ESM can be efficacious for seizures In ABPE patients, especially for ENM [6].…”