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Biomedical subjects

F Woimant

Publications and source records attributed to F Woimant.

At least 73 records · Page 4Linked to original sources

Platelet surface glycoprotein changes in patients with cerebral ischemia.

In vitro abnormalities of platelet behaviour have been described in patients with ischemic cerebrovascular disease (ICD) suggesting that changes in platelet receptors and/or platelet a granules may occur in the circulation. We investigated the frequency of such alterations in 95 patients that were studied within a few days after acute stroke. Using specific antibodies to two intrinsic plasma membrane glycoproteins (GPs), the GPIIb-IIIa complex and GPIV, and to thrombospondin (TSP), a a-granular protein that becomes expressed on the platelet surface upon activation, we were able to distinguish two groups of patients: 16 patients presented an increased concentration of TSP on their platelets demonstrating in vivo platelet secretion. These patients could constitute a group with increased risk of thrombosis. In contrast, 20 patients presented a decreased concentration of GPIIb-IIIa and GPIV. This decrease in intrinsic plasma membrane GPs was associated with a decrease in mean platelet volume and may suggest the occurrence of platelet fragmentation in the circulation.

Acute Disease↗

[Emergency preoperative embolization using coils of ruptured sylvian aneurysm. Apropos of a case].

The authors report a case of a 73 year old patient who presented with a right temporal lobe hematoma secondary to rupture of a right middle cerebral artery bifurcation aneurysm. Treatment consisted of partial thrombosis of the aneurysm by the endovascular introduction of metallic coils followed by surgical hematoma evacuation and aneurysm clipping. Thrombus of the aneurysm done probably diminished the risk of intraoperative rupture. Partial endovascular treatment has a very small risk and may be done on a emergency basis at the same time as the diagnostic arteriogram. It can also be suggested for patients in poor condition to diminish the risk of recurrent hemorrhage until the patient is well enough to undergo definitive surgical clipping.

Aged↗

[Benign cerebral angiopathies and phenylpropanolamine].

Heroin, cocaine, amphetamines, sympathomimetic drugs can cause cerebral angiopathy. We report 2 patients with cerebrovascular disorders after ingestion of a nasal vasoconstrictor containing phenylpropanolamine (P.P.A.). The first patient had two acute repetitive attacks of severe headache and vomiting, occurring after a daily treatment with 180 mg of P.P.A. during 6 weeks. The second patient had an intracerebral hemorrhage, occurring some hours after taking for the first time 120 mg of P.P.A. In both cases, cerebral angiography, performed in the next week, demonstrated segmental narrowing and dilatations of medium-size intracranial arteries. None of the usual causes of cerebral vasculitis were present. The outcome was favorable and follow-up angiograms showed the disappearance of the beading pattern. P.P.A. is widely used over the counter in diet pills and stimulants. Cerebral vascular complications have been rarely reported, always hemorrhagic and often associated with cerebral vasculitis. They are unrelated to duration or dosage of treatment. The mechanism is unclear but could result from several factors: chronic or paroxystic high blood pressure, immuno-allergic vasculitis, arterial spasm, direct "toxic" effect of the P.P.A. on the arterial wall may be increased by other drugs and caffeine.

Adult↗

[Cerebral ischemic accidents and chronic disseminated intravascular coagulation of cancerous origin].

Cerebral infarcts in 3 patients revealed the presence of disseminated intravascular coagulation (DIVC) of cancerous origin before any clinical manifestations of the neoplasm. Neurologic manifestations of these consumption coagulopathies almost constantly produce a picture of diffuse encephalopathy, expression of disseminated microinfarcts; however, transient or constituted focalized ischemic accidents by occlusion of a medium sized artery are also possible, and this in the absence of non-bacterial thrombotic endocarditis. Biologic diagnosis of DIVC is not always simple, and screening tests (platelet count, prothrombin and fibrinogen levels) can remain within normal limits during chronic forms, as a result of a subjacent inflammatory syndrome, frequently associated with cancer. Two other specific serum tests are therefore of fundamental interest: assay of fibrin degradation products and tests for soluble complexes.

Adenocarcinoma↗

[Clinical and developmental aspects of small brain stem hematomas. Contribution of x-ray computed tomography].

In a review of 16 cases, the authors emphasize that small brainstem haemorrhages, diagnosed by CT-scan, can have a good outcome, most often spontaneously. Twelve hematomas were in the pons, four in the mesencephalon. Several clinical features were remarkable: consciousness was not or moderately impaired, focal symptoms and signs predominantly neuro-ophthalmologic were present. Involvement of the cranial nerves and long tracts occurred rarely in isolation. Arterial hypertension was the usual cause (50 p. cent); one normotensive patient with neurological disorders prior to the bleeding had an arteriovenous malformation, demonstrated angiographically. In two cases an obstructive hydrocephalus was surgically treated. Expected advances from CT-scan and magnetic resonance imaging (M.R.I.) are discussed.

Adult↗

[Cerebral vascular accidents in anticoagulant therapy].

Thirty-three patients hospitalized as they presented with cerebral vascular lesions during anticoagulant therapy (25 intracerebral hemorrhages, 7 subdural hematoma, and one ischemia lesion). Frequency of intra-cerebral hemorrhages along with anticoagulant therapy was about 11 p. 100, this of subdural hematoma ranged from 12 to 38 p. 100. Intra-cerebral hemorrhages failed to show any peculiar topography and volume was variable. A predisposing factor thus existed in about 50 p. 100 of cases: high blood pressure or arterial aneurysm. Previous cranial traumatism was only demonstrated in 48 p. 100 patients presenting with a subdural hematoma. Prognosis as for these intracranial hemorrhages might be compared to this of hemorrhagic lesions appearing under other etiologic conditions. Ischemia lesion was secondary to a severe thrombopenia to heparin.

Acute Disease↗

[Myelopathy manifesting as macroglobulinemia].

Slowly progressive cervical cord symptoms over a 2 year period led to the diagnosis of Waldenström macroglobulinemia in a 32 year old man. Diagnosis was made on the finding of circulating monoclonal IgM and lymphocyte infiltration of the bone marrow. Perimedullary infiltration of cervico-dorsal cord was visualized by CT scan. No other tumor tissue was found. Intrathecal secretion of IgM in the CSF was demonstrated. Cervico-dorsal cord radiotherapy followed by systemic chemotherapy led to a rapid improvement in the neurological signs. Reports of spinal cord lesions in Waldenström macroglobulinemia are rare and the relationship of this condition with respect to so-called secreting neurolymphomatosis is discussed.

Adult↗

[Treatment of cerebrovascular accidents in an intensive care unit. 230 cases].

Over a 20 months' period, 230 patients were treated in an intensive care unit for acute cerebral vascular accident. There were 157 ischaemic accidents and 73 haemorrhages. The mean age of the patients was 61.7 years. Mechanical ventilation was used in a quarter of the cases, and tracheotomy was performed in 7%. Surgery was considered necessary in only less than 5%. The overall mortality in the unit was 20% for patients with established ischaemia and 44% for those with cerebral haemorrhage. After 6 months, 64% of patients with ischaemia and 44% of patients with haemorrhage were still alive; 82% were independent, usually without sequelae, and 6% were bed-ridden; 15% of those who had mechanical ventilation survived. Prognostic factors are analyzed and the role of intensive care units in the management of cerebral vascular accidents is discussed.

Adult↗

[Acute interhemispheric subdural hematomas].

Three cases of acute interhemispheric subdural hematomas, one of which bilateral, are reported. These are secondary to cranial traumatism and/or to treatment by anticoagulants and have stereotyped clinical signs. Following a lucid period, intracranial hypertension appears, then a sudden predominantly crural hemiparesis or even paraplegia. The aspects shown by computerized tomography are characteristic. The literature and our experience suggest that the best treatment is complete evacuation of the hematoma by craniotomy performed before alteration of consciousness.

Aged↗