Is there a link between traumatic experiences and self-injurious behaviors in eating-disordered patients?

To find out more about the relationship between the presence of self-injurious behavior (SIB) and a history of traumatic experiences, we studied this link in 70 patients with an eating disorder (ED). The sample showed a high frequency of SIB (38.6%), particularly in patients with bulimia nervosa. We also found high percentages of self-reported experiences of physical (32.3%) and sexual abuse (47.7%). The presence of SIB turned out to be associated with a history of physical and/or sexual abuse. Patients who had suffered interpersonal abuse before the age of 15 were more likely to develop self-destructive behaviors. In line with other investigations, we found that high levels of dissociation and self-criticism differentiated sexually abused ED patients with SIB from those without SIB. We discuss some clinical implications of our findings, with suggestions for treatment.     

Is there a relationship between Parkinson's disease and obsessive-compulsive disorder?

Obsessive-compulsive (OC) symptoms and obsessive-compulsive disorder (OCD) have been reported in Parkinson's disease (PD). This is interpreted as an indirect evidence for the involvement of frontobasal ganglia circuitry in OCD. However, the evidence for relationship between the OC symptoms and PD is inconsistent. This study systematically assessed OC symptoms and OCD in non-demented idiopathic PD patients (n=69) and matched medically ill controls (n=69). The cases did not differ from controls with respect to OC symptoms, clinical and subclinical OCD, tics and other psychiatric diagnoses. There was no relationship between severity of PD and OC symptoms. The findings do not support relationship between OCD and PD. While the findings of this study do not in any way rule out the involvement of frontobasal ganglia circuitry in OCD, it is speculated that the involvement of different circuitry in the pathophysiology of OCD and PD explain the lack of association between PD and OCD.     

Is social anxiety disorder in childhood associated with developmental deficit/delay?

Children with social anxiety disorder (SAD) have been reported to display reduced social skills. Less attention has been paid to whether neurodevelopmental deficits/delays (NDD’s) in language and motor function may contribute to their impaired social skills. The present study aimed to assess the extent of language and motor impairment in children with SAD. A population-based screened sample consisting of 150 children (11–12 years) was assessed with a diagnostic interview (Kiddie-SADS), the Wechsler Abbreviated Scale of Intelligence (WASI) and the Motor Assessment Battery for Children (MABC). Test results were compared across five diagnostic groups: SAD (n = 29); ADHD (n = 23); SAD and ADHD (n = 6); “other disorder” (n = 44) and “no disorder” (n = 48). Delays in language and motor development as reported by mother were also investigated. Verbal IQ and motor skills were reduced and maternally reported delay was more frequent in the SAD group compared to the “other disorder” and “no disorder” group.     

Is there a negative association between anxiety sensitivity and arousal-increasing substances and activities?

Little research has addressed McNally's hypothesis [(1996). Anxiety sensitivity is distinguishable from trait anxiety. In: R. M. Rapee (Ed.), Current controversies in the anxiety disorders (pp. 214-227). New York: The Guilford Press.] that anxiety sensitivity (AS) should be negatively associated with the use of arousal-increasing substances. In the present study, we examined the relationship between AS and the self-reported use of two widely available stimulants--nicotine and caffeine--and exercise frequency in a sample of 256 university students. A measure of trait anxiety was also incorporated within the design. The associations between use of both substances and levels of AS and trait anxiety were weak and nonsignificant. Although inconsistent with McNally's hypothesis, some significant findings were found when the lower-order components of AS (i.e., fears of physical, psychological, and publicly observable symptoms of anxiety) were examined. The associations between exercise frequency and the anxiety measures, indicating a negative relationship, were generally consistent with McNally's hypothesis. Implications of these findings are discussed with reference to future investigation.     

Is childhood separation anxiety disorder a predictor of adult panic disorder and agoraphobia? A seven-year longitudinal study

OBJECTIVE: To examine whether separation anxiety disorder (SAD) in childhood is a risk factor for panic disorder and agoraphobia in adulthood. METHOD: Patients (n = 85) who had completed treatment for SAD, generalized anxiety disorder, and/or social phobia 7.42 years earlier (on average) were reassessed using structured diagnostic interviews. RESULTS: Subjects with a childhood diagnosis of SAD did not display a greater risk for developing panic disorder and agoraphobia in young adulthood than those with other childhood anxiety diagnoses. Subjects with a childhood diagnosis of SAD did not more frequently meet full diagnostic criteria for panic disorder and agoraphobia, generalized anxiety disorder, social phobia, or major depressive disorder in adulthood than subjects with childhood diagnoses of generalized anxiety disorder or social phobia, but were more likely to meet criteria for other anxiety disorders (i.e., specific phobia, obsessive compulsive disorder, posttraumatic stress disorder, and acute stress disorder). CONCLUSIONS: These results argue against the hypothesis that childhood SAD is a specific risk factor for adult panic disorder and agoraphobia.     

Exercise,sleep and cytokines: Is there a relation?

Physical exercise is a modality of non-pharmacological treatment for sleep disorders. Contradicting results are still found in studies of the effect of exercise on sleep. Among the substances that have been described as sleep modulators, cytokines produced during the recovery period after an acute exercise session are very important. Various studies have verified that physical exercise may alter the plasma concentration of the many pro-inflammatory cytokines that may in turn modulate sleep. A number of factors seem to mediate this effect of exercise, including duration, intensity, and form of exercise, in addition to temperature and metabolic alterations. The mechanisms through which exercise promotes alterations in sleep architecture remain to be clarified. Researchers speculate that many hormones and substances produced by metabolism may affect sleep. Therefore, the object of this review is to discuss the effects of exercise and cytokines on sleep, and the relation between these two sleep-regulating components, raising the hypothesis that the alterations in sleep promoted by exercise are mediated by cytokines, which, by increasing the nREM sleep phase, would stimulate the regenerating characteristics of sleep.     

Is there a link between childhood trauma, cognition, and amygdala and hippocampus volume in first-episode psychosis?

Patients with psychosis have higher rates of childhood trauma, which is also associated with adverse effects on cognitive functions such as attention, concentration and mental speed, language, and verbal intelligence. Although the pathophysiological substrate for this association remains unclear, these cognitive deficits may represent the functional correlate of changes observed in relation to trauma exposure in structures such as the amygdala and the hippocampus. Interestingly, these structures are often reported as altered in psychosis. This study investigated the association between childhood trauma, cognitive function and amygdala and hippocampus volume, in first-episode psychosis. We investigated 83 patients with first-episode psychosis and 63 healthy controls. All participants underwent an MRI scan acquired with a GE Sigma 1.5-T system, and a standardized neuropsychological assessment of general cognition, memory, processing speed, executive function, visuo-spatial abilities, verbal intelligence, and language. In a subsample of the patients (N=45) information on childhood trauma was collected with the Childhood Experience of Care and Abuse Questionnaire (CECA.Q). We found that amygdala, but not hippocampus, volume was significantly smaller (p=0.001) in patients compared to healthy controls. There was a trend level interaction for hippocampus volume between group and sex (p=0.056). A history of childhood trauma was associated with both worse cognitive performance and smaller amygdala volume. This smaller amygdala appeared to mediate the relationship between childhood trauma and performance on executive function, language and verbal intelligence in patients with psychosis. This points to a complex relationship between childhood trauma exposure, cognitive function and amygdala volume in first-episode psychosis.     

Is there an association between haemoglobin, depression, and anxiety in cancer patients?

OBJECTIVE: The aim of this study was to examine the association between haemoglobin levels, anxiety disorder, and depression in cancer patients. METHODS: Cancer patients attending The Norwegian Radium Hospital (NRH) rated themselves on the Hospital Anxiety and Depression Scale (HADS). Five hundred thirty-two patients also had valid measurements of haemoglobin at the same time. The associations between tertile haemoglobin levels (7.0-12.3 g/dl, 12.4-13.8 g/dl, 13.9-17.1 g/dl) and HADS-defined anxiety disorder and depression were analysed by logistic regression. RESULTS: HADS-defined depression was identified in 116 cases (22%) and anxiety disorder in 149 (28%). The haemoglobin levels of the lower and middle tertiles were associated with depression (OR=3.85, 95% CI: 2.06-7.21, and OR=2.45, 95% CI: 1.25-4.81, respectively). Adjustment for covariates did not change the association significantly. No association between haemoglobin and anxiety disorder was found. CONCLUSION: In cancer patients, the risk of depression increases with decreasing haemoglobin levels. This should be taken into account when treatment of anaemic or depressed cancer patients is decided upon.     

Is obsessive-compulsive disorder an anxiety disorder?

Obsessive-compulsive disorder (OCD) is classified as an anxiety disorder in the DSM-IV-TR [American Psychiatric Association, 2000. Diagnostic and statistical manual of mental disorders, Fourth ed., rev. Washington, DC: Author]; however, the notion of a spectrum of obsessive-compulsive (OC) related disorders that is comprised of such disparate disorders as OCD, body dysmorphic disorder, certain eating disorders, pathological gambling, and autism, is gaining acceptance. The fact that these disorders share obsessive-compulsive features and evidence similarities in patient characteristics, course, comorbidity, neurobiology, and treatment response raises the question of whether OCD is best conceptualized as an anxiety or an OC spectrum disorder. This article reviews evidence from comorbidity and family studies, as well as biological evidence related to neurocircuitry, neurotransmitter function, and pharmacologic treatment response that bear on this question. The implications of removing OCD from the anxiety disorders category and moving it to an OC spectrum disorders category, as is being proposed for the DSM-V, is discussed.     

Discriminating between generalized anxiety disorder and anxiety disorder not otherwise specified in a Hispanic population: Is it only a matter of worry?

One hundred and two Hispanic persons who presented for treatment at a specialized anxiety disorders clinic were evaluated at intake using the Anxiety Disorders Interview Schedule-Revised (ADIS-R; DiNardo and Barlow [1988] Albany: Center for Stress and Anxiety Disorders, State University of New York at Albany). Results indicated that 14% of these patients suffered from anxiety and/or affective disorders that were not adequately captured by our current diagnostic system. Given that the majority of these cases were characterized by predominantly anxious features, further investigation was undertaken to determine the degree of overlap between these patients (anxiety disorder, not otherwise specified; NOS) and those with generalized anxiety disorder (GAD). The two groups differed only with regard to the number of excessive worries they reported and not in terms of somatic symptomatology, psychosocial stressors, or demographic variables. These data suggest that excessive worry may be a discriminating factor between the GAD and NOS groups, providing support for the notion of GAD as a disorder of chromic worry. Future research is needed to tease apart the relative influences of culture and socioeconomic status on our findings. Depression and Anxiety 5:1–6, 1997. © 1997 Wiley-Liss, Inc.     

What is the threshold for symptomatic response and remission for major depressive disorder, panic disorder, social anxiety disorder, and generalized anxiety disorder?

OBJECTIVE: Symptom-free remission is a goal for treatment in depression and anxiety disorders, but there is no consensus regarding the threshold for determining remission in individual disorders. We sought to determine these thresholds by comparing, in a post hoc analysis, scores on the Clinical Global Impressions scale (CGI) and disorder-specific symptom severity rating scales from all available studies of the treatment of major depressive disorder, panic disorder, generalized anxiety disorder, and social anxiety disorder with the same medication (escitalopram). We also sought to compare the standardized effect sizes of escitalopram for these 4 psychiatric disorders. DATA SOURCES AND STUDY SELECTION: Raw data from all randomized, double-blind, placebo-controlled, acute treatment studies sponsored by H. Lundbeck A/S (Copenhagen, Denmark) or Forest Laboratories, Inc. (New York, N.Y.), published through March 1, 2004, with patients treated with escitalopram for DSM-IV major depressive disorder (5 studies), panic disorder (1 study), generalized anxiety disorder (4 studies), or social anxiety disorder (2 studies) were compared with regard to the standardized effect sizes of change in CGI score and scores on rating scales that represent the "gold standard" for assessment of these disorders (the Montgomery-Asberg Depression Rating Scale, the Panic and Agoraphobia Scale, the Hamilton Rating Scale for Anxiety, and the Liebowitz Social Anxiety Scale, respectively). DATA SYNTHESIS: In all indications, treatment with escitalopram showed differences from placebo in treatment effect from 0.32 to 0.59 on the CGI-S and CGI-I and standardized effect sizes from 0.32 to 0.50 on the standard rating scales. There were no significant differences among the different disorders. Moderate to high correlations were found between scores on the CGI and the standard scales. The corresponding standard scale scores for CGI-defined "response" and "remission" were determined. CONCLUSION: Comparison of scores on the standard scales and scores on the CGI suggest that the traditional definition of response (i.e., a 50% reduction in a standard scale) may be too conservative.     

Is impulsivity a link between childhood abuse and suicide?

Childhood abuse and neglect are known to affect psychological states through behavioral, emotional, and cognitive pathways. They increase the risk of having psychiatric diseases in adulthood and have been considered risk factors for suicidal behavior in all diagnostic categories. Early, prolonged, and severe trauma is also known to increase impulsivity, diminishing the capacity of the brain to inhibit negative actions and to control and modulate emotions. Many neurobiological studies hold that childhood maltreatment may lead to a persistent failure of the inhibitory processes ruled mainly by the frontal cortex over a fear-motivated hyperresponsive limbic system. Multiple neurotransmitters and hormones are involved in the stress response, but, to our knowledge, the two major biological consequences of the chronic exposure to trauma are the hypofunction of the serotonergic system and changes in the hypothalamic-pituitary-adrenal axis function. Some of these findings overlap with the neurobiological features of impulsivity and of suicidal behavior. Impulsivity has also been said to be both a consequence of trauma and a risk factor for the development of a pathological response to trauma. Thus, we suggest that impulsivity could be one of the links between childhood trauma and suicidal behavior. Prevention of childhood abuse could significantly reduce suicidal behavior in adolescents and adults, in part, through a decrease in the frequency of impulsive behaviors in the future.     

Why take social anxiety disorder seriously?

Social anxiety disorder (social phobia) is a disabling psychiatric condition, characterized by a fear of negative evaluation by others. Epidemiological studies have shown a high prevalence of the condition in the general population; the disorder is more common in women than in men. Social anxiety disorder has a typical onset during adolescence and a chronic course; remission rarely occurs without therapeutic intervention. Comorbid psychiatric conditions such as depression and alcoholism commonly occur in patients with preexisting social anxiety disorder, and increase the burden of the condition. Two subtypes of social anxiety disorder have been identified: "nongeneralized" and "generalized"; the latter form causes greater disability and is more often associated with comorbidity. The socioeconomic impact of social anxiety disorder on both sufferers and the community is considerable. For a person with social anxiety disorder, quality of life is greatly reduced; work, social, and personal relationships are all affected. Social anxiety disorder demands increased recognition, so that sufferers receive the treatment they need, in order to improve their quality of life through better social functioning.