How imagery changes self-motion perception.

Imagery and perception are thought to be tightly linked, however, little is known about the interaction between imagery and the vestibular sense, in particular, self-motion perception. In this study, the observers were seated in the dark on a motorized chair that could rotate either to the right or to the left. Prior to the physical rotation, observers were asked to imagine themselves rotating leftward or rightward. We found that if the direction of imagined rotation was different to the physical rotation of the chair (incongruent trials), the velocity of the chair needed to be higher for observers to experience themselves rotating relative to when the imagined and the physical rotation matched (on congruent trials). Accordingly, the vividness of imagined rotations was reduced on incongruent relative to congruent trials. Notably, we found that similar effects of imagery were found at the earliest stages of vestibular processing, namely, the onset of the vestibular-ocular reflex was modulated by the congruency between physical and imagined rotations. Together, the results demonstrate that mental imagery influences self-motion perception by exerting top-down influences over the earliest vestibular response and subsequent perceptual decision-making.

The Tullio phenomenon: a neurologically neglected presentation.

The Tullio phenomenon refers to sound-induced disequilibrium or oscillopsia. Patients with this condition frequently present to neurologists, many of whom are unfamiliar with the condition and its diagnostic criteria. Indeed, due to the unusual nature of the symptoms patients are often misdiagnosed as having psychiatric disturbances. Tullio patients describe disequilibrium, auditory and visual symptoms, which are recurrent, brief, and often triggered by loud noises or middle ear pressure changes, e.g. the Valsalva manoeuvre. Many cases are associated with superior semicircular canal dehiscence (SCCD). Early work suggested that the presence of sound-induced torsional eye movements and visual field tilts were consequent upon a utricular-mediated ocular tilt reaction. However, more recent evidence from imaging and oculographic research, as well as data from our patient series indicates that these ocular abnormalities are usually the result of superior semicircular canal stimulation. The clinical history and a focussed examination are often sufficient to make the diagnosis, which can be confirmed with high resolution CT imaging of the temporal bones. In some patients, surgical occlusion or resurfacing of the affected canal can ameliorate symptoms and signs. The aim of this paper is two-fold: Firstly, to review the clinical features of the Tullio phenomenon, and secondly, to highlight our own observations in three cases with a new clinical syndrome consisting of Tullio's phenomenon with bilateral vestibular failure, a pure horizontal nystagmus in response to sound, and no evidence of canal dehiscence.

Vestibular hypersensitivity to clicks is characteristic of the Tullio phenomenon.

OBJECTIVES: The frequency of pathologically reduced click thresholds for vestibular activation was explored in patients with the Tullio phenomenon (sound induced vestibular activation). METHODS: Seven patients (eight affected ears) with symptoms of oscillopsia and unsteadiness in response to loud external sounds or to the patient's own voice were examined. In all but one patient, vestibular hypersensitivity to sound was confirmed by the fact that eye movements could be produced by pure tones of 110 dB intensity or less. Conventional diagnostic imaging was normal in all cases and three of the patients had normal middle ears at surgical exploration. Thresholds for click evoked vestibulocollic reflexes were compared with those of a group of normal subjects. Galvanic stimulation was used as a complementary method of examining the excitability of vestibular reflexes. RESULTS: All the patients showed a reduced threshold for click activation of vestibulocollic reflexes arising from the affected ear. Short latency EMG responses to clicks were also present in posterior neck and leg muscles, suggesting that these muscles receive vestibular projections. Galvanic stimulation produced a normal pattern of body sway in four of the five patients tested. CONCLUSIONS: A pathologically reduced threshold to click activation (< or = 70 dB NHL (average normal hearing level)) seems to be a consistent feature of the Tullio phenomenon and a useful diagnostic criterion. This in turn is most likely to be due to an increased effectiveness of the transmission of sound energy to saccular receptors. Activation of these receptors probably contributed to the vestibular symptoms experienced by the patients.

The effects of hyperventilation on postural control mechanisms.

The effect of hyperventilation on postural balance was investigated. Voluntary hyperventilation increased body sway in normal subjects, particularly in the sagittal plane. The possibility that this hyperventilation-induced unsteadiness is due to interference with lower limb somatosensory input, vestibular reflexes or cerebellar function was assessed. (i) The effect of hyperventilation on peripheral compound sensory action potentials (SAPs) and somatosensory evoked potentials (SEPs) (recorded centrally, from the scalp) elicited by electrical stimulation of the sural nerve was measured in six normal adults. A reduction in the scalp SEP amplitude and an increase in the peripheral SAP amplitude were observed during hyperventilation, which reversed during the recovery period. These changes indicate increased peripheral neural excitability which could lead to a higher level of ectopic activity; the latter would interfere with central reception of peripheral input. (ii) The click-evoked vestibulo-collic reflex was recorded to study the effect of hyperventilation on vestibulo-spinal activity. EMG recordings from both sternocleidomastoid muscles of six healthy subjects were made in response to loud clicks presented to either ear. Neither the amplitude nor the latency of the response were altered significantly by hyperventilation. (iii) Eye-movement recordings were obtained in the six normal subjects to assess the effect of hyperventilation on the vestibulo-ocular reflex and its visual suppression, the latter being a function largely mediated by the cerebellum; no changes were detected. (iv) Three-dimensional eye-movement recordings and body-sway measurements were obtained in six patients with longstanding unilateral vestibular loss in order to evaluate if hyperventilation disrupts vestibular compensation. In all patients, a horizontal nystagmus either appeared or was significantly enhanced for > or = 60 s after voluntary hyperventilation. Sway was also enhanced by hyperventilation in these patients, particularly in the frontal plane. This study suggests that hyperventilation disrupts mechanisms mediating vestibular compensation. The increase in sway may be, at least partly, mediated by deranged peripheral and central somatosensory signals from the lower limbs. Hyperventilation seems to spare vestibular reflex activity and cerebellar-mediated eye movements.

Clinical and electrophysiological findings in the Tullio phenomenon.

A 55 year old female with idiopathic Tullio phenomenon is presented. Binocular, scleral search eye coil recordings demonstrated a predominantly torsional left-beating and vertical down-beating nystagmus in response to sound intensities over 100 dB HL to the left ear, increasing in amplitude and slow phase velocity with sound intensity and removal of visual fixation. The vertical ocular movement was conjugate, i.e. without skew deviation. Neuro-imaging, all other neuro-otological features, including ipsilateral-contralateral stapedius muscle reflexes, and surgical exploration of the middle ear, were normal. Click-evoked vestibulo-collic potentials were normal from the right ear but showed low threshold (70 dB) and increased amplitude from the left. There was no evidence that the Tullio phenomenon in this patient arises from stapes footplate hypermobility. The findings suggest that some cases of the Tullio phenomenon may be due to a hyperexcitability of the normal vestibular response to sound.

Responses in neck and facial muscles to sudden free fall and a startling auditory stimulus.

EMG responses elicited by sudden onset of free fall and a startling auditory stimulus were investigated in healthy subjects while lying on a couch with their eyes closed. Muscle responses were recorded from masseter (V cranial nerve), orbicularis oculi and mentalis (VII nerve) and sternomastoid and trapezoid (XI nerve). A similar sequence of muscle activation and absolute latencies occurred in response to both stimulus modalities, consisting of a blink (30 msec) followed simultaneously by mentalis, sternomastoid and trapezoid (55 msec). Masseter could either be simultaneously activated with the latter muscles or follow after a delay of 10-20 msec. A patient with bilateral cochleo-vestibular nerve section had responses at comparable latencies in the free fall experiment. The similarities between the reaction to free fall and a startling auditory stimulus indicate that the early response to free fall constitutes a startle and that various stimuli converge onto a common response generator. The latency pattern of neck and facial muscles does not follow a sequence of innervation with increasing segmental distance from a single centre. Therefore, our data do not support the concept that the startle response is produced by a caudally and rostrally spreading volley from a putative pontomedullary centre. It is suggested that the startle response is a polysynaptically generated patterned muscle activation.

Testing the vestibular-ocular reflexes: abnormalities of the otolith contribution in patients with neuro-otological disease.

Conventional vestibular rotation testing with the head centered on the axis stimulates the semicircular canals evoking compensatory eye movements. If the head is placed forwards of the axis in an eccentric position the otoliths are also stimulated by a tangential linear acceleration acting laterally to the skull. In normal subjects the additional otolithic stimulus evokes compensatory eye movements with a higher gain than with head centred, particularly for high frequency (greater than 0.1 Hz) stimuli. The responses with head centred and eccentric in various patients with known/suspected neuro-otological abnormalities have been compared. Patients with vestibular neurinectomies who have asymmetrical head centred responses showed greater asymmetry with head eccentric at higher stimulus frequencies. Some patients with cerebellar lesions showed abnormally enhanced or depressed and asymmetrical responses with head eccentric in comparison with head centred responses, which could be normal. The enhancing effects could be specific to low frequency stimuli. All patients who showed abnormal responses with head eccentric also had positional nystagmus provoked by the gravity acceleration vector when the head was tilted laterally. The direction of the positional nystagmus with respect to the gravity vector was not necessarily the same as the direction of the effect on eye movements of lateral acceleration during eccentric oscillation. Patients with benign paroxysmal vertigo or chronic linear vertigo in whom otolithic abnormalities are suspected were not found to have abnormal responses with head eccentric. We conclude that this method of testing may be useful in elucidating pathophysiology but is not a decisive clinical test for the presence of disordered otolith function.