Thesis (M.S.)--Oregon State University, 2010. / Printout. Includes bibliographical references (leaves 87-92). Also available on the World Wide Web.

Thesis (M.A.) - Simon Fraser University, 2007. / Theses (Faculty of Education) / Simon Fraser University. Senior supervisor: Stephen Smith -- Faculty of Education. Also issued in digital format and available on the World Wide Web.

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Psychopathy is a complex personality disorder denned by a constellation of affective and behavioral characteristics. There is accumulating behavioral evidence suggesting that the condition is associated with impairments in affective, cognitive, and language functions. However, relatively little is known regarding the neural systems underlying these abnormalities. The present thesis is comprised of five experiments designed to elucidate and characterize the abnormal functional architecture underlying these abnormalities in psychopathic criminals. In Experiments 1 and 2, functional magnetic resonance imaging (fMRI) was used to elucidate the neural systems underling abnormal semantic and affective processes in these individuals. In Experiments 3, 4 and 5, event-related potentials (ERPs) were used to characterize the temporal features of cognitive and language functions in psychopaths. The results from Experiment 1 revealed that compared to control participants, psychopaths performed more poorly and failed to showed the appropriate neural differentiation between abstract and concrete stimuli during a lexical decision task. These deficits were located in the right anterior superior temporal gyrus. The results from Experiment 2 indicated that psychopaths, relative to control participants, showed less activation for processing affective stimuli than for neutral stimuli in several neural regions, including the right amygdala/hippocampal formation, left parahippocampal gyrus, ventral striatum, and in the anterior and posterior cingulate. Psychopaths did show greater activation for processing affective than for neutral stimuli in regions located outside the limbic system, including bilateral inferior frontal gyrus. These latter data suggesting that psychopaths used different neural systems than did controls for performing the task. The results from Experiments 3 and 4 indicated that psychopathy is associated with abnormalities in the P3 ERP component elicited by target stimuli during visual and auditory oddball tasks. In addition, the psychopaths' ERPs to visual and auditory target stimuli were characterized by large fronto-central negativities in the 350-600 millisecond time window. These fronto-central ERP negativities are similar to those observed for patients with temporal lobe damage. In Experiment 5, using a standard sentence processing paradigm, no group differences were observed between psychopaths and nonpsychopaths in the amplitude of the N400 potential elicited by terminal words of sentences that were either congruent or incongruent with the previous sentence context. These results indicate that the abnormal fronto-central ERP negativities observed in previous studies of language function in psychopaths are not related to processes involved in the generation of the N400. Taken together, these data suggest that one of the cardinal abnormalities in psychopathy is abnormal semantic processing of conceptually abstract information and affective information and that these abnormalities are related to the function of neural circuits in the anterior temporal lobes and lateral frontal cortex.

Purpose: To highlight the histopathological characteristics of the skin in congenital clubfoot and correlate the clinical findings in clubfoot with the changes in the dermal layers. Materials and methods: One hundred skin specimens, from 77 infants (6 to 12 months), were studied between 2004 and 2008. Using the Pirani scoring system, the clinical severity was recorded. The mobility of the skin and the correctability of the medial ray were assessed clinically. A skin specimen (1cm x 1mm) was taken from the medial side of the foot at surgery following failed plaster treatment. The layers were studied under light microscopy. The thickness of the dermis and the histopathological features of clubfoot skin were compared with 10 normal skin specimens. Results: The dermis of clubfoot skin showed significant fibrosis with thick bundles of collagen fibres (P = .001) on Haematoxylin and Eosin staining (H&E). The dermal thickness ranged between 1.0mm and 5.2mm in clubfoot skin, compared with controls (0.64-1.28mm). Fibrosis extended into the subcutis in a septolobular fashion in 95% of the cases. Significant atrophy of eccrine glands was seen in 98% (P = .001). Hair follicles were absent in 78%. The elastic fibres of clubfoot skin, stained with Elastic van Gieson staining (EVG), showed hypertrophy in varying degrees in all skin specimens. They were fragmented, with loss of their parallel arrangement. There was no significant inflammatory reaction in the dermis. The Pirani score was significantly increased (mean 7.8). Discussion: Fibrosis and thickening of the dermis were the most significant histopathological features of the clubfoot skin. The elastic fibres were also abnormal. There was atrophy of the skin appendages due to the fibrosis. There was a strong correlation between the Pirani score and the severity of the deformity(P 0.016). The cases with poor outcome had a higher score than those with a satisfactory outcome.Lack of a significant inflammatory reaction suggests that neither the serial manipulations of the foot, nor the repeated plaster cast changes, were responsible for the dermal fibrosis, which is probably present from birth and contributes to the deformity. / Thesis (Ph.D.)-University of KwaZulu-Natal, Durban, 2012.

Title:EFFECTS OF THE PROMINENCE OF FIRST HARMONIC ON THE PERCEPTION OF BREATHINESS AND VOWEL IDENTITY Authors: Emily Lin, Samuel Sloane,and Donal Sinex Background: Human communication relies on adequate speech intelligibility to enable the comprehension of verbal messages. Dysphonia (i.e., aberrant voice) may not only result in distraction during communication but also interfere with speech intelligibility leading to a communication barrier. One voice quality commonly found in dysphonia is breathiness, which is related to the presence of excessive airflow during phonation due to incomplete glottal closure. Breathiness has been associated with the prominence of the first harmonic (H1) in the acoustic analysis of voice. Objectives: This study aimed to determine whether excessiveness in the first harmonic (H1) dominance, which has been associated with breathy voice, may result in the perception of breathiness and compromise vowel intelligibility. Methods: Participants included 10 female and 10 male normal-hearing adults, aged between 19 to 40 years. Participant’s tasks included a “breathiness rating” and a “vowel identification” task. For the “breathiness rating” task, a direct magnitude method was employed for the participant to rate a 500-ms long vowel (/i/ and /a/) segmented from sustained vowel phonation. For the “vowel identification” task, the vowel stimuli were segmented out from running speech (“Rainbow passage”) and the participants were asked to listen to one vowel stimulus (/i/, /a/, or /o/; duration: 60 ms) at a time and indicate which vowel (i.e., /i/, /e/, /a/, /o/, or /u/) they perceived the stimulus to be. The vowel stimuli included processed and unprocessed voice recordings of individuals with and without voice disorders. Voices showing the lowest, median, and highest amplitude differences between the first two harmonics (H1-H2) were chosen from a voice database for female and male voices respectively. The 18 selected vowel signals (3 vowels X 3 H1-H2 levels X 2 speaker genders) were processed through 12 signal manipulation conditions. The 12 signal conditions involved increasing or decreasing the H1 amplitude of the original signals in six 2-dB interval steps in both directions. Results: For the “breathiness rating” task, the five-way (3 vowels X 2 speaker genders X 3 H1-H2 levels X 13 signal conditions X 2 listener genders) Mixed Model Analysis of variance (ANOVA) conducted on the breathiness scores for normal speakers and voice patients separately showed significant findings for various main and interaction effects, such as a significant speaker gender by signal condition by vowel interaction effect on the perception of breathiness [F(12, 96) = 1.95, p = 0.038] for normal voice. An increase of H1-H2 through signal manipulation led to an increase of perceived breathiness only when performed on the vowel /i/ produced by female normal speakers. As for the “vowel identification” task, a relationship between H1-H2 increment and vowel intelligibility was found but the relationship was affected by vowel type, speaker gender, and H1-H2 level. With all vowel types, speaker genders, and H1-H2 levels combined, a significant signal condition effect on the number of incorrect vowel identification was found (2 = 188.585, df = 10, p < 0.001). Generally, it appeared that an increase of H1-H2 would worsen the identification of /i/ but enhance that of /o/. Conclusion: The relationship between H1 dominance and perceived breathiness was non-linear. Factors found to disrupt the linear relationship included speaker gender, vowel type, and the extent of H1 dominance. In addition, there was evidence that acoustic manipulation of the H1 amplitude would affect vowel intelligibility and the relationship between vowel intelligibility and H1-H2 values also vary by speaker genders and vowel types.

Pathological Gambling (PG) is an impulse control disorder with lifetime prevalence of 1-3%. Available treatments are limited by uncertain classification and complexity of implicated neurotransmitter systems. Dopamine (DA), a key neurotransmitter implicated in addictive behavior and reward is elevated in response to gambling and psychostimulants. Based on previous research, it was hypothesized that the D2 blocker, haloperidol (HAL), will enhance slot machine reinforcement in PG but not in Healthy Controls (HC). If this increase reflects preferential stimulation of D1 receptors and group differences in D1 sensitivity, D1-D2 blocker (fluphenazine, FLU) should offset increase in reinforcement seen with HAL in PG subjects. In line with DA's implicated role in 'wanting' vs. 'liking' of the addictive reinforcer, the results suggest that DA release mediated partial D1 activation under FLU led to clear differentiation between groups with increased 'wanting' seen in controls but not in gamblers. DA's role in 'liking' however remains elusive.

Pathological Gambling (PG) is an impulse control disorder with lifetime prevalence of 1-3%. Available treatments are limited by uncertain classification and complexity of implicated neurotransmitter systems. Dopamine (DA), a key neurotransmitter implicated in addictive behavior and reward is elevated in response to gambling and psychostimulants. Based on previous research, it was hypothesized that the D2 blocker, haloperidol (HAL), will enhance slot machine reinforcement in PG but not in Healthy Controls (HC). If this increase reflects preferential stimulation of D1 receptors and group differences in D1 sensitivity, D1-D2 blocker (fluphenazine, FLU) should offset increase in reinforcement seen with HAL in PG subjects. In line with DA's implicated role in 'wanting' vs. 'liking' of the addictive reinforcer, the results suggest that DA release mediated partial D1 activation under FLU led to clear differentiation between groups with increased 'wanting' seen in controls but not in gamblers. DA's role in 'liking' however remains elusive.

This thesis examines the pathophysiology of motor neurone dysfunction, along with site of disease onset, in amyotrophic lateral sclerosis (ALS). The rationale for this thesis is the "dying forward" hypothesis, which suggests that corticomotoneurons cause anterograde excitotoxic degeneration of motor neurons in ALS. Initially, axonal excitability studies were applied to ALS patients and revealed widespread axonal ion channel dysfunction, with increases in persistent Na+ conductances and reduction in K+ currents. Such changes result in axonal hyperexcitability, thereby resulting in generation of fasciculations and cramps. Subsequently, axonal excitability studies were applied to Kennedy's disease (KD) patients, a pathological control group, revealing similar changes to ALS and suggesting that upregulation of persistent Na+ conductances was responsible for generation of fasciculations. To better understand the mechanisms underlying fatigability and to assess whether Na+/K+ pump dysfunction contributes to neurodegeneration in ALS, activity-dependent changes in axonal excitability were measured after a maximal voluntary contraction. The increase in threshold was more pronounced in ALS patients with predominantly lower motor neuron involvement, suggesting that peripheral factors were responsible for fatigue in ALS and that Na+/K+ pump function was preserved. Having documented abnormalities of axonal excitability, a novel threshold tracking transcranial magnetic stimulation (TMS) technique was developed for assessment of cortical excitability. This technique overcomes the marked variability in the motor evoked potential with consecutive stimuli, a major limitation of the previous "constant stimulus" technique. After establishing normative data, threshold tracking TMS established that cortical hyperexcitability was an early and prominent feature in ALS. Similar changes were found in flail-arm variant ALS, a pure lower motor neuron form of ALS. In KD patients, cortical excitability was normal, thereby suggesting that cortical hyperexcitability is a primary event in ALS rather than a down-regulation of inhibitory control over the motor cortex in order to compensate for anterior horn cell loss. In order to determine whether cortical hyperexcitability underlies motor neurodegeneration, longitudinal studies were undertaken in familial ALS subjects with the copper/zinc superoxide-dismutase-1 gene mutation. These studies established that cortical hyperexcitability precedes the development of clinical ALS, thereby suggesting that cortical hyperexcitability underlies the basis of motor neurodegeneration in familial ALS.

Thesis (M.S.)--Missouri State University, 2008. / "May 2008." Includes bibliographical references (leaves 58-64). Also available online.