We investigated whether 24-item Hamilton Rating Scale for Depression (HamD24)-based melancholia ratings correlated with treatment outcome, with special focus on whether electroconvulsive therapy (ECT) was used in depressed patients treated on an in-patient mood disorders unit.

We analysed the data on ECT- versus non-ECT-treated patients' outcomes relative to melancholia subscale scores. Two HamD24-based melancholia rating scale scores were computed for 201 depressed in-patients at admission and discharge. Baseline melancholia ratings were analysed to see if they correlated with improvement in total HamD24 scores. We also tested to see if the melancholia subscales followed unimodal or bimodal distributions.

Melancholic symptoms as assessed by one of the HamD24-based subscales directly correlated with overall improvement. Although ECT treatment was associated with greater improvement than was noted in non-ECT-treated patients, severity of melancholia ratings did not affect this relationship. Finally, both melancholia subscale scores followed approximately unimodal distributions.

HamD24-based methods to assess severity of melancholic symptoms have limited clinical utility on an in-patient mood disorders unit in general, and for predicting ECT response in particular. Furthermore, these methods do not seem to identify bimodal populations of depressed patients (i.e. melancholic vs. non-melancholic).

To compare the frequency of psychiatric disorders and the severity of psychiatric symptoms between patients with blepharospasm (BS) and hemifacial spasm (HS).

BS is a type of primary focal dystonia characterised by recurrent and involuntary eye blinking. HS is a condition with different pathophysiology but similar clinical phenotype. Twenty-two patients with BS and 29 patients with HS participated in this study. They underwent a comprehensive psychiatric evaluation that included a structured clinical interview for current psychiatric diagnosis according to Diagnostic Statistical Manual, fourth edition (DSM-IV) (MINI-Plus) and psychometric scales, including the Yale-Brown Obsessive-Compulsive Scale (YBOCS), the Beck Depression Inventory (BDI), the Hamilton Rating Scale for Depression (HRSD), the Hamilton Anxiety Scale (HAS) and the Liebowitz Social Anxiety Scale (LSAS).

BS and HS groups did not differ in most demographic and clinical parameters, such as gender, age and length of symptoms. The frequency of psychiatric disorders and the severity of psychiatric symptoms were similar in both groups.

BS does not seem to have more psychiatric disorders than HS.

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.

To compare the variability of patterns of depressive symptoms between two consecutive depressive episodes in patients with bipolar disorder type I.

Review of prospectively collected data from 136 subjects of an out-patient bipolar unit from 1997 to 2007. Binomial statistics was used for the analysis of Hamilton Depression Rating Scale (HDRS)-31 items of the first and second episodes, and the correlation of the HDRS-31 item scores of both episodes was determined using the Spearman coefficient.

Ten depressive symptoms showed a significant correlation between index and subsequent episodes: psychological anxiety, somatic anxiety, somatic symptoms, diurnal variation, paranoid symptoms, obsessive and compulsive symptoms, hypersomnia, loss of appetite and helplessness. Only four symptoms were stable in both statistical tests: paranoid symptoms, obsessive–compulsive symptoms, loss of appetite and hypersomnia.

Paranoid and obsessive–compulsive symptoms, loss of appetite and hypersomnia tended to be found in successive episodes. However, the moderate correlations of the symptoms across two depressive recurrences suggested that clinical presentations in bipolar depression may not be predicted by symptom profiles presented in previous episodes.

Recently, a reduction in efferent vagal regulation has been found in schizophrenic patients.

Therefore, the brainstems of nine schizophrenic patients and nine normal controls were stereologically analysed. The number of neurons using the optical fractionator method and nuclear volumes applying the Cavalieri principle was estimated in Nissl stained sections of the dorsal motor nucleus of the vagus (DMNV) and the hypoglossal nucleus.

The neurons in the right DMNV were significantly increased in the schizophrenic group compared to normal controls (p = 0.047), while the volumes of the DMNV did not differ. In contrast, no such differences were found in the hypoglossal nucleus.

Although this pilot study is limited by its small sample size, the analysis of the solitarius–ambiguus–vagus system in schizophrenic patients is an interesting target in schizophrenia research. The most reasonable background for increased neuron numbers in the DMNV could be a system-specific neurodevelopmental disturbance in schizophrenia.

Impulsivity has been shown to load on two separate factors, rash impulsivity and sensitivity to reward (SR) in several factor analytic studies. The aims of the current study were to explore the nature of impulsivity in women with borderline personality disorder (BPD) and matched controls, and the underlying neuronal correlates for rash impulsivity and SR.

Fifteen females diagnosed with BPD and 15 matched controls were recruited. All completed the impulsiveness-venturesomeness scale (I7), the sensitivity to punishment (SP) - sensitivity to reward (SR) questionnaire, and performed a Go-NoGo block-design functional magnetic resonance imaging (fMRI) paradigm at 3T. Correlation analyses were done with I7, SP and SR scores with the level of activation in different brain areas in the whole group. An independent group t-test was used to explore any differences between the BPD group and the matched controls.

I7 scores correlated negatively with activity in the left orbitofrontal cortex, amygdala and precuneus, and bilaterally in the cingulate cortices during response inhibition for the entire sample. SP yielded negative correlations in the right superior frontal gyrus and parahippocampal gyrus. No activity related to response inhibition correlated to SR. The Go-NoGo task gave similar brain activity in BPD and matched controls, but behaviourally the BPD group had significantly more commission errors in the NoGo blocks. The BPD group had increased I7 and SP scores indicating rash impulsiveness combined with heightened SP.

These results imply that successful impulse inhibition involves interaction between the impulsive and the emotional systems. Furthermore, impulsivity in BPD is described as rash impulsivity, coexisting with increased SP.

A female adult patient with mild to moderate mental retardation and minor dysmorphisms was referred for neuropsychiatric examination because of psychotic and autistic symptoms and impulsive behaviours.

Standardized neuropsychiatric and neuropsychological assessment as well as detailed somatic and neurological examination was performed. For genetic analysis, karyotyping, whole genome array analysis, and high-resolution detailed analysis of chromosome 21 were carried through.

Karyotyping showed a de novo ring chromosome 21: 46,XX,der(21)r(21)(p11q22.3). High-resolution array analysis demonstrated a complex aberration consisting of an interstitial duplication in 21q21.1, an interstitial deletion in 21q22.2q22.3, an interstitial deletion in 21q22.3 and a terminal deletion of 21q22.3. Apart from mild dysmorphisms, visual and auditory impairments, and infertility, no somatic or neurological abnormalities were found. A formal psychiatric diagnosis could not be established. The behavioural problems and the supposed psychiatric symptoms could be related to her disharmonic social cognitive profile. The behaviour normalized after the patient returned to a stable and structured living environment.

High-resolution micro-array analysis techniques are essential to substantiate the genotype–phenotype correlation in patients with r(21) and other genetic disorders. Moreover, the results of this study stress the importance of the recognition of alexithymia as a potential cause for behavioural problems and psychiatric symptoms in patients with mental retardation in general.

Long-acting injectible antipsychotic agents are rarely considered in the treatment of bipolar patients [bipolar disorder (BPD)]. We posited that BPD patients receiving risperidone long-acting injections [Risperidone long-acting injections (RLAIs)] would experience fewer negative clinical events than those receiving oral atypical antipsychotic agents (AAP).

Adult BPD patients in a hypomanic, manic or mixed episode were randomised to either oral risperdone followed by RLAI (n = 23) or an AAP (n = 25) for 15 months. Any mood stabilizers were continued. An independent clinician board declared any clinical events that occurred but the treatment assignment was concealed.

Nine of the 48 patients who participated in this study did not improve, leaving 39 patients in 1-year extension. RLAI patients received the following bi-weekly dosages: 25 mg (n = 9), 37.5 mg (n = 8), and 50 mg (n = 6). The AAP group included aripiprazole (n = 11, 15–30 mg/day), quetiapine (n = 8, 300–700 mg/day), olanzapine (n = 5, 15–25 mg/day), and ziprasidone, (n = 1, 160 mg/day). In total, 47 clinical events were declared. The RLAI-treated group experienced significantly fewer clinical events (mean: 0.86 ± 0.73) compared with the AAP group (1.61 ± 1.29), t = 2.29, d.f. = 37, p = 0.028 (95% CI = 0.087–1.421). Of all, 50% of the AAP subjects gained ≥ 7% of their baseline body weight as did 38% of the RLAI-treated patients.

RLAI-treated patients experienced significantly fewer negative clinical events. Further exploration should focus on which subtypes of BPD patients might benefit from RLAI treatment. Weight gain in BPD subjects requires clinical attention. Limitations include an open design, small sample size and the inability to conclude on whether this strategy is useful for depressive episodes.

The present study examined whether low birth weight, prematurity or low birth weight adjusted for gestational age are risk factors for the subsequent development of affective disorder, especially depression.

A population-based case–control design was applied to the Danish Medical Birth Register and the Danish Psychiatric Central Register to identify all individuals born between 1 January 1974 and 31 December 1990 and diagnosed prior to 29 August 2003 with affective disorder alone (ICD-10 F3; 4297 females, 1861 males), schizophrenia alone (ICD-10 F2; 1364 females, 2292 males) or both disorders (ICD-10 F3 + F2; 450 females, 405 males). The association between low birth weight and the risk of developing affective disorder and/or schizophrenia was analysed by conditional logistic regression analysis.

Low birth weight was found to be associated with a significantly elevated risk of developing schizophrenia alone (p = 0.021) and both affective disorder and schizophrenia (p = 0.024), and a non-significantly elevated risk of developing affective disorder alone (p = 0.063). The effect remained significant in the affective disorder and schizophrenia groups (p = 0.039) when correcting for gestational age (premature birth), but was lost in the group with both disorders. Premature birth per se was found to be associated with a significantly elevated risk of developing both affective disorder and schizophrenia (p = 0.00018), an effect that remained significant after adjustment for low birth weight.

Prematurity and low birth weight were found to be risk factors for subsequent development of affective disorder (especially depression) and schizophrenia.

The purpose of this study was to investigate deficient inhibitory control in individuals with pathological Internet use (PIU) using a visual go/no-go task by event-related potentials (ERPs).

Subjects were 26 individuals with PIU and 26 controls. Barratt Impulsiveness Scale-11 (BIS-11) was used for measures of impulsivity. A go/no-go task involved eight different two-digit numerical stimuli. The response window was 1000 ms and the inter-trial-interval (ITI) was 1500 ms. Electroencephalography (EEG) was recorded when participants performed the task. Brain electrical source analysis (BESA) 5.2.0 was used to perform data analysis and the no-go N2 amplitude was analysed for investigation of inhibitory control.

BIS-11 total scores, attentional key and motor key scores in PIU group were higher than that of the control group. In the go/no-go task, false alarm rate of PIU group was higher, and hit rate was lower than that of the control group. A repeated measure ANOVA revealed a significant group, frontal electrode sites and group × frontal electrode sites main effect for N2 amplitudes of no-go conditions (for group: F = 3953, df = 1, p = 0.000; for frontal electrode sites: F = 541, df = 9, p = 0.000; for group × frontal electrode sites: F = 306, df = 9, p = 0.000), and a significant group, central electrode sites and group × central electrode sites main effect for N2 amplitudes of no-go conditions (for group: F = 9074, df = 1, p = 0.000; for central electrode sites: F = 163, df = 2, p = 0.000; for group × central electrode sites: F = 73, df = 2, p = 0.000). N2 amplitudes of no-go conditions were lower than those at control group.

Individuals with PIU were more impulsive than controls and shared neuropsychological and ERPs characteristics of compulsive-impulsive spectrum disorder, which supports that PIU is an impulse disorder or at least related to impulse control disorder.

Although bipolar disorder (BD) with comorbid obsessive-compulsive disorder (OCD) is highly prevalent, few controlled studies have assessed this comorbidity. The objective of this study was to investigate the clinical characteristics and expression of comorbid disorders in female BD patients with OCD.

We assessed clinically stable female outpatients with BD: 15 with comorbid OCD (BD+OCD group) and 15 without (BD/no-OCD group). All were submitted to the Structured Clinical Interview for DSM-IV, with additional modules for the diagnosis of kleptomania, trichotillomania, pathological gambling, onychophagia and skin picking.

The BD+OCD patients presented more chronic episodes, residual symptoms and previous depressive episodes than the BD/no-OCD patients. Of the BD+OCD patients, 86% had a history of treatment-emergent mania, compared with only 40% of the BD/no-OCD patients. The following were more prevalent in the BD+OCD patients than the BD/no-OCD patients: any anxiety disorder other than OCD; impulse control disorders; eating disorders; and tic disorders.

Female BD patients with OCD may represent a more severe form of disorder than those without OCD, having more depressive episodes and residual symptoms, and being at a higher risk for treatment-emergent mania, as well as presenting a greater anxiety and impulse control disorder burden.

The phenomenology of unipolar and bipolar disorders differ in a number of ways, such as the presence of mixed states and atypical features. Conventional depression rating instruments are designed to capture the characteristics of unipolar depression and have limitations in capturing the breadth of bipolar disorder.

The Bipolar Depression Rating Scale (BDRS) was administered together with the Montgomery Asberg Rating Scale (MADRS) and Young Mania Rating Scale (YMRS) in a double-blind randomised placebo-controlled clinical trial of N-acetyl cysteine for bipolar disorder (N = 75).

A factor analysis showed a two-factor solution: depression and mixed symptom clusters. The BDRS has strong internal consistency (Cronbach's alpha = 0.917), the depression cluster showed robust correlation with the MADRS (r = 0.865) and the mixed subscale correlated with the YMRS (r = 0.750).

The BDRS has good internal validity and inter-rater reliability and is sensitive to change in the context of a clinical trial.

Recently, we reported that mitochondrial respiratory chain complexes I, III and IV were inhibited in the cerebral cortex and cerebellum of rats submitted to chronic mild stress (CMS) and that acute ketamine administration reversed this effect. Therefore, we investigated whether the inhibition of these enzymes may be reversed by chronic administration of ketamine.

Adult male Wistar rats were submitted to CMS and chronically treated with ketamine. After 40 days of CMS, consumption of sweet food, adrenal gland weight, body weight and enzymatic activity of the complexes were measured.

We verified that CMS decreased the intake of sweet food, increased the adrenal gland weight and the control group gained weight after 40 days but the stressed group did not; ketamine administration reversed these effects. We also verified that chronic administration of ketamine reversed the inhibition of complexes I, III and IV in cerebral cortex. However, in cerebellum, only complex IV inhibition was reversed. The chronic ketamine administration partially reverses the inhibition caused by CMS.

We hypothesise that CMS inhibits complexes I, III and IV activities and that chronic administration of ketamine administration partially reverses such an effect. Therefore, it seems reasonable to propose that ketamine administration might be a useful therapy for patients affected by major depression.

This pilot study examines the utility of a novel, standardised brief neuropsychological assessment tool (the ARCS, Audio Recorded Cognitive Screen) in a different clinical setting to that in which it was initially developed. We hypothesised that the ARCS would be feasible to administer to individuals with a psychotic illness and that it would detect cognitive deficits similar to those identified by an established instrument (the RBANS, Repeatable Battery for the Assessment of Neuropsychological Status).

Twenty-five people with psychosis (mean age = 43.72, SD = 9.78) and 25 age- and gender-matched controls were recruited from the Newcastle community (NSW, Australia). The ARCS and RBANS were completed about 1 week apart in a counterbalanced order.

The ARCS was well received, performed satisfactorily and both the ARCS and RBANS were sensitive to deficits typically associated with psychosis (e.g. memory and attention). After controlling for memory deficits, the largest disparity between the psychosis and control groups was on the ARCS fluency domain [p < 0.001, partial Eta-squared (ηp2) = 0.21].

The ARCS uses audio administration (approximately 34 min) to reduce clinician time (to 3–5 min for scoring) and appears to be a useful brief assessment tool for examining the cognitive deficits associated with psychosis. However, the potential clinical utility of the ARCS needs to be investigated further in larger samples drawn from a wider variety of specialist and non-specialist settings.