Early-stage psychosis is characterized by increased affective reactivity to everyday stressors. Studies on individuals with psychosis and those at heightened risk of psychosis reveal changes in neural reactions to stress, affecting limbic regions (the hippocampus and amygdala), prelimbic areas (ventromedial prefrontal cortex and ventral anterior cingulate cortex), and salience areas (anterior insula). In our study, we determined if a similar neural reactivity pattern was present in people with early psychosis and analyzed its connection to daily-life stress reactivity in their brain activity. Utilizing functional MRI, 29 participants categorized as experiencing early psychosis, featuring 11 individuals at-risk for mental state and 18 individuals at the first-episode psychosis stage, successfully completed the Montreal Imaging Stress Task. read more An acceptance and commitment therapy-based ecological momentary intervention's efficacy in treating early psychosis was assessed in a large-scale, randomized, controlled trial, including this study. All participants, through experience sampling methodology (ESM), documented their momentary affect and stressful activities in their daily environments. Employing multilevel regression models, researchers investigated whether daily-life stress reactivity was influenced by activity in (pre)limbic and salience areas. Increased activation of the right AI was observed in response to task-induced stress, alongside decreased activation in the vmPFC, vACC, and hippocampus. Changes in vmPFC and vACC activity levels during tasks were associated with affective stress responses, while changes in HC and amygdala activity were correlated with increased overall stress ratings. The initial findings point to regionally differentiated effects of daily life stressors on mood and psychosis in early psychosis. The observed pattern reveals a connection between chronic stress and neural stress reactivity.
Measurements of acoustic phonetics have exhibited a relationship with the negative symptoms of schizophrenia, presenting a route for quantifying these symptoms. Measurements of F1 and F2, integral parts of acoustic properties, are contingent upon tongue height and the position of the tongue in the oral cavity (forward or back), ultimately defining a generalized vowel space. We analyze vowel space in both patient and control groups using two phonetic measures. The first is the average Euclidean distance from the participant's mean F1 and mean F2 coordinates, and the second is the density of vowels within one standard deviation of the mean F1 and F2 values.
The acoustic properties of the structured and spontaneous speech of 70 patients and 78 control subjects, a total of 148 participants, were meticulously recorded and analyzed. We studied the association of phonetic measurements of vowel space with aprosody ratings using the Scale for the Assessment of Negative Symptoms (SANS) and the Clinical Assessment Interview for Negative Symptoms (CAINS).
Patient/control status was demonstrably correlated with vowel space measurements, imputable to a group of 13 patients whose phonetic values, as evaluated by both phonetic measures, point to a contraction in vowel space. The phonetic measures demonstrated no association with the related items and the mean ratings of the SANS and CAINS questionnaires. Reduced vowel space may be a characteristic specific to a portion of patients with schizophrenia, likely those on a higher dosage of antipsychotic medications.
The accuracy of clinical research scales for assessing aprosody or monotone speech in recognizing constricted vowel spaces might be surpassed by acoustic phonetic measures. A full interpretation of this novel finding, including its potential medication effects, will rely on subsequent replications.
When evaluating constricted vowel space, acoustic phonetic measures may yield more sensitive results than clinical research rating scales for aprosody or monotone speech. To ascertain the validity of this groundbreaking discovery, including its prospective impact on medication, independent replications are needed.
Schizophrenia patients' brains may exhibit an imbalance of noradrenaline, contributing to both the symptoms and impairments in fundamental information processing. The current study examined whether augmentation with the noradrenergic 2-agonist, clonidine, might bring about a reduction in these symptoms.
Thirty-two patients with chronic schizophrenia, enrolled in a randomized, double-blind, placebo-controlled clinical trial, were randomly allocated to receive either a six-week augmentation treatment with 50g of clonidine or a placebo in addition to their existing medication. read more At the baseline, three-week, and six-week marks, the effects on symptom severity, as well as sensory and sensorimotor gating, were ascertained. A comparison of results was made against 21 age- and sex-matched healthy controls (HC) who were untreated.
When compared to baseline, clonidine-treated patients, and only clonidine-treated patients, displayed significantly diminished PANSS negative, general, and total scores at the follow-up point. Typically, even patients receiving a placebo exhibited slight (statistically insignificant) improvements in these measurements, suggesting a placebo effect. The sensorimotor gating of patients at baseline showed a significantly lower value when compared to controls. For patients treated with clonidine, the parameter showed an increase during the treatment period, in direct opposition to the decrease seen in the healthy control (HC) and placebo groups. The results of both treatments and groups showed no influence on sensory gating. read more The effects of clonidine treatment were remarkably well-tolerated by those receiving it.
Only those patients undergoing clonidine treatment demonstrated a substantial decrease in two of the three PANSS subscales, maintaining their sensorimotor gating levels. The current research, highlighting the limited data on successful treatments for negative symptoms, advocates for the exploration of antipsychotic augmentation with clonidine as a promising, low-cost, and safe treatment approach in schizophrenia.
Patients administered clonidine displayed a statistically significant decrease in two PANSS subscales, whilst concurrently retaining their sensorimotor gating. Our investigation into effective treatments for negative symptoms, despite few reports, suggests that adding clonidine to existing antipsychotic regimens as a low-cost and safe strategy holds promise for managing schizophrenia.
Cognitive impairment is a potential consequence of tardive dyskinesia (TD), a common side effect of extended antipsychotic treatment. Discrepancies in cognitive impairment stemming from sex have been observed in schizophrenia research; however, the presence or absence of similar sex-linked variances in cognitive function among schizophrenia patients with TD has not been investigated.
The research involved 496 schizophrenia inpatients and 362 healthy controls. Our approach to assess patients' psychopathological symptoms involved the Positive and Negative Syndrome Scale (PANSS), while the severity of TD was assessed using the Abnormal Involuntary Movement Scale (AIMS). In a study of 313 inpatients and 310 healthy controls, cognitive function was evaluated by administering the Repeatable Battery for Assessment of Neuropsychological Status (RBANS).
Schizophrenia patients demonstrated significantly diminished cognitive function across all domains, as evidenced by significantly worse performance compared to healthy control participants (all p<0.001). Patients with TD achieved higher PANSS total, PANSS negative symptom subscale, and AIMS scores than patients without TD (all p<0.0001); conversely, RBANS total, visuospatial/constructional, and attention subscale scores were significantly lower in the TD group (all p<0.005). Furthermore, the visuospatial/constructional and attention indices were significantly lower in male patients with TD compared to those without TD (both p<0.05), but this pattern was not seen in female patients. Visuospatial/constructional and attention indices demonstrated a negative correlation with the total AIMS scores; this correlation was specific to male patients (both p<0.05).
Potential sex-related differences in cognitive impairment exist in schizophrenia patients with comorbid tardive dyskinesia, implying a possible protective influence of female gender against cognitive decline resulting from tardive dyskinesia.
Schizophrenia patients with comorbid tardive dyskinesia demonstrate potential sex-specific impacts on cognitive function, potentially indicating a protective effect of female gender in mitigating cognitive impairment linked to this condition.
Delusions, in both clinical and non-clinical contexts, are hypothesized to be influenced by reasoning biases as a risk factor. However, the causal relationship, if any, between these biases and delusions over time, in the general population, is not definitively established. Consequently, our study investigated the longitudinal connection between reasoning errors and delusional beliefs among the general public.
We performed an online study, a cohort study, with 1184 adults from the general German and Swiss public. Participants, at baseline, completed assessments of reasoning biases (jumping-to-conclusion bias [JTC], liberal acceptance bias [LA], bias against disconfirmatory evidence [BADE], and possibility of being mistaken [PM]) and delusional ideation. Delusional ideation was also assessed 7 to 8 months later.
Participants with a more significant JTC bias were more likely to exhibit a greater increase in delusional ideation over the succeeding months. The association's relationship could be best characterized by a positive quadratic relationship. The factors BADE, LA, and PM exhibited no association with the subsequent development of alterations in delusional ideation.
The research suggests a potential link between jumping to conclusions and delusional ideation in the wider population, though this relationship might manifest as a quadratic trend. Though no other linkages proved meaningful, subsequent studies incorporating shorter timeframes might offer more insight into how cognitive biases might influence delusional thoughts in non-clinical individuals.