Although poor sleep accompanies depression, it is unknown which specific sleep abnormalities precede depression. This is similarly the case for depression developing during interferon-α (IFN-α) therapy. Because vulnerability becomes evident in those who slept poorly before IFN-α, we prospectively determined which specific aspect of sleep could predict subsequent depression.

Two nights of polysomnography with quantitative electroencephalogram (EEG) were obtained in 24 adult, euthymic subjects – all subsequently treated with IFN-α for hepatitis C. Every 2 weeks, a Beck Depression Inventory-II (BDI-II) score was obtained, and the maximal increase in BDI-II from pre-treatment baseline – excluding the sleep question – was determined.

The delta sleep ratio (DSR; an index of early-night restorative delta power) was inversely associated with BDI-II increases (p<0.01), as was elevated alpha power (8–12 Hz; p<0.001). Both delta (0.5–4 Hz) and alpha power exhibited high between-night correlations (r=0.83 and 0.92, respectively). In mixed-effect repeated-measure analyses, there was an interaction between alpha power and DSR (p<0.001) – subjects with low alpha power and elevated DSR were resilient to developing depression. Most other sleep parameters – including total sleep time and percentage of time in slow wave sleep – were not associated with subsequent changes in depression.

Both high DSR and low alpha power may be specific indices of resilience. As most other aspects of sleep were not associated with resilience or vulnerability, sleep interventions to prevent depression may need to specifically target these specific sleep parameters.

Disturbances in the noradrenergic system, including alterations in the densities of α2-adrenoceptors, are posited to be involved in the pathophysiology of depression. In this study, we investigate the binding of α2-adrenoceptors in regions relevant to depression in an animal model of depression.

Using in vitro autoradiography techniques and the selective α2-ligand, [3H]RX 821002, we investigated the density of α2-adrenoceptors in female Flinders-sensitive line (FSL) rats, a validated model of depression, and in two traditional control groups – female Flinders-resistant line (FRL) and Sprague-Dawley (SD) rats.

The α2-adrenoceptor density was increased in most regions of the FSL rat brain when compared with SD rats (10% across regions). Moreover, the α2-adrenoceptor density was further increased in the FRL rats compared with both FSL (10% across regions) and SD rats (24% across regions).

The increase in α2-adrenoceptor binding in cortical regions in the FSL strain compared with the SD control strain is in accord with α2-adrenoceptor post-mortem binding data in suicide victims with untreated major depression. However, the differences in binding observed in the two control groups were unexpected and suggest the need for further studies in a larger cohort of animals of both sexes.

Glutamatergic dysfunction in the brain has been implicated in the pathophysiology of schizophrenia. Previous studies suggested that l-theanine affects the glutamatergic neurotransmission and ameliorates symptoms in patients with schizophrenia. The aims of the present study were twofold: to examine the possible effects of l-theanine on symptoms in chronic schizophrenia patients and to evaluate the changes in chemical mediators, including glutamate + glutamine (Glx), in the brain by using 1H magnetic resonance spectroscopy (MRS).

The subjects were 17 patients with schizophrenia and 22 age- and sex-matched healthy subjects. l-Theanine (250 mg/day) was added to the patients’ ongoing antipsychotic treatment for 8 weeks. The outcome measures were the Positive and Negative Syndrome Scale (PANSS), Pittsburgh Sleep Quality Index scores and MRS results.

There were significant improvements in the PANSS positive scale and sleep quality after the l-theanine treatment. As for MRS, we found no significant differences in Glx levels before and after the 8 week l-theanine treatment. However, significant correlations were observed between baseline density of Glx and change in Glx density by l-theanine.

Our results suggest that l-theanine is effective in ameliorating positive symptoms and sleep quality in schizophrenia. The MRS findings suggest that l-theanine stabilises the glutamatergic concentration in the brain, which is a possible mechanism underlying the therapeutic effect.

We investigated whether the nitric oxide (NO) precursor, l-arginine, can prevent the antidepressant-like action of the fast-acting antidepressant, ketamine, in a genetic rat model of depression, and/or induce changes in the glutamate (Glu)/N-methyl-d-aspartate receptor (NMDAR)/NO/cyclic guanosine monophosphate (cGMP) signalling pathway. Hereby it was evaluated whether the NO signalling system is involved in the antidepressant mechanism of ketamine.

Flinders sensitive line (FSL) rats received single i.p. injections of ketamine (15 mg/kg) with/without pre-treatment (30 min prior) with l-arginine (500 mg/kg). Depression-like behaviour was assessed in the forced swim test (FST) in terms of immobility, and the activation state of the Glu/NMDAR/NO/cGMP pathway was evaluated ex vivo in the frontal cortex and hippocampus regions in terms of total constitutive NOS (cNOS) activity and cGMP concentration.

l-Arginine pre-treatment prevented the antidepressant-like effect of ketamine in the FST, as well as a ketamine-induced increase in cGMP levels in the frontal cortex and hippocampus of FSL rats. Ketamine reduced cNOS activity only in the hippocampus, and this effect was not reversed by l-arginine.

Both the behavioural and molecular results from this study indicate an involvement for the NO signalling pathway in the antidepressant action of ketamine. Although not easily interpretable, these findings broaden our knowledge of effects of ketamine on the NO system.

A recent clinical study demonstrated that sodium benzoate (SB), a prototype competitive d-amino acid oxidase inhibitor, was effective in the treatment of several symptoms, such as positive and negative symptoms, and cognitive impairment in medicated patients with schizophrenia. The objective of the study was to examine the effects of SB on behavioural abnormalities such as pre-pulse inhibition (PPI) deficits and hyperlocomotion in mice after a single administration of the N-methyl-d-aspartate (NMDA) receptor antagonist, phencyclidine (PCP).

The effects of SB on behavioural abnormalities (PPI deficits and hyperlocomotion) in mice after PCP administration were examined. Furthermore, effects of SB on tissue levels of amino acids were also examined.

A single oral dose of SB (100, 300, or 1000 mg/kg) attenuated PPI deficits in mice after administration of PCP (3.0 mg/kg, s.c.) in a dose-dependent manner. In contrast, L-701,324 (10 mg/kg), an antagonist at the glycine site of the NMDA receptor, did not affect the effect of SB (1000 mg/kg) on PCP-induced PPI deficits. Furthermore, a single oral dose of SB (1000 mg/kg) significantly attenuated the hyperlocomotion in mice after administration of PCP (3.0 mg/kg, s.c.). However, a single oral dose of SB (1000 mg/kg) caused no changes to d-serine levels in plasma or in the frontal cortex, hippocampus, and striatum of these animals.

This study suggests that SB induced antipsychotic effects in the PCP model of schizophrenia, although it did not increase d-serine levels in the brain.

NRGN is one of the most promising candidate genes for schizophrenia based on function and position. Therefore, this study aimed to examine the genetic association of this polymorphism with schizophrenia in the Zhuang and Han populations of south China.

A total of 282 patients (188 Han and 94 Zhuang) and 282 healthy subjects (188 Han and 94 Zhuang) were recruited. Of these, 246 schizophrenia patients underwent an assessment of psychotic symptoms using the Positive and Negative Syndrome Scale (PANSS). A TaqMan genotyping assay method was used to determine the genotypes.

We did not find a significant association of rs12807809 polymorphism with schizophrenia in the total pooled samples, or in the separate ethnic groups. However, in Han schizophrenia patients, quantitative data analyses showed that the CC genotype of the rs12807809 polymorphism was associated with PANSS aggression subscale score and activation subscale score. Furthermore, carriers of the C allele of rs12807809 polymorphism among Han schizophrenia patients had higher scores of general, activation, depression, aggression, and global symptoms than the T allele carriers.

In conclusion rs12807809 polymorphism may not contribute to the risk of schizophrenia but influence the clinical symptoms of schizophrenia in the Han population.

Glucagon-like peptide 1 (GLP-1) receptor agonists are a new group of antidiabetic medications quickly gaining popularity. We aimed to examine behavioural and neuroendocrine changes following chronic treatment with GLP-1 receptor agonists in animal models.

The effects of chronic treatment with GLP-1 receptor agonists were determined on behavioural parameters [anxiety level in the light–dark compartment test, the motor activity in automated activity cages, immobility in the forced swimming test (FST)] and on corticosterone release in mice. The possible antidepressant effect of chronic liraglutide treatment was also studied in Flinders Sensitive Line (FSL) rats, a genetic model of depression.

Two weeks of treatment with exenatide (10 µg /kg twice daily) or liraglutide (1200 µg/kg once daily) did not affect the anxiety level in a light–dark compartment test nor induce an antidepressant-like effect in the FST in mice. Moreover, chronic treatment with liraglutide had no effect on depression-related behaviour in FSL rats. Interestingly, hypolocomotion induced by the drugs in mice disappeared after chronic dosing. Both of the GLP-1 receptor agonists induced robust increases in corticosterone levels in mice under basal conditions as well as in the case of combination with swimming stress. Remarkably, exenatide was as potent a stimulator of corticosterone release after 2 weeks as after acute administration.

The increases in corticosterone release seen after acute exenatide or liraglutide treatment do not abate after 2 weeks of treatment demonstrating that tolerance does not develop towards this particular effect of GLP-1 agonists.

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.

Gut microbiota (GM) has previously been associated with alterations in rodent behaviour, and since the GM is affected by the diet, the composition of the diet may be an important factor contributing to behavioural changes. Interestingly, a magnesium restricted diet has been shown to induce anxiety and depressive-like behaviour in humans and rodents, and it could be suggested that magnesium deficiency may mediate the effects through an altered GM.

The present study therefore fed C57BL/6 mice with a standard diet or a magnesium deficient diet (MgD) for 6 weeks, followed by behavioural testing in the forced swim test (FST) to evaluate depressive-like behaviour. An intraperitoneal glucose tolerance test (GTT) was performed 2 day after the FST to assess metabolic alterations. Neuroinflammatory markers were analysed from hippocampus. GM composition was analysed and correlated to the behaviour and hippocampal markers.

It was found that mice exposed to MgD for 6 weeks were more immobile than control mice in the FST, suggesting an increased depressive-like behaviour. No significant difference was detected in the GTT. GM composition correlated positively with the behaviour of undisturbed C57BL/6 mice, feeding MgD diet altered the microbial composition. The altered GM correlated positively to the hippocampal interleukin-6.

In conclusion, we hypothesise that imbalances of the microbiota–gut–brain axis induced by consuming a MgD diet, contributes to the development of depressive-like behaviour.

Prisoners categorised as ‘dangerous’ are a category of prisoners that require and/or force into using special measures of caution, protection and security. The aim of the study was to examine the intensity of anxiety (as a state and as a trait) experienced by officers working with ‘dangerous’ prisoners and styles of coping with stress they adopt.

A total of 40 officers working with ‘dangerous’ prisoners (the study group, SG) and 60 officers of the security department not working with ‘dangerous’ prisoners (the reference group, RG) were studied. The intensity of anxiety was assessed applying the Polish version of ‘State-Trait Anxiety Inventory’ (STAI); styles of coping with stress were explored employing the Polish version of ‘Coping Inventory for Stressful Situations’ (CISS) and the author’s own questionnaire. Data were analysed using the mean, standard deviation, difference testing (the Mann–Whitney U test), correlation–regression procedure (Kendall’s tau, τ correlation coefficient and forward stepwise multiple regression).

Officers in the SG faced verbal and physical aggression; nevertheless, scores of officers in both the groups were within the interval of mean scores for all the studied STAI and CISS variables. Officers in the SG achieved significantly higher scores on the state-anxiety scale and the Emotion-Oriented Style (EOS), and lower scores on the Task-Oriented Style (TOS) and Social Diversion (SD). The correlation-regression procedure indicated that there were relationships between anxiety and styles of coping with stress but they differed slightly between the groups.

Officers in the SG feel state anxiety stronger and display a stronger preference for the EOS than officers in the RG. Officers in the RG more strongly prefer the TOS and SD. State anxiety is a variable negatively explaining the TOS in the SG, whereas anxiety as a trait is a variable explaining the EOS in both the groups. The coping styles of warders dealing with dangerous prisoners are different and may need specific psychological counselling and training programmes.

In major depressive disorder (MDD), single nucleotide polymorphisms (SNPs) in monoaminergic genes may impact disease susceptibility, treatment response, and brain volume. The objective of this study was to examine the effect of such polymorphisms on hippocampal volume in patients with treatment-resistant MDD and healthy controls. Candidate gene risk alleles were hypothesised to be associated with reductions in hippocampal volume.

A total of 26 outpatients with treatment-resistant MDD and 27 matched healthy controls underwent magnetic resonance imaging and genotyping for six SNPs in monoaminergic genes [serotonin transporter (SLC6A4), norepinephrine transporter (SLC6A2), serotonin 1A and 2A receptors (HTR1A and HTR2A), catechol-O-methyltransferase (COMT), and brain-derived neurotrophic factor (BDNF)]. Hippocampal volume was estimated using an automated segmentation algorithm (FreeSurfer).

Hippocampal volume did not differ between patients and controls. Within the entire study sample irrespective of diagnosis, C allele-carriers for both the NET−182 T/C [rs2242446] and 5-HT1A−1019C/G [rs6295] polymorphisms had smaller hippocampal volumes relative to other genotypes. For the 5-HTTLPR (rs25531) polymorphism, there was a significant diagnosis by genotype interaction effect on hippocampal volume. Among patients only, homozygosity for the 5-HTTLPR short (S) allele was associated with smaller hippocampal volume. There was no association between the 5-HT2A, COMT, and BDNF SNPs and hippocampal volume.

The results indicate that the volume of the hippocampus may be influenced by serotonin- and norepinephrine-related gene polymorphisms. The NET and 5-HT1A polymorphisms appear to have similar effects on hippocampal volume in patients and controls while the 5-HTTLPR polymorphism differentially affects hippocampal volume in the presence of depression.

In this study, we aimed to find out whether sexual dysfunction in patients with Parkinson’s Disease (PD) was associated to PD-related disability and whether this relationship was modulated by depressive and anxiety symptoms.

Eighty-nine consecutive patients with idiopathic PD who attended to our movement disorders outpatient clinics between January 2011 and June 2014 were included in this study. The diagnosis of PD was confirmed by a movement disorders specialists in Neurology, according to UK Parkinson’s Disease Society Brain Bank Criteria. The Unified PD Rating Scale (UPDRS) motor was used to assess motor disability and Hoehn and Yahr stage (H&Y) was used to establish disease severity. Cognitive function was assessed by the Mini-Mental State Examination. Patients were also administered the Hamilton depression (HAMD) and anxiety (HAMA) rating scales. The sexual functions of the patients were rated by applying the Turkish version of the Arizona Sexual Experiences Scale (ASEX).

The mean age at the time of the study visit was 67.74±9.05. Male/female ratio was 1.87. Mean UPDRS total was 29.06±13.96 and mean UPDRS motor was 17.62±9.07. Mean HAMD score was 13.92±10.86, 58.4% of the patients had minor or major depression; and mean HAMA score was 7.94±6.49, 56.2% of the patients had minor or major anxiety. The mean ASEX score was 18.54±7.27 out of a maximum of 30. ASEX total scores were correlated with age, H&Y stage and HAMA scores. Age and also age at onset were correlated with ASEX subdomains except sexual desire. There was no correlation between disease duration and ASEX subdomains. UPDRS motor score was correlated with erection/lubrication. HAMD was only correlated with orgasm satisfaction. HAMA score was correlated with stimulation and orgasm.

In patients with PD, there may be a common factor that modulates both depression, anxiety and sexual function. Further studies are needed to clarify the exact relationship.

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.

Autosomal recessive intellectual disability (ID) is genetically heterogeneous and most of the genes causing it remain undiscovered.

We have ascertained 11 consanguineous families multiplex for IDs in order to identify new loci for autosomal recessive genes for non-syndromic ID, or to aid pinpointing mutations in known causative gene/loci.

Microarray genotyping (Affymatrix 250K) was performed to identify homozygosity-by-descent (HBD) in all affected families.

Analysis of genotypes revealed 45 potential HBD regions across the families, although these may be rationalised down to 39. Two families share an overlapping HBD region on 7q11.21. In one family, X-linkage also looks plausible, and a new ID gene near the centromere may be a likely cause. In one family, no HBD region was found, and thus we exclude autosomal recessive mutation as the likely cause in this family. Copy-number variation (CNV) was also performed and revealed no CNVs, homozygous or heterozygous, segregating with the phenotype.

The homozygous loci identified in this study might harbour candidate genes for ID in these studied families. Therefore, we are proceeding with next-generation sequencing analysis of the families, using whole-exome approaches, and anticipate that this will identify the causative gene/mutation within the identified HBD regions for many of the families studied here.

Magnesium deficiency has been associated with anxiety in humans, and rodent studies have demonstrated the gut microbiota to impact behaviour.

We investigated the impact of 6 weeks of dietary magnesium deficiency on gut microbiota composition and anxiety-like behaviour and whether there was a link between the two. A total of 20 C57BL/6 mice, fed either a standard diet or a magnesium-deficient diet for 6 weeks, were tested using the light-dark box anxiety test. Gut microbiota composition was analysed by denaturation gradient gel electrophoresis.

We demonstrated that the gut microbiota composition correlated significantly with the behaviour of dietary unchallenged mice. A magnesium-deficient diet altered the gut microbiota, and was associated with altered anxiety-like behaviour, measured by decreased latency to enter the light box.

Magnesium deficiency altered behavior. The duration of magnesium deficiency is suggested to influence behaviour in the evaluated test.

Attention-deficit hyperactivity disorder (ADHD) is a chronic neurobiological disorder with childhood onset and persistence through adolescence and adulthood. ADHD patients frequently show exaggerated emotional responses. The amygdala plays an important role in emotion processing and in the activation of the frontal lobe. We hypothesised that smaller amygdala volumes in ADHD patients would be associated with less control of impulsivity and emotional instability.

We studied nine adult patients with ADHD and nine group-matched healthy volunteers using a 1.5 T magnetic resonance imaging scanner. We manually obtained morphometric measurements, which were later processed and compared.

Significant negative correlation between the right amygdala volume and Barratt’s impulsivity scores was observed (r=−0.756, p=0.018). No correlation was found between impulsivity scores and the volume of the left amygdala. Age was not found to be a contributor of the results.

Smaller amygdala volumes have been observed in patients with ADHD. Our results suggest that greater emotional processing and less control of impulsivity are associated with smaller amygdala volumes in ADHD patients. Furthermore, the right amygdala would play a bigger role in impulsivity and behaviour control than the left amygdala. Further studies involving larger samples of adult patients with ADHD and using multimodal designs are needed.

Carcinoembryonic antigen (CEA) is an oncofetal glycoprotein that is widely used as a tumour marker in adenocarcinomas. However, several non-neoplastic conditions, including acute and chronic inflammation and other inflammation-related conditions, are characterised by increased CEA concentrations.

Bipolar disorder (BD) ranks seventh among the worldwide burden of non-fatal diseases. Inflammatory biomarkers have been considered as one of the main key pillars of a multifactorial approach for prediction of BD in an at-risk population.

BP is accompanied by activation of inflammatory, cell-mediated and negative immunoregulatory cytokines.

We measured the levels of CEA in serum samples from 44 individuals with euthymic BP out-patients and 45 healthy controls. Patients were diagnosed according to the DSM-IV criteria. CEA was measured by an electrochemiluminescence immunoassay.

The mean serum CEA concentration was 2.36±1.52 and 1.77±0.98 µg/l in patients and controls, respectively. CEA levels were significantly increased in euthymic BP patients when compared with controls (p=0.031).

This study suggests that CEA is increased in BD and supports a role for immune activation in the core pathological mechanisms of BP. CEA levels may be a secondary marker for diagnosing BP.

Although the cognitive-enhancing abilities after modafinil have been demonstrated, its effects on memory consolidation remain overlooked. We investigated the effects of repeated modafinil administration on consolidation of a discriminative avoidance task.

Mice were trained in the plus-maze discriminative avoidance task. After training, mice received intraperitonial modafinil (doses of 32, 64 or 128 mg/kg). Animals were treated for more 9 consecutive days; 30 min after the last injection, testing was performed. In addition, the effects of 32 mg/kg modafinil on consolidation at different time points were examined.

The smaller dose of modafinil (32 mg/kg) impaired memory consolidation, without modifying anxiety or locomotion. Still, modafinil post-training administration at 1 or 2 h impaired memory persistence.

Modafinil impaired memory consolidation in a dose- and time-dependent fashion.

Schizophrenia is associated with a reduction of the lifespan by 20 years, with type II diabetes and cardiovascular disease contributing the most to the increased mortality. Unrecognised or silent myocardial infarction (MI) occurs in ~30% of the population, but the rates of unrecognised MI in patients with schizophrenia have only been sparsely investigated.

Electrocardiograms (ECG) from three psychiatric hospitals in Denmark were manually interpreted for signs of previous MI. Subsequently, ECGs were linked to the National Patient Registry in order to determine whether patients had a diagnosis consistent with previous MI.

A total of 937 ECGs were interpreted, 538 men (57.4%) and 399 women (42.6%). Mean age at the time of ECG acquisition was 40.6 years (95% CI: 39.7–41.5, range: 15.9–94.6). We identified 32 patients with positive ECG signs of MIs. Only two of these patients had a diagnosis of MI in the National Patient Registry. An additional number of eight patients had a diagnosis of MI in the Danish National Patient Registry, but with no ECG signs of previous MI. This means that 30 out of 40 (75%) MIs were unrecognised. Only increasing age was associated with unrecognised MI in a stepwise multiple logistic regression model compared with patients with no history of MI, OR: 1.03 per year of age, 95% CI: 1.00–1.06, p=0.021.

Unrecognised MI is common among patients with schizophrenia and may contribute to the increased mortality found in this patient group.

Asymmetry in brain structure and function is implicated in the pathogenesis of psychiatric disorders. Although right hemisphere abnormality has been documented in obsessive–compulsive disorder (OCD), cerebral asymmetry is rarely examined. Therefore, in this study, we examined anomalous cerebral asymmetry in OCD patients using the line bisection task.

A total of 30 patients with OCD and 30 matched healthy controls were examined using a reliable and valid two-hand line bisection (LBS) task. The comparative profiles of LBS scores were analysed using analysis of covariance.

Patients with OCD bisected significantly less number of lines to the left and had significant rightward deviation than controls, indicating right hemisphere dysfunction. The correlations observed in this study suggest that those with impaired laterality had more severe illness at baseline.

The findings of this study indicate abnormal cerebral lateralisation and right hemisphere dysfunction in OCD patients.