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Biomedical subjects

F Dubeau

Publications and source records attributed to F Dubeau.

At least 109 records · Page 6Linked to original sources
PubMed1995

Frequency and characteristics of dual pathology in patients with lesional epilepsy.

We studied 167 patients who had identifiable lesions and temporal or extratemporal partial epilepsy. Pathology included neuronal migration disorders (NMDs) (48), low-grade tumors (52), vascular malformations (34), porencephalic cysts (16), and gliotic lesions as a result of cerebral insults early in life (17). MRI volumetric studies using thin (1.5- or 3-mm) coronal images were performed in all patients and in 44 age-matched normal controls. An atrophic hippocampal formation (HF), indicating dual pathology, was present in 25 patients (15%). Abnormal HF volumes were present in those with lesions involving temporal (17%) but also extratemporal (14%) areas. Age at onset and duration of epilepsy did not influence the presence of HF atrophy. However, febrile seizures in early childhood were more frequently, although not exclusively, found in patients with hippocampal atrophy. The frequency of hippocampal atrophy in our patients with low-grade tumors (2%) and vascular lesions (9%) was low. Dual pathology was far more common in patients with NMDs (25%), porencephalic cysts (31%), and reactive gliosis (23.5%). Some structural lesions, such as NMDs, are more likely to be associated with hippocampal atrophy, independent of the distance of the lesion from the HF. In other types of lesions, such as vascular malformations, dual pathology was found when the lesion was close to the HF. A common pathogenic mechanism during pre- or perinatal development may explain the occurrence of concomitant mesial temporal sclerosis and other structural lesions because of either (1) associated developmental abnormalities or (2) predisposition to prolonged febrile convulsions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Operative strategies for patients with cortical dysplastic lesions and intractable epilepsy.

Cortical dysplastic lesions (CDLs) are usually identified by magnetic resonance imaging (MRI). Clinical, electrographic and histologic findings suggest that focal CDLs (FCDLs) are highly epileptogenic, often involve the rolandic cortex, and can present variable degrees of histopathologic abnormalities. An ictal or "ictal-like" bursting pattern of electrographic activity was recorded over dysplastic cortex in 65% of our patients. Resective surgery can eliminate or significantly reduce seizure frequency in many medically intractable patients, depending on lesion location, degree, and extent of histopathologic abnormalities. Best results are achieved when complete or major excision of both the MRI-visible lesion and the cortical areas displaying ictal electrographic activity can be performed. This is more likely when the degree of histopathologic abnormality is mild to moderate or when the lesion is in a temporal lobe. More severe histopathologic abnormalities and central insular or multilobar lesions usually lead to less favorable results: either major excision of the visualized lesion is impractical or the lesion is microscopically more extensive than shown by MRI. Multilobar resection or hemispherectomy for patients with infantile spasms associated with CDLs and for patients with hemimegalencephaly are often associated with dramatic improvement in seizure control. Callosotomy can be performed in selected patients with diffuse CDLs who have intractable drop attacks.

Adolescent↗
PubMed1994

Morbidity of chronic recording with intracranial depth electrodes in 170 patients.

A consecutive series of 170 patients who have been submitted to intracranial depth electrode recordings is reviewed to assess the overall morbidity of the technique. Most patients had bitemporal and frontal electrodes inserted and were monitored for an average period of 18 days. A surgically amenable focus was found in 85% of the cases. There were 4 cases of infection including 2 cerebral abscesses which required surgical evacuation. One patient with frontal lobe atrophy developed an acute subdural hematoma after electrode implantation. There was no death or neurological deficit in the entire series. Morbidity was encountered mainly in the neuropsychological sphere, several patients having developed transient postictal psychosis after repetitive seizures. Our recording technique has been associated with low surgical morbidity. Patients undergoing depth electrode recordings should be closely monitored to minimize the occurrence of psychotic episodes associated with drug withdrawal and increased seizure frequency.

Adult↗
PubMed1994

Late-onset drop attacks in temporal lobe epilepsy: a reevaluation of the concept of temporal lobe syncope.

We report the clinical, radiologic, and EEG features of six patients with temporal lobe drop attacks (TLDA), all of whom underwent temporal resection. Postoperative follow-up of at least 1 year was available in all. TLDA were never the first manifestation but followed the onset of epilepsy after a long delay ranging from 7 to 43 years (mean, 24.4 years). Seizures were of unilateral temporal origin. In one patient, stereo EEG recording of TLDA showed rapid spread of the ictal discharge away from the temporal lobe in less than 1 second. Postoperatively, three patients were seizure free; one has had no TLDA but experiences sporadic auras; another, despite a reduction of more than 50%, continues to have complex partial seizures and TLDA; and the sixth has had sporadic secondarily generalized seizures upon reduction of antiepileptic medication. In conclusion, drop attacks may occur in temporal lobe epilepsy, usually long after the onset of epilepsy. They lead to increased disability and suggest a rapid spread of the ictal discharge and possible involvement of the pontine reticular formation rather than the presence of bitemporal foci or an extratemporal origin.

Adult↗
PubMed1993

Life-threatening focal status epilepticus due to occult cortical dysplasia.

OBJECTIVE: Neuronal migration disorders are usually, but not necessarily, demonstrated by magnetic resonance imaging. Preoperative suspicion of these anomalies in the presence of normal magnetic resonance studies has important practical implications. This study delineates some clinical features that permit early suspicion of focal cortical dysplasia localized in the central and precentral regions. DESIGN: In a retrospective case series, we studied the clinical presentation of four consecutive patients with normal preoperative magnetic resonance images in whom focal cortical dysplasia was found in the surgical specimen. SETTING: Patients were seen in three referral centers specializing in epilepsy surgery. PATIENTS: Four patients (three female), between the ages of 4 and 21 years, had intractable partial seizures leading to resective brain surgery. INTERVENTION: Three patients had corticectomies in the central (two patients) or frontal (one patient) regions. One underwent an en bloc resection of the central area after two unsuccessful corticectomies and cortical transection. RESULTS: Three patients presented with life-threatening focal motor status epilepticus necessitating intubation, and one had epilepsia partialis continua. All had had seizures previously, and the attacks progressed to intractability after 1 1/2 to 3 years. Surgery led to control of the seizures, but only two patients became seizure free (mean follow-up, 15.7 months). All but one developed a postoperative deficit, which eventually improved. CONCLUSIONS: Focal cortical dysplasia should be suspected when life-threatening focal motor status epilepticus or epilepsia partialis continua occur in children or young persons without another obvious cause. Normal magnetic resonance studies do not exclude neuronal migration disorders.

Adolescent↗
PubMed1993

Increased neocortical spiking and surgical outcome after selective amygdalo-hippocampectomy.

We studied the electrocorticogram (ECoG) before and immediately after transcortical selective amygdalo-hippocampectomy, prospectively in 13 consecutive patients and retrospectively in three others. ECoG was performed with surface and two depth electrodes inserted through T2 aimed at the amygdala and anterior hippocampus. Before resection the ECoG showed a variable amount of interictal spiking, recorded either independently from the depth and surface, or synchronously. A small cortical incision (2-3 cm) was made in T2. The hippocampus, amygdala and parahippocampal gyrus were removed subpially. After the resection, increased epileptiform abnormality was observed in all 16 patients and a different ECoG pattern emerged. It consisted of repetitive, high amplitude spikes and polyspikes, separated by attenuated background, recorded from the most anterior temporal area. Similar observations were reported by Niemeyer in 1958. The outcome was comparable to that of standard anterior temporal resection: 62.5% class I and 25% class II (Engel's scale). ECoG is often used to tailor the amount of resection, and the persistence of epileptic abnormalities correlates with worse outcome. This is not the case in selective amygdalo-hippocampectomy, suggesting that a different underlying mechanism is responsible for the increased interictal spiking following this procedure.

Adolescent↗
PubMed1993

Early childhood prolonged febrile convulsions, atrophy and sclerosis of mesial structures, and temporal lobe epilepsy: an MRI volumetric study.

We performed MRI volumetric measurements of the amygdala (AM) and hippocampal formation (HF) in a group of 43 patients with temporal lobe epilepsy not controlled by optimal drug treatment. Fifteen patients (35%) had a history of prolonged febrile convulsions (PFC) in early childhood; 30 patients underwent surgery, and histopathology was available in twenty-four. The mean values of AM and HF volumes ipsilateral to the EEG focus were significantly smaller than those of normal controls. The volumetric measurements showed a more pronounced atrophy of the AM in patients with a history of PFC, although the HF volumes were also smaller in this group. Patients with a history of PFC had a higher proportion of more severe mesial temporal sclerosis (MTS) compared with those with no PFC. These findings confirm a correlation between early childhood PFC, the severity of atrophy of mesial structures, and MTS.

Adolescent↗
PubMed1991

Biochemical markers of excitability in human neocortex.

We measured biochemical markers of excitability in brain excised for neurosurgical therapy of epilepsy. Intraoperative electrocorticography was used to identify and compare samples from regions of persistent interictal spike discharges and areas of the cerebral convexity which were free of interictal spiking. We found that interictal spiking was associated with elevated tissue levels of the excitatory amino acids glutamic acid (26%, p less than 0.001) and aspartic acid (25%, p less than 0.05). There was also a significant increase in the activity of the enzymes glutamic acid dehydrogenase (20%, p less than 0.01) and aspartate acid aminotransferase (18%, p less than 0.01) which are involved in their formation. There was no change in the levels of the inhibitory neurotransmitters GABA or taurine. We also found a significant increase in the activity of tyrosine hydroxylase (52%, p less than 0.001), the rate controlling enzyme in catecholamine biosynthesis. There was a reduction in the density (Bmax) of cortical alpha-1 adrenoceptors (26%, p less than 0.01) and a concomitant diminution of receptor coupled phosphatidylinositide metabolism (21%, p less than 0.01). This blunting of inhibitory noradrenergic transmembrane signaling may contribute to a relative imbalance between excitatory and inhibitory mechanisms in epileptogenic neocortex.

Amino Acids↗
PubMed1989

Adrenergic mediated phosphatidylinositol metabolism is modulated by epileptic discharges in human neocortex.

Adrenergic mediated phosphatidylinositol (PI) hydrolysis was measured in tissues obtained from 21 patients immediately following surgery for focal epilepsy. Accumulation of [3H]inositol monophosphate (IP1) was significantly reduced (21%, P less than 0.01) in actively spiking neocortex (n = 15) versus samples from non-spiking regions (n = 9). Epileptic discharges may blunt alpha 1-adrenoceptor stimulated transmembrane signalling in human neocortical epileptic foci.

Action Potentials↗
PubMed1989

Effect of repeated versus single electroconvulsive seizures on adrenergic-mediated phosphatidylinositol hydrolysis in rat neocortex.

Adrenergic-stimulated phosphatidylinositol (PI) hydrolysis was measured in cortical slices obtained from adult rats following electroconvulsive seizures (ECS). One group of animals received ECS daily for 15 days and a second group received a single ECS. Rats were then sacrificed at intervals of 15 min, 60 min, 4 h, and 24 h after the last ECS. Inositol 1-monophosphate (IP1) accumulation was transiently reduced (20%, P less than 0.01), at 15 min, in repeatedly shocked versus sham-shocked control animals. No changes were observed at later intervals nor at any time in rats submitted to a single ECS. These findings suggest that repeated but not single convulsive seizures transiently desensitize adrenergic-mediated PI metabolism. Although repeated ECS significantly increased the density (Bmax) of alpha 1 recognition sites in cortical slices at 15 min, 4 h, and 24 h, this upregulation was not coupled to a functional change in PI hydrolysis.

Animals↗
PubMed1984

Brain abscess due to Petriellidium boydii.

A 22 year-old man died from multiple cerebral abscesses due to Petriellidium boydii 4 1/2 months after an episode of near drowning. The autopsy showed dissemination to heart and kidney. This patient had no immunocompromising disease but was treated with corticosteroids. The treatment of this condition with ventricular shunting and amphotericin B is discussed and compared with the experience of ten other cases reported in the literature.

Adult↗
PubMedDate not supplied

Increased activity of choline acetyltransferase and acetylcholinesterase in actively epileptic human cerebral cortex.

We measured the activities of the cholinergic marker synthetic and catabolic enzymes choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) in surgical specimens obtained from 38 patients immediately following anterior temporal lobectomy for intractable epilepsy. Samples from patients with actively spiking lateral temporal cortex were compared to non-spiking lateral temporal cortex obtained from patients in whom the epileptic discharges were confined to the hippocampus. Mean activities of ChAT and AChE were increased by 25% (P less than 0.01) and 30% (P less than 0.025) respectively in the spiking vs. non-spiking cortex. We suggest that the above-normal activity of these cholinergic marker enzymes may reflect sprouting of cholinergic nerve terminals in spontaneously spiking cortex of some patients and/or increased acetylcholine metabolism secondary to the stimulatory effect of the ongoing epileptic discharge.

Acetylcholinesterase↗
PubMedDate not supplied

Transient changes in cortical alpha 1 adrenoceptors and seizure threshold following electroconvulsive seizures in rats.

Alpha 1 adrenoceptor density (Bmax) is consistently decreased in actively spiking human cortical epileptic foci. Interpretation of these unique human data is limited because all surgical excisions are completed shortly after a period of active seizure discharge. To determine the temporal profile of seizure-induced changes in cortical alpha 1 adrenoceptors we examined rats primed by 15 daily electroconvulsive seizures (ECS). Since the noradrenergic system has an inhibitory effect on epileptic activity, we also measured the postictal rise in minimal ECS seizure threshold. Animals were sacrificed immediately before or at intervals after the last scheduled seizure. Cortical membranes were assayed using [3H]prazosin as specific radioligand. Repeated ECS produced an increase in the number of cortical alpha 1 sites from 4 to 24 h postictally, but following the last seizure there was a transient 'normalization' of alpha 1 receptor density which persisted for 3 h. The postictal ECS seizure threshold also remained elevated for a 2 h period. Both these transient postictal changes may in part result from activation of the central NA system. Decreased alpha 1 adrenoceptors in surgical specimens of spiking cerebral cortex may also be a secondary response to focal seizure activity.

Animals↗
PubMedDate not supplied

Excitatory amino acids modulate phosphoinositide signal transduction in human epileptic neocortex.

Stimulation of phosphoinositide (PI) hydrolysis by norepinephrine (NE), carbachol (Carb), and excitatory amino acids (EAAs) was measured in slices prepared from neocortex excised during epilepsy surgery. NE and Carb markedly enhanced PI turnover (EC50: NE, 12 microM; Carb, 661 microM) as reflected by [3H]inositol monophosphate (IP1) accumulation in tissue slices prelabeled with [3H]myoinositol. These effects were dose-dependent, saturable, and five to six times higher than basal IP1 accumulation. A weaker stimulation (twofold) was observed with quisqualate (QUIS; EC50, 1.1 microM) and glutamate (GLU; EC50, greater than 1 mM), while minimal or no stimulation was seen with kainate (KA) and N-methyl-D-aspartate (NMDA). Agonist-stimulated PI turnover was significantly reduced in samples from actively spiking epileptic neocortex versus nonspiking areas as defined by electrocorticography (NE, -23%, p less than 0.05; Carb, -44%, p less than 0.01). Preincubation of slices with various EEAs inhibited Carb-induced IP1 formation. The maximal extent of inhibition (1 mM) was both amino acid-dependent (IC50: NMDA, 5 microM; KA, 3.3 microM; QUIS, 47 microM; GLU, greater than 1 mM). These data suggest that epileptic activity modulates PI metabolism and alters receptor-effector coupling. As important mediators of epileptogenesis, EAAs may interfere++ with the efficiency of this second messenger system.

Carbachol↗
PubMedDate not supplied

Occipitotemporal epilepsies: evaluation of selected patients requiring depth electrodes studies and rationale for surgical approaches.

In 8 patients in whom it was uncertain whether they had occipital or temporal lobe (TL) epilepsy, clinical, scalp EEG, and radiologic features were correlated with the sites of seizure onset as determined by depth EEG. The 8 patients were selected from > 40 with occipital epilepsy because they had (a) an aura considered to be of occipital lobe (OL) origin, (b) an occipital interictal epileptic focus, (c) an OL lesion, or (d) a combination of all of these. Scalp EEG and clinical patterns suggested temporal involvement in all, however. Extracranial EEG recordings were often misleading, showing multilobar interictal epileptic abnormalities, and seizure onset was of poor localizing value and did not clarify the problem sufficiently. Intracranial EEG recordings showed that seizure onset could be ordered along an occipitotemporal gradient. Consistent OL seizure onset was observed in patients who had only elementary visual auras. Those who had inconsistent aura or no aura, suggesting OL origin, had onset of most attacks in the TL. All patients had a seizure spread pattern suggesting early TL involvement. To prevent visual field defect, surgical approaches included temporal resection when temporal seizure origin or spread was demonstrated; although occasionally this produced excellent results, it was of limited benefit in most patients, even when some seizures were proven to originate in TL structures. In patients with malignant epilepsy and in those with an occipital lesion, occipital resection should be considered.

Adolescent↗