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M G Bousser

Publications and source records attributed to M G Bousser.

At least 163 records · Page 9Linked to original sources
PubMed1993

Migraine and risk of ischaemic stroke: a case-control study.

OBJECTIVES: To determine whether migraine is a risk factor for ischaemic stroke. DESIGN: A case-control study. SETTING: Two hospitals in Paris. SUBJECTS: 212 patients with stroke (137 men and 75 women) and 212 controls matched for sex, age (to within five years), and history of hypertension. MAIN OUTCOME MEASURES: Ischaemic stroke, confirmed by brain computed tomography or magnetic resonance imaging, and history of headache, recorded with structured questionnaire during interview. RESULTS: Prevalence of migraine did not differ between patients with stroke and controls: 18/137 v 17/137 for men (odds ratio 1.1 (95% confidence interval 0.5 to 2.2), p = 0.86); 23/75 v 17/75 for women (odds ratio 1.6 (0.7 to 3.5), p = 0.24); and 41/212 v 34/212 for both sexes (odds ratio 1.3 (0.8 to 2.3), p = 0.33). When subjects were split into two age groups, however, prevalence of migraine was significantly higher among younger women (aged < 45) with stroke compared with their controls (13/20 v 6/20, odds ratio 4.3 (1.2 to 16.3), p = 0.03). Furthermore, the risk of ischaemic stroke was higher among younger women who smoked (7/20 v 1/20, odds ratio 10.2 (1.1 to 93.3)). CONCLUSIONS: Prevalence of migraine was not different between patients with stroke and matched controls except among women aged < 45, when migraine and stroke were significantly associated.

Adolescent↗
PubMed1993

A gene for familial hemiplegic migraine maps to chromosome 19.

Familial hemiplegic migraine is an autosomal dominant disorder of unknown pathogenesis in which the migrainous attacks are marked by the occurrence of a transient hemiplegia during the aura. While investigating CADASIL, mapped previously to chromosome 19, we observed that some patients had recurrent attacks of migraine with aura. Although the clinical and neuroimaging features of familial hemiplegic migraine differ markedly from CADASIL, we hypothesized that the same gene could be involved in the pathogenesis of both conditions. We chose two large pedigrees for linkage analysis of familial hemiplegic migraine. A maximum lod score > 8 was found with two markers that are also strongly linked to CADASIL. Multilocus linkage analysis suggested that the loci responsible for the two diseases reside within an interval of about 30 cM on chromosome 19.

Adolescent↗
PubMed1993

Very small (border zone) cerebellar infarcts. Distribution, causes, mechanisms and clinical features.

Computerized tomography (CT) and magnetic resonance imaging (MRI) allow accurate anatomical localization of large thromboembolic cerebellar infarcts in the territories of the cerebellar arteries and their branches. In addition, MRI and CT show very small cerebellar infarcts as discrete foci of signal change that are not easily localizable within well-defined arterial territories. They could be border zone infarcts. Their anatomy, mechanism and clinical features have not been studied. By reviewing our CT and MRI files over a 2-year period, we found 47 patients with very small cerebellar infarcts; 23 patients had angiography. Infarcts were cortical (32 patients), deep (10 patients) and both (five patients). Most lesions corresponded to border zone cerebellar infarcts. The mechanisms of infarction were (i) global hypoperfusion due to cardiac arrest (two patients); (ii) small or end (pial) artery disease due to intracranial atheroma or hypercoagulable states (nine patients); (iii) focal cerebellar hypoperfusion due to large artery (vertebral or basilar) occlusive disease (16 patients) or brain embolism (11 patients) resulting in infarcts in the watershed areas (27 patients total); (iv) unknown mechanism (nine patients, 19%). Large artery occlusive disease was more frequently observed in deep than in cortical infarcts (9 out of 15 versus 11 out of 37; P < 0.0001). The most frequent symptoms were dizziness, lightheadedness, unsteadiness with axial lateropulsion, dysarthria and limb clumsiness. These symptoms were either transient or recurrent, at times related to positional changes of the head or trunk. Position-related symptoms often persisted for weeks or months after the ischaemic event, and occurred mainly in patients with combined carotid and vertebrobasilar occlusive disease. Physical findings were either absent or included wide-based gait, lateropulsion, mild ipsilateral dysmetria, dysarthria or dysdiadochokinesia. We conclude that very small cerebellar infarcts are often found on CT and MRI. Their border zone distribution and frequent posturally related symptoms most often result from large or pial artery disease rather than from systemic hypotension.

Adult↗
PubMed1993

Efficacy of subcutaneous sumatriptan in the acute treatment of early-morning migraine: a placebo-controlled trial. Early-Morning Migraine Sumatriptan Study Group.

OBJECTIVES: To evaluate the efficacy of self-administered subcutaneous sumatriptan in the acute treatment of early-morning migraine attacks. DESIGN: A double-blind, randomized, placebo-controlled, cross-over study. SETTING: Thirteen neurology centres in France. SUBJECTS: Patients of either sex, 18-65 years old, with two to six attacks of migraine (according to the International Headache Society (IHS) criteria, with or without aura) per month, of which at least two had to be early-morning migraine attacks. One-hundred-and-one patients were included, 96 being evaluable for the first attack and 81 for the cross-over design. INTERVENTIONS: Two migraine attacks (grade 2/3) were treated with sumatriptan (6 mg) or placebo, with an optional second injection 1-24 h later. Main outcome measures. The primary end-point was headache relief: reduction in headache severity from grade 2/3 (moderate/severe) to grade 1/0 (mild/none) 2 h after treatment. RESULTS: Sumatriptan was superior to placebo for headache relief (32 [78%] vs. 11 [28%] at the first attack; 29 [73%] vs. 8 [20%] at the second; P < 0.001). Because of a significant carry-over effect for some of the secondary end-points, a parallel-group analysis of the first attack was performed, which confirmed a significantly higher efficacy of sumatriptan for all end-points: pain-free rate (22 [46%] vs. 7 [15%]; P = 0.001) and use of a second injection (26 [53%] vs. 38 [81%]; P = 0.004). Sumatriptan was preferred by 74% of patients vs. 17% for placebo, and 9% expressed no preference (P < 0.0001). After complete relief, headache reappeared in 8/23 (35%) patients with sumatriptan and 3/7 (43%) with placebo. Adverse events were significantly more frequent with sumatriptan but they were minor and transient. CONCLUSION: Subcutaneous sumatriptan auto-injection is an effective and well-tolerated acute treatment of early-morning migraine attacks allowing earlier return to normal activity.

Adult↗
PubMed1993

Autosomal dominant leukoencephalopathy and subcortical ischemic stroke. A clinicopathological study.

BACKGROUND AND PURPOSE: We recently described an autosomal dominant syndrome characterized mainly by recurrent strokes and neuroimaging evidence of leukoencephalopathy. We now report the pathological findings in one of the affected subjects. CASE DESCRIPTION: A 40-year-old woman experienced her first grand mal seizure in 1971. From 1983 on she suffered recurrent strokes, seizures, and psychiatric disturbances with depressions, manic episodes, and dementia. In 1988, after her fourth stroke, she became tetraplegic with a severe pseudobulbar palsy, and she died in 1990. Pathological examination disclosed a recent capsulolenticular hematoma, multiple small deep infarcts, a diffuse myelin loss and pallor of the hemispheric white matter, and a widespread vasculopathy of the small arteries penetrating the white matter. The arterial wall was markedly thickened with an extensive nonamyloid eosinophilic deposit in the media and reduplication of the internal elastic lamella. CONCLUSIONS: The underlying lesion of this hereditary disorder is located in the small arteries and is of unknown etiology. It differs from arteriosclerotic and amyloid angiopathies but is similar to that described in some cases of hereditary multi-infarct dementia.

Adult↗
PubMed1993

Patent foramen ovale: is stroke due to paradoxical embolism?

BACKGROUND AND PURPOSE: A patent foramen ovale has been reported to be significantly more frequent in young stroke patients than in matched control subjects, and paradoxical embolism has been suggested as the main mechanism of stroke in this situation. The present study was designed to test this hypothesis. METHODS: Sixty-eight consecutive patients under 55 years of age presenting with an ischemic stroke had an extensive workup, including transesophageal echocardiography with contrast. We compared the prevalence of criteria for the diagnosis of paradoxical embolism in patients with and without a patent foramen ovale. RESULTS: A patent foramen ovale was found in 32 patients (47%). A Valsalva-provoking activity was present at stroke onset in six patients with a patent foramen ovale and in eight patients with no patent foramen ovale (chi 2 = 0.1, nonsignificant). Clinical/radiological features suggestive of an embolic mechanism were not more frequent in patients with a patent foramen ovale. Clinical evidence of deep vein thrombosis was present in one patient with a patent foramen ovale and in none of the others. No occult venous thrombosis was found in a subgroup of patients with a patent foramen ovale and no definite cause for stroke who underwent venography (n = 13). CONCLUSIONS: Our results do not support the hypothesis that paradoxical embolism is the primary mechanism of stroke in patients with a patent foramen ovale.

Adult↗
PubMed1993

Atrial septal aneurysm and patent foramen ovale as risk factors for cryptogenic stroke in patients less than 55 years of age. A study using transesophageal echocardiography.

BACKGROUND AND PURPOSE: An association between atrial septal aneurysm and embolic events has been suggested. Atrial septal aneurysm has been shown to be associated with patent foramen ovale and, in some reports, with mitral valve prolapse. These two latter cardiac disorders have been identified as potential risk factors for ischemic stroke. The aim of this prospective study was to assess the role of atrial septal aneurysm as an independent risk factor for stroke, especially for cryptogenic stroke. METHODS: We studied the prevalence of atrial septal aneurysm, patent foramen ovale, and mitral valve prolapse in 100 consecutive patients < 55 years of age with ischemic stroke who underwent extensive etiological investigations. We compared these results with those in a control group of 50 consecutive patients. The diagnosis of atrial septal aneurysm and patent foramen ovale relied on transesophageal echocardiography with a contrast study and that of mitral valve prolapse, on two-dimensional transthoracic echocardiography. RESULTS: Stepwise logistic regression analysis showed that atrial septal aneurysm (odds ratio, 4.3; 95% confidence interval, 1.3 to 14.6; P = .01) and patent foramen ovale (odds ratio, 3.9; 95% confidence interval, 1.5 to 10; P = .003) but not mitral valve prolapse were significantly associated with the diagnosis of cryptogenic stroke. The stroke odds of a patient with both atrial septal aneurysm and patent foramen ovale were 33.3 times (95% confidence interval, 4.1 to 270) the stroke odds of a patient with neither of these cardiac disorders. For a patient with atrial septal aneurysm of > 10-mm excursion, the stroke odds were approximately 8 times the stroke odds of a patient with atrial septal aneurysm of < 10 mm. CONCLUSIONS: This study shows that atrial septal aneurysm and patent foramen ovale are both significantly associated with cryptogenic stroke and that their association has a marked synergistic effect. Atrial septal aneurysms of > 10-mm excursion are associated with a higher risk of stroke.

Adolescent↗
PubMed1993

Cerebral infarction due to painless thoracic aortic and common carotid artery dissections.

BACKGROUND: Aortic arch dissection is usually lethal unless emergency surgery is performed. The dissection rarely may have a benign outcome or may occur without pain and be revealed by cerebral infarction. It is then likely to be seen primarily by a neurologist. In such cases, the value of new noninvasive diagnostic testing has not been reported. CASE DESCRIPTION: A 51-year-old man had a sudden left-sided hemiplegia due to hemorrhagic capsular and caudate infarcts on the right side. Cervical ultrasound examination with color flow imaging showed a bilateral common carotid artery dissection extending up to the bifurcation. Transesophageal echocardiography showed an aortic arch dissection, involving the innominate and left common carotid artery origins, which was confirmed by magnetic resonance imaging and aortography. The patient spontaneously fully recovered and is still alive 24 months after the stroke onset. CONCLUSIONS: This case emphasizes the usefulness of new noninvasive techniques such as transesophageal echocardiography and color-coded Doppler echocardiography in the diagnosis and follow-up of painless dissection of aortic and common carotid arteries. This cause of stroke may be underestimated.

Aortic Dissection↗
PubMed1993

[Incidental finding of an isolated thrombus in the left atrium in a young woman with sinus rhythm 5 years after cerebral ischemic accident].

The authors report the case of a 40 year old woman who had an ischemic stroke. The initial investigation including a complete blood clotting analysis, failed to demonstrate the cause. Five years later, the investigations were completed systematically by transesophageal echocardiography which demonstrated an isolated thrombus localised in the left atrial appendage though the localisation heart was in sinus rhythm and morphologically normal. This case illustrates in the diagnostic yield of transesophageal echocardiography in the investigation of systemic embolism in young patients who have had a cerebral ischemic event of unknown cause, even in the absence of predisposing cardiac cause.

Adult↗
PubMed1993

[Evolution of symptomatic carotid stenoses under medical treatment].

Data from the 2 major studies (ECST and NASCET) carried out to evaluate surgery of symptomatic carotid artery stenosis provided more information on the evolution (during medical treatment) of these lesions than all previous work. The essential risk, that of a cerebral infarction homolateral to the stenosis, is closely related to the degree of stenosis; for occlusions greater than 70% it was 5% annually in the ECST and 13% in the NASCET, more severe occlusions being treated in the latter study. Inversely, it was only 0.5% annually for stenoses involving less than 30% (ECST). For occlusions of between 30 and 70%, the risk has not yet been determined exactly, since the 2 studies are ongoing, but everything suggests that the risk is related to the degree of stenosis for this range also. Factors increasing this risk include: the cerebral site--and not only retinal--of the initial stenosed carotid, the ulcerative nature of the stenosis, the existence of contralateral carotid occlusion and the presence of vascular risk factors. Therapy is dependent on the evaluation of total risk factors, surgery being indicated increasingly as there is the greater high risk of stenosis. Surgery is then additional to medical treatment of vascular risk factors, mainly hypertension and antithrombotic therapy: generally aspirin and perhaps Ticlopidine.

Carotid Stenosis↗
PubMed1992

Migraine.

Explore the source record for details and available documents.

Administration, Topical↗
PubMed1992

The prevalence of ulcerated plaques in the aortic arch in patients with stroke.

BACKGROUND AND METHODS: The cause of cerebral infarction is obscure in up to 40 percent of patients with this disorder who are studied prospectively. In this investigation, we determined the frequency of ulcerated plaques in the aortic arch and explored the part they may play in the formation of cerebral emboli. Using an autopsy data bank, we studied the prevalence of ulcerated plaques in the aortic arch in 500 consecutive patients with cerebrovascular and other neurologic diseases who were studied at autopsy. RESULTS: Ulcerated plaques were present in 26 percent of the 239 patients with cerebrovascular disease but in only 5 percent of the 261 patients with other neurologic diseases (P less than 0.001). After we controlled for age and heart weight, the adjusted rates were 16.9 percent and 5.1 percent, respectively (adjusted odds ratio, 4.0; 95 percent confidence interval, 2.1 to 7.8; P less than 0.001). Among the patients with cerebrovascular disease, the prevalence of ulcerated plaques in the aortic arch was 28 percent in the 183 patients with cerebral infarcts and 20 percent in the 56 patients with brain hemorrhage. The prevalence of ulcerated plaques was 61 percent among the 28 patients with no known cause of cerebral infarction, as compared with 22 percent among the 155 patients with a known cause of cerebral infarction (P less than 0.001). After adjustment for covariates, the prevalence was 57.8 percent among patients with no known cause of cerebral infarction and 20.2 percent among those with a known cause (adjusted odds ratio, 5.7; 95 percent confidence interval, 2.4 to 13.6; P less than 0.001). The presence of ulcerated plaques in the aortic arch was not correlated with the presence of extracranial internal-carotid artery stenosis, suggesting that these were two independent risk factors for stroke. CONCLUSIONS: Ulcerated plaques in the aortic arch may play a part in causing cerebral infarction, especially in patients in whom cerebral infarction has no known cause.

Adult↗
PubMed1992

Pain as the only manifestation of internal carotid artery dissection.

Internal carotid artery dissection is a major cause of ischemic stroke in the young. Pain is the leading symptom and is associated with other focal signs such as Horner's syndrome and painful tinnitus or with signs of cerebral or retinal ischemia. We report two patients with angiographically confirmed extracranial internal carotid artery dissection presenting with cephalic pain as the only manifestation. The first patient had a diffuse headache and a latero-cervical pain lasting for 12 days, reminiscent of carotidynia. The second patient experienced an exploding headache suggestive of subarachnoid hemorrhage, which was ruled out by computed tomography of the head and cerebrospinal fluid study. These patients demonstrate that recognition of carotid artery dissection as a cause of carotidynia and headache suggestive of subarachnoid hemorrhage may permit an earlier diagnosis and possibly the prevention of a stroke through the use of anticoagulation.

Adult↗
PubMed1992

Ipsilateral cluster headache and chronic paroxysmal hemicrania: two case reports.

We report two patients with ipsilateral attacks of cluster headache and chronic paroxysmal hemicrania. The first patient, a 33-year-old man, started having attacks of chronic cluster headache at the age of 27. At 33, they were replaced by typical attacks of ipsilateral chronic paroxysmal hemicrania which showed a dramatic improvement with indomethacin 150 mg daily. After two days of complete remission, cluster headache attacks reappeared and persisted until verapamil, 360 mg a day, was added to indomethacin. The second patient, a 45-year-old man, first developed attacks of episodic cluster headache at the age of 35. At 44, he experienced ipsilateral typical attacks of chronic paroxysmal hemicrania, and two months later attacks of cluster headache. Under verapamil 240 mg daily, attacks of cluster headache disappeared, but those of chronic paroxysmal hemicrania increased in frequency until indomethacin 150 mg daily was added. These observations suggest a close relationship but not a similarity between cluster headache and chronic paraoxysmal hemicrania, and show the practical therapeutic interest of maintaining this distinction.

Adult↗
PubMed1992

Headache following carotid endarterectomy: a prospective study.

The occurrence of headache in the 28 days following surgery was studied in 50 consecutive patients (14F and 36M, mean aged 70 years) who underwent carotid endarterectomy for atheromatous carotid stenosis. Thirty-one patients (62%) reported headache. Headache occurred in the first five days after surgery in 87% of cases. Its characteristics and temporal profile were highly variable but it was mostly bilateral (74%), mild or moderate (78%), requiring no treatment (77%). No correlation was found between the occurrence of headache and degree of stenosis, intraoperative characteristics and past history of headache. In none of our patients was severe ipsilateral headache, cerebral hyperperfusion syndrome, or cluster-like hemicrania encountered and only five patients met the IHS criteria for post-endarterectomy headache. Post-endarterectomy headache is frequent when specifically looked for and is therefore not a single entity. The present IHS criteria are unsatisfactory and should be modified accordingly.

Aged↗
PubMed1992

Transesophageal echocardiographic detection of aortic arch disease in patients with cerebral infarction.

BACKGROUND AND PURPOSE: Ulcerated plaques in the aortic arch are frequent autopsy findings in patients with cerebral infarctions, particularly those of unknown cause. It has been suggested that they could be a source of cerebral emboli. Using transesophageal echocardiography, we prospectively studied 12 consecutive patients with cerebral infarction of undetermined cause after noninvasive workup to evaluate the frequency of aortic plaques or mural thrombi that could embolize in cerebral arteries. SUMMARY OF REVIEW: Six patients (50%) had an intraluminal echogenic mass of the aortic arch, mainly located at the junction of the ascending aorta and arch. This material was pedunculated (in one patient) or broad based (in five patients) with a markedly irregular surface and intraluminal extension from 3 to 15 mm. In addition, we found cholesterol emboli in two of the four patients who underwent quadriceps biopsy. CONCLUSIONS: These results show that transesophageal echocardiography has capabilities in detecting such lesions and point to the aortic arch as a possible source of cerebral emboli in patients with cerebral infarction of unknown cause.

Aged↗
PubMed1992

Cerebral venous thrombosis in Behçet's disease: clinical study and long-term follow-up of 25 cases.

Among 250 patients with Behcet's disease, we describe 25 cases of angiographically proven cerebral venous thrombosis. Intracranial hypertension was the most frequent manifestation. Two initially untreated patients relapsed. Treatment of cerebral venous thrombosis consisted of combined heparin and steroids in 19 patients, steroids alone in three, and heparin alone in three others. Neurologic symptoms improved rapidly in all. Nineteen patients received long-term anticoagulation, and two received aspirin. Relapse of cerebral venous thrombosis or development of optic atrophy did not occur in treated patients. Partial or total recanalization of the occluded sinus was frequent. After more than 3 years of follow-up, the prognosis of dural sinus thrombosis is satisfactory.

Adolescent↗