R. John Leigh

Ocular flutter and ataxia associated with AIDS-related complex

Saccadic oscillations and ataxia have been described in association with viral encephalitis. The authors describe two patients with AIDS-related complex who developed ocular flutter and ataxia. CSF analysis revealed a pleocytosis. Magnetic resonance imaging of the brain in one showed cerebellar atrophy. Ocular flutter, prominent with horizontal saccadic eye movements, was documented by electro-oculography. Blinking induced flutter in one patient while convergence induced it in the other. This is the first report of patients with probable HIV-related brainstem encephalitis suffering ocular flutter.

Dynamic modulation of vestibuloocular reflex gain during passive head rotation

To measure the performance of the visually enhanced vestibuloocular reflex (VEVOR), we exposed four normal subjects to the onset and subsequent offset of t 15 deg/second velocity steps of passive horizontal head rotation while they viewed a stationary light spot. Gaze and head movement data were collected using the search coil technique, and, after saccade removal and digital filtering, the measured position waveforms were differentiated to obtain gaze and head velocity. We used a modeling approach to analyze the data. Based on currently accepted schemes,*X2 a simple model of the VOR was created that incorporated elements characterizing semicircular canal dynamics and VOR latency, as well as an element providing a constant gain value. We coupled this with a model describing how visual inputs may augment VOR signals to maintain target fixation during rotation (based on Robinson et al.).3 Optimal parameter estimation techniques were employed to determine values for model parameters that caused model simulations to accurately reflect measured data.4 If the VOR acts perfectly with a gain of near 1.0, one would expect that gaze would not be significantly perturbed, despite perturbations of the head, because the generated eye movements would be almost completely compensatory. However, as depicted in FIGURE 1, the VE-VOR data showed substantial gaze perturbations when the head begins to move from rest (at 0.0 seconds), but much lower level perturbations when the head was subsequently stopped (at 2.0 seconds). This asymmetric degree of gaze perturbation was typical for all of our subjects and could not be predicted using the aforementioned model. The improved performance when the head was stopped could not have arisen due to augmentation of the VOR with signals derived from visual inputs; the latency of visual processing (requiring at least 50 mseconds for visual pro~essing)~ would delay such visual contributions until long after the observed compensatory eye motion had already occurred. Also, if vision did play a role when the head stopped, one might expect it to play a similar role at the onset of head motion, which it clearly does not. We reasoned that if the internal VOR gain were initially at some value less than 1.0 when a head rotation is initiated, the magnitude of the induced eye rotations will