Schizophrenia (SZ) is a chronic illness that is treated symptomatically. Cognitive dysfunction is a core feature of SZ that is relatively intractable to pharmacotherapy. Yoga can improve cognitive function among healthy individuals. A recent open trial indicated significant benefits of yoga training (YT) in conjunction with conventional pharmacotherapy among patients with SZ.

To describe the protocol for an ongoing randomised controlled trial designed to test whether the reported beneficial effects of YT on cognitive function among SZ patients can be replicated. Secondarily, the effects of YT on daily functioning living skills are evaluated.

Consenting patients with SZ receive routine clinical treatment and are randomised to adjunctive YT, adjunctive physical exercise (PE) or treatment as usual (proposed N = 234 total, N = 78 in each group). The trial involves YT or PE 5 days a week and lasts 3 weeks. Participants are evaluated thrice over 6 months. Cognitive functions measured by Trail Making Test, University of Pennsylvania Neurocognitive Computerised Battery were primary outcome measures while clinical severity and daily functioning measured by Independent Living Skills Survey were secondary outcome measures.

A total of 309 participants have been randomised as of 31 August 2013, which exceeded beyond 294 proposed after attrition. Once participants begin YT or PE they generally complete the protocol. No injuries have been reported.

Short term YT is feasible and acceptable to Indian SZ patients. If beneficial effects of YT are detected, it will provide a novel adjunctive cognitive remediation strategy for SZ patients.

There has been fairly consistent empirical support for the association between major depressive disorder and marital dissatisfaction. However, this evidence is limited mostly to out-patient and population-based samples. Further, the role of possible mediating factors such as attachment style and conflict communication are less well investigated in major depression.

The present study aims to investigate whether couples with a depressed partner and nonclinical couples differ in marital satisfaction, attachment style, psychological distress and conflict communication. Gender differences are also investigated.

Seventy-seven couples, who participated in a family intervention trial, were compared with 77 age- and gender-matched nonclinical couples.

The depressed patients reported more psychological distress and attachment difficulties and less marital satisfaction than their partners and the nonclinical couples. Partners perceived their relationship as more satisfying than the nonclinical couples. The clinical couples reported less mutual constructive and more mutual avoidant communication in their relationship compared with the nonclinical couples. Finally, female depressed patients reported higher levels of psychological symptoms and were more avoidant attached than male patients.

This study shows important differences in several individual and relational characteristics between couples with a depressed partner and nonclinical couples. Further research will be necessary to clarify whether the investigated psychosocial variables play a causal and/or a maintaining role in depression.

To report a case of Pisa syndrome in a patient with idiopathic normal pressure hydrocephalus, who had never been exposed to psychotropic medications.

A 26-year-old, Colombian, male patient, was referred because he had cognitive abnormalities, gait disturbances and urinary incontinence. This patient also displayed pleurothotonos. Neurofunctional evaluations of sensory and motor integration at peripheral and central nervous system levels were done. Idiopathic normal pressure hydrocephalus (NPH) was diagnosed.

Pisa syndrome disappeared after spinal tap drainage with further gait, balance and behavioural improvement. A brainstem-thalamocortical deregulation of the central sensory and motor programming, due to the chaotic enlargement of brain ventricles was thought to be the pathophysiological mechanism underlying this case.

NPH must not be longer considered as an exclusive geriatric disorder. Further, uncommon movement disorders may appear with this disorder, which should be carefully approached to avoid iatrogenic and deleterious pharmacological interventions.

To examine associations between IgA responses to Gram-negative gut commensal bacteria and peri-menstrual symptoms and sex hormone levels during the menstrual cycle in women with and without premenstrual symptoms.

Forty women aged 18–45 years completed the Daily Record of Severity of Problems (DRSP) during all 28 consecutive days of the menstrual cycle. We assayed, in plasma, IgA responses to six Gram-negative bacteria, that is, Hafnei alvei, Pseudomonas aeruginosa, Morganella morganii, Klebsiella pneumoniae, Pseudomonas putida and Citobacter koseri, progesterone and oestradiol at days 7, 14, 21 and 28 of the menstrual cycle.

Significant changes in Δ (actual − 1 week earlier) IgA to lipopolysaccharides (LPS) of the six Gram-negative bacteria during the menstrual cycle were observed with peak IgA levels at T4 (day 28) and lows at T1 or T2 (day 7 or 14). The ΔIgA changes in H. alvei, M. Morganii, P. putida during the menstrual cycle were significantly and positively associated with changes in the total DRSP score, and severity of physio-somatic, anxiety and breast-craving, but not depressive, symptoms. The changes in IgA responses to LPS were largely predicted by changes in progesterone and steady-state levels of progesterone averaged over the luteal phase.

Menstrual cycle-associated changes in IgA directed against LPS and by inference bacterial translocation may be driven by the effects of progesterone on transcellular, paracellular and vascular pathways (leaky gut) thereby contributing to the severity of physio-somatic and anxiety symptoms as well as fatigue, breast swelling and food cravings.

This study aims to document the nature and progression of the spontaneous writing impairment observed in patients with Alzheimer's disease (AD) over a 12-month period using both a cross-sectional and prospective longitudinal design.

Thirty-one minimal–moderate AD patients and 30 controls matched for age and socio-cultural background completed a simple and complex written description task at baseline. The AD patients then had follow-up assessments at 6 and 12 months.

Cross-sectional comparisons indicated that minimal–moderate AD patients produced more semantic paraphasias, phonological paraphasias, and empty and indefinite phrases, whilst producing fewer pictorial themes, repairing fewer errors, and producing shorter and less complex sentences than controls. The two groups could not be distinguished on visual paraphasias. Longitudinal follow-up, however, suggested that visual processing deteriorates over time, where the prevalence of visual errors increased over 12 months.

The findings suggest that the deterioration of writing skills observed in the spontaneous writings of AD patients shows a pattern of impairment dominated by semantic errors with a secondary impairment in phonological processing, which is later joined by a disruption of visuospatial and graphomotor processing.

Background: A well-known technique to assess (psychological) arousal is to measure the skin conductance level (SCL). Although widely used in experimental psychological research, this technique has not been used often in (locked) psychiatric admission settings on patients who are at a high risk of engaging in aggressive behaviour. One of the obvious reasons for this is that measuring skin conductance, until recently, required a substantial amount of equipment.

Methods: As technology developed, it became possible to develop small wearable devices in the form of regular watches to measure the SCL as well as other psycho-physiological parameters. To illustrate the potential this may have for the prevention of aggressive behaviour, a case description is provided of a patient in crisis who became physically aggressive while wearing a skin conductance measurement device.

Results: Interestingly, the SCL of the patient had been rising sharply before the first signs of aggressive behaviour were visible.

Conclusion: Although it concerns an anecdotal case study, this finding suggests that measuring SCL on a continuous basis in patients who are at a high risk of becoming violent, without this procedure having to interfere with their daily life, may open new avenues for preventing aggression at an earlier stage. A large-scale empirical study in a substantial number of (potentially aggressive) patients is needed, however, to investigate the predictive validity of mobile skin conductance assessments on imminent inpatient aggression in a reliable way.

The N-methyl-d-aspartate receptor (NMDAR) antagonist ketamine, produces rapid and enduring antidepressant effect in patients with treatment-resistant depression. Similar dramatic effects have not been observed in clinical trials with other NMDAR antagonists indicating ketamine may possess unique pharmacological properties. Tetrabenazine induces ptosis (a drooping of the eyelids), and the reversal of this effect, attributed to a sympathomimetic action, has been used to detect first-generation antidepressants, as well as ketamine. Because the actions of other NMDAR antagonists have not been reported in this measure, we examined whether reversal of tetrabenazine-induced ptosis was unique to ketamine, or a class effect of NMDAR antagonists.

The effects of ketamine and other NMDAR antagonists to reverse tetrabenazine-induced ptosis were examined and compared with their antidepressant-like effects in the tail suspension test (TST) in mice.

All the NMDAR antagonists tested produced a partial reversal of tetrabenazine-induced ptosis and, as expected, reduced immobility in the TST. Ketamine, memantine, MK-801 and AZD6765 were all about half as potent in reversing tetrabenazine-induced ptosis compared to reducing immobility in the TST, while an NR2B antagonist (Ro 25-6981) and a glycine partial agonist (ACPC) were equipotent in both tests.

The ability to reverse tetrabenazine-induced ptosis is a class effect of NMDAR antagonists. These findings are consistent with the hypothesis that the inability of memantine, AZD6765 (lanicemine) and MK-0657 to reproduce the rapid and robust antidepressant effects of ketamine in the clinic result from insufficient dosing rather than a difference in mechanism of action among these NMDAR antagonists.

The ability to accurately judge facial expressions is important in social interactions. Individuals with bipolar disorder have been found to be impaired in emotion recognition; however, the specifics of the impairment are unclear. This study investigated whether facial emotion recognition difficulties in bipolar disorder reflect general cognitive, or emotion-specific, impairments. Impairment in the recognition of particular emotions and the role of processing speed in facial emotion recognition were also investigated.

Clinically stable bipolar patients (n = 17) and healthy controls (n = 50) judged five facial expressions in two presentation types, time-limited and self-paced. An age recognition condition was used as an experimental control.

Bipolar patients’ overall facial recognition ability was unimpaired. However, patients’ specific ability to judge happy expressions under time constraints was impaired.

Findings suggest a deficit in happy emotion recognition impacted by processing speed. Given the limited sample size, further investigation with a larger patient sample is warranted.

The present study was designed to test the hypothesis that there is a reduction in the activity of the enzyme cytochrome c oxidase (Cox) in Alzheimer’s disease (AD).

Systematic review of literature and meta-analysis were used with data obtained from the PubMed, Scopus, MEDLINE, Lilacs, Eric and Cochrane. The keywords were Alzheimer’s AND Cox AND mitochondria; Alzheimer’s AND Cox AND mitochondria; Alzheimer’s AND complex IV AND mitochondria. A total of 1372 articles were found, 23 of them fitting the inclusion criteria. The data were assembled in an Excel spreadsheet and analysed using the RevMan software. A random effects model was adopted to the estimative of the effect.

The data shows a significant decrease in the activity of the Cox AD patients and animal models.

Cox enzyme may be an important molecular component involved in the mechanisms underlying AD. Therefore, this enzyme may represent a possible new biomarker for the disease as a complementary diagnosis and a new treatment target for AD.

Catatonic features are observed in several psychiatric illnesses but can also be found following substance misuse. Loperamide is an anti-diarrhoeal medication that acts on opioid receptors in the intestine, reducing peristalsis. It is normally unable to pass through the intestinal wall or the blood–brain barrier; however, high dosages can in fact induce the effects on the central nervous system.

We describe the case of a 20-year-old man who presented with severe catatonia following excessive intake of loperamide, fully remitted with lorazepam.

We speculate on a possible increase of loperamide's bioavailability after overdose owing to reduced expression and functioning of P-glycoprotein.

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.

Transcranial direct current stimulation (tDCS) is a non-invasive and well-tolerated brain stimulation technique with promising efficacy as an add-on treatment for schizophrenia and for several other psychiatric disorders. tDCS modulates neuroplasticity; psychiatric disorders are established to be associated with neuroplasticity abnormalities. This review presents the summary of research on potential genetic basis of neuroplasticity-modulation mechanism underlying tDCS and its implications for treating various psychiatric disorders.

A systematic review highlighting the genes involved in neuroplasticity and their role in psychiatric disorders was carried out. The focus was on the established genetic findings of tDCS response relationship with BDNF and COMT gene polymorphisms.

Synthesis of these preliminary observations suggests the potential influence of neuroplastic genes on tDCS treatment response. These include several animal models, pharmacological studies, mentally ill and healthy human subject trials.

Taking into account the rapidly unfolding understanding of tDCS and the role of synaptic plasticity disturbances in neuropsychiatric disorders, in-depth evaluation of the mechanism of action pertinent to neuroplasticity modulation with tDCS needs further systematic research. Genes such as NRG1, DISC1, as well as those linked with the glutamatergic receptor in the context of their direct role in the modulation of neuronal signalling related to neuroplasticity aberrations, are leading candidates for future research in this area. Such research studies might potentially unravel observations that might have potential translational implications in psychiatry.

Road traffic injuries are the leading cause of death among young people. Recognition of the contribution of impulsive behaviour may help novice drivers to behave more safely. Previously a brief intervention focusing on impulsive traffic behaviour conducted by psychologists in driving schools had been effective. The aim of this study was an independent re-evaluation of the effect of the intervention, as conducted by driving school teachers, and assessment of the potential associations with candidate genotypes.

Driving school students (mean age 22.5, SD=7.9) were divided into intervention (n=704) and control (n=737) groups. Driving school teachers were trained to administer the intervention which consisted of a lecture and group work (1.5 h in total) on impulsivity. Traffic offences and crashes were monitored during 3 years, using police and traffic insurance fund databases. Functional polymorphisms of the dopamine transporter (DAT) and serotonin transporter genes (DAT1 VNTR and 5-HTTLPR) were assessed.

The intervention significantly lowered general traffic risk and prevalence of traffic accidents. DAT1 VNTR 9R carriers, particularly males, had higher general traffic risk in the whole sample. Female 5-HTTLPR s’ allele carriers of the intervention group had the lowest general traffic risk. Intervention was most effective in female DAT1 VNTR 10R/10R homozygotes.

Brief impulsivity-centred intervention appears as a promising strategy for preventing risk-taking behaviour in novice drivers and can be fully integrated to driving school curriculum.

There is a growing interest in the role of kynurenine pathway and tryptophan metabolites in the pathophysiology of depression. In the present study, the metabolism of tryptophan along the kynurenine pathway was analysed in a rat model of depression.

Kynurenic acid (KYNA) and 3-hydroxykynurenine (3-HK) were measured by high-performance liquid chromatography (HPLC) in prefrontal cortex (PFC) and frontal cortex (FC) in a rat model of depression, the Flinders Sensitive Line (FSL) and their controls, the Flinders Resistant Line (FRL) rats. In addition, KYNA was also measured in hippocampus, striatum and cerebellum.

KYNA levels were reduced in the PFC of FSL rats compared with FRL rats, but did not differ with regard to the FC, hippocampus, striatum or cerebellum. 3-HK levels in PFC and FC, representing the activity of the microglial branch of the kynurenine pathway, did not differ between the FSL and FRL strains.

Our results suggest an imbalanced metabolism of the kynurenine pathway in the PFC of FSL rats.

The transient receptor potential vanilloid type-1 channel (TRPV1) is expressed in the midbrain periaqueductal grey (PAG), a region of the brain related to aversive responses. TRPV1 antagonism in the dorsolateral PAG (dlPAG) induces anxiolytic-like effects in models based on conflict situations. No study, however, has investigated whether these receptors could contribute to fear responses to proximal threat. Thus, we tested the hypothesis that TRPV1 in the PAG could mediate fear response in rats exposed to a predator.

We verified whether exposure to a live cat (a natural predator) would activate TRPV1-expressing neurons in the PAG. Double-staining immunohistochemistry was used as a technique to detect c-Fos, a marker of neuronal activation, and TRPV1 expression. We also investigated whether intra-dlPAG injections of the TRPV1 antagonist, capsazepine (CPZ), would attenuate the behavioural consequences of predator exposure.

Exposure to a cat increased c-Fos expression in TRPV1-positive neurons, mainly in the dorsal columns of the PAG, suggesting that TRPV1-expressing neurons are activated by threatening stimuli. Accordingly, local injection of CPZ inhibited the fear responses.

These data support the hypothesis that TRPV1 channels mediate fear reactions in the dlPAG. This may have an implication for the development of TRPV1-antagonists as potential drugs for the treatment of certain psychiatric disorders.

To verify the prevalence and clinical impact of excessive daytime sleepiness (EDS) in outpatients with bipolar disorder.

Eighty‐one outpatients with bipolar disorder and 79 healthy control subjects were recruited. Patients were required not to be acutely manic or depressed. We used the Epworth Sleepiness Scale, the Pittsburgh Sleep Quality Index and the Functioning Assessment Short Test to assess sleepiness, sleep problems and functioning, respectively.

Patients had a higher prevalence of sleepiness (40%) than the control group (18%). Sleepiness and sleep disturbance had independent impacts on disability in the multivariable model.

This study suggests that EDS is a relevant clinical dimension in patients with bipolar disorder. It is a frequent symptom that often overlaps with other sleep disturbances. This study also reveals that once present it has the potential to increase functional impairment.

G protein-coupled receptor 55 (GPR55) is an orphan G protein-coupled receptor with various physiological functions. Recent evidence suggests that this receptor may be involved in the control of motor functions. Therefore, in the present study, we evaluated the effects of intra-striatal administration of GPR55 selective ligands in a rat model of Parkinson’s disease.

Experimental Parkinson was induced by unilateral intra-striatal administration of 6-hydroxydopamine (6-OHDA, 10 µg/rat). L-α-lysophosphatidylinositol (LPI, 1 and 5 µg/rat), an endogenous GPR55 agonist, and ML193 (1 and 5 µg/rat), a selective GPR55 antagonist, were injected into the striatum of 6-OHDA-lesioned rats. Motor performance and balance skills were evaluated using the accelerating rotating rod and the ledged beam tests. The sensorimotor function of the forelimbs and locomotor activity were assessed by the adhesive removal and open field tests, respectively.

6-OHDA-lesioned rats had impaired behaviours in all tests. Intra-striatal administration of LPI in 6-OHDA-lesioned rats increased time on the rotarod, decreased latency to remove the label, with no significant effect on slip steps, and locomotor activity. Intra-striatal administration of ML193 also increased time on the rotarod, decreased latency to remove the label and slip steps in 6-OHDA-lesioned rats mostly at the dose of 1 µg/rat.

This study suggests that the striatal GPR55 is involved in the control of motor functions. However, considering the similar effects of GPR55 agonist and antagonist, it may be concluded that this receptor has a modulatory role in the control of motor deficits in an experimental model of Parkinson.