Post-stroke psychosis (PSP) is a rare but serious neuropsychiatric condition characterized by delusions and/or hallucinations following a stroke. Despite its impact on prognosis and quality of life, PSP remains underdiagnosed and undertreated, with limited data on its prevalence and risk factors. The purpose of this study is to assess the prevalence and determinants of post-stroke psychosis (PSP), as well as to compare PSP and non-PSP patients in terms of improvement and daily living outcomes. This nested case–control study included 2,624 acute stroke patients from a university hospital between May 2017 and April 2022. Patients who developed PSP within 6 months post-stroke were identified as cases (n = 108), and 119 patients without PSP were randomly selected as controls. Comprehensive assessments included clinical, laboratory, and imaging evaluations at baseline. After 6 months, follow-up evaluations were conducted, including neurological examinations, psychiatric assessments, and stroke severity assessments using the Barthel index (BI). The psychiatric assessments included the Hamilton Depression Rating Scale for depression and the Mini-Mental State Examination for cognitive status.
The prevalence of PSP was 5.4%. risk factors significantly associated with PSP included older age, male patients, lower education level (≤ 5 years), hemiplegia, sphincter affection, cortical lesion, brain atrophy, small vessel disease, ischemic stroke, post-stroke dementia, and seizures. Non-specified psychosis and delusional disorder were the most common psychosis subtypes. There was a significantly higher percentage of excellent patients in the non-PSP group compared to those who had PSP regarding the observed improvement in the patient's condition. Also, there is a higher percentage of deteriorated patients in the PSP group (46.6%) compared to another group (18.9%) regarding BI.
PSP is a prevalent post-stroke complication associated with distinct risk factors and poor functional outcomes. Early screening and identification of high-risk patients, along with multidisciplinary management strategies, are crucial for optimizing recovery and quality of life in stroke survivors.
This study aimed to evaluate the efficacy of rTMS in treating sleep disorders in PD. It included 24 patients with PD who had sleep disorders. Group allocations (active or sham with a ratio of 2:1) were placed in serially numbered closed envelopes. Each patient was evaluated with the following: MDS-UPDRS, Parkinson’s Disease Sleep Scale (PDSS), Beck Depression Inventory (BDI), and polysomnography (PSG) before and 10 days after the treatment sessions. Each session consisted of 10 trains, 20 Hz, 10 sec for each, over the parietal cortex (bilaterally). Scores of UPDRS, BDI, and PDSS improved significantly in the active group but not in the sham group. The PSG data showed that sleep onset and rapid eye movement (REM) latencies (min), REM duration, and time spent awake (both as %TST) were improved after rTMS in the active group compared with the sham group. The number of awakenings, the wake-after-sleep onset index, the arousal index, and periodic leg movements (PLMs) were all significantly reduced in the active group but not in the sham group. Ten sessions of 20 Hz rTMS over parietal cortexes improved sleep quality and PLMs in patients with PD. The improvement in PSG and PDSS were correlated with improvements in UPDRS and BDI scores.
Schizophrenia is a severe mental illness affecting approximately 1% of the population worldwide. While its exact causes remain unknown, emerging evidence suggests that infections and inflammation may contribute to disease development in a subset of individuals. This review comprehensively summarizes the evidence linking infections, immune system dysfunction, and schizophrenia risk.
Several population-based studies have linked serious prenatal or childhood infections requiring hospitalization to increased risk of later schizophrenia diagnosis, especially in individuals with genetic predisposition. Both central nervous system infections and systemic infections appear to confer risk. Specific pathogens including Toxoplasma gondii, herpesviruses, Chlamydophila, and more have been implicated. Autoimmune diseases are also associated with increased schizophrenia susceptibility, possibly due to blood-brain barrier disruption allowing brain-reactive antibodies access. The recent Coronavirus disease 2019 (COVID-19) pandemic raises questions about SARS-CoV-2 as a risk factor for new-onset psychosis. The mechanisms underlying the infection-schizophrenia link likely involve inflammation, cytokines, microglial activation, and tryptophan/kynurenine pathway modulation. Treatments targeting inflammation showed some efficacy in schizophrenia, further supporting an inflammation hypothesis. While the epidemiological and mechanistic evidence is substantial, further research is needed to conclusively determine the exact mechanisms linking immune dysfunction to schizophrenia requires further study.
The evidence suggests immune system abnormalities likely play a role, perhaps by interacting with genetic and environmental factors, in instigating schizophrenia pathophysiology in a subset of patients. More research is needed to understand these connections more clearly which may aid future prevention and personalized treatment approaches tailored to specific illness subtypes.