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Carbon monoxide (CO) has been the leading cause of poisoning mortality in many countries and hyperbaric oxygen (HBO) is a widely accepted treatment for CO poisoning. However, some patients with CO poisoning will still develop neurocognitive sequelae regardless of HBO therapy, which can persist since CO poisoning or be present days to weeks after a recovery from CO poisoning. HBO has been used in the prevention and treatment of neurocognitive sequelae after CO poisoning, and some mechanisms are also proposed for the potential neuroprotective effects of HBO on the neurocognitive impairment after CO poisoning, but there is still controversy on the effectiveness of HBO on neurocognitive sequelae after CO poisoning. In this paper, we briefly introduce the neurocognitive sequelae after CO poisoning, summarize the potential predictive factors of neurocognitive sequelae, and discuss the use of HBO in the treatment and prevention of neurocognitive sequelae after CO poisoning.

Cerebral malaria is considered a leading cause of neuro-disability in sub-Saharan Africa among children and about 25% of survivors have long-term neurological and cognitive deficits or epilepsy. Their development was reported to be associated with protracted seizures, deep and prolonged coma. The study was aimed to determine the discharge pattern and to identify potential and informative predictors of neurological sequelae at discharge, complicating childhood cerebral malaria in central Sudan. A cross-sectional prospective study was carried out during malaria transmission seasons from 2000 to 2004 in Wad Medani, Sinnar and Singa hospitals, central Sudan. Children suspected of having cerebral malaria were examined and diagnosed by a Pediatrician for clinical, laboratory findings and any neurological complications. Univariate and multiple regression model analysis were performed to evaluate the association of clinical and laboratory findings with occurrence of neurological complications using the SPSS. Out of 940 examined children, only 409 were diagnosed with cerebral malaria with a mean age of 6.1 ± 3.3 yr. The mortality rate associated with the study was 14.2% (58) and 18.2% (64) of survivors (351) had neurological sequelae. Abnormal posture, either decerebration or decortication, focal convulsion and coma duration of >48 h were significant predictors for surviving from cerebral malaria with a neurological sequelae in children from central Sudan by Univariate analysis. Multiple logistic regression model fitting these variables, revealed 39.6% sensitivity for prediction of childhood cerebral malaria survivors with neurological sequelae (R² = 0.396; p=0.001). Neurological sequelae are common due to childhood cerebral malaria in central Sudan. Their prediction at admission, clinical presentation and laboratory findings may guide clinical intervention and proper management that may decrease morbidity and improve CM consequences.

Gray matter (GM) atrophy and white matter (WM) lesions may contribute to cognitive decline in patients with delayed neurological sequelae (DNS) after carbon monoxide (CO) poisoning. However, there is currently a lack of evidence supporting this relationship. This study aimed to investigate the volume of GM, cortical thickness, and burden of WM lesions in 33 DNS patients with dementia, 24 DNS patients with mild cognitive impairment, and 51 healthy controls. Various methods, including voxel‐based, deformation‐based, surface‐based, and atlas‐based analyses, were used to examine GM structures. Furthermore, we explored the connection between GM volume changes, WM lesions burden, and cognitive decline. Compared to the healthy controls, both patient groups exhibited widespread GM atrophy in the cerebral cortices (for volume and cortical thickness), subcortical nuclei (for volume), and cerebellum (for volume) ( p  < .05 corrected for false discovery rate [FDR]). The total volume of GM atrophy in 31 subregions, which included the default mode network (DMN), visual network (VN), and cerebellar network (CN) ( p  < .05, FDR‐corrected), independently contributed to the severity of cognitive impairment ( p  < .05). Additionally, WM lesions impacted cognitive decline through both direct and indirect effects, with the latter mediated by volume reduction in 16 subregions of cognitive networks ( p  < .05). These preliminary findings suggested that both GM atrophy and WM lesions were involved in cognitive decline in DNS patients following CO poisoning. Moreover, the reduction in the volume of DMN, VN, and posterior CN nodes mediated the WM lesions‐induced cognitive decline.

Delayed neurological sequelae (DNS) is a devastating consequence following acute carbon monoxide (CO) poisoning. This study aims at exploring the independent predictors of DNS in patients with CO exposure. Data of patients with diagnosis of CO poisoning was retrospectively collected and reviewed in 5 regional medical facilities. Patients were classified into the DNS group and non-DNS group according to clinical findings during a follow-up period of 6 months. Demographic characteristics, co-morbidities, clinical manifestations, and treatment strategies were compared to identify possible correlative factors. Multivariate analysis was performed to determine the independent predictors of DNS. We screened 1129 patients and enrolled 326 cases (158 males, average age 44.56 ± 16.08 years) in the analysis. Thirty-seven (11.35%) developed DNS at a median interval of 33 days. Uni-variable analysis identified older age, higher body mass index, hypertension, loss of consciousness, longer CO exposure, lower Glasgow Coma Scale (GCS) on-site/at emergency room, and elevation of lactate as relevant factors for DNS; while multivariable logistic regression revealed that older age (OR = 1.11; p < 0.001), longer duration of CO exposure (OR = 1.54; p = 0.023), GCS on-site (OR = 2.06; p < 0.001), and GCS at emergency room (OR = 1.33; p = 0.048) were independent predictors for DNS. Our multicenter study demonstrated older age, longer duration of CO exposure, and GCS score were independent predictors of DNS in COP patients. GCS scored on-site might be a more sensitive and specific parameter compared with GCS evaluated at the emergency room. Further prospective studies in a larger patient cohort are warranted to draw a comprehensive conclusion.

Bacterial meningitis is a devastating infection, with a case fatality rate of up to 30% and 50% of survivors developing neurological complications. These include short-term complications such as focal neurological deficit and subdural effusion, and long-term complications such as hearing loss, seizures, cognitive impairment and hydrocephalus. Complications develop due to bacterial toxin release and the host immune response, which lead to neuronal damage. Factors associated with increased risk of developing neurological complications include young age, delayed presentation and Streptococcus pneumoniae as an etiologic agent. Vaccination is the primary method of preventing bacterial meningitis and therefore its complications. There are three vaccine preventable causes: Haemophilus influenzae type b (Hib), S. pneumoniae, and Neisseria meningitidis. Starting antibiotics without delay is also critical to reduce the risk of neurological complications. Additionally, early adjuvant corticosteroid use in Hib meningitis reduces the risk of hearing loss and severe neurological complications.

BACKGROUND:Carbon monoxide poisoning (COP) accounts for a large number of emergency department visits worldwide and is fatal in many cases. In surviving patients, neurological sequelae (NS) attributable to cerebral hypoxia are the most devastating outcome, but reliable predictors are limited. Therefore, we conducted a study to identify predictors of NS in patients with COP and evaluate their effects. METHODS:In this retrospective case–control study, we identified patients with COP in a medical center in Southern Taiwan between January 2005 and December 2014. Cases were patients with NS, and controls were patients without NS. We obtained information on potential predictors of NS from medical records and evaluated their association with NS, including demographic characteristics, exposure source, suicide attempts, duration of exposure (by tertile), histories, symptoms, signs, laboratory data, treatment, and the length of hospital stay. RESULTS:We included 371 patients with COP. Of them, 93 developed NS, and their mean ages (41.4 ± 14.7 years vs. 39.7 ± 14.2 years) and proportions of males (59.1% vs. 58.6%) were similar to those in the 298 controls. Multivariate logistic regression showed that a history of hypertension (adjusted odds ratio = 2.1; 95% confidence interval = 1.0, 4.5) and a longer duration of carbon monoxide exposure (adjusted odds ratio = 1.7; 95% confidence interval = 1.1, 2.8; the longest tertile [>5 hours] vs. the other two tertiles [≤5 hours]) were independent predictors for NS, but not the level of carboxyhemoglobin. CONCLUSIONS:This study identified two independent predictors for NS that may be useful for public healthcare workers and physicians in predicting outcomes and deciding on treatment strategies for COP patients.

This study retrospectively analyzed children admitted to the Fourth Affiliated Hospital of Guangxi Medical University for CO (carbon monoxide) poisoning from January 2018 to December 2022 and followed up on their neurological sequelae for a long time. The study was approved by the Ethics Committees of the Fourth Affiliated Hospital of Guangxi Medical University (the identification code was KY2023131) and informed consent was obtained from all participants and/or their legal guardians. The study complied with the Declaration of Helsinki. Through Global Deterioration Scale [GDS], we further compared the differences between children with and without cognitive impairment, and identified some risk factors for long-term cognitive impairment in children after CO poisoning. The GDS score of the patient was based on the follow-up score, and we only conducted one follow-up and recorded the GDS score throughout the entire study period. The follow-up time interval is defined as the time from the first discharge of the patient to our follow-up. A total of 113 children were encompassed in the study, with an average follow-up of 3.6 years (3.6 ± 1.5 years). Among them, 13 children (11.5%, 13/113) had cognitive abnormalities. The utilization of gas water heaters in enclosed bathrooms (101 cases, 89.4%) constituted the most frequent cause of CO poisoning among children in this study, followed by heating with fire (11 cases, 9.7%). Furthermore, one child was left by his father in a running car, thereby resulting in poisoning. The clinical manifestations of CO poisoning in children were mainly consciousness disorders (67 cases, 59.3%), dizziness or headache (37 cases, 32.7%), and other manifestations including irritability, crying, vomiting, limb weakness, and limb twitching, a total of 9 cases. The duration of consciousness disorders in children with cognitive abnormalities was mostly more than one day, with a median of 5 days, and the hospitalization time was longer. Children with cognitive abnormalities had higher C-reactive protein (CRP) levels, higher D-dimer levels, and higher liver enzyme levels. The most common imaging change after CO poisoning in children was cerebral edema, with two cases of subarachnoid hemorrhage observed and one case of demyelinating changes observed. For children with coma time less than one hour, there were few abnormal changes in cranial imaging. Children with cognitive abnormalities were more likely to develop epilepsy (38.5%, 5/13) and other system damage (53.8%, 7/13) during hospitalization, including pulmonary infection (3 cases), stressful gastrointestinal bleeding (2 cases), electrolyte imbalance (2 cases), dysfunction of liver, kidney or myocardial (3 cases), and some children had multiple system damage at the same time. There were statistical differences in the admission CO hemoglobin level, fibrinogen, D-dimer, high-sensitivity CRP, neuron enolase, alanine aminotransferase or aspartate aminotransferase (ALT or AST), lactate dehydrogenase, length of hospital stay, discharge and admission Glasgow Coma Scale (GCS), seizure frequency, duration of consciousness disorders more than one day, cranial imaging changes, use of ventilators, presence of other system damage, the number of hyperbaric oxygen (HBO) treatments, and whether the patients were transferred to another hospital between the two groups of children. Multivariate logistic regression analysis showed that head imaging changes and consciousness disorders lasting for more than a day were statistical differences. For children with unconsciousness lasting for more than one hour, it is advisable to contemplate conducting a head imaging examination as soon as possible within 3 days after CO exposure to guide the treatment during the acute phase.Characteristic alterations in cranial imaging and a longer duration of consciousness disorders (exceeding one day) might be correlated with subsequent neurological sequelae. For children with CO poisoning presenting these characteristics, active treatment can be implemented, encompassing but not restricted to HBO treatments, to minimize subsequent damage to the greater extent possible. So, for children who were unconscious for more than one day or presented characteristic changes in cranial imaging, long-term follow-up should be carried out to determine whether delayed encephalopathy or subsequent cognitive impairment occurs.

The main objective of the treatment of acute carbon monoxide (CO) poisoning is to prevent delayed neurological sequelae (DNS). However, today there is still no objective screening tool to identify patients at high risk of developing DNS. The aim of this study was to identify clinical factors that could predict DNS after acute charcoal-burning CO poisoning. This prospective observational study was conducted from September 1, 2019 to August 31, 2020 in a single academic medical center. Patients older than 18 years of age suffering from charcoal-burning CO poisoning were included in the study. After acute recovery, patients were followed up for six weeks to investigate for DNS development. The clinical predictors of DNS were determined using a multivariate logistic regression model. Of the 217 patients—113 males (52.1%), median age 37.0 (27.5–51.5) years—included, 49 (22.6%) developed DNS. The multivariate logistic regression analysis revealed the independent predictors of DNS as a lower initial Glasgow Coma Scale (GCS) score (adjusted odds ratio (AOR): 0.73, 95% confidence interval (CI): 0.62–0.87), a longer duration of CO exposure (AOR: 2.18, 95% CI: 1.65–2.88), and the presence of acute brain lesions with high signal intensity on diffusion-weighted imaging (AOR: 5.22, 95% CI: 1.50–18.08). The created multivariate regression model predicted DNS development with high accuracy (area under the curve: 0.93, 95% CI: 0.89–0.97). A low initial GCS score, longer exposure to CO and abnormal findings on diffusion-weighted magnetic resonance imaging can assist in the early identification of patients at high risk of DNS development.

The purpose of this study is to evaluate childhood bacterial meningitis (BM): incidence, clinical presentation, causative pathogens, diagnostics, and outcome (neurological sequelae, hearing loss, and death). A retrospective review of all children aged ≤ 16 years and 1 month diagnosed with BM at a tertiary children’s centre in the period 2010–2020. The Glasgow Outcome Scale (GOS) was used to assess outcome, with a GOS score of 1–4 considered to be an unfavourable outcome. Logistic regression univariate analysis was used to determine predefined risk factors for death, unfavourable outcome, and long-term neurological sequelae. Seventy-four patients (44 males) with a median age of 8.0 months (range 1 day to 16 years and 1 month) and 77 BM episodes were included in the study. The average incidence rate of BM was 2.2/100,000/year, the majority (91%) being community-acquired BM. Streptococcus pneumonia and Neisseria meningitidis were the most common pathogens 12/77 (16%) each. Neurological sequelae at discharge were present in 24 (34%) patients, unfavourable outcome in 19 (25%), and hearing loss (deafness) in two (3%) survivors of BM. Seven (9%) patients died. Long-term neurological sequelae were observed in 19/60 (32%), aphasia/dysphasia being the most common in 10 (17%) BM children. No independent risk factors were identified for long-term neurological sequelae in univariate analysis. Conclusion: The risk for a fatal course of BM is still remarkable. Neurological sequelae persisted in a substantial proportion of BM survivors in long-term follow-up, aphasia/dysphasia being the most common. Hearing loss (deafness) occurred in 3%. However, no specific risk factors predicting the long-term sequelae were found. What is Known: • Streptococcus pneumonia and Neisseria meningitidis were the most common pathogens causing bacterial meningitis. • Risk for fatal course of bacterial meningitis (BM) remains remarkable despite advances in modern medicine. What is New: • In long-term follow-up, 1/3 of BM children suffered from neurological sequelae in the 2010s, aphasia and dysphasia being the most common sequelae. • Hearing loss was diagnosed in only two (3%) children, whom of both were deaf.

Survivors of Powassan encephalitis often have persistent neurological disease. A new mouse model replicates some elements of the human disease and demonstrates the presence of viral RNA in the brain as well as myelitis more than 2 mo after the acute infection. The related tick-borne encephalitis and West Nile Neuroinvasive Disease (WNND) also have common neurological sequelae, and models for these better-studied diseases provide evidence for prolonged virus, RNA, and inflammation in some cases, in addition to damage from the acute encephalitic disease. A better understanding of the biological basis for persistent signs and symptoms after Powassan encephalitis, currently a rare disease, could benefit from further studies of the more prevalent flaviviral encephalitides.