[The causes of intracranial hemorrhagic complications induced by antivitamins K]. / Conditions de survenue des accidents hémorragiques intracrâniens des antivitamines K.

Cerebral haemorrhage is the main life-threatening complication of oral anticoagulant therapy. In order to identify a means of prevention, the authors undertook a retrospective study of 68 consecutive cases of anticoagulant-related intracerebral haemorrhage. The mortality was 38.5%. The respective frequency of intracerebral haemorrhage, subarachnoid haemorrhage, acute and chronic subdural haematomas was 63.2, 16.2, 10.3 and 10.3%, respectively. On admission, nearly half the patients (53%) had prothrombin ratios inferior to 25%. A predisposing factor was found in 58% of cases: hypertension (30.6%), head injury (14.5%), alcoholism or drug interaction (11.2%), and one case of intracerebral aneurysm. A history of a transient ischaemic attack or of a cerebrovascular accident was found in 10.2% of cases and 11.7% had a previous anticoagulant related extracranial haemorrhage. The initial indications for oral anticoagulation were ischaemic heart disease (32%), atrial fibrillation (20.5%), secondary prevention of venous thromboembolic disease (17.6%) and primary prevention of venous thrombosis (11.7%). The duration of treatment for isolated ischaemic heart disease was over 6 months in all cases: the average duration of treatment was 12.4 months in phlebitis and pulmonary embolism. A critical review of the indications of treatment in the light of recent recommendations showed that if inappropriate indications were rare, the sometimes unnecessary prolongation of treatment was more common. Nearly half of these cases were receiving anticoagulants when the potential benefits were questionable at the time of the haemorrhagic complication. Clinical and biological follow-up is necessary for patients on anticoagulants; minor bleeding complications may be the prelude to major haemorrhage. Biological follow-up is based on control of the international normalised ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Lack of association between peripheral neuropathy and HTLV-I infection in west Africa. Epidemiological, serological and nerve biopsy study.

Patients (n = 1166) with various neurological disorders hospitalized in Dakar, Abidjan, Lomé and Ouagadougou were examined prospectively over a 42-month period. Seropositivity for HTLV-I alone was found to be 1.8%, which is comparable to that estimated for the general population in Africa. Eighteen of the patients with TSP and only 5 with PN were HTLV-I positive, but co-infections were found in 30-40% of cases. Discrete and unspecific lesions were observed on light and electron microscopic examination of peripheral nerve biopsies from 11 patients. Since spastic paraparesis emerges as the disorder containing the largest number of HTLV-I-positive individuals, it may be premature to conclude that HTLV-I is a causal agent in PN. Nevertheless, their rarity and the frequency of retroviral co-infections distinguish these cases of African HTLV-I-associated myelopathy from comparable cases observed in other parts of the world.

Acute or subacute alcoholic neuropathy mimicking Guillain-Barré syndrome.

Over the last 10 years we have encountered 8 patients with chronic alcoholism who presented with severe symmetrical polyneuropathy, primarily proximal in 6, which evolved over a period of 24 h to 3 weeks. In 3 cases, artificial ventilation was required. Sensory symptoms were in all instances intense, and tendon reflexes absent. CSF protein levels were normal. The course was one of gradual improvement, often incomplete with residual motor and distal sensory deficits. Three patients died within 2 months to 2 years with multiple and severe pathologies attributable to chronic alcoholism. There was no evidence for disorders other than the alcoholism and malnutrition. Electrophysiological findings were consistent with predominantly axonal lesions and nerve biopsy specimens confirmed acute and severe axonal lesions. Several of these patients had been referred to us with a possible diagnosis of Guillain-Barré syndrome due to the severity of the neuropathy and the rapidity of its onset (Landry syndrome). Acute alcoholic neuropathy is distinguishable, however, on clinical, electrophysiological and morphological grounds.