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Biomedical subjects

J L Mas

Publications and source records attributed to J L Mas.

At least 73 records · Page 4Linked to original sources
PubMed1995

Incidence and causes of strokes associated with pregnancy and puerperium. A study in public hospitals of Ile de France. Stroke in Pregnancy Study Group.

BACKGROUND AND PURPOSE: The incidence, causes, and prognosis of nonhemorrhagic strokes and intraparenchymal hemorrhages occurring in association with pregnancy or puerperium are poorly understood. METHODS: We carried out a retrospective (1989 through 1991) and prospective (1992) study in 63 public maternities (348,295 deliveries) of the region of Ile de France (10,660,554 inhabitants) and in the neurology, neurosurgery, and intensive care units of the same geographic area. Records of women who suffered a cerebrovascular event during pregnancy or the first 2 weeks postpartum were reviewed by two study neurologists. Stroke was defined according to the criteria of the World Health Organization. RESULTS: Thirty-one cases of strokes were identified, including 15 nonhemorrhagic strokes (including strokelike deficits associated with eclampsia) and 16 intraparenchymal hemorrhages, assessed in all cases by CT scan and/or MRI. The incidence of nonhemorrhagic strokes in women who delivered in public maternities of Ile de France was 4.3 per 100,000 deliveries (95% confidence interval, 2.4 to 7.1) and that of intraparenchymal hemorrhage was 4.6 per 100,000 deliveries (95% confidence interval, 2.6 to 7.5). Eclampsia accounted for 47% of cases of nonhemorrhagic strokes. The other causes were extracranial vertebral artery dissection, postpartum cerebral angiopathy, inherited protein S deficiency, and disseminated intravascular coagulation associated with amniotic fluid embolism. The cause remained undetermined in four cases despite extensive investigations. Eclampsia accounted for 44% of intraparenchymal hemorrhages. Another 37% were due to rupture of a vascular malformation. The cause remained undetermined in three cases. There were four maternal deaths (all associated with intraparenchymal hemorrhage), three of them in eclamptic women. Fetal mortality and prematurity were associated with eclampsia. CONCLUSIONS: The incidence of nonhemorrhagic stroke does not seem to be much increased during pregnancy and early puerperium. In contrast to that in the nonpregnant state, the frequency of intraparenchymal hemorrhage in pregnancy appears to be similar to that of nonhemorrhagic strokes, suggesting that pregnancy may increase the risk of cerebral hemorrhage. Eclampsia is the main cause of both nonhemorrhagic stroke and intraparenchymal hemorrhage. Intraparenchymal hemorrhage associated with eclampsia carries a poor prognosis.

Adult↗
PubMed1994

Magnetic resonance imaging and dynamic CT scan in cervical artery dissections.

BACKGROUND AND PURPOSE: The typical magnetic resonance imaging picture of arterial dissection, namely, a narrowed eccentric signal void surrounded by a semilunar signal hyper-intensity (corresponding to the mural hematoma) on T1- and T2-weighted images, has been repeatedly reported, but the sensitivity of magnetic resonance imaging for the diagnosis of cervical dissection is poorly known. Another technique, dynamic computed tomography, may provide evidence of mural hematoma, but there has been no systematic evaluation of this technique. The aims of this study were to assess both the sensitivity of routine 0.5-T magnetic resonance imaging for the detection of a typical picture of cervical artery dissection and the value of dynamic computed tomographic scans to provide evidence of dissecting hematoma. METHODS: Fifteen consecutive patients with angiographically confirmed extracranial internal carotid (n = 9) or vertebral (n = 10) dissections were studied using a standardized 0.5-T spin-echo magnetic resonance imaging protocol with axial slices. Twelve of these patients had dynamic computed tomographic scans at the site of the dissection suggested by angiography. RESULTS: A typical magnetic resonance imaging picture of cervical artery dissection was observed in 12 of 15 (80%) patients and in 13 of 19 (68%) dissected vessels. The sensitivity of magnetic resonance imaging was higher in internal carotid (78%) than in vertebral (60%) dissections and in stenotic-type dissections (85%) than in occlusive or aneurysmal-type dissections. The dynamic computed tomographic scan showed the mural hematoma in 11 of the 12 (92%) patients and in 12 of 15 (80%) dissected vessels. CONCLUSIONS: Routine 0.5-T magnetic resonance imaging with axial slices is a sensitive technique for the diagnosis of dissection, but in about 20% of patients with cervical artery dissection magnetic resonance imaging will demonstrate no typical abnormality. Dynamic computed tomographic scans are a sensitive neuroimaging procedure to confirm the presence of the mural hematoma, but it needs to be directed by prior angiography.

Adult↗
PubMed1994

[Epidemiology of cerebral infarction].

The annual incidence of strokes (all types) is estimated to be between two and four per thousand in the 55 to 64 year age-group and reaches about 15 per thousand over the age of 75 years. Population registries and hospital registries show that cerebral infarcts represent about 80% of all strokes and indicate the respective roles of the principal causes. A significant reduction in mortality related stroke in general and cerebral infarction in particular has been observed in many countries over recent decades. Hypertension constitutes the principal risk factor for ischaemic and haemorrhagic stroke. This risk varies by about 40% when the mean diastolic blood pressure varies from 5 to 10 mmHg, even in normotensive subjects. Several studies have demonstrated that treatment of moderate or severe hypertension lowers the incidence of stroke. Smoking, diabetes, chronic alcoholism (> 3 standard glasses per day), hypercholesterolaemia and raised plasma fibrinogen also constitute independent risk factors for cerebral infarction. Of the emboligenic heart diseases, non-valvular atrial fibrillation (80% of all cases of atrial fibrillation) is the most potent risk factor for cerebral infarction: subjects with this disease have a risk of cerebral infarction of approximately 5% per year. The presence of asymptomatic carotid artery stenosis is associated with an annual risk of cerebral infarction generally estimated to be between 1 and 2% which, in reality, increases with the degree of stenosis. Even in the case of tight stenosis, the risk of ipsilateral cerebral infarction remains low (< 3% per year for stenosis > 75%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

[Medical treatment of atherosclerotic carotid stenoses].

Patients with atherosclerotic carotid artery stenosis commonly have arterial disease elsewhere, especially coronary artery disease. The aim of the medical treatment is to reduce the incidence of stroke, myocardial infarction and vascular death. Both primary and secondary prevention of these vascular events requires control of vascular risk factors, particularly lowering elevated blood pressure, lowering of elevated blood cholesterol and stopping smoking. Aspirin and ticlopidine are effective in reducing vascular events in patients with atherosclerosis, with a relative reduction of about 25% for the composite outcome event "stroke, myocardial infarction or vascular death". Whether low dose (less than 100 mg/d), medium (300 mg/d) or high dose (1,000 mg/d or more) of aspirin confer the same degree of protection against vascular events is unclear. The gastrointestinal side effects are greater for the high dose than for the medium dose, but the difference between the medium dose and the low dose is very small. Ticlopidine conveys a modest risk of reversible severe neutropenia and is often used as a second-line drug, but this is a controversial issue. Heparin is often used as a short-term preventive treatment in patients with transient ischaemic attacks or minor stroke, especially in those with "crescendo" transient ischaemic attacks, progressing stroke, severe carotid stenosis or intraluminal thrombus.

Arteriosclerosis↗
PubMed1993

[Internal carotid artery dissection].

Arterial dissection results from bleeding into the vessel wall. Some cases are associated with cervical trauma or have evidence of an underlying vascular disease; many occur without any history of injury or detectable arterial disease. Among the cervical cephalic arteries, the extracranial segment of the internal carotid artery is the vessel most commonly involved; intracranial carotid dissections are much rare. Carotid dissection occurs predominantly in young or middle-aged adults and shows no sex predominance. Although clinical manifestations can be extremely diverse (from isolated headache to rapidly lethal stroke), the most common and suggestive syndrome associates "local" symptoms (such as head or neck pain, Horner's syndrome, pulsatile tinnitus or lower cranial nerves palsy) and delayed (up to several weeks) symptoms of cerebral ischaemia in the territory of the internal carotid artery territory. Dissection can be bilateral or associated with dissection of the vertebral artery. Angiography has long been considered the gold standard for the diagnosis. As this procedure carries a risk of cerebral complications, noninvasive diagnostic approaches such as magnetic resonance imaging and ultrasound have been developed and are increasingly used. The prognosis of carotid dissections depends on the presence and severity of ischaemic brain damage. Recurrent dissections seem extremely rare. Normalization or improvement of the vascular abnormalities during the subsequent weeks is frequent and is an excellent argument in favour of the diagnosis. Although no controlled trial has ever been performed, anticoagulant treatment is often used for a few months when the dissection involves the extracranial segment of the carotid artery. No standard treatment of intracranial carotid dissection has emerged.

Adult↗
PubMed1993

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy maps to chromosome 19q12.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) has been recently reported as a cause of stroke. It is characterized, in the absence of hypertension, by recurrent subcortical ischaemic strokes, starting in early or midadulthood and leading in some patients to dementia. Magnetic resonance imaging and pathological examination show numerous small subcortical infarcts and a diffuse leukoencephalopathy underlaid by a non-arteriosclerotic, non-amyloid angiopathy. We performed genetic linkage analysis in two unrelated families and assigned the disease locus to chromosome 19q12. Multilocus analysis with the location scores method established the best estimate for the location of the affected gene within a 14 centimorgan interval bracketed by D19S221 and D19S222 loci.

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

[Secondary prevention of cerebral embolism of cardiac origin].

About 20% of cerebral ischemic strokes are the consequence of embolism arising from the heart. Their secondary prevention is based on the treatment of the causal heart disease, which is most often associated with an anticoagulant treatment. In case of nonrheumatismal atrial fibrillation (AF), the most frequent cause of cerebral embolism of cardiac origin, the benefits of a long-standing anticoagulant treatment in comparison with a placebo or with aspirin for the prevention of recurrence is being investigated in a European multicenter trial. However, considering the very favorable results reported recently for primary prevention, it seems logical to think that many patients with nonrheumatismal AF will also benefit from this treatment as secondary prevention. The optimal delay to begin an anticoagulant during the acute phase of cardioembolic brain infarcta remains controversial. Physicians must weight the spontaneous risk of embolic recurrence against the risk of symptomatic brain hemorrhage with anticoagulants (caused by worsening of a spontaneous hemorrhagic transformation) for the individual patients. Recommendations of the Cerebral Embolism Study Group include delaying the start of the heparin course by 48 hours or more after checking for hemorrhage on CT. In case of large infarction, of hemorrhagic infarction or of uncontrolled arterial hypertension, it seems safer to delay the treatment for at least a week. However, these are only empirical recommendations, which must be adapted to each case according to the individual risks.

Anticoagulants↗
PubMed1992

Meningeal sarcoidosis, pseudo-meningioma, and pachymeningitis of the convexity.

Two cases of meningeal sarcoidosis with unusual and misleading presentations are reported. In the first case, CT scan, angiographic, and MRI findings were indistinguishable from those of meningioma. CSF pleiocytosis may help in diagnosing sarcoid pseudo-meningioma. The second patient had transient focal deficits and pachymeningitis of the convexity. The transient deficits were probably of epileptic origin based on their response to antiepileptic treatment. The diagnosis of neurosarcoidosis was made only after meningeal biopsy, despite thorough investigations.

Adult↗
PubMed1992

A familial disorder with subcortical ischemic strokes, dementia, and leukoencephalopathy.

A family had a disorder characterized by (1) a pattern suggestive of autosomal dominant inheritance, (2) recurrent attacks of focal brain deficits starting in mid adulthood and often leading to severe motor disability with pseudobulbar palsy and dementia of the subcortical type, and (3) neuroimaging evidence of leukoencephalopathy and well-circumscribed lesions consistent with small deep infarcts. Some affected members were clinically asymptomatic but had MRI signs of leukoencephalopathy. Extensive investigations failed to uncover a previously described recognizable genetic disorder.

Adult↗
PubMed1992

[Epidemiology of cerebrovascular accidents].

Recent studies concerning secular trends in stroke incidence and mortality and identification of independent risk factors for stroke are reviewed. Stroke mortality has declined in many industrialized countries in recent decades. In France, it has been declining by more than 30% between 1968 and 1982 in all age groups and in both sexes except for women under 40 years. The decline in stroke mortality seems to be partly real and partly apparent. In the community-based study of Rochester, Minnesota, stroke incidence decreased by 54% between 1945-49 and 1975-79. Recent data from Rochester, however, suggest that the incidence of stroke may no longer be declining. Survival after stroke has also apparently been improving but several sources of potential bias may also have influenced the decrease in reported survival rates. Hypertension is a major risk factor for stroke. Prolonged differences in "usual" diastolic blood pressure of 5 to 10 mmHg are associated with about 40% difference in stroke incidence. Recent analysis suggests that stroke incidence reduction could arise rapidly after hypertension control and that a lower blood pressure should confer a lower risk of vascular disease, even in individuals conventionally considered as "normotensive". There is evidence that cigarette smoking is an important risk factor for stroke with an overall relative risk of 1.5 and that the risk of stroke declines rapidly after the cessation of smoking. A cardiac condition may be a marker for another risk factor or the primary substrate for cerebral embolism. In patients with atrial fibrillation, the risk of stroke is increased through both of these mechanisms. Diabetes mellitus, chronic alcohol consumption (> 3 drinks/day), and high fibrinogen levels are other independent risk factors for stroke. While high levels of cholesterol may be associated with ischemic stroke, an inverse association of the serum cholesterol with the occurrence of intracerebral hemorrhage in men has been reported. In patients with asymptomatic internal carotid stenosis, higher degrees of stenosis convey a higher risk of stroke. However, far from all these strokes are due to thromboembolism from an atheromatous plaque in the ipsilateral internal carotid artery. The relative risk of stroke during the first 5 years following a transient ischemic attack is 7 times that in persons without transient ischemic attack. More than a third of the subsequent strokes occur in a vascular territory different from that of the incident TIA. While the use of oral contraceptives may increase the relative risk of stroke, postmenopausal estrogen treatment may have a protective effect on the risk of vascular diseases.

Age Factors↗