Yaw Head Tilt Research Articles

Head movements suggest canal and otolith projections are activated during galvanic vestibular stimulation

Three-dimensional changes in the angular orientation of the head were monitored during galvanic vestibular stimulation (GVS) delivered through electrodes implanted bilaterally in the tensor tympani muscle of the guinea-pig middle ear. Bilateral GVS was delivered by passing current between both ears with the anode situated in one ear and the cathode in the other ear. Unilateral GVS was also delivered between one ear and an indifferent electrode on the skull. Constant-current stimulation caused the head to tilt predominantly within the roll and yaw planes toward an ear stimulated with anodal current and away from an ear stimulated with cathodal current. No significant head tilt in the pitch plane was observed with either bilateral or unilateral GVS. Bilateral GVS was found to induce significantly greater roll head tilt (RHT) and yaw head tilt (YHT) than the same intensity of unilateral anodal or cathodal GVS, but not the sum of responses induced by the two polarities of unilateral GVS. Significant asymmetries were observed in the responses of YHT and RHT for unilateral anodal and cathodal GVS; unilateral cathodal stimulation generated greater head deviation compared with the same intensity of unilateral anodal stimulation. These asymmetric responses are consistent with activation of irregularly discharging afferents, which have been shown previously to exhibit asymmetric responses for anodal and cathodal GVS (Kim and Curthoys, 2004). Together with the observations of previous guinea-pig studies, the results suggest that head movements induced by GVS may be mediated by irregularly discharging afferents innervating the otoliths, and possibly the horizontal semicircular canals.

Effects of Chronic Infusion of a GABAA Receptor Agonist or Antagonist into the Vestibular Nuclear Complex on Vestibular Compensation in the Guinea Pig

The aim of this study was to determine the effects of chronic infusion of a GABA(A) receptor agonist/antagonist into the ipsilateral or contralateral vestibular nuclear complex (VNC) on vestibular compensation, the process of behavioral recovery that occurs after unilateral vestibular deafferentation (UVD). This was achieved by a mini-osmotic pump that infused, over 30 h, muscimol or gabazine into the ipsilateral or contralateral VNC. Spontaneous nystagmus (SN), yaw head tilt (YHT), and roll head tilt (RHT) were measured. Infusion of muscimol or gabazine into either the ipsilateral or the contralateral VNC had little effect on SN compensation. In contrast, infusion of muscimol (250, 500, and 750 ng) into the contralateral VNC and gabazine (31.25, 62.5, and 125 ng) into the ipsilateral VNC significantly affected YHT and RHT (p < 0.05), but not their rate of compensation (p > 0.05). Interestingly, the effects of muscimol and gabazine on YHT and RHT were consistent throughout the first 30 h post-UVD. Infusion of muscimol (62.5, 125, and 250 ng) into the ipsilateral VNC and gabazine (125, 375, and 750 ng) into the contralateral VNC had little effect on YHT and RHT or their rate of compensation. These results suggest that the ipsilateral gabazine and contralateral muscimol infusions are modifying the expression of the symptoms without altering the mechanism of compensation. Furthermore, the neurochemical mechanism responsible for vestibular compensation can cope with the both the GABA(A) receptor-mediated and the UVD-induced decrease in resting activity.

Rapid vestibular compensation in guinea pig even with prolonged anesthesia

The results of previous studies have suggested that prolonged anesthesia following unilateral labyrinthectomy (UL) results in a retardation of vestibular compensation, the process of behavioral recovery that occurs following the lesion. In this study we investigated the effects of short-term (25 min) and long-term (4 h) anesthesia with isoflurane on the time course of vestibular compensation following UL in guinea pig. Although there were significant differences in the frequency of spontaneous nystagmus (SN) ( p < 0.05) and its rate of compensation ( p < 0.05) between the 25 min and 4 h isoflurane groups, these differences appeared to be due largely to the 5, 9 and 13 h time points. There was also a significant difference in the rate of yaw head tilt (YHT) compensation, largely due to the 5 h time point. When exponential regression analysis was performed to evaluate the overall pattern of compensation, there was no significant difference in the time required to reach 100% SN or YHT compensation between the 25 min and 4 h isoflurane groups. Furthermore, there were no significant differences in roll head tilt (RHT) compensation between the two groups. These results suggest that the time course of vestibular compensation is largely independent of the duration of the anesthesia used for UL surgery.

Effect of Low Body Temperature During Unilateral Labyrinthectomy on Vestibular Compensation in the Guinea Pig

Objectives - Vestibular compensation, the recovery that follows unilateral vestibular deafferentation (UVD), is a model for central nervous system plasticity. Recovery from the static symptoms of UVD may involve temperature-dependent processes that modulate the immediate effects of UVD and/or the capability of the central nervous system to undergo adaptive plasticity. In this study we investigated changes in oculomotor and postural vestibular symptoms resulting from low body temperature during UVD. Material and methods - To study the effect of low temperatures at the time of UVD on vestibular compensation, we compared the rate of compensation and peak values for postural [roll head tilt (RHT) and yaw head tilt (YHT)] and oculomotor [spontaneous nystagmus (SN)] symptoms in three groups of guinea pigs. Animals in Group 1 (n=6) were maintained at 38°C throughout unilateral labyrinthectomy (UL). Animals in Group 2 (n=6) were not temperature-controlled and animals in Group 3 (n=4) were cooled with ice to 25°C throughout UL. Results - Cooled animals showed significantly higher rates of SN upon recovery from anaesthesia and took a significantly longer time to compensate. Cooled animals were also slower to compensate for postural symptoms (RHT and YHT), with 2 animals showing no compensation for RHT 52 h after UL. Conclusion - Hypothermia (25°C) during UVD surgery exacerbates postural and oculomotor symptoms following UL and significantly slows recovery.

The Contribution of Nitric Oxide to Vestibular Compensation: Are There Species Differences?

Nitric oxide (NO) has been implicated in the processes by which animals recover from peripheral vestibular damage (''vestibular compensation''). However, there is little systematic data available on the effects of NO inhibition on the vestibular compensation process. In the present study we administered the nitric oxide synthase (NOS) inhibitor N G -nitro-L-arginine methyl ester (L-NAME) using a subcutaneous osmotic minipump and examined its effects on the compensation of spontaneous nystagmus (SN), yaw head tilt (YHT) and roll head tilt (RHT) in guinea pigs. Following unilateral labyrinthectomy (UL), treatment with 5, 10, 50 or 100 mM L-NAME had no effect on the expression of any of these symptoms or their rate of compensation. By contrast, pre-UL treatment with 100 mM L-NAME resulted in a decrease in SN frequency at 10 h post-UL and an increase in its rate of compensation. Lower concentrations had no effect on SN. Pre-UL treatment with L-NAME had no significant effect on YHT or RHT at any particular time point. Analysis of NOS activity demonstrated that the highest concentration of L-NAME inhibited NOS activity in the contralateral vestibular nucleus complex, bilateral cerebellum and bilateral cortices. These results suggest that L-NAME may have different effects on vestibular compensation in guinea pigs compared to other species, such as the rat and frog.

The effects of protein kinase C and calmodulin kinase II inhibitors on vestibular compensation in the guinea pig

Previous studies have demonstrated that vestibular compensation, the process of behavioural recovery which occurs following unilateral deafferentation of the vestibular labyrinth (UVD), is correlated with changes in in vitro phosphorylation of various protein substrates in the brainstem vestibular nucleus complex (VNC). The aim of the present study was to investigate the possible causal relationship between protein kinase activity and the induction of the vestibular compensation process, by delivering inhibitors of protein kinase C (PKC) or Ca 2+/calmodulin-dependent kinase II (CaMKII) into the ipsilateral VNC at the time of the UVD and determining their effects on three static symptoms of UVD, spontaneous nystagmus (SN), yaw head tilt (YHT) and roll head tilt (RHT) in guinea pigs. Infusion of the PKC inhibitor, 3-[1-(3-dimethylaminopropyl)-1H-indol-3-yl]-4-(1H-indol-3-yl)-1H-pyrrole-2,5-dione, HCl (bisindolylmaleimide I, HCl/GF 109203X, HCl) (‘Bis I’), at a concentration of 5 or 50 μM, significantly increased SN frequency at the earliest time points (6 and 8 h post-UVD) compared to vehicle controls and the less selective analogue, 2,3-bis(1H-indol-3-yl)- N-methylmaleimide (bisindolylmaleimide V) (‘Bis V’). However, the compensation of YHT and RHT was unaffected by the PKC inhibitor. By contrast, the cell-permeable CaMKII inhibitor, myristoylated autocamtide-2 related inhibitory peptide ( N-Myr-Lys-Lys-Ala-Leu-Arg-Arg-Gln-Glu-Ala-Val-Asp-Ala-Leu-OH) (‘myr-AIP’) or the cell-impermeable analogue, autocamtide-2 related inhibitory peptide ( N-Lys-Lys-Ala-Leu-Arg-Arg-Cln-Glu-Ala-Val-Asp-Ala-Leu-OH) (‘AIP’), failed to alter the compensation of SN, YHT or RHT at any dose compared to vehicle controls. These results implicate PKC-, but not CaMKII-, signal transduction pathways in the initiation of SN compensation in guinea pig.

The effects of l-NAME on vestibular compensation and NOS activity in the vestibular nucleus, cerebellum and cortex of the guinea pig

Nitric oxide (NO) has been implicated in the processes by which animals recover from peripheral vestibular damage (‘vestibular compensation’). However, few data exist on the dose–response effects of systemic administration of the nitric oxide synthase (NOS) inhibitor, N G-nitro- l-arginine methyl ester ( l-NAME), on the vestibular compensation process. The aim of this study was to investigate the effects on compensation of 5, 10, 50 or 100 mM l-NAME administered by s.c osmotic minipump for 50 h following unilateral vestibular deafferentation (UVD) in guinea pig, either commencing the drug treatment at 4 h pre-UVD or at the time of the UVD (i.e., post-UVD). Post-UVD treatment with l-NAME, at any of the four concentrations used, had no effect on the compensation of spontaneous nystagmus (SN), yaw head tilt (YHT) or roll head tilt (RHT). By contrast, pre-UVD treatment with 100 mM l-NAME resulted in a significant decrease in SN frequency ( P<0.05) and a change in the rate of its compensation ( P<0.0005). Pre-UVD l-NAME resulted in a significant increase in the overall magnitude of YHT ( P<0.005); however, post-hoc comparisons revealed no significant differences between any specific l-NAME and vehicle groups. Pre-UVD l-NAME had no effect on RHT at any concentration. Analysis of NOS activity in the pre-UVD l-NAME treatment groups at 50 h post-UVD showed that only 100 mM l-NAME resulted in a significant decrease in NOS activity in the contralateral medial vestibular nucleus (MVN)/prepositus hypoglossi (PH) ( P<0.05) and that NOS activity in the ipsilateral MVN/PH was not significantly affected. However, NOS activity was significantly inhibited in the bilateral cerebellum and cortices for several concentrations of l-NAME. These results suggest that pre-UVD systemic administration of l-NAME can significantly increase the rate of SN compensation in guinea pig and that this effect is correlated with inhibition of NOS activity in several regions of the CNS.

Effects of intra-vestibular nucleus injection of the group I metabotropic glutamate receptor antagonist AIDA on vestibular compensation in guinea pigs.

Removal of the peripheral vestibular receptor cells in one inner ear (unilateral vestibular deafferentation, UVD) results in a syndrome of ocular motor and postural disorders, many of which disappear over time in a process of behavioural recovery known as vestibular compensation. Excitatory amino acid receptors, in particular the N-methyl-D-aspartate (NMDA) receptor, have been implicated in vestibular compensation; however, the metabotropic glutamate receptors (mGluRs) have not been studied in this context. The aim of this study was to determine whether group I mGluRs in the brainstem vestibular nucleus complex (VNC) ipsilateral to the UVD are involved in vestibular compensation of the static symptoms of UVD in guinea pig. The selective group I mGluR antagonist (RS)-1-aminoindan-1,5,dicarboxylic acid (AIDA) was continuously infused into the ipsilateral VNC for 30-min pre-UVD and 30-min post-UVD by cannula, at a rate of 1 microl/h, using one of four doses: 0.1 fg, 0.1 pg, 0.1 ng or 0.1 microg (n=5 animals in each case). In control conditions, a 0.1-fg (n=4) or 0.1-microg (n=5) NaOH vehicle was infused into the ipsilateral VNC using the same protocol. In order to control for the possibility that AIDA disrupted spontaneous neuronal activity in the VNC in normal animals, 0.1 microg AIDA (n=4) or 0.1 microg NaOH (n=2) was infused into the VNC in labyrinthine-intact animals. In both groups, static symptoms of UVD (i.e. spontaneous nystagmus, SN, yaw head tilt, YHT and roll head tilt, RHT) were measured at 8, 10, 12, 15, 20, 25, 30, 35, 45 and 50 h post-UVD. In addition, the righting reflex latency (RRL) was measured in labyrinthine-intact animals in order to assess whether AIDA impaired motor coordination in labyrinthine-intact animals. In UVD animals, the highest dose of AIDA significantly reduced SN frequency and changed its rate of compensation (P<0.001 and P<0.0001, respectively). This dose of AIDA also caused a significant reduction in YHT (P<0.005) as well as a significant change in its rate of compensation (P<0.0001). However, RHT was not significantly affected. In the labyrinthine-intact animals, AIDA infusion did not induce a UVD syndrome, nor did it significantly affect RRL. These results suggest that group I mGluRs in the ipsilateral VNC may be involved in the expression of ocular motor and some postural symptoms following UVD. Furthermore, group I mGluRs may not contribute to the resting activity of vestibular nucleus neurons.

The effects of intra-vestibular nucleus administration of brain-derived neurotrophic factor (BDNF) on recovery from peripheral vestibular damage in guinea pig.

Brain-derived neurotrophic factor (BDNF), at doses of 0.04, 0.4 or 4.0 microg/day, was delivered by cannula and s.c osmotic minipump into the ipsilateral vestibular nucleus complex from 0 to 50 h following unilateral labyrinthectomy (UL) in guinea pigs. Compared to the vehicle control group, the frequency of spontaneous nystagmus was significantly reduced (p < 0.02) and the rate of yaw head tilt compensation increased (p < 0.02). However, roll head tilt was not signifcantly affected. There were also no significant effects of BDNF administration into the IVth ventricle (4.0 microg/day) on any UL symptom. These results further support the hypothesis that neurotrophins such as BDNF may enhance the vestibular compensation process.

Effectiveness and Utility of Chemical Labyrinthectomy with Streptomycin Using Osmotic Pump

To investigate the utility of osmotic pumps, labyrinthectomy was performed surgically (surgical group) or chemically with 30% streptomycin sulfate (SM) using osmotic pumps (SM group) in guinea pigs. After treatment, no statistical difference was observed in the frequency of spontaneous nystagmus and the degree of yaw head tilt between the groups. These data indicate the reliability and efficacy of osmotic pumps, and it might be possible to make guinea pig models using osmotic pumps to predict various grades of damage in the vestibular periphery of humans.

An antisense oligonucleotide to brain-derived neurotrophic factor delays postural compensation following unilateral labyrinthectomy in guinea pig.

An antisense oligonucleotide to brain-derived neurotrophic factor (BDNF) was delivered by osmotic mini-pump at a 1 mM concentration via a cannula into the ipsilateral vestibular nucleus complex from 15 to 56h following unilateral labyrinthectomy in guinea pigs. Compared with the control groups, vestibular compensation of roll head tilt was significantly delayed (p < 0.05), while compensation of spontaneous nystagmus and yaw head tilt was unaffected. These results suggest that neurotrophins such as BDNF may be involved in specific aspects of the vestibular compensation process.

Evidence that the ginkgo biloba extract, EGb 761, neither accelerates nor enhances the rapid compensation of the static symptoms of unilateral vestibular deafferentation in guinea pig

The concentrated Ginkgo biloba extract, EGb 761, has previously been reported to enhance and accelerate vestibular compensation following unilateral vestibular deafferentation (UVD), in particular, compensation of the dynamic postural symptoms such as locomotor dysequilibrium. However, many of these studies have not included a complete analysis of the static symptoms of UVD, such as spontaneous nystagmus (SN), yaw head tilt (YHT), and roll head tilt (RHT), nor have they included a dose-response analysis or vehicle controls for EGb 761. The aim of the present study was to examine the effects of the EGb 761 extract on static vestibular compensation in guinea pig, using a dose-response analysis and both vehicle and saline controls. Analysis of variance showed that there was a significant decrease in SN frequency (P < 0.05) and a significant change in the rate of SN compensation (P < 0.05), using 3 i.p. injections of EGb 761 (25, 50, or 100 mg/kg), or vehicle, or saline, at 0, 25, and 40 h post-UVD. However, post-hoc testing revealed that this was due entirely to significant differences between the saline and vehicle groups at 35, 40, and 50 h post-UVD (P < 0.05 in all cases) and between the saline and the 100 mg/kg and 25 mg/kg EGb 761 groups at 35 and 50 h post-UVD, respectively (P < 0.05 for both comparisons); there were no significant differences between the vehicle and drug groups at any time. YHT and RHT were not significantly different between the drug, saline, and vehicle groups. In a second set of experiments, the 50 and 100 mg/kg EGb 761 i.p. injection frequencies were doubled. However, once again, neither SN nor YHT were significantly different between the EGb 761 groups and the vehicle controls. These results suggest that 1) EGb 761 does not significantly enhance or accelerate compensation of the static symptoms of UVD in guinea pig and 2) the EGb 761 vehicle may exert some effects on its own. Therefore, EGb 761 may be of limited use in the treatment of acute vestibular dysfunction in humans.

Vestibular compensation in guinea pigs given intravenous lidocaine after unilateral labyrinthectomy

Intravenous lidocaine has been reported to alleviate vertigo in Meniere’s disease and suggested as a possible antivertigo agent after unilateral labyrinthectomy in a study of cats. To further evaluate the effects of intravenous lidocaine on the acute phase of postural compensation, we subjected 13 pigmented guinea pigs to unilateral labyrinthectomy. Seven received intravenous lidocaine (4 mg/kg) immediately after labyrinthectomy. The other six served as controls and received an equivalent-volume injection of normal saline solution. Total body curvature, trunk curvature, yaw head tilt, and roll head tilt were measured at frequent intervals for up to 30 hours after surgery. Both groups had immediate difficulties with posturing that gradually improved. The lidocaine group tended to exhibit delayed postural compensation, but this was only statistically significant for roll head tilt. These results do not show improvement in postural compensation from unilateral labyrinthectomy after the administration of intravenous lidocaine. A species-specific effect on the vestibular pathways is suggested, and we conclude that further evaluation of lidocaine and the vestibular system is warranted. (Otolaryngol Head Neck Surg 1999;120:12-6.)

The role of N-methyl- d-asparate receptor in the guinea pig inner ear after unilateral labyrinthectomy

To investigate the role of the N-methyl- d-aspartate (NMDA) receptor in the vestibular periphery, vestibular compensation in the guinea pig was studied following chemical unilateral labyrinthectomy by osmotic pump administration of streptomycin sulfate (SM) with or without d-2-amino-5-phosphonovalerate ( d-APV), one of the NMDA receptor antagonists. All animals administrated SM (SM group) or SM and d-APV (SM+ d-APV group) showed spontaneous nystagmus and head tilt. The maximum degree of yaw head tilt in the SM+ d-APV group was statistically smaller than that in the SM group. Moreover the time constant for head tilt in the SM+ d-APV group was statistically shorter than that in the SM group. These results indicate that the NMDA receptor in the vestibular periphery influences vestibular compensation after unilateral labyrinthectomy.

The Opioid Receptor Antagonist, Naloxone, Enhances Ocular Motor Compensation in Guinea Pig Following Peripheral Vestibular Deafferentation

The opioid receptor antagonist, naloxone, has been demonstrated to enhance recovery from spinal cord injury and fluid percussion brain injury. The present study investigated, for the first time, the effects of naloxone on behavioral recovery following unilateral peripheral vestibular deafferentation (unilateral labyrinthectomy, UL) in guinea pig. An ip injection of 5 mg/kg naloxone 30 min pre-UL and 5 h post-UL was found to significantly reduce the frequency of spontaneous nystagmus relative to the vehicle control group (P<0.005). However, a lower dose (2.5 mg/kg) had no effect. At either dose, the effects on the postural symptoms, yaw head tilt and roll head tilt, were small by comparison and in most cases nonsignificant. These results suggest that naloxone can reduce the ocular motor effects of UL in a dose-dependent fashion.

Evidence that short ACTH fragments enhance vestibular compensation via direct action on the ipsilateral vestibular nucleus

The aim of the present study was to determine whether administration of the synthetic ACTH-(4-9) analogue, Org 2766, directly into the ipsilateral vestibular nucleus complex (VNC), would enhance vestibular compensation following unilateral labyrinthectomy (UL). Either artificial cerebrospinal fluid (ACSF; n = 4) or Org 2766 (0.67 nmol kg-1 every 4 h for 52 h; n = 4), was administered directly into the VNC via a stainless steel cannula connected to an osmotic minipump implanted s.c. Three symptoms of UL, spontaneous ocular nystagmus (SN), roll head tilt (RHT) and yaw head tilt (YHT), were measured at 10, 20, 25, 30, 40, 45 and 50 h post-UL. Org 2766 produced a significant decrease in the frequency of SN and accelerated its compensation. Org 2766 had no significant effect on either the compensation of RHT or YHT. This result suggests that vestibular compensation is enhanced by short ACTH fragments as a result of direct action on the ipsilateral VNC itself.

高齢モルモットの前庭代償機能

To determine age-related changes in vestibular compensation we measured the frequency of spontaneous nystagmus and yaw head tilt after unilateral labyrinthectomy. Albino guinea pigs were divided into two groups: the control group (3 to 12 months of age; n=8) and the aged group (36 to 39 months of age; n=3). We found that the frequency of spontaneous nystagmus in the aged group was significantly lower than in the control group (p<.05). The time constant for spontaneous nystagmus in the aged group was shorter than that in the control group. No significant difference was found in yaw head tilt between the two groups. We conclude that the function of vestibular compensation is not affected by aging. We suggest that the decline of spontaneous nystagmus in the aged group may be due to the diminution of resting activity in two vestibular nuclei.

Methylprednisolone reduces spontaneous nystagmus following unilateral labyrinthectomy in guinea pig

The present study investigated the effects of methylprednisolone on the vestibular compensation process following unilateral labyrinthectomy in guinea pigs. A single injection of methylprednisolone (15, 30 or 60 mg/kg s.c.), 15 min pre-labyrinthectomy, had no significant effect on either the severity or the rate of compensation of spontaneous ocular nystagmus or yaw head tilt; roll head tilt showed a significant change in the rate of compensation ( P < 0.005), due to increased roll head tilt in the 60 mg/kg group. However, a pre-labyrinthectomy injection of 30 mg/kg s.c. methylprednisolone followed by a second 30 mg/kg injection at 4 h post-labyrinthectomy resulted in a significant reduction in spontaneous nystagmus frequency ( P < 0.005) and a significant change in the rate of spontaneous nystagmus compensation ( P < 0.005). The additional 30 mg/kg injection had no significant effect on the magnitude or compensation of the postural symptoms. These results indicate that, at the optimal dose of 30 mg/kg, 2 injections of methylprednisolone (15 min pre-labyrinthectomy and 4 h post-labyrinthectomy) result in a significant reduction in spontaneous nystagmus frequency.

Ginkgolide B accelerates vestibular compensation of spontaneous ocular nystagmus in guinea pig following unilateral labyrinthectomy

The aim of this study was to investigate the effects of ginkgolide B on the behavioral recovery process (vestibular compensation) which occurs following surgical removal of the vestibular receptor cells in one labyrinth (unilateral labyrinthectomy, UL). Guinea pigs received a single ip injection of ginkgolide B at the time of the UL (25, 50, or 100 mg/kg) and the effects on the compensation of the UL symptoms, spontaneous ocular nystagmus (SN), yaw head tilt (YHT), and roll head tilt (RHT), were evaluated. The effects of a single vehicle injection or a similar injection of ginkgolide A were used for comparison. Twenty-five mg/kg ginkgolide B significantly increased the rate of SN compensation compared to the vehicle control group ( P < 0.02). However, 50 mg/kg ginkgolide B had no significant effect on either SN frequency or the rate of SN compensation. Ginkgolide B (100 mg/kg) significantly altered the rate of SN compensation ( P < 0.02); however, SN frequency values were higher at most measurement times. YHT and RHT were not significantly affected by ginkgolide B at any of the doses used. Twenty-five mg/kg ginkgolide A had no significant effect on any of the UL symptoms. These results suggest that, at the optimal dose of 25 mg/kg, a single ip injection of ginkgolide B at the time of the UL can produce an acceleration of SN compensation.

Effect of sensory deprivation or electrical stimulation on acute vestibular symptoms following unilateral labyrinthectomy in rabbit.

The effect of sensory deprivation or electrical stimulation on vestibular compensation was investigated for 7 days after unilateral labyrinthectomy (ULX) in 50 rabbits. Eye movements induced by sinusoidal rotation of the whole body and spontaneous nystagmus were measured for vestibulo-ocular compensation, and head deviation was measured for vestibulospinal compensation. The rabbits were divided into 4 groups: one with ULX only (LX only), ULX with bilateral tarsorrhaphy (LX+TX), ULX with cervical dorsal root ganglionectomy (LX+GX), and a group stimulated electrically on the lesion-sided vestibular system with square pulse for 8 h/day (LX+ES). In LX only, the frequency of spontaneous nystagmus was 2.93 +/- 0.19 beats/sec just after ULX, declining to zero in 4 days. In eye movements induced by sinusoidal rotation on the 7th day after ULX, directional preponderance was 24-43% and gain decreased to 32-48% by rotation toward the intact side and 17-29% by rotation toward the lesion side, compared with that before ULX. Roll head tilt and yaw head tilt were 82 +/- 9 degrees, 45 +/- 6 degrees, respectively, on the 7th day. Recovery of vestibulo-ocular reflex and head deviation was delayed in LX+TX and LX+GX compared with that in ULX only, but recovery was enhanced in LX+ES. Therefore, in this study, electrical stimulation of the lesion side seemed to have a favorable effect on suppression of acute vestibular symptoms induced by unilateral vestibular lesion.