We report 2 survivors of severe methanol poisoning who developed, apart from blindness, a Parkinson-like extrapyramidal syndrome characterized by reduced initiative, poor voice volume, masked facies, mild tremor, rigidity, and bradykinesia. Both patients were mildly demented and 1 had hyperreflexia and bilateral Babinski responses. Computed tomographic scans in both patients demonstrated bilateral symmetrical infarction of the frontocentral white matter and putamen. Electromyography in 1 patient showed extensive denervation, mainly involving the legs, but normal motor conduction velocities. L-Dopa administered to the more severely affected patient had no effect on the parkinsonian features. Autopsy revealed cystic resorption of the putamen and the frontocentral subcortical white matter in additon to widespread neuronal damage throughout the cerebrum, cerebellum, brainstem, and spinal cord.

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✓ A detailed study of posttraumatic syringomyelia is reported. The interior of the syrinx was outlined by positive contrast and gas myelography. The contrast material entered the syrinx via a communication between the cavity and the subarachnoid space at the site of spinal cord injury. The syrinx also communicated with the fourth ventricle. It is postulated that posttraumatic syringomyelia results from the dissection of cystic remnants of hematomyelia known to be present at the site of serious spinal cord injury. Dissection occurs when pressure within the cyst is increased by elongation of the spinal cord during neck movements, principally flexion. Posttraumatic syringomyelia should be treated by a surgical procedure, which allows permanent drainage of the syrinx into the subarachnoid space.

We describe the cases of 2 adult patients who developed respiratory arrest and were found to have Arnold-Chiari malformation on magnetic resonance imaging. Following posterior fossa decompression both patients improved, though one of them subsequently died during sleep. Imaging of the craniocervical junction should be part of the workup of patients with unexplained apneic episodes.

We describe two patients with post‐partum cerebral angiopathy. (Case 1) A 24‐year‐old patient developed vaginal bleeding 1 day post‐partum. She received blood transfusion and ergometrine. Four days later she experienced severe occipital headache, loss of vision and generalized seizures. An MRI showed right occipital lesion. She was treated with phenytoin and prednisone. Her vision returned to normal within 2 days. Cerebral angiography showed multiple segmental narrowing; 6 h later severe occipital headache and cortical blindness recurred. She was treated with nimodipine and prednisone with complete recovery in 10 days. (Case 2) On the 7th post‐partum day a 24‐year‐old patient was given ergometrine. One day later she developed severe headache and hypertension, followed by drowsiness, right hemiplegia and aphasia. A left frontal hematoma was seen on the CT scan. Cerebral angiography showed multiple segemental narrowing. Resolution of this angiography was confirmed on follow‐up angiography. Post‐partum cerebral angiopathy is a rare complication of a normal pregnancy. It may present as an ischemic or hemorrhagic stroke. The transience of this severe complication and its association with the administration of drugs with strong vasoconstrictive properties suggest and etiological relationship. Other factors and the exact mechanism are unclear.