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To investigate the association between cytokine peripheral levels and the risk of cardiovascular disease in patients with schizophrenia and controls.A sample of 40 patients and 40 control subjects participated in the study. Psychiatric diagnosis was established following structured clinical assessment. The Framingham Score was used to assess cardiovascular risk (CVR). Serum levels of the cytokines IL-1β, IL-6, IL-8, IL-10, IL-12p70 and TNF-α were determined by cytometric bead array (CBA) technique, and the serum levels of IL-33, sST2, sTNFR1, sTNFR2, Leptin and Adiponectin by Enzyme-Linked Immunosorbent assay (ELISA).Patients with schizophrenia showed greater frequency of moderate CVR when compared with controls (p = 0.14). In addition, patients showed higher levels of sTNFR2 and Adiponectin compared to controls (p = 0.007 and p 0.001, respectively). Adiponectin and sTNFR2 were associated with CVR only in patients (p = 0.0002 and p = 0.033, respectively). In multivariate analysis controlling for socio-demographic and clinical confounders, illness duration (r = 0.492; p 0.002) and sTNFR2 (r = 0.665; p 0.004) were independent predictors of CVR.Our results reinforce the concept that patients with schizophrenia are at greater risk to develop cardiovascular diseases, and suggest that the associated chronic low-grade inflammation might play a role in this process.

This study aimed at evaluating changes in the renin-angiotensin system (RAS) in patients with schizophrenia in comparison with controls. Plasma levels of angiotensin-converting enzyme (ACE), ACE2, angiotensin (Ang)-(1-7) and Ang II were assessed in 25 patients with schizophrenia and 20 controls. Patients with schizophrenia presented decreased levels of ACE compared to controls [median (25th-75th percentiles) = 434.79 (341.15-524.02) vs. 508.49 (396.34-608.72); p 0.05]. No significant differences were found regarding ACE2, Ang-(1-7) and Ang II levels. There were no associations between the measured molecules and clinical parameters. Our results corroborate the hypothesis that the RAS is involved in the pathophysiology of schizophrenia.

Objectives to evaluate cannabinoid receptors (CBRs) expression on peripheral immune cells, i.e., blood monocytes, neutrophils, lymphocytes, and NK cells, and their relationship to a wide range of serum cytokine levels in subjects with schizophrenia and controls. Methods A sample of 55 people with chronic schizophrenia and 48 controls were enrolled in the study. The expression of the cannabinoid receptors CB1R and CB2R was evaluated in peripheral blood leukocytes by flow cytometry. Serum levels of cytokines/chemokines were simultaneously analyzed by cytometric bead array. Results We found higher expression of cannabinoid receptors on cells of the innate immune system in subjects with schizophrenia when compared with controls. Serum levels of interleukin-4 (IL-4), IL-6, IL-10, IL-17, interferon (IFN-γ), and (C-X-C motif) ligand 10/interferon gamma-induced protein 10 (CXCL10/IP10) were decreased, while levels of the chemokine (C-C motif) ligand 2/monocyte chemoattractant protein-1 (CCL2/MCP-1) were increased in the schizophrenia group in comparison with controls. Patients with schizophrenia showed simpler correlation network between cytokines and CBRs expression than controls. Conclusion Patients with schizophrenia showed increased CBRs expression in cells of the innate immune system and simpler correlation network between cytokines and CBRs expression when compared with controls. These results suggest a defective endocannabinoid system-mediated immunomodulation in patients with schizophrenia.

Objective Changes in immune system have been reported in schizophrenia. This study aimed to evaluate the involvement of IL-33, a member of the IL-1 cytokine family, in schizophrenia and its association with cognitive performance in these patients. Methods Forty patients with chronic schizophrenia and 40 healthy subjects participated in the study. Serum levels of IL-33 and sST2 (soluble form of the IL-33 receptor) were measured using enzyme-linked immunosorbent assay (ELISA). Patients were evaluated with the Brief Assessment of Cognition in Schizophrenia (BACS) and the Schizophrenia Cognition Rating Scale (SCoRS). Results Patients with schizophrenia and controls presented similar serum levels of IL-33 and sST2. Levels of both markers were positively correlated with cognitive performance in patients with schizophrenia. Conclusion We found a significant correlation between IL-33 and sST2 levels and cognition in schizophrenia. Our results might help in the understanding of how immune markers are associated with cognitive impairment in schizophrenia. It remains to be determined whether the association between IL-33/sST2 and cognition is restricted to patients with schizophrenia.

Deficits in neurocognition and social cognition play a critical role in the functional impairment of patients with schizophrenia. Increased oxidative stress has been evidenced in schizophrenia. Increased oxidative stress can affect neuronal function and lead to impairments in neurocognitive functions (especially working memory) and social cognition.To investigate deficits in neurocognition and social cognition and their potential association with oxidative stress biomarkers in schizophrenia.Eight-five clinically stable patients with schizophrenia and 75 controls were enrolled in this study. Neurocognition was evaluated through the Brief Assessment of Cognition in Schizophrenia (BACS). Social cognition was assessed through the Hinting Task - a test of theory of mind - and an emotion processing test, Facial Emotion Recognition Test (FERT-100). Oxidative stress was assessed by measuring serum levels of glutathione (GSH) and thiobarbituric acid reactive substances (TBARS).Patients had decreased serum levels of GSH (Z=3.56; p0.001) and increased TBARS (Z=5.51; P0.001) when compared with controls. TBARS levels are higher in patients using first generation antipsychotics. Higher serum levels of TBARS in patients were associated with poor performance in working memory test (r=-0.39; p=0.002), even when controlling for age and negative symptoms (Standard Beta: -0.36; CI= -2.52 a -13.71).The association between greater lipid peroxidation, as assessed by TBARS, and worse performance in working memory corroborates theoretical models of greater vulnerability of schizophrenia to oxidative stress.

Purpose The purpose of this study was to test the psychometric properties of the Neurobehavior Inventory (NBI) in a group of temporal lobe epilepsy (TLE) patients from a tertiary care center, correlating its scores with the presence of psychiatric symptoms. Methods Clinical and sociodemographic data from ninety-six TLE outpatients were collected, and a neuropsychiatric evaluation was performed with the following instruments: Mini-Mental State Examination (MMSE), structured psychiatric interview (MINI-PLUS), Neurobehavior Inventory (NBI), and Hamilton Depression Rating Scale (HAM-D). Results Some traits evaluated by the NBI showed adequate internal consistency (mean inter-item correlation between 0.2 and 0.4) and were frequent, such as religiosity (74%) and repetitiveness (60.4%). Principal component analysis showed three factors, named here as emotions (Factor 1), hyposexuality (Factor 2), and unusual ideas (Factor 3). Depressive symptoms on HAM-D showed a strong association with emotions and hyposexuality factors. When patients with left TLE and right TLE were compared, the former exhibited more sadness (p = 0.017), and the latter, a greater tendency toward sense of personal destiny (p = 0.028). Conclusion Depression influences NBI scoring, mainly emotionality and hyposexuality traits. Neurobehavior Inventory subscales can be better interpreted with an appropriate evaluation of comorbid mood and anxiety disorders. Compromise in left temporal mesial structures is associated with increased tendency toward sad affect, whereas right temporal pathology is associated with increased beliefs in personal destiny.

BACKGROUND: Despite the old Kraepelinean concept that bipolar disorder (BD) does not evolve with cognitive decline, the presence of cognitive impairment, especially executive dysfunction has been recognized in BD patients. Brain-derived neurotrophic factor (BDNF) and pro-inflammatory molecules are important contributors to the pathophysiology of BD, and imbalance in peripheral levels of these molecules may be implicated in the cognitive decline observed in BD patients. We aimed to investigate the executive performance of BD type I euthymic patients and its relation with the plasma levels of BDNF, TNF-α and its related soluble receptors (sTNFR1 and sTNFR2). METHODS: We evaluated executive functioning through the Frontal Assessment Battery (FAB). Plasma levels of BDNF, TNF-α, sTNFR1 and sTNFR2 were measured using enzyme-linked immunosorbent assay (ELISA) in 25 euthymic type I BD patients and 25 age and gender matched healthy controls. RESULTS: BD patients had an impairment in executive functioning (p

Objective The aim of the work described here was to measure the role of psychopathological features, specifically impulsivity and depression, in suicidality in patients with temporal lobe epilepsy (TLE). Methods Neuropsychiatric evaluation of 66 outpatients with TLE was performed with the following instruments: a structured clinical interview (Mini International Neuropsychiatric Interview Plus), the Barratt Impulsiveness Scale, the Hamilton Anxiety Scale, the Beck Depression Inventory, and the Brief Psychiatric Rating Scale. Results A current Axis I psychiatric diagnosis, mainly mood and anxiety disorders, was assigned to 37 subjects (56.1%) Presence of suicide risk was identified in 19 patients (28.8%), and 14 (21.2%) had attempted suicide. Frequency of seizures ( P = 0.012), current major depression ( P = 0.001), and motor impulsivity ( P = 0.005) were associated with suicide risk on univariate analysis. Logistic regression stressed the main relevance of major depression (OR = 12.82, 95% CI = 2.58–63.76, P = 0.002) and motor impulsivity (OR = 1.21, 95% CI = 1.06–1.38, P = 0.005) to suicide risk. Conclusion Depression has a major influence on suicidality in epilepsy. Motor impulsivity is also relevant and may be an important component of depression in TLE associated with suicide risk.

Objective The purpose of this research was to evaluate the Brazilian-Portuguese version of the Neurological Disorders Depression Inventory for Epilepsy (NDDI-E) and to assess its psychometric properties. Methods This study involved 98 outpatients who underwent psychopathological evaluation with the Mini International Neuropsychiatric Interview—Plus Version, Hamilton Depression Scale (HAM-D), and a Portuguese version of the NDDI-E. Results The NDDI-E was easily understood and quickly administered to most of the patients. At a cutoff score > 15, NDDI-E had a sensitivity of 81.5%, a specificity of 83.1%, and a negative predictive value of 92.2% for diagnosis of major depression. Internal consistency reliability of the NDDI-E was 0.79, and there was also a positive correlation between the NDDI-E and the HAM-D (P Conclusion The Brazilian-Portuguese version of NDDI-E can be used as a practical screening tool to improve recognition of depression in Brazilian people with epilepsy.

Prefrontal cortex (PFC) dysfunction can lead to impairment in planning and behavioral inhibition, as well as personality changes. As ascending monoaminergic brainstem systems modulate PFC functioning, it is possible that lesions in the brainstem lead to symptoms similar to prefrontal dysfunction. A 29-year-old man developed several cognitive and behavioral symptoms after neurosurgery for resection of a pilocytic astrocytoma in the pontine-mesencephalic area. A careful analysis of symptoms indicated PFC dysfunction that could be attributed to lesions in the ascending monoaminergic brainstem systems. Interestingly, the cognitive symptoms improved after treatment with methylphenidate, which is a drug that modules catecholaminergic neurotransmission, thereby supporting this hypothesis. This is a unique case of PFC dysfunction that may be related to post-operative lesion of the catecholaminergic nuclei in the brainstem.

Background Bipolar disorder (BD) diagnosis is based on specific set of mood and behavioural symptoms although they also exhibit cognitive dysfunction. Immune/inflammatory mechanisms have been implicated in the pathophysiology of BD. Objective To investigate whether cognitive functioning is associated with clinical parameters and immune profile in patients with BD in remission. Methods Twenty patients with BD type I in remission (15/20 female; age [mean ± SD] 43.80 ± 11.72 years; years of education [mean ± SD] 12.40 ± 3.39) and 25 healthy controls (16/25 female; age [mean ± SD] 43.52 ± 11.72 years; years of education [mean ± SD] 11.16 ± 2.66) matched for age, gender, and years of education were enrolled in this study. Subjects were evaluated with the Mini-Plus; Young Mania Rating Scale; Hamilton Depression Rating Scale; and with Brief Assessment of Cognition in Affective Disorders a comprehensive test battery to evaluate visuomotor, immediate affective and non-affective memory, verbal fluency, delayed affective and non-affective memory, inhibition, and problem solving domains. We assessed IL2, IL4, IL6, IL10, IL17, INF, TNF and its soluble receptors in plasma by flow cytometry. Results Patients with BD exhibited poorer performance on all cognitive domains in comparison with controls. Patients with BD also had high levels of soluble TNF receptors, and Th1/Th2/Th17 cytokines (p Conclusion Our data suggest that inflammatory dysfunction might contribute to the cognitive impairment in BD.

The study investigates the effects of acute and chronic oral treatment with Hypericum perforatum L. (HP LI 160, 62.5-500 mg/kg) in rats submitted to different anxiety models: the elevated T-maze (for inhibitory avoidance and escape measurements), the light/dark transition, and the cat odor test. These models were selected for their presumed capacity of evidencing specific subtypes of anxiety disorders as recognized in clinical practice. The results showed that acute HP (125 mg/kg) impaired elevated T-maze inhibitory avoidance, an anxiolytic effect, without altering escape performance. Chronic HP (250 mg/kg) enhanced avoidance latencies only in animals that were preexposed to the open arms of the maze. Preexposure shortens escape latency, improving it as an escape index. Differently from the reference drug imipramine (IMP, 15 mg/kg), chronic HP did not impair escape from the open arms of the maze. On the other hand, similarly to IMP, the extract increased the number of transitions between the two compartments in the light/dark transition model. Treatment regimens with HP and IMP did not alter behavioral responses of rats to a cloth impregnated with cat odor. These observations suggest that HP LI 160 exerts anxiolytic-like effects in a specific subset of defensive behaviors, particularly those related to generalized anxiety.

We report the case of a patient with temporal lobe epilepsy, nonresponsive to antiepileptic drugs, who became seizure-free, but developed recurrent excessive irritability and psychotic symptoms after successful mesial temporal lobectomy. This patient was refractory to various pharmacological treatments including antipsychotics, mood stabilizers, and benzodiazepines before being successfully treated with olanzapine.