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A 13-year-old boy was the victim of attempted strangulation. His condition had returned to normal by the sixth day after the assault; however, from the seventh day, choreoathetosis, dystonia, and marked pseudobulbar paralysis developed in the boy. The computed tomographic scans and T2-weighted magnetic resonance images that were obtained at this time revealed low-density and high-signal intensities in the region of the bilateral putamen and caudate nucleus. These symptoms and the changes in his computed tomographic scans and magnetic resonance images subsided gradually during a 2-month period. Sequential analysis of the cerebrospinal fluid for gamma-aminobutyric acid and dopamine concentrations during his illness revealed reciprocal changes with normal recovery. Because of the delayed onset of neurological changes and the cerebrospinal fluid showing reversible symptoms, the delayed encephalopathy after strangulation had been related to the biochemical alterations that followed anoxia in the vulnerable basal ganglia.

A 13-year-old boy was the victim of a strangulation attempt. His behavior was normal by the 6th day after the assault. However, from the 7th day, he developed choreoathetosis, dystonia and marked pseudobulbar palsy. CT and T2-weighted MRI at this time revealed a low density and high signal intensity in the region of the bilateral putamen and caudate respectively for the first time. Thereafter, these symptoms and changes in CTs and MRIs subsided gradually over two months. Sequential analysis of CSF for GABA and dopamine during illness revealed reciprocal changes each other with normal recovery. Because of delayed onset of neurological changes, and findings of CSF with reversible symptoms the delayed encephalopathy after strangulation is probably related to biochemical alteration secondary to anoxia in vulnerable basal ganglia.

This study reports a case of MELAS with epileptic seizure, and reviews the characteristics of seizures in patients with this syndrome. They are characterized by: (1) generalized and/or partial seizures, (2) frequent association with visual symptoms and hemiparesis, and (3) posteriorly predominant EEG abnormalities.

A case of multiple intracerebral tuberculoma occurred in the course of anti-tuberculous therapy is reported. A 16-year-old high school boy had been treated with isoniagid, streptomycin and paramino-salicylic acid on the tuberculous pleulitis for 3 months previously. He was admitted to our hospital because of progressive headache associated with vomiting. Neurological examination revealed bilateral full papilledema and incomplete bilateral abducens palsy. An immediate CT study with contrast enhancement demonstrated two small ring-like mass with considerable perifocal edema in the left temporal and occipital lobe, respectively. Intracerebral tuberculoma was considered to be most likely, so the patient was given antituberculous therapy with steroid and mannitol. However, despite of medical decompression, he developed intracranial hypertension aggravated, leading to removal of tumor 7 days after admission. Initially left temporal tuberculoma, which had more extensive and prominent perifocal edema, was successfully excised. The specimen was a walnut-sized granuloma with hard capsule including pus inside. Numerous tuberculous bacilli were identified with Ziel-Nielsen staining technique from the pus. Postoperative course was gratifying, and other tumor in the left occipital lobe, which was also diagnosed as tuberculoma, was treated with continuing administration of isoniagid, ethanbutol and rifampicin. However, the former two drugs were forced to be discontinued because of agranulocytosis. Only rifampicin was maintained for 2 months thereafter but no decrease of the size was observed in serial CT studies. Then left occipital tuberculoma was removed. The pathology was tuberculoma with positive bacilli staining. He discharged 1 month later without any neurological deficit but was on antituberculous therapy (rifampisin) as an outpatient for 3 years.(ABSTRACT TRUNCATED AT 250 WORDS)