Plasma anti-serotonin and serotonin anti-idiotypic antibodies are elevated in panic disorder.

The psychoneuroimmunology of panic disorder is relatively unexplored. Alterations within brain stress systems that secondarily influence the immune system have been documented. A recent report indicated elevations of serotonin (5-HT) and ganglioside antibodies in patients with primary fibromyalgia, a condition with documented associations with panic disorder. In line with our interest in dysregulated 5-HT systems in panic disorder (PD), we wished to assess if antibodies directed at the 5-HT system were elevated in patients with PD in comparison to healthy volunteers. Sixty-three patients with panic disorder and 26 healthy volunteers were diagnosed by the SCID. Employing ELISA, we measured anti-5-HT and 5-HT anti-idiotypic antibodies (which are directed at 5-HT receptors). To include all subjects in one experiment, three different batches were run during the ELISA. Plasma serotonin anti-idiotypic antibodies: there was a significant group effect [patients > controls (p = .007)] and batch effect but no interaction. The mean effect size for the three batches was .76. Following Z-score transformation of each separate batch and then combining all scores, patients demonstrated significantly elevated levels of plasma serotonin anti-idiotypic antibodies. Neither sex nor age as covariates affected the significance of the results. There was a strong correlation between anti-serotonin antibody and serotonin anti-idiotypic antibody measures. Plasma anti-serotonin antibodies: there was a significant diagnosis effect [patients > controls (p = .037)]. Mean effect size for the three batches was .52. Upon Z-score transformation, there was a diagnosis effect with antibody elevations in patients. Covaried for sex and age, the result falls below significance to trend levels. The data raise the possibility that psychoimmune dysfunction, specifically related to the 5-HT system, may be present in PD. Potential interruption of 5-HT neurotransmission through autoimmune mechanisms may be of pathophysiologic significance in certain patients with panic disorder. It remains to be demonstrated if the peripheral autoimmunity is representative of CNS 5-HT neuronal alterations. Replication appears warranted.

Discrimination accuracy and decision biases in different types of reality monitoring in schizophrenia.

A reality monitoring task was administered to 31 schizophrenic patients and 31 normal controls. Twenty-four items were produced, either orally by the experimenter, orally by the subjects, or seen as pictures. Subjects were later read a list of 48 items and were asked to indicate if each item was new, self-generated, experimenter-generated, or presented as a picture. Results showed that schizophrenic patients were impaired in discriminating old items from new, with a higher bias than controls toward reporting new items as if they were old (false alarms). In addition, patients were impaired in discriminating self-generated items from externally generated items, with a higher bias than controls toward attributing self-generated items to an external source. Lastly, they were significantly impaired in discriminating the modality (auditory versus visual) in which the event was presented. The bias toward remembering orally produced items as pictures was correlated with positive symptomatology and was significantly higher than controls in patients with high levels of positive symptoms. This suggests that mental imagery may play a role in positive symptomatology. These results demonstrate the relevance of studying decision biases along with discrimination performance for the understanding of the mechanisms of reality monitoring impairment in schizophrenia.

Instructional set does not alter outcome of respiratory challenges in panic disorder.

In an attempt to reproduce the findings of Rapee et al (1986) that instructional set could alter the anxiogenic effects of carbon dioxide inhalation, 45 patients with panic disorder received two sets of instructions and then underwent a series of respiratory challenges (room air hyperventilation, 5% and 7% CO2 inhalation). The instructions failed to alter the anxiogenic response to any of the interventions.

Psychological distress and natural killer cells in gay men with and without HIV infection.

OBJECTIVE: The variability of the decline in immune function among those infected by HIV raises the possibility that psychological factors might help to explain the differences. Since studies of other populations have shown natural killer (NK) cells to be affected by psychiatric conditions, the authors examined this relationship in the context of HIV infection, expecting to find fewer NK cells to be associated with greater psychological distress. METHOD: Forty-six HIV-negative and 74 HIV-positive gay men who were participating in a longitudinal study had NK cells enumerations performed (by staining for CD56) 36 months after entry into the study. Comparisons were made between HIV-negative, HIV-positive asymptomatic, and HIV-positive symptomatic men by using a variety of clinician-rated and self-report measures of psychological function and absolute NK cell number. RESULTS: HIV-negative men had more NK cells than the groups of HIV-positive men. The groups' measures of psychological distress did not differ in any clinically meaningful ways. In general, the presence of DSM-III-R diagnoses and the measures of distress did not relate to NK cell number. CONCLUSIONS: NK cell number is not related to measures of psychological distress in these gay men with and without HIV infection.

Psychoneuroimmunology and HIV infection.

Advances in the neurosciences and immunology provide a framework for understanding how mental health status may be a co-factor in the progression of human immunodeficiency virus (HIV) infection. The authors discuss the interrelatedness of the central nervous system and the immune system, discuss the possible relevance of such connections to HIV immunopathology, and review research that demonstrates the effect of psychiatric and psychosocial factors on immunological status and medical outcome. An application of psychoneuroimmunology to HIV infection warrants careful consideration of the many complexities involved.

Response of the melatonin cycle to phototherapy for Seasonal Affective Disorder. Short note.

It is well-established that human nocturnal melatonin secretion is suppressed by presentation of artificial light greater than 2,000 lux, a level that is also therapeutically effective in alleviating winter depression symptoms of Seasonal Affective Disorder [SAD]. Furthermore, early-morning bright light induces phase advances of the melatonin cycle in SAD patients (Lewy et al., 1987a). The functional significance of melatonin in SAD remains unclear. With plasma melatonin sampled at 20-min intervals in a series of overnight studies, we found marked phase delays of the cycle, relative to that previously reported for normals, in 4/5 depressed SAD patients. 2,500 lux light exposure at 6-8 a.m. resulted in exponentially declining melatonin levels that approached low daytime baselines within two hours (t1/2 = 45.52 min). All five patients showed clinical remissions as well as phase advances of the melatonin cycle of 0.75 to 3.27 hours (mean, 1.94 +/- 0.84 hours) after one week of daily exposure from 6-8 a.m. and p.m. These results suggest that the combination of early morning and early evening light exposures induces circadian phase adjustments similar to those of morning light alone, by impacting a photosensitive interval when, in SAD, melatonin secretion overshoots its normal nocturnal phase.