Marcel Chatel

European Stroke Initiative Recommendations for Stroke Management

This article summarises recommendations for acute management of stroke by the European Stroke Initiative (EUSI), on behalf of the European Stroke Council (ESC), the European Neurological Society (ENS), and the European Federation of Neurological Societies (EFNS).

Long-term outcome of oligodendrogliomas

Background: Favorable prognostic factors for oligodendroglial tumors include age younger than 40 years, low tumor grade, and extent of resection. Objective: To assess survival time and prognostic factors of 100 patients with oligodendrogliomas diagnosed between 1995 and 2002. Methods: The tumors were rated histologically by the WHO classification as low grade (grade II) or anaplastic (grade III). One hundred patients were categorized into three groups: group A: grade II, group B: secondary grade III (low grade with anaplastic transformation during the follow-up), group C: de novo grade III. All patients were symptomatic at presentation and underwent neurosurgical procedure for histologic diagnosis. Follow-up was performed with clinical assessment, brain MRI, and MIBI scintigraphy. Results: There were 66 men and 34 women (mean age at diagnosis 46.7 years). The most common first symptom was partial epileptic seizure (75%). Fifty-six patients had initial gadolinium enhancement (A: 15.6%; B: 36.8% as grade II, 95% as grade III; C: 90%), generally associated with MIBI hypermetabolism (p < 0.0001). Survival rates at 2, 5, and 10 years were A: 88%, 88%, 85%; B: 79%, 64%, 42%; C: 43%, 16%, 15%. Conclusions: Secondary anaplastic oligodendroglioma patients were younger than patients with de novo anaplastic oligodendrogliomas. Histologic confirmation is mandatory because some low grade oligodendrogliomas had gadolinium enhancement on MRI and some anaplastic did not. Survival time was longer for secondary than for de novo anaplastic oligodendrogliomas without difference in the duration of the malignant phase of the disease.

De novo absence status epilepticus as a benzodiazepine withdrawal syndrome

Summary: A 67‐year‐old woman with a history of psychotropic drug abuse developed confusion. EEG was consistent with absence status epilepticus (AS). Intravenous (i.v.) flumazenil 1 mg, a benzodiazepine antagonist with anticonvulsant properties, increased both confusion and paroxysmal activity. Complete resolution was obtained after diazepam was administered i.v., and the patient then admitted that she had abruptly discontinued long‐standing treatment with carpipramine, amitryptiline, bromazepam, and flunitrazepam. The aggravating effect of flumazenil indicates that benzodiazepine withdrawal was probably the elective triggering factor of this de novo absence status epilepticus.

Expression of vascular endothelial growth factor-b in human astrocytoma

Growth of human malignant gliomas is stringently dependent on an angiogenic process that probably involves vascular endothelial growth factor (VEGF). Expressions of mRNA coding for the different forms of VEGF were analyzed in surgical specimens from human astrocytomas. Low levels of placental growth factor (PGF) and VEGFC mRNA were observed in polymerase chain reaction, but not in Northern blot experiments. VEGF mRNA was found in some but not all grade and grade IV astrocytomas. VEGFB mRNA was observed in all tissue samples analyzed irrespective of the tumor grade. A new splice variant of VEGFB (VEGFB155) that lacks exons 5 and 6 is described. Expressions of VEGF mRNA in cultured glioblastomas cells were upregulated by hypoxia, but the sensitivity of the cells to hypoxia was reduced as compared with normal rat astrocytes. VEGF expression was depressed by dexamethasone. Expressions of VEGFB mRNA were affected neither by hypoxia nor by dexamethasone. The results indicate a coexpression of VEGF mRNA and VEGFB mRNA in human astrocytomas. Expression of VEGFB is markedly different from that of VEGF. Possible roles of VEGFB as a cofactor for hypoxia-induced angiogenesis in human astrocytomas are discussed.

Opercular Myoclonic‐Anarthric Status Epilepticus

Summary: We report 3 cases of opercular myoclonic status epilepticus (OMASE), characterized by fluctuating cortical dysarthria without true aphasia associated with epileptic myoclonus involving bilaterally the glossopharyngeal musculature. In this syndrome, the inferior rolandic area of either one or the other hemisphere is involved by an epileptogenic lesion of various etiology. Ictally, clonic expression was consistent with epilepsia partialis continua (EPC) and bilaterally and symmetrically involved palatal muscles (cases 1–3), tongue (cases 2 and 3), lips and chin (case 3), and inferior jaw (case 1) due to In adulthood, rhythmical palatal movements of bilateral projections of the inferior corticonuclear pathways. Postictally, the main clinical sign was pseudobulbar palsy, consistent with Todds palsy. In our cases, OMASE was either of vascular (cases 1 and 2) or tumoral origin (case 3). In adulthood, early recognition of OMASE, although nonspecific, may be important for early management of carotid occlusive disease because it usually indicates an acute opercular infarction.

Early 99mTc-Ethylcysteinate Dimer Brain SPECT Patterns in the Acute Phase of Stroke as Predictors of Neurological Recovery

Objectives: Accurate prediction of outcome in acute stroke would help in identifying subgroups of patients for therapeutic trials and intravenous thrombolysis. The purpose of this study was to prospectively test the hypothesis that brain SPECT, with 99mTc-L,L-ethylcysteinate dimer (ECD), a tracer sensitive to cell function, performed in the first hours after stroke onset, adds predictive power to concomitant neurological evaluation. Methods: Twenty-four patients with a first-ever middle cerebral artery stroke were prospectively studied with ECD-SPECT within 12 h after stroke onset. Neurological evaluation was performed using Orgogozo’s scale at admission and 3 months later in order to calculate the percent Martinez-Vila evolution indices (EI%). Semiquantitative visual analysis of SPECT images was performed in 6 cortical regions relevant for carotid artery territory. Both the extent and the intensity of cortical reduced ECD uptake were calculated, leading to an ‘ischemia’ score, corresponding to the sum of regions of interest (ROI) where ECD uptake was between 40 and 80% of the contralateral healthy hemisphere, and an ‘irreversibly damaged tissue’ (IDT) score, corresponding to an uptake below 40%, and a total score (ischemia + IDT). Each patient was assigned to one of three patterns: (1) pattern I with severe ECD cortical uptake reduction defined by at least one ROI with uptake under 40%, (2) pattern II with moderate ECD cortical uptake reduction (40–80%) only and (3) pattern III with normal ECD uptake. Results: There were 11 patients (46%) with pattern I ECD-SPECT. This group had almost invariably (10/11 patients) a poor outcome. The 12 patients (50%) classified in pattern II had a variable clinical outcome, ranging from improvement to deterioration. The single patient with a normal SPECT (pattern III) had a full clinical recovery. Both total score and IDT score were strongly significantly correlated with neurological recovery EI% (respectively p = 0.006 and 0.004). Their predictive value was significantly higher than, and independent of, day 0 neurological evaluation. No patient had an increased ECD uptake. Conclusion: Our results show that the degree of ECD cortical uptake reduction, measured on early brain SPECT, is a strong predictor of neurological recovery. ECD-SPECT data have a higher predictive value than day 0 neurological evaluation. The apparently better predictive value of ECD over hexamethylpropyleneamine oxime may reflect this tracer’s brain retention mechanisms which are weighted more towards cell function than towards perfusion. ECD-SPECT is easily obtainable and may help in selecting out from therapy those patients who are likely to have either very good or very poor spontaneous outcome, and thus improve the assessment of acute stroke and the choice of therapeutic strategy.

Fluorescence In Situ Hybridization Study of Aneuploidy of Chromosomes 7, 10, X, and Y in Primary and Secondary Glioblastomas

The aneuploidy of autosomes 7, 10, and sex chromosomes (X and Y) was analyzed in a series of 44 primary (de novo) and 20 secondary glioblastomas using fluorescence in situ hybridization (FISH) on smear preparations of glioma tissue. The tumors were screened for trisomy 7, monosomy 10, as well as loss of the Y chromosome and disomy of the X chromosome in male subjects, and monosomy of the X chromosome in female subjects. We found that taken alone or in combination, these chromosomal abnormalities do not appear to be characteristic of a glioblastoma subtype; therefore, they do not allow the differentiation between primary and secondary glioblastomas. Also, the loss of a chromosome 10 appears to be an earlier event than a gain of a chromosome 7 for the genesis of a secondary glioblastoma.

Cytogenetics of malignant gliomas: I. The autosomes with reference to rearrangements

Autosomal chromosome abnormalities are far from always detectable and, when detected, far from fully consistent in malignant gliomas. In 15 of 41 malignant gliomas, we found autosomal chromosome aberrations ranging from solitary trisomy to a wildly abnormal polyploid complement. The sequence of chromosome events appears to proceed from the normal to the near-diploid state (via structural and numerical changes) to near-tetraploidy (via polyploidization), and finally toward near-triploidy (via chromosome loss and additional rearrangements). Characteristic chromosome changes of trisomy 7 and monosomy 10 were repeatedly found, usually together in the same cell clones. In only one case was trisomy 7 an isolated change. We observed structural rearrangements of chromosomes 7 and 10 which may be of some use in mapping specific genes duplicated or deleted by the whole-chromosome changes of chromosomes 7 and 10. Nonrandom structural changes of other autosomes, including chromosomes 1, 5, and 11, fit with the model of malignant glioma as a process involving multiple genes. An unusual concentration of breakpoints in 12q13, juxtaposing it to at least five other regions, reflects the presence of genetic information in 12q13 important to the development of malignant gliomas.

Ictal asomatognosia with hemiparesis

A 69-year-old woman presented with an ictal Anton-Babinski syndrome(asomatognosia with hemiparesis). Except for head and eye deviation to the side of the paralyzed limb, epileptic nystagmus, brief episodes of impaired consciousness, and automatisms, clinical symptomatology was identical to Anton-Babinski syndrome of vascular origin. Results of MRI imaging were normal. EEG showed a simple partial nonconvulsive status epilepticus of right parieto-temporal origin. Anton-Babinski syndrome may thus be a functional expression of focal status epilepticus.

Single photon emission computed tomography study of subclinical rhythmic electrographic discharge in adults

Subclinical rhythmic electrographic discharge in adults (SREDA) is considered a benign EEG pattern of uncertain significance, although it may closely resemble an EEG seizure pattern. We investigated a 57-year-old man with a very lateralized epileptiform activity localized to the occipito-temporal areas of the right hemisphere. Neuropsychological tests, clonazepam injection and 99m Tc-HMPAO-SPECT were performed during the SREDA and compared to the interparoxysmal data, providing further evidence that SREDA cannot be considered as an epileptic pattern and that, in some instances, it may be related to chronic hypoxic/ischemic mechanisms.