Dynamic Modification of the Vestibulo-Ocular Reflex by the Nodulus and Uvula

Abstract

The time constant of the decay of slow-phase eye velocity of postrotatory nystagmus or optokinetic after-nystagmus is reduced during exposure to a stationary visual surround (visual suppression). It is also reduced after tilting the head (tilt suppression). A "dump" mechanism in the vestibulo-ocular reflex has been proposed to rapidly discharge activity from the central vestibular system during both types of suppression. Monkeys lost this mechanism after lesions of the nodulus and uvula. They also lost the ability to habituate the time constant of nystagmus on repeated exposure to optokinetic and vestibular stimuli. Periodic alternating nystagmus, which is believed to represent an instability in the vestibulo-ocular reflex, was observed in two of three monkeys. These data indicate that the nodulus and uvula play an important role in suppressing, habituating, and stabilizing the vestibulo-ocular reflex.

Effects of 4-aminopyridine on nystagmus and vestibulo-ocular reflex in ataxia-telangiectasia

“…Individuals with damage to this region, including those with A-T in whom Purkinje neuron dropout is pan-cerebellar, thus manifest disinhibited velocity storage. When severe, disinhibition of velocity storage can manifest with PAN, which emerges in this state as a consequence of an adaptive vestibular mechanism that normally acts to minimize sustained unidirectional nystagmus, even to the point of causing the oscillating reversals of direction [12,17,18,31]. Although we saw PAN in our subjects with A-T, we did not observe an increase in the VOR time constant.…”

“…The indirect pathway features the neural integrator, the velocity storage, that stabilizes the eye velocity during whole field rotation and extends the band-width over which the VOR is compensatory for head movement [22]. Gammaaminobuteric acid (GABA) mediated inhibition through the Purkinje neurons of cerebellar nodulus and ventral uvula determines the fidelity of the velocity storage, its function is measured by the decay rate of the velocity storage output, the slow phase eye velocity of rotational nystagmus during en bloc constant velocity rotations [31]. It is therefore anticipated that cerebellar disease might affect the velocity storage, while drugs influencing the cerebellar function might affect the decay time constant of the velocity storage.…”

The cerebellar nodulus: Perceptual and ocular processing of graviceptive input

“…Lack of PAN in our patient suggests that bilateral damage of the nodulus is required for this peculiar spontaneous nystagmus. 11,[18][19][20] At the same time, we propose that based on our case and on one case with heminodular stroke in the literature, 11 not only bilateral lesions of the nodulus 6 or combined bilateral uvulo-nodular lesions 18 result in direction-changing (apogeotropic) positional nystagmus, but that heminodular damage is sufficient to cause such position-dependent ocular motor instability. Both spontaneous horizontal nystagmus beating towards the lesioned side 11 and contralesional lateropulsion 11 were previously described and matched findings in our patient.…”

Testing of the Semicircular Canal Function in Vertigo and Dizziness

“…By analysing the postrotatory response to step stimuli not only side differences but additionally the central processing of the VOR, including the 'velocity storage', could be quantified [9]. The 'velocity storage' is known as the indirect pathway, which acts parallel to the direct VOR pathway [10] and is realized by a commissural inhibitory network [11][12][13][14] under cerebellar control of the uvula and nodulus [15]. One function of the 'velocity storage' is to increase the cupula time constant to improve the ability to transduce the low-frequency components of the VOR [16].…”