Ictal motor signs and interictal regional cerebral hypometabolism.
ABSTRACT Early motor manifestations are the main components of focal seizures involving the frontal lobe. We examined the relationship between the initial ictal motor manifestations and interictal abnormalities of cerebral glucose consumption (rCMRGlc) as assessed by PET in 48 consecutive patients with focal seizures of neocortical origin. Group data analysis revealed that patients with predominantly unilateral clonic seizures had a significant contralateral perirolandic hypometabolism and to a lesser degree a contralateral frontomesial hypometabolism. Patients with predominantly focal tonic manifestations showed a hypometabolism within the frontomesial and perirolandic regions that was unilateral in all patients with lateralized tonic seizures. Patients with versive seizures had mainly contralateral metabolic depressions without a consistent regional pattern. Patients with hypermotor seizures had metabolic depressions involving frontomesial, anterior cingulate, perirolandic, and anterior insular/frontal operculum areas. In all patient groups, bilateral and symmetric hypometabolism of the thalamus and cerebellum was observed. We propose that this pattern of distinctly abnormal metabolic brain regions demonstrates not only possible epileptogenic zones but also symptomatogenic brain regions as shown by the associations between clinical manifestations and sets of abnormal brain regions, particularly if epileptogenic zones are in a clinically silent neocortical brain region. The detection and possible differentiation of symptomatogenic and epileptogenic zones might improve the effectiveness of presurgical noninvasive studies.
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ABSTRACT: To describe the clinical, electrophysiologic, neuroradiologic, and histologic findings in our patients with drug-resistant hypermotor seizures (HMSs) and to evaluate the outcome of their surgical treatment. Twenty-three patients were identified by criteria for drug-resistant HMS. Surgical treatment and presurgical evaluation modalities including semiology, magnetic resonance imaging (MRI), interictal/ictal scalp video-EEG (electroencephalography), and intracranial recording were analyzed retrospectively. The common seizure frequency of 60-300 per month was observed among 15 patients. Sixteen patients (69.6%) experienced auras such as fear and palpitation. Marked agitation was observed in 12 patients and mild agitation in 11 patients. Groaning/shouting and asymmetric posturing were common accompanying symptoms. Asymmetric posturing was observed more often in patients with mild agitation than in those with marked agitation (p = 0.027). MRI detected focal abnormalities in six patients. Intracranial recording was conducted in 16 patients. The origins of seizures were localized in mesial frontal cortex in four patients, dorsolateral frontal cortex in four patients, and mesial temporal cortex in two patients. The epileptogenic zones (EZs) were resected from the frontal lobe in 21 patients and from the temporal lobe in 2 patients. The follow-up ranged from 12-60 months. Seventeen patients (73.9%) had been seizure-free, 11 of whom had presented with marked agitation (11 of 12) and 6 with mild agitation (6 of 11) (p = 0.069). Histologic examinations demonstrated focal cortical dysplasia (FCD) in 18 patients. The HMSs can originate from both the mesial and dorsolateral frontal cortex, and occasionally from the temporal lobe. Patients with drug-resistant HMSs should be recommended for resective surgical treatment.Epilepsia 10/2010; 51(10):2124-30. · 3.96 Impact Factor
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ABSTRACT: Aims. To build up a coherent shared pathophysiology of NFLE and AP and discuss the underlying functional network. Methods. Reviewing relevant published data we point out common features in semiology of events, relations to macro- and microstructural dynamism of NREM sleep, to cholinergic arousal mechanism and genetic aspects. Results. We propose that pathological arousals accompanied by confused behavior with autonomic signs and/or hypermotor automatisms are expressions of the frontal cholinergic arousal function of different degree, during the condition of depressed cognition by frontodorsal functional loss in NREM sleep. This may happen either if the frontal cortical Ach receptors are mutated in ADNFLE (and probably also in genetically not proved nonlesional cases as well), or without epileptic disorder, in AP, assuming gain in receptor functions in both conditions. This hypothesis incorporates the previous "liberation theory" of Tassinari and the "state dissociation hypothesis" of Bassetti and Terzaghi). We propose that NFLE and IGE represent epileptic disorders of the two antagonistic twin systems in the frontal lobe. NFLE is the epileptic facilitation of the ergotropic frontal arousal system whereas absence epilepsy is the epileptic facilitation of burst-firing working mode of the spindle and delta producing frontal thalamocortical throphotropic sleep system. Significance. The proposed physiopathogenesis conceptualize epilepsies in physiologically meaningful networks.Epilepsy research and treatment. 01/2012; 2012:312693.
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ABSTRACT: The article summarises the role of input and consequent phasic events in the dynamism of non-rapid eye movement (NREM) sleep and in homeostatic slow-wave economy during sleep. Then, an overview of the mechanism of how micro-arousals in NREM sleep gate epileptic events in absence epilepsy (AE) and in sporadic and autosomal dominant nocturnal frontal lobe epilepsy (NFLE/ADNFLE) is presented. The ictal type of generalised spike-wave discharges (SWDs) are associated with a special vigilance level in between NREM, rapid-eye movement (REM) and wake state. This transitional state is characterised by input-driven bidirectional fluctuations. Among them, SWDs are linked to A1 type A phases of CAP and therefore seem to be associated with shifts towards NREM sleep (sleep induction). In ADNFLE (and presumably in NFLE), micro-arousals release epileptic events in NREM sleep probably due to epileptic sensitisation of the cholinergic arousal system by the known acetylcholine (ACh) receptor mutations affecting the arousal system, giving rise to the epileptic (and also parasomniac) episodes. In both kinds of these system epilepsies (AE and NFLE), epileptic events can be released by phasic events during NREM sleep. The difference is that absences are activated in reactive states with a sleep-promoting, antiarousal effect, while in NFLE the epileptic disorder is interwoven with the cholinergic arousal function. The role of arousal/antiarousal in NFLE and AE fits nicely with the hypothesis that these epilepsies are disorders of two antagonistic thalamo-frontal systems involved in functions NREM sleep and wakefulness.Epilepsy research 08/2013; · 2.48 Impact Factor