A dissertation on a study presented to the Discipline of Speech Pathology and Audiology , School of Human and Community Development , Faculty of Humanities , University of the Witwatersrand , In fulfilment of the requirements for the degree M.A. Audiology , March 2017 / In health care, there appears to be greater consideration for the biopsychosocial model of disability and viewing disability in terms of functional health. Recently, the effect of impairment on the significant other’s (SO’s) quality of life (QOL) has been explored. In audiology, there appear to be very few published studies in this area, particularly related to vestibular disorders. The purpose of this study was to investigate the experiences of vestibular disorders on the SO’s QOL. A qualitative research design was employed, including 11 interviews and two focus groups. Participants were SO’s of individuals with chronic vestibular disorders, and were recruited from a private audiology practice in Gauteng through purposive sampling strategies. Data were analysed using thematic analysis. Eight primary themes emerged in the data analysis: social implications, financial implications, searching for a diagnosis, emotional effects, changes in family dynamics, support systems, comparison-oriented coping mechanisms, and referrals for psychological services. Findings suggested that SO’s experienced third-party vestibular disability; however, having the appropriate support systems, including family and friends, was pertinent. It was also indicated that the relationship with the audiologist was essential in providing better understanding of the condition and prognosis thereof, resulting in less frustration and improved adaptation to the reported changes. A key finding was the lack of referral for psychological or counselling services. These findings suggest the need to account for third-party vestibular disability in clinical, theoretical, and academic settings, and they call for the inclusion of third-party disability in policy-making. / MT 2018

Thesis (M. Sc. Med.)--Discipline of Medicine, Faculty of Medicine, University of Sydney, 2007. / Title from title screen (viewed June 20, 2007). Submitted in fulfilment of the requirements for the degree of Master of Science in Medicine to the Faculty of Medicine. Degree awarded 2007; thesis submitted 2005. Includes bibliography. Also issued in print.

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.

Exposure to abnormal motion produces a variety of behavioural effects in both human and non-human species. The general purpose of the present studies was to produce and investigate some of these effects in the laboratory rat. In the first series of experiments, rats displayed appreciable decreases in reactivity to noxious stimuli presented after exposure to brief periods of different types of motion. This motion-induced antinociception was found to persist for periods of up to 15 min. A second series of experiments examined the role of the vestibular system in this motion-induced antinociception phenomenon. Rats whose peripheral vestibular apparatus had been rendered insensitive to accelerative stimuli did not exhibit motion-induced antinociception. Subsequent experiments attempted to delineate the role of some individual components of the central vestibular system but no single component investigated was found to play a major role in the production of antinociception. Experiments in this and the preceding series of experiments also demonstrated that the antinociceptive effect could be dissociated from dizziness or acute vestibular dysfunction. In the third series of experiments, the physiological mechanisms by which vestibular stimulation produces antinociception were investigated. Experiments in this series demonstrated that motion-induced antinociception could be blocked by opiate antagonists and that the motion-induced antinociceptive effect showed cross-tolerance with chronic morphine administration. These two findings strongly implicate an endogenous opiate peptide (endorphin) system as the underlying mechanism for mot ion-induced antinociception. The brief duration of the antinociceptive effect and the fact that disruption of the pituitary-adrenal axis did not affect motion-induced antinociception suggested that the opiate peptides involved were the enkephalins rather than B-endorphin. Other behavioural effects of abnormal motion were reported in the the fourth series of experiments. The resemblance between the symptoms of motion sickness and those of opiate administration suggested that endogenous opiate peptides may mediate motion sickness. Although exposure to abnormal motion did produce a substantial conditioned taste aversion (a behavioural assay for motion sickness in the rat), attempts to attenuate the aversion with two different opiate antagonists were unsuccessful. These results suggested that abnormal motion exerts its illness-producing effects through some mechanism other than an endogenous opiate system. In the final experiment, rats that were exposed to a brief period of abnormal motion subsequently exhibited a suppression of defensive burying behaviour that was similar to that produced by anxiolytic drugs. The results of this study indicate that abnormal vestibular stimulation may have a variety of different behavioural effects in rats. However, it appears that no single mechanism can account for all of these effects. / Arts, Faculty of / Psychology, Department of / Graduate

published_or_final_version / Physiology / Doctoral / Doctor of Philosophy

Thesis. 1977. Ph.D.--Massachusetts Institute of Technology. Dept. of Aeronautics and Astronautics. / MICROFICHE COPY AVAILABLE IN ARCHIVES AND AERO / Vita. / Bibliography : leaves 323-333. / by Greg L. Zacharias. / Ph.D.

Damage to one vestibular apparatus (unilateral vestibular deafferentation, UVD) results in severe postural and ocular motor disturbances (such as spontaneous nystagmus, SN) that recover over time in a process known as vestibular compensation. However, the underlying neurochemical mechanisms of vestibular compensation are poorly understood. While UVD affects many areas in the CNS, attention has focused upon the partially deafferented second order neurons in the vestibular nuclei complex (VNC). Several converging lines of evidence suggest that Ca�⁺-permeable ion channels (N-methyl-D-aspartate receptors and L-type voltage-gated Ca�⁺-channels) and intracellular Ca�⁺-dependent protein kinases play an important role in vestibular compensation. However, the nature of this involvement and the locus of these changes are unknown. The aim of this thesis was to investigate the role of Ca�⁺ signalling pathways in the VNC during vestibular compensation in guinea pig. These issues were investigated in three separate experiments that utilised two methodological approaches: i) in vitro assays were used to determine the nature and extent of protein phosphorylation within the VNC at various stages of compensation; and ii) ion channel blockers or cell-permeable kinase inhibitors were injected directly into the VNC immediately before UVD to determine whether or not these systems were causally involved in compensation. The results of experiment 1 (Chapter 5) showed that a bolus intra-VNC injection of an uncompetitive NMDA receptor antagonist, but not an L-type voltage-gated Ca�⁺ channel antagonist, temporarily reduced SN frequency at the earliest measurement time (6 hours post-UVD). These results suggested that the initial expression of SN required, in part, the activation of NMDA receptors in the VNC on the side of the UVD, and by inference, Ca�⁺ entry through the ion channel. The results of experiment 2 (Chapter 6) revealed that the medial VNC contains abundant Ca�⁺/calmodulin-dependent and Ca�⁺/phospholipid-dependent protein kinase activities. The same VNC tissue removed from animals at various times after UVD, showed that vestibular compensation is accompanied by specific changes in the phosphorylation of several major protein kinase C substrates. These included an unidentified 46-kDa band, and a 75-kDa band with similar characteristics to the myristoylated alanine-rich C kinase substrate (MARCKS). These results suggest that protein kinase C signalling pathways may be involved in vestibular compensation. The results of experiment 3 (Chapter 7) are consistent with these results showing that intra-VNC infusion of a protein kinase C inhibitor, but not a Ca�⁺/calmodulin-dependent protein kinase II inhibitor, significantly increased SN at the earliest measurement times (6 and 8 hours), but had no effect upon the time taken to achieve compensation or on postural compensation. These results suggest that the induction of SN compensation involves protein kinase C activity in the VNC. Taken together, these findings suggest that the mechanisms underlying the expression of SN (e.g., Ca�⁺ influx via NMDA receptors) are possibly distinct from those that initiate its compensation (e.g., PKC activation). The downstream effects of raised intracellular Ca�⁺ may involve protein kinase C-dependent phosphorylation of key intracellular proteins that initiate long-lasting changes in cellular function within the VNC.

Loss of sensory input from one vestibular labyrinth by unilateral vestibular deafferentation (UVD) results in a severe ocular motor (i.e., spontaneous nystagmus (SN)) and postural syndrome (i.e., yaw head tilt, (YHT) and roll head tilt (RHT)) which compensates over time in a behavioural recovery process known as vestibular compensation. It is generally accepted that the UVD-induced neuronal imbalance in the resting activity between the two vestibular nuclear complexes (VNCs) generates the ocular motor and postural syndrome and that the restoration of the resting activity in the ipsilateral VNC plays a causal role in the compensation of the static symptoms. γ-Aminobutyric acid (GABA) and the GABAA and GABAB receptors within the VNC are involved in normal vestibulo-ocular and --spinal pathways and it has been suggested that modification of GABAergic inhibition may be a mechanism responsible for the recovery of resting activity in the ipsilateral VNC. Behavioural, western blotting, and immunoassay techniques were used to address the role of the GABAA receptor in the VNC during vestibular compensation. The first study involved the characterization of SN, YHT, and RHT compensation in guinea pigs that had been anaesthetized with isoflurane during the UVD. These animals compensated rapidly (i.e., 30 hrs) and the time to compensate was independent of the duration of the anaesthesia. Using the 30 hrs time frame, the effects of the chronic infusion of the GABAA receptor agonist (muscimol) / antagonist (gabazine) into either the ipsilateral or the contralateral VNC on the compensation of SN, YHT, and RHT, were determined. 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 hrs post-UVD. At 30 hrs post-UVD, the pumps were disconnected. In both experimental groups, the value and direction of the YHT and RHT returned to vehicle levels. 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. At 30 hrs post-UVD, the pumps were disconnected. In both experimental groups, the value and direction of the YHT and RHT returned to vehicle levels. These results suggest that the ipsilateral gabazine and contralateral muscimol infusions were modifying the expression of the symptoms without altering the mechanism of compensation. Furthermore, the mechanism responsible for vestibular compensation can cope with the both the GABAA receptor-mediated and the UVD-induced decrease in resting activity. Results from the western blotting study indicated that compensation of SN, YHT, and RHT is not associated with changes in the protein levels of the GABAA receptor α₁, β₂, or γ₂ subunits. Compensation of SN, YHT, and RHT is associated with an elevation in cortisol salivary levels. Overall, the results suggest that the GABAA receptors are involved in the expression of YHT and RHT, but not in the mechanism that is responsible for their compensation.

Thesis (M.S.)--Ohio University, June, 2006. / Title from PDF t.p. Includes bibliographical references (p. 104-111)

Thesis (M. Sc.)--York University, 1998. / Typescript. Includes bibliographical references (leaves. Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://wwwlib.umi.com/cr/yorku/fullcit?pMQ39249.