Disturbed EEG Sleep, Paranoid Cognition and Somatic Symptoms Identify Veterans With Post-Traumatic Stress Disorder

Background Chronic post-traumatic stress disorder (PTSD) behavioural symptoms and medically unexplainable somatic symptoms are reported to occur following the stressful experience of military combatants in war zones. Aims To determine the contribution of disordered EEG sleep physiology in those military combatants who have unexplainable physical symptoms and PTSD behavioural difficulties following war-zone exposure. Method This case-controlled study compared 59 veterans with chronic sleep disturbance with 39 veterans with DSM-IV and clinician-administered PTSD Scale diagnosed PTSD who were unresponsive to pharmacological and psychological treatments. All had standardised EEG polysomnography, computerised sleep EEG cyclical alternating pattern (CAP) as a measure of sleep stability, self-ratings of combat exposure, paranoid cognition and hostility subscales of Symptom Checklist-90, Beck Depression Inventory and the Wahler Physical Symptom Inventory. Statistical group comparisons employed linear models, logistic regression and chi-square automatic interaction detection (CHAID)-like decision trees. Results Veterans with PTSD were more likely than those without PTSD to show disturbances in non-rapid eye movement (REM) and REM sleep including delayed sleep onset, less efficient EEG sleep, less stage 4 (deep) non-REM sleep, reduced REM and delayed onset to REM. There were no group differences in the prevalence of obstructive sleep apnoeas/hypopnoeas and periodic leg movements, but sleep-disturbed, non-PTSD military had more EEG CAP sleep instability. Rank order determinants for the diagnosis of PTSD comprise paranoid thinking, onset to REM sleep, combat history and somatic symptoms. Decision-tree analysis showed that a specific military event (combat), delayed onset to REM sleep, paranoid thinking and medically unexplainable somatic pain and fatigue characterise chronic PTSD. More PTSD veterans reported domestic and social misbehaviour. Conclusions Military combat, disturbed REM/non-REM EEG sleep, paranoid ideation and medically unexplained chronic musculoskeletal pain and fatigue are key factors in determining PTSD disability following war-zone exposure

Effects of a nuclear polyhedrosis virus of the western tent caterpillar on individual performance and population dynamics

Viral diseases are an important feature of fluctuating populations of Lepidoptera. I examined the potential for a nuclear polyhedrosis virus (NPV) to explain the changes in abundance and fecundity observed in populations of the western tent caterpillar, Malacosoma californicum pluviale. Fluctuating populations are characterized by prolonged declines following high density. In M. c. pluviale, decreases in fecundity track these declines. While viral diseases of Lepidoptera are usually recognized for their ability to kill infected hosts, they may also reduce the fitness of individuals which survive infection. I surveyed studies in the literature which evaluated qualitative characteristics of individuals following treatment with virus. Debilitating effects of viral diseases of Lepidoptera included slower development rates, lower pupal and adult weights, reduced reproductive capacity and shorter adult longevity. These sublethal effects were observed more frequently in studies of less virulent pathogens (cytoplasmic polyhedrosis viruses or CPVs) than in studies of NPVs. Debilitating effects of both CPVs and NPVs could potentially suppress host population growth. In the laboratory, I treated M. c. pluviale larvae with NPV to assess whether viral infection could potentially reduce fecundity as observed in declining field populations of the host. Weights of male and female pupae and female fecundity were reduced in survivors of virus treatment, which suggests that NPV could reduce fecundity of field populations of the western tent caterpillar. In small-scale field and related laboratory experiments, I examined immediate and delayed effects of NPV introduction and density on M. c. pluviale. In a factorial experiment, larvae at high density showed increased feeding and development rates and decreased reproductive potential. The introduction of NPV significantly increased mortality of the host, particularly at high density, and generally reduced host reproductive potential. Adults from this experiment were mated and their offspring reared in the laboratory. No treatment effects on egg viability or larval performance occurred. Treatments did have significant delayed effects on pupal weights of female offspring. However, in a correlational field study maternal fecundity was not related to pupal weights of offspring. M. c. pluviale introduced to host trees used in the initial factorial experiment showed no effects of previous caterpillar density on performance as predicted by host plant induction theory. However an interactive effect of previous virus introduction and density on mortality was observed owing to persistence of NPV particles in the environment. Female pupal weights were also slightly reduced in the year following NPV introduction. I assessed the potential for NPV and density to reduce population growth by calculating net reproductive rates for treatments from the above field experiments. The introduction of NPV had a large immediate impact on population growth, particularly at high host density. Delayed effects of NPV introduction at high density were insufficient to prolong this decline, but did appreciably suppress predicted population growth. Treatment effects on individual quality (fecundity) had little effect on predicted population change. Because delayed density dependence may lead to population instability, I concluded that viral disease may have a more destabilizing influence on tent caterpillar populations than density alone. Persistence of virus particles in the environment could contribute to, but not explain prolonged declines in field populations of M. c. pluviale. High density may be sufficient to initiate decreases in fecundity in these populations while viral disease may explain continued fecundity decreases during prolonged declines.Science, Faculty ofZoology, Department ofGraduat