No description available.

Animal research has elucidated the neurobiological substrates and environmental determinants of pain modulation. Despite these advances, relatively little is known about how psychological processes activate pain modulatory systems. One psychological process that is thought to play an important role in regulating pain sensitivity is emotion. In addition, previous research into the human menstrual cycle and the animal estrous cycle have determined that either the presence of certain gonadal hormones or the fluctuations of these hormones may lead to changes in how females perceive pain, regulate emotion, and modulate pain. The present study examines both the role of emotion and the human menstrual cycle in pain modulation. Participants were 39 female undergraduate students with a mean age of 18.7 years (SD=1.46). Results are consistent with prior studies indicating that progesterone has antiinflammatory effects. Specifically, significant effects were observed primarily in the luteal phase. Subjects in the luteal phase demonstrated less sympathetic arousal during the experiment but greater autonomic arousal during the noise stressor. Participants in the luteal phase also demonstrated an analgesic/anti-inflammatory response evidenced by an observed decrease in secondary hyperalgesia for those that did not receive the noise stressor. No such changes in pain perception were discovered in the ovulation and follicular phases. Finally, in response to the noise stressor, an inhibition of the analgesic/anti-inflammatory effects was observed in the luteal phase. No such evidence of stress-induced pain modulation was discovered in the ovulation and follicular phases. Although the specific mechanisms of this action still remain unclear, prior evidence points to the role of centrally-mediated pain modulation. It is likely that the stressor worked to inhibit the anti-inflammatory effects commonly observed in the luteal phase to persistent inflammatory pain through centrally-mediated pain modulatory mechanisms. It is hypothesized that hormone-mediated effects at the level of the amygdala influenced the impact of affective pain modulation.

No description available.

Unlike men, women’s genital arousal is category-nonspecific with respect to sexual orientation, such that their genital responses do not differentiate stimuli by gender. A possible explanation for women’s nonspecific sexual response is the inclusion of women at different phases of the menstrual cycle or women using hormonal contraceptives in sexual psychophysiology research, which may be obscuring a specificity effect. The present study employs the ovulatory-shift hypothesis – used to explain a shift in women’s preferences for masculine traits during peak fertility – as an explanatory model for women’s nonspecific sexual arousal. Twenty-nine naturally-cycling women were tested at two points in their menstrual cycles (follicular and luteal) to determine the role of hormonal variation, as estimated by fertility status, on the specificity of genital (using vaginal photoplethysmograph) and subjective sexual arousal. Cycle phase at the time of first testing was counterbalanced; however, no effect of order was observed. Inconsistent with the ovulatory-shift model, the predicted mid-cycle shift in preferences for masculinity or sexual activity at peak fertility was not obtained. Category-specificity of genital arousal did not increase during the follicular phase. A statistical trend was observed for higher genital arousal to couple sex stimuli during the follicular phase compared to the luteal phase, suggesting that women’s genital arousal may be sensitive to fertility status with respect to sexual activity (specifically, couple sex), but not gender. Subjective arousal was not influenced by fertility status. This study is the first to provide evidence that women’s genital arousal may be influenced by the probability of conception. / Thesis (Master, Psychology) -- Queen's University, 2011-09-29 08:51:26.973

Scores from high-stakes tests such as the Scholastic Aptitude Test (SAT) are commonly used as criteria for college admission decisions. So, it is of implied importance to identify factors that contribute to susceptibility to failure on these tests. One potential factor addressed in the current study was whether emotional cognitive load differentially impacts those with low working memory capacity or trait anxiety. Individual differences in subjective arousal were also tested as a mechanism contributing to this effect. In Experiment 1, a reading comprehension task revealed that type of cognitive load affected accuracy. In Experiment 2, state anxiety was induced using methods from previous research. The results revealed that, again, only type of cognitive load affected comprehension accuracy. Together, results suggest that arousal induced via disturbing words negatively influence reading performance regardless of superior working memory capacity. These findings are not based on cognitive load in general, but the semantic value of the words processed, in particular, that led to comprehension difficulty. Results are discussed in terms of theoretical and practical implications.

This study investigated the differences between right and left hemisphere brain damaged (BD) patients and controls in response to verbal and spatial-affective stimuli. The three null hypotheses explored in this study were: (a) Right hemisphere BD patients would not display significantly different arousal levels from controls in response to verbal and spatial-affective stimuli, (b) left hemisphere BD patients would not display significantly different arousal levels from controls in response to verbal and spatial-affective stimuli, and (c) left hemisphere BD patients would not display significantly different arousal levels from right hemisphere BD patients in response to verbal and spatial-affective stimuli. A One-Way Analysis of Variance was used to determine if differences in arousal existed between right and left hemisphere BD patients and controls. Planned comparisons (t-tests) were used in analyzing the hypotheses.A total of 48 subjects was used in this study. Experimental subjects were composed of 16 left and 16 right hemisphere BD patients from Community Hospital, Indianapolis, Indiana. Sixteen control subjects were obtained from the community of Muncie, Indiana. All subjects were volunteers. No significant differences were found between right and left hemisphere BD patients and controls with respect to age, education, and post injury.The instruments used in this study were a J & J electrodermal unit, the Affective Behavior Test, and the Comprehension subtest of the Wechsler Adult Intelligence Scale-Revised. All tests were individually administered while GSR recordings were obtained. Administration, scoring, computer analyses, and interpretation was completed between May 1982 and February 1984.All three null hypotheses were rejected. Right and left hemisphere BD patients' arousal levels in response to affective stimuli were significantly different from those of controls (p <.001). These results suggested that arousal levels in right and left hemisphere BD patients were lower than non-brain damaged individuals. Additionally, right hemisphere BD patients were found to have significantly lower arousal levels than left hemisphere BD patients (p<.01). In light of these findings, it was recommended that future research explore the value of increasing arousal levels for cerebrovascular accident patients in the rehabilitative process.

In our pilot study investigating Texas Hold ‘em poker, we found that players bluffing (with a losing hand) elicits a similar physiological arousal response (as measured by skin conductance levels) to those in a position of strength and poised to win. Since arousal has been suggested to be a reinforcing factor in problematic gambling behaviour, we sought to replicate the findings of our pilot study in the current investigation. We aimed to extend our previous findings further by: isolating truthful betting (strong betting) to disambiguate deception when players are in positions of strength (i.e. trapping), measuring subjective excitement levels and risk assessments, investigating the physiological arousal responses following wins versus losses, and finally, exploring group differences (i.e. problem gambling status, experience levels). 71 participants played 20 naturalistic rounds of Texas Hold ‘em poker for monetary rewards. We were able to replicate our previous findings that bluffing triggers a physiological arousal (as measured by skin conductance responses) similar to truthful strong betting. Trapping was also found to elicit a skin conductance response similar to both bluffing and strong betting. Measures of subjective excitement revealed a pattern that converged with physiological data. Furthermore, wins were found to be more arousing than losses. Finally, our exploratory analysis of group differences (i.e. problem gambling status, experience) proved to be an insignificant factor with all measures. We conclude that the effect of bluffing on physiological arousal is so powerful that it pervades all participants; which is problematic due to its risky nature and potential to be self-triggered. With its ever increasing popularity and availability, more research on Texas Hold ‘em poker is warranted for treatment implications.

Obstructive sleep apnoea (OSA) is a common condition characterized by recurrent complete and partial upper airway obstruction. OSA sufferers have been shown to have a significantly smaller upper airway lumen compared to non-OSA sufferers. However, non-anatomical factors of sleep stage, arousability and neuromechanical responses to airway occlusion and chemosensitivity are likely to play a significant part in influencing OSA severity across the night. An exploration of these non-anatomical factors forms the basis for the experiments in this thesis. In the first experimental chapter presented in this thesis, a detailed retrospective epoch by epoch analysis of nocturnal polysomnography in 253 patients referred to a clinical sleep service was performed to examine differences in sleep apnoea severity and arousal indices across the different stages of sleep, while controlling for posture. Both patients with and without OSA demonstrated significant reductions in respiratory and arousal event frequencies from stage 1 to 4 with intermediate frequencies in REM sleep. Lateral posture was also associated with significant improvements in OSA and arousal frequencies, with an effect size comparable to that of sleep stage. The majority of patients showed significant reductions in OSA severity during slow wave sleep. In non-REM sleep, there was a strong correlation between OSA severity and arousal frequency. These results confirm in a large group of patients, a strong sleep stage dependence of both OSA and arousal frequencies. The second study in this thesis explores the development of a CO2 stabilising or ‘clamp’ device to enable the provision of positive airway pressure, and by proportional rebreathing, the maintenance of relatively constant end-tidal CO2 despite significant hyperventilation. Healthy volunteers performed brief periods of significant voluntary hyperventilation at 2 levels of CPAP with the rebreathing function off and with active CO2 clamping in randomized order. Compared to CPAP alone, the device substantially attenuated hypocapnia associated with hyperventilation. The third study of the thesis was designed to investigate if increasing and stabilizing end-tidal CO2 could improve obstructive breathing patterns during sleep. 10 patients with severe OSA underwent rapid CPAP dialdown from therapeutic to a sub-therapeutic level to experimentally induce acute, partial upper airway obstruction over 2 minute periods repeated throughout the night. The CO2 clamp device developed and validated in Study 2 was used to determine whether during periods of partial upper airway obstruction with severe flow limitation, (1) increased end-tidal CO2 resulted in improved airflow and ventilation and (2) clamping end-tidal CO2 lessened post-arousal ventilatory undershoot. Three conditions were studied in random order: no clamping of CO2, clamping of end-tidal CO2 3-4 mmHg above eucapnic levels during the pre-dialdown baseline period only, and clamping of CO2 above eucapnia during both baseline and dialdown periods. Elevated CO2 in the baseline period alone or in the baseline and dialdown periods together resulted in significantly higher peak inspiratory flows and ventilation compared to the no clamp condition. Breath-by-breath analysis immediately pre- and post-arousal showed higher end-tidal CO2 despite hyperventilation immediately post-arousal and attenuation of ventilatory undershoot in CO2 versus non-CO2 clamped conditions. These results support that modulation of ventilatory drive by changes in pre- and post-arousal CO2 are likely to importantly influence upper airway and ventilatory stability in OSA. The fourth study was designed to explore several possible pathophysiological mechanisms whereby obstructive sleep apnoea is improved in stages 3 & 4 (slow wave) versus stage 2 sleep. 10 patients with severe OSA who demonstrated significant reductions in OSA frequency during slow wave sleep on diagnostic investigation were studied. Patients underwent rapid dialdowns from therapeutic CPAP to 3 different pre-determined sub-therapeutic pressures to induce partial airway obstruction and complete airway occlusions in a randomised sequence during the night in both stage 2 and slow wave sleep. Partial airway obstructions and complete occlusions were maintained until arousal occurred or until 2 minutes had elapsed, whichever came first. After airway occlusions, time to arousal, peak pre-arousal negative epiglottic pressure and the rate of ventilatory drive augmentation were significantly greater, suggesting a higher arousal threshold and ventilatory responsiveness to respiratory stimuli during slow wave compared to stage 2 sleep. Post dialdowns, the likelihood of arousal was lower with less severe dialdowns and in slow wave compared to stage 2 sleep. Respiratory drive measured by epiglottic pressure progressively increased post-dialdown, but did not translate into increases in peak flow or ventilation pre-arousal and was not different between sleep stages. These data suggest that while arousal time and propensity following respiratory challenge are altered by sleep depth, there is little evidence to support that upper airway and ventilatory compensation responses to respiratory load are fundamentally improved in slow wave compared to stage 2 sleep. In summary, sleep stage, arousal threshold and chemical drive appear to strongly influence upper airway and ventilatory stability in OSA and are suggestive of important non-anatomical pathogenic mechanisms in OSA.

Thesis (M.D.)--University of Adelaide, 1986. / Includes bibliographical references (leaves 317-350).

Thesis (Ph.D.)--University of Utah, 1998. / Includes bibliographical references (leaves 296-313).