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.
"In non-lesional cases, the assumption that minor motor events coming from the medial surface are epileptic in nature was proved by invasive stereo-EEG recording (Nobili et al., 2007). Functional neuro-imaging studies had congruent results: fronto-polar and orbito-frontal seizure-onset zones were found by singlephoton emission computed tomography (SPECT) and frontal hypometabolic areas by positron emission tomography (PET) in idiopathic cases (Harvey et al., 1993; Schlaug et al., 1997). Finally, the frontal lobe origin of these attacks was confirmed by seizure freedom after surgery (Nobili et al., 2003). "
[Show abstract][Hide abstract] 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; 107(1-2). DOI:10.1016/j.eplepsyres.2013.06.021 · 2.02 Impact Factor
"Functional neuroimaging data have provided further support of the frontal origin in these patients. SPECT studies have found frontopolar and orbitofrontal seizure onset zones  and PET studies interictal frontal hypometabolic areas . In one study singular hyperperfusion zone was described with ictal SPECT . "
[Show abstract][Hide abstract] 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.
"Our hypothesis that the topography of glucose hypometabolism relates to the pathways of seizure propagation is further supported by studies that have correlated seizure semiology with FDG-PET. Schlaug et al. (1997) found prominent contralateral perirolandic glucose hypometabolism in patients with focal clonic seizures and contralateral frontomesial glucose hypometabolism in patients with unilateral tonic seizures, corresponding, respectively, to the involvement of primary motor area and supplementary motor area. Ictal dystonic posturing is correlated with contralateral basal ganglia hypometabolism (Dupont et al., 1998; Rusu et al., 2005), and the extent of cerebral hypometabolism is related to the complexity of seizure semiology (Savic et al., 1997; Chassoux et al., 2004). "
[Show abstract][Hide abstract] ABSTRACT: This study aims to map the temporal and extratemporal 18-fluorodeoxyglucose positron emission tomography (FDG-PET)-defined hypometabolism in mesial temporal lobe epilepsy (MTLE). We hypothesize that quantitative analysis will reveal extensive extratemporal glucose hypometabolism (EH), that the EH is related to seizure propagation beyond the temporal lobe, hypometabolism restricted to one temporal lobe predicts a good outcome following surgery, and EH predicts a poor outcome.
Sixty-four patients were studied who had undergone temporal lobectomy for intractable MTLE and had at least 2 years of postoperative follow-up. Spatial preprocessing and statistical analysis on preoperative interictal FDG-PET using statistical parametric mapping (SPM 2) identified significant regions of hypometabolism compared to normal controls. The predictors of outcome were determined by univariable and multiple logistic regression analyses.
EH was common and widespread, occurring most frequently in the ipsilateral insula and frontal lobe. The extent of EH was not significantly associated with age of onset or the duration of epilepsy. Presence of secondarily generalized tonic--clonic seizures (SGTCS) was associated with a larger extent of remote hypometabolism (RH, p < 0.005). Multiple logistic regression analysis identified the extent of RH and the age at surgery as independent predictors of seizure outcome.
Our results indicate that RH in MTLE is associated with a poorer surgical outcome, especially if seen in the contralateral hemisphere. The extent of RH relates to SGTCS but not to duration of epilepsy.
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