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Biomedical subjects

B Pépin

Publications and source records attributed to B Pépin.

At least 19 recordsLinked to original sources
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

[Neurological manifestations in relation to vitamin E deficiency, caused by a defect of biliary acid synthesis].

A progressive neurological syndrome with cerebellar signs, abnormal proprioception, areflexia and Babinski response was observed in a child with chronic intestinal malabsorption. There was no ophtalmoplegia or retinitis pigmentosa. Electromyography and biopsy showed no axonopathy or myopathy. Two other members of the family were also affected. The serum Vitamin E corrected the serum Vitamin E levels within a few months and led to secondary neurological improvement. The authors underline the importance of searching for Vitamin E deficiency and its cause in patients, especially children, with signs of spino cerebellar degeneration. Substitative therapy may have a favorable influence on the neurological condition even when administered late.

Bile Acids and Salts↗
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

Familial juvenile parkinsonism with multiple systems degenerations. A clinicopathological study.

An unusual case of familial multisystemic degeneration is reported. Two siblings had juvenile parkinsonism, areflexia, and retinal degeneration of slow progression. The main neuropathological findings in case 1 were pallidoluysian, nigral, dentate, and dorsal columns degeneration. The authors draw a comparison between this case and juvenile parkinsonism, dentato-rubro-pallido-luysian atrophy, and spino-cerebello-nigral degeneration.

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↗
PubMed1985

[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↗
PubMed1984

[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↗
PubMed1983

[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↗
PubMed1976

[Familial form of centronuclear myopathy in the adult].

Two adult cases of centronuclear myopathy are described in a family from French Guyana. One of them, aged 23, has a slight weakness despite hypertrophic muscles. A typical picture of centronuclear myopathy was seen on muscle biopsy with atrophy of type I fibers and hypertrophy of II A fibers. His uncle, aged 53, had a progressive weakness of the lower limbs for the last 25 years, with also a pattern of centronuclear myopathy, but with more dystrophic features and atrophy of both type I and II A fibers. The mode of inheritance is dominant. These two cases are compared with the previously published reports. The pathogenesis of centronuclear myopathy is discussed.

Adult↗
PubMed1975

[Familial case of myotonia with muscular hypertrophy, weakness corrected by effort and atrophy of type II fibers].

A 35 years old man has a non progressive muscle disease which appeared when he was 6. Clinically, there is a slight muscle hypertrophy, an important spontaneous myotonia and a curious muscle weakness, quite marked on the first efforts, but disappearing entirely after a few muscle contractions. The E.M.G. is normal but for the myotonic reaction. Muscle biopsy shows a selective atrophy of type II fibers. The disease is a genetic one, a sister and a brother of our patient having noticed the same symptom. The place of this disease among the congenital myotonias is discussed.

Adult↗