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It is well admitted now that gliosis participates in epileptogenesis, particularly in symptomatic focal epilepsies, like temporal lobe epilepsy. Indeed, astrocytic and microglial activation was shown to release numerous inflammatory factors that modify neuronal excitability or contribute to neuronal loss. These redundant processes maintain chronic epilepsy. However, other sources of inflammation exist. Several studies pointed out the epileptogenicity of blood-brain barrier disruption due to the leakage of leukocytes and serum proteins, triggering inflammatory and immune responses which disturb the neuronal environment. Recently, it was proposed that peripheral inflammation plays a key-role in epilepsy, mainly mediated by circulating cytokines which promote leukocyte extravasation., (© Société de Biologie, 2011.)

Epilepsy surgery is possible in specific cases of localisation-related pharmaco-resistant epilepsy and can often lead to seizure-freedom condition. A presurgical diagnostic workup is necessary to localise the epileptic focus and assess the risks of post-operative neurological or cognitive deficits. Even when the brain MRI does not reveal any lesion, other imaging techniques and in some cases intracranial EEG recordings can lead to successful surgery. All patients suffering from pharmaco-resistant epilepsy should be referred to an expert centre to confirm the diagnosis and evaluate the possibility of epilepsy surgery. In children, early epilepsy surgery can allow better continuation of cognitive development and education.

The notion that cognitive and behavioural dysfunctions of epileptic origin can be prolonged and with an insidious onset, has meant a radical conceptual change about epilepsy considered so far uniquely as a paroxysmal disorder. Also, these dysfunctions can be the only observable manifestations of the disorder. It is particularly true in some epileptic syndromes with onset in childhood. Epileptic dysfunctions are characterized by a discontinuity in time (intermittent, recurrent), in space (cerebral localization of the dysfunction and its spread). They often have a significant relationship with sleep. These features, with sometimes the existential dimension of some symptoms (intermittent loss of the flux of consciousness, intermittent perceptual distortions or cognitive-emotional dysfunction) are not seen in any other congenital or acquired disorders of the human brain. Longitudinal clinical studies in which the epileptic variable can be directly correlated with the precise study of the cognitive dysfunction (also with increasingly complex methods of brain imaging) are a difficult, relatively new multidisciplinary task, especially in the very young child. Case examples of children followed from early childhood to adulthood will illustrate the diversity of observed cognitive and behavioural abnormalities directly caused by the epileptic activity which can be massive or very discrete. One is only beginning to document precisely the late consequences (or absence of) of some early childhood epilepsies that had a direct impact on developing brain function at some point.

Purpose: The aim of the study was to define the usual and pathological modifications arising in the brain following hemispherotomy for intractable epilepsy in children., Methods: Preoperative MRI and postoperative imaging scans (CT in the first week, MRI at 3 months and 1 year after surgery) were reviewed in a series of 52 patients, average age 8 years and 7 months, with intractable epilepsy due to dysplasia, Rasmussen's encephalitis, ischemic lesions and/or Sturge-Weber disease. The posterior fossa, brain parenchyma, ventricles and subdural space were also analyzed., Results: Hemispheric scarring was a typical finding on CT and MRI as a consequence of the surgical procedure. Also frequently seen were small subdural effusions, bleeding along the surgical scar on early CT, and chronic subdural effusions with no mass effect on mid-term and late MRI scans. Other features - such as large subdural effusions that required external shunts and hydrocephalus - were rare, but severe, and considered to be postoperative complications. In contrast to the complications associated with other surgical techniques such as hemispherectomy, infection, extensive edema or hemosiderosis were never found in our series., Conclusion: Hemispherotomy is a surgical technique performed to treat intractable epilepsy. Our findings will help to identify the typical morphology of postsurgical scars, and to differentiate the usual features and complications seen in the postoperative period on CT and MRI brain scans.

Malformations of cortical development (MCD) represent a major cause of developmental disabilities and severe epilepsy. Advances in imaging and genetics have improved the diagnosis and classification of these conditions. Up to now, eight genes have been involved in different types of MCD. Lissencephaly-pachygyria and subcortical band heterotopia (SBH) represent a malformative spectrum resulting from mutations of either LIS1 or DCX genes. LIS1 mutations cause a more severe malformation in the posterior brain regions. DCX mutations usually cause anteriorly predominant lissencephaly in males and SBH in female patients. Additional forms are X-linked lissencephaly with corpus callosum agenesis and ambiguous genitalia associated with mutations of the ARX gene. Lissencephaly with cerebellar hypoplasia (LCH) encompass heterogeneous disorders named LCH type a to d. LCHa are related with mutation in LIS1 or DCX, LCHb with mutation of RELN gene, and LCHd could be related with TUBA1A gene. Polymicrogyria encompass a wide range of clinical, aetiological and histological findings. Among several syndromes, recessive bilateral fronto-parietal polymicrogyria has been associated with mutations of the GPR56 gene. Bilateral perisylvian polymicrogyria showed a linkage to chromosome Xq28 in some pedigrees, and mutations in SRPX2 gene in others conditions. X-linked bilateral periventricular nodular heterotopia (BPNH) consists of BPNH with focal epilepsy in females and prenatal lethality in males. Filamin A (FLNA) mutations have been reported in some families and in sporadic patients. It is possible to infer the most likely causative gene by brain imaging studies and other clinical findings. Based on this experience, a detailed phenotype analysis is needed to develop the most efficient research on MCD in the future.

The definition of the epileptogenic zone is a concept proposed by Jean Bancaud and Jean Talairach based on the anatomical, electrical and clinical correlations established from stereoelectroencephalographic recordings. They believed the epileptogenic zone to be the "region of the beginning and the primary organization" of ictal discharges. The opinion of North American authors is different: the epileptogenic zone is the "what to remove area" to produce freedom from seizures. This surgical definition assumes postsurgical validation. The aim of this paper is to show how to define the epileptogenic zone from all the stereoelectroencephalographic recording data.

The insula is the only cortical part of the brain that is not visible on the surface of the hemisphere, because it is totally covered by the frontoparietal and temporal opercula. The insula is triangular in shape and is separated from the opercula by the anterior, superior, and inferior peri-insular sulci. It is morphologically divided into two parts by the central insular sulcus. The anterior part of the insula bears three short gyri, and its posterior part contains two long gyri. The vascular supply of the insula is mainly provided by the M2 segment of the middle cerebral artery, a substantial obstacle to any open or stereotactic procedure aiming at the insular region. The insula is functionally involved in cardiac rhythm and arterial blood pressure control, as well as in visceromotor control and in viscerosensitive functions. There is substantial evidence that the insula is involved as a somesthetic area, including a major role in the processing of nociceptive input. The role of the insula in some epilepsies was recently investigated by means of depth electrode recordings made following Talairach's stereoelectroencephalography (SEEG) methodology. It appears that ictal signs associated with an insular discharge are very similar to those usually attributed to mesial temporal lobe seizures. Ictal symptoms associated with insular discharges are mainly made up of respiratory, viscerosensitive (chest or abdominal constriction), or oroalimentary (chewing or swallowing) manifestations. Unpleasant somatosensory manifestations, always opposite the discharging side, are also frequent. Ictal signs arising from the insula occur in full consciousness; these are always simple partial seizures. Seizures arising from the temporal lobe always invade the insular region, but in approximately 10% of cases, the seizures originate in the insular cortex itself. These data explain that there has been a rebirth of interest in the insula from a surgical perspective over the past few years. The literature contains no reports of cases of resection of insular cortex alone; most insular resections are performed in the context of temporal resection, when there is some evidence of seizures originating in the insula itself. Such procedures are risky and their efficacy, in terms of postoperative surgical outcome, has not yet been clearly assessed. In this context, less invasive procedures, such as SEEG-guided radiofrequency thermolesions of the insular cortex, are under investigation.

In psychopathology, few studies have been focused on the psychiatric complications of medically refractory mesial temporal lobe epilepsy (MTLE). The aim of the present study was to study NG's capacities, who presented emotional change after right temporal epilepsy surgery with phobias and empathy disorders. NG was examined in two emotional judgment tasks: one explicit and another implicit. For negative stimuli, NG had attraction in the explicit task and dependency in the implicit task. This study suggests that surgical intervention might be one of the causes of postoperative psychiatric disorders in patients with MTLE. MTLE patients have to be explored with neuropsychological paradigms.

Surgery of partial epilepsies in childhood has largely benefited from the recent advances of imaging techniques, which carry a triple goal: (1) to contribute to the localization of the epilepsy onset zone, (2) to detect and delineate an underlying lesion, and (3) to study the spatial relationship between the epileptogenic zone and the neighboring functional cortex, in order to select patients and plan the resection. This noninvasive presurgical imaging workup must be compared to clinical and electrical data to estimate the postoperative prognosis, while invasive techniques such as SEEG, cortical stimulations, and IAT often remain indispensable in difficult cases, i.e., in cryptogenic epilepsies. As in adults, advances in MRI allow us to detect more and more subtle underlying lesions, but this requires repeating MR studies during early childhood and using adapted sequence parameters to account for ongoing myelination. Ictal SPECT and PET imaging prove especially useful in planning depth electrode placement when video-EEG is not contributive, when MRI looks normal or shows multiple abnormalities, or in cases of discrepant findings. Multimodal imaging greatly enhances the sensitivity of all of these techniques. Finally, functional MRI of motor and language functions provide noninvasive cortical mapping of essential functions, using age-adapted paradigms, in cooperating children from age five to six and from IQs around 60.

Nontumoral epileptogenic lesions account for the major pathological group of surgical specimens obtained from patients with temporal or extratemporal drug-resistant epilepsy. Hippocampal sclerosis remains the predominant etiology, but cerebral cortical dysplasias actually make up the second major cause of nontumoral epilepsy and are increasingly recognized. The percentage of vascular lesions or glial/glio-mesodermal scars remains stable, but the minor or nonspecific lesion group is decreasing because of imaging investigation technique improvement.

We report here the results of the first survey on epilepsy surgery activity in France. Data from a questionnaire sent to 17 centers practicing epilepsy surgery were analyzed. All centers responded; however, all items were not completely documented. Over 50 years, more than 5000 patients have been operated on for drug-resistant epilepsy and more than 3000 patients underwent some invasive monitoring, most often SEEG. Currently, nearly 400 patients (including more than 100 children) are operated on yearly for epilepsy in France. Over a study period varying among centers (from two to 20 years; mean, 9.5 years), results from more than 2000 patients including one-third children were analyzed. Important differences between adults and children, respectively, were observed in terms of location (temporal: 72% versus 4.3%; frontal: 12% versus 28%; central: 2% versus 11%), etiology (hippocampal sclerosis: 41% versus 2%; tumors 20% versus 61%); and procedures (cortectomy: 50% versus 23%; lesionectomy: 8% versus 59%), although overall results were identical (seizure-free rates following temporal lobe surgery: 80.6% versus 79%; following extratemporal surgery: 65.9% versus 65%). In adults, the best results were observed following temporomesial (TM) resection associated with hippocampal sclerosis or other lesions (class I: 83% and 79%, respectively), temporal neocortical (TNC) lesional (82%), while resections for cryptogenic temporal resections were followed by 69% (TM) and 63% (TNC) class I outcome. Extratemporal lesional resections were associated with 71% class I outcome and cryptogenic 43%. In children, the best results were obtained in tumor-associated epilepsy regardless of location (class I: 80%). A surgical complication occurred in 8% after resective surgery - with only 2.5% permanent morbidity - and 4.3% after invasive monitoring (mostly hemorrhagic). Overall results obtained by epilepsy surgery centers were in the higher range of those reported in the literature, along with a low rate of major surgical complications. Growing interest for epilepsy surgery is clearly demonstrated in this survey and supports further development to better satisfy the population's needs, particularly children. Activity should be further evaluated, while existing epilepsy surgery centers as well as healthcare networks should be expanded.

Magnetic resonance imaging is an imaging technique allowing morphological and functional study of the brain. Algorithmic and technical advances offer new insights in such brain studies using new approaches to search epileptogenic lesion. Voxel based analysis appears as the dominant methodology to study grey and white matter using the following contrast: T1, T2, T2 relaxometry, magnetization transfert and diffusion weighted imaging. Ongoing development focuses on sulcal morphometry and gyrification index, to improve our understanding of developmental epilepsy. Magnetic resonance spectroscopy appears as a promising tool following availability of high field strength clinical MRI and evidence about its utility in the field of epileptology. Functional MRI benefits from such high field strength and new pulse sequence using diffusion gradients to probe neuronal firing.

Background and Purpose: Taylor-type focal cortical dysplasias (TTFCD) represent a particular pathological entity responsible for severe drug-resistant epilepsy of extratemporal location. Epilepsy can be surgically cured if complete removal of the lesion can be performed. However, identification on imaging may be difficult and negative standard MRIs are not rare. The frequent location of TTFCD in the central region restrains the possibilities of complete resection. We report a series of patients operated on for intractable epilepsy associated with TTFCD in the central area., Patients and Methods: Between 2000 and 2006, of 34 consecutive patients with TTFCD, 17 had a lesion located in the central area. MRI was considered normal in eight, although in five a subtle gyral abnormality was disclosed on further analysis. A (18)FDG PET scan performed in 16 cases demonstrated focal hypometabolism in 15 that correlated with abnormalities on MRI when visible. SEEG performed in 13 cases revealed typical abnormalities for TTFCD in 10 cases. At resection, cortical and subcortical stimulations of the dysplastic cortex did not elicit a motor response., Results: Postoperative motor or sensory deficit was observed in 13 patients--severe in four--which subsequently resolved completely in seven. Six patients had a minor permanent, motor or sensory deficit. Four patients were reoperated for seizure recurrence and residual dysplastic tissue was found at reoperation in three cases. Average postoperative follow-up was 3.7 years. Sixteen patients (94%) were in Engel Class I (65% in Class IA)., Conclusion: This study suggests that surgical resection of central region TTFCD may be associated with favorable seizure outcome and no or minor functional permanent disability. In cases of seizure relapse, reoperation can be performed without further permanent deficit and lead to seizure-free outcome. Future techniques for intraoperative detection of these lesions could optimize their complete resection in functional areas.

Background and Purpose: Animal models have provided very valuable data to specify the physiopathological mechanisms of the various forms of epilepsy. However, the question arises of knowing which of these experimental results are relevant to the human epileptic brain. The development of epileptic surgery makes it possible to directly study the functional properties of human brain tissue in vitro and to analyze the mechanisms underlying seizures and epileptogenesis. We review some of the results obtained over the last few years in our laboratory based on electrophysiological, immunocytochemical and molecular experiments conducted on human brain tissue., Results: This review covers a number of the mechanisms of neuronal synchronizations generating epileptiform discharges, including the role of electrical synapses connecting the inhibitory interneurons, particularly in Taylor-type focal cortical dysplasia and the functional lability of GABAergic inhibition in epileptogenic human cortical tissue, which may sustain triggering and propagation of seizures. Some of these mechanisms have not been described in animal models., Conclusions: Studies on human tissue, when carefully designed, are necessary to validate the data collected on animal models and will continue to provide us with new and important information on the cerebral changes related to epilepsy. Moreover, these studies allow development of a class of antiepileptic drugs that have a completely new mechanism of action, which could be effective in the treatment of drug-resistant epilepsies.

Vagus Nerve Stimulation (VNS) is recognized as an efficient procedure for controlling seizures in patients with drug-refractory epilepsies. It is used as a palliative procedure as a complement to conventional treatment by antiepileptic (AE) drugs and, according to literature, 40 to 50p.cent of patients report a decrease in seizures frequency >or=50p.cent, which is usually accepted to classify patients as responders in add on AE drug trials. The objectives of this study based on retrospective analysis of 50 consecutive patients with partial (39) or generalized (11) refractory epilepsy non eligible for surgery were; firstly to evaluate the global long term VNS efficacy and secondly to identify potential predictors of the VNS effects on seizure frequency. No patient has been seizure free at any moment of the follow up (2.8+/-1.8 years, max: 6 years) and the AE has been maintained in all. During follow up 44, 66, 61 and 58p.cent of patients were classified as responders at 6 months, 1, 2 and 3 years, respectively. Logistic regression analysis showed that: the percentage of responders at 6 months of follow up and later was significantly higher than that before 6 months (p=0.002); generalized epilepsy was predictive of a better outcome as compared to partial epilepsy (p=0.03); there was a trend for a better outcome in partial epilepsies symptomatic of a focal lesion than in those with normal brain MRI (p=0.06). These results are in line with previously published data in terms of global efficiency and confirm that seizures control does not reach its maximal level before at least one year of VNS. In severe generalized epilepsies (either secondary or cryptogenic) manifesting by frequent falls due to atonic or tonic-clonic generalized seizures VNS is a useful palliative procedure, which entails much les of surgical risk than callosotomy. The better VNS effects in patients with partial epilepsy possibly reflect the high incidence in our series of Malformations of Cortical Development, which have been identified as one the few variables possibly predictive of a response over 50p.cent of seizures frequency reduction.

Epilepsy is the more frequent clinical manifestation of hemispheric cavernomas in 50 to 75% of symptomatic cases; the annual risk of a first seizure is evaluated from 1.5 to 2.5%. As for all epileptogenic lesions, many questions arise: Is the pathologic tissue or the perilesional cortex responsible for the epileptic symptoms? Is the risk related with the topography of the lesion? Is the prognosis of the epilepsy related with the number of seizures? Can the epilepsy become drug-resistant? Can surgical treatment cure the epilepsy? When surgery is indicated, should lesionectomy alone or lesionectomy plus perilesional tissue resection be performed? The iron and the hemosiderin deposits induce metabolic perturbations and tissue reorganization (gliosis and sclerosis) around the cavernoma. These cortical modifications seem to be responsible for the epileptic discharges but this is difficult to demonstrate. Epileptic discharges have been recorded in the perilesional tissue in only one study of the literature. Drug therapy can usually control the seizures, but it appears that surgery is more effective when the epilepsy is recent and the seizures are not too frequent. For these reasons it would appear licit to propose the resection of the lesion when the surgical risk is not too great. In case of drug-resistant epilepsy, the same function-targeted surgical strategy may be used as for the management of any severe epilepsy.

Introduction: Parry-Romberg's syndrome or progressive facial hemiatrophy is a rare disorder of unknown etiology which may be accompanied by neurological complications, frequently epilepsy, usually focal refractory epilepsy. The associated brain lesions are located on the same side as the half face atrophy and may progress., Observation: We report the cases of two patients with Parry-Romberg's syndrome and epilepsy. Neurosurgery was performed in one patient, enabling a histological study., Conclusion: The link between Parry-Romberg's syndrome and epilepsy is discussed and the neurodevelopmental theory with vascular dysgenesis is suggested.

In neuropediatry, paroxysmal phenomenons characteristic of the child can be of an epileptic or non epileptic origin. A correct clinical diagnosis has to be done straightaway in order to best select the complementary exams, establish the prognosis and decide the treatment. We will describe the clinical presentation of the main paroxysmal phenomenons found in children.

In Senegal, as in other under developed countries, the delays before seeking medical treatment are long varying from 2 to 12 according to studies. This is related to the fact that in traditional African communities, prejudices and believes delayed medical management which is seeked after failure of traditionnal treatments. The objectives of this study concerning therapeutic itinerary of epileptics in the EEG laboratory at the Neurology Department at CHU in Dakar were to evaluate the average latency of medical consultation and to identify the recourse path by patients receiving antiepileptic treatment. We conducted from March to may 2001, a cross disciplinary study, with a sample size of 212 patients. 79.2% of patients were less than 30 years old. They first seek treatment in hospitals in 36.8%, traditional practionners in 35.8%, health centers in 23%, and private clinics in 4%. The average delay of treatment in modern structures was by 13.4 +/- 4.7 months. The towards the healers was linked to faulty beliefs in 61.8% of the cases, lack of information (22.4%), or a lack of financial means (2.6%). The patients were refeared to traditional healers in 6.7% of the cases for reasons of confidence in traditional medecine. The orientation to neurology clinic was recommended by health personal in 83% of the cases, family (14.6%), or the healer (1.4%). The long and difficult journey of epileptics in Senegal remains marked by exclusion, absence or delay of medical attention.

Intermittent left vagus nerve stimulation is a novel therapeutic modality that can be proposed to patients with a refractory epilepsy and for whom resective surgery is not an option. Its precise mechanism of action is not known. Controlled studies have shown that its efficacy is similar to that of antiepileptic drugs: 50% decrease in seizure frequency in 40% patients after two years. Side effects which are generally mild to moderate are the result of a diffusion of the stimulation to the larynx. No CNS side effect has been reported.

Convulsions and epilepsy in the child include widely diverse disorders, ranging from simple and benign to complex and severe. Initially, the general practitioner must consider the various diagnoses in order to prescribe appropriate investigations and treatment (now complex and numerous), or to orient the diagnosis. In the case of paroxysm, the initial step is to affirm the diagnosis of epileptic seizure, especially on the basis of the descriptions made by the child and by witnesses, possibly with the aid of an EEG. The second step is to determine the etiology, differentiating isolated seizures occurring in a particular context (for example febrile convulsions) from epileptic seizures with no special context. The description of the seizure and the inter-critical EEG lead to classifying the seizure as partial or generalised and, if it is repeated, to consider it as composing one of the childhood epileptic syndromes.

The decision to treat and the choice of the right antiepileptic drug depend on frequency, severity, type of seizures, epileptic syndrome, familial and school life, impact of seizures. On the other hand it is important to know the pediatric characteristics of pharmacology, tolerance, possible side effects and efficacy of each antiepileptic drug. Some antiepileptic drugs could also worsen some types of seizures. Other therapies can be efficient in refractory epilepsies: steroids, vague nerve stimulation, ketogenic diet and surgery. Clinical informations are essential to appreciate drugs efficacy and safety. Physician could be very important for the social and school insertion of epileptic children.

Study of idiopathic epilepsy in childhood can distinguish various syndromes on the basis of clinical and electroencephalographic criteria. There is much overlapping between the syndromes described. The aim of the classification is to define precisely the prognosis of each disorder and to approach treatment effectively and safely, avoiding aggravation of a condition by poorly adapted prescription. The main distinction is between partial seizures, among which the principal is centro-temporal with spikes, and generalised seizures of which the most common are absence epilepsy and juvenile myoclonic epilepsy. Since the phenotypes are well defined, molecular genetic studies should lead to better knowledge of the complex biochemical mechanisms of idiopathic epilepsy. Seizures that occur without lesions are well managed by treatment in most cases and have a good psychosocial prognosis. The possibility of acquiring autonomy, familial overprotection, restrictions and interdictions must all be kept in mind in the psychological, social and educational handling of persons with epilepsy, most of which are benign cases.

The syndrome of coeliac disease, epilepsy and cerebral calcifications is a rare complication of coeliac disease. The pathological changes consist in a patchy pial angiomatosis and resemble those of Sturge-Weber syndrome, whose variant without port-wine angioma must be ruled out. Typical course includes three stages leading to a severe encephalopathy. However, the mental impairment is extremely variable. The pathogenetic process is so for unknown; main clues involve a chronic folic acid deficiency or a HLA-related autoimmune disorder. Treatment requires early gluten-free diet and anti-epileptic drug.

Inactivation of an epileptogenic focus by dividing it into sub-unities unable to maintain epileptic activity has been demonstrated in animals. Based on these experiments, multiple subpial transections have been performed in patients suffering from partial drug-resistant epilepsies when resection of the epileptogenic cortex was not possible. In order to develop a new surgical technique for such epilepsies, the authors present an initial study of multiple cortical laser photolesions on the rabbit brain. The aim of this study is to assess the histological lesions created on the cortex with a laser at a chronic stage, and to compare the electrical paroxysmal activity of a penicillin focus on the laser irradiated cortex and on the non radiated cortex in the same animal. Twenty-five adult albino rabbits were used for this study. Both hemispheres of 19 rabbits have been exposed; 14 to 35 photolesions in a network were performed on one hemisphere using a 1.064 microns wavelength Nd-YAG laser. Six to twenty-one days later, a penicillin-induced focus was created on both hemispheres, a corticographic study was performed, and each animal was sacrificed for histological study of the brain. For the 6 last animals a high-power 0.805 micron wavelength diode laser was used with the same protocol. Histological study was solely performed in order to compare the effects of both lasers. In 11 animals electrocorticographic control was reliable. Time to first spike occurrence after penicillin application was significantly increased on the treated hemisphere as compared to the untreated one (1' to 14'30" and 10" to 6', respectively; p < 0.01) and the number of spikes per minute at early and late counts was significantly smaller on the treated hemisphere as compared to the untreated one (1 to 29 and 2 to 70, respectively; p < 0.02). Histologically the lesions appeared as cone-shaped coagulation necrosis surrounded by an area of macrophagic reaction, angiogenesis and gliosis. With the diode laser, some lesions included ischemic changes extended in the white matter. This study demonstrated the possibility of creating limited and reproducible photolesions using the laser light energy, without extensive destruction of the cortex. These lesions were reaching from one third to the totality of the cortical depth, depending on laser exposure parameters. This study also demonstrated that these photolesions arranged in a network and at a chronic stage were associated with a significantly reduced paroxysmal activity of a penicillin focus when compared to intact cortex. Since such lesions did not totally isolate cortical sub-unities, spiking was still recorded from the irradiated cortex, but at a lower rate, suggesting a disorganization of the local neuronal network responsible for paroxysmal activity.

Histopathologic findings in 110 cortical resections performed for medically intractable epilepsy are reported. The abnormalities observed in our series fell into seven categories: vascular lesions, tumors, non-vascular malformative lesions, focal accumulation of polyglucosan bodies, non infectious inflammatory lesions, hippocampal sclerosis, and mild non-specific lesions. There was no microscopic abnormality in 14 cases. Several patients presented a double pathology, most often an hippocampal sclerosis as one part of the dual pathology.

Morphological brain asymmetries of the planum temporale, Sylvian fissure and insula were assessed by stereotactic-stereoscopic angiography in 70 epileptic patients without neuroradiological abnormalities, at angiography and CT in these regions. Fifty four patients were right-handers and 16 not right-handers. In 57 patients hemispheric speech dominance was evaluated by the Wada test and electroclinical correlations: in 8 patients, 4 men and 4 women, speech was located in right hemisphere or bilaterally. Lateral asymmetry was present in the regions examined. Correlations between the morphological measurements were not identical in the left and the right hemisphere. No significant relationship was found between anatomical asymmetries and handedness. In men, but not in women, significant differences were observed between the right-bilateral speech group (4 subjects) and the left speech group (31 subjects): right hemisphere regions, including the insula, were larger in the former than in the later whereas, left hemisphere regions were identical in both groups.

We report two cases of gradual facial hemiatrophy (Parry-Romberg syndrome). The first patient, an adolescent girl under treatment for hypothyroidism, presented with a very severe form combining advanced facial hemiatrophy, epilepsy with hemi-generalized seizures and hemiatrophy of the brain. The second patient was a girl who presented with localized scleroderma resembling a saber injury, homolateral cerebral atrophy and contralateral hemiparesis. Our two cases are evidence in support of a close relationship between saber injury-like scleroderma and the Parry-Romberg syndrome.

In former investigations on human focal epilepsy and on experimental epilepsy by cobalt implantation, the authors have demonstrated the signaletic importance of "activated astrocytes": cortical astrocytes endowed with a modified metabolism and an accelerated turnover. The present study concerns the results of the intra-amygdaloid injections of kainic acid, a strong excitatory and neurotoxic amino acid. Injections in semi-chronic conditions in the rat lead to electrical and motor seizures and to the production of activated astrocytes not only in regions that might trigger off epileptic seizures (cerebral cortex, amygdala, possibly hippocampus), but also in the neostriatum. Stimulation of this last region results in a Huntington chorea-like syndrome. Thus, the importance of activated astrocytes must be extended to include other conditions of intense hyperactivity of neurons than epilepsy.

The author reports the discovery of an original entity, the activated astrocyte, which is an essential component and the first anatomical sign of the epileptogenic focus. The importance of the activated astrocyte is demonstrated by the fact that it is observed before the clinical signs appear and as soon as the first spikes are recorded on the electrocortigram. Cautious conclusions are drawn. The authors recognizes the essential role of the neurons and does not suggest that astrocytes are the cause of epilepsy. However, since astrocyte activation is observed before the first electrical signs announce the beginning of an epileptogenic focus, he suggests that activated astrocytes probably offer morphological evidence of certain mechanisms closely concerned in the formation of the epileptogenic focus. The metabolic activation of the astrocyte is not surprising, and is probably related to the increase in loco-regional metabolism due to neuronal hyperactivity, the starting point of epilepsy. It confirms current opinion, especially in biochemistry, on the importance of the glial cells in the neuronastrocyte association. This work opens up certain prospects. First, the significance of the activated astrocyte in the context of current biochemical, neuro-physiological and morphological studies of the glial compartment is a promising research field. Second, from the clinical angle, it is very important to be able to identify an epileptogenic gliosis on the basis of activated astrocytes. Used in conjunction with modern neuro-physiological techniques to locate the epileptogenic focus, the search for activated astrocytes in biopsy material obtained stereotactically should permit better detection of the affected area and thus ensure more successful surgery in cases of focal epilepsy resistant to medication.

Previous anatomochemical and experimental investigations had resulted in the histochemical characterisation of the epileptogenic focus by the presence of "activated astrocytes"; cortical reactive astrocytes acquiring an intense activity of sundry dehydrogenases (DH) and becoming visible in spite of the positivity of the neuropil, and stopping at the amylose step in the synthesis of glycogen. This activation exists from the first electrical sings of epilepsy and even preceeds them in the case of glucose-6-phosphate DH. The present study deals with the fate of activated astrocytes after the disappearance of electrical signs of the epileptogenic focus produced by implantation of a cobalt powder-gelatin pellet into the cerebral cortex of the rat. After extinction of the focus, high activity of DH persists in astrocytes only in the immediate vicinity of the glial scar surrounding the implant. Later, among the DH investigated only glutamate and specially glucose-6-phosphate DH maintain an activity intense enough to reveal these cells on the background of the neuropil. These results point to a progressive return to a normal metabolism of astrocytes after the disappearance of the electrical signs of epilepsy by way of steps similar to those preceeding these signs.

A node of Ranvier in which the nodal axon is post-synaptic to a terminal axon was found in the cerebral cortex of the rat near by an epileptic focus. This type of synapse is in itself a rare observation but is also worthwile considering because of its vicinity with this focus.

In the preoperative investigation of partial epilepsies, electrical characteristics of the so-called epileptogenic area are of critical interest to localize this area. We have always emphasized that the analysis of ictal events themselves, is more valuable than that of inter-ictal anomalis. One reason for this emphasis has been the absence of a reliable method to evaluate the relationship between the topography of ictal and interictal events. An technique for imaging an intracerebral potential field is reported. It allows to analyse the spatio-temporal distribution of interictal events recorded during the SEEG exploration. This technique applied to an illustrative patient shows that the temporo-spatial distribution of interictal spikes is related to that of the ictal discharge itself. A new hypothesis concerning the build up of an epileptogenic area in man is presented.

Hypopigmented macules of epiloia have been studied by photonic and electron microscopy in 7 cases. The number of melanocytes was not decreased but these cells were hypotrophic and had a low tyrosinae activity. The melanosomes were smaller in size and their maturation rate was greatly reduced; many abnormal round and granular melanosomes, phaeomelanosome-like, were observed. In one case, such abnormal melanocytes were also occasionally found in normally pigmented control skin.

The evaluation of M.R.I. in the presurgical management of epilepsies requires establishing the significance of the abnormal signals. In 15 cases, correlations among M.R.I., electrophysiological data obtained by chronic intracerebral recordings and histological examination were studied. Abnormalities were detected by M.R.I. in 12 cases (80%). An accurate epileptic-focus topographical orientation was obtained by M.R.I. in 10 cases. But M.R.I. findings did not coincide with functional data obtained by S.E.E.G. recordings. Abnormalities detected by M.R.I. led to rectify the previous hypothesis about the epileptic focus localization in two cases. One false positive and one case of incomplete data would have been misleading if S.E.E.G. had not been performed. M.R.I. abnormalities included two morphological changes and ten high intensity T2 signals. The increased T2 intensity was more often focal (9) than diffuse (1). Among the 8 cases of increased T2 intensity correlated to the epileptic focus, 1 was histologically normal, 3 corresponded to specific lesions (astrocytoma: 1, hamartoma: 2) and 4 corresponded to non specific lesions (gliosis: 2, spongiosis: 2). When M.R.I. was normal at the site of the epileptic focus, either no alteration (2) or non specific lesions (2) were found. Uncus herniation could not be identified with M.R.I. M.R.I. has proven sensitive, detecting small epileptogenic lesions missed by C.T. Moreover in some cases, high T2 signals have been correlated topographically with the epileptic focus and histologically with non specific lesions. These signals are more likely related to a functional phenomenon such as an increase in water content than to the histopathological findings themselves.

The authors, referring to 29 observed cases, review the characteristics of true renal epilepsy with regard both to attacks and to interictal periods. Their research shows that this type of epilepsy cannot be explained by any specific anatomical lesion but is probably functional and more specifically metabolic; it disappears when renal dialysis is performed. The authors accept that the factors liable to provoke this kind of epilepsy include cellular hyperhydration possibly associated with hypocalcaemia and with a genetic predisposition to convulsions. They reject the role of uraemia. This type of renal epilepsy is compared to the epileptic attacks provoked by renal dialysis.