Abstract
Lesions were placed in the paramedian pontine reticular formation ( PPRF ) of monkeys and the resulting gaze palsies studied. Brainstem regions were identified by single cell recordings before kainic acid was injected to selectively destroy neuronal cell bodies in the vicinity. Unilateral PPRF lesions led to a loss of all rapid eye movements towards the ipsilateral side. Deficits were identical to those after experimental electrolytic lesions in monkeys, or structural lesions in humans. Bilateral PPRF lesions produced two different syndromes. Rostral PPRF lesions led to a selective loss of horizontal rapid eye movements leaving vertical movements intact. Caudal PPRF lesions led in addition to a severe disruption of vertical rapid eye movements.
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