Here, we examined the cingulum bundle, a long-range white matter tract mediating dorsal limbic connectivity, using diffusion tensor imaging (DTI) tractography, in children and adolescents with autism spectrum disorder (ASD) versus controls. We hypothesised that cingulum bundle microstructure would be altered in ASD, based on evidence implicating abnormal white matter connectivity in this disorder.

DTI data were acquired for 19 ASD participants (IQ ⩾ 70; 7–18 years; mean = 12.4 ± 3.1) and 16 age-matched controls (7–18 years; mean = 12.3 ± 3.6) on a 3 T magnetic resonance imaging system. Deterministic tractography was used to isolate the cingulum bundle. Left and right cingulum bundles were examined for differences in several DTI metrics in ASD children/adolescents versus controls, including: fractional anisotropy (FA), mean, axial, and radial diffusivity.

Significant age × group interaction effects were found for all DTI metrics (mean diffusivity: F1,28 = 9.5, p = 0.005, radial diffusivity: F1,28 = 7.8, p = 0.009, axial diffusivity: F1,28 = 5.2, p = 0.03, FA: F1,28 = 4.4, p = 0.04). Interaction effects were driven by increases in cingulum bundle diffusivity (mean, radial, and axial diffusivity), and decreased FA, in younger ASD participants within our sample versus controls.

Our results point to immature microstructural organisation of the cingulum bundle in ASD, particularly during the early years of life, with implications for limbic network synchronisation and complex socio-emotional performance.

To investigate whether patients with Alzheimer's disease (AD) were able to alter their awareness of memory deficits after exposure to a memory task.

Thirty normal older adults and 23 mild AD patients participated in the study. Anosognosia was assessed using discrepancies between self- and informant-evaluations of cognitive and functional performance. Participants estimated their performance on the Verbal Paired Associates task at different points in time (before, immediately after the task and after a 1-h delay).

AD patients were generally less able to judge their memory abilities than healthy older adults, and tended to overestimate their task performance beforehand. Their prediction accuracy increased immediately after the task, but after a 1-h delay, they again misjudged their abilities at pretesting accuracy levels. Self-carer discrepancy scores of awareness of deficits in memory and other areas correlated significantly with memory tests but not with other neuropsychological tasks in the assessment, and larger discrepancy scores were associated with poorer performance.

AD patients can monitor their task performance online, but are unable to maintain awareness of their deficits over time. Loss of awareness of memory deficits (or of any other deficits) in early stage AD may indicate damage to a system which updates a personal knowledge base with recent information. Failure to retain this information impedes abstraction from episodic to semantic memory.

The aim of this paper was to provide a systematic review and update on the pharmacotherapy of social anxiety disorder (SAD), including the efficacy and tolerability of these agents, the ranking of interventions, and the grading of results by quality of evidence.

The Common Mental Disorder Controlled Trial Register and two trial registries were searched for randomised controlled trials (RCTs) comparing any pharmacological intervention or placebo in the treatment of SAD. We performed a standard pairwise meta-analysis using a random effects model and carried out a network meta-analysis (NMA) using the statistical package, R. Quality of evidence was also assessed.

We included 67 RCTs in the review and 21 to 45 interventions in the NMA. Paroxetine was most effective in the reduction of symptom severity as compared to placebo. Superior response to treatment was also observed for paroxetine, brofaromine, bromazepam, clonazepam, escitalopram, fluvoxamine, phenelzine, and sertraline. Higher dropout rates were found for fluvoxamine. Brofaromine, escitalopram, fluvoxamine, paroxetine, pregabalin, sertraline, and venlafaxine performed worse in comparison to placebo for the outcome of dropouts due to adverse events. Olanzapine yielded a relatively high rank for treatment efficacy and buspirone the worse rank for dropouts due to any cause.

The differences between drugs and placebo were small, apart from a significant reduction in symptom severity and response for paroxetine. We suggest paroxetine as a first-line treatment of SAD, with the consideration of future research on the drug olanzapine as well as brofaromine, bromazepam, clonazepam, escitalopram, fluvoxamine, phenelzine, and sertraline because we observed a response to treatment.

Bipolar disorder (BD) patients have recently been shown to exhibit increased proinflammatory cytokine levels indicating the role of inflammation in this disease. As inflammatory responses often include complement level alterations and complement production is influenced by cytokines, we aimed to find out whether complement system is activated in BD in a time-dependent manner and complement factors are involved in BD pathogenesis.

Serum C4, factor B, sC5b-9 and neuron-specific enolase levels were measured by enzyme-linked immunosorbent assay, whereas peripheral blood mononuclear cell messenger RNA (mRNA) expression levels of C1q, C4, factor B and CD55 were measured by real-time polymerase chain reaction in chronic BD patients (n=22), first episode BD patients (n=24) and healthy controls (n=19).

Serum complement levels were significantly reduced in chronic BD patients as compared with first episode BD patients and healthy controls. Serum levels of complement factors showed significant inverse correlation with disease duration, severity of manic symptoms and serum neuron-specific enolase levels. In chronic BD patients, peripheral blood mononuclear cell mRNA expression levels of C1q, C4 and factor B were significantly elevated, whereas the mRNA expression level of the complement inhibitor CD55 was significantly reduced.

Our results suggest that complement factor levels are reduced in BD presumably due to overconsumption of the complement system and complement production is increased at mRNA level possibly as a compensation measure. Complement factors might potentially be used as indicators of disease severity, neuronal loss and cognitive dysfunction.

Patients with functional memory disorder (FMD) report significant memory failures in everyday life. Differentiating these patients from those with memory difficulties due to early stage neurodegenerative conditions is clinically challenging. The current study explored whether distinctive neuropsychological profiles could be established, suitable to differentiate patients with FMD from healthy individuals and those experiencing amnestic mild cognitive impairment (a-MCI).

Patients with a clinical diagnosis of FMD were compared with patients with a-MCI, and healthy matched controls on several tests assessing different cognitive functions. Patients with clinically established mood disorders were excluded. Patients with FMD and a-MCI were broadly comparable on the level of their subjective memory complaints as assessed by clinical interview.

The neuropsychological profile of the FMD patients, although they expressed subjective memory and attention concerns during their clinical interview was distinct from patients with a-MCI on tests of memory [semantic fluency, age of acquisition (AoA) analysis of semantic fluency, verbal and non-verbal memory]. FMD patients did not differ significantly from healthy controls, but their scores on the letter fluency and digit cancellation tasks were not significantly different from those of the a-MCI patients indicating a possible sub-threshold deficit on these tasks.

Whilst subjective complaints are common within the FMD population, no objective impairment could be detected, even on a sensitive battery of tasks designed to detect subtle deficits caused by an early neurodegenerative brain disease. This study indicates that FMD patients can be successfully differentiated from patients with neurodegenerative memory decline by characterising their neuropsychological profile.

This study aimed to explore effects of adjunctive N-acetylcysteine (NAC) treatment on inflammatory and neurogenesis markers in unipolar depression.

We embarked on a 12-week clinical trial of NAC (2000 mg/day compared with placebo) as an adjunctive treatment for unipolar depression. A follow-up visit was conducted 4 weeks following the completion of treatment. We collected serum samples at baseline and the end of the treatment phase (week 12) to determine changes in interleukin-6 (IL6), C-reactive protein (CRP) and brain-derived neurotrophic factor (BDNF) following NAC treatment.

NAC treatment significantly improved depressive symptoms on the Montgomery–Asberg Depression Rating Scale (MADRS) over 16 weeks of the trial. Serum levels of IL6 were associated with reductions of MADRS scores independent of treatment response. However, we found no significant changes in IL6, CRP and BDNF levels following NAC treatment.

Overall, this suggests that our results failed to support the hypothesis that IL6, CRP and BDNF are directly involved in the therapeutic mechanism of NAC in depression. IL6 may be a useful marker for future exploration of treatment response.

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.

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.

Negative symptoms in schizophrenia have been associated with structural and functional alterations of the amygdala. We hypothesised that there would be between-group differences in amygdala volume and neural activation patterns during processing of affective stimuli among patients with schizophrenia and healthy controls. We further hypothesised correlations between neuroimaging metrics and clinical ratings of negative symptoms in patients with schizophrenia.

We used structural and functional magnetic resonance imaging to assess volume and neural activation of the amygdala in 28 patients with schizophrenia and 28 healthy controls.

We found no between-group differences in amygdala volume or neural activation. However, we found a significant negative correlation between emotional blunting and neural activation in the left amygdala during processing of positive affect. We also found a significant negative correlation between stereotyped thinking and the volume of right amygdala.

Our findings implicate the amygdala in a subgroup of negative symptoms in schizophrenia that are characterised by reduced expression with blunted affect and stereotyped thinking.

Our understanding of the neural circuitry involved in mood disorders is rapidly expanding through the ever-increasing application of functional brain imaging techniques.

A selective review of functional neuroimaging studies in patients with primary mood disorders was undertaken in order to identify points of commonality and controversy in the existing literature.

Articles published between 1980 and July 2005 were identified using a range of keywords from relevant on-line databases and key journals.

Increased activity within limbic regions has been consistently associated with depressive states and may also be present in manic states too. Dorsal and ventral prefrontal regions appear compromised as suggested by emerging evidence of cortical inefficiency within prefrontal regions or reductions in their connectivity with limbic areas. Most of the functional changes observed are at least partly reversible following clinical remission although deficits in prefrontal regions may be state-related.

Despite the use of disparate functional imaging modalities, there is a convergence of findings, and the results described do not appear to differ between unipolar and bipolar depression. However, further data are required in order to fully determine the functional changes occurring during manic states. Future work will also need to elucidate the effects of medication, the utility of specific cognitive tasks, and blood oxygenation level-dependent interactions within these affective states.

Severely malnourished patients with anorexia nervosa (AN) are reported to show fewer symptomatic viral infections and a poorer response to bacterial infection than controls. They are also reported to show mild immune system changes, although the relevance of these to altered infection disease presentation in AN and AN pathophysiology is unknown. Thus, in this paper, we suggest a range of immune system changes that might underpin these altered responses to common pathogens, and review a number of recent infectious disease findings for their utility in explaining the pathophysiology of AN.

A systematic review of the literature pertaining to immunity and infectious disease in AN was performed.

AN is associated with leucopenia, and the increased spontaneous and stimulated levels of proinflammatory cytokines [i.e. interleukin (IL)-1β, IL-6 and tumour necrosis factor α). A range of less consistent findings are also reviewed. Most of these data were not controlled for length of illness, degree of malnutrition, micronutrient or vitamin deficiencies or recent refeeding and starvation.

Cytokine disturbances have been suggested to be causally related to AN symptomatology and pathophysiology of AN, although the evidence supporting this assertion is lacking. Immune and cytokine changes in AN do, however, occur in association with a decreased incidence of symptomatic viral infection, decreased clinical response to bacterial infection leading to delayed diagnosis and increased morbidity and mortality associated with the infections.

The relationship between cannabis use and the onset of psychosis is well established. Aberrant salience processing is widely thought to underpin many of these symptoms. Literature explicitly investigating the relationship between aberrant salience processing and cannabis use is scarce; with those few studies finding that acute tetrahydrocannabinol (THC) administration (the main psychoactive component of cannabis) can result in abnormal salience processing in healthy cohorts, mirroring that observed in psychosis. Nevertheless, the extent of and mechanisms through which cannabis has a modulatory effect on aberrant salience, following both acute and chronic use, remain unclear.

Here, we systematically review recent findings on the effects of cannabis use – either through acute THC administration or in chronic users – on brain regions associated with salience processing (through functional MRI data); and performance in cognitive tasks that could be used as either direct or indirect measures of salience processing. We identified 13 studies either directly or indirectly exploring salience processing. Three types of salience were identified and discussed – incentive/motivational, emotional/affective, and attentional salience.

The results demonstrated an impairment of immediate salience processing, following acute THC administration. Amongst the long-term cannabis users, normal salience performance appeared to be underpinned by abnormal neural processes.

Overall, the lack of research specifically exploring the effects of cannabis use on salience processing, weaken any conclusions drawn. Additional research explicitly focussed on salience processing and cannabis use is required to advance our understanding of the neurocognitive mechanisms underlying the association between cannabis use and development of psychosis.

This study provides a comprehensive review of the literature on memory impairment and the potential effective factors in patients with chronic pain.

A literature search of databases PubMed, EMBASE, SpringerLink, and PsycINFO until September 2012 was conducted using the keywords ‘memory’ and ‘chronic pain’. The study emphasises on publications over the past 20 years.

Memory impairment in chronic pain patients is substantial, but the aspects of memory (e.g. working memory, long-term memory, and autobiographical memory) in chronic pain patients and the potentially related factors (e.g. age, level of education, pain conditions, emotion, neural network, and use of analgesics) are modest. Memory impairment is interpreted with the attention-narrowing hypothesis and the capacity-reduction hypothesis.

The currently available data and theory have explained memory impairment in chronic pain patients, but many controversies remain. Future research should focus on the subclinical characteristics of chronic pain, enlarging the sample size, and emphasise on the experimental intervention method and the cognitive neuroscience method.