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SUMMARY Objective of the study. To assess the need of nursing care for patients with spinal cord injury during the early in-patient rehabilitation period. Methods. During the study, thirty-two patients following an acute spinal cord injury, hospitalized in the Neurorehabilitation Unit of the Rehabilitation Division at the Kaunas University of Medicine Hospital, were inquired, examined and cared for. The contingent of studied patients consisted of paraplegic individuals with retained upper limb functions who could fill in themselves a questionnaire, which included 22 questions. Results. The obtained data have shown that 10 women participating in the study were older than 22 men (p £ 0.05): the average age of the women (in the range of 28 to 70 years) was 41 years whereas of the men (in the range of 19 to 52 years), 33.86 years. A reliable correlation according to the Kendall coefficient was determined between the patients self–assessment and the real mobility of the studied individuals. The data of the study have shown that 17 (54.5 percent) of the patients with disturbed urinary function were febrile. The fever was assessed in all 7 patients with continuously indwelled Foley catheters (p £ 0.05), whereas in 15 cases of intermittent catheterization just 5 (33.3 percent) of the patients were febrile (p £ 0.05). The employment of the Fisher criterion has shown that in cases of continuously indwelled Foley catheters for the urinary bladder drainage and the presence of fever... [to full text]

Neuropathic pain is a significant and frequent outcome of spinal cord injury (SCI), and is often refractory to treatment. A better understanding of the pathological processes following injury that contribute to the development of neuropathic pain will aid the search for novel therapeutics. In the second chapter of this thesis a murine model of post-SCI below-lesion neuropathic pain was utilized to investigate changes in GABAergic tone. The gad1:GFP transgenic mouse line allowed the study of a subpopulation of GFPlabeled GABAergic neurons under control of the GABA synthesizing glutamate decarboxylase enzyme. SCI was observed to result in a loss of GABAergic neurons, and secondary markers of GABAergic tone supported this observation. This finding suggests that GABAergic interneuron cell death accounts for the decreased GABAergic tone previously reported post-SCI. In the third chapter of this thesis it was attempted to prevent the death of GABAergic neurons post-SCI using a transgenic mouse line expressing increased levels of the X-linked inhibitor of apoptosis (XIAP) under the ubiquitin C promoter. No differences were observed between ubXIAP and wildtype mice, indicating that increased expression of XIAP is not sufficient to prevent the development of neuropathic pain post- SCI. The fourth chapter of this thesis attempted to prevent the development of neuropathic pain through a novel treatment schedule of the drug pregabalin. Pregabalin administered shortly after SCI prevented the development of neuropathic pain. Pregabalin initiated 1 week post-SCI had no effect. Early pregabalin treatment did not appear to dramatically alter glial activation, or expression of the pregabalin receptor, but we observed changes in markers associated with synaptic plasticity. My findings build upon our knowledge of the mechanisms underlying post-SCI below-lesion neuropathic pain, and suggest new avenues of research, such as the uses of preemptive treatment with pregabalin, that offer promise for translation to clinical use.

Following spinal cord injury (SCI), up to 70% of patients develop a condition known as autonomic dysreflexia (AD). This study investigates the use of Pregabalin as a preemptive treatment to mitigate the development of AD following SCI in an animal model. Saline-treated and dPGB rats (first Pregabalin treatment 7 days post-SCI) demonstrated typical signs of AD, with mean arterial pressure (MAP) increases of 23.5% and 27.4% respectively, following colon distension. In contrast, iPGB animals (first Pregabalin treatment 1 hour post-SCI) had MAP increases of 14.6%; significantly lower than saline-treated animals. Additionally, iPGB animals had significantly lower urine volumes than saline-treated animals on days 9 and 10 post-SCI, indicating a more rapid return of spontaneous bladder voiding. It was concluded that only treatment with Pregabalin immediately following SCI can alleviate large increases in blood pressure that accompany AD episodes. Immunostaining for substance P revealed a significantly higher density in both the dorsal horn and central autonomic area in iPGB animals when compared to saline-treated and uninjured animals, indicating a possible mechanism of sympathetic inhibition following iPGB treatment.

Approximately two-thirds of patients will experience pain following spinal cord injury (SCI). This pain can arise as an immediate consequence of SCI, or can develop over time into chronic, neuropathic pain. Individuals are frequently prescribed opioid analgesics, including morphine, for the treatment of pain in both the acute and chronic phases of SCI. Yet, despite the prevalence of opioid use, no studies have examined the addictive potential of opioids, or their secondary effects, following spinal injury. These experiments used a clinically relevant self-administration paradigm to examine both addiction and functional recovery after morphine administration. To assess morphine administration in the acute phase of SCI, animals were placed in operant chambers 24-hours following spinal injury. In the chambers, depression of a reinforced lever resulted in an intravenous infusion of morphine (or vehicle). Animals were placed in the chambers for 7, 12-hour sessions and could administer up to 30 mg of morphine per session. Morphine self-administration was also examined in the chronic phase of injury. Animals were placed into operant chambers for 7, 12-hour sessions beginning 14 or 35 days after injury. The amount of morphine administered, as well as recovery of locomotor function and general health, was compared across subjects with SCI and sham (no injury) controls. In the acute phase of injury, SCI significantly reduced self-administration of morphine, but administration led to decreased recovery of locomotor function and weight loss. In the chronic phase of injury, self-administration did not differ between contused and sham animals. All subjects administered the full amount of morphine available each day. In this phase of injury, morphine administration led to significant weight loss, but did not attenuate recovery of locomotor function. These studies suggest that spinal injury reduced the addictive potential of morphine in the acute, but not the chronic, phase of SCI. However, acute administration of high doses of morphine decreased recovery of locomotor function. Morphine should not be used in this phase of injury for the clinical treatment of pain. In the chronic phase, opioid use must be closely monitored as use may result in addictive behavior.

Altered sexual function is one of the most devastating consequences of spinal cord trauma (SCT). Despite this fact, current knowledge of the neural circuitry regulating sexual response in the spinal cord (SC) in healthy humans is remarkably incomplete. In order to better understand the changes that occur to sexual responses following SCT, we must elucidate the neural transmission of sexual function in healthy humans. Functional magnetic resonance imaging (fMRI) techniques to map neuronal function have been adapted for the SC and can now reveal this neural circuitry. We mapped, with spinal fMRI, neuronal activity in the lower thoracic, lumbar and sacral SC in healthy men (n = 10) and women (n = 9) that occurs in response to intermittent audiovisual stimulation (AVS), intermittent genital self-stimulation (GSS) and the combination of the former and latter, applied continuously and simultaneously until orgasm (AVGSS). MR images revealed predominantly increased signal intensity changes (ΔS+) in the autonomic preganglionic nuclei of the lower thoracic, lumbar and sacral SC in women and mostly decreased signal intensity changes (ΔS-) in comparable regions in men. In functional MR images, ΔS+ are related to increased neuronal input while ΔS- are associated with diminished neuronal input to a particular region. Linear regression analyses uncovered a greater number of inverse correlations between SC ΔS and scores of sexual function in women than in men indicating greater descending modulation of SC circuits regulating sexual responses in women than in men. Taken together, our results demonstrate that spinal fMRI is an effective and sensitive technique that can reveal signal intensity changes in the lower thoracic, lumbar and sacral SC associated with AVS, GSS and AVGSS in healthy men and women. / Thesis (Master, Neuroscience Studies) -- Queen's University, 2009-10-06 21:26:15.011

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Compared with our knowledge concerning the responses to exercise of able-bodied athletes there is relatively little known about the exercise responses of athletes who have a spinal cord injury (SCI). The purpose of this thesis was to examine the physiological characteristics of endurance trained wheelchair athletes; to assess the importance of various physiological factors to the endurance performance of wheelchair athletes; to describe and examine the physiological and metabolic responses and performances of wheelchair athletes to endurance and brief high intensity exercise; and to assess the influence of level of SCI or wheelchair racing class on these responses to exercise. The mean peak oxygen uptake (V02 pk) achieved by the group of 27 wheelchair athletes during wheelchair treadmill exercise was 2.11 ±0.53 I. min-1. When the athletes were grouped according to the paralympic racing classification system (TK2; TK3; TK4) the V02 pk values were 1.28 ±0.16 l. min-1,2.10 ±0.43 I. min-1 and 2.32 ±0.52 I. min-1 respectively. The mean peak heart rates of these groups were 112 ±4 b. min-1,190 ±9 b. min-i, and 200 ±9 b. min-1 respectively. The relationship between V02 pk and endurance performance (r=-0.69; p<0.01) was not as high as found between % V02 pk utilised at a given submaximal propulsion speed (r=0.89; p<0.01) or a propulsion speed equivalent to a reference blood lactate concentration (BLA) of 4 mmol. l-1 (r=-0.87; p<0.01). During a 10 km treadmill trial the group of athletes maintained a speed equivalent to 78.4 ±13.6% V02 pk. The TK2 racing class appeared to exhibit lower heart rates and respiratory exchange ratio (R) values throughout the test than the other racing classes. During a one hour endurance test at 80% of top speed (TS), an exercise intensity meaningful to the wheelchair athlete, the group were working at 64.6 ±13.5% V02 pk. The responses observed were indicative of steady state exercise. Oxygen uptake and ventilation rate remained stable, there was no cardiovascular drift, there was a decrease in R value, BLA peaked after 15 minutes and then decreased throughout the remainder of the test. Blood glucose (BGL) concentrations remained similar to the value observed at rest throughout the test. In general, it was found that wheelchair athletes were able to maintain a propulsion speed equivalent 75% V02 pk for prolonged periods of time, irrespective of their level of SCI. There were no differences between the physiological and metabolic responses of the two paraplegic racing classes. The tetraplegic group appeared to exhibit lower heart rates, BLA, BGL and R values throughout the duration of the test. The concentrations of plasma free fatty acid, glycerol, ammonia and urea postexercise indicated a tendency towards higher values in the wheelchair racing class with the lowest lesion level athletes (TK4). During a 20 s high intensity exercise fixed work test there was greater metabolic activity in the TK2 racing class than the TK4 racing class. The metabolic responses of the TK3 racing class to this test were, in general, between these two groups. A 30 s arm sprint resulted in a decrease in power output of greater than 50% for each racing class. The mean power outputs (MPO) generated by the TK2, TK3 and TK4 racing classes were 100.2 ±21.7 W, 188.3 ±48.9 W and 247.2 ±40.3 W respectively. The physiological and metabolic responses showed a similar tendency. A 30 s test at 80% MPO showed that the metabolic responses of each racing class were similar. The results of the thesis suggest that the amount of muscle mass available for recruitment during exercise and the degree of disruption to the sympathetic nervous system play an important role in determining the responses to exercise and the racing performance of wheelchair athletes with a SCI.

Previous research has demonstrated that the spinal cord is capable of a simple form of instrumental learning. In this instrumental learning paradigm, rats typically receive a complete spinal transection at the second thoracic vertebra, and are tested 24 hours after surgery. Subjects that receive shock to a hind leg quickly learn to maintain the leg in a flexed position, which reduces net shock exposure (Grau et al., 1998). Prior studies have examined the mechanisms that mediate this learning, but little is known about how or where the consequences of learning are stored (memory). The goal of this dissertation proposal is to examine the neural modification(s) that preserve learned behavioral effects over time. It is clear that the central nervous system plays an essential role in instrumental learning. During the acquisition of instrumental learning, the connections between the peripheral nervous system (PNS) and the central nervous system must remain intact (Crown et al., 2002a). Acquisition is also disrupted by intrathecal application of pharmacological agents (lidocaine) that inhibit spinal reflexes (Crown et al., 2002a). The experiments outlined in this dissertation are motivated by an unexpected observation: while application of lidocaine to the spinal cord prior to training blocks acquisition of the instrumental response, inactivating spinal neurons has no effect on the maintenance of the instrumental response. These data suggest that, after the instrumental response is acquired, a peripheral component is capable of maintaining the instrumental response. Aim 1 examined how inhibiting the spinal cord influenced the maintenance of instrumental learning. Intrathecal lidocaine inhibited a spinal withdrawal reflex and instrumental learning, but did not affect the maintenance of the learned response. Expanding on these results, Aim 2 examined how disconnecting the PNS from the spinal cord would influence the maintenance of instrumental learning. If a PNS to spinal cord connection is needed for the maintenance of instrumental learning, then removing that connection by a sciatic transection should disrupt performance of the instrumental response. Together, the results of Aims 1 & 2 confirm that a peripheral alteration contributions to the maintenance of instrumental behavior. In Aim 3, I developed a procedure that would allow for drug delivery directly to the tibialis anterior muscle. If the neuromuscular junction is capable of influencing a spinal reflex, then blocking the neuromuscular junction with an antagonist (curare) should disrupt the acquisition and maintenance of the instrumental response. Based on the results of Aim 3, Aim 4 investigated how other pharmacological manipulations at the neuromuscular junction can influence the acquisition and maintenance of the instrumental response. Using glutamate receptor antagonists (CNQX and MK-801), I showed that glutamatergic signaling plays an essential role.