Biomedical subjects
Publications and source records attributed to M G Bousser.
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OBJECTIVE: To describe neurological complications occurring after roller-coaster rides. PATIENTS AND METHODS: We report 6 cases of complications occurring after roller-coaster rides and analyze published data. RESULTS: Complications seen our patients included 5 cervicoencephalic arterial dissections, one with brainstem dysfunction due to extending syringobulbia. Reported data include one cervicoencephalic arterial dissection, one case of carotid artery occlusion, 3 cases of subdural hematoma, one with subarachnoid hemorrhage, one with cerebrospinal fluid leak, and one with Brown-Séquard syndrome secondary to an enterogenous cyst of the spinal cord. In all patients, pain was the first symptom experienced. In 71.4% of cases, it occurred immediately after the trauma. Marfanís syndrome may be the only risk factor identifiable prior to exposure. The mechanisms of most complications are poorly understood but are likely to involve sudden head and neck flexion-extension movements. CONCLUSION: Neurological complications occurring after roller-coaster rides are highly uncommon, but may leave invalidating sequelae or be fatal. Clinicians should be aware of these complications so these patients can be given proper care early, particularly at the stage when pain is the only sign. Early management could help limit the consequences of these complications.
We report a reversible reduction of water diffusion in the brain during a prolonged attack of hemiplegic migraine. The patient had a sporadic mutation of the CACNA1A gene. The diffusion changes were observed in the contralateral hemisphere 3 and 5 weeks after the onset of hemiplegia. These results suggest the occurrence of hemispheric cytotoxic edema during severe attacks of hemiplegic aura. The mechanisms underlying such ultrastructural modifications are unknown but an abnormal release of excitatory amino acids can be hypothesized.
In contrast to arterial stroke, cerebral venous thrombosis (CVT) is an infrequent condition which presents with a wide spectrum of signs and with a highly variable mode of onset. The clinician must therefore consider it systematically in all brain syndromes and perform the appropriate neuroimaging investigations: computed tomography (CT) with computed tomography angiography and/or magnetic resonance imaging with magnetic resonance angiography and, if necessary intra-arterial angiography. Once the diagnosis is established, a wide investigation for should be carried out in search of the cause, and treatment started as soon as possible. Treatment is based on the combination of intravenous heparin (followed by oral anticoagulants for 3-6 months), symptomatic treatment (anticonvulsants, analgesics, treatment of increased intracranial pressure) and treatment of the cause. Local thrombolysis is indicated if there is deterioration due to thrombosis extension despite adequate anticoagulation. Diagnosis and treatment of CVT should be considered as an emergency because of the considerable potential for full recovery in this condition.
At the acute phase of cerebral infarction, two recent large studies found that the use of aspirin reduces both mortality and the risk of the recurrence of stroke. In primary prevention, aspirin nearly halves the risk of myocardial infarction but does not reduce that of stroke. Concerning the secondary prevention of atherothrombotic brain infarcts, aspirin has been the most extensively studied drug, and is efficient between 50 mg and 1.3 g. In spite of the efficacy of other antiplatelets in this indication--ticlopidine (500 mg), clopidogrel (75 mg) and dipyridamole (400 mg)--aspirin remains the most cost-effective, doses between 100 and 300 mg being the most widely used. Cardiac diseases with a high embolic risk require the use of oral anticoagulation. In nonvalvular atrial fibrillation, the choice of antithrombotic drugs depends on risk stratification: oral anticoagulants are indicated in high-risk subjects, whereas aspirin is recommended in low-risk subjects and when oral anticoagulants are contraindicated. Studies with associations of aspirin and other antiplatelets are required to increase the yield of this medication in high-risk subjects, in parallel with efforts to detect and to treat the vascular risk factors.
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Since 1962, more than 25 studies have been devoted to the relationship between oral contraceptives and stroke. They are all case-control or cohort epidemiological studies and thus contain the difficulties and biases that are inherent in these types of studies. The following conclusions can be drawn from these studies: High oestrogen content (> or = 50 microg) increases the risk of stroke, all stroke subtypes, and stroke death. Low oestrogen content (<50 microg) carries a very low or no risk of stroke. There are no data on progestogen only oral contraceptives. Stroke risk is greatly increased if associated risk factors are present, in particular hypertension, cigarette smoking and migraine. Oral contraceptives, even at low doses, significantly increase the risk of cerebral venous thrombosis, which is further enhanced if congenital thrombophilia is present. The attributable risk of stroke in young women using oral contraceptives is about 1 per 200000 woman-years. The contraceptive and non-contraceptive benefits of low dose oral contraceptives vastly outweigh their risks provided that other risk factors are absent or well controlled.
In this paper we review the evidence that migraine is associated with ischaemic stroke in young women, emphasizing potential biases, factors that may influence the association, potential mechanisms, and potential public health impact. Consistency of case-control findings from several countries and supporting evidence from prospective data suggest that the association is not an artifact of study design or execution, although, due to methodological limitations, none of the studies mentioned can be considered definite proof of the association. However, it is less clear whether migraine without aura is associated with stroke or whether the association is restricted to migraine with aura. Similarly, there are few data examining the magnitude of the association among nonusers of oral contraceptives compared with those who use low oestrogen oral contraceptives. As a consequence, there is a lack of data concurrently stratifying both by the presence vs. the absence of aura and by the use of low oestrogen oral contraceptives vs. non-use of oral contraceptives. Moreover, there is still no convincing evidence on the mechanisms that would be implied and on the groups of migraineurs really at risk of ischaemic stroke. Despite the considerable advances in our understanding of the relationship between migraine and stroke, there are many gaps in the data needed for public health recommendations.
This paper will review available data bearing on the relationship of post-menopausal hormone replacement therapy to the risk of first or recurrent ischaemic stroke. Although experimental data from both human and animal studies will be briefly mentioned, the bulk of evidence is from observational epidemiological studies. As such, the limitations of observational studies, particularly as applied to the health effects of post-menopausal hormone replacement therapy, will be emphasized. We conclude that there is no compelling consistent evidence that post-menopausal hormone replacement therapy either decreases or increases stroke risk. There are, however, reasons to be concerned that this therapy may contribute to stroke risk.
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BACKGROUND AND PURPOSE: Atrial septal abnormalities have been associated with cryptogenic ischemic stroke in young patients, but the causal link has not yet been established. Paradoxical embolism is considered the most likely mechanism but is rarely proven. It can be hypothesized that, in those patients, paroxysmal atrial arrhythmias, potentially favored by the anatomic abnormalities, can be another cause of thrombus formation and subsequent embolism to the brain. In this study we assessed the relationship between atrial vulnerability, reflecting arrhythmogenic properties of the atria, and atrial septal abnormalities in young patients with cryptogenic ischemic stroke. METHODS: We enrolled 62 consecutive patients aged <55 years who had ischemic stroke of unknown cause and transesophageal echocardiography to assess atrial septal aneurysm (ASA) or patent foramen ovale (PFO) (ie, atrial septal abnormalities). These patients underwent electrophysiological study to measure atrial refractoriness and conduction time defining a vulnerability index (ie, latent atrial vulnerability) and to assess the inducibility of sustained (lasting >60 seconds) atrial fibrillation with the use of programmed atrial stimulation. Actual atrial vulnerability was defined by the presence of both latent vulnerability and inducibility of sustained atrial fibrillation lasting >60 seconds. RESULTS: We found atrial vulnerability in 58% of patients with atrial septal abnormalities and in 25% of patients without (odds ratio=4.1 [95% CI, 1.3 to 12.7; P<0.02]). The difference between patients with and without PFO or between patients with both PFO and ASA and those without were also significant. Patients with inducible sustained atrial fibrillation had more frequent past history of palpitations and syncope than patients without (P<0.02). CONCLUSIONS: Atrial vulnerability is associated with atrial septal abnormalities in patients with cryptogenic stroke. This result raises the question of the potential role of transient atrial arrhythmias in thrombus formation in the presence of PFO or ASA.
BACKGROUND: White matter lesions in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) are underlaid by severe ultrastructural changes of the arteriolar wall. Although chronic ischemia is presumed to cause the tissue lesions, the pattern of perfusion abnormalities and hemodynamic reserve in CADASIL, particularly within the white matter, remains unknown. METHODS: We used the MRI bolus tracking method in 15 symptomatic patients with CADASIL (5 with dementia) and 10 age-matched control subjects before and 20 minutes after the intravenous injection of acetazolamide (ACZ, 17 mg/kg). Cerebral blood flow (CBF), blood volume (CBV), and mean transit time (MTT) were calculated both in the cortex and in the white matter according to the singular value decomposition technique. Perfusion parameters were obtained in regions of hyperintensities and within the normal-appearing white matter as observed on T2-weighted images. Analysis was performed with both absolute and relative (region/whole brain) values. RESULTS: A significant reduction in absolute and relative CBF and CBV was found within areas of T2 hyperintensities in white matter in the absence of significant variations of MTT. This reduction was more severe in demented than in nondemented patients. No significant change in absolute CBF and CBV values was observed in the cortex of patients with CADASIL. A decrease in relative CBF and CBV values was detected in the occipital cortex. After ACZ administration, CBF and CBV increased significantly in both the cortex and white matter of affected subjects, but the increase in absolute CBF was lower within areas of increased signal on T2-weighted images in patients than in the white matter of control subjects. CONCLUSIONS: In CADASIL, both basal perfusion and hemodynamic reserve are decreased in areas of T2 hyperintensities in the white matter. This hypoperfusion appears to be related to the clinical severity. The significant effect of ACZ on CBF and CBV suggests that cerebral perfusion might be increased using pharmacological vasodilation in CADASIL.
CADASIL, an autosomal dominant arteriopathy responsible for stroke and dementia, is caused by strongly stereotyped mutations in the Notch3 gene. We report a patient with a condition strongly suggestive of CADASIL (migraine, stroke, and white matter abnormalities), except that this patient did not have any first-degree relatives with similar symptoms. This patient carried a heterozygous Arg182Cys mutation in the Notch3 gene; this mutation was absent in his two biological parents. These data demonstrate the occurrence of a de novo noninherited mutation in the Notch3 gene, which indicates that CADASIL should not be rejected in the absence of a family history. Therefore, our finding suggests that CADASIL may be more frequent than anticipated.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
In this paper we review the evidence that migraine is associated with ischemic stroke, emphasizing potential biases, factors which may influence the association, potential mechanisms, and potential public health impact. Consistency of case-control findings from several countries and supporting evidence from prospective data suggest that the association is not an artifact of study design or execution. However, it is less clear whether migraine without aura is associated with stroke or whether the association is restricted to migraine with aura. Similarly, there are few data examining the magnitude of the association among nonusers of oral contraceptives compared to those who use low estrogen oral contraceptives. Moreover, there is still no convincing evidence on the mechanisms that would be implied and on the groups of migraineurs really at risk of ischemic stroke. Despite the considerable advances in our understanding of the relationship between migraine and stroke, there are many gaps in the data needed for public health recommendations.