2017 Volume 76 Issue 1 Pages 17-25
The oculomotor signs resulting from lesions affecting specific cerebellar regions have not yet been precisely defined in humans. The purpose of this study was therefore to analyze findings of electronystagmography (ENG) quantitatively in a patient with a posterior fossa meningioma mainly compressing the posterior vermis.
A-70-year-old woman had often experienced a paroxysmal positional dizziness (or a faint sensation) on raising her head from prone position or on turning round, accompanied with no auditory symptoms with recent onset. Such dizziness usually resolved in a moment even though the provoking position was maintained. At our outpatient clinic, no induced nystagmus was observed by positioning or positional changing tests. MRI disclosed a meningioma approximately 2 cm in diameter to the left of the midline at the posterior fossa. The tumor seemed to compress the surface of the cerebellar vermis, mainly the culmen (Lobulus-V) and declive (VI). The other parts of the vestibular-cerebellum (such as flocculus, nodulus or uvula) and the brainstem were apparently not affected. The characteristic findings of the ENG were as follows: (1) lateral beating nystagmus (rightwards>leftwards) in the dark; (2) rebound nystagmus; (3) impairment of vertical smooth pursuit, while the horizontal pursuit was preserved; (4) upbeating nystagmus mainly during shifting eyes rightward or upward in the dark; (5) abnormal eye movements such as double saccadic pulses or ocular flutter were frequently intermingled both in the light and dark; (6) The peak slow phase velocity of OKN was mildly reduced, while frequencies of the slow phase velocity of OKN were preserved; (7) the left OKAN was within normal limits, while the right OKAN (slow phase was left) was not so inhibited and prolonged; and (8) vestibular caloric nystagmus was well induced bilaterally. Both sides of visual suppression of the caloric nystagmus were well preserved. Among these findings, it would be presumed that (3), (4) and (5) were especially ascribed in the present case to compression of the cerebellar vermis by the tumor, though the definite pathophysiological mechanism has not yet been clarified.
