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The use of psychiatric services has been associated with a wide range of clinical variables. However, information about the impact of adolescent personality pathology related to hospital admissions is limited.
To analyze the different combination of personality pathology associated to variables of psychiatric hospital admissions (number of admissions, total of days spent as psychiatric inpatient, average of days for admission, and number of admissions in a day care hospital).
The ICD-10 and DSM-IV modules of the semi-structured interview IPDE (International Personality Disorders Examination) were administered, in a sample of 107 adolescent psychiatric patients (M=15.8, SD=0.8 years old; age rank 15-17; 79% female).
Personality pathology group identified by the IPDE showed significantly higher number (p< .001) of psychiatric admissions (M=1.48) than no personality pathology group (M=0.57), but not significant higher number of admissions in a day care hospital. Psychotic patients showed the highest rate of admissions (M=2.88). In present sample, between 30% and 38% of all hospital admitted patients showed a Cluster B personality disorder (PD).The users of psychiatric inpatient services with a complex PD (two o more PD from different clusters) presents in average: 2-2.5 admissions, 34-53 total days spent as psychiatric inpatient, and 11-16 days on each admission.
Patients with psychotic disorders or complex PD were the highest users of inpatients services, but not of day care hospital admissions.
This study was designed to verify whether fluoxetine (FL), a serotonin (5-HT) re-uptake inhibitor, would interfere with nortriptyline (NT), a biphasic U-shaped curvilinear dose-response relationship recently described in our laboratory. We associated 10 mg/kg NT or vehicle to 0, 5, 10, 20 and 40 mg/kg FL, in one group, and 10 mg FL or vehicle to 0, 5, 10, 20 and 40 mg/kg NT, in another group, 30 min before the tail suspension test (TST) in mice. Although we were not able to confirm a synergistic effect between FL and NT, FL-NT association seems to require higher doses of NT to block its own anti-immobility effect at high doses, thus widening NT effective antidepressant-like dose range in mice submitted to TST.
Early-onset psychosis (EOP) are a heterogeneous group, with high diagnostic stability for schizophrenia and bipolar disorder, in contrast to the lack of diagnostic stability of other EOP.
We recruited 24 adolescents consecutively admitted, who presented a first psychotic episode, in the adolescent psychiatric unit of the Gregorio Marañón General Hospital in Madrid, between May 2002 and May 2003, for a two year follow-up. Only one was lost at the two-year assessment.
Diagnosis of the psychotic disorders was assessed using the Kiddie-Sads-Present and Lifetime Version (K-SADS-PL).
The agreement between the baseline and the one-year follow-up diagnoses was 54.2%. Positive Predictive Value (PPV) was 100% for schizophrenia and depression with psychotic features, and 71.4% for bipolar disorder, while only 50.0% for schizo-affective disorder and 16.7% for psychosis NOS. From the one-year to the two-year follow-up, only one patient changed the diagnosis, so the agreement was 95.7%.
Eight patients were diagnosed with schizophrenia at the follow-up, but only four of them had received this diagnosis at the baseline assessment. The diagnosis of bipolar disorder was given at the follow-up to eight patients, from whom only four subjects received this diagnosis at baseline.
The results of the our longitudinal study on diagnostic stability support the Kraepelinean distinction between dementia praecox and manic-depressive psychosis.
Psychosis with onset prior to 18 years of age, or early-onset psychosis (EOP), have a poorer prognosis than adult-onset psychosis. Further, a worse functional outcome of patients with EOP has been related to diagnosis of schizophrenia, severity of negative symptoms, behavioral problems, premorbid functioning, childhood onset, and insidious onset. We aim to examine the functional outcome of patients with EOP over a two-year follow-up.
A total of 24 patients with first episode psychosis were enrolled. Subjects underwent a cross-sectional evaluation at the baseline visit that consisted of collecting sociodemographic data, including parental socioeconomic status as measured by the Hollingshead-Redlich Scale. Psychotic symptoms were assessed using the Spanish version of the Positive and Negative Syndrome Scale (PANSS). Social disability was measured with the Global Assessment of Functioning disability scale (GAF). Patients were assessed at a two-year follow-up. A linear regression analysis was used to predict the level of functioning (based on GAF scores) over the two-year follow-up. Variables entered into this equation were: GAF at two-year follow-up (as dependent variable), and gender, age at first onset, parental socioeconomic status, diagnosis, positive symptoms at baseline, and negative symptoms at baseline (as independent variables).
Negative symptoms at baseline were the only significant variable that predict the functional outcome at the two-year follow-up (p= 0.010).
Functional prognosis of early-onset psychosis depends on the severity of negative symptoms, independently of diagnosis.
It is commonly accepted that in most patients with schizophrenia external factors act on genetic predisposition to produce active psychotic symptoms. It is known that patients with schizophrenia have an abnormal peripheral autonomic response to psychological stress. We sought to characterize the brain activity patterns of such response in these patients.
We studied the pattern of brain activation in response to a mental arithmetic stress paradigm in 14 patients and 14 healthy subjects aged 18 to 50 years, using 3T-fMRI. A period of 6 minutes of resting state acquisition were followed by a block design with three 1-minute CONTROL task (one digit sum), 1 minute STRESS task (two digit substraction) and 1 minute rest after task. Data were analyzed with SPM and SPSS software.
While controls showed bilateral activation of hippocampi, parahippocampi, insulae, amygdalae, anterior cinguli and basal ganglia during mental stress, patients displayed less left hemisphere activation, specifically in insula, orbitofrontal cortex and frontal cortex, along with activation of pons. Moreover, patients did not show activation of hippocampi, parahippocampi and amygdalae.
After stress healthy subjects recovered its basal pattern. However, patients showed sustained activation of right posterior cingulum and temporal pole, along with bilateral orbitofrontal cortex, frontal cortex, precuneus, cuneus and angular gyrus for the observation period.
Present results suggest that abnormal activation of limbic structures underlies extensively documented peripheral autonomic abnormalities in patients with schizophrenia. Abnormal fronto-temporal connectivity may be the pathophysiological link for these results.
Previous studies have reported progressive brain changes and cognitive deficits in early-onset psychosis (EOP). Little is known on the relationship between longitudinal changes in brain structure and neurocognition.
Naturalistic 5-year prospective study comparing frontal gray matter (GM) volume and executive functions in adolescents with a first episode of EOP and a sample of healthy controls at baseline, 2-year and 5-year follow-up.
Thirty-six patients (age at baseline 15.8 ±.7, 66.6% male) and 34 controls (15.4±1.4, 55.9% male) comprised the study sample. Both patients and controls presented with frontal GM loss during the first five years of follow-up. During the first two years, patients presented with significantly greater GM loss than controls in the left (F=9.642, p=0.003) and right frontal lobe (F=7.585, p=0.008), with no significant differences between year 2 and 5. Patients with EOP performed significantly worse in executive tasks than controls in all visits. During the first two years of follow-up, controls, but not patients, presented with a significant improvement in executive functioning (F=7.523, p=0.009), with similar evolution of cognitive functioning between years 2 and 5 in both groups (F=0.908, p=0.346). Changes in frontal GM volume and executive functioning were not significantly correlated within the entire follow-up period.
Over the first two years of illness, patients with EOP show greater frontal GM loss and less improvement in executive functions than expected. This could be a critical period for the development of deficits in EOP, in which more intensive interventions would be warranted.
Bulimia is a psychopathological disorder characterized by the presence of episodes of binge eating, followed by compensatory mechanisms that aim to prevent weight gain. These episodes of uncontrolled ingestion of food are related with deficits in the inhibitory control of behavior (Fairburn & Harrison, 2003). The basal ganglia namely the Nucleus Accumbens (NA) and the Caudate nucleus (CN) are involved in the fronto-striatal circuits that allow the control of impulses.
The main goal of this study was to investigate the presence of structural alterations in the NAc and the CN in a sample of bulimic patients, when compared to normal controls.
Our sample was composed by 41 female participants, 21 diagnosed with bulimia and 20 healthy controls (CG) matched in socio-demographic features. The participants were submitted to the clinical assessment and to a structural magnetic resonance imaging (MRI) acquisition. The NA and the CN of the 41 MRIs were manually segmented using the software Slicer 3D.
No differences between patients with bulimia and healthy controls were found for the volume of the NA. However, the NC volume is significantly decreased in BN.
The reduction of volume in the CN of bulimic patients that was found in this study may be possibly associated with a lower functional activation of this brain structure, contributing to a lack of control of the excessive eating behavior of these patients.
Comorbidity between alcoholism and depression has long been acknowledged, and the possibility that similar brain mechanisms, involving both serotonergic (5-HT) and noradrenergic systems (NE), underlie both pathologies has been suggested. Thus, inhibitors of NE and 5HT uptake have been proposed for the treatment of alcoholism, as they have shown to reduce alcohol intake in various animal models. However, most of the studies mentioned were carried out acutely and there is a lack of knowledge of the possible long-term effects. Clinical studies report an overall low efficacy of antidepressant treatment on alcohol consumption, or even a worsened prognosis. In addition, several cases of alcohol dependence following antidepressant treatment have been reported in the literature.
We aimed at comparing the acute and chronic effects of the treatment with the antidepressant drug reboxetine on alcohol consumption.
We used a rat model of alcohol self-administration, and two different schedules of reboxetine administration (acute and chronic).
Our results confirm the acute suppressant effects of reboxetine on alcohol consumption but indicate that, when this drug is administered chronically in a period of abstinence from alcohol, it can significantly increase the rate of alcohol self-administration.
These results are important for the understanding of the clinical reports describing cases of increased alcohol consumption after antidepressant treatment, and suggest that much more research is needed to fully understand the long term effects of antidepressants, which remain the most widely prescribed class of drugs.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
Glutamatergic neurotransmission dysfunction has classically been related to the aetiology of psychotic disorders. A substantial polygenic component shared across these disorders has been reported and molecular genetics studies have associated glutamatergic-related genes, such as d-amino acid oxidase activator (DAOA) and regulator of G-protein signalling 4 (RGS4) with the risk for psychotic disorders. Our aims were to examine: (i) the relationship between DAOA and RGS4 and the risk for psychotic disorders using a family-based association approach, and (ii) whether variations in these genes are associated with differences in patients’ cognitive performance.
The sample comprised 753 subjects (222 patients with psychotic disorders and 531 first-degree relatives). Six SNPs in DAOA and 5 SNPs in RGS4 were genotyped. Executive cognitive performance was assessed with Trail Making Test B (TMT-B) and Wisconsin Card Sorting Test (WCST). Genetic association analyses were conducted with PLINK, using the transmission disequilibrium test (TDT) for the family-based study and linear regression for cognitive performance analyses.
The haplotype GAGACT at DAOA was under-transmitted to patients (P = 0.0008), indicating its association with these disorders. With regards to cognitive performance, the DAOA haplotype GAGGCT was associated with worse scores in TMT-B (P = 0.018) in SZ patients only. RGS4 analyses did not report significant results.
Our findings suggest that the DAOA gene may contribute to the risk for psychotic disorders and that this gene may play a role as a modulator of executive function, probably through the dysregulation of the glutamatergic signalling.
Parasomnias are a category of sleep disorders in which abnormal events occur during sleep, due to inappropriately timed activation of physiological systems.
we report the case of a 41-year-old female who has no psychiatric history. The patient went to emergency department because when she was starting to sleep, in the first state of sleep, she felts a sensation of paralysis in all her body, with incapacity for breathing, chest oppression and tactile hallucinations like something or someone was touching her entire body. Due to that, the patient awoke frightened, with high levels of anxiety, with heart palpitations, shortness of breath, trembling, choking feeling, sweating, nausea and fear of dying. When the patient arrived to the emergency department, she was suffering a panic attack, thinking that she could have some kind of neurological disease or she was suffering a heart attack. after treating the panic attack with 1 mg of lorazepam, all the symptoms subsided gradually.
in this case report, we present a patient with a new-onset parasomnia, with hypnagogic hallucinations and a panic attack at the awakening. It is known that stress factors are closely associated with parasomnias, as we can see in this case because the patient was moving and she was sleeping in a new place.
Parasomnias are very frequently present in general population and they can trigger intense anxiety status that can lead to panic attacks.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
β-glucans are naturally occurring polysaccharides which have isoform specific immunomodulatory and metabolic properties(1). Certain yeast (1→3)-β-D-glucan isoforms improve cholesterol(2), glucose(3) and lipid homeostasis(4). Feeding (1→3)-β-D-glucan alters the microbiome of high-fat diet (HFD) induced obese (DIO)/type 2 diabetic (T2D) mice(5). Here we investigated the potential impact of baker's yeast (1→3)-β-D-glucan in mice humanized with gut microbiomes from either obese healthy versus obese diabetic subjects on immune-metabolism within the context of high-fat feeding.
C57Bl/6J male mice received an antibiotic cocktail of Ampicillin, Metronidazole, Vancomycin, Imipenem and Ciprofloxacin HCl in their drinking water for 6 weeks to diminish the endogenous gut microbiota. Mice were inoculated with microbiota samples obtained from obese healthy (OBH) or diabetic (OBD) humans twice daily for 3 days by oral dosing. Mice were fed a low-fat diet (LFD) (10% kcal) for 4 weeks followed by HFD (45% kcal) with/without baker's yeast (1→3)-β-D-glucan (βG), for 9 weeks. Weight, feed intake, glucose tolerance (1.5g/kg), insulin tolerance (0.5U/kg), hepatic and skeletal lipid levels were examined. Tissue specific molecular markers of metabolism and inflammation, and gut microbiome analysis are being determined to compliment the phenotypic data.
OBH mice were more glucose tolerant and insulin sensitive than OBD mice, despite equal weight gain and adipose tissue mass. Fasting HOMA-IR, attributable to higher insulin concentrations, was higher in OBD compared to OBH mice. βG supplementation reduced HOMA-IR in OBD mice (P < 0.0611). Hepatic triacylglycerol (TAG) and cholesterol levels were also higher in OBD mice, which were prevented by βG supplementation. Hepatic proteomic, caecal microbiomic and metabolomic analysis is on-going in order to ascertain the impact of the OBD versus OBH dysbosis with/without βG supplementation with specific attention on immune-metabolism.
Social cognition has been associated with functional outcome in patients with first episode psychosis (FEP). Social cognition has also been associated with neurocognition and cognitive reserve. Although cognitive reserve, neurocognitive functioning, social cognition, and functional outcome are related, the direction of their associations is not clear. Therefore, the main aim of this study was to analyze the influence of social cognition as a mediator between cognitive reserve and cognitive domains on functioning in FEP both at baseline and at 2 years.
The sample of the study was composed of 282 FEP patients followed up for 2 years. To analyze whether social cognition mediates the influence of cognitive reserve and cognitive domains on functioning, a path analysis was performed. The statistical significance of any mediation effects was evaluated by bootstrap analysis.
At baseline, as neither cognitive reserve nor the cognitive domains studied were related to functioning, the conditions for mediation were not satisfied. Nevertheless, at 2 years of follow-up, social cognition acted as a mediator between cognitive reserve and functioning. Likewise, social cognition was a mediator between verbal memory and functional outcome. The results of the bootstrap analysis confirmed these significant mediations (95% bootstrapped CI (−10.215 to −0.337) and (−4.731 to −0.605) respectively).
Cognitive reserve and neurocognition are related to functioning, and social cognition mediates in this relationship.
Heat shock may disrupt oocyte function by increasing the generation of reactive oxygen species (ROS). We evaluated the capacity of the antioxidant melatonin to protect oocytes using two models of oxidative stress – heat shock and the pro-oxidant menadione. Bovine cumulus–oocyte complexes (COC) were exposed in the presence or absence of 1 µM melatonin to the following treatments during maturation: 38.5°C, 41°C and 38.5°C+5 µM menadione. In the first experiment, COC were matured for 3 h with 5 µM CellROX® and analyzed by epifluorescence microscopy to quantify production of ROS. The intensity of ROS was greater for oocytes exposed to heat shock and menadione than for control oocytes. Melatonin reduced ROS intensity for heat-shocked oocytes and oocytes exposed to menadione, but not for control oocytes. In the second experiment, COC were matured for 22 h. After maturation, oocytes were fertilized and the embryos cultured for 7.5 days. The proportion of oocytes that cleaved after fertilization was lower for oocytes exposed to heat shock and menadione than for control oocytes. Melatonin increased cleavage for heat-shocked oocytes and oocytes exposed to menadione, but not for control oocytes. Melatonin tended to increase the developmental competence of embryos from heat-shocked oocytes but not for embryos from oocytes exposed to menadione or from control oocytes. In conclusion, melatonin reduced production of ROS of maturing oocytes and protected oocytes from deleterious effects of both stresses on competence of the oocyte to cleave after coincubation with sperm. These results suggest that excessive production of ROS compromises oocyte function.
We propose a multi-layer approach to simulate hyperpycnal and hypopycnal plumes in flows with free surface. The model allows to compute the vertical profile of the horizontal and the vertical components of the velocity of the fluid flow. The model can describe as well the vertical profile of the sediment concentration and the velocity components of each one of the sediment species that form the turbidity current. To do so, it takes into account the settling velocity of the particles and their interaction with the fluid. This allows to better describe the phenomena than a single layer approach. It is in better agreement with the physics of the problem and gives promising results. The numerical simulation is carried out by rewriting the multilayer approach in a compact formulation, which corresponds to a system with nonconservative products, and using path-conservative numerical scheme. Numerical results are presented in order to show the potential of the model.