Modulation of muscle sympathetic nerve activity by low-frequency physiological activation of the vestibular utricle in awake humans

We recently showed that selective stimulation of one set of otolithic organs—those located in the utricle, sensitive to displacement in the horizontal axis—causes a marked entrainment of skin sympathetic nerve activity (SSNA). Here, we assessed whether muscle sympathetic nerve activity (MSNA) is similarly modulated. MSNA was recorded via tungsten microelectrodes inserted into cutaneous fascicles of the common peroneal nerve in 12 awake subjects, seated (head vertical, eyes closed) on a motorised platform. Slow sinusoidal accelerations–decelerations (±4 mG) were applied in the X (antero-posterior) or Y (medio-lateral) direction at 0.08 Hz. Cross-correlation analysis revealed partial entrainment of MSNA: vestibular modulation was 32 ± 3 % for displacements in the X-axis and 29 ± 3 % in the Y-axis; these were significantly smaller than those evoked in SSNA (97 ± 3 and 91 ± 5 %, respectively). For each sinusoidal cycle, there were two peaks of modulation—one associated with acceleration as the platform moved forward or to the side and one associated with acceleration in the opposite direction. We believe the two peaks reflect inertial displacement of the stereocilia within the utricle during sinusoidal acceleration, which evokes vestibulosympathetic reflexes that are expressed as vestibular modulation of MSNA as well as of SSNA. The smaller vestibular modulation of MSNA can be explained by the dominant modulation of MSNA by the arterial baroreceptors.     

Low-frequency galvanic vestibular stimulation evokes two peaks of modulation in skin sympathetic nerve activity

We have previously shown that sinusoidal galvanic vestibular stimulation (sGVS), delivered bilaterally at 0.2–2.0 Hz, evokes a potent entrainment of sympathetic outflow to muscle and skin. Most recently, we showed that stimulation at 0.08–0.18 Hz generates two bursts of modulation of muscle sympathetic nerve activity (MSNA), more pronounced at 0.08 Hz, which we interpreted as reflecting bilateral projections from the vestibular nuclei to the medullary nuclei responsible for the generation of MSNA. Here, we test the hypothesis that these very low frequencies of sGVS modulate skin sympathetic nerve activity (SSNA) in a similar fashion. SSNA was recorded via tungsten microelectrodes inserted into the left common peroneal nerve in 11 awake-seated subjects. Bipolar binaural sGVS (±2 mA, 100 cycles) was applied to the mastoid processes at 0.08, 0.13 and 0.18 Hz. As with MSNA, cross-correlation analysis revealed two bursts of modulation of SSNA for each cycle of stimulation but, unlike MSNA, this modulation was equally pronounced at all frequencies. These results further support our conclusion that bilateral sGVS causes cyclical modulation of the left and right vestibular nerves and a resultant modulation of sympathetic outflow that reflects the summed activity of bilateral projections from the vestibular nuclei onto, in this case, the primary output nuclei responsible for SSNA—the medullary raphé. Furthermore, these findings emphasise the role of the vestibular system in the control of skin sympathetic outflow, and the cutaneous expression of motion sickness: pallor and sweat release. Indeed, vestibular modulation of SSNA was higher in those subjects reporting nausea than in those who did not report nausea during this low-frequency sGVS.     

Vestibular and pulse-related modulation of skin sympathetic nerve activity during sinusoidal galvanic vestibular stimulation in human subjects

We have previously shown that sinusoidal galvanic vestibular stimulation (sGVS), a means of a selectively modulating vestibular afferent input without affecting other inputs, can cause partial entrainment of muscle sympathetic nerve activity (MSNA). Given that motion sickness causes sweating and pallor, we tested the hypothesis that sGVS also entrains skin sympathetic nerve activity (SSNA), but that the optimal frequencies are closer to those associated with slow postural changes (0.2 Hz). SSNA was recorded via tungsten microelectrodes inserted into the common peroneal nerve in 11 awake-seated subjects. Bipolar binaural sinusoidal GVS (±2 mA, 200 cycles) was applied to the mastoid processes at frequencies of 0.2, 0.5, 0.8, 1.1, 1.4, 1.7 and 2.0 Hz. All subjects reported strong postural illusions of ‘rocking in a boat’ or ‘swaying in a hammock’. Sinusoidal GVS caused a marked entrainment of SSNA at all frequencies. Measured as the modulation index, vestibular modulation ranged from 81.5 ± 4.0% at 0.2 Hz to 76.6 ± 3.6% at 1.7 Hz; it was significantly weaker at 2.0 Hz (63.2 ± 5.4%). Interestingly, pulse-related modulation of SSNA, which is normally weak, increased significantly during sGVS but was stronger at 0.8 Hz (86.2 ± 2.0%) than at 0.2 Hz (69.3 ± 8.3%), the opposite of the pattern seen with vestibular modulation of MSNA. We conclude that vestibular inputs can entrain the firing of cutaneous sympathetic neurones and increase their normally weak pulse-related rhythmicity.     

Modulation of muscle sympathetic bursts by sinusoidal galvanic vestibular stimulation in human subjects

There is controversy as to whether the vestibulosympathetic reflexes demonstrated in experimental animals actually exist in human subjects. While head-down neck flexion and off-vertical axis rotation can increase muscle sympathetic nerve activity (MSNA) in awake subjects, we recently showed that bipolar galvanic vestibular stimulation (GVS) does not. However, it is possible that our stimuli (2 mA, 1 s)—although capable of causing strong postural and occulomotor responses—were too brief. To address this issue we activated vestibular afferents using continuous sinusoidal (0.5–0.8 Hz, 60–100 cycles, ±2 mA) bipolar binaural GVS in 11 seated subjects. Sinusoidal GVS evoked robust vestibular illusions of “rocking in a boat” or “swinging from side to side.” Cross-correlation analysis revealed a cyclic modulation of MSNA ranging from 31 to 86% across subjects (mean ± SE 58 ± 5%), with total MSNA increasing by 156 ± 19% (P = 0.001). Furthermore, we documented de novo synthesis of sympathetic bursts that were coupled to the sinusoidal input, such that two bursts—rather than the obligatory single burst—could be generated within a cardiac interval. This demonstrates that the human vestibular apparatus exerts a potent facilitatory influence on MSNA that potentially operates independently of the baroreceptor system.     

Low-frequency sinusoidal galvanic stimulation of the left and right vestibular nerves reveals two peaks of modulation in muscle sympathetic nerve activity

Studies previously performed in our laboratory have shown that sinusoidal galvanic vestibular stimulation (sGVS), a means of selectively modulating vestibular input without affecting other inputs, can cause partial entrainment of muscle sympathetic nerve activity (MSNA) at frequencies ranging from 0.2 to 2.0 Hz. Here we test the effect of sGVS on sympathetic outflow when stimulating the vestibular system at lower frequencies. MSNA was recorded via tungsten microelectrodes inserted into the left common peroneal nerve in 12 awake, seated subjects. Bipolar binaural sinusoidal GVS (±2 mA, 100 cycles) was applied to the mastoid processes at 0.08, 0.13 and 0.18 Hz. Cross-correlation analysis revealed two bursts of modulation of MSNA for each cycle of stimulation. We believe the primary peak is related to the positive phase of the sinusoid, in which the right vestibular nerve is hyperpolarised and the left vestibular nerve depolarised. Furthermore, we believe the secondary peak is related to the negative phase of the sinusoid (depolarisation of the right vestibular nerve and hyperpolarisation of the left vestibular nerve). This was never observed at higher frequencies of stimulation, presumably because at such frequencies there is insufficient time for a second peak to be expressed. The incidence of double peaks of MSNA was highest at 0.08 Hz and lowest at 0.18 Hz. These observations emphasise the role of the vestibular apparatus in the control of blood pressure, and further suggest convergence of bilateral inputs from vestibular nuclei onto the output nuclei from which MSNA originates, the rostral ventrolateral medulla (RVLM).     

Biphasic effects of tonic stimulation of muscle nociceptors on skin sympathetic nerve activity in human subjects

Skin sympathetic nerve activity (SSNA) controls skin blood flow and sweat release, and acute noxious stimulation of skin has been shown to cause a decrease in SSNA in the anaesthetised or spinal cat. In awake human subjects, acute muscle pain causes a transient rise in SSNA, but the impact of long-lasting (tonic) stimulation of muscle nociceptors on skin sympathetic outflow, blood flow and sweat release is unknown. We tested the hypothesis that tonic stimulation of muscle nociceptors causes a sustained increase in sympathetic outflow to the skin. SSNA was recorded from the common peroneal nerve of 10 awake human subjects. Tonic muscle pain was induced by infusing hypertonic saline (7 %) into the tibialis anterior muscle over ~40 min, titrated to achieve a constant level of muscle pain. SSNA initially increased following the onset of the infusion, reaching a peak of 164 % of baseline within 5 min, but then showed a prolonged and sustained decrease, reaching a nadir of 77 % in 20 min. Conversely, skin blood flow (and vascular conductance) initially decreased, followed by a progressive increase; there were no consistent changes in sweat release. In 9 of 10 subjects, SSNA and skin blood flow were inversely related. We conclude that sympathetic outflow to the skin exhibits a biphasic response to long-lasting stimulation of muscle nociceptors: an initial increase presumably related to the ‘arousal’ or ‘alerting’ component of pain, characterised by increased SSNA and decreased skin blood flow, followed by a prolonged decrease in SSNA and increased skin blood flow. The latter may be a purposeful response that contributes to wound healing.     

Vestibular modulation of muscle sympathetic nerve activity by the utricle during sub-perceptual sinusoidal linear acceleration in humans

We assessed the capacity for the vestibular utricle to modulate muscle sympathetic nerve activity (MSNA) during sinusoidal linear acceleration at amplitudes extending from imperceptible to clearly perceptible. Subjects (n = 16) were seated in a sealed room, eliminating visual cues, mounted on a linear motor that could deliver peak sinusoidal accelerations of 30 mG in the antero-posterior direction. Subjects sat on a padded chair with their neck and head supported vertically, thereby minimizing somatosensory cues, facing the direction of motion in the anterior direction. Each block of sinusoidal motion was applied at a time unknown to subjects and in a random order of amplitudes (1.25, 2.5, 5, 10, 20 and 30 mG), at a constant frequency of 0.2 Hz. MSNA was recorded via tungsten microelectrodes inserted into muscle fascicles of the common peroneal nerve. Subjects used a linear potentiometer aligned to the axis of motion to indicate any perceived movement, which was compared with the accelerometer signal of actual room movement. On average, 67 % correct detection of movement did not occur until 6.5 mG, with correct knowledge of the direction of movement at ~10 mG. Cross-correlation analysis revealed potent sinusoidal modulation of MSNA even at accelerations subjects could not perceive (1.25–5 mG). The modulation index showed a positive linear increase with acceleration amplitude, such that the modulation was significantly higher (25.3 ± 3.7 %) at 30 mG than at 1.25 mG (15.5 ± 1.2 %). We conclude that selective activation of the vestibular utricle causes a pronounced modulation of MSNA, even at levels well below perceptual threshold, and provides further evidence in support of the importance of vestibulosympathetic reflexes in human cardiovascular control.     

Frequency-dependent modulation of muscle sympathetic nerve activity by sinusoidal galvanic vestibular stimulation in human subjects

We have previously demonstrated that selective modulation of vestibular inputs, via sinusoidal galvanic vestibular stimulation (GVS) delivered at 0.5–0.8 Hz, can cause partial entrainment of muscle sympathetic nerve activity (MSNA). Given that we had seen interaction between the dynamic vestibular input and the normal cardiac-locked MSNA rhythm, we tested the hypothesis that frequencies of GVS remote from the cardiac frequency would cause a greater modulation of MSNA than those around the cardiac frequency. Bipolar binaural sinusoidal GVS (±2 mA, 200 cycles) was applied to the mastoid processes in 11 seated subjects at frequencies of 0.2, 0.5, 0.8, 1.1, 1.4, 1.7 and 2.0 Hz. In all subjects, the stimulation evoked robust vestibular illusions of “rocking in a boat” or “swinging from side to side.” Cross-correlation analysis revealed a cyclic modulation of MSNA at all frequencies, with the modulation index being similar between 1.1 Hz (78.5 ± 3.7%) and 2.0 Hz (77.0 ± 4.3%). However, vestibular modulation of MSNA was significantly stronger at 0.2 Hz (93.1 ± 1.7%) and significantly weaker at 0.8 Hz (67.2 ± 1.8%). The former suggests that low-frequency changes in vestibular input, such as those associated with postural changes, preferentially modulate MSNA; the latter suggests that vestibular inputs compete with the stronger baroreceptor inputs operating at the cardiac rhythm (~0.8 Hz), with vestibular modulation of MSNA being greater when this competition with the baroreceptors is reduced.     

Absence of short-term vestibular modulation of muscle sympathetic outflow,assessed by brief galvanic vestibular stimulation in awake human subjects

There is evidence in experimental animals for a potent vestibulosympathetic reflex, but its existence in humans is controversial. Static head-down neck flexion and off-vertical axis rotation have been shown to increase muscle sympathetic nerve activity (MSNA), but not skin sympathetic nerve activity (SSNA), whereas horizontal linear acceleration decreases MSNA in humans. However, both forms of stimuli also activate other receptors. To examine the effects of a pure vestibular stimulus on MSNA and SSNA, and its potential interaction with the baroreceptors, we used galvanic vestibular stimulation (GVS) in 12 healthy seated subjects. MSNA was recorded in ten subjects via a percutaneous microelectrode in the peroneal nerve; ECG, blood pressure, respiration, skin blood flow and sweating were also recorded. GVS (2 mA, 1 s pulse) was delivered via surface electrodes over the mastoid processes at unexpected times, triggered from the R-wave with a delay of 0, 200, 400 or 600 ms. In addition to causing robust postural illusions, GVS caused cutaneous vasoconstriction and sweat release in all subjects (due to a short-latency increase in SSNA, three subjects), but no significant change in MSNA. The failure of GVS to elicit a change in muscle sympathetic nerve activity, as documented by averaging, suggests that the vestibular system is not engaged in short-term modulation of muscle sympathetic activity. Conversely, phasic vestibular inputs do excite cutaneous sympathetic neurones, consistent with the observation that motion sickness is accompanied by pallor and sweating.     

Horizontal otolith-ocular responses in humans after unilateral vestibular deafferentation

We studied horizontal eye movements evoked by lateral whole body translation in nine patients who underwent vestibular nerve section. Preoperatively, all had preserved caloric function on both sides. Testing was performed before, 1 week and 6–10 weeks after surgery. Patients were seated upright in an electrically powered car running on a linear track. The car executed acceleration steps of 0.24 g, randomly to the left and right in the dark. The normal response consisted of a bidirectionally symmetrical nystagmus with compensatory slow phases. Response asymmetry of the slow-phase velocity of the desaccaded and averaged eye position signal was less than 13% in normals (n = 21). Before surgery, patients’ responses were mostly symmetrical. Postoperatively, responses were diminished or absent with head acceleration towards the operated ear in all patients, causing a marked asymmetry which averaged 56% after correction for spontaneous nystagmus. On follow-up, responses regained symmetry. Thus, early after vestibular nerve section, a single utricle produces a normal LVOR only with ipsilateral head translation. Therefore, afferents for the LVOR seem to originate from the mid-lateral area of the macula, where hair cells are stimulated in their on-direction during ipsilateral head translation. Compensation may depend on recovery of the off-directional responses from lateral hair cells of the remaining utricle. Received: 9 December 1996 / Accepted: 15 July 1997     

Vestibulo-collic reflex (VCR) in mice

The vestibulo-collic reflex (VCR) attempts to stabilize head position in space during motion of the body. Similar to the better-studied vestibulo-ocular reflex, the VCR is subserved by relatively direct, as well as indirect pathways linking vestibular nerve activity to cervical motor neurons. We measured the VCR using an electromagnetic technique often employed to measure eye movements; we attached a loop of wire (head coil) to an animal’s head using an adhesive; then the animal was gently restrained with its head free to move within an electromagnetic field, and was subjected to sinusoidal (0.5–3 Hz) or abrupt angular acceleration (peak velocity approximately 200°/s). Head rotation opposite in direction to body rotation was assumed to be driven by the VCR. To confirm that the compensatory head movements were in fact vestibular in origin, we plugged the horizontal canal unilaterally and then retested the animals 2, 8 and 15 days after the lesion. Two days after surgery, the putative VCR was almost absent in response to abrupt or sinusoidal rotations. Recovery commenced by day 8 and was nearly complete by day 15. We conclude that the compensatory head movements are vestibular in origin produced by the VCR. Similar to other species, there are robust compensatory mechanisms that restore the VCR following peripheral lesions.     

Effects of deep and superficial experimentally induced acute pain on skin sympathetic nerve activity in human subjects

There is evidence in experimental animals that deep and superficial pain exert differential effects on cutaneous sympathetic activity. Skin sympathetic nerve activity (SSNA) was recorded from the common peroneal nerve of awake human subjects and injections of 0.5 ml hypertonic saline was made into the tibialis anterior muscle (causing a deep, dull ache) or 0.2 ml into the overlying skin (causing a sharp burning pain) at unexpected times. Both deep and superficial pain caused increases in SSNA immediately on injection and preceding the onset of pain for both muscle and skin pain (10.1 ± 2.4 vs. 15.3 ± 5.3 s; muscle versus skin, respectively). SSNA increases were short lasting (104.2 ± 13.4 vs. 81.8 ± 11.7 s; muscle versus skin pain) and did not follow muscle and skin pain profiles. Sweat release occurred following both intramuscular and subcutaneous injections of hypertonic saline. While muscle or skin pain invariably caused changes in skin blood flow as well as increases in sweat release, skin blood flow increased in females and decreased in males. We conclude that both acute muscle and skin pain cause an increase in SSNA, sweat release and gender-dependent changes in skin blood flow.     

Vertical (Z-axis) acceleration alters the ocular response to linear acceleration in the rabbit

Whether ocular orientation to gravity is produced solely by linear acceleration in the horizontal plane of the head or depends on both horizontal and vertical components of the acceleration of gravity is controversial. Here, we compared orienting eye movements of rabbits during head tilt to those produced by centrifugation that generated centripetal acceleration along the naso-occipital (X-), bitemporal (Y-) and vertical (Z-) axes in a constant gravitational field. Sensitivities of ocular counter-pitch and vergence during pitch tilts were ≈25°/g and ≈26°/g, respectively, and of ocular counter-roll during roll tilts was ≈20°/g. During X-axis centripetal acceleration with 1 g of gravity along the Z-axis, pitch and vergence sensitivities were reduced to ≈13°/g and ≈16°/g. Similarly, Y-axis acceleration with 1g along the Z-axis reduced the roll sensitivity to ≈16°/g. Modulation of Z-axis centripetal acceleration caused sensitivities to drop by ≈6°/g in pitch, ≈2°/g in vergence, and ≈5°/g in roll. Thus, the constant 1g acceleration along the Z-axis reduced the sensitivity of ocular orientation to linear accelerations in the horizontal plane. Orienting responses were also modulated by varying the head Z-axis acceleration; the sensitivity of response to Z-axis acceleration was linearly related to the response to static tilt. Although the sign of the Z-axis modulation is opposite in the lateral-eyed rabbit from that in frontal-eyed species, these data provide evidence that the brain uses both the horizontal and the vertical components of acceleration from the otolith organs to determine the magnitude of ocular orientation in response to linear acceleration.

Different thermal dependency of cutaneous sympathetic outflow to glabrous and hairy skin in humans

We investigated the effects of ambient temperature on the sudomotor and vasoconstrictor components of skin sympathetic nerve activity (SSNA). The sympathetic traffic was measured by simultaneous microneurographic recording from post-ganglionic nerve fibres in the tibial and the peroneal nerves. When the ambient temperature was raised from 25° C to 34° C, both sudomotor and vasoconstrictor components of SSNA were enhanced in the peroneal nerve but were suppressed in the tibial nerve. The sudomotor and vasoconstrictor sympathetic outflows were elevated in both nerves when the temperature was lowered from 34° C to 18° C. Our results suggested that the sudomotor and the vasoconstrictor components of SSNA are differently modulated by ambient temperature. The difference in sudomotor and vasoconstrictor components of SSNA in the tibial and the peroneal nerves at different ambient temperature may have been responsible for the differences observed in sweating and vasoconstriction in glabrous and hairy skin.     

Head position modulates optokinetic nystagmus

Orientation and movement relies on both visual and vestibular information mapped in separate coordinate systems. Here, we examine how coordinate systems interact to guide eye movements of rabbits. We exposed rabbits to continuous horizontal optokinetic stimulation (HOKS) at 5°/s to evoke horizontal eye movements, while they were statically or dynamically roll-tilted about the longitudinal axis. During monocular or binocular HOKS, when the rabbit was roll-tilted 30° onto the side of the eye stimulated in the posterior → anterior (P → A) direction, slow phase eye velocity (SPEV) increased by 3.5–5°/s. When the rabbit was roll-tilted 30° onto the side of the eye stimulated in the A → P direction, SPEV decreased to ~2.5°/s. We also tested the effect of roll-tilt after prolonged optokinetic stimulation had induced a negative optokinetic afternystagmus (OKAN II). In this condition, the SPEV occurred in the dark, “open loop.” Modulation of SPEV of OKAN II depended on the direction of the nystagmus and was consistent with that observed during “closed loop” HOKS. Dynamic roll-tilt influenced SPEV evoked by HOKS in a similar way. The amplitude and the phase of SPEV depended on the frequency of vestibular oscillation and on HOKS velocity. We conclude that the change in the linear acceleration of the gravity vector with respect to the head during roll-tilt modulates the gain of SPEV depending on its direction. This modulation improves gaze stability at different image retinal slip velocities caused by head roll-tilt during centric or eccentric head movement.     

Primate disconjugate eye movements during the horizontal AVOR in darkness and a plausible mechanism

Disconjugate eye movements during the horizontal angular vestibulo-ocular reflex (AVOR) evoked in response to steps or pulses of head velocity have been previously reported in lateral eyed animals. In this study, we measured binocular responses to sustained sinusoidal and pseudo-random vestibular stimuli in yaw, delivered in darkness, in both human and monkey. The vestibular stimuli used in our experiments had peak velocities in the range of 120–200°/s, frequencies in the range of 0.17–0.5 Hz, and durations between 60 and 75 s. Our results show a large vergence component to the AVOR response that systematically modulated with head velocity. We also examined our results for temporal–nasal preponderance in slow eye velocity. Although each subject showed some degree of directional preference, we did not find a systematically greater eye velocity for temporal–nasal direction across all subjects. Here, we present these findings and discuss that at least two possible sources could result in disconjugate eye movements during the horizontal rotational VOR in darkness: peripheral and central mechanisms.     

Content-Based Estimation of Brain MRI Tilt in Three Orthogonal Directions

In a general scenario, the brain images acquired from magnetic resonance imaging (MRI) may experience tilt, distorting brain MR images. The tilt experienced by the brain MR images may result in misalignment during image registration for medical applications. Manually correcting (or estimating) the tilt on a large scale is time-consuming, expensive, and needs brain anatomy expertise. Thus, there is a need for an automatic way of performing tilt correction in three orthogonal directions (X, Y, Z). The proposed work aims to correct the tilt automatically by measuring the pitch angle, yaw angle, and roll angle in X-axis, Z-axis, and Y-axis, respectively. For correction of the tilt around the Z-axis (pointing to the superior direction), image processing techniques, principal component analysis, and similarity measures are used. Also, for correction of the tilt around the X-axis (pointing to the right direction), morphological operations, and tilt correction around the Y-axis (pointing to the anterior direction), orthogonal regression is used. The proposed approach was applied to adjust the tilt observed in the T1- and T2-weighted MR images. The simulation study with the proposed algorithm yielded an error of 0.40 ± 0.09°, and it outperformed the other existing studies. The tilt angle (in degrees) obtained is ranged from 6.2 ± 3.94, 2.35 ± 2.61, and 5 ± 4.36 in X-, Z-, and Y-directions, respectively, by using the proposed algorithm. The proposed work corrects the tilt more accurately and robustly when compared with existing studies.

     

Human discrimination of translational accelerations

Human perception of self-motion is the result of combining information from many sensory systems such as visual, vestibular, and proprioceptive systems. Research on vestibular thresholds has mainly focused on estimating absolute thresholds for translational and rotational motions and estimating difference thresholds for rotational velocities. In this study, psychophysical methods are used to determine the ability of normal subjects to discriminate among sinusoidal accelerations in the horizontal plane. Difference thresholds were estimated using four different acceleration amplitudes ranging from peak amplitude of 0.5–2.0 m/s² and three different frequencies ranging from 0.25 to 0.6 Hz. Difference thresholds ranged from 0.05 m/s² for a sinusoidal acceleration with peak amplitude of 0.5 to 0.13 m/s² for a sinusoidal acceleration with peak amplitude of 2.0 m/s². The relationship between difference threshold estimates and peak accelerations is found to compare favorably to Weber’s law, which is often used to represent changes in threshold values in other sensory systems. Moreover, the threshold estimates tend to decrease as frequency increases. The effect of visual condition on thresholds was also investigated. It was shown that when the visual scene is stationary with respect to the subject, there are no significant differences between threshold estimates based on closed-eye and open-eye scenarios.     

Bone conducted vibration selectively activates irregular primary otolithic vestibular neurons in the guinea pig

The main objective of this study was to determine whether bone-conducted vibration (BCV) is equally effective in activating both semicircular canal and otolith afferents in the guinea pig or whether there is preferential activation of one of these classes of vestibular afferents. To answer this question a large number (346) of single primary vestibular neurons were recorded extracellularly in anesthetized guinea pigs and were identified by their location in the vestibular nerve and classed as regular or irregular on the basis of the variability of their spontaneous discharge. If a neuron responded to angular acceleration it was classed as a semicircular canal neuron, if it responded to maintained roll or pitch tilts it was classified as an otolith neuron. Each neuron was then tested by BCV stimuli—either clicks, continuous pure tones (200–1,500 Hz) or short tone bursts (500 Hz lasting 7 ms)—delivered by a B-71 clinical bone-conduction oscillator cemented to the guinea pig's skull. All stimulus intensities were referred to that animal's own auditory brainstem response (ABR) threshold to BCV clicks, and the maximum intensity used was within the animal's physiological range and was usually around 70 dB above BCV threshold. In addition two sensitive single axis linear accelerometers cemented to the skull gave absolute values of the stimulus acceleration in the rostro-caudal direction. The criterion for a neuron being classed as activated was an audible, stimulus-locked increase in firing rate (a 10% change was easily detectable) in response to the BCV stimulus. At the stimulus levels used in this study, semicircular canal neurons, both regular and irregular, were insensitive to BCV stimuli and very few responded: only nine of 189 semicircular canal neurons tested (4.7%) showed a detectable increase in firing in response to BCV stimuli up to the maximum 2 V peak-to-peak level we delivered to the B-71 oscillator (which produced a peak-to-peak skull acceleration of around 6–8 g and was usually around 60–70 dB above the animal's own ABR threshold for BCV clicks). Regular otolithic afferents likewise had a poor response; only 14 of 99 tested (14.1%) showed any increase in firing rate up to the maximum BCV stimulus level. However, most irregular otolithic afferents (82.8%) showed a clear increase in firing rate in response to BCV stimuli: of the 58 irregular otolith neurons tested, 48 were activated, with some being activated at very low intensities (only about 10 dB above the animal's ABR threshold to BCV clicks). Most of the activated otolith afferents were in the superior division of the vestibular nerve and were probably utricular afferents. That was confirmed by evidence using juxtacellular injection of neurobiotin near BCV activated neurons to trace their site of origin to the utricular macula. We conclude there is a very clear preference for irregular otolith afferents to be activated selectively by BCV stimuli at low stimulus levels and that BCV stimuli activate some utricular irregular afferent neurons. The BCV generates compressional and shear waves, which travel through the skull and constitute head accelerations, which are sufficient to stimulate the most sensitive otolithic receptor cells.     

Coordination between breathing and forearm movements during sinusoidal tracking

Time relationships (coordination) between breathing and rhythmical limb movements were analyzed during sinusoidal tracking movements of the forearm in 11 healthy subjects. The tracking rate was varied systematically between 0.1 and 1.0 Hz in 0.1-Hz steps. The aim of the study was to elucidate whether rhythmical tracking movements can entrain breathing, and whether this entrainment depends upon the movement rate. Subjects exhibited coordination between tracking movements and breathing at various rate ratios (1:1, 1:2, 1:3). At tracking rates of between 0.2 and 0.6 Hz, 1:1 coordination occurred with a maximum at 0.3 Hz; this rate range was called the 1:1 entrainment band. Coordination of 1:2 occurred at between 0.5 and 1.0 Hz (the 1:2 coordination band) with a maximum at 0.7 Hz. Coordination of 1:3 could be detected at between 0.5 and 1.0 Hz. Different subjects showed 1:n entrainment bands at similar locations but different widths of the rate range studied. The breathing rate during tracking was significantly higher than at rest, and it was correlated positively with tracking rate. This correlation, however, depended upon the width of the entrainment bands. Breathing rates varied between 0.2 and 0.6 Hz for all coordination patterns. We conclude that the occurrence of fixed time relationships is an expression of the strength of central nervous system coupling between the two processes. The frequency of coordination between breathing and rhythmical tracking movements depends critically upon the movement rate. Accepted: 7 October 1999