ObjectiveTo determine whether saccadic velocity in the suppression head impulse paradigm (SHIMP) test is a reliable indicator of vestibular loss at the acute and at the chronic stage in patients suffering from different vestibular pathologies.MethodsThirty-five normal subjects and 57 patients suffering from different vestibular pathologies associated with unilateral vestibular loss (UVL) or bilateral vestibular loss (BVL) were tested in the SHIMPs paradigm. SHIMPs were performed by turning the head 10 times at high velocities to the left or right side, respectively. The patients were instructed to fixate on a red spot generated by a head-fixed laser projected on the wall. In this SHIMPs paradigm, healthy subjects made a large anti-compensatory saccade at the end of the head turn (a SHIMP saccade). The peak saccadic velocity, the percentage of the trials completed with saccades in 10 trials, and the latency of the saccades were quantified in each group. A video-head impulse test (v-HIT) was systematically performed in all of our subjects as well as a caloric test. The dizziness handicap inventory questionnaire was also given to chronic UVL and BVL patients.ResultsAt the acute stage after a complete UVL, patients had zero or a few anti-compensatory saccades for low velocity head turns toward the lesioned side. These saccades had lower velocity than the anti-compensatory saccades recorded during head rotation toward the intact side and/or compared with the saccades measured in control subjects. At the chronic stage, some of the patients recovered the ability to perform SHIMP saccades at each head turn toward the lesioned side, but very often these saccades were of significantly lower velocity. In BVL patients, no anti-compensatory saccades, or only significantly smaller ones, could be detected for head turns to both sides.ConclusionSHIMP is a specific and sensitive test to detect a complete horizontal canal loss at the acute stage. In addition, it reflects the ability of patients with moderate horizontal vestibulo–ocular reflex gain decrease to generate anti-compensatory saccades in the chronic stage. In association with v-HIT, it allows determination of the residual vestibular function and to detect anti-compensatory saccades.

LE. Control of neuronal persistent activity by voltage-dependent dendritic properties. J Neurophysiol 100: 1278 -1286. First published July 16, 2008 doi:10.1152/jn.90559.2008. Neural integrators and working memory rely on persistent activity, a widespread neural phenomenon potentially involving persistent sodium conductances. Using a unique combination of voltage-clamp, dynamicclamp, and frequency-domain techniques, we have investigated the role of voltage-dependent conductances on the dendritic electrotonic structure of neurons of the prepositus hypoglossi nucleus (PHN), which is known to be involved in oculomotor integration. The PHN contains two main neuronal populations: type B neurons with a double afterhyperpolarization and type D neurons, which not only are oscillatory but also have a greater electrotonic length than that of type B neurons. The persistent sodium conductance is present in all PHN neurons, although its effect on the dynamic electrotonic structure is shown to significantly differ in the two major cell types present in the nucleus. The electrotonic differences are such that the persistent sodium conductance can be almost perfectly manipulated in a type B neuron using an on-line dynamic clamp to add or subtract virtual sodium ion channels. The dynamic-clamp results are confirmed by data-fitted models, which suggest that the persistent sodium conductance has two different roles depending on its somatic versus dendritic location: perisomatic conductances could play a major role in maintaining action potential discharge and dendritic conductances would be more involved in other computational properties, such as those involving remote synaptic processing or bistable events.

ObjectiveWe examined the eye movement response patterns of a group of patients with bilateral vestibular loss (BVL) during suppression head impulse testing. Some showed a new saccadic strategy that may have potential for explaining how patients use saccades to recover from vestibular loss.MethodsEight patients with severe BVL [vestibulo-ocular reflex (VOR) gains less than 0.35 and absent otolithic function] were tested. All patients were given the Dizziness Handicap Inventory and questioned about oscillopsia during abrupt head movements. Two paradigms of video head impulse testing of the horizontal VOR were used: (1) the classical head impulse paradigm [called head impulse test (HIMPs)]—fixating an earth-fixed target during the head impulse and (2) the new complementary test paradigm—fixating a head-fixed target during the head impulse (called SHIMPs). The VOR gain of HIMPs was quantified by two algorithms.ResultsDuring SHIMPs testing, some BVL patients consistently generated an inappropriate covert compensatory saccade during the head impulse that required a corresponding large anti-compensatory saccade at the end of the head impulse in order to obey the instructions to maintain gaze on the head-fixed target. By contrast, other BVL patients did not generate this inappropriate covert saccade and did not exhibit a corresponding anti-compensatory saccade. The latencies of the covert saccade in SHIMPs and HIMPs were similar.ConclusionThe pattern of covert saccades during SHIMPs appears to be related to the reduction of oscillopsia during abrupt head movements. BVL patients who did not report oscillopsia showed this unusual saccadic pattern, whereas BVL patients who reported oscillopsia did not show this pattern. This inappropriate covert SHIMPs saccade may be an objective indicator of how some patients with vestibular loss have learned to trigger covert saccades during head movements in everyday life.