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.

To evaluate the absence and size of massa intermedia (MI), a midline thalamic structure, and its gender-specific alteration in patients with schizophrenia and bipolar disorder.

Thirty-five patients with schizophrenia (17 females and 18 males), 21 patients with bipolar disorder (15 females and 6 males) and 89 healthy controls (50 females and 39 males) were evaluated by magnetic resonance imaging. Thin-slice magnetic resonance images of the brain were evaluated. MI was determined in coronal and sagittal images, and area of the MI was measured on the sagittal plane.

Females had a significantly lower incidence of absent MI compared with males in the healthy control group. The absence of MI in schizophrenia and bipolar patients was not higher than the incidence in healthy controls. The size of MI showed a gender difference. The mean MI area size was smaller in female schizophrenia patients than in female controls, while no significant difference was observed between male schizophrenia patients and their controls.

The size of MI, a gender difference midline structure, is smaller in females with schizophrenia, and the results of this study support other studies of structural aberration of the thalamus and other midline structures in the brains of patients with schizophrenia.

Schizophrenia has been associated with limited abilities to interact effectively in social situations. Face perception and ability to recognise familiar faces are critical for social interaction. Patients with chronic schizophrenia are known to show impaired face recognition. Studying first-episode (FE) patients allows the exclusion of confounding effects of chronicity, medication and institutionalisation in this deficit.

To determine brain (dys)functions during a face encoding and recognition paradigm in FE schizophrenia.

Thirteen antipsychotic-naïve FE schizophrenia patients and 13 age- and sex-matched healthy controls underwent functional magnetic resonance imaging during a face encoding and recognition paradigm. Behavioural responses were recorded on line.

Patients recognised significantly fewer of previously presented faces than the controls (p = 0.008). At the neural level, both groups activated a network of regions including the fusiform area, occipital, temporal and frontal regions. In brain activity, the two groups did not differ in any region during encoding or recognition conditions (p > 0.05, corrected or uncorrected).

Our findings show impaired face recognition without a significant alteration of related brain activity in FE schizophrenia patients. It is possible that neural changes become more strongly evident with progression of the illness, and manifest themselves as behavioural impairments during the early course.

Studies investigating the cognitive effects of serotonin depletion, using the technique of acute tryptophan depletion (ATD) by dietary means, have generally suggested that ATD impairs delayed verbal recall and recognition. In two previous studies in the elderly, this result has not been replicated and ATD impaired working memory. These results may be susceptible to type II error but a similar testing schedule in the individual studies allows data to be pooled in a larger analysis.

Data from two separate double-blind placebo-controlled studies of the effects of ATD on cognitive function in the elderly were combined. In one study, a low dose and in the other a high dose of amino acids was used. In a repeated measures analysis of variance, the effects of ATD and the interaction of this with the other factors (age, gender and dose) on cognitive measures was examined.

Data from 31 healthy subjects aged between 60 and 81 years were analysed. There were no main effects of ATD or consistent interactions between ATD and age, gender or dose. There were significant interactions between ATD, gender and dose. When tryptophan depleted, females having the higher dose drink had reduced scores on Digit span and immediate recall on the Rey Auditory Verbal Learning Test.

The enlarged data set did not confirm an overall effect of ATD on working memory or on delayed word recall but does suggest an effect of ATD on encoding or registration in the subgroup of females receiving a higher strength drink.

The aims of this study were to determine the dominant affective temperament changes in stroke survivors and whether temperament affects the disability.

A total of 63 stroke patients were included in this study. Temperament Evaluation of Memphis, Pisa, Paris and San Diego Autoquestionnaire was used to determine the dominant affective temperament (depressive, hyperthymic, cyclothymic, irritable or anxious). The disability level was measured with the Barthel index (BI).

Depressive temperament (17.5%) and anxious temperament (12.7%) were the most common dominant affective temperaments. The frequencies of irritable, cyclothymic and hyperthymic temperaments were 4.8, 3.2 and 0%, respectively. The mean BI score was 78.1 ± 18.3 in patients with depressive temperament and 67.4 ± 28.4 in patients without depressive temperament (p = 0.403). The mean BI score was 78.1 ± 15.3 in patients with anxious temperament and 68.0 ± 28.3 in patients without anxious temperament (p = 0.541). Multiple linear regression analysis indicated that BI score was not associated with affective temperament changes.

The results of the current study suggest that depressive and anxious temperaments are the most common affective temperaments and that there appears to be no association between disability level and dominant affective temperament in stroke survivors.

Although there are rapidly growing concerns about the high rates of cognitive dysfunction in Korea, the knowledge of risk factors for Alzheimer’s disease (AD) among the general public in Korea remains to be elucidated.

A total of 2767 randomly selected subjects from the Ansan Geriatric Study were questioned on their knowledge of putative risk factors for AD. Their answers were compared with their sociodemographic data and other variables.

The most common stated risk factor was being older (59.6%), followed by head trauma (33.6%) and cerebrovascular disease (30.4%). However, a substandard education, which is a known risk factor, was considered significant by only 9.5% of the subjects. Predictors for a worse knowledge of the risk factors for AD were being older, a lower level of education, lower economic status and the attitude that dementia is not curable.

This study revealed that misunderstanding about AD is more prevalent in older subjects and those with a lower level of education, and so public health education on the basic concepts of AD should be targeted at this population.

The aim of the present study was to assess the association between previous suicide attempts and functional impairment among euthymic patients with bipolar disorder (BD).

Seventy-one Diagnostic Statistical Manual IV (DSM-IV) patients with BD and 61 healthy volunteers were recruited from the Bipolar Disorder Program at the Clinic Hospital of Barcelona. Patients with (n = 36, 50.7%) and without (n = 35, 49.3%) previous suicide attempts were assessed using the Structured Clinical Interview for DSM-IV-TR (SCID-P). Previous suicide attempts were carefully investigated by means of patient and caregiver interview and by a standard structured interview from the protocol of our BD Program. The Functioning Assessment Short Test (FAST) was employed to assess functional impairment.

Euthymic patients with previous suicide attempts showed functional impairment, particularly in occupational (F = 30.39; p = 0.001) and cognitive functioning (F = 18.43; p = 0.001). In addition, family history of psychiatric illness (χ2: 6.49; degrees of freedom (df) = 2;132; p = 0.010), family history of affective disorders (χ2 = 5.57; p = 0.017), psychotic symptoms (χ2 = 5.88; p = 0.014) and axis II comorbidity were associated with previous suicide attempts (χ2 = 5.16; p = 0.021).

Bipolar patients with previous suicide attempts had lower overall functioning than patients who did not attempt suicide. Previous suicide attempts were particularly associated with the occupational and cognitive domains of functioning.

The present study aims to investigate the association of unipolar depression (UPD) with six serotonergic gene polymorphisms in Han Chinese.

One hundred and thirty-two UPD patients and 180 healthy controls were genotyped for polymorphisms of six serotonergic genes, including tryptophan hydroxylase (TPH1 A218C), serotonin transporter promoter region (5-HTTLPR), serotonin receptor 2A (5-HT2AR −1438G/A), serotonin receptor 2C (5-HT2CR Cys23Ser), serotonin receptor 6 (5-HT6R C267T) and serotonin receptor 1Dβ (5-HT1DβR T371G). Symptomatic clusters were evaluated by the 24-item Hamilton Rating Scale for Depression (HAMD).

The frequencies of S/S genotype and S allele in 5-HTTLPR polymorphism were significantly higher in UPD patients than in healthy controls. There was a significant difference in distributions of genotypes in 5-HT2CR Cys23Ser polymorphism between UPD patients and control subjects, but the difference became no significant when the data were further stratified by gender. The patients with genotypes G/G and T/G of 5-HT1DβR T371G polymorphism had significantly lower scores of diurnal variation evaluated by HAMD than those with genotype T/T, while the patients with genotype T/G had significantly higher scores of hopelessness than those with genotypes G/G and T/T. There were no significant differences in genotypic and allelic distributions of TPH1 A218C, 5-HT2AR −1438G/A or 5-HT6R C267T polymorphisms between the case and control groups.

The study demonstrates that 5-HTTLPR and 5-HT2CR Cys23Ser polymorphisms might contribute to susceptibility of UPD, and the genotype T/T in 5-HT1DβR T371G polymorphism might be a risk factor for diurnal variation, while T/G might be a protective factor against hopelessness in Han Chinese populations.

There have been limited data available on the prevalence of structural brain abnormalities in asymptomatic individuals and a growing interest in the various ethical issues related to reporting of such findings. This study evaluated the prevalence of incidental abnormalities on brain magnetic resonance imaging (MRI) in a random sample of 60- to 64-year-old community-dwelling individuals as well as successfully followed a referral pathway taking into account of the various ethical issues related to the referral process. The Personality and Total Health (PATH) Project was designed to study the risk and protection factors of normal ageing, dementia and other neuropsychiatric disorders.

MRI scans were performed in randomly selected 478 healthy, community-dwelling 60- to 64-year-old individuals. All scans were reported for abnormalities by a radiologist.

Abnormalities were detected in 22 (4.8%) subjects, comprising 10 tumours (pituitary adenoma 4, meningioma 3, suprasellar tumour 1, cavernous haemangioma 1, subarachnoid lipoma 1), 6 infarct-like lesions, 2 arachnoid cysts, 1 possible normal pressure hydrocephalus, and 1 each of unconfirmed aneurysm and mesial temporal sclerosis. Further evaluation led to novel intervention in one case of pituitary adenoma, and adjustment of drug treatment to modify risk factors in two cases with subclinical infarction.

While no case required immediate referral or urgent surgical intervention, the change in the outcome of treatment of some cases suggests that appropriate referral process should be in place when researchers study large number of subjects in the community using MRI of the brain.

Previous studies have suggested that antidepressant treatment of depression may potentiate dopamine transmission through increased sensitivity of postsynaptic D2 receptors.

D2 receptor function was assessed in 24 patients with major depression before and 16 patients after 16 weeks of treatment with cognitive behavioural therapy (CBT) using a challenge with a selective D2 antagonist, sulpiride. Four hundred milligrams of sulpiride was administered orally on two test days and response was measured by the change in prolactin levels and changes in self-rating scale measures of mood, anxiety and pleasure.

The prolactin response to sulpiride (as measured by the maximum prolactin level) was significantly increased after CBT (z = −2.792, p = 0.005). Sulpiride resulted in an improvement on mood ratings on both test days, but after CBT, this effect was significantly diminished as measured by the Profile of Mood States score (t = −2.27, p = 0.038).

After 16 weeks of CBT, we detected an enhanced prolactin response to sulpiride, suggesting an increased sensitivity of D2 receptor functioning.

Neuropsychiatric disturbances are common among patients with genital herpes simplex virus (HSV) infection. To date, no studies have examined the possible role of immune activation in the aetiology of these disturbances. The aim of this study was to examine the relationship between markers of immune activation and measures of emotional and somatic dysfunction among patients with symptomatic genital herpes.

Twenty-two patients with documented genital herpes were assessed when herpetic lesions were present and when they were not. Each assessment included a clinical examination, self-reported symptom measures as well as a blood and urine collection. Markers of immune activation [neopterin and interleukin (IL)-6] in serum and urine were quantified by enzyme-linked immunoassay. These measures were also obtained from a group of healthy control subjects.

Urine, but not serum, levels of neopterin and IL-6 correlated significantly with measures of reported psychological distress and fatigue. These associations were not confined to periods of overt clinical lesions.

HSV-related neuropsychiatric morbidity correlates selectively with regional, but not systemic, measures of immune activation. We hypothesise that communication between the local inflammatory site in the pelvis and the brain occurs through autonomic afferent pathways.

The perception of music without a stimulus, or musical hallucination, is reported in both organic and psychiatric disorders. It is most frequently described in the elderly with associated hearing loss and accompanied by some degree of insight. In this setting it is often referred to as ‘musical hallucinosis’. The aim of the authors was to present examples of this syndrome and review the current understanding of its neurobiological basis.

We describe three cases of persons experiencing musical hallucinosis in the context of hearing deficits with varying degrees of associated central nervous system abnormalities.

Putative neurobiological mechanisms, in particular those involving de-afferentation of a complex auditory recognition system by complete or partial deafness, are discussed in the light of current information from the literature.

Musical hallucinosis can be experienced in those patients with hearing impairment and is phenomenologically distinct for hallucinations described in psychiatric disorders.

The prevalence of body dysmorphic disorder (BDD) in patients with borderline personality disorder (BPD) is unidentified. We hypothesised that BDD would be more common than realised in patients with BPD and comorbidity with BDD would result in a more severe clinical profile. Also, childhood trauma may play a predictive role in this association.

The study included 70 BPD in-patients and 70 matched healthy controls. The subjects were evaluated with a comprehensive assessment battery using Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I), Structured Clinical Interview for DSM-III-R Personality Disorders (SCID-II) diagnostic tool for BDD, Global Assessment of Functioning, Traumatic Experiences Checklist and Hamilton Depression Rating Scale.

The prevalence of BDD was 54.3% in the borderline sample. The BPD patients with BDD had significantly lower overall functioning and higher levels of BPD pathology, childhood traumatic experiences, suicide attempts, substance abuse and self-mutilation than those without BDD. Traumatic experiences were significant predictor of comorbid BDD diagnosis in BPD patients.

Our results suggest a relatively high prevalence of BDD among patients with BPD, and co-occurrence of BDD and BPD remains to be clarified. The additional diagnosis of BDD in patients with BPD may cause a more severe global illness, and these two disorders may share, at least partly, a common psychopathologic mechanism.

The mechanism of action of antidepressant drugs is not fully understood. Application of genomic methods enables the identification of biochemical pathways that are regulated by antidepressants, and this may provide novel clues to the molecular and cellular actions of these drugs. The present study examined gene expression profiles in the hippocampus of rats exposed to chronic antidepressant treatment.

Animals were treated for 12 days with the selective serotonin reuptake inhibitor paroxetine; then, hippocampal ribonucleic acid was recovered, and changes in gene expression were assessed by microarray analysis.

A total of 160 genes that showed differential expression after paroxetine exposure were identified. Using functional relevance and observed fold change as selection criteria, the expression changes in a subset of these genes were confirmed by quantitative polymerase chain reaction.

Of this subset, only two genes, cyclin D1 (Ccnd1) and hairy and enhancer of split 6 (Hes6), showed robust and consistent changes in expression. Both genes were downregulated by paroxetine, and both have been previously implicated in neurogenesis. Further investigation of these two genes may provide new insight into the mechanism of action of antidepressants.

Psychopathological, neuropsychological and genetic findings indicate an association between ASD Spectrum Disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). The goal of this study was to compare the neuropsychological profiles of attention functions in children with ADHD and with ASD and without comorbid ADHD. The hypothesis was that either ADHD and autistic children with comorbid ADHD symptoms were more impaired in inhibition and sustained attention performance and that all individuals with ASD show more deficits in divided attention.

Children aged 6 to 18 years old with ADHD (n = 30) or ASD with (n = 21) and without comorbid ADHD (n = 20) and 30 healthy children were included consecutively. Psychopathology was evaluated using the KIDDIE-SADS and symptom checklists for ADHD and ASD according to DSM-IV. Assessed neuropsychological functioning included inhibition, sustained as well as divided attention and alertness tasks.

Age and IQ-corrected z-scores were used. Statistically significant group effects were found for the variables sustained attention median (F = 3.2, = .02), hits (F = 3.3, p = .02) and false alarms (F = 3.9, p = .01), divided attention hits (F = 3.3, p = .02), errors (F = 3.1, p = .03) and false alarms (F = 3.3, p = .03) and alertness false alarms (F = 2.9, p = .04). Pearson Correlations revealed associations between ADHD symptoms and sustained attention in the ADHD group and between ADHD symptoms and inhibition in the ASD+ group.

Our hypothesis was partly confirmed as ADHD children showed more deficits in sustained attention and ASD children in divided attention tasks. However there was no evidence that children with ASD and comorbid ADHD symptoms have a specific profile in comparison to pure ASD children.