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Biomedical subjects

E Roullet

Publications and source records attributed to E Roullet.

At least 91 records · Page 5Linked to original sources
PubMed1987

[Cerebral cysticercosis: 4 cases].

Four cases of cerebral cysticercosis are reported, occurring in an immigrant population. Two patients presented with periodic epileptic fits and cerebral calcifications. One patient presented with an acute hemiparesis associated with lymphocytic meningitis and cerebral calcifications; the fourth patient had chronic meningitis with epileptic fits. Three patients were treated with praziquantel: an acute reaction occurred during treatment in two cases with an increase in the titres of the immunological reaction of hydatid cyst disease in one case. The authors suggest classifying this condition in three types: acute (parenchymatous or subarachnoid), chronic (chronic meningitis, hydrocephalus, progressive dementia), and sequelae (epilepsy with or without headaches). This classification seems the most appropriate way of summarizing the variable clinical presentation of this condition which is rarely observed in France. The most valuable diagnostic investigation is CT brain scanning. Immunological reaction to hydatid cyst (CSF and blood) are sometimes negative. Treatment with praziquantel often causes an acute reaction with a rise in antibody titres; this is a clinically benign reaction, and it could be used as a diagnostic test.

Adolescent↗
PubMed1986

Comparison of the response to phytohemagglutinin, of peripheral blood mononuclear cells and cerebrospinal fluid lymphocytes in multiple sclerosis and other neurological diseases. Determination of the frequency of the precursor cells by a limiting dilution analysis.

Proliferative response to phytohemagglutinin (PHA) of cerebrospinal fluid lymphocytes (CSF-L) and peripheral blood mononuclear cells (PMBC) from patients with multiple sclerosis (MS) and other neurological diseases (OND) was tested using either bulk culture conditions or limiting dilution techniques in the presence of additional exogenous IL2. CSF-L response to PHA was found significantly lower than that of PBMC in both MS and OND patients. There was no significant difference in the response of CSF-L between the two groups. The limiting dilution analysis of the frequency of the precursors of PHA-responsive cells showed a strikingly decreased frequency of these precursors among CSF-L.

Adolescent↗
PubMed1986

[Double-blind treatment of 49 cases of chronic multiple sclerosis using hyperbaric oxygen].

Forty nine patients with a chronic form of multiple sclerosis (MS) [progressive or stable] were treated with hyperbaric oxygen (HO) in a double blind trial. Patients were divided in three groups: the first group (group I) received a course of 2.3 ATA HO with diazepam (5 mg); the second group (group II) received a course of 2 ATA HO; the third group (group III) was the control group. Each patient breathed an adapted gaseous mixture in high pressure. Each patient received 20 sessions of this procedure during 4 weeks. Patients were evaluated with clinical, neurophysiological and immunological parameters. Clinical examination consisted in the evaluation of the Kurtzke's Disability Status Scale (DSS) and Functional Status Scale (FSS). This evaluation was done in the week before the procedure, the week following the treatment, then in the third and sixth month. The neurophysiological study was a comparative analysis from the variations of visual, somesthesic and brain stem auditory potentials. The immunological study was the analysis of the lymphocyte populations (OKT4/OKT8 ratio). Each examination was carried out the week before, then the week following the procedure. We found no amelioration into three groups. Subjectively, some patients thought to be better, but this was true in the two treated groups (I, II) and in the control group (III). There was not an FSS significant variation. We also found no significant variation of evoked potentials and OKT4/OKT8 ratio. We observed some incidental effects of the treatment, particularly in group I, in which patients were treated with a higher pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain↗
PubMed1985

Leukoencephalopathy in diffuse hemorrhagic cerebral amyloid angiopathy.

We have studied 12 patients with diffuse hemorrhagic cerebral amyloid angiopathy clinically and at postmortem examination. The brains in 8 patients had diffuse bilateral loss of myelin in the hemispheric white matter sparing the U fibers, corpus callosum, and internal capsules. The periventricular areas were predominantly affected. Microscopic examination of the white matter showed an association with subacute or chronic edematous lesions: spongiosis, swollen oligodendroglia, widening of the perivascular spaces with edema fluid or siderophages, hyalinization of the blood vessel walls, incomplete myelin loss, and astrocytic gliosis. Three of 8 autopsied patients had undergone computed tomographic examination, which showed bilateral hypodensity of the hemispheric white matter. The brains of 4 patients with illnesses of shorter duration showed only discrete but similar lesions in the centrum semiovale. These white matter changes are similar to those observed in Binswanger's subcortical encephalopathy. We suggest that a common mechanism of hypoperfusion of the distal white matter causes the leukoencephalopathy.

Aged↗
PubMed1985

[Arteriopathic leukoencephalopathy (17 anatomo-clinical cases)].

Seventeen clinico-pathological cases of leukoencephalopathy due to vascular diseases are reported. All of them had diffuse, often spotty demyelination sparing the U fibers, the corpus callosum, the internal capsule and the optic radiations. Microscopic examination of the white matter showed the association of the following lesions: oedema, swollen oligodendroglia, spongiosis, incomplete loss of myelin, astrocytic gliosis with Rosenthal's fibers, widening of the perivascular spaces with oedema fluid or hemosiderin laden macrophages, thickening and hyalinization of the blood vessels walls. Among those cases, 8 were consistent with Binswanger's subcortical encephalopathy (5 males, 3 females, mean age at death: 64 years, mean illness duration: 6, 7 years); all of them were hypertensive and had lacunae in the basal ganglia, hemispheric white matter and pons. Another case could be considered as a cortico-subcortical chronic hypertensive encephalopathy (77 y.o., female, illness duration: 4 years); she was hypertensive and had small cortical infarcts and perivascular bleedings, lobar and cerebellar hematomas, but no amyloid deposits in the blood vessels walls. Eight patients (5 males, 3 females mean age at death: 72 years, mean illness duration: 5, 4 years, 6 normotensive, 2 hypertensive) had diffuse meningocortical amyloid angiopathy with multiple small cortical infarcts, small cortical perivascular bleedings, slit haemorrhages and one or more lobar hematomas. Four of them had numerous senile plaques and neurofibrillary tangles. To our knowledge such a leukoencephalopathy in cerebral amyloid angiopathy has not been yet pointed out. It was present in 8 out of 12 cases of diffuse haemorrhagic form of cerebral amyloid angiopathy observed in the Charles Foix Laboratory of la Salpêtrière, during the last 10 years. A common mechanism with hypoperfusion of the distal white matter and alteration of the blood brain-barrier is suggested for this leukoencephalopathy.

Aged↗
PubMed1985

[Late syringomyelobulbia complicating spinal cord injury. Improvement after syringoperitoneal shunt].

A patient suffered from paraplegia of T-10 level at age 29, and he complained of new symptoms in the upper limbs at age 42. Gradual ascending worsening occurred, and the diagnosis of post-traumatic syringomyelobulbia was made 23 years after the initial accident. CT scan with metrizamide transit at the medulla level confirmed the diagnosis. Definite clinical improvement was seen after syringo-peritoneal shunting. Clinical, radiological and therapeutic aspects are briefly discussed.

Adult↗
PubMed1985

[Myopathy with tubular aggregates. Clinical, biological and histological study of 2 cases].

Two male patients, aged 46 and 48, presented with muscle pain on exercise, generalized or limited to the upper extremities. Physical signs were limited to mild muscle wasting in one case. There was no myoglobinuria. Electromyography was normal in one case, and showed some polyphasic units in the other. An ischaemic lactate test was normal in the one case in which it was performed. Serum creatine kinase activity was normal or only mildly elevated. Histochemical and ultrastructural study of muscle showed tubular aggregates in type II fibers in both cases, and otherwise gave normal results. Symptoms were unchanged with a follow-up of 2 and 16 years, respectively. Tubular aggregates are found in a number of unrelated clinical and experimental conditions, which are reviewed. In these cases and in 3 similar patients, previously reported, tubular aggregates seem to be the hallmark of hitherto unrecognized metabolic disorders.

Alcoholism↗
PubMed1984

[Prolonged treatment of multiple sclerosis with average doses of azathioprine. An evaluation of 15 years' experience].

Since 1967, 211 probable or definite multiple sclerosis (MS) patients have received azathioprine (100 mg daily) as primary immunosuppressive treatment. Treatment results are evaluated in 145 patients who have received prolonged (one year or more) continuous therapy and whose disability had been evaluated prospectively. The main characteristics of these patients are the following: male 45, female 100; mean age of onset of MS: 27 years; mean duration of treatment and follow-up: 67 and 115 months, respectively. 48 patients were in the progressive phase of MS at the onset of treatment; 17 of these had a stable disability score during therapy; however, the number of stabilized patients decreased significantly with duration of treatment. Among 97 patients in the remittent phase of the disease, 22 had no further bout during treatment, 41 had bouts but had no increase in disability, and 34 were aggravated; in 14 of these, secondary progression occurred during therapy. Haematologic, cutaneous, digestive and infectious side-effects occurred but were always reversible. In the subgroup of 131 patients who had received no other immunosuppressive treatment than azathioprine and in whom information was obtained at the end of 1982, 10 cancers (all of them epitheliomas) were diagnosed. The frequency of malignancy in the patients followed for 5 years or more was 10 p. 100. Five patients died from cancer (4 of 6 deaths in the remittent group). These results are compared with those of other series. It is suggested that the use of azathioprine in MS should be restricted.

Adult↗
PubMed1984

[Intention and action myoclonus disclosing occupational mercury poisoning].

A 58-year-old laboratory-glassware manufacturer was referred to hospital because of coarse "tremor" of the upper extremities of 16-months-duration. Examination showed severe intention and action myoclonus, confirmed by electromyographic recording, slight memory impairment but was otherwise normal. Mercury levels were high in blood and urine (not in CSF) and, as other causes of myoclonus were excluded, inorganic mercury poisoning, was diagnosed. Only slight unilateral intention tremor persisted after dimercaprol treatment. Inhalation of mercury vapor was the mode of contamination. Myoclonus is the hallmark of severe inorganic mercury intoxication, the main clinical and pathological aspects of which are briefly discussed.

Humans↗
PubMed1983

[Cerebrovascular accidents and migraine].

Twenty-three clinical cases are reported, illustrating the difficulties of diagnosing migrainous focal cerebrovascular accidents. Cases of constituted cerebral infarcts and transient cerebral ischemia occurring during the cephalalgic phase, without headache and in patients with no previous history of typical migrainous attacks are described. Migraine may be considered to be the cause on convincing clinical criteria, but the diagnosis can only be established after negative results of investigations to exclude other causes of focal cerebral ischemia.

Acute Disease↗