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Biomedical subjects

F Woimant

Publications and source records attributed to F Woimant.

At least 19 recordsLinked to original sources
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

Watershed cerebral infarcts: retrospective study of 24 cases.

Twenty-four patients presenting an acute stroke with watershed cerebral infarct on CT scan or MRI were included in this retrospective study. Age was 63 +/- 14 years (mean +/- SD), and sex ratio was 2 men for 1 woman. Main clinical features were: in anterior location, lower limb weakness and frontal syndrome with transcortical motor aphasia in left lesions or spatial dyscalculia in right ones; in posterior location, brachiofacial weakness with constant quadranopsia and hypoesthesia, and Gerstmann syndrome in left lesion. There was no distinctive feature for subcortical and multiple infarcts. In bilateral infarcts, there were one pseudobulbar syndrome, and 2 pseudo brainstem syndromes with neuropsychological signs. Aetiologies were severe carotid artery disease in 14 cases, severe cardiopathy in 6, isolated cerebral angiitis in 1, essential thrombocythemia in 1, protein C deficiency with sickle cell disease in 1, and cholesterol emboli in 1 anatomical case. CBF performed in carotid artery occlusions or tight stenoses showed evidence of haemodynamic changes. Microembolic process can be proposed in the case with cholesterol emboli. Preventive treatment is discussed.

Cerebral Infarction↗
PubMed1991

MRI in spontaneous dissection of vertebral and carotid arteries. 15 cases studied at 0.5 tesla.

Fifteen patients were observed between 1987 and 1990: there were six with angiographically confirmed vertebral artery dissection, and 9 with carotid artery dissection. Results showed concordance of MRI and angiographic findings, in all cases but one. The dissected portion consistently showed a semilunar hyperintensity narrowing the residual eccentric signal void of the lumen when the artery was not completely occluded. In one angiographically occluded vessel, MR detected a small signal void within the hyperintensity, indicating that the artery was not completely occluded. The length of the dissected portion was clearly demonstrated by MR. Follow up MR and angiographic studies confirmed the regression of the dissection, and also allowed examination of the cerebral parenchyma.

Aortic Dissection↗
PubMed1991

Granulomatous angiitis and cerebral amyloid angiopathy presenting as a mass lesion.

A woman, who presented with clinical and radiological signs of a right temporal mass suggestive of a brain tumour, was found to have granulomatous angiitis associated with cerebral amyloid angiopathy; the diagnosis was confirmed by biopsy. She is still well 13 years after excision of the lesion. The association of granulomatous angiitis and cerebral amyloid angiopathy constitutes a peculiar variety of central nervous system micro-angiopathy. Only a few similar cases have been described.

Amyloidosis↗
PubMed1991

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↗
PubMed1991

[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↗
PubMed1988

[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↗
PubMed1988

[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↗
PubMed1986

[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↗
PubMed1986

[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↗