Subtraction ictal SPECT co-registered to MRI (SISCOM) in Sturge-Weber syndrome.
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Adult↗
Biomedical subjects
C Marescaux
Publications and source records attributed to C Marescaux.
Modifications of local cerebral glucose utilization in thalamic structures following injection of a dopaminergic agonist in the nucleus accumbens--involvement in antiepileptic effects?
Dopaminergic transmission in the nucleus accumbens (NAcc) is implicated in different aspects of reward and motivational mechanisms. More recently, it has been suggested that this nucleus could also be involved in the modulation of generalized epileptic seizures. In particular, microinjection of dopaminergic agonists in the NAcc suppresses the occurrence of epileptic seizures in a model of absence seizures, the GAERS (generalized absence epileptic rats from Strasbourg). The aim of this study was to identify the structures involved in this effect. Local cerebral metabolic rates for glucose utilization (LCMRglc) were measured in different parts of the basal ganglia and output structures after apomorphine injection in the NAcc in GAERS and in the inbred non-epileptic rats (NE), concomitantly with seizure suppression. Apomorphine injection in the NAcc induced a significant increase of glucose intake in the anteromedial, mediodorsal and ventrolateral nuclei of the thalamus in NE rats, while no significant changes were observed in the basal ganglia structures (globus pallidus, subthalamic nucleus, substantia nigra). Furthermore, microinjections of muscimol (100 and 200 pmol/side) in the mediodorsal nucleus of the thalamus in GAERS rats suppressed seizures. These results suggest that the mediodorsal nucleus of the thalamus could be involved in absence seizures modulation. Along with data from the literature, our data suggest that this nucleus could participate in the control of the basal ganglia over generalized epileptic seizures.
Animals↗
Suppression of absence seizures by electrical and pharmacological activation of the caudal superior colliculus in a genetic model of absence epilepsy in the rat.
Activation of the superior colliculus has been shown to reproduce the antiepileptic effect of the inhibition of the substantia nigra reticulata. A circuit involving neurons of the caudal deep layers of the superior colliculus has been suggested to control brain stem convulsive seizures. The present study was designed to examine whether a similar circuit is also involved in the control of absence seizures. For this, activation of either the rostral or caudal parts of the deep and intermediate layers of the superior colliculus was applied in a genetic model of absence seizures in the rat (GAERS). Single-shock (5 s) electrical stimulation of the rostral and caudal superior colliculus interrupted ongoing spike-and-wave discharges at an intensity (antiepileptic threshold) significantly lower than the intensity inducing behavioral effects. At this intensity, no interruption of licking behavior was observed in water-deprived rats. Repeated stimulations (5 s on/5 s off) at the antiepileptic threshold reduced absence seizures only during the first 10 min. Bilateral microinjection of a GABA antagonist (picrotoxin, 33 pmol/side) significantly suppressed spike-and-wave discharges when applied in the caudal aspect of the superior colliculus. This antiepileptic effect appears dissociated from an anxiogenic effect, as tested in an elevated plus maze test. Finally, bilateral injection of picrotoxin (33 pmol/side) appeared more effective in the superficial and intermediate layers of the caudal superior colliculus, whereas such injections had only weak effects on absence seizures when applied in the deep layers. These results suggest that a specific population of neurons located in the intermediate and superficial layers of the caudal superior colliculus is involved in the inhibitory control of absence seizures. It may constitute an important relay for the control of absence seizures by the basal ganglia via the substantia nigra reticulata.
Animals↗
Evolution of hippocampal epileptic activity during the development of hippocampal sclerosis in a mouse model of temporal lobe epilepsy.
Unilateral intrahippocampal injection of kainic acid in adult mice reproduces most of the morphological characteristics of hippocampal sclerosis (neuronal loss, gliosis, reorganization of neurotransmitter receptors, mossy fiber sprouting, granule cell dispersion) observed in patients with temporal lobe epilepsy. Whereas some neuronal loss is observed immediately after the initial status epilepticus induced by kainate treatment, most reorganization processes develop progressively over a period of several weeks. The aim of this study was to characterize the evolution of seizure activity in this model and to assess its pharmacological reactivity to classical antiepileptic drugs. Intrahippocampal electroencephalographic recordings showed three distinct phases of paroxystic activity following unilateral injection of kainic acid (1 nmol in 50 nl) into the dorsal hippocampus of adult mice: (i) a non-convulsive status epilepticus, (ii) a latent phase lasting approximately 2 weeks, during which no organized activity was recorded, and (iii) a phase of chronic seizure activity with recurrent hippocampal paroxysmal discharges characterized by high amplitude sharp wave onset. These recurrent seizures were first seen about 2 weeks post-injection. They were limited to the injected area and were not observed in the cerebral cortex, contralateral hippocampus or ipsilateral amygdala. Secondary propagation to the contralateral hippocampus and to the cerebral cortex was rare. In addition hippocampal paroxysmal discharges were not responsive to acute carbamazepine, phenytoin, or valproate treatment, but could be suppressed by diazepam. Our data further validate intrahippocampal injection of kainate in mice as a model of temporal lobe epilepsy and suggest that synaptic reorganization in the lesioned hippocampus is necessary for the development of organized recurrent seizures.
Action Potentials↗
Contribution of SISCOM imaging in the presurgical evaluation of temporal lobe epilepsy related to dysembryoplastic neuroepithelial tumors.
PURPOSE: Dysembryoplastic neuroepithelial tumors (DNTs) are a group of glioneuronal supratentorial and intracortical lesions often associated with the early onset of intractable and crippling partial seizures. They are characterized by their location, multinodular architecture, and heterogeneous cell composition, with a specific glioneuronal element in the specific form. Foci of cortical dysplasia may be associated with the tumoral lesion, and identifying the presence and the extent of cortical dysplasia is not always easy on magnetic resonance images (MRIs). The purpose of this article is to evaluate, retrospectively, the usefulness of ictal single-photon emission computed tomography (SPECT) imaging to assess the presence and the extent of cortical dysplasia associated with DNTs in nine patients with intractable temporal lobe epilepsy related to histopathologically confirmed DNTs. METHODS: The results of the subtraction of ictal and interictal SPECT coregistered to MRI (SISCOM) were compared with the results of the examinations of pathological material after surgery. RESULTS: SISCOM showed a strongly hyperperfused area corresponding anatomically to electroclinical abnormalities and to the location of DNTs on MRI. A circumscribed hyperperfusion was present in DNTs without cortical dysplasia, limited to the location of the tumor on MRI. In cases of associated cortical dysplasia, a widespread hyperperfusion including areas corresponding to normal perilesional regions on MRI was found. CONCLUSIONS: SISCOM, used among presurgical investigations, contributes to detecting cortical dysplasia associated with DNTs. Concordance between the symptomatogenic zone (defined from the medical history and electroclinical data), MRI scans, SISCOM pattern, and complete resection of the epileptic zone was predictive of a good postsurgical outcome.
Adolescent↗
EEG criteria predictive of complicated evolution in idiopathic rolandic epilepsy.
BACKGROUND: Although so-called "benign" epilepsy with centrotemporal spikes (BECTS) always has an excellent prognosis with regard to seizure remission, behavioral problems and cognitive dysfunctions may sometimes develop in its course. To search for clinical or EEG markers allowing early detection of patients prone to such complications, the authors conducted a prospective study in a cohort of unselected patients with BECTS. METHODS: In 35 children with BECTS, academic, familial, neurologic, neuropsychological, and wake and sleep EEG evaluations were repeated every 6 to 12 months from the beginning of the seizure disorder up to complete recovery. RESULTS: In 25 of 35 patients (72%), behavioral and intellectual functioning remained unimpaired. In 10 of 35 patients (28%), educational performance and familial maladjustment occurred. These sociofamilial problems were correlated with impulsivity, learning difficulties, attention disorders, and minor (7/35 cases, 20%) or serious (3/35 cases, 8%) auditory-verbal or visual-spatial deficits. Worsening phases started 2 to 36 months after onset and persisted for 9 to 39 months. Occurrence of atypical evolutions was significantly correlated with five qualitative and one quantitative interictal EEG pattern: intermittent slow-wave focus, multiple asynchronous spike-wave foci, long spike-wave clusters, generalized 3-c/s "absence-like" spike-wave discharges, conjunction of interictal paroxysms with negative or positive myoclonia, and abundance of interictal abnormalities during wakefulness and sleep. Clinical deterioration was not linked with seizure characteristics or treatment. CONCLUSION: Different combinations of at least three of six distinctive interictal EEG patterns and their long-lasting (> or =6-month) persistence seem to be the hallmarks of patients with BECTS at risk for neuropsychological impairments.
Adolescent↗
Alterations of hippocampal GAbaergic system contribute to development of spontaneous recurrent seizures in the rat lithium-pilocarpine model of temporal lobe epilepsy.
Reorganization of excitatory and inhibitory circuits in the hippocampal formation following seizure-induced neuronal loss has been proposed to underlie the development of chronic seizures in temporal lobe epilepsy (TLE). Here, we investigated whether specific morphological alterations of the GABAergic system can be related to the onset of spontaneous recurrent seizures (SRS) in the rat lithium-pilocarpine model of TLE. Immunohistochemical staining for markers of interneurons and their projections, including parvalbumin (PV), calretinin (CR), calbindin (CB), glutamic acid decarboxylase (GAD), and type 1 GABA transporter (GAT1), was performed in brain sections of rats treated with lithium-pilocarpine and sacrificed after 24 h, during the silent phase (6 and 12 days), or after the onset of SRS (10-18 days after treatment). Semiquantitative analysis revealed a selective loss of interneurons in the stratum oriens of CA1, associated with a reduction of GAT1 staining in the stratum radiatum and stratum oriens. In contrast, interneurons in CA3 were largely preserved, although GAT1 staining was also reduced. These changes occurred within 6 days after treatment and were therefore insufficient to cause SRS. In the dentate gyrus, extensive cell loss occurred in the hilus. The pericellular innervation of granule cells by PV-positive axons was markedly reduced, although the loss of PV-interneurons was only partial. Most strikingly, the density of GABAergic axons, positive for both GAD and GAT1, was dramatically increased in the inner molecular layer. This change emerged during the silent period, but was most marked in animals with SRS. Finally, supernumerary CB-positive neurons were detected in the hilus, selectively in rats with SRS. These findings suggest that alterations of GABAergic circuits occur early after lithium-pilocarpine-induced status epilepticus and contribute to epileptogenesis. In particular, the reorganization of GABAergic axons in the dentate gyrus might contribute to synchronize hyperexcitability induced by the interneuron loss during the silent period, leading to the onset of chronic seizures.
Animals↗
Relationship between neuronal loss and interictal glucose metabolism during the chronic phase of the lithium-pilocarpine model of epilepsy in the immature and adult rat.
The lithium-pilocarpine (Li-Pilo) model of epilepsy reproduces most of the features of human temporal lobe epilepsy. After having studied the metabolic changes occurring during the silent phase, in the present study, we explored the relationship between interictal metabolic changes and neuronal loss during the chronic phase following status epilepticus (SE) induced by Li-Pilo in 10-day-old (P10), 21-day-old (P21), and adult rats. Rats were observed and their EEG was recorded to detect the occurrence of spontaneous recurrent seizures (SRS). Local cerebral glucose utilization was measured during the interictal period of the chronic phase, between 2 and 7 months after SE, by the [(14)C]2-deoxyglucose method in rats subjected to SE at P10, P21, or as adults. Neuronal damage was assessed by cell counting on adjacent cresyl violet stained sections. When SE was induced at P10, rats did not become epileptic, did not develop lesions and cerebral glucose utilization was in the normal range 7 months later. When SE was induced in adult rats, they all became epileptic after a mean duration of 25 days and developed lesions in the forebrain limbic areas, which were hypometabolic during the interictal period of the chronic phase, 2 months after SE. When SE was induced in P21 rats, 24% developed SRS, and in 43% seizures could be triggered (TS) by handling, after a mean delay of 74 days in both cases. The remaining 33% did not become epileptic (NS). The three groups of P21 rats developed quite comparable lesions mainly in the hilus of the dentate gyrus, lateral thalamus, and entorhinal cortex; at 6 months after SE, the forebrain was hypometabolic in NS and TS rats while it was normo- to slightly hypermetabolic in SRS rats. These data show that interictal metabolic changes are age-dependent. Moreover, there is no obvious correlation, in this model, between interictal hypometabolism and neuronal loss, as reported previously in human temporal lobe epilepsy.
Action Potentials↗
Controlling attentional priority by preventing changes in oculomotor programs: a job for the premotor cortex?
Abruptly presented items capture attention automatically so they constitute the first items to be examined [Yantis and Jonides, Journal of Experimental Psychology: Human Perception and Performance, 1984;10:601; Jonids and Yantis, Perception and Psychophysics, 1988;43:346; Theeuwes, Perception and Psychophysics, 1992;51:599; Theeuwes, Journal of Experimental Psychology: Human Perception and Performance, 1994;20:799]. This attentional priority can be controlled in a top-down manner by directing attention towards the locus of interest [Yantis and Johnson, Journal of Experimental Psychology: Human Perception and Performance, 1990;16:812; Theeuwes. Perception and Psychophysics, 1991;49:83; Miller, Perception and Psychophysics, 1989;45:567; Folk et al., Journal of Experimental Psychology: Human Perception and Performance, 1992; 18:1030]. The premotor theory of attention [Rizzolatti et al., Neuropsychologia 1987;25:31; Rizzolatti et al., Attention and Performance XV, 1994, p. 231] assumes that the mechanism responsible for the attentional shifts is strictly linked to that responsible for eye movements, and several studies [Corbetta et al., Society of Neuroscience Abstracts 1997;23:122.12; Nobre et al., Brain 1997;120:515; Theeuwes et al., Journal of Experimental Psychology: Human Perception and Performance, 1999;25:1595] suggested that the premotor cortex plays a role in the control of attention. However, the nature of this involvement is still unclear. We have been asking a patient (RJ) with a damage of the right premotor cortex to decide whether a target had a discontinuity on its right or left side. The absolute location of the target was pre-cued. In Section 2, an interference was observed when a sudden onset occurred in the visual space, suggesting that RJ was not able to control attentional capture. The possibility to attribute this interference to an insufficient focalization of attention or a grouping effect were discarded by Sections 3 and 4, respectively. Section 5 revealed that this interference followed exclusively the onset occurring in the hemifield opposite the one containing the target (meridian effect [Rizzolatti et al., Neuropsychologia 1987;25:31]). The results suggest that the control of attentional capture may be achieved by keeping constant the parameters of the appropriate oculomotor program.
Adult↗
Pathophysiological aspects of Landau-Kleffner syndrome: from the active epileptic phase to recovery.
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Epilepsy↗
Neuropeptide Y and epilepsy: varying effects according to seizure type and receptor activation.
In vitro and in vivo experiments suggest antiepileptic properties for NPY. In this study, the pharmacology of these effects was examined and compared in different rat models of seizures. Agonists for Y(1), Y(2) and Y(5) receptors reduced seizure-like activity in hippocampal cultures. Intracerebral injection of NPY or Y(5) agonists reduced the expression of focal seizures produced by a single electrical stimulation of the hippocampus. Conversely, NPY agonists increased the duration of generalized convulsive seizures induced by pentylenetetrazol. These results suggest that NPY reduces seizures of hippocampal origin through activation of Y(5) receptors. They also point to probable modulatory effects of NPY in brain structures other than the hippocampus, involved in initiation, propagation or control of seizures.
Animals↗
Inhibition of the substantia nigra suppresses absences and clonic seizures in audiogenic rats, but not tonic seizures: evidence for seizure specificity of the nigral control.
GABAergic inhibition of the substantia nigra pars reticulata has been shown to suppress seizures in most models of epilepsy involving forebrain networks, such as absences or clonic seizures. No such antiepileptic effects were observed, however, in genetically audiogenic rats exhibiting tonic seizures generated in the brainstem. This suggests a constitutive dysfunction of the nigral GABAergic neurotransmission in this strain of rat or a selective action of the nigral control on specific networks. In the present study, we first confirmed that bilateral injection of muscimol (700 pmol/side) in the substantia nigra had no effect in Wistar rats with audiogenic seizures (Wistar AS). [3H]Muscimol autoradiography suggested a 40% reduced density of GABA(A) receptors in the substantia nigra of Wistar AS, whereas no change was observed in the cortex and the superior colliculus (superficial and intermediate layers), as compared to control animals. In Wistar AS where 40 repetitions of audiogenic stimulations progressively induced generalised convulsive seizures with both tonic and clonic components, bilateral injection of muscimol (350 pmol/side) in the substantia nigra suppressed the clonic component but had no effect on tonic seizures. In hybrid rats issued from cross-breeding between Wistar AS and rats with spontaneous absence seizures, bilateral injection of muscimol (18 pmol/side) in the substantia nigra abolished cortical spike-and-wave discharges, but had no effect on tonic audiogenic seizures at doses up to 700 pmol/side. These results show that despite a decreased number of GABA(A) receptors in the substantia nigra, inhibition of this structure in Wistar AS still leads to inhibition of seizures involving forebrain structures. These results confirm that GABAergic inhibition of the substantia nigra has antiepileptic effects through the control of forebrain circuits. They suggest that this control mechanism has no inhibitory effect on circuits underlying audiogenic tonic seizures.
Acoustic Stimulation↗
Medium-voltage 5-9-Hz oscillations give rise to spike-and-wave discharges in a genetic model of absence epilepsy: in vivo dual extracellular recording of thalamic relay and reticular neurons.
In humans with absence epilepsy, spike-and-wave discharges develop in the thalamocortical system during quiet immobile wakefulness or drowsiness. The present study examined the initial stage of the spontaneous development of spike-and-wave discharges in Genetic Absence Epilepsy Rats from Strasbourg. Bilateral electrocorticograms were recorded in epileptic and non-epileptic rats under freely moving and undrugged conditions and under neuroleptanalgesia. Short-lasting episodes of medium-voltage 5-9-Hz (mean=6-Hz) oscillations usually emerged spontaneously from a desynchronized electrocorticogram and in bilateral synchrony in both rat strains. These oscillations were distinguishable from sleep spindles regarding their internal frequency, duration, morphology, and moment of occurrence. Spontaneous spike-and-wave discharges developed from such synchronized medium-voltage oscillations, the spike-and-wave complex occurring at the same frequency as the 5-9-Hz wave. Because the thalamus is thought to play a significant role in the generation of spike-and-wave discharges, dual extracellular recording and juxtacellular labelling of relay and reticular neurons were conducted to study the thalamic cellular mechanisms associated with the generation of spike-and-wave discharges. During medium-voltage 5-9-Hz oscillations, discharges of relay and reticular cells had identical patterns in epileptic and non-epileptic rats, consisting of occasional single action potentials and/or bursts (interburst frequency of up to 6-8 Hz) in relay cells, and of rhythmic bursts (up to 12-15 Hz) in reticular neurons, these discharging in the burst mode almost always before relay neurons. The discharge frequency of reticular bursts decelerated to 6 Hz by the beginning of the spike-and-wave discharges. During these, relay and reticular neurons usually fired in synchrony a single action potential or a high-frequency burst of two or three action potentials and a high-frequency burst, respectively, about 12 ms before the spike component of the spike-and-wave complexes. The frequency of these corresponded to the maximal frequency of the thalamocortical burst discharges associated with 5-9-Hz oscillations. The patterns of relay and reticular phasic cellular firings associated with spike-and-wave discharges had temporal characteristics similar to those associated with medium-voltage 5-9-Hz oscillations, suggesting that these normal and epileptic oscillations are underlain by similar thalamic cellular mechanisms. In conclusion, medium-voltage 5-9-Hz oscillations in the thalamocortical loop give rise to spike-and-wave discharges. Such oscillations are not themselves sufficient to initiate spike-and-wave discharges, meaning that genetic factors render thalamocortical networks prone to generate epileptic electrical activity, possibly by decreasing the excitability threshold in reticular cells. While these GABAergic neurons play a key role in the synchronization of glutamatergic relay neurons during seizures, relay cells may participate significantly in the regulation of the recurrence of the spike-and-wave complex. Furthermore, it is very likely that synchronization of relay and reticular cellular discharges during absence seizures is generated in part by corticothalamic inputs.
Action Potentials↗
Differential sensitivity to inverse agonists of GABA(A)/benzodiazepine receptors in rats with genetic absence-epilepsy.
A strain of Wistar rats, genetic absence epilepsy rats from Strasbourg (GAERS), was selected and inbred over 40 generations for occurrence of spontaneous spike-wave discharges characteristic of absence seizures, simultaneously with a strain of non-epileptic rats (NER). GAERS demonstrate an excessive sensitivity to antagonists of the GABA(A) receptor. The sensitivity to convulsions induced by various inverse agonists of the GABA(A)/benzodiazepine receptor was compared in GAERS and NERs. The beta-carbolines FG 7142 and DMCM, and the imidazobenzodiazepines RO 19-4603 and the alpha 5-selective RY 024 were several times more convulsant in GAERS than in NERs. The largest differences were found with the non-selective RO 19-4603- and FG 7142. The proconvulsant imidazobenzodiazepine RO 15-4513, binding also to diazepam-insensitive receptors, had low efficacy. The high affinity binding of GABA(A)/BZD receptors with (3H) RO 15-1788 in the brain of naive rats and after administration of FG 7142 did not differ in GAERS and NERs. The data indicate that the hypersensitivity of GAERS to various inverse agonists of the GABA(A)/benzodiazepine receptor involves cortical GABA(A) receptors and is not related to differential activity of a subunit-selective receptor.
Animals↗
Vigabatrin protects against hippocampal damage but is not antiepileptogenic in the lithium-pilocarpine model of temporal lobe epilepsy.
In temporal lobe epilepsy (TLE), the nature of the structures involved in the development of the epileptogenic circuit is still not clearly identified. In the lithium-pilocarpine model, neuronal damage occurs both in the structures belonging to the circuit of initiation and maintenance of the seizures (forebrain limbic system) as well as in the propagation areas (cortex and thalamus) and in the circuit of remote control of seizures (substantia nigra pars reticulata). In order to determine whether protection of some brain areas could prevent the epileptogenesis induced by status epilepticus (SE) and to identify the cerebral structures involved in the genesis of TLE, we studied the effects of the chronic exposure to Vigabatrin (gamma-vinyl-GABA, GVG) on neuronal damage and epileptogenesis induced by lithium-pilocarpine SE. The animals were subjected to SE and GVG treatment (250 mg/kg) was initiated at 10 min after pilocarpine injection and maintained daily for 45 days. These pilo-GVG rats were compared with rats subjected to SE followed by a daily saline treatment (pilo-saline) and to control rats not subjected to SE (saline-saline). GVG treatment induced a marked, almost total neuroprotection in CA3, an efficient protection in CA1 and a moderate one in the hilus of the dentate gyrus while damage in the entorhinal cortex was slightly worsened by the treatment. All pilo-GVG and pilo-saline rats became epileptic after the same latency. Glutamic acid decarboxylase (GAD67) immunoreactivity was restored in pilo-GVG rats compared with pilo-saline rats in all areas of the hippocampus, while it was increased over control levels in the optical layer of the superior colliculus and the substantia nigra pars reticulata. Thus, the present data indicate that neuroprotection of principal cells in the Ammon's horn of the hippocampus is not sufficient to prevent epileptogenesis, suggesting that the hilus and extra-hippocampal structures, that were not protected in this study, may play a role in the genesis of spontaneous recurrent seizures in this model. Furthermore, the study performed in non-epileptic rats indicates that chronic treatment with a GABAmimetic drug upregulates the expression of the protein GAD67 in specific areas of the brain, independently from the seizures.
Animals↗
[Cognitive consequences of Rolandic Epilepsy].
Idiopathic focal epilepsies and particularly rolandic epilepsy are considered to have an excellent outcome with spontaneous recovery during adolescence. The characterization of this syndrome in 1959 by Beaussart and Nayrac was a great progress for childhood epileptology: the existence of a focal epilepsy with a good prognosis and no underlying brain lesion, so-called "benign" epilepsy, was recognized. Since the first descriptions, numerous neuropsychological studies were performed showing variable results. All the studies agree with the fact that children with rolandic epilepsy keep a normal global intellectual efficiency and a good long-term outcome. Nevertheless, some children may suffer transiently during the active phase of the epilepsy from oromotor dysfunction, neuropsychological deficits, or attention deficits with learning disorders. The analysis of cognitive and neurophysiological correlations evidenced a significant correlation between the epileptic focus localization and few specific dysfunctions. We evidenced mainly a significant effect of the persistence of a prolonged slow focus and a strong activation of night EEG spike and waves on cognitive decline and attention disorders. These abnormalities are mainly observed during severe or atypical evolutions of rolandic epilepsy. Preliminary longitudinal studies show that these cognitive deficits are transient. Thus, the presence of an active epileptic focus, without underlying brain lesion, could interfere with normal maturation of cognitive function.
Adolescent↗
Semiology of typical and atypical Rolandic epilepsy: a video-EEG analysis.
Since the first descriptions of Rolandic Epilepsy or benign epilepsy with centrotemporal spikes (BECTS), typical and atypical forms have been reported. Indeed, classical focal seizures are sometimes associated with various atypical ictal symptoms and cognitive or behavioural disorders. In an effort to define early clinical and EEG criteria allowing early distinction between typical and atypical forms, we recently conducted a prospective study in a cohort of children with Rolandic Epilepsy. The results of this study have been reported elsewhere. We now discuss the semiological characteristics, and comment on the video-EEG data collected during this study. Symptoms were classified into three major categories: "classical focal seizures"; "spike and wave related symptoms"; and "paraictal symptoms". Classical focal seizures constitute the electroclinical expression of the development and the propagation of a focal cortical neuronal discharge. "Spike and wave related symptoms" are brief neurological or neuropsychological phenomena having a relatively strict temporal relation with individual components of isolated focal or generalized spikes and waves. "Paraictal symptoms" consist of acquired progressive and fluctuating motor or cognitive deficits and are not directly correlated with Todd paralysis. We present detailed video-EEG material of selected cases and discuss the usefulness of such distinctions in terminology. We suggest that variability in clinical expression probably reflects the implication of different pathophysiological mechanisms, which in turn could explain differences in sensitivity to treatment. (Published with videosequences.)
Arm↗
Benign childhood epilepsy with centrotemporal spikes: is it always benign?
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Brain↗