Crossed adductor reflexes were recorded electromyographically in ten patients with bilateral lesions of the upper motor neuron. Three of these had a femoral neuropathy. Following blows directed to either the tendon of the adductor muscle or to the medial epicondyle of the femur, large amplitude responses of short latency were recorded from the ipsilateral adductor muscle while small amplitude responses of short latency and large amplitude responses of long latency were recorded from the contralateral adductor. The responses of short latency which were recorded from the ipsilateral and contralateral adductor muscles ranged from 18 to 27 ms. The contralateral responses of long latency ranged from 60 to 67 ms. On tapping the patella or patellar tendon, large amplitude responses of short latency were recorded from the contralateral adductor muscles while the ipsilateral adductor responses were absent. These responses resulted from stretch of the ipsilateral and contralateral adductor muscles. The contralateral responses were mediated across the midline by an extraspinal mechanical pathway.

Filamentous axonalmasses, similar to the abnormal enlargements found in the ventral horns, were found in Clarke’s nucleus in six cases of sporadic A LS. Clarke’s nucleus is generally thought to be normal in sporadic A LS, but the present findings, in conjunction with distal spinocerebellar degeneration which is often described, suggest that this system is also pathologically involved.

John W. Magladery was born in New Liskeard, Ontario on October 11, 1911. He graduated from Upper Canada College in 1929 and the University of Toronto Medical School in 1935. As a Rhodes scholar, he received the degree of D. Phil, in Neurophysiology from Oxford University in 1937. During World War II, he was a major in the Royal Canadian Army Medical Corps. Post-graduate studies were undertaken at the University of Toronto and the National Hospital, Queen Square.

Anoxic tonic seizures are reported as a complication of severe asthma in two adults. The nature of these attacks can be misinterpreted. They do not indicate the presence of a recurrent seizure problem unconnected to the episodes of anoxia caused by asthma. These attacks do not respond to antiepileptic medication, but cease if the asthma can be controlled. One of our patients developed an anoxic encephalopathy and the other died. The need for prompt diagnosis and appropriate treatment is emphasized.

The authors report a single case of Huntington’s chorea associated with a unilateral focus of ectopic gray matter. The patient’s symptoms began at age 45 and included typical involuntary jerking movements of all extremities and face. Mental deterioration may have proceeded the choreiform movements. The family history was positive for Huntington’s chorea. Pneumoencephalogram showed atrophy of the caudate nuclei bilaterally early in the disease. The patient improved transiently with haloperidol therapy.

The major pathologic features included mild generalized cerebral atrophy with marked atrophy of the caudate nuclei and putamen. Within the white matter of the left frontal lobe, there were irregular nodules of ectopic gray matter with an overall diameter of 2 cm.

The rarity of either unilateral ectopia or Huntington’s chorea alone, makes it impossible to judge if the two lesions might be linked by a common pathologic mechanism. The significance such a linkage might hold is discussed in light of several currently postulate pathologic mechanisms.

A case of spinal subdural hematoma occurring in association with anticoagulant therapy is reported. Seven similar cases from the literature are reviewed with emphasis on the clinical features, investigation, and the results of treatment. The prognosis for recovery is good, only if the condition is diagnosed and the clot evacuated before severe spinal cord compression and subsequent ischemic necrosis has occurred.

Five patients were studied to determine whether kinetic interaction occurs between valproic acid and primidone. During concurrent administration of primidone and valproic acid no significant interaction was observed. Primidone and derived phenobarbital levels did not change significantly. No adjustment of primidone dose was required when valproic acid was used as adjunctive therapy.