Cognitive impairment is the most consistent neurological complication of acquired and degenerative brain disorders. Historically, most focus was on dementia but now has been broadened to include the important construct of mild cognitive impairment.

Systematic search and review of articles linked quality of life (QoL) and cognitive complications of neurological disorders. We excluded QoL in dementia.

Our search identified 249 publications. Most research examined patients with brain tumours, stroke, epilepsy, head injury, Huntington's disease, motor neuron disease, multiple sclerosis and Parkinson's disease. Results suggested that the majority of patients with epilepsy, motor neuron disease, multiple sclerosis, Parkinson's disease, stroke and head injury have subtle cognitive deficits early in their disease course. These cognitive complaints are often overlooked by clinicians. In many cases, the cognitive impairment is progressive but it can also be relapsing-remitting and in some cases reversible. Despite the importance of severe cognitive impairment in the form of dementia, there is now increasing recognition of a broad spectrum of impairment, including those with subclinical or mild cognitive impairment. Even mild cognitive difficulties can have functional and psychiatric consequences–especially when they are persistent and untreated. Specific cognitive deficits such an inattention, dysexecutive function and processing speed may affect a number of quality of life (QoL) domains. For example, cognitive impairment influences return to work, interpersonal relationships and leisure activities. In addition, fear of future cognitive decline may also impact upon QoL.

We recommend further development of simple tools to screen for cognitive impairments in each neurological condition. We also recommend that a thorough cognitive assessment should be a part of routine clinical practice in those caring for individuals with neurological disorders.

This study is the first to examine the effect of bereavement of a first-degree family member on subsequent morbidity over a 10-year follow-up period.

A sample of bereaved subjects (n = 72) were compared with a control group (n = 80) recruited in the same period with respect to morbidity experience during follow-up. Morbidity events were ascertained from the subject themselves, their health care providers and these sources were also compared.

Bereavement was associated with an elevated total burden of illness as well as with mental health and circulatory system categories diagnosed according to the International Classification of Diseases - Clinically Modified (ICD-9) classification system. The elevation ranged from approximately 20% for any illness to 60–100% among circulatory system disorders. Although in an earlier study there was a downregulation of T-cell function in the bereaved during the first 8 weeks, there was no evidence that the bereavement was associated with increased morbidity in the respiratory or immune system ICD-9 categories long-term.

Past epidemiological research has indicated that bereavement of a close family member is associated with adverse health consequences of a generalised morbidity. Our study suggests an increase in mental health and circulatory system effects in particular. Further research is required to determine whether other systems are also affected by bereavement.

Mindfulness meditations (MM) are a group of meditation practices which are increasingly receiving attention. The aim of the present work is to review current findings about the neural correlates of MM and compare such findings with other specific and non-specific treatments.

A literature search was undertaken using MEDLINE, ISI web of knowledge, the Cochrane database and references of retrieved articles. Studies which focused on the functional neural correlates of MM, psychotherapy, pharmacotherapy and placebo published up to August 2009 were screened in order to be considered for the inclusion.

Main findings suggest that long-term MM practice allows a more flexible emotional regulation by engaging frontal cortical structures to dampen automatic amygdala activation. A large overlap exists between cerebral areas activated during MM, psychotherapy, pharmacotherapy and those activated by placebo. However, while MM, psychotherapy and placebo seem to act through a top-down regulation, antidepressants seem to act through a bottom-up process.

MM seem to target specific brain areas related to emotions and emotional regulation. Similar mechanisms have been observed also in other interventions, particularly psychotherapy.

One of the main utilities of staging in bipolar disorder is enhancing the formulation of pharmacological and non-pharmacological treatment strategies. Hence, it is essential to ascertain whether the number of previous episodes influences treatment response. Hereby, we present a 5-year post hoc study on the efficacy of group psychoeducation for bipolar disorders according to the number of previous episodes.

For this subanalysis, we have compared the 5-year outcome of 120 euthymic psychoeducated versus non-psychoeducated bipolar patients according to the number of previous episodes at study entry.

Patients with more than seven episodes at study entry did not show any significant improvement with psychoeducation according to time to recurrence. Patients with more than 14 episodes did not benefit from psychoeducation in terms of a reduction of time spent ill. Patients with 7 or 8 episodes showed a benefit in terms of fewer days spent in hypomania, depression, mixed episodes or any episodes but not mania, while patients with 9–14 episodes showed a benefit in terms of fewer days spent in hypomania and depression but not in mixed states or mania. Only patients who presented up to 6 episodes showed reduction in time spent in any episode polarity.

The number of previous episodes clearly worsens response to psychoeducation, perhaps in a more subtle way than that observed with other psychological therapies. Psychoeducation should be delivered as soon as possible in the illness course, supporting the idea of early intervention.

There is evidence that, even in remission, patients with bipolar disorder (BD) have deficits in cognitive function and emotional regulation. Siblings of patients with BD are also reported to exhibit minor dysfunction in neuropsychological domains. In this study, we examined the interference of acute mood state with reaction time (RT) and response inhibition in euthymic patients with BD, in their healthy siblings and in healthy controls.

A total of 34 patients with bipolar I disorder, 22 healthy siblings and 33 healthy controls performed a stop-signal paradigm after induction of a transient intense sadness and a relaxed mood state. The differences in RT and the response inhibition were compared between the groups.

Euthymic patients with BD displayed a higher emotional reactivity compared with their siblings and with controls. Compared with controls, patients with BD showed longer RTs in a relaxed mood state and a delay in response inhibition during emotional activation.

The present study provides evidence for the clinical observation that patients with BD have shorter RTs when in a state of emotional arousal rather than in a relaxed state. Inhibitory deficits in these patients may be because of a too strong emotional arousal. The results show that in patients with BD, relaxation and emotional arousal are inversely associated with performance in a neuropsychological task. This is in contrast to findings in healthy individuals suggesting a dysbalance in emotional regulation in these patients.

Myeloperoxidase (MPO) is an enzyme involved in the production of hypochloric acid as well as other reactive oxygen species. This enzyme plays a significant role in inflammatory processes. In view of the observed associations between depression and such inflammatory processes, as well as of the reports that confirm the presence of oxidative stress in depression, this study was designed to assess the correlation, if any, between the single nucleotide polymorphism G-463A of the MPO gene and the risk of recurrent depressive disorders (DD).

The study was carried out in a group of 149 patients with recurrent DD and 149 healthy control subjects. Genotyping was performed by PCR/restriction fragment length polymorphism.

A comparison between healthy controls and depressive patients showed a statistically significant difference in genotype distribution and allele frequency in the studied groups. Genotype distribution and allele frequency did not correlate with clinical variables of the patients.

The obtained results of the study allow us to draw a cautious conclusion about the role of the analysed G-463A MPO polymorphism in recurrent DD development, which, however, requires eventual confirmation in further studies.

Several studies have suggested that cytokine alterations could be related to the pathophysiology of schizophrenia. Transforming growth factor-beta1 (TGF-β1) is believed to be an important factor in regulation of inflammatory responses and to have anti-inflammatory effects. TGF-β1 also has trophic effects on dopaminergic neurons. We tested the hypothesis TGF-β1 is associated with the pathophysiology of schizophrenia.

The polymorphisms at codon 10 (T869C) and codon 25 (G915C) of TGF-β1 were analysed in 99 schizophrenia patients and 130 normal controls. At baseline and after 8 weeks of treatment, clinical symptoms were evaluated on Positive and Negative Syndrome Scale (PANSS).

None of the subjects were polymorphic at codon 25. However, the C allele at codon 10 was more frequent in schizophrenia (p = 0.05). Although schizophrenia group showed a higher tendency of allele frequency in the subjects with C allele (p = 0.05), the allelic difference did not reach statistical significance after correction for multiple comparisons (p = 0.1).

PANSS scores showed no significant correlation with genotypes. The genotype distribution was not significantly different between responders and non-responders. However, the C allele was more frequent among responders (p = 0.03).

These results suggest that the TGF-β1 polymorphism is associated with therapeutic response to antipsychotics. However, further studies with larger numbers of subjects are needed to confirm the effect of TGF-β1 in schizophrenia.

To investigate for the first time in a prospective study the relationship between depressive state and the neuropathological hallmarks of Alzheimer's disease, using a scale for depressive symptoms in dementia, while controlling for clinical severity of dementia.

Within the framework of a prospective longitudinal study of depression in Alzheimer's disease, patients with dementia underwent a clinical evaluation every six months during the last years of their lives, using the Cornell scale for depression in dementia to assess depressive symptoms and using the Functional Assessment Staging scale to control for clinical severity of dementia. The brains of 43 Alzheimer patients were obtained. The last clinical evaluations prior to death together with post-mortem neuropathology measures were analysed.

We found a correlation between the Cornell scores and the sum score for the density of neuritic plaques in the entire cortex (p = 0.027), and even stronger in the temporal cortex (p = 0.012). The observed correlations were independent of sex, age of death, clinical dementia severity and duration of Alzheimer's disease.

This study shows a positive relationship between depressive state at time of death and the presence of neuritic plaques in Alzheimer's disease, which is independent of the clinical severity of dementia.

Major depressive disorder (MDD) is characterised by predominately negatively valenced emotional symptoms that are often accompanied by cognitive impairments. We posited that cognitive impairments in MDD are related to altered emotional processing in prefrontal cortex.

We compared 20 medication-free patients with MDD and 29 matched healthy controls. Both groups performed an emotional task during functional magnetic resonance imaging (fMRI). Furthermore, they completed the intra–extra dimensional set shift (IED) test probing for cognitive impairments. Then we correlated the results of the IED with the changes in fMRI BOLD signal in MDD patients and healthy subjects.

The subcategory of the IED applying extradimensional shift (EDS) showed a divergent performance of the MDD group committing significantly more errors than the control group. Correlating the EDS errors with fMRI signal changes, the healthy subjects showed a positive correlation with the right ventrolateral prefrontal cortex and the right orbitofrontal cortex. MDD subjects, in contrast, showed a positive correlation in right dorsolateral prefrontal cortex (DLPFC) and a negative correlation in the left dorsomedial prefrontal cortex (DMPFC).

We hypothesise that the differential correlation in healthy controls and MDD patients may reflect the use of different strategies in their performance. The impaired executive functions, as reflected by altered processing in right DLPFC and left DMPFC, may implicitly influence emotional processing in patients suffering from MDD.

This study examined changes in brain grey matter in victims of rape (VoR) with and without post-traumatic stress disorder (PTSD). Previous research has focused on PTSD caused by various traumatic events, such as war and disaster, among others. Although considerable research has focused on rape-related PTSD, limited studies have been carried out in the context of Mainland China.

The study included 11 VoR with PTSD, 8 VoR without PTSD and 12 healthy comparison (HC) subjects. We used voxel-based morphometry to explore changes in brain grey-matter density (GMD) by applying statistical parametric mapping to high-resolution magnetic resonance images.

Compared with HC, VoR with PTSD showed significant GMD reductions in the bilateral medial frontal cortex, left middle frontal cortex, middle temporal gyrus and fusiform cortex and significant GMD increases in the right posterior cingulate cortex, postcentral cortex, bilateral precentral cortex and inferior parietal lobule. Compared to VoR without PTSD, VoR with PTSD showed significant GMD reductions in the right uncus, left middle temporal gyrus, and the fusiform cortex, and increases in the left precentral cortex, inferior parietal lobule and right post-central cortex.

The findings of abnormal GMD in VoR with PTSD support the hypothesis that PTSD is associated with widespread anatomical changes in the brain. The medial frontal cortex, precentral cortex, posterior cingulate cortex, post-central cortex and inferior parietal lobule may play important roles in the neuropathology of PTSD.

There is a paucity of data about risk factors for suicide attempts in bipolar disorder. The aim of this study is to examine the association between suicide attempts and obesity in people with bipolar disorder.

Two hundred fifty-five DSM-IV out-patients with bipolar disorder were consecutively recruited from the Bipolar Disorder Program at Hospital das Clínicas de Porto Alegre and the University Hospital at the Universidade Federal de Santa Maria, Brazil. Diagnosis and clinical variables were assessed with Structured Clinical Interview for DSM-IV-axis I (SCID I) and Program structured protocol. History of suicide attempts was obtained from multiple information sources including patients, relatives and review of medical records. Patients with body mass index (BMI) ≥ 30 were classified as obese.

Over 30% of the sample was obese and over 50% had a history of suicide attempt. In the multivariate model, obese patients were nearly twice (OR = 1.97, 95% CI: 1.06–3.69, p = 0.03) as likely to have a history of suicide attempt(s).

Our results emphasise the relevance of obesity as an associated factor of suicide attempts in bipolar disorder. Obesity may be seen as correlate of severity and as such, must be considered in the comprehensive management of bipolar patients.

Aberrant electrophysiological and haemodynamic processing of auditory oddball stimuli is among the most robustly documented findings in patients with schizophrenia. However, no study to date has directly examined linked patterns of electrical and haemodynamic differences in patients and controls.

In a recent paper we demonstrated a data-driven approach, joint independent component analysis (jICA) to fuse together functional magnetic resonance imaging (fMRI) and event-related potential (ERP) data and elucidated the chronometry of auditory oddball target detection in healthy control subjects. In this paper we extend our fusion method to identify specific differences in the neuronal chronometry of target detection for chronic schizophrenia patients compared to healthy controls.

We found one linked source, consistent with the N2 response, known to be related to cognitive processing of deviant stimuli, spatially localized to bilateral fronto-temporal regions. This source showed significant between-group differences both in amplitude response and in the fMRI/ERP distribution pattern. These findings are consistent with previous work showing N2 amplitude and latency abnormalities in schizophrenia, and provide new information about the linkage between the two.

In summary, we use a novel approach to isolate and identify a linked fMRI/ERP component which shows marked differences in chronic schizophrenia patients. We also show that jointly using both fMRI and ERP measures provides a fully picture of the underlying haemodynamic and electrical changes which are present in patients. Our approach also has broad applicability to other diseases such as autism, Alzheimer's disease, or bipolar disorder.