THE LOCALIZING VALUE OF NYSTAGMUS IN BRAIN-STEM DISORDERS

As causes for conjugate jerk nystagmus at the midposition of the eye, vestibular imbalance, a neural integrator deficit, smooth pursuit imba lance and a saccade generator deficit have been considered. The author s investigated anatomically brainstem lesions of patients with downbea t, upbeat, torsional and horizontal nystagmus. Although relatively com mon, downbeat nystagmus is only rarely seen with brainstem lesions. In these instances it is localized in midline medullary structures. Upbe at nystagmus is more often caused by a discrete brainstem lesion in th e medulla, which can be as far caudal as the cranio-cervical junction. Lesions have also been found at the pontine level. In the mesencephal on, torsional nystagmus occurs with lesions to the interstitial nucleu s of Cajal and the rostral interstitial nucleus of the MLE In addition torsional nystagmus is seen after vestibular nuclei and lateral medul lary lesions. Both lesion sites are also found with horizontal nystagm us. Although in some instances pathophysiology of anatomical structure s can largely explain the nystagmus (e.g., torsional nystagmus) this i s not the case in others. This applies particularly for the caudal med ullary lesions seen with upbeat nystagmus, since the oculomotor relate d structures of the vestibular nuclei and the nucleus praepositus hypo glossi do not extend so far caudally. A possible anatomical candidate are the cell groups of the paramedian tract (pmt). They do extend so f ar caudally, receive an input from virtually all ocular premotor struc tures in the brainstem, and project to the parts of the cerebellum, kn own to be involved in gaze-holding.