The principal clinical and pathological findings in 16 fatal cases of human African trypanosomiasis caused by T.b. Gambiense are described. The changes in the brain took the form of a non-specific lymphoplasmacytic meningo-encephalitis of varying intensity. Other features included morular cells, diffuse microglial hyperplasia, and large reactive astrocytes in the white matter. Carditis was identified in 10 cases. Acute reactive arsenical encephalopathy appeared to be the principal cause of death in 10 patients. Convulsions figured prominently in this type of encephalopathy in seven patients and were sufficiently severe to produce hypoxic brain damage. In three cases of acute reactive arsenical encephalopathy the structural changes in the brain were those of acute haemorrhagic leucoencephalopathy.

The hippocampus is known to be frequently involved in head injury. In adults, such hippocampal lesions frequently include regions of selective neuronal necrosis. The present report examines the frequency and distribution of hippocampal damage in 37 cases of fatal head injury in children. Damage to the hippocampus was noted in 27 of 37 cases (73%). Lesions were often focal areas of selective neuronal necrosis located in the CA-1 subfield. Other subfields of the hippocampus were involved to lesser degrees. The frequency and distribution of hippocampal damage in fatal childhood head injury is similar to that reported for fatal head injuries of all ages. Pathological evidence of high intracranial pressure and/or hypoxic brain damage in other anatomical locations was present in the majority of cases. Clinical seizures prior to death occurred in 22% of the cases studied. However, these factors could not account for all cases of hippocampal damage in the present report. Thus, the hippocampus is frequently damaged in fatal head injury in children. The mechanisms involved in the production of such damage may involve hypoxia, raised intracranial pressure and altered cerebral perfusion. However, other, yet to be elucidated, mechanisms may be involved.

A case of delayed onset of paraplegia following minor head injury and meningitis is presented. At operation extensive necrosis of the thoracic spinal cord was demonstrated. The possibility of spinal cord infarction is discussed.

SUMMARY A case of acquired hepatocerebral degeneration secondary to biliary cirrhosis is described. It differs from the conventional type because of the clinical predominance of cerebellar symptomatology and because the principal neuropathological abnormalities were restricted to the pallidum and to the cerebellum.