Thesis (Ph.D.)--University of Nebraska-Lincoln, 2009. / Title from title screen (site viewed January 12, 2010). PDF text: v, 128 p. : ill. ; 1 Mb. UMI publication number: AAT 3360500. Includes bibliographical references. Also available in microfilm and microfiche formats.

published_or_final_version / Physiology / Doctoral / Doctor of Philosophy

published_or_final_version / abstract / Physiology / Doctoral / Doctor of Philosophy

published_or_final_version / Physiology / Doctoral / Doctor of Philosophy

Vestibular-dependent surface potentials can be recorded from over the scalp following stimulation with intense air- (AC) and bone-conducted (BC) sound. However, sound-evoked responses may be confounded by parallel stimulation of the auditory system. To demonstrate the pure vestibular origin of the cortical potentials, patients with severe to profound bilateral hearing loss were stimulated with AC and BC sound. The responses had the same amplitude as those recorded in normal subjects, and were only present in patients with preserved vestibular function, confirming their vestibular origin. One negative surface potential, the N15, was largest when measured over the forehead, and detailed mapping of this potential localised it to the eyes. This extraocular response had the same polarity on each side of the eye and was altered by changing gaze direction, suggesting an extraocular muscle origin (i.e. an ocular vestibular evoked myogenic potential, or OVEMP). Galvanic vestibular stimulation (GVS) produces large eye movements with horizontal and torsional components directed away from the cathode. A modified electrode montage was used to characterise the OVEMPs produced by GVS. OVEMPs recorded from beneath the eyes had the appropriate polarity to produce the torsional eye movement and likely originated in the inferior oblique muscles. Sound-evoked OVEMPs were investigated in patients with superior canal dehiscence (SCD), as they have vestibular hypersensitivity to sound. The SCD patients had large sound-evoked OVEMPs with low threshold, similar to the VEMP. OVEMP amplitude was much larger in the patients than controls and could be an additional diagnostic marker for this condition. Although SCD patients have large VEMPs and eye movements evoked by AC sound, little is known about other vestibular reflexes. It was shown that patients also have large sound-evoked vestibulo-spinal reflexes, similar to those evoked by GVS. However, despite these large reflexes, there was little consistent whole body sway. Finally, a case is reported in which the combination of VEMP and OVEMP results indicated the location and nature of a central nervous system lesion. The patient had delayed potentials when stimulated on the left side, indicating a demyelinating lesion in the root entry zone of the left vestibulocochlear nerve.

The vestibular system provides us with sensory information that is essential for maintaining balance and stability. When sensory input is lost due to unilateral vestibular damage (UVD), our ability to maintain stable gaze and posture becomes compromised. Over time, vestibular function is partially restored through a process known as vestibular compensation, which is associated with the rebalancing of activity in the vestibular nuclear complex (VNC) of the brainstem. However, the physiological mechanisms associated with vestibular compensation remain elusive. We addressed several different experimental objectives pertaining to plasticity and sensory adaptation associated with vestibular compensation. First, we demonstrated that systemic manipulation of γ-amino-butyric acid type B (GABAB) receptors altered the course of vestibular behavioural recovery within the first several hours after UVD. Second, we showed that immunohistochemical labeling of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluR4 was elevated in the VNC on the intact compared to lesioned side acutely following UVD. Third, we produced preliminary data suggesting that excitatory responses to vestibular nerve stimulation may be acutely potentiated by UVD on the intact side. Finally, we established that rapid sensory adaptation may increase the dynamic ranges of vestibular neurons and perhaps improve limited vestibular reflex function in the long term. Acutely following UVD, potentiation of vestibular nerve synapses appear to be associated with an increase in GluR4 subunit expression in the contralesional VNC. Also, such potentiation could be enhanced by acute modifications in pre-synaptic GABAB receptor activation. In the long term, and independent of these plastic changes, sensory adaptation may enable the vestibular system to overcome the persistent limitations imposed by UVD.

The vestibular system provides us with sensory information that is essential for maintaining balance and stability. When sensory input is lost due to unilateral vestibular damage (UVD), our ability to maintain stable gaze and posture becomes compromised. Over time, vestibular function is partially restored through a process known as vestibular compensation, which is associated with the rebalancing of activity in the vestibular nuclear complex (VNC) of the brainstem. However, the physiological mechanisms associated with vestibular compensation remain elusive. We addressed several different experimental objectives pertaining to plasticity and sensory adaptation associated with vestibular compensation. First, we demonstrated that systemic manipulation of γ-amino-butyric acid type B (GABAB) receptors altered the course of vestibular behavioural recovery within the first several hours after UVD. Second, we showed that immunohistochemical labeling of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit GluR4 was elevated in the VNC on the intact compared to lesioned side acutely following UVD. Third, we produced preliminary data suggesting that excitatory responses to vestibular nerve stimulation may be acutely potentiated by UVD on the intact side. Finally, we established that rapid sensory adaptation may increase the dynamic ranges of vestibular neurons and perhaps improve limited vestibular reflex function in the long term. Acutely following UVD, potentiation of vestibular nerve synapses appear to be associated with an increase in GluR4 subunit expression in the contralesional VNC. Also, such potentiation could be enhanced by acute modifications in pre-synaptic GABAB receptor activation. In the long term, and independent of these plastic changes, sensory adaptation may enable the vestibular system to overcome the persistent limitations imposed by UVD.

Thesis--M. Phil., University of Hong Kong, 1980.

Thesis--Ph. D., University of Hong Kong, 1979.

published_or_final_version / Medical Sciences / Master / Master of Medical Sciences