Dissertation submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in fulfilment of the requirements for the degree Master of Science. 2013 / The Babinski sign is a pathological response elicited by a stimulus to the lateral plantar border of thesole of the foot. The resulting reflex involves dorsiflexion (upward motion) of the toes, most notably the hallux, with accompanying flexion in the ankle, knee and hip. It is an important part of the clinical neurological examination and aids in the diagnosis of central nervous system dysfunction. There is however no wholly standardised method to elicit this reflex or interpret it, resulting in possible variation in its utility. The resulting aim of the studies constituting this dissertation were therefore to: 1) assess what techniques and pressures are used to elicit the reflex in a group of neurologists;2) to investigate the relationship between input variables of the reflex and the resultant output variables as measured with the use of electromyography and kinematics;3) compare objective variables, relating to toe, foot and leg movement, of the pathological reflex to the healthy response; 4) assess the inter-rater reliability of the reflex and 5) determine what aspects of the reflex are most closely related to the ratings of the students and neurologists. A specialized custom-built Babinski hammer was constructed to measure the duration of the stroke and pressures exerted on the foot of a single healthy subject by neurologists (n=12). The relationship between the recorded pressures and the movement of the toes (measured kinematically), muscle activity in the tibialis anterior and the pain felt by the subject (gauged using a visual analogue scale) were evaluated. Following this, the average pressure used by the neurologists was used to elicit the reflex in six patients with known positive Babinski responses and six healthy gender and age matched controls. These reflexes were compared with kinematic (measurement of toe, foot and leg movement) and electromyographic (muscle activity of the involved muscles) methods. These reflexes were recorded and the recorded footage was shown to 12 medical students and 12 neurologists who were asked to interpret if 3 the responses were pathological or non-pathological. Kinematic and electromyographic descriptions of each reflex made it possible to assess what aspects of the reflex are important for classification of a pathological response for both medical students and neurologists. A large amount of intra- and inter-rater variability was shown amongst the neurologists in how they elicited the reflex. The amount of pressure applied was shown to be significantly related to hallux movement (p<0.01) as well as to the degree of pain felt by the subject (p<0.01). Significant differences were found between the patients and controls for change in hallux angle (p<0.0001), movement latency (p<0.05)and the maximum electromyographic amplitude of tibialis anterior(p<0.01). The inter-rater reliability of the medical students and the neurologists showed substantial agreement between raters (kappa = 0.67 and 0.72 respectively). Both neurologists and students made use of the change in hallux angle, time taken to reach maximum ankle angle, movement latency and the maximum amplitude of gastrocnemius when rating the reflex. Neurologists alone observed time taken to reach maximum hallux angle and change in ankle angle as being important while medical students‘ alone looked at maximum amplitude of biceps femoris. In conclusion, I found a large variation between the techniques of neurologists when assessing the Babinski reflex. This variation is related to variation in aspects of the resultant reflex. The pathological response (the Babinski sign) has shorter movement latency and less activity in the tibialis anterior muscle than the flexor response seen in healthy individuals. Ratings of pre-recorded Babinski responses had substantial agreement when both neurologists and medical students assessed pathology. In order to assess them both groups made use of the speed of the reflex, the direction of hallux movement and concurrent withdrawal activity in the leg to differentiate between a pathological and a healthy response.

Dissertation submitted to the Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, in fulfilment of the requirements for the degree of Master of Science in Occupational Therapy Johannesburg, 2015 / Many factors have been shown to play a role in employment after a spinal cord injury. Globally the rates of employment post-injury have been disappointing with a rate of 36.8% 1. METHODS This mixed methods study was divided into two phases. During phase one qualitative data was gathered. This data was used to design a questionnaire which was emailed to members of the Quadpara Association of South Africa in phase two. Bivariate data analysis was performed and a logistic regression. RESULTS Eleven themes emerged from phase one. There was a high employment rate of 79.55% at the time of the study and 92.13% had worked for remuneration since injury. There was a statistically significant association between employment at the time of the study and six factors. CONCLUSION This study had a surprisingly high employment rate post-injury. Despite few results being statistically significant there were many that are of clinical importance.

by Tseung Chu Man Yee, Miriam. / Thesis (M.S.W.)--Chinese University of Hong Kong, 1987. / Bibliography: leaves 169-177.

Rowlands Dewi Kenneth. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (leaves 113-121). / Abstract --- p.i / Acknowledgements --- p.iii / Publications --- p.iv / Abbreviations --- p.v / Contents --- p.vii / Chapter Chapter 1 --- Prostaglandins --- p.1 / Chapter 1.1 --- Introduction --- p.1 / Chapter 1.2 --- Prostanoid biosynthesis and metabolism --- p.1 / Chapter 1.3 --- Prostaglandin receptors --- p.3 / Chapter 1.3.1 --- DP-receptors --- p.3 / Chapter 1.3.2 --- EP1-receptors --- p.4 / Chapter 1.3.3 --- EP2-receptors --- p.4 / Chapter 1.3.4 --- EP3-receptors --- p.5 / Chapter 1.3.5 --- EP4-receptors --- p.6 / Chapter 1.3.6 --- FP-receptors --- p.7 / Chapter 1.3.7 --- IP-receptors --- p.8 / Chapter 1.3.8 --- TP-receptors --- p.11 / Chapter 1.4 --- Agonists and antagonists --- p.11 / Chapter Chapter 2 --- Role of prostacyclin in pain modulation --- p.14 / Chapter 2.1 --- Pain --- p.14 / Chapter 2.2 --- Prostaglandins and pain --- p.15 / Chapter 2.3 --- Prostacyclin and pain --- p.16 / Chapter 2.3.1 --- [3H]-Iloprost binding sites --- p.16 / Chapter 2.3.2 --- IP-receptor mRNA --- p.17 / Chapter 2.3.3 --- IP-receptor knockout mice --- p.17 / Chapter 2.3.4 --- Direct nociceptive action of prostacyclin --- p.18 / Chapter 2.4 --- Treatment of prostanoid-induced pain --- p.19 / Chapter Chapter 3 --- Dorsal root ganglion cells --- p.21 / Chapter 3.1 --- In vitro model of pain --- p.21 / Chapter 3.2 --- Characteristics of cultured DRG cells --- p.22 / Chapter 3.2.1 --- Size and distribution --- p.22 / Chapter 3.2.2 --- Biochemical and physiological characteristics --- p.22 / Chapter 3.2.2.1 --- Gapsaicin-sensitive neurones --- p.23 / Chapter 3.2.2.2 --- Neuropeptide content --- p.23 / Chapter 3.2.2.3 --- Elevation of [Ca2+］i --- p.24 / Chapter 3.3 --- Effect of nerve growth factor --- p.24 / Chapter Chapter 4 --- Materials and solutions --- p.26 / Chapter 4.1 --- Materials --- p.26 / Chapter 4.2 --- Solutions --- p.30 / Chapter 4.2.1 --- Culture medium --- p.30 / Chapter 4.2.2 --- Buffers --- p.31 / Chapter 4.2.3 --- Solutions --- p.32 / Chapter Chapter 5 --- Development of dorsal root ganglion cell preparation --- p.33 / Chapter 5.1 --- Introduction --- p.33 / Chapter 5.2 --- Methods --- p.34 / Chapter 5.2.1 --- Dissection of dorsal root ganglia --- p.34 / Chapter 5.2.2 --- Preparation of a single-cell suspension --- p.34 / Chapter 5.2.2.1 --- Effect of trimming dorsal root ganglia --- p.34 / Chapter 5.2.2.2 --- Enzymatic dissociation --- p.35 / Chapter 5.2.2.3 --- Mechanical dissociation --- p.36 / Chapter 5.2.3 --- Neuronal cell enrichment --- p.36 / Chapter 5.2.3.1 --- Differential adhesion --- p.36 / Chapter 5.2.3.2 --- BSA gradient --- p.37 / Chapter 5.2.3.3 --- Combination of BSA gradient and differential adhesion --- p.37 / Chapter 5.2.4 --- Cell counting --- p.37 / Chapter 5.2.5 --- Culture conditions --- p.38 / Chapter 5.2.6 --- Size distribution of DRG cells --- p.39 / Chapter 5.2.7 --- Immunocytochemistry --- p.39 / Chapter 5.3 --- Results and discussion --- p.40 / Chapter 5.3.1 --- Preparation of single-cell suspension --- p.40 / Chapter 5.3.2 --- Neuronal cell enrichment --- p.42 / Chapter 5.3.3 --- Size distribution of DRG cells --- p.32 / Chapter 5.3.4 --- Effects of mitotic inhibitors and NGF --- p.45 / Chapter 5.3.5 --- Immunocytochemistry --- p.48 / Chapter 5.4 --- Conclusions --- p.48 / Chapter Chapter 6 --- Methods --- p.53 / Chapter 6.1 --- Dorsal root ganglion cell preparation --- p.53 / Chapter 6.1.1 --- Preparation of tissue culture plates and coverslips --- p.54 / Chapter 6.1.2 --- Preparation of Pasteur pipettes --- p.54 / Chapter 6.2 --- Measurement of adenylate cyclase activity --- p.55 / Chapter 6.2.1 --- Introduction --- p.55 / Chapter 6.2.2 --- Preparation of columns --- p.55 / Chapter 6.2.3 --- Measurement of [3H]-cyclic AMP production --- p.56 / Chapter 6.2.4 --- Data analysis --- p.57 / Chapter 6.3 --- Measurement of phospholipase C activity --- p.58 / Chapter 6.3.1 --- Introduction --- p.58 / Chapter 6.3.2 --- Preparation of columns --- p.58 / Chapter 6.3.3 --- Measurement of [3H]-inositol phosphate production --- p.59 / Chapter 6.3.4 --- Data analysis --- p.60 / Chapter 6.4 --- Measurement of [Ca2+]i --- p.60 / Chapter 6.4.1 --- Introduction --- p.60 / Chapter 6.4.2 --- Preparations of cells --- p.61 / Chapter 6.4.3 --- Measurement of Fura-2 fluorescence --- p.62 / Chapter 6.5 --- Measurement of neuropeptides --- p.62 / Chapter 6.5.1 --- Introduction --- p.62 / Chapter 6.5.2 --- Preparation of cells --- p.63 / Chapter 6.5.3 --- CGRP assay --- p.64 / Chapter 6.5.4 --- Substance P assay --- p.64 / Chapter 6.5.5 --- Purification of samples using Sep-Pak cartridges --- p.65 / Chapter Chapter 7 --- Characterisation of prostacyclin receptors on adult rat dorsal root ganglion cells --- p.66 / Chapter 7.1 --- Stimulation of adenylate cyclase --- p.66 / Chapter 7.1.1 --- Introduction --- p.66 / Chapter 7.1.2 --- Agonist concentration-response curves --- p.67 / Chapter 7.1.3 --- Cross-desensitisation experiments --- p.72 / Chapter 7.1.4 --- Evidence for EP3-receptors --- p.77 / Chapter 7.1.5 --- G-protein coupling of the IP-receptor --- p.77 / Chapter 7.1.6 --- Discussion --- p.78 / Chapter 7.1.7 --- Conclusions --- p.82 / Chapter 7.2 --- Stimulation of phospholipase C --- p.82 / Chapter 7.2.1 --- Introduction --- p.82 / Chapter 7.2.2 --- Agonist concentration-response curves --- p.83 / Chapter 7.2.3 --- G-protein coupling --- p.83 / Chapter 7.2.4 --- Discussion and Conclusions --- p.84 / Chapter 7.3 --- Stimulation of changes in [Ca2+]i --- p.87 / Chapter 7.3.1 --- Introduction --- p.87 / Chapter 7.3.2 --- Preliminary results --- p.87 / Chapter 7.3.3 --- Discussion and conclusions --- p.89 / Chapter Chapter 8 --- Neuropeptide release by adult rat dorsal root ganglion cells --- p.90 / Chapter 8.1 --- Introduction --- p.90 / Chapter 8.2 --- Methods and Results --- p.91 / Chapter 8.3 --- Discussion --- p.91 / Chapter 8.4 --- Conclusions --- p.92 / Chapter Chapter 9 --- Regulation of prostacyclin receptors on adult rat DRG cells --- p.93 / Chapter 9.1 --- Introduction --- p.93 / Chapter 9.2 --- Contribution of non-neuronal cells --- p.93 / Chapter 9.3 --- Effect of DRG cell density --- p.94 / Chapter 9.4 --- Effect of indomethacin --- p.99 / Chapter 9.5 --- Contribution of endogenously-produced non-prostanoid ligands --- p.100 / Chapter 9.6 --- Effect of PKC activation --- p.102 / Chapter 9.7 --- Discussion --- p.104 / Chapter 9.8 --- Conclusions --- p.106 / Chapter Chapter 10 --- General Discussion and Conclusions --- p.107 / Chapter 10.1 --- Development of DRG cell preparation --- p.107 / Chapter 10.2 --- Effect of prostanoid mimetics on intracellular messengers --- p.108 / Chapter 10.3 --- Regulation of prostacyclin receptors --- p.109 / Chapter 10.4 --- Role of prostacyclin in pain modulation --- p.111 / References --- p.113

The hallmark of an adult mammalian central nervous system is the inability to regenerate after an injury. Zebrafish, on the other hand, have an astounding regenerative capacity. After a spinal cord lesion, zebrafish can re-establish the damaged neuronal network and regain their swimming ability within weeks. This is partly due to the presence of the ependymal radial glia (ERGs), which line the wall of the central canal and act as the stem/progenitor cells of the spinal cord. Under homeostatic conditions the ERGs are largely quiescent, however, the lesion triggers them to proliferate and replace cells that have been lost due to the damage. Previous studies have shown that the regeneration of the motor neurons is affected by the signalling pathways similar to those governing the first development of these cells during embryogenesis, such as Sonic hedgehog, Notch and dopamine signalling. Serotonin (5-HT), similar to dopamine, is a monoaminergic neurotransmitter with a wide range of physiological and behavioural functions. It has also been shown to play a role during development of the nervous system. In this doctoral thesis I address the hypothesis that 5-HT has a positive effect on the development and adult regeneration of motor neurons. In addition, I expand on the previously discovered augmenting effect of dopamine on motor neuron development, by analysing the downstream pathways of its action. I show that during the development, incubating embryos in 5-HT increases the proliferation of the motor neuron progenitor (pMN) cells, which leads to augmented motor neuron production. RT-PCR on FAC sorted pMN cells highlights a number of serotonergic receptors that might be responsible for this effect. Although the downstream pathways are still unknown, 5-HT appears not to act on the sonic hedgehog canonical pathway, as shown by the unchanged expression of the hedgehog effector gene, patched2 after 5-HT treatment. I show that 5-HT does not affect the generation of vsx1+ or pax2a+ interneurons, suggesting that it has a predominant effect on motor neuron production. In the intact spinal cord of an adult zebrafish, the pMN-like ERGs express serotonergic receptors, indicating they are responsive to 5-HT stimulation. After a lesion, 5-HT administration enhances the proliferation of the pMN-like ERGs caudal to the lesion site resulting in an increase in the number of newborn motor neurons. Rostral to the lesion site, administration of exogenous 5-HT does not have an effect on the ERG proliferation, possibly due to the fact that the endogenous source of 5-HT, in the form of the descending axons, is still present and might already elicit a maximal response of the progenitor cells. 5-HT does not have an effect on the proliferation of the progenitor cells dorsal or ventral to the pMNlike domain, nor does it affect the regeneration of the serotonergic interneurons. These results suggest that 5-HT from the brain preferentially contributes to the regeneration of the motor neurons. Dopamine is another monoamine shown to enhance motor neuron production during the development and regeneration. To investigate the downstream pathways of dopamine signalling on motor neuron production during embryogenesis, RNA-sequencing was performed on FAC sorted pMN cells after a treatment with a dopamine agonist, pergolide. The results yielded 14 differentially expressed genes (FDR < 0.05) with diverse functions in the cell, indicating that dopamine might act on multiple targets to promote motor neuron production. Taken together, these results demonstrate the positive effect of monoaminergic stimulation on motor neuron development and regeneration. They provide an insight into the pathways that govern the proliferation of stem/progenitor cells in the embryonic and adult spinal cord, which might contribute to the research working on enhancing adult neurogenesis in mammals.

Thesis (M.D.) -- University of Texas Southwestern Medical Center at Dallas, 2007. / Vita. Bibliography: pp. 42-45.

This investigation was conducted to determine the effectiveness of Personal Achievement Skills (PAS), a structured group psychotherapy approach, on the productivity, social functioning, self-esteem, locus of control, and life satisfaction of individuals with traumatic spinal cord injury. Subjects for the study were recruited through disability advocacy organizations, state disability service agencies, and local colleges, universities, and rehabilitation centers. The research design utilized was a randomized, pretest, posttest control group design with 15 experimental and 14 control group subjects. A behavioral Activity Questionnaire was specially designed for the study to assess productivity. It included activities such as employment, educational pursuits, social and community involvement, volunteer work, and family responsibilities. Other measures included: (a) the Affiliative Tendency Scale, (b) the Rosenberg Self-Esteem Scale, (c) the Nowicki-Strickland Locus of Control Scale, and (d) the Life Satisfaction Index. The results of the investigation indicated that PAS group participants, in comparison to the control group, improved significantly on the self-esteem measure. No such improvement was found on the other measures in the study. With regard to the self-esteem finding, male subjects responded more favorably to the PAS approach than female subjects. The issues and concerns of using the PAS approach with individuals with physical limitations were discussed along with recommendations and modifications for future research. / Graduation date: 1992

Thesis (Ph. D.)--Ohio State University, 2006. / Title from first page of PDF file. Includes bibliographical references (p. 127-155).

Injury to the cervical spinal cord is a devastating event that results in a transient to permanent loss of sensory and motor functions following injury. Moderate recovery has been reported to occur in individuals and in animal models after spinal cord injury (SCI). One approach to promote recovery after SCI is rehabilitative training. This thesis examines the relation of reaching training with adaptive changes (i.e. plasticity) and functional recovery following SCI. In my first experiment, I investigated whether plasticity of the corticospinal tract (CST) is the cause for reaching recovery after ablation of the dorsal and lateral CST. Rats that received reaching training were significantly better in reaching than their untrained counterparts. A relesion of the CST revealed that the reaching recovery mainly depended on plasticity of the CST itself. Since it is controversial whether training should be initiated immediately after SCI, I investigated whether a delayed initiation of reaching training after SCI is beneficial. I compared the reaching success of rats that received reaching training on day 4 post SCI with rats that received training on day 12 post SCI. I found that the reaching success in rats that either received reaching training on day 4 or 12 following SCI was similar. Lastly, I investigated whether training efficacy is declined in chronically injured rats. Since it has been shown that the inflammatory response after SCI declines, it is questionable whether there is a relation between the inflammatory response after SCI and training efficacy. In my last experiment I injected chronically injured rats with a substance that induces a systemic inflammation. I found that rehabilitative reaching training in chronic injured rats only resulted in an improved reaching recovery when the training was combined with the administration of the substance that induces inflammation (lipopolysaccharide). Although there are still unanswered questions regarding the underlying mechanism for functional recovery after SCI, the results of this thesis could be used as a basic to improve future rehabilitative training strategies and therefore improve the quality of life in individuals that suffer from SCI.

Thesis (Ph. D.)--Ohio State University, 2006. / Available online via OhioLINK's ETD Center; full text release delayed at author's request until 2007 May 24