[Acute motor polyradiculopathy revealing neurosyphilis in an immunocompetent patient].
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Biomedical subjects
Publications and source records attributed to Y Lanoë.
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We report a case of neurosyphilis of the spinal cord in a 38-year-old-man presenting with urinary incontinence and Argyll-Robertson sign. Anamnesis revealed the congenital origin of the disease. Urodynamics findings were consistent with a conus medullaris involvement and CSF study revealed a specific lymphocytic meningitis. A specific spinal arteritis was found by angiography. A quarterly 15 to 20 days course of intravenous penicillin was then instituted during 2 years. A specific treatment of urinary symptoms resulted in complete disappearance of sphincter dyssynergia. Antibiotic therapy was followed by clinical improvement and regression of most of the CSF abnormalities.
The authors report a case of acute polyneuropathy revealing a solitary osseous plasmacytoma with osteo-dense and osteolytic bone lesions. Initially, the rapid progression of the sensory and motor loss led to treatment by plasma exchanges and irradiation of the plasmacytoma. Four months later, despite a significant improvement of the neurological condition, serum protein electrophoresis continued to show a peak of monoclonal immunoglobulin. Chemotherapy with cyclophosphamide and prednisone was administered for one year whilst the neuropathy continued to regress. This case, which presents many classical features of plasma cell dyscrasia (polyneuropathy with albumino-cytological dissociation, radiological osseous condensation, low concentrations of lambda light chain protein), illustrates some unusual features of solitary plasmacytomas associated with peripheral neuropathy: the young age of our patient, an acute progression of the neuropathy in the early stages, tumoral localisation in the diaphysis of a long bone.
A myopathy revealed the presence of a vitamin-sensitive osteomalacia in a patient with congenital hypoalbuminemia. The severe myopathy and osteomalacia recovered after treatment with 25-hydroxycholecalciferol. Hypoalbuminemia was detected in two brothers of the patient; parents and grandparents were consanguineous. Various tests demonstrated that the patient's hypoalbuminemia was due to faulty synthesis. Albumin reactions to several drugs were normal, but those normally transported by albumin have to be administered cautiously because of the low plasma concentrations. The possible relationship between hypovitaminosis D and congenital hypoalbuminemia, an association considered to be fortuitous by Montgomery, remains debatable.