Pain during depression and relationship to rejection sensitivity

Objective: Approximately 50% of patients with depression report symptoms of pain, yet the clinical and biological mechanisms underlying this association remain unclear. Recent neuroimaging studies, however, support the contention that depression, as well as pain distress and rejection distress, share the same neurobiological circuits. In this study, we aimed to examine the hypothesis that perception of increased pain during depression is related to increased rejection sensitivity. Method: The present study analysed data from a study of 186 treatment‐resistant depressed patients who met DSM‐IV criteria for depression and had completed a self‐report questionnaire regarding currently perceived pain and rejection sensitivity. Results: A major increase in the experience of pain during depression was predicted by a major increase in rejection sensitivity during depression. Conclusion: The experience of increased pain during depression is related to increased rejection sensitivity. Research to further elucidate this relationship is required.     

Structural and functional models of depression: from sub-types to substrates

OBJECTIVE: To present a functional model of depression facilitating research and clinical understanding. METHOD: The authors conducted a systematic literature search and reviewed articles pertaining to the neurochemistry and pathophysiology of depressive disorders, focusing on the contribution made by the principal monoamines to three differing depressive structural sub-types (i.e. psychotic, melancholic and non-melancholic). RESULTS: We suggest that the three structural depressive subtypes appear functionally underpinned by differential contributions of serotonergic, noradrenergic and dopaminergic neurotransmitters, so influencing phenotypic distinction (our structural model) and allowing an aetiological model to be derived with treatment specificity implications. CONCLUSION: The functional model logically iterates with the structural model of depression and provides a useful framework for conceptualizing the depressive disorders. This model provides a logic for distinguishing between principal depressive subtypes, pursuing their functional underpinnings and explaining treatment differential effects across the three sub-types.     

Recognizing the anxious face of depression

"Anxious depression" is used variably both by researchers and clinicians to describe admixtures of anxiety and depressive symptoms. The authors sought to determine the best model for conceptualizing anxious depression by studying a sample of depressed patients referred to a tertiary referral unit. Anxiety and depression were assessed using a comprehensive set of mixed symptoms that were subsequently refined to provide separate anxiety and depressive factors, and patients were trichotomized into groups of low, medium, and high anxiety on the basis of their total anxiety factor scores. Associations between the constructs of anxiety and depression in different depressive subgroups were explored, and the severity of depressive symptoms and other clinical variables across the three anxiety groupings was assessed. Depression variables were not linearly associated in a consistent pattern with anxiety-defined groups, arguing against a simple interdependence model driven by a higher-order variable such as depression severity. By contrast, the state anxiety categories were linked strongly with lifetime anxiety disorder prevalence, with some associations linear and with others evidencing a trend break association. The authors found support for a model of anxious depression, whereby anxiety both predisposes to nonmelancholic depression and contributes to its presentation by shaping its clinical features. Such a model and its definition assist in clarifying the cause of anxious depression and its treatment.     

Drug interaction between rifampicin and cotrimoxazole in patients with tuberculosis.

1. Patients (n = 15) who were admitted with complications of tuberculosis, were given antitubercular therapy (ATT) with rifampicin (RIF), for a minimum period of 15 d, and cotrimoxazole (CTZ), concurrently, for 5-10 d. 2. The serum RIF levels were measured before the start of CTZ treatment and at the end of its administration. 3. The plasma half-life (t1/2) of RIF increased significantly from 1.92 +/- 0.57 h to 2.31 +/- 0.134 h after CTZ treatment. 4. The mean serum levels of RIF increased significantly at 4 and 6 h after CTZ administration.     

Valid assessment of the clinical features of depression by relatives appears to slip under the RADAR

OBJECTIVE: We report on the development of an observational measure designed for completion by relatives, the Recent Appearance of Depression Assessed by Relatives (RADAR), and consider its validity. METHOD: One hundred and one patients with a current major depressive episode had a relative or close friend complete the RADAR, while psychiatrists and research assistants collected extensive data. RESULTS: Correlated against both patient self-report and psychiatrist-rated depression severity measures, RADAR scores evidenced poor validity overall. Recent Appearance of Depression Assessed by Relatives scores also failed to differentiate depressive subtypes, in that scores for patients with melancholic depression were not significantly higher than for those with non-melancholic depression. CONCLUSIONS: Results are consistent with previous findings of poor agreement between clinicians and corroborative witnesses in assessing clinical depressive features, and argue against reliance on corroborative witness reports.     

Psychosocial issues in the management and treatment of children and adolescents with asthma

Asthma is one of the most common chronic childhood illness. Studies have reported higher incidence of psychosocial adaptation problems in children with asthma, particularly severe asthma, than children in the general population. Increased psychosocial problems in children with asthma have been ascribed to adverse developmental impact of having a chronic health problems, increased demands on the family and dysfunctional familial interactional patterns. Treatment models include education and self management training programs, family therapy, relaxation therapy and biofeedback. These programs have been found to produce improved adjustment, increased medication compliance and greater perceived self competence in managing symptoms and decreased use of medical services. It is concluded that children with asthma require a comprehensive management strategy that pays attention not only to physiological control of asthma symptoms but also emotional and behavioural problems of children and their families.     

A typical mood stabilizers: a "typical role for atypical antipsychotics

OBJECTIVE: To assess the potential role of atypical antipsychotics as mood stabilizers.METHOD: A MedLine, PsychLIT, PubMed, and EMBASE literature search of papers published up to December 2004 was conducted using the names of atypical antipsychotics and a number of key terms relevant to bipolar disorder. Additional articles were retrieved by scrutinizing the bibliographies of review papers and literature known to the authors. Data pertinent to the objective was reviewed according to the various phases of bipolar disorder.RESULTS: The data is most substantive for the use of atypical antipsychotics in mania, to the extent that an argument for a class effect of significant efficacy can be made. This does not extend to bipolar depression, however, good data is now emerging for some agents and will need to be considered for each individual agent as it accumulates. As regards mixed states and rapid cycling the evidence is thus far sparse and too few maintenance studies have been conducted to make any firm assertions. However, with respect to long-term therapy the atypical antipsychotics do have clinically significant side-effects of which clinicians need to be aware.CONCLUSION: Based on the evidence thus far it is perhaps premature to describe the atypical antipsychotics as mood stabilizers. Individual agents may eventually be able to claim this label, however, much further research is needed especially with respect to maintenance and relapse prevention.     

Hypothalamo-pituitary-adrenal axis dysfunction in chronic fatigue syndrome, and the effects of low-dose hydrocortisone therapy

These neuroendocrine studies were part of a series of studies testing the hypotheses that 1) there may be reduced activity of the hypothalamic-pituitary-adrenal axis in chronic fatigue syndrome and 2) low-dose augmentation with hydrocortisone therapy would improve the core symptoms. We measured ACTH and cortisol responses to human CRH, the insulin stress test, and D-fenfluramine in 37 medication-free patients with CDC-defined chronic fatigue syndrome but no comorbid psychiatric disorders and 28 healthy controls. We also measured 24-h urinary free cortisol in both groups. All patients (n = 37) had a pituitary challenge test (human CRH) and a hypothalamic challenge test [either the insulin stress test (n = 16) or D-fenfluramine (n = 21)]. Baseline cortisol concentrations were significantly raised in the chronic fatigue syndrome group for the human CRH test only. Baseline ACTH concentrations did not differ between groups for any test. ACTH responses to human CRH, the insulin stress test, and D- fenfluramine were similar for patient and control groups. Cortisol responses to the insulin stress test did not differ between groups, but there was a trend for cortisol responses both to human CRH and D-fenfluramine to be lower in the chronic fatigue syndrome group. These differences were significant when ACTH responses were controlled. Urinary free cortisol levels were lower in the chronic fatigue syndrome group compared with the healthy group. These results indicate that ACTH responses to pituitary and hypothalamic challenges are intact in chronic fatigue syndrome and do not support previous findings of reduced central responses in hypothalamic-pituitary-adrenal axis function or the hypothesis of abnormal CRH secretion in chronic fatigue syndrome. These data further suggest that the hypocortisolism found in chronic fatigue syndrome may be secondary to reduced adrenal gland output. Thirty-two patients were treated with a low-dose hydrocortisone regime in a double-blind, placebo-controlled cross-over design, with 28 days on each treatment. They underwent repeated 24-h urinary free cortisol collections, a human CRH test, and an insulin stress test after both active and placebo arms of treatment. Looking at all subjects, 24-h urinary free cortisol was higher after active compared with placebo treatments, but 0900-h cortisol levels and the ACTH and cortisol responses to human CRH and the insulin stress test did not differ. However, a differential effect was seen in those patients who responded to active treatment (defined as a reduction in fatigue score to the median population level or less). In this group, there was a significant increase in the cortisol response to human CRH, which reversed the previously observed blunted responses seen in these patients. We conclude that the improvement in fatigue seen in some patients with chronic fatigue syndrome during hydrocortisone treatment is accompanied by a reversal of the blunted cortisol responses to human CRH.