The Role of Momentary Dissociation in the Sensory Cortex: A Neurophysiological Review and its Implications for Maladaptive Daydreaming.

Daydreaming, a form of spontaneous and self-generated mental process, may lead to the disintegration of attention from the immediate external environment. In extreme cases, patients may develop maladaptive daydreaming comorbid with dissociation. The examination of dissociative alterations frequently occurs within the framework of complex cognitive processes. While dissociation may be a neurological and psychological dysfunction of integration, transient dissociative occurrences, i.e., momentary dissociation may signify a dynamic interplay between attentional division and orientation within the sensory cortex. Furthermore, previous studies have recorded the interactivity of attention by stimuli onset with P3 event-related potentials and the active suppression of distractor positivity. In this context, during auditory and visual mismatch negativity, the sensory cortex may interact with attentional orientation. Additionally, distractor positivity during task-relevant stimuli may play a crucial role in predicting momentary dissociation since sensory cortices share cerebral correlates with attentional fluctuations during mental imagery. Thus, this theoretical review investigated the cerebral activities associated with attentional orientation and may be extended to mindfulness. By integrating these findings, we aim to provide a comprehensive understanding of dissociative states which may lead to a resolution for dissociative psychopathology.

Attention-Deficit/Hyperactivity Disorder (ADHD) and Time Perception in Adults: Do Adults with Different ADHD Symptomatology Severity Perceive Time Differently? Findings from the National Czech Study.

BACKGROUND Studies show neurological differences between patients with attention-deficit/hyperactivity disorder (ADHD) and healthy controls. Furthermore, it is possible that poor timing is linked with impairments in neural circuitry. This study aimed to test the hypothesis that there is a difference in time perception between adults with severe ADHD symptomatology and adults with no ADHD symptomatology. MATERIAL AND METHODS Previously, we collected data from a more extensive set of participants (n=1518) concerning the prevalence of ADHD in adulthood. We recruited participants from 3 groups defined by increasing ADHD severity out of this participant pool. Each participant was presented with 2 experimental tasks (in counterbalanced order): duration estimation and duration discrimination. RESULTS In general, we did not find any specific differences in time perception related to the severity of ADHD. Regarding duration estimation, we found that the difference between the actual and estimated durations increased with the actual duration (F(1, 7028.00)=2685.38, P<0.001). Although the differences between groups were not significant, the group×duration interaction was (F[1, 7028.00]=10.86, P<0.001), with a very small effect size (ηp²<0.001, 95% CI [0.00, 0.01]). CONCLUSIONS The results suggest that although individuals may demonstrate increased ADHD symptomatology, they may not have objectively more significant difficulties in time perception tasks than their counterparts with mild symptomatology. Nonetheless, time perception should be further studied because, as qualitative research suggests, participants with more severe ADHD symptomatology subjectively perceive more significant differences in time management in real life.

A Real-World Study on the Use of the Alcohol Use Disorders Identification Test (AUDIT) in Men Admitted to a Psychiatric Hospital.

BACKGROUND This real-world study aimed to investigate the use of the Alcohol Use Disorders Identification Test (AUDIT) in men admitted to a psychiatric hospital. MATERIAL AND METHODS The AUDIT questionnaire (10 items) was consecutively administered for a period of 3 years to male patients admitted to a psychiatric hospital (n=636). Laboratory blood tests of biochemical parameters were measured as biomarkers of alcohol consumption. Data were evaluated using linear models with mixed effects in the case of continuous dependent variables and logistic regression models with mixed effects in the case of categorical dependent variables. RESULTS We found that 45.3% of the patients had a high risk of alcohol consumption or alcohol dependence and 54.7% had a low risk of alcohol consumption. The ICD-10 diagnoses of alcohol-related disorders (F1x), psychotic disorders (F2x), affective disorders (F3x), neurotic and psychosomatic disorders (F4x) were statistically significantly associated with total AUDIT score (P<0.001). There was a statistically significant association between the total AUDIT score and length of hospitalization (P=0.004) and the incidence of suicidal thoughts (P=0.003). Plasma concentrations of alanine aminotransferase (P=0.005), aspartate aminotransferase (P<0.001), gamma glutamyltransferase (P=0.001), total cholesterol (P=0.027) and mean corpuscular value of erythrocytes (P<0.001) were statistically significantly increased with a higher AUDIT score. CONCLUSIONS This real-world study showed that the AUDIT questionnaire evaluated the severity of disorders caused by alcohol and their impact on comorbid mental disorders. These results may be helpful in improving targeted interventions in this group of patients.

Interactions Among Polymorphisms of Susceptibility Loci for Alzheimer's Disease or Depressive Disorder.

BACKGROUND Several genetic susceptibility loci for major depressive disorder (MDD) or Alzheimer's disease (AD) have been described. Interactions among polymorphisms are thought to explain the differences between low- and high-risk groups. We tested for the contribution of interactions between multiple functional polymorphisms in the risk of MDD or AD. MATERIAL AND METHODS A genetic association case-control study was performed in 68 MDD cases, 84 AD cases (35 of them with comorbid depression), and 90 controls. The contribution of 7 polymorphisms from 5 genes (APOE, HSPA1A, SLC6A4, HTR2A, and BDNF) related to risk of MDD or AD development was analyzed. RESULTS Significant associations were found between MDD and interactions among polymorphisms in HSPA1A, SLC6A4, and BDNF or HSPA1A, BDNF, and APOE genes. For polymorphisms in the APOE gene in AD, significant differences were confirmed on the distributions of alleles and genotype rates compared to the control or MDD. Increased probability of comorbid depression was found in patients with AD who do not carry the ε4 allele of APOE. CONCLUSIONS Assessment of the interactions among polymorphisms of susceptibility loci in both MDD and AD confirmed a synergistic effect of genetic factors influencing inflammatory, serotonergic, and neurotrophic pathways at these heterogenous complex diseases. The effect of interactions was greater in MDD than in AD. A presence of the ε4 allele was confirmed as a genetic susceptibility factor in AD. Our findings indicate a role of APOE genotype in onset of comorbid depression in a subgroup of patients with AD who are not carriers of the APOE ε4 allele.

Plasma homocysteine in Alzheimer's disease with or without co-morbid depressive symptoms.

OBJECTIVE: Elevated homocysteine is associated with a variety of diseases, including Alzheimer's disease (AD) and depressive disorder. This study was designed to detect an association between plasma homocysteine and AD with or without co-morbid depressive symptoms. METHODS: Plasma homocysteine concentrations were measured in 85 AD patients (36 of them with depressive symptoms), 33 non-AD patients with a depression diagnosis and 44 healthy controls, all aged above 50 years. RESULTS: Positive correlation between age and homocysteine was confirmed. Significantly higher mean plasma homocysteine was found in AD patients, but not in depressive patients, when compared with controls. We confirmed significant correlation between homocysteine concentration and the degree of cognitive impairment in AD patients. There was no incremental effect of concurrent depressive symptoms on homocysteine concentration in AD patients. CONCLUSION: The association of high homocysteine with degree of cognitive impairment or stage of dementia in AD indicate potential role of high plasma homocysteine as a biomarker of the disease and/or indicator of brain damage during the progression of AD dementia.

Plasma cortisol in Alzheimer's disease with or without depressive symptoms.

BACKGROUND: Cortisol is presumed to be a risk factor for stress- and age-related disorders, such as depressive disorder and Alzheimer's disease (AD). The aim of this study was to investigate the association of plasma cortisol concentration with AD in presence or absence of comorbid depressive symptoms. MATERIAL AND METHODS: Plasma cortisol concentration was measured in 80 AD patients (35 of them with depressive symptoms), 27 elderly depressive patients without AD, and 37 elderly controls. RESULTS: Compared to controls, a significant increase of mean plasma cortisol was found in AD patients but not in depressive patients. Plasma cortisol was positively correlated with cognitive impairment in AD patients. We confirmed a U-shaped association between plasma cortisol and major depression and a linear association between plasma cortisol and AD without depressive symptoms. Significantly increased relative risk of disease in people with high plasma cortisol was found for AD with depressive symptoms and for AD with mild dementia. CONCLUSIONS: Plasma cortisol reflects the degree of cognitive impairment in AD rather than the severity of comorbid depression. We confirmed that both hypercortisolemia and hypocortisolemia are associated with depressive disorder. Significant association between high plasma cortisol and AD was found, supporting the use of high plasma cortisol as a component of a panel of biochemical markers for AD with depressive symptoms as well as AD in the early stage of dementia development.

Age-Dependent Alterations in Platelet Mitochondrial Respiration.

Mitochondrial dysfunction is an important cellular hallmark of aging and neurodegeneration. Platelets are a useful model to study the systemic manifestations of mitochondrial dysfunction. To evaluate the age dependence of mitochondrial parameters, citrate synthase activity, respiratory chain complex activity, and oxygen consumption kinetics were assessed. The effect of cognitive impairment was examined by comparing the age dependence of mitochondrial parameters in healthy individuals and those with neuropsychiatric disease. The study found a significant negative slope of age-dependence for both the activity of individual mitochondrial enzymes (citrate synthase and complex II) and parameters of mitochondrial respiration in intact platelets (routine respiration, maximum capacity of electron transport system, and respiratory rate after complex I inhibition). However, there was no significant difference in the age-related changes of mitochondrial parameters between individuals with and without cognitive impairment. These findings highlight the potential of measuring mitochondrial respiration in intact platelets as a means to assess age-related mitochondrial dysfunction. The results indicate that drugs and interventions targeting mitochondrial respiration may have the potential to slow down or eliminate certain aging and neurodegenerative processes. Mitochondrial respiration in platelets holds promise as a biomarker of aging, irrespective of the degree of cognitive impairment.

Violence risk and personality assessment in adolescents by Structured Assessment of Violence Risk in Youth (SAVRY) and high school personality questionnaire (HSPQ): Focus on protective factors strengthening.

Background: Adolescents are most at risk of engaging in violent interaction. Targeting violence risk and protective factors is essential for correctly understanding and assessing their role in potential violence. We aimed to use the Structured Assessment of Violence Risk in Youth (SAVRY) tool within the sample of adolescents to capture violence risk and protective factors and personality variables related to risk and protective factors. We further aimed to identify which violence risk and protective factors were positively or negatively related to violence within personal history and if any personality traits are typical for violent and non-violent adolescents. Identifying broader or underlying constructs within the SAVRY tool factor analysis can enable appropriate therapeutic targeting. Methods: We used the Czech standardized version of the SAVRY tool. The study sample comprised 175 men and 226 women aged 12-18 years divided into two categories according to the presence or absence of violence in their personal history. Mann-Whitney U test was used to compare numerical variables between the two groups. SAVRY factor analysis with varimax rotation was used to determine the item factors. We administered the High School Personality Questionnaire (HSPQ) to capture adolescents' personality characteristics. Results: In our sample, there were 151 participants with violence in their personal histories and 250 non-violent participants. Non-violent adolescents had higher values for all six SAVRY protective factors. The strongest protective factor was P3, Strong attachment and bonds across gender or a history of violence. Using factor analysis, we identified three SAVRY internal factors: social conduct, assimilation, and maladaptation. The SAVRY protective factors were significantly positively related to several factors in the HSPQ questionnaire. Conclusion: The results highlight the significance of protective factors and their relationship with violence prevalence. HSPQ diagnostics could be helpful in clinically targeting personality-based violence risks and protective factors. The therapeutic focus should be on tension, peer rejection, and anxiety. It is also essential to foster positive attitudes toward authority, prosocial behavior, and attitudes toward school. These strategies can help strengthen protective factors of the SAVRY.

Novel approaches in schizophrenia-from risk factors and hypotheses to novel drug targets.

Schizophrenia is a severe psychiatric disorder characterized by emotional, behavioral and cognitive disturbances, and the treatment of schizophrenia is often complicated by noncompliance and pharmacoresistance. The search for the pathophysiological mechanisms underlying schizophrenia has resulted in the proposal of several hypotheses to explain the impacts of environmental, genetic, neurodevelopmental, immune and inflammatory factors on disease onset and progression. This review discusses the newest insights into the pathophysiology of and risk factors for schizophrenia and notes novel approaches in antipsychotic treatment and potential diagnostic and theranostic biomarkers. The current hypotheses focusing on neuromediators (dopamine, glutamate, and serotonin), neuroinflammation, the cannabinoid hypothesis, the gut-brain axis model, and oxidative stress are summarized. Key genetic features, including small nucleotide polymorphisms, copy number variations, microdeletions, mutations and epigenetic changes, are highlighted. Current pharmacotherapy of schizophrenia relies mostly on dopaminergic and serotonergic antagonists/partial agonists, but new findings in the pathophysiology of schizophrenia have allowed the expansion of novel approaches in pharmacotherapy and the establishment of more reliable biomarkers. Substances with promising results in preclinical and clinical studies include lumateperone, pimavanserin, xanomeline, roluperidone, agonists of trace amine-associated receptor 1, inhibitors of glycine transporters, AMPA allosteric modulators, mGLUR2-3 agonists, D-amino acid oxidase inhibitors and cannabidiol. The use of anti-inflammatory agents as an add-on therapy is mentioned.

[Education in schizophrenia: how patients and their relatives assess the relapse prevention programme PREDUKA]. / Edukace u schizofrenie: Jak pacienti a príbuzní hodnotí program prevence relapsu PREDUKA.

Antipsychotic medication and early relapse warning signs detection are the cornerstone of relapse prevention in schizophrenia spectrum disorders. Many patients do not use antipsychotic medication because of lack of information about its preventive effects and the risk of relapse. We introduce PREDUKA--PREventive EDUcational programme for relapse prevention. The goal of the programme is to deliver the information about schizophrenia to patients and their relatives. 178 patients and 252 relatives (118 mothers and 51 fathers) took part in 25 one-day psychoeducational programmes in 6 centres in the Czech Republic between January 2008 and June 2009 and anonymously fulfilled a short questionnaire. Patients and relatives assessed the programme with an average mark 1.4 (1 best, 5 worst). 49.4% patients and 49.0% relatives had received enough information about psychotic disorders during their hospitalization. Moreover 94.1% patients and 95.7% relatives confirmed acquiring new information on how to live with psychosis as a result of PREDUKA programme. 59.6% patients and 73.8% relatives were interested in ITAREPS - Information Technology Aided Relapse Prevention Programme. Mothers were significantly more interested (82.2%) than fathers (62.2%) (p = 0.031). Expressed high interest of patients and their relatives in both programmes indicates their readiness to become active and competent partners in the long-term treatment of schizophrenia spectrum disorders.

Activities of mitochondrial respiratory chain complexes in platelets of patients with Alzheimer's disease and depressive disorder.

We analyzed activities of complex I, II, III, and IV, and citrate synthase (CS) in patients with major depressive disorder (MDD) or Alzheimer's disease (AD) presenting with or without depression. Associations of these parameters with disease or disease severity were observed in both AD and MDD; however, mean values of mitochondrial parameters were significantly altered in AD but not in MDD. Potential mitochondrial dysfunction in MDD seems not to be caused by disturbed activity of CS or respiratory complexes. In AD, a decrease in the activity of CS and complex IV may cause mitochondrial dysfunction, whereas an increase in activities of other mitochondrial complexes or their ratios to CS may be an adaptive response. The data indicate that comorbid depression in AD is associated with increased complex II activity. The mitochondrial parameters measured can be included in the panel of biomarkers of AD.

Disturbances of mitochondrial parameters to distinguish patients with depressive episode of bipolar disorder and major depressive disorder.

BACKGROUND: Mitochondrial dysfunctions are implicated in the pathophysiology of mood disorders. We measured and examined the following selected mitochondrial parameters: citrate synthase (CS) activity, electron transport system (ETS) complex (complexes I, II, and IV) activities, and mitochondrial respiration in blood platelets. PATIENTS AND METHODS: The analyses were performed for 24 patients suffering from a depressive episode of bipolar affective disorder (BD), compared to 68 patients with MDD and 104 healthy controls. BD and unipolar depression were clinically evaluated using well-established diagnostic scales and questionnaires. RESULTS: The CS, complex II, and complex IV activities were decreased in the depressive episode of BD patients; complex I and complex I/CS ratio were significantly increased compared to healthy controls. We observed significantly decreased complex II and CS activities in patients suffering from MDD compared to controls. Decreased respiration after complex I inhibition and increased residual respiration were found in depressive BD patients compared to controls. Physiological respiration and capacity of the ETS were decreased, and respiration after complex I inhibition was increased in MDD patients, compared to controls. Increased complex I activity can be a compensatory mechanism for decreased CS and complex II and IV activities. CONCLUSION: We can conclude that complex I and its abnormal activity contribute to the defects in cellular energy metabolism during a depressive episode of BD. The observed parameters could be used in a panel of biomarkers that could selectively distinguish BD depression from MDD and can be easily examined from blood elements.

Mitochondrial Dysfunction in Blood Platelets of Patients with Manic Episode of Bipolar Disorder.

OBJECTIVES: The bipolar affective disorder (BAD) pathophysiology is multifactorial and has not been fully clarified. METHOD: We measured selected mitochondrial parameters in peripheral blood components. The analyses were performed for patients suffering from a manic episode during remission and were compared to those performed for healthy controls. BAD was clinically evaluated using well-established diagnostic scales and questionnaires. Mitochondrial respiration was examined in intact and permeabilized blood platelets using high-resolution respirometry. The citrate synthase (CS) and electron transport system (ETS) complex (complex I, II, and IV) activities were examined in platelets. RESULTS: The CS, complex II and complex IV activities were decreased in the BAD patients, complex I activity was increased, and the ratio of complex I to CS was significantly increased. In the intact platelets, respiration after complex I inhibition and residual oxygen consumption were decreased in the BAD patients compared to the healthy controls. In the permeabilized platelets, a decreased ETS capacity was found in the BAD patients. No significant differences were found between BAD patients in mania and remission. CONCLUSION: Increased complex I activity can be a compensatory mechanism for decreased CS and complex II and IV activities. We conclude that complex I and its abnormal activity contribute to defects in cellular energy metabolism during a manic episode and that the deficiency in the complex's functioning, but not the availability of oxidative phosphorylation substrates, seems to be responsible for the decreased ETS capacity in BAD patients. The observed parameters can be further evaluated as 'trait' markers of BAD.

Interplay between the APOE Genotype and Possible Plasma Biomarkers in Alzheimer's Disease.

BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder with a complex pathogenesis and a common occurrence of comorbid diseases such as depression. It is accepted that the presence of the ε4 allele of the gene that encodes apolipoprotein E (APOE) is the strongest genetic risk factor for the development of sporadic AD. Melatonin, cortisol, homocysteine, and prolactin are presumed to be risk factors or biomarkers for stress- and age-related disorders. OBJECTIVE: The interplay between the APOE genotype and plasma biomarkers was examined in patients with AD presenting with or without depression to contribute to understanding the interdependence of various molecular mechanisms in the pathophysiology of AD. METHOD: The APOE genotype and morning plasma melatonin, cortisol, homocysteine, and prolactin concentrations were measured in 85 patients with AD and 44 elderly controls. RESULTS: A significant association between AD and the allele (ε4) or genotype (ε3/ε4 or ε4/ε4) frequencies of APOE was confirmed. Plasma homocysteine and cortisol levels were significantly increased in patients with AD compared to those in controls, independent of the presence of comorbid depressive symptoms or the severity of dementia. Significantly lower plasma melatonin concentration was found in patients with AD but not in controls, who were noncarriers of the APOE ε4 allele, regardless of the presence of depression or the severity of dementia in AD. CONCLUSION: Our findings indicate the existence of a little-known specific APOE-mediated mechanism that increases the plasma melatonin level in a subgroup of patients with AD who are carriers of the APOE ε4 allele.

The role of some new factors in the pathophysiology of depression and cardiovascular disease: overview of recent research.

Depressive disorders and cardiovascular disease are inter-connected by a whole range of pathophysiological mechanisms. Three biological mechanisms are fundamental: activation of the hypothalamus-hypohysis-adrenal axis with a subsequent increase in sympathetic-adrenal system activity, decrease in vagal tone with a decrease in heart rate variability, and alterations of thrombogenesis with increased platelet aggregability. Behavioural mechanisms and psycho-social factors are also integral to this common pathophysiology. Recently, research has focused mainly on studying various forms of stress, as well as changes and possibilities of influencing the autonomous vegetative system. Temporal aspects of the incidence and development of depressive episodes in relation to cardiovascular disease and subsequent cardiovascular morbidity and mortality are being studied, as well as general mortality risk factors. These findings are important for clinical practice. It is evident that in patients with untreated depressive disorder, the risk of developing cardiovascular disease is significantly higher than in patients suffering from a depressive disorder being treated with anti-depressants. From the data published so far, it may be surmised that depressive disorders in patients with cardiovascular disease may be reliably and safely treated with anti-depressants that act as inhibitors of serotonin re-uptake.

Evaluation of psychopathology in patients with paroxysmal supraventricular tachycardia.

BACKGROUND: A higher prevalence of anxiety- and depression-related symptoms are expected in patients with at least one somatic disease and who are on medications compared with the general population. OBJECTIVES: To determine if patients with paroxysmal supraventricular tachycardia (PSVT) show a higher prevalence of anxiety and depressive symptoms compared with a control population. The induction of depressive symptoms by beta-blockers or calcium channel blockers was also evaluated. METHODS: Twenty-five patients (17 women, eight men) with documented PSVT (atrioventricular re-entrant tachycardia or atrioventricular nodal re-entrant tachycardia) were evaluated by a battery of questionnaires and inventories, which provide information about the presence of symptoms of anxiety and/or depression. All patients were examined by a psychiatrist and completed the following five scales: Symptom Checklist-90, Hamilton Anxiety Scale, Hamilton Depression Rating Scale, Zung's Self-Rating Depression Scale and Beck Self-Assessment Depression Scale. RESULTS AND CONCLUSIONS: The majority of the evaluations (Hamilton Anxiety Scale, Beck Self-Assessment Depression Scale, Zung's Self-Rating Depression Scale), did not show a higher incidence of severe symptoms of depression in the group of patients with PSVT. However, the Hamilton Depression Rating Scale rated the symptoms of depression as significant, but the score was low enough to be considered nonsignificant. According to the Symptom Checklist-90, men perceived the presence of the cardiological disease more intensively and more negatively than women (P=0.1). Psychiatric history and therapy with psychopharmacological agents were comparable in both groups. It was noted that patients had sporadic contacts with a psychiatrist or a psychologist, but this was not directly associated with PSVT.

GSK3ß, CREB, and BDNF in peripheral blood of patients with Alzheimer's disease and depression.

BACKGROUND: Glycogen synthase kinase-3ß (GSK3ß), cAMP-response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) play critical roles in neuronal survival, synaptic plasticity and memory and participate in the pathophysiology of both depressive disorder and Alzheimer's disease (AD). METHODS: This study was designed to determine the association of GSK3ß activity, CREB activity and BDNF concentration in peripheral blood of patients with AD with or without depressive symptoms and in depressive patients without AD. GSK3ß activity in platelets, CREB activity in lymphocytes and BDNF concentration in plasma, platelet-rich plasma or platelets were measured in 85 AD patients (36 of whom displayed co-morbid depressive symptoms), 65 non-AD patients with depressive disorder and 96 healthy controls. AD patients were clinically assessed for stage of dementia, cognitive impairment and severity of depressive symptoms. Depressive patients were clinically assessed for severity of depression. RESULTS: We observed increased CREB activity and GSK3ß activity in AD with depressive symptoms or in AD at mild stage of dementia. Decreased BDNF concentration was found in platelet-rich plasma of AD patients at moderate to severe stages of dementia or in AD without depressive symptoms. An association was revealed of the severity of cognitive impairment with the increase of GSK3ß in the platelets of AD patients with mild dementia. In depressive patients, a lower concentration of phosphorylated GSK3ß was associated with a higher severity of depression. Association was confirmed between severity of depression, CREB activation, and BDNF concentration in drug-naïve depressive patients. CONCLUSION: Our data demonstrated that AD is accompanied by increased CREB activity in lymphocytes and a decreased concentration of BDNF in platelet-rich plasma. The decreased BDNF concentration appears to correlate with moderate to severe stages of dementia in AD. Observation of decreased phosphorylation of GSK3ß in platelets of both AD patients with depressive symptoms and depressive patients after treatment confirms the role of increased GSK3ß activity in the pathophysiology of both AD and depressive disorder. Associations were confirmed between AD and platelet GSK3ß activity, lymphocyte CREB activity and plasma BDNF. CREB activity and platelet BDNF concentration seems to be related to depressive disorder.

Mitochondrial respiration in blood platelets of depressive patients.

Recent evidences include mitochondrial dysfunctions in pathophysiology of mood disorders. We examined association between depressive disorders and mitochondrial respiration using both intact and permeabilized blood platelets. In intact platelets, physiological respiration, maximal capacity of electron transport system and respiratory rate after complex I inhibition were decreased in depressive patients, who reached partial remission, compared to healthy controls. Respiratory rates were unchanged in several respiratory states in permeabilized platelets. Results indicate that changes in respiratory rate in intact platelets can be used as biological marker of depressive disorder. The hypothesis that decreased mitochondrial respiratory rate participate in pathophysiology of depression was supported.

Use of coercive measures during involuntary hospitalization: findings from ten European countries.

OBJECTIVE: Involuntary treatment in mental health care is a sensitive but rarely studied issue. This study was part of the European Evaluation of Coercion in Psychiatry and Harmonization of Best Clinical Practice (EUNOMIA) project. It assessed and compared the use of coercive measures in psychiatric inpatient facilities in ten European countries. METHODS: The sample included 2,030 involuntarily admitted patients. Data were obtained on coercive measures (physical restraint, seclusion, and forced medication). RESULTS: In total, 1,462 coercive measures were used with 770 patients (38%). The percentage of patients receiving coercive measures in each country varied between 21% and 59%. The most frequent reason for prescribing coercive measures was patient aggression against others. In eight of the countries, the most frequent measure used was forced medication, and in two of the countries mechanical restraint was the most frequent measure used. Seclusion was rarely administered and was reported in only six countries. A diagnosis of schizophrenia and more severe symptoms were associated with a higher probability of receiving coercive measures. CONCLUSIONS: Coercive measures were used in a substantial group of involuntarily admitted patients across Europe. Their use appeared to depend on diagnosis and the severity of illness, but use was also heavily influenced by the individual country. Variation across countries may reflect differences in societal attitudes and clinical traditions.