Depression and sickness behavior are Janus-faced responses to shared inflammatory pathways

It is of considerable translational importance whether depression is a form or a consequence of sickness behavior. Sickness behavior is a behavioral complex induced by infections and immune trauma and mediated by pro-inflammatory cytokines. It is an adaptive response that enhances recovery by conserving energy to combat acute inflammation. There are considerable phenomenological similarities between sickness behavior and depression, for example, behavioral inhibition, anorexia and weight loss, and melancholic (anhedonia), physio-somatic (fatigue, hyperalgesia, malaise), anxiety and neurocognitive symptoms. In clinical depression, however, a transition occurs to sensitization of immuno-inflammatory pathways, progressive damage by oxidative and nitrosative stress to lipids, proteins, and DNA, and autoimmune responses directed against self-epitopes. The latter mechanisms are the substrate of a neuroprogressive process, whereby multiple depressive episodes cause neural tissue damage and consequent functional and cognitive sequelae. Thus, shared immuno-inflammatory pathways underpin the physiology of sickness behavior and the pathophysiology of clinical depression explaining their partially overlapping phenomenology. Inflammation may provoke a Janus-faced response with a good, acute side, generating protective inflammation through sickness behavior and a bad, chronic side, for example, clinical depression, a lifelong disorder with positive feedback loops between (neuro)inflammation and (neuro)degenerative processes following less well defined triggers

Sleep and quality of life in depression

Major depression is a common disorder; nearly 10% of the population suffers from a depressive illness in any given year. There is a strong association between sleep disturbances and depression. The most common sleep disturbance associated with major depressive disorder is insomnia. The relationship between insomnia and depression is bidirectional in that insomnia is one of the symptoms of depression and chronic insomnia can be a risk factor for depression. Depression causes changes in sleep patterns and sleep quality. Depressed patients showed prolonged sleep latency, increased wakefulness during sleep, early morning awakening, decreased sleep efficiency, decreased amounts of slow wave sleep and rapid eye movement (REM) sleep abnormalities. Depression is currently one of the leading causes of disability in the world. There is a direct association between the severity of depression and the level of disability. Depression has a big impact on quality of life of patients. Studies have showed that patients with major depressive disorder have poorer quality of life than persons from the general population. Effects of depression on quality of life are equal to or greater than those of patients with chronic medical conditions. Untreated depression usually does not go away by itself and often gets worse with time and increases a person's risk of suicide; it is a fact that up to 15% of those who are clinically depressed die through suicide. Clinical depression is treatable with counseling and medication. The majority of people with depressive disorders improve when they receive appropriate treatment. Improvement in depressive symptoms during the treatment is related to improvement in the quality of life. Antidepressants are shown to improve quality of life. There are some tools for evaluating quality of life in depressive patients, today. These tools help us to assess improvement in depressive patients beyond the extent to which depression rating scales do. In clinical settings, quality of life instruments can show us when patients begin to feel benefits of antidepressant therapy. © 2008 Humana Press, Totowa, NJ

Relationship between fast-acting antidepressant properties of total sleep deprivation and serum BDNF levels

Sleep deprivation therapy is a treatment option for major depressive disorder. Total sleep deprivation for one night improves depressive symptoms in 40–60% of treatments. Recent reports have suggested that brain-derived neurotrophic factor (BDNF) levels are reduced in individuals suffering major depressive disorder and these levels normalize following antidepressant treatment.In a recent study we have shown that the effects of total sleep deprivation therapy on BDNF levels in major depression. Results were compared between depressive patients that were treated with sertraline and healthy volunteers who experienced single total sleep deprivation. The baseline BDNF levels were significantly lower in both patient groups than the controls. Single sleep deprivation therapy was shown to decrease HAM-D scores and increase BDNF levels significantly in depressive patients. Effects of single sleep deprivation therapy on HAM-D scores was correlated with changes in BDNF levels. A series of three sleep deprivation therapies in a week accelerated the treatment response and increased the BDNF levels rapidly compared to the patients treated with sertraline alone. Better treatment response in the TSD group was also correlated with the statistically significant increase of BDNF levels in the 7th day compared to the sertraline group.In conclusion, our results support the BDNF reduction in major depression. Rapid antidepressant effects of sleep deprivation therapy appear to relate to the rapid BDNF increase in major depressive patients. These results give an opportunity to explore the relationship between fast antidepressant response and BDNF changes in major depression.</jats:p

RELATIONSHIP BETWEEN FAST-ACTING ANTIDEPRESSANT PROPERTIES OF TOTAL SLEEP DEPRIVATION AND SERUM BDNF LEVELS

[Abstract Not Available

Aortic aneurysm and electroconvulsive therapy in elderly depressive patient

We report the case of a 67-year-old single man with aortic aneurysm whose depression was successfully treated with electroconvulsive therapy. Metoprolol succinate was used for blood pressure control, and there were no cardiovascular side effects and no significant increase in blood pressure detected

Cotard's syndrome with schizophreniform disorder can be successfully treated with electroconvulsive therapy: case report

We report a case of Cotard's syndrome associated with psychotic symptoms. A 27-year-old man was admitted to hospital with the diagnosis of schizophreniform disorder. His presenting symptoms, which had started 1 month before hospital admission, were somatic delusions of gastrointestinal and cardiovascular malfunction and the absence of a stomach, which resulted in a decrease in weight from 75 kg to 63 kg in 1 month. Cranial computed tomographic images showed dilatation of the lateral and third ventricles, whereas magnetic resonance imaging revealed central atrophy and lateral ventricle dilatation. Single-photon emission computed tomography demonstrated left temporal, left frontal and left parietal hypoperfusion. The patient did not respond to antipsychotic therapies, but he was successfully treated with electroconvulsive therapy. This report emphasizes that Cotard's syndrome may be accompanied by lesions of the left hemisphere and that electroconvulsive therapy could be the first-line therapy in such patients with psychotic disorder

Sleep quality and psychopathological features in obese binge eaters

The objectives of this study were to determine the prevalence of Binge Eating Disorder (BED) and to investigate the subjective sleep qualities and the psychopathological features of BED in treatment-seeking obese patients. Thirty-six treatment-seeking obese subjects and 37 control subjects were interviewed with the DSM-IV research criteria for BED, The Pittsburgh Sleep Quality Index (PSQI), Bulimic Investigatory Test, Edinburg (BITE) and SCL-90-R scales. Eight out of 36 treatment-seeking obese patients (22.2 per cent) met the criteria for BED. The PSQI global scores, sleep latencies and SCL-PSDI, SCL-interpersonal sensitivity subscale results were all significantly higher in treatment-seeking BED obese subjects than non-BED (N-BED) subjects and controls. Our findings suggest that BED appears to be a common disorder in treatment-seeking obese patients. The treatment-seeking obese BED patients suffer from more psychopathological problems than N-BED obese patients and controls, and the subjective sleep qualities are likely to be disrupted in patients with BED. Copyright (C) 2004 John Wiley Sons, Ltd