Mindfulness meditation (MM) practices constitute an important group of meditative practices that have received growing attention. The aim of the present paper was to systematically review current evidence on the neurobiological changes and clinical benefits related to MM practice in psychiatric disorders, in physical illnesses and in healthy subjects.

A literature search was undertaken using Medline, ISI Web of Knowledge, the Cochrane collaboration database and references of retrieved articles. Controlled and cross-sectional studies with controls published in English up to November 2008 were included.

Electroencephalographic (EEG) studies have revealed a significant increase in alpha and theta activity during meditation. Neuroimaging studies showed that MM practice activates the prefrontal cortex (PFC) and the anterior cingulate cortex (ACC) and that long-term meditation practice is associated with an enhancement of cerebral areas related to attention. From a clinical viewpoint, Mindfulness-Based Stress Reduction (MBSR) has shown efficacy for many psychiatric and physical conditions and also for healthy subjects, Mindfulness-Based Cognitive Therapy (MBCT) is mainly efficacious in reducing relapses of depression in patients with three or more episodes, Zen meditation significantly reduces blood pressure and Vipassana meditation shows efficacy in reducing alcohol and substance abuse in prisoners. However, given the low-quality designs of current studies it is difficult to establish whether clinical outcomes are due to specific or non-specific effects of MM.

Despite encouraging findings, several limitations affect current studies. Suggestions are given for future research based on better designed methodology and for future directions of investigation.

Although guided self-help for depression and anxiety disorders has been examined in many studies, it is not clear whether it is equally effective as face-to-face treatments.

We conducted a meta-analysis of randomized controlled trials in which the effects of guided self-help on depression and anxiety were compared directly with face-to-face psychotherapies for depression and anxiety disorders. A systematic search in bibliographical databases (PubMed, PsycINFO, EMBASE, Cochrane) resulted in 21 studies with 810 participants.

The overall effect size indicating the difference between guided self-help and face-to-face psychotherapy at post-test was d=−0.02, in favour of guided self-help. At follow-up (up to 1 year) no significant difference was found either. No significant difference was found between the drop-out rates in the two treatments formats.

It seems safe to conclude that guided self-help and face-to-face treatments can have comparable effects. It is time to start thinking about implementation in routine care.

Several studies have reported reduction of auditory hallucinations (AH) after repetitive transcranial magnetic stimulation (rTMS) to the left temporal cortex. This study explored the effects of rTMS to the left and right temporal cortex.

Eighteen subjects with schizophrenia and frequent AH were enrolled in a double-blind, cross-over trial of 3 days of active rTMS to the left or right temporal cortex, or sham rTMS to the vertex (control condition), followed by an open treatment phase. The effects on AH were assessed by a blinded rater, using the Auditory Hallucination Rating Scale (AHRS).

During the double-blind phase, active temporal rTMS did not result in significantly greater improvement in hallucination scores than sham rTMS to the vertex, apart from a reduction in distress scores. Hallucination scores improved during the open continued treatment phase.

This study did not demonstrate an advantage for left temporal rTMS compared to right temporal and sham stimulation, over a 3-day stimulation period, but found modest improvement in hallucinations during continued open label treatment.

Schizophrenia out-patients have deficits in affective theory of mind (ToM) but also on more basal levels of social cognition, such as the processing of neutral and emotional expressions. These deficits are associated with changes in brain activation in the amygdala and the superior temporal sulcus (STS). However, until now there have been no studies that examined these different levels of social cognition and their neurobiological underpinnings in patients within one design.

Sixteen medicated schizophrenia out-patients and 16 matched healthy controls were studied with functional magnetic resonance imaging (fMRI) during a social cognition task that allows the investigation of affective ToM (aToM), emotion recognition and the processing of neutral facial expressions.

Patients showed a deficit in emotion recognition and a more prominent deficit in aToM. The performance in aToM and in emotion recognition was correlated in the control group but not in the schizophrenia group. Region-of-interest analysis of functional brain imaging data revealed no difference between groups during aToM, but a hyperactivation in the schizophrenia group in the left amygdala and right STS during emotion recognition and the processing of neutral facial expressions.

The results indicate that schizophrenia out-patients have deficits at several levels of social cognition and provide the first evidence that deficits on higher-order social cognitive processes in schizophrenia may be traced back to an aberrant processing of faces per se.

Post-traumatic stress disorder (PTSD) has been called one of the signature injuries of the Iraq War. In this review prevalence estimates of PTSD are summarized and discrepancies are discussed in relation to methodological differences between studies.

We searched for population-based studies with a minimum sample size of 300. Studies based on help-seeking samples were excluded. We identified 60 possible papers, of which 19 fulfilled the inclusion criteria. Prevalence estimates and study characteristics were examined graphically with forest plots, but because of high levels of heterogeneity between studies, overall estimates of PTSD prevalence were not discussed.

The prevalence of PTSD in personnel deployed to Iraq varied between 1.4% and 31%. Stratifying studies by PTSD measure only slightly reduced the variability in prevalence. Anonymous surveys of line infantry units reported higher levels of PTSD compared to studies that are representative of the entire deployed population. UK studies tend to report lower prevalence of PTSD compared with many US studies; however, when comparisons are restricted to studies with random samples, prevalences are similar. US studies that have assessed personnel more than once since return from deployment have shown that PTSD prevalence increases over the 12 months following deployment.

Differences in methodologies and samples used should be considered when making comparisons of PTSD prevalence between studies. Further studies based on longitudinal samples are needed to understand how the prevalence of PTSD changes over time.

Cognitive models suggest that auditory verbal hallucinations arise through defective self-monitoring and the external attribution of inner speech. We used a paradigm that engages verbal self-monitoring (VSM) to examine whether this process is impaired in people experiencing prodromal symptoms, who have a very high risk of developing psychosis.

We tested 31 individuals with an At-Risk Mental State (ARMS) and 31 healthy volunteers. Participants read single adjectives aloud while the source and pitch of the online auditory verbal feedback was manipulated, then immediately identified the source of the speech they heard (Self/Other/Unsure). Response choice and reaction time were recorded.

When reading aloud with distorted feedback of their own voice, ARMS participants made more errors than controls (misidentifications and unsure responses). ARMS participants misidentified the source of their speech as ‘Other’ when the level of acoustic distortion was severe, and misidentification errors were inversely related to reaction times.

Impaired VSM is evident in people with an ARMS, although the deficit seems to be less marked than in patients with schizophrenia. Follow-up of these participants may clarify the extent to which the severity of this impairment predicts the subsequent onset of psychosis and development of positive symptoms.

Although cognitive behavioural therapy (CBT) is claimed to be effective in schizophrenia, major depression and bipolar disorder, there have been negative findings in well-conducted studies and meta-analyses have not fully considered the potential influence of blindness or the use of control interventions.

We pooled data from published trials of CBT in schizophrenia, major depression and bipolar disorder that used controls for non-specific effects of intervention. Trials of effectiveness against relapse were also pooled, including those that compared CBT to treatment as usual (TAU). Blinding was examined as a moderating factor.

CBT was not effective in reducing symptoms in schizophrenia or in preventing relapse. CBT was effective in reducing symptoms in major depression, although the effect size was small, and in reducing relapse. CBT was ineffective in reducing relapse in bipolar disorder.

CBT is no better than non-specific control interventions in the treatment of schizophrenia and does not reduce relapse rates. It is effective in major depression but the size of the effect is small in treatment studies. On present evidence CBT is not an effective treatment strategy for prevention of relapse in bipolar disorder.

Most information about the lifetime prevalence of mental disorders comes from retrospective surveys, but how much these surveys have undercounted due to recall failure is unknown. We compared results from a prospective study with those from retrospective studies.

The representative 1972–1973 Dunedin New Zealand birth cohort (n=1037) was followed to age 32 years with 96% retention, and compared to the national New Zealand Mental Health Survey (NZMHS) and two US National Comorbidity Surveys (NCS and NCS-R). Measures were research diagnoses of anxiety, depression, alcohol dependence and cannabis dependence from ages 18 to 32 years.

The prevalence of lifetime disorder to age 32 was approximately doubled in prospective as compared to retrospective data for all four disorder types. Moreover, across disorders, prospective measurement yielded a mean past-year-to-lifetime ratio of 38% whereas retrospective measurement yielded higher mean past-year-to-lifetime ratios of 57% (NZMHS, NCS-R) and 65% (NCS).

Prospective longitudinal studies complement retrospective surveys by providing unique information about lifetime prevalence. The experience of at least one episode of DSM-defined disorder during a lifetime may be far more common in the population than previously thought. Research should ask what this means for etiological theory, construct validity of the DSM approach, public perception of stigma, estimates of the burden of disease and public health policy.

Longitudinal studies indicate that future schizophrenia patients exhibit lower IQ than healthy controls. Recent studies suggest that future patients with other mental illnesses obtain lower pre-morbid IQ. The aims of this study were to compare pre-morbid IQ among five diagnostic categories and normal controls, to examine the distribution of pre-morbid IQ, and to investigate the relationship between pre-morbid IQ and risk of mental illness.

A total of 7486 individuals hospitalized with psychiatric disease and 20 531 controls. IQ was measured at the draft board and hospital diagnoses [schizophrenia (Sz), non-schizophrenic, non-affective psychoses (NSAP), affective (AD), personality (PD) and neurotic/stress disorders (ND)] were followed up to ages 43–54 years. Individuals hospitalized ⩽1 year after appearing before the draft board were excluded.

All future patients obtained significantly lower pre-morbid IQ than controls (3–7 IQ points), AD had the highest IQ and PD the lowest. In each diagnostic category, decreasing IQ was associated with an increasing risk of becoming a patient [odds ratios (ORs) 0.5–2.5 over the full IQ spectrum]. IQ distributions was nearly normal and uni-modal.

IQ deficits in each diagnostic category may reflect different functional patterns and temporal vicissitudes of the specific pathogenetic processes involved in different mental disorders.

Cognitive problems are commonly reported in persons with chronic fatigue syndrome (CFS) and are one of the most disabling symptoms of this condition. A number of cognitive deficits have been identified, although the findings are inconsistent and hindered by methodological differences. The current study therefore conducted a meta-analysis of research examining cognitive functioning in persons with CFS in order to identify the pattern and magnitude of any deficits that are associated with this condition.

A comprehensive search of the PubMed and PsycINFO databases for studies that examined cognitive functioning in CFS between 1988 and 2008 identified 50 eligible studies. Weighted Cohen's d effect sizes, 95% confidence intervals and fail-safe Ns were calculated for each cognitive score.

Evidence of cognitive deficits in persons with CFS was found primarily in the domains of attention, memory and reaction time. Deficits were not apparent on tests of fine motor speed, vocabulary, reasoning and global functioning.

Persons with CFS demonstrate moderate to large impairments in simple and complex information processing speed and in tasks requiring working memory over a sustained period of time.

Weight gain is a long-recognized side-effect of antipsychotic (AP) drugs and a major health concern in the treatment of psychosis. The strength of the causal relationship between AP drug exposure and weight gain can only be gauged by a drugs trial conducted on AP-naive patients.

We conducted a review of the literature regarding the amount of weight gain induced by APs in AP-naive patients and carried out a meta-analysis of mean weight gains.

We found 11 primary studies reporting the effects of APs on body weight or body mass index (BMI) in AP-naive patients. The mean body weight and BMI gains in AP-naive patients were highly significant from the first weeks of treatment. When we limited the analysis to studies conducted on patients hospitalized and without any adjunctive treatment potentially affecting weight, the resultant sample showed less heterogeneity and confirmed the final picture of weight gain at around 3.8 kg and 1.2 points BMI.

Weight gain associated with AP therapy in AP-naive patients occurs rapidly in the first few weeks and continues during the following months. Clinicians should be aware of the high probability of causing weight gain in AP-naive patients and should strictly monitor such patients.

To estimate the spectrum of familial risk for psychopathology in first-degree relatives of children with unabridged DSM-IV bipolar-I disorder (BP-I).

We conducted a blinded, controlled family study using structured diagnostic interviews of 157 children with BP-I probands (n=487 first-degree relatives), 162 attention deficit hyperactivity disorder (ADHD) (without BP-I) probands (n=511 first-degree relatives), and 136 healthy control (without ADHD or BP-I) probands (n=411 first-degree relatives).

The morbid risk (MR) of BP-I disorder in relatives of BP-I probands (MR=0.18) was increased 4-fold [95% confidence interval (CI) 2.3–6.9, p<0.001] over the risk to relatives of control probands (MR=0.05) and 3.5-fold (95% CI 2.1–5.8, p<0.001) over the risk to relatives of ADHD probands (MR=0.06). In addition, relatives of children with BP-I disorder had high rates of psychosis, major depression, multiple anxiety disorders, substance use disorders, ADHD and antisocial disorders compared with relatives of control probands. Only the effect for antisocial disorders lost significance after accounted for by the corresponding diagnosis in the proband. Familial rates of ADHD did not differ between ADHD and BP-I probands.

Our results document an increased familial risk for BP-I disorder in relatives of pediatric probands with DSM-IV BP-I. Relatives of probands with BP-I were also at increased risk for other psychiatric disorders frequently associated with pediatric BP-I. These results support the validity of the diagnosis of BP-I in children as defined by DSM-IV. More work is needed to better understand the nature of the association between these disorders in probands and relatives.

Only one previous randomized controlled trial (RCT) has examined the efficacy of cognitive behaviour therapy (CBT) for chronic fatigue syndrome (CFS) in children. The aim of this study was to compare family-focused CBT with psycho-education for CFS in adolescents.

Sixty-three 11- to 18-year-olds (43 girls, 20 boys) with CFS were randomly assigned to either family-focused CBT or psycho-education delivered over 6 months. School attendance was the main outcome, which was assessed at the end of treatment and at 3, 6 and 12 months follow-up.

At the main outcome point (the 6-month follow-up) both groups had improved similarly. However, although those who received family-focused CBT were attending school for longer than those who received psycho-education, at discharge from treatment and at 3 months follow-up, they improved less quickly across the follow-up period.

Adolescents with CFS get back to school more quickly after family-focused CBT. This is important as they are at a crucial stage of their development. However, the finding that psycho-education was as effective as family-focused CBT at 6 and 12 months follow-up has important implications for health service delivery.