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<p>In recent years, many studies have reported that the tactile spatial acuity of blind participants is enhanced relative to that of sighted participants, but it is unclear what factors drive this enhancement. In the series of three psychophysics studies (of tactile spatial acuity) presented in this thesis, we attempted to tease apart two hypotheses explaining tactile spatial acuity enhancement in the blind: visual deprivation and tactile experience. To measure tactile spatial acuity in these studies, we used a grating orientation task. In the first study (Chapter 2), we found that blind participants outperformed sighted participants, but only on body parts where tactile experience is presumably greater in blind than in sighted participants (i.e., fingertips, not lips); we found additionally that blind participants’ tactile acuity correlated with their Braille reading behaviour (e.g., style, frequency of reading). In the second study (Chapter 3), we found that visual deprivation of sighted participants for periods up to 110 minutes did not enhance their sense of touch. In the third study (Chapter 4), we found that extensive training on a tactile task can substantially improve sighted participants’ sense of touch. The findings from our three studies thus provide consistent support for the hypothesis that tactile experience, but not visual deprivation, drives tactile spatial acuity enhancement in the blind.</p> / Doctor of Philosophy (PhD)

Having an appropriate understanding of the behavioral and physiological impact of a disease requires thoroughly fielded tests and wide-ranging animal models to properly deduce generalized impacts of the disease under investigation. Through novel animal models, we acquire diverse insights into the mechanisms at play so that we may approach the problem at hand with fresh perspective and renewed vigor. Using the naked mole-rat (Heterocephalus glaber), a species becoming increasingly common in the medical sciences, my dissertation aimed to accomplish the aforementioned goals in two parts: 1) take the naked mole-rat through a battery of behavioral tasks to bolster our capabilities of using this animal model in medical research; and 2) introduce the naked mole-rat as an alternative model for the investigation of how loss of dental sensation alters behavior and neuroanatomy. Chapter two describes the many methods with which I tested the naked mole-rat across a variety of typical behavioral tasks for social dominance, learning and memory, anxiety, depression, and sociability. Included herein were tests to determine appropriate motivators for this subterranean species to perform such tasks. Additionally, due to the naked mole-rat’s unique disposition for biting, I measured their biting behaviors and compared them across rodent and other mammalian species. The results show that naked mole-rats exhibit large evolutionary divergence in their sensory capabilities and great consideration needs to be given to the proper behavioral tasks and subsequent evaluations of these behavioral paradigms. In chapter three, I evaluated the impact of tooth extraction on affective behaviors, learning and memory, and sociability. Chapter four sought to uncover underlying neuroplasticity associated with the behavioral tasks performed in chapter three. Additionally, in chapter four, I investigated plasticity of the traditional somatosensory pathway for tooth sensation. Tooth loss decreased neuronal density of contralateral ventral posteromedial nucleus of the thalamus and increased the neuronal density of the contralateral ventral dentate gyrus, indicating that tooth-loss induced neuronal plasticity may be more related to plasticity of pain circuitry or resultant from alterations in the muscles of mastication following tooth loss. Though no significant changes in the hippocampus arose from one year of living with no right incisor, I theorized as to which of the physiological idiosyncrasies exhibited by Heterocephalus glaber may have inhibited any observable plasticity due to tooth loss.

No / The effect of refractive blur upon postural stability was investigated under three conditions: normal standing, standing with input from the somatosensory system disrupted and standing with input from the somatosensory and vestibular systems disrupted. Standing stability was assessed using the centre of pressure (COP) signal from force plate data in four young subjects (mean 23.9 ± 3.1 years) and five repeated sets of measurements were taken. The subjects looked straight ahead at a horizontal and vertical square wave pattern of 2.5 cycles (degree)¿1. Under each of the three test conditions, standing stability was measured with the optimal refractive correction and under binocular blur levels of 0, + 1, + 2, + 4, and + 8 D and with eyes closed. In the normal standing condition, dioptric blur had only a mild effect on postural stability. However refractive blur produced large increases in postural instability when input from one or both of the other two sensory systems were disrupted. We hypothesized that dioptric blur would have an even great effect on postural stability if the visual target used was of higher spatial frequency. This was confirmed by repeated measurements on one subject using a target of 8 cycles (degree)¿1. The study highlights the possible importance of an optimal correction to postural stability, particular in situations (or people) where input from the somatosensory and/or vestibular systems are disrupted, and where the visual surrounds are of high spatial frequency.

Copies of author's previously published articles inserted. Bibliography: leaves I-LXIV. Assesses the diagnostic and prognostic value of early electroencephalography (EEG) and somatosensory evoked potential studies in cortical and non-cortical ischaemic stroke. Both conventional and topographic/quantitative studies were performed. A parallel study was carried out on healthy volunteers to provide an effective control. Equipment and quantitative EEG (qEEG) variability was also assessed.

Copies of author's previously published articles inserted. / Bibliography: leaves I-LXIV. / xxxviii, 239 [77], Lxiv leaves : ill. (chiefly col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Assesses the diagnostic and prognostic value of early electroencephalography (EEG) and somatosensory evoked potential studies in cortical and non-cortical ischaemic stroke. Both conventional and topographic/quantitative studies were performed. A parallel study was carried out on healthy volunteers to provide an effective control. Equipment and quantitative EEG (qEEG) variability was also assessed. / Thesis (Ph.D.)--University of Adelaide, Dept. of Medicine, 1998?

Thesis (Ph. D.)--University of Adelaide, Dept. of Medicine, 1998? / Copies of author's previously published articles inserted. Includes bibliographical references (leaves I-LXIV).

Performance of efficient and precise motor output requires proper planning of movement parameters as well as integration of sensory feedback. Peripheral sensory information is projected not only to parietal somatosensory areas but also to cortical motor areas, particularly the supplementary motor area (SMA). These afferent sensory pathways to the frontal cortices are likely involved in the integration of sensory information for assistance in motor program planning and execution. It is not well understood how and where sensory information from the limb contralateral to motor output is modulated, but the SMA is a potential cortical source as it is active both before and during motor output and is particularly involved in movements that require coordination and bilateral upper-limb selection and use. A promising physiological index of sensory inflow to the SMA is the frontal N30 component of the median nerve (MN) somatosensory-evoked potential (SEP), which is generated in the SMA. The SMA has strong connections with ipsilateral areas 2, 5 and secondary somatosensory cortex (S2) as well as ipsilateral primary motor cortex (M1). As such, the SMA proves a fruitful candidate to assess how sensory information is modulated across the upper-limbs during the various stages of motor output. This thesis inquires into how somatosensory information is modulated in both the SMA and primary somatosensory cortical areas (S1) during the planning and execution of a motor output contralateral to sensory input across the upper-limbs, and further, how and what effect ipsilateral primary motor cortex (iM1) has upon modulation of sensory inputs to the SMA.

Performance of efficient and precise motor output requires proper planning of movement parameters as well as integration of sensory feedback. Peripheral sensory information is projected not only to parietal somatosensory areas but also to cortical motor areas, particularly the supplementary motor area (SMA). These afferent sensory pathways to the frontal cortices are likely involved in the integration of sensory information for assistance in motor program planning and execution. It is not well understood how and where sensory information from the limb contralateral to motor output is modulated, but the SMA is a potential cortical source as it is active both before and during motor output and is particularly involved in movements that require coordination and bilateral upper-limb selection and use. A promising physiological index of sensory inflow to the SMA is the frontal N30 component of the median nerve (MN) somatosensory-evoked potential (SEP), which is generated in the SMA. The SMA has strong connections with ipsilateral areas 2, 5 and secondary somatosensory cortex (S2) as well as ipsilateral primary motor cortex (M1). As such, the SMA proves a fruitful candidate to assess how sensory information is modulated across the upper-limbs during the various stages of motor output. This thesis inquires into how somatosensory information is modulated in both the SMA and primary somatosensory cortical areas (S1) during the planning and execution of a motor output contralateral to sensory input across the upper-limbs, and further, how and what effect ipsilateral primary motor cortex (iM1) has upon modulation of sensory inputs to the SMA.

The main goal of the dissertation was to determine task-dependent modulation of corticospinal descending output. From this main goal, I conducted three different studies to determine how corticospinal output to muscles of the upper arm and hand changed as a function of the task demands. In study 1, I examined how a somatosensory-motor circuit changes when a muscle needs to be active in a task and found that this circuit may be dependent on the movement phase, type of afferent input, and the task demands. In study 2, I examined how this same somatosensory-motor circuit acts to both allow and prevent muscle activity before movement. I revealed that this somatosensory-motor circuit may function to prevent muscle activity when a muscle is not needed in a task and creates facilitation of corticospinal output when it needs to be active in a task. These effects, however, are dependent on the movement phase and the digit the muscle is controlling. Study 3 determined how corticospinal output is modulated to upper arm muscles when performing movements that required different combinations of segmental interactions to achieve the task successfully. Corticospinal output was increased when inertia and the BBC moment at a joint resisted the intended joint rotation and these effects were dependent on the muscle and movement phase. I propose a model of the connectivity between the primary motor and somatosensory cortices that would increase, modulate, or decrease corticospinal output to a muscle depending on its role in the task. The findings from this work provides information to guide future neural rehabilitative interventions for individuals who have movement disorders arising from altered somatosensory-motor processing such as Cerebellar Ataxia, Developmental Coordination Disorder, Focal Hand Dystonia, Parkinson’s disease, and stroke. / Dissertation / Doctor of Philosophy (PhD) / On a day to day basis, we perform a variety of movements without giving much thought to how complicated it is for our nervous system to perform said movements. There are many different areas of the brain that are responsible for controlling movement. This dissertation focuses on two key areas that are critical for movement performance, namely the primary motor and somatosensory cortices. The primary motor cortex is largely responsible for sending signals to the muscles to control movement, while the primary somatosensory cortex plays a crucial role in receiving and understanding sensory input from our body. The studies in this dissertation describe how these two areas of the brain communicate during finger and arm movements to produce or prevent muscle activity. This work has implications for individuals with disorders that impact their everyday movements.