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F Bartolomei

Publications and source records attributed to F Bartolomei.

At least 55 records · Page 3Linked to original sources
PubMed1997

Increase in mRNAs encoding neonatal II and III sodium channel alpha-isoforms during kainate-induced seizures in adult rat hippocampus.

Subtypes I, II and III of sodium channel alpha-subunit mRNAs were analyzed in adult rat brain areas after kainate-induced seizures. Tissue samples were microdissected from occipital neocortex, CA1 and CA3 hippocampus areas and dentate gyrus. Three reverse transcriptase-polymerase chain reaction (RT-PCR) protocols were undertaken to amplify these mRNAs. Amplification products were then distinguished after digestion by restriction enzymes, electrophoresis separation and densitometric analysis of gel profiles. PCR 1 evidenced the relative percentage of mRNAs I, II and III as well as neonatal II and III subtype isoforms, which resulted from an alternative splicing. PCR 2 and 3 were performed to focus on the neonatal vs. adult ratio in II and III subtypes, respectively. Seizures were shown to induce an increase in both neonatal subtypes, which suggested an alteration at the splicing level. These changes exhibited a peculiar brain regional distribution, the maximal effect being observed in dentate gyrus and hippocampus CA1 area. In situ hybridization experiments, using a digoxigenin-labeled oligonucleotide probe-specific for neonatal II and III mRNAs, confirmed this increase in neonatal mRNA subtypes. These changes were transient, reaching a maximum 6 h after drug injection, then disappearing between 12 and 48 h. They were prevented by a pre-treatment of animals by MK-801, a non-competitive antagonist of NMDA receptors. This work, thus, suggested that KA-induced seizures can be accompanied by transient alteration in the splicing pattern of sodium channel alpha-subunit mRNAs which resulted in an increase in expression of their neonatal isoforms within localized areas of adult rat brain.

Animals↗
PubMed1997

Changes in the mRNAs encoding subtypes I, II and III sodium channel alpha subunits following kainate-induced seizures in rat brain.

Several lines of evidence underscore a possible role of voltage-gated Na+ channels (NaCH) in epilepsy. We compared the regional distribution of mRNAs coding for Na+ channel alpha subunit I, II and III in brains from control and kainate-treated rats using non-radioactive in situ hybridization with subtype-specific digoxigenin-labelled cRNA probes. Labelling intensity was evaluated by a densitometric analysis of digitized images. Heterogeneous distribution of the three Na+ channel mRNAs was demonstrated in brain from adult control rats, which confirmed previous studies. Subtype II mRNAs were shown to be abundant in cerebellum and hippocampus. Subtype I mRNAs were also detected in these areas. Subtype III mRNAs were absent in cerebellar cortex, but significantly expressed in neurons of the medulla oblongata and hippocampus. The three subtypes were differentially distributed in neocortical layers. Subtype II mRNAs were present in all of the layers, but mRNAs for subtypes I and III were concentrated in pyramidal cells of neocortex layers IV-V. During kainate-induced seizures, we observed an increase in Na+ channel II and III mRNA levels in hippocampus. In dentate gyrus, subtype III mRNAs increased 3 h after KA administration to a maximum at 6 h. At this latter time, a lower increase in NaCh III mRNAs was also recorded in areas CA1 and CA3. NaCh III overexpression in dentate gyrus persisted for at least 24 h. In the same area, NaCh II mRNAs were also increased with a peak 3 h after KA injection and a return to control levels by 24 h. No changes in NaCh I mRNAs were seen. The KA-induced up-regulation in NaCh mRNAs probably resulted in an increase in hippocampal neuronal excitability.

Animals↗
PubMed1997

Migraine with visual aura and photosensitive epileptic seizures.

A relationship between epilepsy and migraine has long been postulated, but the nature of this interaction is still debated. We observed this association in a 23-year old man with a history of migraine with visual aura who had seizures at age 15 years while watching television. Waking EEG was normal, but sleep recordings demonstrated posterior spike-waves during sleep. During intermittent photic stimulation (IPS), a photoparoxysmal response occurred, maximum in occipital areas. Brain magnetic resonance imaging scan was normal. Seizures did not recur after 4-year treatment with valproate. He is currently seizure-free, but continues to have rare migraine with visual aura. The role of spreading depression or of a putative dopaminergic failure in occipital cortex is discussed.

Adult↗
PubMed1997

Alcoholic epilepsy: a unified and dynamic classification.

The interactions between alcohol and the CNS are complex and there are experimental data suggesting that chronic and acute effects are different and often opposite. An intriguing hypothesis is that repeated alcohol withdrawal seizures (AWS) may render the brain more excitable, leading to an epileptogenic state reminiscent of the 'kindling' model. To gain insight into this question we compared alcoholic patients with seizures related to episodes of AW (AWS) and patients with seizures unrelated to episodes of AW (UAWS). There were several significant differences between the AWS and UAWS groups. Age at admission for seizure was younger in the AWS groups (p < 0.005), seizure number was higher among patients with a history of seizures before admission in the UAWS group (p < 0.05). Neurologic signs were more frequent in the UAWS group (p < 0.05). Duration of intoxication was longer in the UAWS group and brain atrophy demonstrated by CT scan was more common in the UAWS group than the AWS group. Based on these findings, we propose a dynamic classification in which patients presenting seizures unrelated to any cause other than alcohol are classified in several successive stages of 'alcoholic epilepsy', the first being characterized by AWS and the last by persistent chronic seizures.

Adult↗
PubMed1997

Prognostic factors for childhood and juvenile absence epilepsies.

To assess prognostic factors for absence epilepsy (AE), we analyzed data from 80 patients treated for childhood AE (CAE; n = 53) or juvenile AE (JAE; n = 27) in our epilepsy clinic between 1985 and 1992. All patients were classified according to the International Classification of Epileptic Syndromes which was proposed by the International League against Epilepsy in 1989. Patients were separated into two groups based on the course of disease under adequate treatment: Complete response group (CRG): disappearance of absence seizures (AS) or generalized tonic-clonic seizures (GTCS). Poor response group (PRG): persistence of AS and/or GTCS. Approximately 40% of both CAE and JAE patients had poor response. One parameter was associated with poor prognosis in CAE patients, the presence of polyspikes or polyspikes and waves during sleep. No statistical correlation was made for JAE patients. GTCS were frequent in JAE and GTCS occurrence in CAE patients was associated significantly with age at onset after 8 (p < 0.05). The fact that social and educational performance was poorer in the PRG of both types of AE underlines the importance of therapeutic response in patient rehabilitation.

Adolescent↗
PubMed1996

Cryptogenic partial epilepsies with anti-GM1 antibodies: a new form of immune-mediated epilepsy?

PURPOSE: We wished to study immune system dysfunction which has been proposed as a potential cause of epilepsy. Epileptogenic action of antibodies directed against GM1 gangliosides was demonstrated in rats, but the potential role of anti-GM1 antibodies in human epilepsy has not yet been studied. METHODS: We investigated the presence of IgG or IgM anti-GM1 antibodies in the sera of 64 patients with various types of epileptic syndromes: idiopathic generalized epilepsy (IGE) (n = 6), symptomatic or cryptogenic generalized epilepsy (SCGE) (n = 7), symptomatic partial epilepsy (SPE) (n = 26), and cryptogenic partial epilepsy (CPE) (n = 25). RESULTS: Two patients had elevated titers of IgM anti-GM1 antibodies, one patient had elevated titers of both IgM and IgG anti-GM1 antibodies, and 1 patient had elevated titers of IgG anti-GM1 antibodies. All 4 patients had complex partial seizures (CPS) secondarily generalized, drug resistance, psychiatric disorders, and normal brain imaging. Anti-GM1 antibodies were never associated with IGE, SCGE, or SPE. We compared the reactivity of sera from these patients with the sera from 5 patients with motor neuropathies with conduction block (MNCB) against different gangliosides and concluded that epilepsy sera did not react with the Gal(beta 1-3)GalNAc epitope. Two anti-GM1-positive patients were treated successfully with high-dose intravenous immunoglobulins (IgIV). CONCLUSIONS: Our findings suggest that detection of anti-GM1 antibodies could allow identification of a subgroup of patients with partial epilepsy associated with an autoimmune response. If anti-GM1 antibodies prove pathogenic, they could be an important prognostic factor for drug resistance and worsening of seizures.

Adult↗
PubMed1996

Myoclonic alcoholic epilepsy.

We describe 2 patients with chronic alcoholism who over a period of several years developed epilepsy associated with a cerebellar syndrome and action myoclonus. The clinical picture suggested progressive myoclonic epilepsy, but subsequent investigations did not confirm this diagnosis. Myoclonus worsened during abstinence and was relieved during indulgence. We believe that this special clinical syndrome should be recognized as a complication of chronic alcoholism.

Adult↗
PubMed1995

Panic attacks mistaken for relapse of epilepsy.

Panic attacks, a frequent type of pseudoepileptic seizures, occur more frequently in epilepsy patients than in the general population and are often misdiagnosed, leading to pseudosevere epilepsy. We evaluated 4 patients with a past history of epileptic seizures long in remission who were misdiagnosed as having relapsing seizures although they had fairly typical panic attacks. To avoid unnecessary and ineffective antiepileptic drug (AED) treatment, recurrence of seizures after long remission should be carefully evaluated to identify patients with a panic disorder who require specific treatment. In patients who unexpectedly exhibit seizures after long remission, an accurate retrospective diagnosis of the epileptic syndrome and a precise description of the attack symptomatology should be obtained, if possible with EEG-video monitoring.

Adolescent↗
PubMed1995

[Myoclonus of focal action and localized hemispheric lesion. A polygraphic and pharmacological study].

Authors report a case of focal action myoclonus due to a localized hemispheric lesion. The woman had cardiac arrest complicated by ischemic stroke involving the left parietal region. Action myoclonus of the inferior right limb was the sole residual complaint, provoked by movement and maintenance of posture. Patient noted that myoclonus was worsened by carbamazepine and vigabatrin. EEG-EMG polygraphic study demonstrated action myoclonus and showed a particular EEG activity consisting in a volley of spikes on the vertex region during the right inferior limb movements. Contralateral movements did not elicit this activity. Pharmacological response to clonazepam, piracetam and alcohol was studied. A marked improvement of myoclonus was obtained with alcohol. Pathophysiology of this exceptional form of cortical action myoclonus is discussed.

Anticonvulsants↗
PubMed1993

[Partial epilepsy and corpus callosum involvement].

We report two cases of partial complex epilepsy associated with a lesion of the corpus callosum: a cavernoma in one case and a lesion of undetermined nature in the other. Similar cases have already been reported, notably with lipomas or agenesis of the corpus callosum, but they remain exceptional. Two mechanisms could explain such epilepsies: either the lesion extends to the cingulate gyrus whence the epileptic discharge may reach internal temporal structures (our case n. 1), or a temporal focus becomes autonomic after interruption of inhibitory callosal fibres (our case n. 2).

Adult↗
PubMed1992

[Ischemic cerebral vascular stroke after heroin sniffing. A new case].

Three hours after sniffing a dose of heroin, a 30-year old man developed right hemiplegia with aphasia. Magnetic resonance imaging of the brain showed an infarct in the territory of the left anterior choroid artery. Cerebral vascular accidents occurring as complications of heroin addiction are rare: a review of the literature yielded only 13 documented cases. The main characteristics of these strokes are analysed and their pathogenetic mechanisms (immuno-allergic vasculitis, vascular spasm) are discussed.

Administration, Inhalation↗
PubMed1992

[Hemichorea-hemiballismus and toxoplasmosis in AIDS].

The authors report two cases of hemichorea-hemiballism revealing a toxoplasmic abscess in the subthalamic nucleus during AIDS. Despite the great frequency of this opportunistic infection such cases are exceptional. This rarity seems to be explained by the frequent association of other lesions of the basal ganglia which may prevent the movement disorders. Nevertheless an hemichorea-hemiballism in young people must suggest a cerebral toxoplasmosis. Finally a symptomatic treatment is often necessary; in these cases the use of sodium valproate must be considered, this drug being able to induce a clinical improvement.

AIDS-Related Opportunistic Infections↗
PubMed1992

[Systematized cavernous angiomatosis with multiple cerebral and cutaneous localizations].

A 45 year-old woman with no history of familial disease presented with multiple cutaneous and cerebral cavernous angiomas. The diagnosis rested on biopsy for cutaneous angiomas and on MRI for cerebral angiomas. The clinical manifestations of cerebral angiomas were headaches and a cerebellar syndrome, the latter most probably due to progressive growth of cerebellar angiomas. Systematized cavernous angiomatosis is characterized by multiple angiomas of the brain and other viscera and is considered to be a phacomatosis.

Angiomatosis↗
PubMed1991

[Epilepsy seizures in HIV infection. 52 cases].

Fifty-two patients at various stages of human immunodeficiency virus (HIV) infection who had one or several epileptic seizures in the course of that disease were retrospectively studied from 1985 to 1990. Thirty-five percent of these patients were in overt clinical AIDS at the time of the seizure(s). AIDS was revealed by a seizure in 2 cases. Generalized seizures were observed in 71 percent of the patients, and partial seizures in 29 percent. Electroencephalograms showed signs of brain irritation in only 19 percent of the cases. The cause of epileptic seizure(s) could be determined in 36 patients: cerebral toxoplasmosis in 23 cases; progressive multifocal leucoencephalitis in 2 cases; HIV encephalopathy in 3 cases; iatrogenic cause in 4 cases; meningoencephalitis in 3 cases and neurosyphilis in 1 case. No cause other than HIV infection was found in 16 patients. These findings confirm those of previous studies. In about one-third of AIDS patients epileptic seizures are the only clinical manifestation of viral central nervous system infection.

AIDS Dementia Complex↗