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Background: Depressive disorders are significantly more common in the medically ill compared to the general population. Depression is associated with worsening of physical symptoms, greater healthcare utilization and poorer treatment adherence. The present paper provides a critical review on the assessment and management of depression in the medically ill. Methods: Relevant articles pertaining to depression in the medically ill were identified, reviewed and synthesized qualitatively. A systematic review was not performed due to the large breadth of this topic, making a meaningful summary of all published and unpublished studies not feasible. Notable studies were reviewed and synthesized by a diverse set of experts to provide a balanced summary. Results: Depression is frequently under-recognized in medical settings. Differential diagnoses include delirium, personality disorders and depressive disorders secondary to substances, medications or another medical condition. Depressive symptoms in the context of an adjustment disorder should be initially managed by supportive psychological approaches. Once a mild to moderate major depressive episode is identified, a stepped care approach should be implemented, starting with general psychoeducation, psychosocial interventions and ongoing monitoring. For moderate to severe symptoms, or mild symptoms that are not responding to low-intensity interventions, the use of antidepressants or higher intensity psychotherapeutic interventions should be considered. Psychotherapeutic interventions have demonstrated benefits with small to moderate effect sizes. Antidepressant medications have also demonstrated benefits with moderate effect sizes; however, special caution is needed in evaluating side effects, drug–drug interactions as well as dose adjustments due to impairment in hepatic metabolism and/or renal clearance. Novel interventions for the treatment of depression and other illness-related psychological symptoms (e.g. death anxiety, loss of dignity) are under investigation. Limitations: Non-systematic review of the literature. Conclusion: Replicated evidence has demonstrated a bidirectional interaction between depression and medical illness. Screening and stepped care using pharmacological and non-pharmacological interventions is merited. [ABSTRACT FROM AUTHOR]

Objective: Milnacipran is a serotonin noradrenaline reuptake inhibitor (SNRI) approved for treatment of fibromyalgia in Australia, but is used for depression in Europe and elsewhere. This paper will briefly review milnacipran and its utility in psychiatry for the treatment of depression.Conclusion: Milnacipran is a dual reuptake inhibitor of noradrenaline and serotonin, with greater effect on noradrenaline than serotonin, in contrast to the related drugs venlafaxine, desvenlafaxine and duloxetine. Rapidly absorbed irrespective of food, milnacipran has a half-life of approximately 8 hours, reaches steady state in 2 days and is excreted renally. Milnacipran helps a minority of patients with fibromyalgia by reducing pain and fatigue. It is also an effective antidepressant with efficacy comparable to venlafaxine and duloxetine, and a side effect profile characteristic of SNRIs. The dose range is 50-200 mg, in divided doses. Milnacipran may be useful for patients with depression and pain, and endogenous depression characterised by anergia, psychomotor retardation and hypersomnia. Caution is necessary in the presence of heart disease, hypertension, renal impairment, epilepsy, glaucoma, bipolar disorder, and bleeding tendency. Milnacipran is likely to be a useful late antidepressant option in treatment-resistant patients, as well as those with chronic pain, anergia and hypersomnia. [ABSTRACT FROM AUTHOR]

Rationale: In recent decades, the use of ayahuasca (AYA) - a β-carboline- and dimethyltryptamine-rich hallucinogenic botanical preparation traditionally used by Northwestern Amazonian tribes for ritual and therapeutic purposes - has spread from South America to Europe and the USA, raising concerns about its possible toxicity and hopes of its therapeutic potential. Thus, it is important to analyze the acute, subacute, and long-term effects of AYA to assess its safety and toxicity.Objectives: The purpose of this study was to conduct a systematic review of human studies assessing AYA effects on psychiatric symptoms, neuropsychological functioning, and neuroimaging.Methods: Papers published until 16 December 2015 were included from PubMed, LILACS and SciELO databases following a comprehensive search strategy and pre-determined set of criteria for article selection.Results: The review included 28 full-text articles. Acute AYA administration was well tolerated, increased introspection and positive mood, altered visual perceptions, activated frontal and paralimbic regions and decreased default mode network activity. It also improved planning and inhibitory control and impaired working memory, and showed antidepressive and antiaddictive potentials. Long-term AYA use was associated with increased cortical thickness of the anterior cingulate cortex and cortical thinning of the posterior cingulate cortex, which was inversely correlated to age of onset, intensity of prior AYA use, and spirituality. Subacute and long-term AYA use was not associated with increased psychopathology or cognitive deficits, being associated with enhanced mood and cognition, increased spirituality, and reduced impulsivity.Conclusions: Acute, subacute, and long-term AYA use seems to have low toxicity. Preliminary studies about potential therapeutic effects of AYA need replication due to their methodological limitations. [ABSTRACT FROM AUTHOR]

Antidepressants often disrupt sleep. Vortioxetine, a multimodal antidepressant acting through serotonin (5-HT) transporter (SERT) inhibition, 5-HT3, 5-HT7 and 5-HT1D receptor antagonism, 5-HT1B receptor partial agonism, and 5-HT1A receptor agonism, had fewer incidences of sleep-related adverse events reported in depressed patients. In the accompanying paper a polysomnographic electroencephalography (sleep-EEG) study of vortioxetine and paroxetine in healthy subjects indicated that at low/intermediate levels of SERT occupancy, vortioxetine affected rapid eye movement (REM) sleep differently than paroxetine. Here we investigated clinically meaningful doses (80-90% SERT occupancy) of vortioxetine and paroxetine on sleep-EEG in rats to further elucidate the serotoninergic receptor mechanisms mediating this difference. Cortical EEG, electromyography (EMG), and locomotion were recorded telemetrically for 10 days, following an acute dose, from rats receiving vortioxetine-infused chow or paroxetine-infused water and respective controls. Sleep stages were manually scored into active wake, quiet wake, and non-REM or REM sleep. Acute paroxetine or vortioxetine delayed REM onset latency (ROL) and decreased REM episodes. After repeated administration, vortioxetine yielded normal sleep-wake rhythms while paroxetine continued to suppress REM. Paroxetine, unlike vortioxetine, increased transitions from non-REM to wake, suggesting fragmented sleep. Next, we investigated the role of 5-HT3 receptors in eliciting these differences. The 5-HT3 receptor antagonist ondansetron significantly reduced paroxetine's acute effects on ROL, while the 5-HT3 receptor agonist SR57227A significantly increased vortioxetine's acute effect on ROL. Overall, our data are consistent with the clinical findings that vortioxetine impacts REM sleep differently than paroxetine, and suggests a role for 5-HT3 receptor antagonism in mitigating these differences. [ABSTRACT FROM AUTHOR]

Bupropion is an antidepressant that is effective in the treatment of major depressive disorders, smoking cessation, and sexual side effects of selective serotonin reuptake inhibitors. Acute dystonia is characterized by prolonged muscle contraction often represented by spasms of the head and neck muscles as well as occasional jaw clenching and temporomandibular joint syndrome. Although it is believed that dystonia is the result of an abnormality of the basal ganglia, its pathophysiology is still unclear. A few cases of dystonia resulting from bupropion have been reported in prior research papers. This case report discusses a patient who had a neck spasm painful enough to wake him up and dystonic distortion after taking only one dose of 75 mg bupropion. The patient was a young 34-year-old man with a diagnosis of obsessive-compulsive disorder treated with 60 mg fluoxetine. Bupropion was added to his medications because of sexual side effects caused by the fluoxetine. It seems that we must be careful to watch for dystonic symptoms when bupropion is mixed with other drugs that affect serotonin reuptake. Although dystonia is a rare side effect of bupropion, physicians should be aware of it and manage it if it occurs. [ABSTRACT FROM AUTHOR]

Brain diseases and their treatment may help or hurt creativity in ways that shape quality of life. Increased creative drive is associated with bipolar disorder, depression, psychosis, temporal lobe epilepsy, frontotemporal dementia, Parkinson disease treatments, and autism. Creativity depends on goal-driven approach motivation from midbrain dopaminergic systems. Fear-driven avoidance motivation is of less aid to creativity. When serotonin and norepinephrine lower motivation and flexible behaviour, they can inhibit creativity. Hemispheric lateralization and frontotemporal connections must interact to create new ideas and conceptual schemes. The right brain and temporal lobe contribute skill in novelty detection, while the left brain and frontal lobe foster approach motivation and more easily generate new patterns of action from the novel perceptions. Genes and phenotypes that increase plasticity and creativity in tolerant environments with relaxed selection pressure may confer risk in rigorous environments. Few papers substantively address this important but fraught topic. Antidepressants (ADs) that inhibit fear-driven motivation, such as selective serotonin reuptake inhibitors, sometimes inhibit goal-oriented motivation as well. ADs that boost goal-directed motivation, such as bupropion, may remediate this effect. Benzodiazepines and alcohol may be counterproductive. Although dopaminergic agonists sometimes stimulate creativity, their doing so may inappropriately disinhibit behaviour. Dopamine antagonists may suppress creative motivation; lithium and anticonvulsant mood stabilizers may do so less. Physical exercise and REM sleep may help creativity. Art therapy and psychotherapy are not well studied. Preserving creative motivation can help creativity and other aspects of well-being in all patients, not just artists or researchers. [ABSTRACT FROM AUTHOR]

Objective: This paper outlines the process of developing a transcranial magnetic stimulation (rTMS) service in a private hospital setting, to provide a model for similar services elsewhere in Australia and New Zealand. Methods: The practical issues involved in setting up the service, including funding, staffing, equipment, treatment protocols and associated research, are described. Results: The service has been widely accepted by psychiatrists and patients. Forty-five patients have completed treatment and the research results show a significant clinical response to rTMS. Conclusions: Clinicians involved in the service have found both the clinical and research components rewarding. In the longer term, the issue of ongoing funding of rTMS services remains to be resolved. [ABSTRACT FROM AUTHOR]