A clinical and pathological study of myeloneuropathy following abdominal disorders.

Abstract

SUMMARYA man aged 58, who had suddenly an attack of severe watery diarrhoea, abdominal pain and nausea with febricula, which continued for 5 days. For these symptoms he was administrated with chloramphenicol for 7 days (total does 7000 mg). Following this he began to have paresthesia, hypes‐thesia, and disturbance of motility in the lower limbs. Then he had flaccid paralysis, hypotonus of muscles, decrease of tendon reflexes, positive sign of Babinski in the lower limbs. Although he had period of convalescence for a while, the disease gradually grew worse to die. The period of the disease was 510 days. Histopathologi‐cally, noticeable changes were observed on the peripheral nerve and spinal cord; the degeneration of sciatic nerve and Goll's tract from upper part of cervical spinal cord to lower part of lumber spinal cord. In addition to these changes, degeneration or deletion of the nerve cell in Ammon's horn, central chromatolysis of Betz cells and accumulation of fat granules in the anterior horn cells were observed. These histopatho‐logical changes were very similar to those of nicotinic acid deficiency (Pellagra). On the other hand, he had been treated with many kind of drugs. In this point of view, the etiology of SMON was supposed various factors, such as nicotinic acid deficiency, vitamin deficiency, metabolic disturbance and poisoning. However, disposition of the body site must be attached great importance to this disease.In addition to this case, other two cases also had not taken chinoform. Considering these facts, it is the authors opinion that the etiology of SMON can not exclusively be attributed to chinoform intoxication.