Thesis (Ph. D.)--West Virginia University, 2010. / Title from document title page. Document formatted into pages; contains x, 102 p. : ill. (some col.). Includes abstract. Includes bibliographical references.

The present study aimed at investigating the neuropsychological sequelae of transient ischaemic attacks. Transient ischaemic attacks are defined as those neurological disorders in which there is complete resolution of neurological symptoms within twenty·four hours. Transient ischaemic attacks may or may not reveal evidence of brain infarcts on imaging studies. In the present study, the neuropsychological sequelae of transient ischaemic attacks in the carotid circulation were investigated since, within the perspective of cognitive neuropsychology, it was assumed that localized changes in cognitive functions could be demonstrated.Since several psychological, medical and neurological factors are known to influence scores·on neuropsychological tests, regression analyses were performed to determine which factors contributed significantly to the variance of scores on neuropsychological tests in the transient ischaemic attack and control groups. Two transient ischaemic attack groups, each comprising forty left and forty right hemisphere involvement patients, were then compared with each other and with a control group of forty general medical patients. Stenosis of the carotid artery formed a significant predictor of test scores in the combined transient ischaemic attack group. When the groups were·analyzed independently, in the left transient ischaemic attack group stenosis predicted performance on the same tests reaching significance for the combined group, and for the Wisconsin Card Sorting Test (Perseverative Score). In the right transient ischaemic attack group, stenosis significantly predicted performance on Digits Forward, Backward and Total, the PASAT (2.4 seconds) and Trails B. On the other hand, education formed a significant predictor of performance on Digits Forward, Digits Backward and Digits Total and the PASAT (all levels) in the control group. Multivariate comparisons revealed that the left and right transient ischaemic attack groups performed worse than the controls on tests of attention, concentration and conceptual flexibi1ity. The left transient ischaemic attack group performed worse than the right transient ischaemic attack group on all tests of attention and concentration, but there was a significantly better performance of the former group on the Rey Auditory Verbal Learning Test (Trial 1), Block Designs and Verbal Fluency. The findings on the PASAT that left transient ischaemic attack patients performed significantly worse than the right hemisphere group ·were considered to be relatively unreported previously in the literature on transient ischaemic attacks. The findings obtained are discussed from a neurocognitive perspective of neuropsychological functioning in transient ischaemic attacks. / Psychology / Ph. D. (Psychology)

published_or_final_version / Anatomy / Doctoral / Doctor of Philosophy

published_or_final_version / Anatomy / Master / Master of Philosophy

<p>Supratherapeutic doses of anabolic androgenic steroids (AASs) are administered, not only as performance-enhancing drugs in the world of sports, but also in order to modify behaviour. AAS abusers are at risk of developing serious physical and psychological side effects such as dependence and aggressive behaviour. The aim of this thesis was to investigate the impact of supratherapeutic doses of nandrolone decanoate after subchronic administration on dopamine and serotonin pathways involved in drug dependence and aggression, in the male rat brain.</p><p>Adult male Sprague-Dawley rats received intramuscular injections of nandrolone decanoate (3 or 15 mg/kg) or vehicle once daily for 14 days. Nandrolone decanoate pre-exposure abolished the effect of amphetamine on the 3,4-dihydroxyphenylacetic acid (DOPAC) tissue level in the hypothalamus and on the DOPAC/dopamine ratio in the hypothalamus and the hippocampus. A significant decrease of the basal extracellular DOPAC and homovanillic acid (HVA) levels could be detected in the nucleus accumbens, which remained low during the first hour following the amphetamine challenge. Nandrolone decanoate significantly reduced the activity of both monoamine oxidase A and B (MAO-A and -B) in the caudate putamen and amygdala. The gene transcript levels of MAO-B, and the dopamine D1 and D4 receptors were altered in limbic regions. No changes in transcriptional levels could be detected among the serotonin receptor genes examined. However, the density of the serotonin transporter protein was elevated in a range of aggression-related brain regions.</p><p>Taken together, subchronic administration of nandrolone decanoate causes dopaminergic and serotonergic dysregulations in distinct brain regions. These areas of the brain are involved in the development of drug dependence and expression of impulsive and aggressive behaviours. These results may contribute to explain some of the behavioural changes often reported in AAS abusers, such as polydrug use and impaired impulse control.</p>

Arthropods are the most species-rich group of animals, and as such they exhibit an amazing diversity of morphological, behavioral, and ecological adaptations. Because of this diversity, the evolutionary history of this group has been, and still is notoriously difficult to determine because considerations of different traits invariably support alternative evolutionary relationships. Their nervous systems provide an invaluable set of characters for systematic inferences about the origins and evolutionary trajectories of Arthropoda. This is because nervous systems are ubiquitous and contain a wealth of structures from which to infer shared ancestry. Considerations of ancestral arthropod relationships have further provided insights into how arthropod nervous systems have maintained some traits through evolutionary time and how others have been modified or acquired as novelties. This dissertation explores the evolution of arthropod brains within an interdisciplinary framework, utilizing comparative neuroanatomical, neural cladistic, and molecular phylogenetic analyses to support novel hypotheses of nervous system evolution in arthropods. The field of neurophylogenetics relies on the characterization of shared derived neural traits to infer ancestry amongst taxa. The first portion of this work describes highly conserved neural elements from the lamina, or first optic neuropil, of several crustaceans. This study is followed by a neural cladistic study that infers evolutionary relationships amongst major arthropod groups based solely on neural traits. The results of this study are then compared to those from a large-scale molecular phylogenomic analysis of hundreds of conserved orthologous genes. Results from neural cladistic and molecular phylogenetics suggest several species whose neuroanatomical characterization would provide support for novel evolutionary hypotheses. The last portion of this dissertation details a comparative neuroanatomical study on one such diagnostic taxa, the copepod Tigriopus californicus. Two principles of arthropod nervous system organization and evolution are repeatedly supported with this approach: 1) many complex neural structures shared amongst arthropod groups have been inherited from ancient common ancestors, suggesting that the neural arrangements seen today have been carried over from antiquity; and 2) these same complex attributes are absent in numerous late-diverging lineages, supporting the hypothesis that secondary simplification of nervous systems is a common property of arthropods.

Capacity to perform prolonged exercise is reduced in high ambient temperatures, but this premature fatigue is not adequately explained by peripheral mechanisms. The aim of this thesis was to examine some possible underlying mechanisms of central fatigue operating during prolonged exercise in a warm environment. The first series of experiments investigated the effect of nutritional manipulation of central serotonergic activity through alterations to the plasma concentration ratio of free-tryptophan to branched-chain amino acids (f-TRP:BCAA). In contrast to previous reports, acute BCAA supplementation failed to alter perceived exertion and delay the onset of fatigue (Chapter 3). This response was similar when exercise was preceded by an exercise and diet regimen designed to reduce glycogen availability (Chapter 4). The ingestion of meals containing added carbohydrate and fat did not alter f-TRP:BCAA at rest (Chapter 5). Acute dopaminergic / noradrenergic reuptake inhibition with bupropion increased exercise perfonnance by 9 % in warm conditions (30C), but this effect was not apparent at 18C (Chapter 6). This response was accompanied by attainment of a higher core temperature and heart rate towards the end of the bupropion trial in the heat despite no detectable difference in perceived exertion and thermal stress. These data suggested that maintenance of catecholaminergic activity may dampen inhibitory signals from the CNS due to the attainment of a high core temperature, allowing power output to be maintained. The blood-brain barrier (BBB) regulates the exchange of substances between the cerebral interstitial fluid and the blood to maintain a stable environment for the CNS. If the BBB is compromised this may adversely influence nonnal brain function. Serum S1OOb, a proposed peripheral marker of BBB penneability, was increased following exercise in a warm environment (Chapter 7). These data indicate that exposure to combined exercise and heat stress may result in a loss of BBB integrity.

Introduction: Pulmonary Surfactant reduces surface tension in the terminal airways thus facilitating breathing and contributes to host's innate immunity. Surfactant Proteins (SP) A, B, C and D were recently identified as inherent proteins of the CNS. Aim of the study was to investigate cerebrospinal fluid (CSF) SP levels in hydrocephalus patients compared to normal subjects. Patients and methods: CSF SP A-D levels were quantified using commercially available ELISA kits in 126 patients (0±84 years, mean 39 years). 60 patients without CNS pathologies served as a control group. Hydrocephalus patients were separated in aqueductal stenosis (AQS, n = 24), acute hydrocephalus without aqueductal stenosis (acute HC w/o AQS, n = 16) and idiopathic normal pressure hydrocephalus (NPH, n = 20). Furthermore, six patients with pseudotumor cerebri were investigated. Results: SP AÐD are present under physiological conditions in human CSF. SP-A is elevated in diseases accompanied by ventricular enlargement (AQS, acute HC w/o AQS) in a significant manner (0.67, 1.21 vs 0.38 ng/ml in control, p<0.001). SP-C is also elevated in hydrocephalic conditions (AQS, acute HC w/o AQS; 0.87, 1.71 vs. 0.48 ng/ml in controls, p<0.001) and in Pseudotumor cerebri (1.26 vs. 0.48 ng/ml in controls, p<0.01). SP-B and SP-D did not show significant alterations. Conclusion: The present study confirms the presence of SPs in human CSF. There are significant changes of SP-A and SP-C levels in diseases affecting brain water circulation and elevation of intracranial pressure. Cause of the alterations, underlying regulatory mechanisms, as well as diagnostic and therapeutic consequences of cerebral SP's requires further thorough investigations.

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Introduction: Aging, comorbid conditions, and use of medications render older adults more susceptible to alcohol-disease or alcohol-drug interactions that may lead to harmful outcomes. In this dissertation project the risk profile of alcohol and medications use among older adults was investigated. Considering the rise in CNS-acting medication use and the adverse effect profile linked to CNS-acting medications, it was also of interest to find if older adults were at risk of falling due to interactions between alcohol and CNS-acting medication. Objectives: The objectives were as follows: 1) to determine the prevalence, pattern and factors associated with at-risk drinking, 2) to determine the prevalence and pattern of potential concurrent use of CNS-acting medication and alcohol, and to identify factors associated with alcohol use among CNS-acting medication users, 3) to assess the effects of potential concurrent use of CNS-acting medications and alcohol on the risk for falls in older adults. Methods: The study population comprised a nationally representative sample of community-dwelling older adults aged 65 years or older. The 2009 Medicare Current Beneficiary Survey (MCBS) data (n=7163) were employed to determine at-risk drinking based on the Comorbidity Alcohol Risk Evaluation Tool (CARET) and to assess the effects of potential concurrent use of CNS-acting medication and alcohol on the risk for falls. The National Health and Nutrition Examination Survey (NHANES) 2005-2010 data (n=3220) were employed to determine potential concurrent use of alcohol and CNS-acting medications. The effect of combined use of alcohol and CNS-acting medications on risk of falls was assessed using logistic regression modeling and adjusting for confounders. Alcohol consumption was measured by the quantity-frequency method and the National Institute on Alcohol Abuse and Alcoholism (NIAAA) recommended drinking limits were utilized in all analyses. Results: In the MCBS study, 5.6% of the older adults were identified as at-risk drinkers. Adults aged between 65-74 years, being male, non-married, former or current smoker, and having no comorbid conditions were factors associated with at-risk drinking. In the NHANES study, 8.9% reported potential concurrent use of alcohol and CNS-acting medication. Use of at least one CNS-acting medication and drinking excessive alcohol, or binge drinking, was significantly associated with odds of falling. Conclusion: Hazardous alcohol use is common among older adults. A substantial proportion of older adults may concomitantly consume alcohol and CNS-acting medications. Odds of falling are greater in the presence of high alcohol intake and CNS-acting medication use. It is important for health care professionals to warn patients against excessive alcohol consumption. Increasing awareness of this issue among older adults and caregivers may help prevent falls. Contributions from healthcare professionals in the form of screening for potentially harmful alcohol use, prescription monitoring, and initiating counseling may help to reduce older adults’ risk for falls or other adverse effects.