Published Article / The link from medical scan images through data manipulation to additive manufacturing is well established. Various types of software are used to deliver the required .STL file(s). Often, the data manipulation will require the generation of new shapes around existing geometry, e.g. an implant that will replace missing bone tissue. This paper reports exploratory work undertaken to assess the feasibility of using haptic modelling and "virtual sculpting" software to generate novel designs of vertebrae implants for correction of spinal curvature. .STL data of several vertebrae, originating from CT scans, was imported into the Freeform system from SensAble technologies. It was used to create immutable "bucks" around which the user "sculpted" three-dimensional implant geometries. It must be noted that the designs have not been medically assessed and were for demonstration purposes only. However, the process route followed did prove to be feasible and offered some particular advantages, e.g. a precise fit between the implant and the vertebra and the possibility of enabling the direct intervention of medics in the implant design process.

Bakgrund Idag används olika medicinsktekniska produkter för helkroppsimmobilisering vid misstanke om spinal skada prehospitalt. Valet av immobiliseringsutrustning som skall användas görs av ansvarig sjuksköterska på plats. Den vanligaste utrustningen är ryggbräda, vaccummadrass, Kendric Extration Device (KED-väst) och nackkrage. Då utbildningen Pre Hospital Trauma Life Support (PHTLS) varit en del av specialistutbildningen för ambulanssjuksköterskor under en längre period har det funnits lite anledning till att ifrågasätta helkroppsimmobilisering och dess utrustning. All immobiliseringsutrustning klassificeras under klass 1 av Läkemedelsverket, vilket kan innebära att få vetenskapliga studier har gjorts för att utvärdera immobilieringsutrustning. Patientsäkerhetslagen ska efterlevas vad gäller vetenskaplig och beprövad metod i omvårdnaden av patienter med misstänkt spinal skada. Syfte Att genom en litteraturgranskning undersöka rekommendationer och eventuella risker med helkroppsimmobilisering vid misstanke av spinal skada prehospitalt utifrån patientsäkerhet och ett historiskt perspektiv. Metod Studien genomförs som litteraturgranskning med artikelgranskning och ett retrospektivt, deskriptivt perspektiv. Resultat Forskning rekommenderade helkroppsimmobilisering på traumapatienter där det fanns misstanke om spinal skada. Behandlingsriklinjerna följde nuvarande forskningsrekommendationer. Forskningskvaliten hade blivit bättre över tid och resultaten hade ökat i trovärdighet. Flera forskare påvisade risker med helkroppsimmobilisering. Riskerna var relaterade till dagens immobiliseringsutrustning. Ett antal alternativ till dagens immobiliseringsutrusning fanns beskrivna, men användes inte och var inte omnämnda i behandlingsriktlinjer. Slutsats Forskning rekommenderar helkroppsimmobilisering på traumapatienter där det finns misstanke om spinal skada. Immobiliseringutrustning har bevisligen flera risker för patienter, vilka orsakar allvarliga konsekvenser för hälsan. En lågt sittande ryggskada kanske inte behöver helkroppsimmobiliseras. Det kanske räcker med halvkroppsimmobilisering för vissa patienter. / Background Today, there are various medical devices for full body immobilisation in cases of suspected spinal injury prehospital. The choice of immobilisation devices to be used is the charge nurse’s on site. The most common equipment is back board, vaccummadrass, Kendric extraction Device (KED - West) and cervical collar. Because When training Pre Hospital Trauma Life Support (PHTLS) has been part of the specialist training of ambulance nurses over a longer period , there has been little reason to question full body immobilisation and its equipment . All immobilisation devices classified under Class 1 of the Medical Product Agency (MPA) , which may mean that few scientific studies have been done to evaluate immobilisation devices. The Patient Safety Act must be complied with in terms of scientific and proven method in the care of patients with suspected spinal injury. Aim Through a literature review examining recommendations and possible risks of full body immobilisation on suspicion of spinal injury pre-hospital based on patient safety and a historical perspective. Method The study is conducted as a literature review with the article review and a retrospective, descriptive perspective. Result Research recommended full body immobilisation on trauma patients where there was suspicion of spinal injury. Treatment guidelines followed the current research recommendations. The research quality had improved over time and results in increased credibility. Several researchers demonstrated the risks of full body immobilisation. The risks were related to today's immobilisation devices. A number of alternatives to current immobilisation devices was described, but was not used and was not mentioned in the treatment guidelines. Conclusion Research recommends full body immobilisation of trauma patients where there is a suspected spinal injury. Immobilisation devices has proven more risks for patients , which cause serious health consequences. A low sitting back injury may not need full body immobilisation. It might suffice with a half body immobilisation for some patients.

published_or_final_version / Orthopaedics and Traumatology / Master / Master of Philosophy

Research has begun to explore the presence and role of health-related injustice perceptions in samples of individuals who experience chronic pain associated with traumatic injury. Existing studies indicate that higher level of injustice perception is associated with poorer physical and psychosocial outcomes. However, to date, few clinical populations have been addressed. The aim of the current study was to explore injustice perceptions in a sample of individuals who have sustained a spinal cord injury (SCI), as research suggests that such individuals are likely to experience cognitive elements characteristic of injustice perception (e.g., perceptions of irreparable loss, blame, and unfairness). The study explored the relationship between participants’ level of perceived injustice and several variables associated with outcomes following SCI (depression, pain, and disability) at initial admission to a rehabilitation unit and at three months following discharge. The Injustice Experience Questionnaire was used to measure injustice perceptions. IEQ was found to significantly contribute to depression and anger at baseline. IEQ significantly contributed to depression, present pain intensity, and anger at follow-up. The implication of these preliminary findings may be beneficial for development of future interventions, as many individuals in the United States experience the lifelong physical and psychological consequences of SCI at a high personal and public cost.

Bakgrund: Fysiskt trauma är den vanligaste dödsorsaken bland människor under 40 år i västvärlden. Spinal immobilisering är en viktig del i det prehospitala omhändertagandet av traumapatienter där skada på kotpelare och ryggmärg kan misstänkas. Spinal immobilisering praktiseras i stora delar av världen men insatsen tar tid och innebär risker för patienten. Det saknas tydlig evidens för nytta med prehospital spinal immobilisering och behovet är stort av att veta mer om skadeutfall av traumapatienter som är vårdade i ambulans. Syfte: Syftet med studien är att undersöka förekomsten av spinal immobilisering i ambulanssjukvård av patienter som utsatts för trubbigt eller penetrerande våld samt vad för verifierade skador dessa patienter har. Metod: Kvantitativ design med retrospektiv datainsamling från ambulans- och sjukhusjournaler. Resultat: Trehundrasjutton patienter bedömda med RETTS ESS 39 granskades, medelåldern var 42 år och det var ingen skillnad i antal mellan män och kvinnor. 229 patienter spinalimmobiliserades och 27 av dessa visade sig ha någon typ av spinalskada. Resultatet visar att ingen statistiskt signifikant skillnad förelåg mellan spinal immobilisering och verifierad spinal skada. Det sågs inte heller något samband mellan andra verifierade skador och val av spinal immobilisering eller inte. Typ av trauma påverkar inte utfall av spinal immobilisering. Den vanligaste indikationen för spinal immobilisering var smärta/ömhet över kotpelaren och det var också denna indikation som visade sig vara starkast associerad till spinal skada. Diskussion: Varför så många patienter utan skada har spinalimmobiliseras kan denna studie inte svara på men slutsatsen dras att algoritmen för spinal immobilisering bör göras snävare. Detta för att undvika att spinal immobilisering utförs mer än nödvändigt. Samtidigt bedöms vidare forskning inom ämnet som nödvändigt.

背根神經節（DRG）上的初級感覺神經元通常負責感覺從環境中有害的刺激，但新出現的證據表明，它亦負責對危險的感覺。Toll-樣受體-4（TLR4）通常見於小膠質細胞，它是負責識別病原體相關分子模式（PAMPs）或損傷相關分子模式（DAMPs）並誘發炎症。奇怪的是，儘管TLR4在中樞神經系統通常見於神經膠質細胞，在DRG發現的TLR4僅見於初級感覺神經元，但從未見於周邊的衛星膠質細胞（SGC）。而重要的是，在感覺神經節中激活TLR4是會導致神經病理性疼痛的，但我們仍然未知道初級感覺神經元上的TLR4是否導致疼痛的唯一來源。本研究旨在探討在DRG細胞的TLR4信號傳導的分子和細胞機理，並探討在DRG的神經元和膠質細胞上TLR4活動的差異，在生物學上有甚麼意義。 / 為了研究在DRG神經元和膠質細胞的相互作用，我們首先在一個既定的混合DRG細胞培養模型上研究了谷氨酰胺合成酶（ GS ）的表達模式。GS是一種只會在SGC上表達的特異性酶，並於神經元和神經膠質細胞之間的谷氨酰胺 - 谷氨酸循環產生相互作用。在典型的DRG細胞培養，神經元通過擴散因子促進了GS在神經膠質細胞上的表達，然而，GS的表達亦受到TLR4激動劑，即脂多醣（LPS），的抑制。這表明DRG神經元和神經膠質細胞的關係受到TLR4介導的炎症之影響。在混合DRG細胞中，我們對TLR4-免疫反應（IR）進行了鑑定，發現TLR4最主要的是表達在神經元細胞的表面。另外，LPS（ 1微克/毫升，2小時）會刺激混合DRG細胞，通過在DRG細胞中MyD88依賴性信令，誘導環加氧酶-2（COX -2），白細胞介素-1β（ IL-1β）和腫瘤壞死因子-α（TNFα）的轉錄。此外，在DRG細胞， LPS（ 1微克/毫升， 24小時）亦會觸發依賴COX-2 的前列腺素E2（PGE₂）和的前列環素（PGI₂）的產生。但在LPS刺激後，我們發現DRG神經元和神經膠質細胞都對 COX-2-IR呈陽性反應。這證明DRG神經膠質細胞對TLR4誘發的神經炎症也擔任一定的角色。 / 為了純粹研究神經膠質細胞有沒有任何TLR4活性，我們把神經元從混合DRG細胞中除去，從而把神經膠質細胞純化。出乎意料的是，在純化後，大約80的神經膠質細胞對TLR4 -IR呈陽性反應。而且，時間和濃度依賴性的研究表明，純化後的神經膠質細胞對LPS刺激的COX-2表達反應在有效性和效率上比混合DRG細胞的顯著更高。明顯地，神經元對神經膠質細胞的TLR4活性有抑制作用。我們並且發現，神經元的抑制作用是透過由細胞與細胞之間的接觸介導，而不是由擴散因子介導。 / 重要的是， LPS也能誘導純化後的神經膠質細胞去產生依賴COX-2活性的前列腺素E2（PGE₂）。反過來， PGE₂能區別地調節依賴TLR4的炎症基因轉錄，說明在DRG 由TLR4介導的神經炎症是受多重複雜的機理控制。然而有趣的是，從受熱休克性損害的感覺神經元所收集的培養基可以激活純化膠質細胞，並通過對TLR4局部依賴性的方式，誘導COX-2的轉錄。此外，我們利用斑馬魚作為疼痛行為反應的模型，發現COXs的活性與瞬時受體電位通道亞家族V1（ TRPV1）有密切關係。斑馬魚幼蟲的疼痛行為反應是一個適合於篩選新型鎮痛化合物的體內模型。 / 總括來說，透過細胞與細胞之間的接觸和擴散因子，感覺神經元可以控制神經膠質細胞的表型。我們的研究確定感覺神經元是在DRG中表達TLR4的主要細胞類型，但當神經元施加的抑制被削弱，SGC可以成為完全勝任TLR4信息傳遞的細胞。因此我們推測TLR4的活性在DRG中被嚴格調控，以防止不必要的神經炎症發生。至於未來，我們認為在DRG中的TLR4/COX-2/PGE₂信號通路可以成為研究方的新型鎮痛化合物的方向。而轉基因斑馬魚則可用作篩選新型鎮痛化合物的工具。 / Primary sensory neurons of the dorsal root ganglia (DRG) are classically responsible for the detection of physiological stimuli from the environment, but emerging evidences suggests that they are also involved in the sensation of danger. Toll-like receptor 4 (TLR4) is commonly found on microglia for the recognition of pathogen- or damage- associated molecular patterns (PAMPs or DAMPs) and to the activation of TLR4 leads to inflammation. Curiously, while commonly found in glial cells in central nervous system, TLR4 expression was only found in primary sensory neurons but not the satellite glial cells (SGCs) in the DRG. Importantly, activation of TLR4 in sensory ganglia mediates neuropathic pain, but it remains unknown whether neurons are the only source of TLR4 activity. The present study aims to study the cellular and molecular mechanism(s) of TLR4 signalings and explore the biological significance of differential cellular TLR4 activity in the DRG. / To investigate neuron-glia interactions in the DRG, the expression of glutamine synthetase (GS), a SGC-specific enzyme in the glutamine-glutamate shuttle between neuron and glia, was studied in an established model of mixed DRG cells culture. In typical mixed DRG cell cultures, neurons promoted the GS expression in glial cells through diffusible factors. However, GS expression was negatively regulated by theTLR4 agonist, lipopolysaccharide (LPS), indicative of a change in neuron-glia relationships by TLR4 mediated inflammation. In mixed DRG cells, cell surface TLR4-immunoreactivity (-ir) was predominantly identified on the neurons. LPS (1 μg/mL, 2 h) stimulation induced cyclooxygenases-2 (COX-2), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNFα) transcription through MyD88-dependent signalings in DRG cells. Furthermore, LPS (1 μg/mL, 24 h) triggered COX-2-dependent production of prostaglandin E₂ (PGE₂) and prostacyclin (PGI₂) in mixed DRG cells. / To study the TLR4 activity of glial cells, glial cell cultures were purified by removing neurons from mixed DRG cell culture. Unexpectedly, approximately 80% of purified glial cells become TLR4-ir positive. Moreover, a time- and concentration-dependent study showed that the efficacy and efficiency of purified glial cells to express COX-2 in response to LPS was significantly higher than that of mixed DRG cells. We found that neuron inhibited glial cells through cell-cell contact, but not by diffusible factors. Importantly, LPS also induced COX-2 dependent PGE₂ production in purified glial cells. In turn, PGE₂ can differentially modulate TLR4-dependent gene transcription, suggestive of a complex regulation of TLR4-mediated inflammation in the DRG. Intriguingly, conditioned media from heat-shocked damaged sensory neurons activated purified glial cells to induce COX-2-transcription through a partially TLR4-dependent mechanism. Using zebrafish as a model of nocifensive behavior, we found that the activity of COXs was closely associated with the transient receptor potential channel subfamily V1 (TRPV1), and the nocifensive behavior of zebrafish larvae is suitable for in vivo screening of novel analgesic compounds. / To conclude, sensory neurons regulate the phenotypes of DRG glial cells through cell-cell contact and diffusible factors. Here, sensory neurons are confirmed to be the predominant cell type expressing TLR4 in the DRG, but SGCs become fully competent for TLR4 signalings when the neuronal inhibitions are diminished. We therefore hypothesize that TLR4 activity is tightly regulated in the DRG to prevent unwanted neuroinflammation. Future studies with genetically modified zebrafish can be used for the screening of novel analgesic compound targeting the TLR4/COX-2/PGE₂ signaling pathway. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Tse, Kai Hei. / Thesis (Ph.D.) Chinese University of Hong Kong, 2014. / Includes bibliographical references (leaves 190-222). / Abstracts also in Chinese.

Advances in health care science are enabling greater numbers of spinal cord injured persons to live to old age. As these persons grow older, there may be additional problems in coping due to stressors such as decreasing health and income and loss of significant others. The purpose of this study was to determine those factors that contribute to the well-being of middle-aged and elderly community-residing spinal cord injured persons. One hundred spinal cord injured persons ranging in age from 40 to 73 were interviewed. Extensive data were collected in order to investigate the relationship among social support, types of social comparisons made, perceived control, health status and psychological well-being and life satisfaction. In general, respondents reported a degree of well-being that was slightly lower than that reported in studies of nondisabled populations on the same measures of psychological well-being, life satisfaction, and depression. Pearson correlations and multiple linear regressions showed that persons reporting high levels of well-being made favorable social comparisons, reported high levels of perceived control over their lives, had high levels of social support, and judged their health status to be good. They also viewed their disability more favorably and tended to have higher incomes, more education, to be employed, and to be more religious than those indicating lower levels of well-being. The severity of the spinal cord injury was not correlated highly with subjective well-being, although there was a tendency for persons with greater disabilities to report lower levels of well-being. Persons who were younger and who incurred their disability at a younger age also tended to report higher levels of well-being. A model of well-being is proposed. This model suggests that social support fosters the perception of control and the making of favorable social comparisons which, in turn, foster a sense of well-being and satisfaction with life. This model provides direction for future research and has valuable implications for clinical application.

Previous in-vivo studies showed that compressive force acting on the spine may exceed 2600 N. However, the ligamentous lumbar spine becomes unstable when subjected to compressive loads less than 100 N. It is generally accepted that the ligamentous spine itself is unstable but can be stabilized by muscle forces (MFs) in vivo. Nevertheless, normal spinal muscle contraction patterns remain unknown. In recent in vitro studies, when the direction of the applied load was controlled along the spinal curvature so that the internal spinal load became perfect compressive follower loads (CFLs) at all lumbar levels, the ligamentous lumbar spine was found to withstand large compressive load (up to 1200 N) without buckling while maintaining its flexibility in neutral or flexed postures. The results of in-vivo animal studies also have shown that shear stress has a more detrimental effect on the rate of disc degeneration compared to compressive stress. These results suggest CFLs in the lumbar spine would be a normal spinal load whereas the transverse (or shear) load abnormal. An initial test of this postulation would be to investigate whether the spinal muscles can create perfect internal CFLs in the lumbar spine in all 3-D postures. In addition, small intrinsic muscles (SIMs) are crucial for better control of the direction of the internal spinal load along the spinal axis was also proposed. A finite element (FE) model together with an optimization model were used for this study. Both models consist of the trunk, sacrolumbar spine and 244 spinal muscles. Different from other studies, 54 SIMs were also included in the models. The FE model was validated by comparing the ROM of the spine with the literature data. Minimization of the summation of the spinal loads and moments was used as the cost function for the optimization model. The geometrical data obtained from the FE model was used as the input for the optimization model; it was then used to calculate the MFs required for creating the CFLs at all lumbar spine levels. The MFs determined in the optimization model were then imported back to the FE model as input loads to check the stability of the spine under this loading condition. Five different postures were studied: neutral, flexion 40°, extension 5°, lateral bending 30° and axial rotation 10°. Many optimization solutions for spinal muscle force combinations creating pure CFLs in the lumbar spine were found available in each posture. However, FE analyses showed that only muscle forces and patterns solved at FLPs along the curve in the vicinity of the baseline curve stabilized the lumbar spine. Stability was determined by small displacement of the trunk (less or equal to 5mm) due to small deformation of the lumbar spine. The magnitudes of joint reaction forces (JRFs) predicted from the optimization model were comparable to those reported in the literature. When the SIMs were removed, optimization solutions were still feasible in all five postures, but JRFs and trunk displacement were increased. This suggests the need of SIM inclusion in future spine biomechanics studies and clinically, damages to the SIMs may have a high risk of future spinal problems, such as spinal instability, early disc degeneration, deformity and/or early failure of spinal fixation devices. The results from this study supported the hypothesis that the perfect CFLs at all lumbar levels could be the normal physiological load under which the lumbar spinal column could support large load without buckling while allowing flexibility. SIMs played an important role in creating CFLs as by including SIMs in the models, the JRFs at all lumbar spine levels were lowered and the stability of the spine was increased.

Doctor of Philosophy / The general aim of this current work was to examine spinal cord injury (SCI), and in particular to examine the pathology of injury as it relates to changes in sensory transmission. Due to the limited possibilities for experimentation in humans, a range of animal models of SCI have been developed and are reviewed here. The weight drop SCI model is the most similar to the clinical presentation of SCI in humans and has been widely used in the rat. It was selected for the series of experiments reported in this thesis. Many of the functional deficits produced by SCI result from a cascade of biochemical events set into motion by the injury. Included amongst these is the activation of the enzyme nitric oxide synthase which produces the gaseous neuromodulator, nitric oxide (NO). NO is amongst the most widely distributed and widely utilised molecule in virtually all living organisms, and it is an important signalling molecule in the nervous system. One of the major functions performed by NO appears to relate to sensory transmission, and thus alterations in sensory transmission observed as a result of SCI may involve alterations to NO synthesis. One of the principal aims of this thesis was to examine the effect of SCI on the NO producing cells of the spinal cord and to consider what any changes in NO synthesis may suggest in regards to sensation. NO producing cells were examined using NADPH diaphorase (NADPH-d) histochemistry. As the symptoms of SCI such as motor loss and changes in sensory processing are functional changes, it was also useful to examine changes in neuronal function as a result of SCI. Widespread neuronal function was examined via immunohistochemical detection of the gene product of the immediate early gene, c-fos. It is not known how extensive the biochemical changes resulting from SCI may be, thus another of the aims of the present thesis was to examine the effects of SCI on NO synthesis not only at the level of injury, but also distant to the injury. Findings of the present thesis indicated that traumatic SCI resulted in a decrease in the number of NADPH-d positive cells from the superficial dorsal horn (SDH) of the spinal cord, while the number of these cells are increased in the ventral horn. These changes were restricted to spinal segments adjacent to the injury. Fos expression was also altered by injury and was found to decrease. The most profound changes were found to occur in lamina III, although the other laminae also demonstrated similar changes. Changes in fos expression however were notably more widespread than those for NADPH-d and were not restricted to the level of the injury, occurring at all levels of the spinal cord examined. It was interpreted that alterations in NO synthesis appear to be modulated by the local injury-induced environment while fos expression may be altered by widespread changes to the global level of activity within the central nervous system. Having observed that the number of NADPH-d positive cells of the SDH is reduced following injury, it was of interest to determine whether these cells were in fact killed, or whether they were still present but with reduced NADPH-d activity. Cell counts suggested that the NADPH-d positive cells, which were likely to represent a population of inhibitory interneurons, were not killed following injury, but rather are disrupted such that their normal biochemistry is altered. Since these cells were likely to be inhibitory and were located in laminae involved in sensory transmission, the question arose how disruption of these cells may relate to the neuropathic pain observed to develop following SCI. Thus both NADPH-d and fos expression were again examined, but this time in conjunction with the sensory function of the rats. Sensory thresholds to pain-like behaviour were determined prior to and after injury using Von Frey filaments. Rats that demonstrated a decrease in sensory threshold of at least two Von Frey filament gradations (>70%) were classed as allodynic, while those with a less than a 70% decrease in threshold were classed as non-allodynic. A subpopulation of each of the groups of rats (uninjured, non-allodynic and allodynic) underwent a somatic stimulation paradigm. It was found that stimulation resulted in an increase in the number of NO producing cells but only in the allodynic group of animals. Since this group of animals by definition would perceive this stimulation as noxious, it is likely that the noxious nature of the stimulation resulted in the increased number of NO producing cells observed. This effect occurred only in segments adjacent to the injury. When fos expression was examined in the uninjured animals it was noted that somatic stimulation resulted in a decrease in fos expression, almost exclusively in lamina III. Following injury, there was no change in fos expression in lamina III observed. Instead the only change observed was an increase in fos expression in the deep dorsal horn (DDH, lamina IV and V). This occurred most profoundly in the allodynic group. These results suggested that SCI may lead to misprocessing of sensory signals such that non-noxious somatic stimuli are processed in the DDH rather than lamina III following SCI. It is proposed here that this change in laminae processing may be responsible for the perception of pain towards a non-noxious stimulus, and that the reported injury-induced loss of NO producing inhibitory interneurons in the SDH may be responsible for this alteration in sensory processing following SCI. Sensation is also processed by a number of supraspinal structures and a number of these have been implicated in the development of neuropathic pain states. The effects of SCI on neuronal activity as well as NO synthesis were examined in the periaqueductal grey region of the mid brain (PAG). SCI was shown to result in reduced neuronal activity in the PAG. This reduction in activity did not follow the somatotopy of the lateral column of the PAG (lPAG). It was suggested the reduced activity may not be solely caused by reduced spinal input as a result of SCI. Reduced neuronal activity in the PAG may indicate reduced PAG function, which includes descending modulation of spinal sensory transmission. Injury was not found to alter NADPH-d expression in the PAG. The effect of traumatic lumbar SCI on the parietal (sensorimotor) cortex of the rat was also examined, as loss of inputs following SCI have been shown to result in a profound reorganisation of the cortex. Results indicated that SCI results in a virtual cessation of neuronal activity in areas 1 and 2 of the parietal cortex, likely as a result of lost afferent drive. Theories of cortical plasticity suggest that while the primary inputs via the lumbar spinal cord may be lost following SCI, other less dominants input will remain and become more dominant. It has been proposed previously that cortical reorganisation involves a rapid reorganisation of the entire sensory system. It was interpreted that a similar process may explain the system-wide reduction in neuronal activity observed in the present series of studies.

Thesis (Ph. D. in Biomedical Engineering)--Vanderbilt University, May 2007. / Title from title screen. Includes bibliographical references.