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Biomedical subjects

B Sauron

Publications and source records attributed to B Sauron.

8 recordsLinked to original sources

Lesions of basal ganglia due to disulfiram neurotoxicity.

Three cases of disulfiram induced Parkinsonism and frontal lobe-like syndrome associated with bilateral lesions of the lentiform nuclei on CT scan are reported. Symptoms developed either after an acute high dose of disulfiram (one case) or after several days to weeks of disulfiram treatment (two cases) and persisted over several years in two patients. These observations suggest that basal ganglia are one of the major targets of disulfiram neurotoxicity. The mechanisms of the lesions of basal ganglia may involve carbon disulfide toxicity.

Adult

Serum and CSF humoral immunity in Guillain-Barré syndrome: clinical correlations.

Paired samples of CSF and serum obtained from 29 patients affected with Guillain-Barré syndrome (GBS) were analyzed for various protein levels, including immunoglobulins and complement components. An attempt was made to correlate these findings to the clinical stage, severity, and duration of the disease. Intrathecal IgG synthesis was detected and quantified by means of a previously reported formula. It is practically constant in the GBS during the stage of stabilized paralysis, and is significantly greater in this stage than in the stage of progressive paralysis. Moreover, it increases with severity and duration (longer than 3 months) of the disease. Evidence of intrathecal C3 consumption is also presented.

Adolescent

Chronic localised encephalitis (Rasmussen's) in an adult with epilepsia partialis continua.

A 29 year old male presented with epileptic fits, progressive left sided focal seizures and epilepsia partialis continua, increasing left hemiparesis and mental slowing. Death occurred 2 years after the onset of the illness. Lesions were limited to the right cerebral hemisphere. Hypertrophic astrocytosis was diffuse throughout the gray and white matter but was more severe in the deep cortical layers and U fibres, where it was associated with vacuolar changes and capillary proliferation. Sparse perivascular lymphocytic cuffs, rod shaped microglia and microglial nodules were present. No inclusion bodies were found. These clinico-pathologic features were similar to the cases described by Rasmussen. Only five necropsy cases of this rare disease have been reported previously, all in children. The aetiology is unknown.

Adult

Miller Fisher syndrome: clinical and electrophysiologic evidence of peripheral origin in 10 cases.

Clinical and electrophysiologic data recorded in patients with Fisher syndrome characterized by ophthalmoplegia, ataxia, and areflexia are presented. Cases with limb weakness or pleocytosis in the CSF were excluded, according to Fisher. Ten patients were selected. All had hand and foot numbness. A large amount of protein without cell reaction was found during the third week of illness in serial CSF examinations. EMGs showed very slight limb involvement without spontaneous activity, and in most cases, facial muscles exhibited a denervation pattern. Distal motor nerve conduction velocity on limbs and F wave latencies were normal, whereas the sensory nerve action potentials were altered in all but one case when tested (seven out of eight cases). By means of blink reflex study performed in four patients, no significant pattern of brainstem dysfunction was discovered. The authors discuss the preeminent role of peripheral nerve lesions with regard to the ataxia and ophthalmoplegia.

Adolescent

[Baló's concentric sclerosis].

A clinico-pathological case of concentric sclerosis (Baló type) is reported. A 30-year-old man experienced dizziness, nausea and vomiting. Twelve days later he developed gait disturbances. Neurological examination showed broad based gait, brisk tendon reflexes, bilateral extensor plantar responses, right hemihypoesthesia, cerebellar dysmetria, and a left lateral gaze palsy. CSF examination showed, 520 mg p. 100 ml protein, 7500 red blood cells, 31 lymphocytes and 9 polymorphonuclear leukocytes/mm3, 18 p. 100 gammaglobulin. Three CT scans were performed and showed a round hypodensity in the parieto-occipital white matter with contrast enhancement on one occasion, and several other hypodensities in the contralateral parieto-occipital white matter and in both frontal lobes. 23 days after the onset of the disease, the patient became comatose. A cerebral biopsy was obtained from one of the frontal lesions. He died from aspiration bronchopneumonia 2 months after the first signs. Neuropathological examination showed numerous concentric zones of demyelination which involved the white matter of both hemispheres, brain stem, and cerebellum. On light microscopy sudanophilic myelin breakdown products were numerous in the bands of demyelinisation. Astrocytic proliferation was marked, with frequent Rosenthal fibers. Edema was noted in some lesions. Myelin-axonal dissociation was obvious, but some axonal swelling were observed. Electron microscopy demonstrated the integrity of oligodendrocytes and of blood vessels and confirmed the prominent alterations of the astrocytes. Fifteen similar cases of the literature have been reviewed. The present case seems to be the first one with CT scan examination and electron microscopic study of a brain biopsy. The nosological situation of Baló's disease among the inflammatory demyelinating diseases of the group of MS is discussed.

Adult

[Whipple's disease with encephalopathy. A case report with review of the literature].

A 58 year-old man developed a progressive encephalopathy four years after Whipple's disease onset with digestive, lymph node, and multiple joint lesions, treated over a period of two years. The diagnosis of neurological manifestations of Whipple's disease was based on clinical findings and the presence of PAS+ inclusion bodies in CSF cells. The outcome was fatal in spite of antibiotic therapy. Diagnostic features of this rare neurological affection are discussed. Preventive treatment and surveillance of patients with Whipple's disease are necessary even after well-conducted therapy.

Anti-Bacterial Agents

[Motor neglect of thalamic origin: report on two cases (author's transl)].

Two cases of thalamic lesions with motor neglect are presented. The syndrome of motor neglect was complete in those cases with a) underutilization of left limbs, but good utilization upon verbal orders, b) loss of placement reaction, c) weakness of movement when hand was approaching the target, d) weakness of motor reaction to nociceptive stimuli. Those cases confirm that motor neglect exists after thalamic lesions and bring pathologic clues for topographic discussion. Motor neglect seems to be a particular case of partial unilateral neglect throwing some doubt on the hypothesis of a global trouble of hemispheric activation. Prevalence of left motor neglects suggests some linkage between propositional motility and language. One may suppose that in the right hemisphere language is able to have a vicarious action when spontaneous activation is lost; at the opposite, in the left hemisphere language and motility would be too linked to let this dissociation be generally possible.

Brain Neoplasms