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France Woimant

Publications and source records attributed to France Woimant.

10 recordsLinked to original sources
PubMed2006

[Stroke centers and stroke networks].

Admission to a stroke unit represents an established and efficient treatment for acute stroke. However, stroke care is yet not enough developed in many countries. In France, the organisational model is based on stroke unit admission for acute stroke patients associated with a network of stroke units covering the majority of the territory. That model fulfils the commitment of equity of access to medical care for the whole population, and optimises use of resources. The task of the five-year organisational plan Schéma régional d'organisation sanitaire is aimed achieve that goal.

Acute Disease↗
PubMed2006

[Wilson's disease].

Wilson's disease is an autosomal recessive disorder of copper excess. This illness results from mutations of the ATP7B gene chromosome 13. The discovery of the gene allowed a better understanding of cytosolic copper trafficking its relationship with ceruloplasmin synthesis. Symptomatic patients may present with hepatic, neurologic or psychiatric forms. Clinical and phenotypic evidences provide only presumptive arguments for this disease which can be routinely assessed by molecular analysis. This disease can be efficiently treated by chelation and zinc therapy. Liver transplantation is the therapy to patients with hepatic fulminant course, or in those with relentless progression of hepatic dysfunction in spite of medical therapy.

Hepatolenticular Degeneration↗
PubMed2005

Extensive cortico-subcortical lesions in Wilson's disease: clinico-pathological study of two cases.

Wilson's disease (WD) with extensive cortico-subcortical lesions represents a rare neuropathological subgroup, the pathogenesis of which is not clearly determined. We report two new cases with identical lesions. In the families of each of the patient, there were mutations in the ATPase7B gene, especially in the family of proband 1, and in the first cousin of proband 2. These cases included massive destruction of the white matter in superior gyri, mostly frontal, extending to the deep cortex with neuronal loss and capillary proliferation. Astrocytes were of Alzheimer type 1 and 2; and type 1 were labeled by anti-metallothionein. Opalski cells were abundant and their macrophagic lineage was confirmed by immunostaining. Among the possible mechanisms proposed, the role of vascular factors and penicillamine treatment could be excluded. Cerebral copper content in white matter and putamen of case 1 was at the same level as in common WD but accumulation of unbound copper in the white matter was a distinctive feature, which suggested a pathological neurotoxic effect.

Adenosine Triphosphatases↗
PubMed2005

A negative D-dimer assay does not rule out cerebral venous thrombosis: a series of seventy-three patients.

BACKGROUND AND PURPOSE: Cerebral venous thrombosis (CVT) is an infrequent variety of cerebrovascular disease with a wide spectrum of clinical presentations and a notoriously difficult diagnosis. Previous reports have emphasized the potential clinical utility of D-dimer assay in CVT diagnosis. METHODS: A rapid sensitive D-dimer assay was performed at entry in 73 patients with CVT <30 days duration, examined in our institution between 1999 and 2003. RESULTS: The mean value of D-dimer levels was 1521 ng/mL; 7 patients (10% of all patients and 26% of those presenting with isolated headache) had values <500 ng/mL. In a multivariate analysis, isolated headache was the only variable associated with a negative D-dimer assay. CONCLUSIONS: A negative D-Dimer assay does not confidently rule out CVT, particularly in the setting of recent isolated headache.

Adult↗
PubMed2005

Blood Pressure, smoking and oral contraceptive control after cryptogenic stroke in young adults in the PFO-ASA Study.

BACKGROUND: Management of vascular risk factors is not optimal in stroke patients. We assessed the control of hypertension, smoking and stopping of oral contraceptive in 581 consecutive young cryptogenic ischemic stroke patients followed in the PFO-ASA study and we identified factors associated with inadequate management. METHODS: At each follow-up visit, blood pressure (BP), smoking and use of oral contraceptive were recorded. Data were analyzed at 6 months, 1 and 2 years. Hypertension was defined as systolic BP > or = 140 or diastolic BP > or = 90 mm Hg, recorded in at least two follow-up visits. Current smoking was defined as more than one cigarette per day reported during at least one follow-up visit. RESULTS: During follow-up, 36% of patients were hypertensive and 30% were smokers. Among the 90 hypertensive patients at baseline, 60-68% remained with high BP and among the 278 patients who were current smokers at baseline, 54-58% still smoked during follow-up. Age (OR = 1.05, 95% CI 1.02-1.08), male sex (OR = 1.42, 95% CI 0.93-2.18), body mass index > or = 27 (OR = 2, 95% CI 1.27-3.17) and known hypertension (OR = 3.08, 95% CI 1.80-5.28) were significantly associated with hypertension during follow-up. Tobacco consumption at baseline (OR = 35.2, 95% CI, 19.3-64.2), alcohol consumption at baseline (OR = 2.7, 95% CI 1.4-5.2) and Rankin < or = 2 (OR = 2.6, 95% CI 1.4-4.9) were independently associated with persistent smoking. Among the 114 women who were using combined estrogen-progesterone pills at baseline, 96.5% stopped. CONCLUSIONS: Major risk factors for stroke are poorly controlled after stroke, even in the context of a prospective clinical study in young adults.

Blood Pressure↗
PubMed2005

Brain damage after heat stroke.

Cerebellar syndromes and radiologic cerebellar atrophy after hyperpyrexia have occasionally been reported, mostly in neuroleptic malignant syndromes, but neuropathologic studies are extremely rare. We studied 3 patients (a 74-year-old woman, a 63-year-old man, and an 80-year-old man) who had heat stroke during heat waves in France. One patient had generalized seizures and died 28 hours after admission. The other patients survived one month and 2 months after admission; both had palatal myoclonus, and in one case, magnetic resonance imaging showed high signal intensity in the cerebral peduncles. The main neuropathology in the 3 cases was severe diffuse loss of Purkinje cells associated with heat shock protein 70 expression by Bergmann glia. In situ end labeling was negative in surviving Purkinje cells, suggesting that the mechanism of neuronal death was not apoptosis. Degeneration of Purkinje cells axons resulted in myelin pallor of the white matter of the folia and of the hilum of the dentate nuclei. DNA internucleosomal breakages were identified by in situ end labeling in the dentate nuclei and centromedian nuclei of the thalamus and were associated with degeneration of the cerebellar efferent pathways: superior cerebellar peduncles, decussation of the superior cerebellar peduncles (Wernekinck commissure), and dentatothalamic tract. These findings suggest that the mechanisms of neuronal death in the dentate nuclei and centromedian nuclei of the thalamus was different from that in Purkinje cells and more likely resulted from deafferentation. Ammon's horn and other areas susceptible to hypoxia were spared. These observations confirm the selective vulnerability of Purkinje cells to heat-induced injury and involvement of the cerebellar efferent pathways in palatal myoclonus.

Aged↗