Alam A, Chengappa KNR. Obstructive sleep apnoea and schizophrenia: a primer for psychiatrists

Objective: The main objective of this review is to improve psychiatric clinician awareness of obstructive sleep apnoea (OSA) and its potential consequences in patients with schizophrenia. This article will also discuss the diagnosis and treatment options for OSA while considering the significant role psychiatrists can play in facilitating the diagnosis and treatment of OSA.

Data sources: Ovid, Medline and PsychInfo databases were searched for articles between 1960 and 2010. Search terms used were Sleep apnoea or apnoea and schizophrenia or psychosis. The number of articles retrieved was 38. Articles were carefully reviewed for any data pertinent to OSA in patients with schizophrenia.

Conclusions: OSA is a common disorder that is frequently unrecognised. As a chronic breathing condition, OSA is associated with adverse health outcomes and high mortality. OSA may co-occur with schizophrenia or evolve over time, especially with weight gain. The diagnosis should be considered whenever a patient presents with risk factors or clinical manifestations that are highly suggestive of OSA. Those who report snoring, daytime sleepiness and are obese or have a large neck circumference should be considered for an OSA diagnosis. Appropriate diagnosis and treatment of OSA can reduce daytime sleepiness, improve cardiovascular and other medical conditions, as well as reduce mortality. Psychiatrists can play very important role in suspecting OSA in their patients and making the initial referral. Furthermore, behavioural management, especially promoting weight loss and smoking cessation, are effective components of OSA treatment that psychiatrists are positioned to facilitate with their patients.

Nielsen RE. Treatment of psychosis during pregnancy – a case report and a mini-review.

Objective: Describe clinical problems in treating a patient with psychotic symptoms during pregnancy by presenting a case report, and review the current evidence on antipsychotic drugs during pregnancy.

Methods: The review consists of a non-systematic clinical review of current data on treatment with antipsychotics during pregnancy. The case, a 27 year old female initially diagnosed with posttraumatic stress disorder (PTSD) after a rape and emotionally unstable personality disorder, illustrates some of the common challenges a clinician meets. The patient initially discontinues all treatment as she is unsure if the drugs could have a teratogenic effect and is changed to a treatment that is regarded as safe during pregnancy.

Results: The current data supports treatment with chlorpromazine although there is a risk of side effects, e.g. extrapyramidal symptoms and hypotension, but also treatment with olanzapine and risperidone. If the patient is currently treated with clozapine, this treatment should be continued, due to clozapines unique efficacy profile. Blood monitoring for six months after birth is recommended when the newborn has been exposed to clozapine treatment.

Conclusion: Current evidence on treatment with antipsychotics during pregnancy is sparse, but not treating is associated with increased risks compared to treatment.

De Luca RD, Fraga DB, Ghedim FV, Kolling J, Ferreira AGK, Cunha AA, Wyse ATS, Zugno AI. Na+,K+-ATPase activity is increased in rats subjected to chronic administration of ketamine.

Objective: Schizophrenia is a devastating psychiatric disorder. Symptoms of schizophrenia can be divided into positive, negative and cognitive, and the physiopathology is still been unknown. Na+,K+-ATPase is a protein in its role as a maintainer of fluid balance in all mammals and alterations in this enzyme could cause brain abnormalities. The aim of our study was to investigate the activity of this enzyme in rats submitted to chronic administration of ketamine.

Methods: Adult male Wistar rats were submitted to sub-anaesthetic doses of the 25 mg/kg ketamine by seven consecutive days and the Na+,K+-ATPase activity was analysed in prefrontal and hippocampus of rats.

Results: We observed an increase in Na+,K+-ATPase activity in prefrontal cortex administration of 25 mg/kg ketamine. However, ketamine has no effect in hippocampus.

Conclusion: This evidence indicates that the alteration in Na+,K+-ATPase may be related with glutamatergic system and consequently could be related to the development of schizophrenia.

Williams LJ, Pasco JA, Jacka FN, Henry MJ, Dodd S, Nicholson GC, Kotowicz MA, Berk M. Bipolar disorder and adiposity: a study using whole body dual energy X-ray absorptiometry scans.

Objective: Previous research has demonstrated a relationship between adiposity and bipolar disorder, although data are derived predominantly from patient samples and use indirect methods of assessing adiposity. This study investigated the association between bipolar disorder and several indices of adiposity, including body fat mass as measured by dual energy X-ray absorptiometry (DXA), in a community-based sample.

Methods: In this study, 21 women with bipolar disorder and 523 healthy controls were drawn from an age-stratified, random, community-based sample of women (20–93 years) participating in the Geelong Osteoporosis Study. Bipolar disorder was diagnosed utilising a semi-structured clinical interview. Anthropometric measurements (weight, height, waist and hip circumference) were taken and fat mass was determined from whole body DXA scans (Lunar DPX-L).

Results Those with bipolar disorder tended to have greater adiposity. Age-adjusted mean (95% CI) values for bipolar versus controls according to adiposity indices were weight 75.6 (68.9–82.3) versus 72.6 (71.3–74.0) kg, waist circumference 89.8 (84.1–95.6) versus 87.3 (86.1–88.5) cm, waist:hip ratio 0.85 (0.82–0.87) versus 0.84 (0.83–0.84), body mass index 27.6 (25.1–30.1) versus 27.5 (27.0–28.0) kg/m2, fat mass 31.4 (26.5–36.3) versus 28.6 (27.5–29.5) kg and %body fat 40.4 (36.9–43.9) versus 38.0 (37.3–38.7)%; all p > 0.05. Further adjustment for height, smoking, alcohol, psychotropic medication, energy intake or physical activity did not influence these patterns.

Conclusion Although a pattern suggestive of greater adiposity among those with bipolar disorder was observed, no significant differences were detected. We cannot exclude the possibility of a type II error. Further research with a larger sample may produce more conclusive results.

Aydemir O, Akkaya C. Association of social anxiety with stigmatisation and low self-esteem in remitted bipolar patients.

Background: In remitted bipolar disorder, it is aimed to show the association between social anxiety, self-esteem and stigmatisation.

Methods: From two university clinics, a sample of 150 remitted bipolar patients was included in this study. Patients were assessed with Liebowitz Social Anxiety Scale, Rosenberg Self-Esteem Scale and sense of stigmatisation subscale of Bipolar Disorder Functioning Questionnaire (Stigma) and were rated with Hamilton Depression Rating Scale and Young Mania Rating Scale for mood symptoms. Confirmatory path analysis was performed.

Results: The mean age of the patients was 39.5, and 52.7% (n = 79) were female. Ninety per cent (n = 135) of the patients had bipolar I disorder. The mean duration of the illness was 13.4 years and the mean number of episodes was 7.8. The model was subjected to confirmatory path analysis and the goodness-of-fit index was calculated to be 0.909, the confirmatory fit index was found to be 0.902 and the root mean square error of approximation was 0.097. Self-esteem was negatively associated with stigmatisation (r = −0.746). Social anxiety was positively associated with self-esteem (r = 0.494). Social anxiety was negatively associated with stigmatisation (r = −0.381).

Conclusions: In remitted bipolar patients, social anxiety is very high and this social anxiety seems to be caused by self-stigmatisation and low self-esteem.

Zhang X, Wang X, Sha W, Zhou H, Zhang Y. Val66Met polymorphism and serum brain-derived neurotrophic factor concentration in depressed patients.

Objective: Accumulating evidence has suggested a pathophysiological role for brain-derived neurotrophic factor (BDNF) in major depressive disorder (MDD). The present study evaluated serum levels of BDNF and explored whether Val66Met BDNF gene polymorphism is correlated with changes in circulating BDNF levels in patients with MDD and control subjects.

Methods: Subjects were 76 patients with MDD and 50 controls. Diagnosis of MDD was determined by the use of a structured clinical interview according to Diagnostic and Statistical Manual of Mental Disorder-IV (DSM-IV) criteria. The concentrations of BDNF were measured by using the enzyme-linked immunosorbent assay. The Val66Met BDNF gene polymorphism was examined by the polymerase chain reaction technique.

Results: Serum BDNF was significantly lower in MDD patients than in normal control subjects (p < 0.001). There were no significant differences either in allele or genotype in the Val66Met polymorphism between the MDD and control groups. Moreover, genotype did not significantly correlate with the BDNF serum levels in the MDD or control groups.

Conclusions: Our study suggests that there is a decrease in serum BDNF levels in untreated MDD patients. However, serum BDNF levels were not associated with the Val66Met polymorphism.

Yang L, Ruan L-M, Ye H-H, Cui H-B, Mu Q-T, Lou Y-R, Ji Y-X, Li W-Z, Sun D-H, Chen X-B. Depression is associated with lower circulating endothelial progenitor cells and increased inflammatory markers.

Objective: To test the hypothesis that depression status in subjects without cardiovascular diseases (CVD) or diabetes is associated with depletion of circulating endothelial progenitor cells (EPCs) and impaired endothelial function.

Method: Thirty depressive persons with the first episode of depression (case group) diagnosed according to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) and 30 healthy people (control group) were investigated. The depression status was estimated using Hamilton Rating Scale of Depression from which the criteria of depression are determined to be >21 score. EPCs labeled with CD34-ECD, CD133-phycoerythrin and kinase insert domain receptor (KDR)-fluorescein isothiocyanate antibodies were counted by flow cytometry in the peripheral blood of patients and control subjects. Mononuclear cells that were positive for CD34/KDR, CD133/KDR and CD34/CD133/KDR within the lymphocyte population were characterised as different phenotypes of EPCs.

Results: There were no significant differences in baseline clinical characteristics between patients and healthy individuals (all p > 0.05). However, patients with depression had significantly lower levels of circulating CD34+CD133+KDR+ EPCs (132.20 ± 17.27 vs. 225.93 ± 9.88, p = 0.000) and endothelial colony-forming units (26.40 ± 3.79 vs. 36.60 ± 2.88, p = 0.000) than that of healthy subjects. Furthermore, CD34+CD133+KDR+ EPCs had a negative correlation with tumour necrosis factor-α (Spearman's ρ = 0.433, p = 0.000) and interleukin-6 (Spearman's ρ = 0.441, p = 0.032).

Conclusion: Our result shows that depression was associated with lower levels of circulating EPCs, which may contribute to the development of endothelial dysfunction and atherosclerosis.

Réus GZ, Stringari RB, Ribeiro KF, Luft T, Abelaira HM, Fries GR, Aguiar BW, Kapczinski F, Hallak JE, Zuardi AW, Crippa JA, Quevedo J. Administration of cannabidiol and imipramine induces antidepressant-like effects in the forced swimming test and increases brain-derived neurotrophic factor levels in the rat amygdala.

Objective: Cannabidiol is a chemical constituent from Cannabis sativa and it has multiple mechanisms of action, including antidepressant effects. The main objective of the present study was to evaluate behavioural and molecular effects induced by administration of cannabidiol and imipramine in rats.

Methods: In the present study, rats were acutely or chronically treated for 14 days once a day with saline, cannabidiol (15, 30 and 60 mg/kg) or imipramine (30 mg/kg) and the animals behaviour was assessed in forced swimming and open-field tests. Afterwards, the prefrontal cortex, hippocampus and amygdala brain-derived neurotrophic factor (BDNF) levels were assessed by enzyme-linked immunosorbent sandwich assay.

Results: We observed that both acute and chronic treatments with imipramine at the dose of 30 mg/kg and cannabidiol at the dose of 30 mg/kg reduced immobility time and increased swimming time; climbing time was increased only with imipramine at the dose of 30 mg/kg, without affecting locomotor activity. In addition, chronic treatment with cannabidiol at the dose of 15 mg/kg and imipramine at the dose of 30 mg/kg increased BDNF levels in the rat amygdala.

Conclusion: In conclusion, our results indicate that cannabidiol has an antidepressant-like profile and could be a new pharmacological target for the treatment of major depression.

Karanasios P, Loukopoulou P, Zampakis P, Tiligadas T, Makridou A, Doukas V, Argyriou AA. Foreign accent syndrome caused by a left temporal–parietal ischaemic stroke.

Aim: We present the first reported case of a Greek patient with foreign accent syndrome (FAS) secondary to a left temporal-parietal ischemic stroke.

Case report: A 76 year-old right-handed, Greek in origin, male was referred because he had suddenly manifested changes in speech expression. The neurological examination revealed that his prior typical English-Australian accent resembled a mixture of Greek and English-Britain accent consistent with FAS, though he had visited only once Greece the last 15 years and never had been to United Kingdom.

Results: A brain Magnetic Resonance Imaging scan depicted an ischemic temporal lesion in the language-dominant left hemisphere, affecting the left posterior superior and middle temporal gyri, as well as the ipsilateral inferior supramarginal angular gyrus and posterior insula.

Conclusion: We might suggest that FAS in our patient was induced because of interrupted cortical-subcortical feedback pathways. The phenomenon of subcortical-cortical diaschisis might also have contributed to its clinical manifestation.

López Arteaga MT, Amo C, Sánchez Morla EM, Sánchez Román M. Induced psychosis after withdrawal of varenicline: a case report.

Objective: Varenicline has been associated with psychiatric side effects, and cases with psychotic symptoms during treatment have been reported, few of them after the withdrawal. We describe a case with no current or previous medical or psychiatric history.

Method: A single case report.

Results: The patient without previous psychiatric pathology, following the withdrawal of treatment with varenicline, experiences delirium and behavioural disturbances. There was a remission of symptoms after 3 weeks of treatment with risperidone.

Conclusion: Discontinuation of treatment with varenicline due to poor tolerance for side effects (nausea and insomnia) could trigger psychotic symptoms in subjects with no personal or family psychiatric history.