As depression is a considerable risk factor for an unfavourable course of myocardial infarction (MI), antidepressant treatment of post-MI depression and, inherent to MI status, polypharmacy has become an important issue.

The present study is the first to evaluate cognitive side effects of fluoxetine, as part of a placebo-controlled double-blind trial, in patients with post-first MI depression.

Cognitive performance of 54 depressed patients post first-MI, treated with fluoxetine or placebo was compared. Cognitive performance was tested before and after 9 weeks of treatment using the Visual Verbal Learning Test, Concept Shifting Task, Stroop Colour-Word Test and Letter-Digit-Substitution Test.

The median number of cardiovascular drugs taken by MI patients was 4.9. There were no differences between the fluoxetine and the placebo group on cognitive performance.

In sum, there were no negative side effects of fluoxetine compared with placebo on cognition in depressed MI patients, simultaneously treated with cardiac drugs.

Hepatitis C virus (HCV) infection is common among intravenous drug users, and because of the long latent period, HCV liver disease is set to increase.

We sought to examine practice guidelines regarding treatment of HCV in drug users and to review the evidence for current practices.

A structured search of the Pubmed database, websites of the National Institute for Clinical Excellence and national and international expert groups and opinion of independent experts in the field.

All those infected with HCV need to be assessed to ascertain whether they have active ongoing viral replication and the extent of liver damage. HCV-infected individuals should be educated about the modes of transmission and means of reducing the risk of infecting others. They should also be advised to avoid cofactors (especially alcohol) that accelerate the progression of liver disease. Specific treatment with antivirals can cause viral clearance and prevent the progression of liver disease. Therapy is effective in those on opiate-replacement treatments and also in motivated individuals who continue to use intravenous drugs. The decision whether to treat drug users should be made jointly by specialists in the management of viral hepatitis and addiction on a case-by-case basis. Current combination drug regimens are expensive but are claimed to be cost-effective, and are certainly much less costly than managing end-stage liver disease. In addition to satisfactory sustained viral response rates, other benefits such as a beneficial effect on drug habit, self-esteem and rehabilitation have been reported. Encouraging suitable drug users to take-up and comply with treatment seems to be more easily achieved in supportive drug dependency unit settings (rather than the more formal surroundings of a hospital clinic).

An area of recent interest in psychiatric research is the application of neuroimaging techniques to investigate neural events associated with the development and the treatment of symptoms in a number of psychiatric disorders.

To examine whether psychological therapies modulate brain activity and, if so, to examine whether these changes similar to those found with relevant pharmacotherapy in various mental disorders.

Relevant data were identified from Pubmed and PsycInfo searches up to July 2005 using combinations of keywords including ‘psychological therapy’, ‘behaviour therapy’, ‘depression’, ‘panic disorder’, ‘phobia’, ‘obsessive compulsive disorder’, ‘schizophrenia’, ‘psychosis’, ‘brain activity’, ‘brain metabolism’, ‘PET’, ‘SPECT’ and ‘fMRI’.

There was ample evidence to demonstrate that psychological therapies produce changes at the neural level. The data, for example in depression, panic disorder, phobia and obsessive compulsive disorder (OCD), clearly suggested that a change in patients' symptoms and maladaptive behaviour at the mind level with psychological techniques is accompanied with functional brain changes in relevant brain circuits. In many studies, cognitive therapies and drug therapies achieved therapeutic gains through the same neural pathways although the two forms of treatment may still have different mechanisms of action.

Empirical research indicates a close association between the ‘mind’ and the ‘brain’ in showing that changes made at the mind level in a psychotherapeutic context produce changes at the brain level. The investigation of changes in neural activity with psychological therapies is a novel area which is likely to enhance our understanding of the mechanisms for therapeutic changes across a range of disorders.

The aim of this study was to search for morphological and hemodynamic changes in hepatic and splanchnic vasculature in alcoholic patients without the signs of hepatic damage and subtyped by Cloninger classification by means of sonography, and compare the subtypes among themselves and with nonalcoholic healthy subjects.

Thirty alcohol dependent patients and 30 healthy subjects with no alcohol problem or hepatic impairment were included in the study. Patients were subtyped by Cloninger classification and all patients were evaluated by gray-scale and spectral Doppler ultrasound. The diameter of the portal vein, portal venous velocity, peak systolic and end diastolic velocities of hepatic and superior mesenteric arteries were assessed. RI, PI and systolic/diastolic velocity ratios were also calculated.

Portal vein diameter (PV diameter), portal vein cross sectional area (PV area), portal vein velocity (PV PSV), hepatic artery peak systolic velocity (HA PSV), hepatic artery end diastolic velocity (HA EDV), hepatic artery resistive index (HA RI), hepatic artery pulsatility index (HA PI), and systolic/diastolic velocity ratios (HA S/D), superior mesenteric artery peak systolic velocity (SMA PSV), superior mesenteric artery end diastolic velocity (SMA EDV), superior mesenteric artery resistive indices (SMA RI), pulsatility index (SMA PI), and systolic/diastolic velocity rates (SMA S/D) showed no significant difference among the groups (P > 0.01). Although there is no significant difference in PV PSV, HA PSV, SMA PSV, SMA EDV values between the groups, mean values of Type II alcoholics is greater than other groups. Portal vein cross-sectional area was greater in alcoholic patients (Type I, II and III) compared to the control group (P = 0.000). Portal vein velocity, hepatic artery peak systolic and end diastolic velocity, superior mesenteric artery peak systolic and end diastolic velocity were significantly greater in alcoholic patients than in the control group (P < 0.001). No statistical difference was detected between other parameters evaluated.

In alcohol dependent patients, some hemodynamic and morphologic changes occur in hepatic and splanchnic circulation, even before the signs of hepatic damage develop, which can be detected by means of Doppler and gray-scale sonography. But as there is no significant difference between the Doppler ultrasonographic findings among alcoholics subtyped by a Cloninger classification, which is a clinical classification, it suggests that psychiatric classification doesn't show any correlation with biological parameters, and because of this Cloninger classification a psychiatric classification cannot be considered as a characteristic determinative factor in the prognosis of hepatic disorder due to alcohol use. However, higher values of Type II alcoholics can be attributed to the longer alcohol intake of this subtype.

Mirtazapine is an antidepressant first approved in the Netherlands in 1994 for the treatment of major depressive disorder. However, evidence suggests its effectiveness in a variety of other psychiatric disorders and non-psychiatric medical conditions.

The present paper reviews the published literature on the off-label indications of Mirtazapine.

A search of the relevant literature from MEDLINE, PsycLIT and EMBASE databases, included in the Science Citation Index and available up to March 2006, was conducted using the terms mirtazapine, case-reports, open-label trials and randomized controlled trials. Only articles referring to conditions other than major depression were included in this present review.

Off-label use of mirtazapine has been reported in panic disorder, post-traumatic stress disorder, generalized anxiety disorder, social phobia, obsessive-compulsive disorder, dysthymia, menopausal depression, poststroke depression, depression as a result of infection with human immunodeficiency virus, elderly depression, Methylenedioxymethamphetamine (MDMA)-induced depression, hot flashes, alcohol and other substance use disorders, sleep disorders, sexual disorders, tension-type headaches, cancer pain, fibromyalgia, schizophrenia and other less frequent conditions.

So far, data on the off-label usefulness of mirtazapine are limited and mainly based on observations from case reports or open-label studies. However, positive cues suggest that confirmation of these preliminary data with randomized controlled trials may give sufficient evidence to warrant the use of mirtazapine in a broad range of disorders.

New evidence is emerging regarding abnormalities of hypothalamic-pituitary-adrenal (HPA) axis function in subtypes of affective disorders. Adverse effects of HPA axis dysregulation may include dysfunction of monoaminergic transmitter systems, cognitive impairment and peripheral effects. Newer treatments specifically targeting the HPA axis are being developed.

To review these developments focusing particularly on the glucocorticoid receptor (GR) antagonist mifepristone.

A selective review of the literature.

The function of GRs is increasingly being defined. The role of corticotrophin-releasing hormone (CRH) and dehydroepiandrosterone (DHEA) in the brain is also increasingly understood. HPA axis function is particularly likely to be abnormal in psychotic depression and bipolar disorder, and it is in these conditions that trials of the GR antagonist mifepristone are being focused. CRH antagonists and DHEA are also being investigated as potential treatments.

Initial studies of mifepristone and other HPA-axis-targeting agents in psychotic depression and bipolar disorder are encouraging and confirmatory studies are awaited.

The enlarged cava septi pellucidi (CSP = 6 mm in length) have been reported as a reliable marker of an underlying neuropsychiatric disease or disorder. Differences in the dimensions of cava longer than 6 mm associated with a neuropsychiatric impairment could be of possible clinical and forensic significance.

We obtained 479 brains from autopsied persons (310 males and 169 females, aged 22–89 years) and observed that 110 brains (75 males and 35 females) had CSP, of which the length of CSP was equal to or longer than 6 mm on 69 (49 males and 20 females) of them. These cava were classified into four groups depending on the past medical histories of the autopsied person: five without neuropsychiatric history (asymptomatic CSP), 25 schizophrenic patients, 22 alcoholics, and 17 with a past head trauma (symptomatic CSP).

The linear parameters of CSP (i.e. length, width) of the symptomatic and asymptomatic groups were measured and were statistically analyzed. Analysis revealed that the cava in the group of schizophrenic patients were significantly longer and wider.

Discriminant function analysis was used to derive a mathematical formula to classify CSP into one of the groups obtained based on width measurements of the cavum.

Depression and pain are both burdensome ailments that affect a major proportion of the population. It is evident that depression and pain frequently coexist, with treatment and outcome implications.

To review the literature on the nature, prevalence and co-morbidity of depression and pain, the biological and psychological mechanisms involved and treatment options, thus presenting a broad overview of the current information available.

Relevant sources were identified from PubMed and Medline databases using a combination of keywords including depression, pain, prevalence, co-morbidity, biological and psychological mechanisms, serotonin (5-HT), norepinephrine (NE), hypothalamic-pituitary-adrenal (HPA) axis, amygdala, functional magnetic resonance imaging (fMRI), antidepressant and psychological therapy.

It is evident from the research that depression and pain are common co-morbidities. Pain as a physical symptom of depression affects approximately 65% of patients, leading to less favourable outcomes and greater health care utilization. Moreover, depression is a common feature in chronic pain patients and can affect pain threshold and tolerance. Evidence from biological and psychological studies has revealed mechanisms that link chronic pain to depression. Several classes of anti-depressants and psychological interventions have been used successfully in the treatment of somatic symptoms of depression and for a variety of pain syndromes.

Pain and depression are linked by overlapping phenomenology, neurobiology and therapy. They are mutually interacting, and the interaction has significant treatment and outcome implications.

Double depression, the combination of major depression and dysthymia, is associated with poor health-related quality of life (HRQoL) and increased health service utilization.

To determine the prevalence of double depression, its associated morbidity and use of health services and antidepressants.

A random and representative sample of the South Australian general population was interviewed. The mood module of the Primary Care Evaluation of Mental Disorders (PRIME-MD), the Short-Form Health Status Questionnaire (SF-36) and Assessment of Quality of Life (AQoL) instruments were administered, and data relating to health service utilization, antidepressant use and role functioning were collected.

Double depression was present in 3.3% of the population. The use of health services was significantly higher in this group than those with no depression, or dysthymia or major depression alone. Only 15.2% had attended a community health service, 18.2% had seen a psychiatrist, 10.1% a psychologist, 16.2% a social worker and 9.1% any other counsellor in the last month. While 41.4% were currently taking an antidepressant, the average doses of the two most commonly prescribed antidepressants were below the maximum recommended doses, and the use of antidepressant augmentation strategies was also minimal.

While double depression is associated with increased morbidity and use of health services, the optimum use of both pharmacological and nonpharmacological treatments is clearly lacking in this community sample.

In this flexible-dose, open-label trial, we examined the efficacy of omega-3 fatty acids for the treatment of depression during pregnancy.

Fifteen pregnant women with major depressive episodes participated. Subjects initially received two capsules per day [0.93 g of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)]; the dose could be increased by one capsule per day every 2 weeks to a maximal dose of 2.8 g. Subjects were assessed with the Edinburgh Postnatal Depression Scale (EPDS) and Hamilton Rating Scale for Depression (HRSD).

Average duration of participation in this treatment trial was 8.3 weeks (SD ± 7.1). Average final dose of EPA + DHA in this flexible dose trial was 1.9 g per day (±0.5). The mean reduction in EPDS scores was 40.9% (SD ± 21.9); the mean decrease in HRSD score was 34.1% (SD ± 27.1).

This open trial provides data to support the need for randomized controlled dose-finding trials of omega-3 fatty acids in major depressive episodes during pregnancy.

Emotion regulation involves the initiation of new emotional responses and continual alteration of current emotions in response to rapidly changing environmental and social stimuli. The capacity to effectively implement emotion regulation strategies is essential for psychological health; impairments in the ability to regulate emotions may be critical to the development of clinical levels of depression, anxiety and mania.

This review provides a summary of findings from current research examining the neural mechanisms of emotion regulation by means of conscious cognitive strategies of reappraisal. These findings are considered in the context of related concepts of emotion perception and emotion generation, with discussion of the likely cognitive neuropsychological contributions to emotion regulation and the implications for psychiatric disorders.

Convergent evidence implicates an inhibitory role of prefrontal cortex and cingulate regions upon subcortical and cortical emotion generation systems in the cognitive control of emotional experience. Concurrent modulation of cortical activity by the peripheral nervous system is highlighted by recent studies using simultaneous physiological and neuroimaging techniques. Individual differences in emotion perception, generation of affect and neuropsychological skills are likely to have direct consequences for emotion regulation.

Emotion regulation relies on synergy within brain stem, limbic and cortical processes that promote the adaptive perception, generation and regulation of affect. Aberrant emotion processing in any of these stages may disrupt this self-sustaining regulatory system, with the potential to manifest in distinct forms of emotion dysregulation as seen in major psychiatric disorders such as depression, bipolar disorder and schizophrenia.