Clinical factors for delayed neuropsychiatric sequelae from acute carbon monoxide poisoning: a retrospective study.

Background: Delayed neuropsychiatric sequelae (DNS), which seriously affect the daily lives of patients, are the most common complications of carbon monoxide (CO) poisoning. No uniform screening tool is available for identifying high-risk groups. Therefore, in this study, we aimed to explore whether conventional laboratory indicators and imaging data from primary hospitals could predict the occurrence of DNS. Methods: This retrospective observational study was conducted in a single-center primary hospital from January 1, 2021 to May 31, 2023. Participants included patients aged >18 years with acute CO poisoning. Patients with complete recovery in the acute phase were followed up by telephone and outpatient visits, and the presence of DNS was determined according to the occurrence of new neurological symptoms within 6 weeks after discharge. We obtained demographic, laboratory, and imaging data from the medical records and performed a univariate analysis. A multivariate logistic regression model was used to identify independent clinical predictors of DNS. Results: A total of 73 patients were included in the study, of whom 25 (34.2%) developed DNS. Multivariate logistic regression analysis revealed that a longer duration of CO exposure (adjusted odds ratio (AOR): 1.262, 95% confidence interval (CI): 1.069-1.490) and the presence of acute brain lesions on diffusion-weighted imaging (DWI) (AOR: 5.117, 95% CI: 1.430-18.315) were independent risk factors for DNS. Receiver operating characteristic analyses of the duration of CO exposure were performed (area under the curve (AUC): 0.825; 95% CI: 0.731-0.918) with a cut-off value of 5.5 h, and DNS was predicted with a sensitivity of 96% and a specificity of 66.7%. Conclusion: High cranial DWI signal within 24 h and duration of poisoning longer than 5.5 h are independent predictors of DNS. The predictive effects of conventional laboratory indicators require further standardized and large-sample studies.

Demographics and clinical characteristics of carbon monoxide poisoning for patients attending in the emergency department at a tertiary hospital in Riyadh, Saudi Arabia.

BACKGROUND: Carbon Monoxide (CO) is one of the most common environmental causes of acute intoxication globally. It can lead to the development of Delayed Neuropsychiatric Sequelae (DNS) which may develop in 2-40 days after remission of acute CO poisoning. DNS is defined by recurrent-transient neurological, cognitive, or psychological manifestations. This study was intended to describe the demographics and characteristics of CO poisoning patients attending at the Emergency Department (ED) and assess the association between CO intoxication and the development of DNS in a tertiary hospital, Riyadh, Saudi Arabia. METHODS: A retrospective descriptive cross-sectional study was conducted in subjects who were diagnosed with CO poisoning and attended to the ED at King Abdulaziz Medical City (KAMC) and King Abdullah Specialist Children's Hospital (KASCH) in Riyadh during the period from January 2016 to December 2021. Patient demographics, vitals, diagnostic tests, and oxygen therapy at initial presentation were documented. Patient medical records were reviewed at 2-40 days following CO poisoning for development of DNS. Ethical approval was obtained from King Abdullah International Medical Research Center (KAIMRC). RESULTS: A total of 85 patients were diagnosed with CO poisoning and met the study inclusion criteria. Of those, 76% were adults with an average age of 32.36 (SD ± 15.20) and 51% were male adults. Five (6%) of the 85 patients developed DNS. Common symptoms included dizziness, nausea, and decreased visual acuity in 40% of the cases. The development of DNS manifestations was most likely (80%) to occur at 2 to 10 days after the initial incident. Inferential statistics showed that BMI (p-value = 0.021) and age group (p-value = 0.029) were significantly associated with COHb level, which was not the case for gender and the presence of clinical manifestation. Furthermore, Gender was significantly associated with the development of DNS (20% male vs. 80% female, p = 0.050). CONCLUSIONS: The findings of this study are consistent with previous published studies showing low proportions of patients who were exposed to CO poisoning at risk of developing DNS. Further larger-scale multicenter studies are needed to assess the factors associated with the development of DNS for patients with CO poisoning.

Delayed neuropsychiatric sequelae due to long-term effects of carbon monoxide poisoning in Ethiopia: A case report.

Background: One emergency that occurs frequently and has high morbidity is carbon monoxide poisoning. After a time of lucidity, some victims who recover from the incident of acute carbon monoxide exposure may later suffer delayed neuropsychiatric sequelae (DNS), which can include cognitive impairments, a wide range of neurological abnormalities, and affective disorders. Below, we report the first documented incident of DNS after carbon monoxide poisoning in Ethiopia. Case presentation: A 40-year-old male patient who developed a coma after he was exposed to burning charcoal in a closed room was admitted to Debre Tabor Comprehensive Specialized Hospital in the northwest region of Ethiopia. He stayed for 12 days during his first admission and was discharged with improvement. One month after discharge, he developed delayed neuropsychiatric sequelae, which manifested as bizarre behavior, being unable to walk unsupported, loss of concentration, and failure to control urine and feces. Brain MRI showed bilateral periventricular and frontoparietal deep white matter subcortical abnormal T1 and T2 prolongation with no restriction of diffusivity, possibly due to demyelinating disorders. He was managed with fluid therapy, benzhexol, risperidone, and rehabilitation therapy. He stayed for two weeks in our hospital and was discharged with improvement. Conclusion: Despite the paucity of delayed neuropsychiatric sequelae from carbon monoxide poisoning, physicians should be highly suspicious in the right situations. The precise mechanisms of delayed toxic effects, prevention measures, and treatment modalities have not yet been determined; therefore, more research and attention are required.

Effectiveness of Initial Troponin I and Brain Natriuretic Peptide Levels as Biomarkers for Predicting Delayed Neuropsychiatric Sequelae in Patients with CO Poisoning: A Retrospective Multicenter Observational Study.

BACKGROUND: Delayed neuropsychiatric sequelae (DNS) are a severe complication of carbon monoxide (CO) poisoning, and predicting DNS is difficult. This study aimed to investigate whether cardiac markers can be used as biomarkers to predict DNS occurrence following acute CO poisoning. METHODS: This was a retrospective observational study that included patients with acute CO poisoning who visited two emergency medical centers in Korea from January 2008 to December 2020. The primary outcome was whether the occurrence of DNS was associated with laboratory results. RESULTS: Of the 1327 patients with CO poisoning, 967 patients were included. Troponin I and BNP were significantly higher in the DNS group. As a result of multivariate logistic regression analysis, it was found that troponin I, mentality, creatine kinase, brain natriuretic peptide, and lactate levels independently influenced DNS occurrence in CO poisoning patients. The adjusted odds ratios for DNS occurrence were 2.12 (95% CI 1.31-3.47, p = 0.002) for troponin I and 2.80 (95% CI 1.81-3.47, p < 0.001) for BNP. CONCLUSION: Troponin I and BNP might be useful biomarkers for predicting the occurrence of DNS in patients with acute CO poisoning. This finding can help to identify high-risk patients who require close monitoring and early intervention to prevent DNS.

Alteraciones cognitivas, neurológicas, neuropsicológicas y neuropsiquiátricas en pacientes post-covid-19. Una revisión sistemática / Cognitive, neurological, neuropsychological and neuropsychiatric alterations. in post-covid-19 patients

Introducción. El virus SARS CoV-2 causante de la enfermedad COVID-19, reporta cientos de contagios diariamente, las alteraciones y secuelas de este nuevo patógeno han sido reportadas a nivel global, por la gravedad que implica ser adulto mayor y evolucionar de manera grave. Metodología. El presente trabajo tiene un enfoque cualitativo, con intenciones exploratorias y descriptivas de las alteraciones a nivel cognitivo, neuropsicológico, neuropsiquiátrico y neurológico. Resultados. En el análisis fueron incluidos 16 artículos que expresan alteraciones en áreas de funcionamiento que comprometen la calidad de vida en pacientes mayores de 18 años, la evidencia científica es fuerte sobre las alteraciones que provoca el nuevo virus SARS Cov-2, desde el deterioro de la cognición, habilidades visuoespaciales y cefaleas constantes entre otros síntomas, que son de atención desde una perspectiva multidisciplinar. Conclusiones. La transmisión del virus en la población adulta supone un riesgo a la salud, este estudio evidencia las alteraciones a nivel cognitivo, motor y neurológico siendo la edad un factor que predispone la aparición de secuelas. (AU)

Introduction. The SARS-CoV-2 virus that causes theCOVID-19 disease, reports hundreds of infections daily,the alterations and sequelae of this new pathogen have been reported globally, due to the seriousness of being anolder adult and evolving seriously. Methodology. The present work has a qualitative approach, with exploratory and descriptive intentions of the alterations at a cognitive, neuropsychological, neuropsychiatric and neurological level. Results. In the analysis, 16 articles were included that express alterations in areas of functioning that compromise the quality of life in patients over 18 years of age, the scientific evidence is strong on the alterations caused by the new SARS-CoV-2 virus, from the deterioration of cognition, visuospatial abilities and constant headachesamong other symptoms, which are of attention from amultidisciplinary perspective. Conclusions. The transmission of the virus in the adult population poses a risk to health, this study shows alterations at the cognitive, motor and neurological level, agebeing a factor that predisposes the appearance of sequelae. (AU)

Dexamethasone therapy prevents delayed neuropsychiatric sequelae after carbon monoxide poisoning: a prospective registry-based study.

BACKGROUND: Delayed neuropsychiatric sequelae are major complications of carbon monoxide poisoning; carbon monoxide triggers brain oxidation and inflammation. Corticosteroids such as dexamethasone modulate neurological damage after carbon monoxide poisoning through anti-inflammatory actions and immune response inhibition. However, it is not known whether corticosteroids prevent delayed neuropsychiatric sequelae. We thus studied whether dexamethasone reduced the incidence of delayed neuropsychiatric sequelae. METHODS: This registry-based study enrolled patients with carbon monoxide poisoning treated in a Korean tertiary care hospital from March 1st, 2020 to November 30th, 2021. Data of patients were prospectively collected during the study period, and retrospectively analyzed. One group received intravenous dexamethasone. We performed multivariable logistic regression analysis to identify factors associated with delayed neuropsychiatric sequelae. RESULTS: A total of 128 patients were enrolled, of which 99 patients received dexamethasone therapy and 29 patients did not. The incidences of delayed neuropsychiatric sequelae in the dexamethasone and non-dexamethasone groups were 16.2% and 37.9%, respectively. Multivariable logistic regression analysis revealed that dexamethasone use (odds ratio = 0.122, 95% confidence interval 0.031-0.489) and a higher Glasgow Coma Scale (odds ratio = 0.818, 95% confidence interval 0.682-0.981) was associated with a lower incidence of delayed neuropsychiatric sequelae. CONCLUSION: Early dexamethasone treatment was significantly associated with a decreased incidence of delayed neuropsychiatric sequelae. A higher Glasgow Coma Scale at presentation also was associated with a lower incidence of delayed neuropsychiatric sequelae.

Neuropsychiatric post-acute sequelae of COVID-19: prevalence, severity, and impact of vaccination.

The potential long-term neuropsychiatric effects of COVID-19 are of global concern. This study aimed to determine the prevalence and predictors of neuropsychiatric post-acute sequelae of COVID-19 among Egyptian COVID-19 survivors and to study the impact of full vaccination before COVID-19 infection on the occurrence and severity of these manifestations. Three months after getting COVID-19 infection, 1638 COVID-19 survivors were screened by phone for possible neuropsychiatric sequelae. Subjects suspected to suffer from these sequelae were invited to a face-to-face interview for objective evaluation. They were requested to rate the severity of their symptoms using visual analogue scales (VAS). The mean age of participants was 38.28 ± 13 years. Only 18.6% were fully vaccinated before COVID-19 infection. Neuropsychiatric post-acute sequelae of COVID-19 were documented in 598 (36.5%) subjects, fatigue was the most frequent one (24.6%), followed by insomnia (16.4%), depression (15.3%), and anxiety (14.4%). Moderate and severe COVID-19 infection and non-vaccination increased the odds of developing post-COVID-19 neuropsychiatric manifestations by 2 times (OR 1.95, 95% CI = 1.415-2.683), 3.86 times (OR 3.86, 95% CI = 2.358-6.329), and 1.67 times (OR 1.67, 95% CI = 1.253-2.216), respectively. Fully vaccinated subjects before COVID-19 infection (n = 304) had significantly lesser severity of post-COVID-19 fatigue, ageusia/hypogeusia, dizziness, tinnitus, and insomnia (P value = 0.001, 0.008, < 0.001, 0.025, and 0.005, respectively) than non-vaccinated subjects. This report declared neuropsychiatric sequelae in 36.5% of Egyptian COVID-19 survivors, fatigue being the most prevalent. The effectiveness of COVID-19 vaccines in reducing the severity of some post-COVID-19 neuropsychiatric manifestations may improve general vaccine acceptance.

The Clinical Observation of Inflammation Theory for Depression: The Initiative of the Formosa Long COVID Multicenter Study (FOCuS).

There is growing evidence that the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with increased risks of psychiatric sequelae. Depression, anxiety, cognitive impairments, sleep disturbance, and fatigue during and after the acute phase of COVID-19 are prevalent, long-lasting, and exerting negative consequences on well-being and imposing a huge burden on healthcare systems and society. This current review presented timely updates of clinical research findings, particularly focusing on the pathogenetic mechanisms underlying the neuropsychiatric sequelae, and identified potential key targets for developing effective treatment strategies for long COVID. In addition, we introduced the Formosa Long COVID Multicenter Study (FOCuS), which aims to apply the inflammation theory to the pathogenesis and the psychosocial and nutrition treatments of post-COVID depression and anxiety.

Chronic neuropsychiatric sequelae of SARS-CoV-2: Protocol and methods from the Alzheimer's Association Global Consortium.

Introduction: Coronavirus disease 2019 (COVID-19) has caused >3.5 million deaths worldwide and affected >160 million people. At least twice as many have been infected but remained asymptomatic or minimally symptomatic. COVID-19 includes central nervous system manifestations mediated by inflammation and cerebrovascular, anoxic, and/or viral neurotoxicity mechanisms. More than one third of patients with COVID-19 develop neurologic problems during the acute phase of the illness, including loss of sense of smell or taste, seizures, and stroke. Damage or functional changes to the brain may result in chronic sequelae. The risk of incident cognitive and neuropsychiatric complications appears independent from the severity of the original pulmonary illness. It behooves the scientific and medical community to attempt to understand the molecular and/or systemic factors linking COVID-19 to neurologic illness, both short and long term. Methods: This article describes what is known so far in terms of links among COVID-19, the brain, neurological symptoms, and Alzheimer's disease (AD) and related dementias. We focus on risk factors and possible molecular, inflammatory, and viral mechanisms underlying neurological injury. We also provide a comprehensive description of the Alzheimer's Association Consortium on Chronic Neuropsychiatric Sequelae of SARS-CoV-2 infection (CNS SC2) harmonized methodology to address these questions using a worldwide network of researchers and institutions. Results: Successful harmonization of designs and methods was achieved through a consensus process initially fragmented by specific interest groups (epidemiology, clinical assessments, cognitive evaluation, biomarkers, and neuroimaging). Conclusions from subcommittees were presented to the whole group and discussed extensively. Presently data collection is ongoing at 19 sites in 12 countries representing Asia, Africa, the Americas, and Europe. Discussion: The Alzheimer's Association Global Consortium harmonized methodology is proposed as a model to study long-term neurocognitive sequelae of SARS-CoV-2 infection. Key Points: The following review describes what is known so far in terms of molecular and epidemiological links among COVID-19, the brain, neurological symptoms, and AD and related dementias (ADRD)The primary objective of this large-scale collaboration is to clarify the pathogenesis of ADRD and to advance our understanding of the impact of a neurotropic virus on the long-term risk of cognitive decline and other CNS sequelae. No available evidence supports the notion that cognitive impairment after SARS-CoV-2 infection is a form of dementia (ADRD or otherwise). The longitudinal methodologies espoused by the consortium are intended to provide data to answer this question as clearly as possible controlling for possible confounders. Our specific hypothesis is that SARS-CoV-2 triggers ADRD-like pathology following the extended olfactory cortical network (EOCN) in older individuals with specific genetic susceptibility.The proposed harmonization strategies and flexible study designs offer the possibility to include large samples of under-represented racial and ethnic groups, creating a rich set of harmonized cohorts for future studies of the pathophysiology, determinants, long-term consequences, and trends in cognitive aging, ADRD, and vascular disease.We provide a framework for current and future studies to be carried out within the Consortium. and offers a "green paper" to the research community with a very broad, global base of support, on tools suitable for low- and middle-income countries aimed to compare and combine future longitudinal data on the topic.The Consortium proposes a combination of design and statistical methods as a means of approaching causal inference of the COVID-19 neuropsychiatric sequelae. We expect that deep phenotyping of neuropsychiatric sequelae may provide a series of candidate syndromes with phenomenological and biological characterization that can be further explored. By generating high-quality harmonized data across sites we aim to capture both descriptive and, where possible, causal associations.

Legacy of neuropsychiatric symptoms associated with past COVID-19 infection: A cause of concern.

Although primarily affecting the respiratory system, growing attention is being paid to the neuropsychiatric consequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infections. Acute and sub-acute neuropsychiatric manifestations of coronavirus disease 2019 (COVID-19) disease and their mechanisms are better studied and understood currently than they had been when the pandemic began; however, many months or years will be necessary to fully comprehend how significant the consequences of such complications will be. In this editorial, we discuss the possible long-term sequelae of the COVID-19 pandemic, deriving our considerations on experiences drawn from past coronaviruses' outbreaks, such as the SARS and the middle east respiratory syndrome, and from the knowledge of the mechanisms of neurotropism and invasiveness of SARS-CoV-2. Acknowledging the global spread of COVID-19 and the vast number of people affected, to date amounting to many millions, the matter of this pandemic's neuropsychiatric legacy appears concerning. Public health monitoring strategies and early interventions seem to be necessary to manage the possible emergence of a severe wave of neuropsychiatric distress among the survivors.

Association between Early Phase Serum Lactate Levels and Occurrence of Delayed Neuropsychiatric Sequelae in Adult Patients with Acute Carbon Monoxide Poisoning: A Systematic Review and Meta-Analysis.

The primary goal of treating carbon monoxide (CO) poisoning is preventing or minimizing the development of delayed neuropsychiatric sequelae (DNS). Therefore, screening patients with a high probability for the occurrence of DNS at the earliest is essential. However, prognostic tools for predicting DNS are insufficient, and the usefulness of the lactate level as a predictor is unclear. This systematic review and meta-analysis investigated the association between early phase serum lactate levels and the occurrence of DNS in adult patients with acute CO poisoning. Observational studies that included adult patients with CO poisoning and reported initial lactate concentrations were retrieved from the Embase, MEDLINE, Google Scholar and six domestic databases (KoreaMED, KMBASE, KISS, NDSL, KISTi and RISS) in January 2022. Lactate values were collected as continuous variables and analyzed using standardized mean differences (SMD) using a random-effect model. The risk of bias was evaluated using the Quality in Prognosis Studies (QUIPS) tool, and subgroup, sensitivity and meta regression analyses were performed. Eight studies involving a total of 1350 patients were included. The early phase serum lactate concentration was significantly higher in the DNS group than in the non-DNS group in adult patients with acute CO poisoning (8 studies; SMD, 0.31; 95% CI, 0.11−0.50; I2 = 44%; p = 0.002). The heterogeneity decreased to I2 = 8% in sensitivity analysis (omitting Han2021; 7 studies; SMD, 0.38; 95% CI, 0.23−0.53; I2 = 8%; p < 0.001). The risk of bias was assessed as high in five studies. The DNS group was associated with significantly higher lactate concentration than that in the non-DNS group.

Potential markers for predicting delayed encephalopathy in patients with acute carbon monoxide poisoning.

BACKGROUND: Acute carbon monoxide poisoning (ACOP) commonly results in delayed neuropsychiatric sequelae (DNS). Currently, there are no reliable predictors. The aim of this article is to establish a practical model for predicting the development of delayed encephalopathy clinically. METHODS: Retrospective analysis of clinical data were performed at a single institution for the past 6 years. 107 patients with ACOP were recruited, of who 67 developed DNS and 40 did not. Clinical characteristics of the patients were analyzed between the two groups. The risk factors associated with DNS development were screened to identify the potential markers for predicting DNS. A predictive model was then built, and the receiver operating characteristic (ROC) curve analysis was used to assess its predictive ability. RESULTS: There were significant differences in 13 clinical features between the two groups. Four potential markers were identified. They were age, source of CO, Glasgow Coma Scale score and the initiation of HBOT. The potential predictive model showed an area under the curve (AUC) of 0.93 in the training set and 0.97 in the testing set. CONCLUSIONS: Our model could calculate the probability of DNS after acute CO poisoning.

Survivors of COVID-19 exhibit altered amplitudes of low frequency fluctuation in the brain: a resting-state functional magnetic resonance imaging study at 1-year follow-up.

Although some short-term follow-up studies have found that individuals recovering from coronavirus disease 2019 (COVID-19) exhibit anxiety, depression, and altered brain microstructure, their long-term physical problems, neuropsychiatric sequelae, and changes in brain function remain unknown. This observational cohort study collected 1-year follow-up data from 22 patients who had been hospitalized with COVID-19 (8 males and 11 females, aged 54.2 ± 8.7 years). Fatigue and myalgia were persistent symptoms at the 1-year follow-up. The resting state functional magnetic resonance imaging revealed that compared with 29 healthy controls (7 males and 18 females, aged 50.5 ± 11.6 years), COVID-19 survivors had greatly increased amplitude of low-frequency fluctuation (ALFF) values in the left precentral gyrus, middle frontal gyrus, inferior frontal gyrus of operculum, inferior frontal gyrus of triangle, insula, hippocampus, parahippocampal gyrus, fusiform gyrus, postcentral gyrus, inferior parietal angular gyrus, supramarginal gyrus, angular gyrus, thalamus, middle temporal gyrus, inferior temporal gyrus, caudate, and putamen. ALFF values in the left caudate of the COVID-19 survivors were positively correlated with their Athens Insomnia Scale scores, and those in the left precentral gyrus were positively correlated with neutrophil count during hospitalization. The long-term follow-up results suggest that the ALFF in brain regions related to mood and sleep regulation were altered in COVID-19 survivors. This can help us understand the neurobiological mechanisms of COVID-19-related neuropsychiatric sequelae. This study was approved by the Ethics Committee of the Second Xiangya Hospital of Central South University (approval No. 2020S004) on March 19, 2020.

Neuropsychiatric sequelae of acute carbon monoxide poisoning: The predictive role of neuron specific enolase and glial fibrillary acidic protein.

BACKGROUND: Acute carbon monoxide (CO) poisoning is one of the most common poisons worldwide and neuropsychiatric sequelae (NS) are the most frequent form of its morbidity. OBJECTIVES: This study aimed to measure the percentage of patients liable to NS, to evaluate the cognitive profile of patients with NS and to assess the role of neuron specific enolase (NSE) and glial fibrillary acidic protein (GFAP) in predicting the development of NS after acute CO poisoning. METHODS: This prospective study included 50 patients with acute CO poisoning presented to the Poison Control Center, Ain Shams University Hospitals during the period from beginning of November 2015 till the end of January 2017. Patients' demographic characteristics, clinical manifestations and blood carboxyhemoglobin levels were recorded. Serum levels of NSE and GFAP were determined on admission. Every patient was invited to participate in a follow-up visit at a dedicated outpatient clinic one month after CO exposure. During the visit, a complete neurological examination, as well as a psychiatric evaluation using the Structured Clinical Interview for Diagnostic and Statistical Manual of Mental Disorders version 4 Axis-I were performed for detection of neurological and psychiatric disorders. Wechsler memory scale test was administrated for detection of cognitive deficits. The patients were divided into two groups based on the presence or absence of NS. RESULTS: Cognitive impairment was found in 38 % of patients in the NS group. The serum levels of NSE and GFAP were significantly high in the NS group in comparison to the non-NS group. Receiver operating characteristic curves (ROC) determined the cut-off level of NSE at 39 ng/mL achieved 100 % sensitivity with 88.64 % specificity to predict the development of NS after acute CO poisoning while GFAP had 95.24 % sensitivity and 69.23 % specificity at a cut-off value of 2.8 ng/mL. CONCLUSION: NSE and GFAP could be useful in the early identification of patients at risk of developing NS after CO poisoning helping in treatment plans and thus improving quality of care.

Dilemma of Treating Psychosis Secondary to Stroke.

Post-stroke psychosis is prevalent and disabling with increased mortality risk. Treatment for post-stroke psychosis is limited in this staggering medical concern. The most commonly used medications are antipsychotics, however, the risk for stroke increases further with the use of antipsychotics. Furthermore, interventional clinical studies have not been carried out to test the efficacy and safety of antipsychotics in the management of post-stroke psychosis. We present a case of post-stroke psychosis to highlight the risks faced by these patients in terms of daily function and safety concerns and the challenges encountered in treatment due to poor response to the conventional antipsychotics; and so calling attention to early diagnosis and improved treatment options. More clinical investigations are needed to address the pathology associated with the clinical presentation and exploring the pharmacotherapies to improve efficacy and safety of treatment for post-stroke psychosis.

Initial creatine kinase level as predictor for delayed neuropsychiatric sequelae associated with acute carbon monoxide poisoning.

INTRODUCTION: The primary goal of treating patients with carbon monoxide (CO) poisoning is preventing delayed neuropsychiatric sequelae (DNS). It is difficult to predict DNS because there is no precise diagnostic method in the early phase of CO poisoning. In this study, we aimed to investigate the optimal cut-off value for creatine kinase level to predict DNS. METHODS: This retrospective observational study included patients with CO poisoning visiting a single tertiary center from January to July 2018. They were divided into two groups according to the presence of DNS. We compared baseline characteristics with variables that could affect the presence of DNS. The optimal cut-off value of initial creatine kinase concentration for DNS was calculated. Additionally, multivariate analysis was performed to confirm whether creatine kinase could be an independent predictor of DNS. RESULTS: Of the 138 patients, 12 patients developed DNS. Univariate analysis showed significant differences in the Glasgow Coma Scale, duration of exposure, laboratory tests, abnormal finding on MRI in acute phase, the number of hyperbaric oxygen therapy sessions, and duration of hospitalization. Receiver operating characteristic analyses of creatine kinase were performed (AUC = 0.92; 95% CI, 0.86-0.96) with a cut-off value of 1603 U/L; DNS was predicted with a sensitivity of 91.7% and specificity of 88.1%. In multivariate analysis, the adjusted odds ratio of creatine kinase was 51.516. CONCLUSION: In patients with CO poisoning, initial creatine kinase concentrations of >1603 U/L can be used as an independent predictor of DNS.

Neuropsychiatric symptoms associated with the COVID-19 and its potential nervous system infection mechanism: the role of imaging in the study.

The epidemic of coronavirus disease 2019 (COVID-19) has broken the normal spread mode of respiratory viruses, namely, mainly spread in winter, resulting in over 230 million confirmed cases of COVID-19. Many studies have shown that severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) can affect the nervous system by varying degrees. In this review, we look at the acute neuropsychiatric impacts of COVID-19 patients, including acute ischemic stroke, encephalitis, acute necrotizing encephalopathy, dysosmia, and epilepsy, as well as the long-term neuropsychiatric sequelae of COVID-19 survivors: mental disorder and neurodegenerative diseases. In particular, this review discusses long-term changes in brain structure and function associated with COVID-19 infection. We believe that the traditional imaging sequences are important in the acute phase, while the nontraditional imaging sequences are more meaningful for the detection of long-term neuropsychiatric sequelae. These long-term follow-up changes in structure and function may also help us understand the causes of neuropsychiatric symptoms in COVID-19 survivors. Finally, we review previous studies and discuss some potential mechanisms of SARS-CoV-2 infection in the nervous system. Continuous focus on neuropsychiatric sequelae and a comprehensive understanding of the long-term impacts of the virus to the nervous system is significant for formulating effective sequelae prevention and management strategies, and may provide important clues for nervous system damage in future public health crises.

Delayed brain injury post carbon monoxide poisoning.

A 66-year-old male was found unresponsive and diagnosed with acute carbon monoxide poisoning, with pathognomonic findings on radiological imaging. During his first day's the patient underwent acute neurological deterioration; however, this was followed 2 weeks later with a subsequent improvement to near baseline. The improvement back to baseline was short-lived, and the patient quickly worsened and underwent neurological decompensation. These findings were consistent with delayed post hypoxic leukoencephalopathy, serious sequelae of carbon monoxide poisoning. This case report shows the importance of recognition of carbon monoxide toxicity and aims to improve accurate diagnosis of the sequelae that may follow using computed tomography and magnetic resonance imaging sequences, magnetic resonance spectroscopy in order to prevent or ameliorate further neurological decline.

Long-Term Neuropsychiatric Sequelae in a Survivor of Cyanide Toxicity Patient With Arterialization.

Cyanide is one of the most rapidly acting poisons and accounts for many suicidal and homicidal deaths. Some natural products such as silk and wool can release cyanide when burned. Most patients who survive cyanide poisoning experience neurological sequelae. This report describes the case of a healthy 45-year-old Yemeni woman who was present during the burning of furniture in a closed space in her home. Upon admission, she displayed signs of inhalational injury, a black discoloration around her mouth and nostrils, and a first-degree burn on the left side of her neck. She experienced neuropsychiatric sequelae of cyanide poisoning, with deficits evolving over three months. Even after three months of treatment and continuous follow-up, she still showed signs of mild cognitive memory impairment along with word-finding difficulties and focal dystonia of her right hand. Full neurological and cognitive assessments are crucial to determine the neuropsychiatric sequelae of acute cyanide toxicity. Magnetic resonance imaging (MRI) can show the extent and structure of lesions in cyanide-sensitive regions of the brain, but it is not always diagnostic. The arterialization of venous blood gases may serve as an early clue to the diagnosis of cyanide poisoning.

Are we facing a crashing wave of neuropsychiatric sequelae of COVID-19? Neuropsychiatric symptoms and potential immunologic mechanisms.

The coronavirus disease 19 (COVID-19) pandemic is a significant psychological stressor in addition to its tremendous impact on every facet of individuals' lives and organizations in virtually all social and economic sectors worldwide. Fear of illness and uncertainty about the future precipitate anxiety- and stress-related disorders, and several groups have rightfully called for the creation and dissemination of robust mental health screening and treatment programs for the general public and front-line healthcare workers. However, in addition to pandemic-associated psychological distress, the direct effects of the virus itself (several acute respiratory syndrome coronavirus; SARS-CoV-2), and the subsequent host immunologic response, on the human central nervous system (CNS) and related outcomes are unknown. We discuss currently available evidence of COVID-19 related neuropsychiatric sequelae while drawing parallels to past viral pandemic-related outcomes. Past pandemics have demonstrated that diverse types of neuropsychiatric symptoms, such as encephalopathy, mood changes, psychosis, neuromuscular dysfunction, or demyelinating processes, may accompany acute viral infection, or may follow infection by weeks, months, or longer in recovered patients. The potential mechanisms are also discussed, including viral and immunological underpinnings. Therefore, prospective neuropsychiatric monitoring of individuals exposed to SARS-CoV-2 at various points in the life course, as well as their neuroimmune status, are needed to fully understand the long-term impact of COVID-19, and to establish a framework for integrating psychoneuroimmunology into epidemiologic studies of pandemics.