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.

Effects of smoking on delayed neuropsychiatric sequelae in acute carbon monoxide poisoning: A prospective observational study.

ABSTRACT: Smoking is a well-known risk factor for cardio-cerebrovascular disease. However, several studies have reported the "smoker's paradox" whereby smokers have a better prognosis for cardio-cerebrovascular diseases. Similar to cardio-cerebrovascular diseases, hypoxia is one of the major mechanisms of injury in carbon monoxide (CO) poisoning. This study investigated the association between smoking and delayed neuropsychiatric sequelae (DNS) in acute CO poisoning.This study involved patients with CO poisoning treated at a university hospital in Bucheon, Korea between September 2017 and March 2020. The exclusion criteria were age <18 years, discharge against medical advice, loss to follow-up, persistent neurological symptoms at discharge, transfer from another hospital 24 hours after exposure, and transfer from another hospital after hyperbaric oxygen therapy. Logistic regression analysis was performed to find factors associated with DNS.Two hundred sixty three patients visited the hospital due to CO poisoning and of these, 54 were excluded. DNS was evaluated up to 3 months after discharge, and until this time, DNS occurred in 35 (16.8%) patients. And the incidence rate of DNS was lower in smokers than non-smokers (15, 12% vs 20, 23.8%, P = .040). Multivariable logistic regression analysis revealed that CO exposure time (odds ratio [OR] 1.003; confidence interval [CI] 1.001-1.005; P = .003), the Glasgow coma scale (GCS) (OR 0.862; CI 0.778-0.956; P = .005), and pack-years (OR 0.947; CI 0.903-0.993; P = .023) were statistically significant for DNS development.These results indicate that more pack-years smoked were associated with reduced risk of the development of DNS in acute CO poisoning, and that CO exposure time and GCS is a predictive factor for DNS occurrence.

Surveillance of suicide deaths involving gases in Australia using the National Coronial Information System, 2006 to 2017.

BACKGROUND: There have been concerns about the increased use of helium and nitrogen gas as a suicide mechanism in Australia. METHODS: National Coronial Information System data were used to investigate gas-specific suicides in Australia over the period 2006-2017. Characteristics were compared between helium or nitrogen, carbon monoxide and seven other gases. RESULTS: Gas inhalation accounted for 10% (3,103/31,002) of all suicide deaths in Australia between 2006 and 2017. The mean age of individuals who died by suicide was 47.6 years (SD 16.9, R 14-97) and 83.3% were male. The number of gas suicides declined over the study period (IRR=0.96). The fall was associated with a 47% decline in carbon monoxide suicides (IRR=0.93). There was an increase in deaths due to argon (IRR=1.60) and nitrogen (IRR=1.27). Compared to individuals using other non-carbon monoxide gases, individuals who died by suicide from helium or nitrogen were significantly more likely to be older, have a physical illness and/or disability, have contacted a euthanasia group and have accessed instructional material and purchased gas online. CONCLUSIONS: Suicides by carbon monoxide decreased between 2006 and 2017 alongside an increase in argon and nitrogen gas use - particularly among older adults. The ease of access to these gases points to new targets for means restriction. Implications for public health: Identifying the types of gases used in suicide deaths and emerging trends may enable targeted interventions that could potentially reduce access.

Longitudinal gray matter changes of the pain matrix in patients with carbon monoxide intoxication: A voxel-based morphometry study.

PURPOSE: Carbon monoxide (CO) intoxication causes gray matter (GM) changes and headache symptom in patients with CO intoxication, but the headache-associated GM changes are not well understood. The purpose of this study was to perform a voxel-based morphometry (VBM) analysis to investigate longitudinal GM changes of brain pain matrix in patients with CO intoxication. METHODS: This prospective study enrolled 24 patients with CO intoxication and 20 healthy controls. Whole brain high-resolution T1-weighted images were acquired in both groups and were repeated in patients at 1 week, and 1, 3, and 9 months after CO exposure. VBM was performed to detect global GM changes in patients with CO intoxication, and the automated anatomical labeling template was utilized to estimate the distribution of significant GM clusters in the brain. RESULTS: GM volumes were significantly decreased mainly in the frontal and occipital lobes, including several pain-matrix regions 1 week after CO intoxication. The regions with significant GM changes further involved the central GM structures and the periaqueductal gray (pain-modulating center) at 1 and 3 months after CO intoxication, but the alterations were partially normalized in the frontal lobe and cerebellum 9 months after CO intoxication. Significant negative correlations were revealed between GM volume and duration of coma in the pain matrix regions. Moreover, five patients exhibited delayed neuropsychiatric sequelae (DNS) and had greater GM volume changes than non-DNS patients. CONCLUSION: VBM analysis is helpful to understand the longitudinal GM changes of the pain matrix in patients with CO intoxication.

Demographic characteristics and delayed neurological sequelae risk factors in carbon monoxide poisoning.

AIM: Carbon monoxide (CO) is a colorless, odorless gas and tasteless. CO poisoning (COP) is one of the most frequently encountered inhalation poisonings. The most common cause of morbidity in COP is delayed neurological sequelae (DNS). DNS is the occurrence of neuropsychiatric findings within 2-240 days after discharge of patients with COP and there are no definitive diagnostic criteria. The aim of our study is; to determine the risk factors and incidence of DNS. METHOD: Our study is a retrospective, observational study. Patients with the diagnosis of COP in the emergency department between 2015 and 2016 were included in the study. Patients age, gender, findings in the initial physical examination (PE) and neurological examination (NE), blood carboxyhemoglobin (COHb) level, relation between hyperbaric oxygen (HBO) treatment and DNS were assessed. RESULTS: Total of 72 patients were included in the study. Mean age was 33.43 ±â€¯20.89. It was determined that pathological findings in the initial NE are a significant predictive factor for DNS (Odds ratio 18.600, p:0.004). Significant relation between NE and HBO treatment was present (p:00.1). There was no statistically significant relationship between initial COHb level and receiving HBO treatment (p:0.9). Median COHb level of patients with DNS was 30 (min:10, max: 43), median COHb level of patients without DNS was 25 (min:10, max:44) and there was no statistically significant relationship between the two groups according to COHb levels (p:0.7). CONCLUSION: Pathological findings in the initial neurological examination had a predictive value for delayed neurological sequelae in patients with carbon monoxide poisoning.

Cerebral Damage after Carbon Monoxide Poisoning: A Longitudinal Diffusional Kurtosis Imaging Study.

BACKGROUND AND PURPOSE: Previous DTI cross-sectional studies have showed the cerebral damage feature was different in the three clinical stages after carbon monoxide poisoning. Diffusional kurtosis imaging (DKI) is an advanced diffusion imaging model and considered to better provide microstructural contrast in comparison with DTI parameters. The primary aim of this study was to assess microstructural changes in gray and white matter with diffusional kurtosis imaging in the acute, delayed neuropsychiatric, and chronic phases after acute carbon monoxide (CO) poisoning. The secondary aim was to relate diffusional kurtosis imaging measures to neuropsychiatric outcomes of acute carbon monoxide poisoning. MATERIALS AND METHODS: In all, 17 patients with acute carbon monoxide poisoning and 30 sex- and age-matched healthy volunteers were enrolled in the study. Patients were scanned within 1 week, 3-8 weeks, and 6 months after acute carbon monoxide poisoning. Diffusional kurtosis imaging metrics including mean kurtosis, mean diffusivity, fractional anisotropy, and kurtosis fractional anisotropy were measured in 11 ROIs and then further correlated with neuropsychiatric scores. RESULTS: In WM, mean kurtosis tended to increase from the acute-to-delayed neuropsychiatric phases and then decrease in the chronic phase, while in GM mean kurtosis showed a constant decline. Contrary to mean kurtosis, mean diffusivity first decreased then tended to increase in WM, while in GM, from the acute to chronic phases, mean diffusivity showed a constant increase. In both WM and GM, the fractional anisotropy and kurtosis fractional anisotropy values progressively declined with time. Kurtosis fractional anisotropy showed the best diagnostic efficiency with an area under the curve of 0.812 (P = .000). Along with neuropsychiatric scores, kurtosis fractional anisotropy of the centrum semiovale and Digit Span Backward were most relevant (r = 0.476, P = .000). CONCLUSIONS: Longitudinally, microstructural changes were inconsistent in WM and GM with time after acute carbon monoxide poisoning. Diffusional kurtosis imaging metrics provided important complementary information to quantify the damage to cognitive impairment.

Forced person-following: a new type of stimulus-bound behavior.

We report a new type of stimulus-bound behavior, denoted forced person-following, which we documented for a patient with hypoxic encephalopathy following a suicide attempt with carbon monoxide poisoning. The patient's brain was damaged in the bilateral frontal, parietal, and temporal lobes and in the basal ganglia. The patient was compelled to follow any person who came into his sight and would continue to do so until the person went out of his sight. The patient also exhibited certain primitive reflexes. The forced person-following exhibited by our patient appears to be a consequence of stimulus-bound behavior due to frontal lobe dysfunction and, to a lesser degree, severe cognitive dysfunctions, e.g., visuospatial deficits, which are related to damage in posterior cortices. The unique behavior exhibited by this patient might contribute to our understanding of innate human behavior.

Time trends in suicide rates by domestic gas or car exhaust gas inhalation in Japan, 1968-1994.

AIMS: A reduction in the carbon monoxide content of domestic gas and car exhaust gas has been associated with a decrease in gassing suicides in many western countries. In Japan, a reduction in the carbon monoxide content of domestic gas supply began in the early 1970s, and carbon monoxide emissions standards of new passenger cars were significantly strengthened in 1978. However, little is known about the impact of detoxification of these gases on gassing-related suicides in Japan. Therefore, we examined the changing patterns of suicide due to domestic gas or car exhaust gas inhalation by gender and age in Japan between 1968 and 1994. METHODS: Suicide mortality data were obtained from the Vital Statistics of Japan. In this study, age was divided into four groups: 15-24, 25-44, 45-64 and 65+ years. Method of suicide was divided into three groups: domestic gas, car exhaust gas and non-gases. We calculated method-specific age-standardised suicide rates by gender within each of the four age groups. We applied joinpoint regression to the data and quantified the observed changes. RESULTS: Suicide rates by domestic gas, regardless of gender and age, increased from 1968 to the mid-1970s and then decreased sharply. The proportion of all suicides accounted for by domestic gas was comparatively high in the mid-1970s among females aged 15-24 and 25-44 years, while for other gender-age-groups the proportion of domestic gas suicides remained small, even at the peak. For females aged 15-44 years, the decrease in domestic gas suicides appeared to cause a substantial decrease in overall suicides in this gender/age group. Car exhaust gas was a more common method for males, particularly those aged 25-64 years. Car exhaust gas suicide rates for males aged 25-64 years peaked in the mid-1980s, followed by a sharp decrease. CONCLUSIONS: A reduction in the carbon monoxide content of the domestic gas, which began in the early 1970s in Japan, was associated with a decrease in domestic gas suicides for both genders of all ages. Concerning females aged 15-44 years, a decrease in domestic gas suicides caused a substantial decrease in overall suicides in this gender/age group since the proportion of domestic gas suicides among all suicides combined was comparatively large. However, it remains uncertain whether the introduction of catalytic converters in the 1970s in Japan resulted in a reduction of suicides from car exhaust gas inhalation.

Predictive Role of QTc Prolongation in Carbon Monoxide Poisoning-Related Delayed Neuropsychiatric Sequelae.

OBJECTIVE: Delayed neuropsychiatric sequelae (DNS) are serious complications of carbon monoxide (CO) poisoning that adversely affect poisoned patients' quality of life as well as socioeconomic status. This study aimed to determine clinical predictors of DNS in patients with CO poisoning. METHODS: This retrospective study included all CO-poisoned patients admitted to the emergency department (ED) of Linkou Chang Gung Memorial Hospital in Taiwan from 1 January 2009 to 31 December 2015. The medical records of all patients with CO poisoning were carefully reviewed, and relevant data were abstracted into a standardised form. Univariate and multivariate logistic regression models were used to identify predictors of DNS after CO poisoning. Receiver operating characteristic (ROC) curve analysis was used to determine the ideal cut-off value for continuous variables that predict the development of DNS. RESULTS: A total of 760 patients with CO poisoning were identified during the study period. Among them, 466 were eligible for the analysis of predictors of DNS. In multivariate analysis, Glasgow Coma Scale <9 (odds ratio [OR], 2.74; 95% confidence interval [CI], 1.21-6.21), transient loss of consciousness (OR, 3.59; 95% CI, 1.31-9.79), longer duration from CO exposure to ED presentation (OR, 1.05; 95% CI, 1.03-1.08), and corrected QT (QTc) prolongation (OR, 2.61; 95% CI, 1.21-5.61) were found to be associated with a higher risk of DNS. The area under the ROC curve (AUC) for QTc interval measured within 6 h after exposure best predicted the development of DNS, with a result of 0.729 (95% CI 0.660-0.791). Moreover, the best cut-off value of the QTc interval was 471 ms, with a sensitivity of 53.3% and a specificity of 85.1%. CONCLUSIONS: We identified several potential predictors of DNS following CO poisoning. Among them, QTc prolongation found within 6 h after exposure is a novel predictor of DNS, which may be helpful in the future care of patients with CO poisoning.

Diffusion kurtosis imaging as a neuroimaging biomarker in patients with carbon monoxide intoxication.

Attempting suicide by burning charcoal can lead to carbon monoxide (CO) intoxication and cognitive deficits. Changes in white matter (WM) quantified by diffusion tensor imaging (DTI)-derived parameters have been validated to reflect cognitive test scores. As diffusion kurtosis imaging (DKI) measures biological microstructures using non-Gaussian diffusivity, we assessed the added-information of DKI with neuropsychological test scores as the major outcome measure. A total of 45 patients were enrolled and compared with 30 age-matched controls. The patients were stratified into acute or chronic phase according to the intervals of intoxication and assessments. WM status was assessed using tract-based spatial statistics for DKI and DTI topographies, and the sensitivity/specificity of either model was tested using area under the curve (AUC) analysis. To evaluate their clinical significance, values of DKI- and DTI-derived parameters were extracted from seven regions of interest (ROI) and correlated with neuropsychiatric scores. The kurtosis parameters were lower in the patients than in the controls but none of the parameters provided differentiations between the acute or chronic phase. Kurtosis fractional anisotropy (KFA) had a higher AUC than fractional anisotropy while the other 3 DTI parameters had higher AUC than the corresponding DKI ones. In clinical correlations, KFA value of right posterior WM correlated with visual memory (r = 0.326, p = 0.029), and KFA values of bilateral posterior WM correlated with the digit forward score (right: r = 0.302, p = 0.043; left: r = 0.314, p = 0.036). Although DTI was more sensitive in reflecting disease status, KFA may be more sensitive and specific than fractional anisotropy in cognitive test score predictions.

[Delayed neuropsychological sequelae after carbon monoxide poisoning]. / Verzögerte Kohlenmonoxidenzephalopathie.

Carbon monoxide poisoning is a very common intoxication worldwide. Its clinical manifestations vary from symptoms like mild headache and dizziness to more serious issues including death. Less well known are symptoms that occur with a delay of 2-40 days, such as movement disorders, cognitive impairment or affective disorders. In this article, we present a case of carbon monoxide poisoning with a delayed neurological sequela. The following review summarizes the literature on clinical presentation, diagnostic options, pathophysiology and therapy of this disease.

iTRAQ-based differential proteomic analysis of the brains in a rat model of delayedcarbon monoxide encephalopathy.

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a difficult-to-manage neurological complication that can severely affect the life quality of patients. Although the central nervous system (CNS) injuries have been reported, the underlying molecular mechanisms are still unclear. Therefore, we established a rat model of DEACMP, applying isobaric tags for a relative and absolute quantification (iTRAQ)-based proteomics approach to identify differentially expressed proteins in cerebral tissue. A total of 170 proteins in the CO exposure groups were identified as differentially changed. Bioinformatics analysis suggested that these proteins are mainly involved in the biological processes, such as energy metabolism and many neurodegenerative diseases. Three proteins, Glial fibrillary acidic protein (GFAP), mitochondrial malate dehydrogenase (MDHM), and isocitrate dehydrogenase [NAD] subunit alpha (IDH3A), were identified as playing important roles in CNS injuries in DEACMP, and were successfully confirmed by immunohistochemistry analysis. Our study not only offers us new insights into the pathophysiological mechanisms of CNS injuries in DEACMP, but also may provide clinicians with important references in early prevention and treatment.

Serum neuron-specific enolase as an early predictor of delayed neuropsychiatric sequelae in patients with acute carbon monoxide poisoning.

Delayed onset of neuropsychiatric symptoms after apparent recovery from acute carbon monoxide (CO) poisoning has been described as delayed neuropsychiatric sequelae (DNS). To date, there have been no studies on the utility of serum neuron-specific enolase (NSE), a marker of neuronal cell damage, as a predictive marker of DNS in acute CO poisoning. This retrospective observational study was performed on adult patients with acute CO poisoning consecutively treated over a 9-month period. Serum NSE was measured after emergency department arrival, and patients were divided into two groups. The DNS group comprised patients with delayed sequelae, while the non-DNS group included patients with none of these sequelae. A total of 98 patients with acute CO poisoning were enrolled in this study. DNS developed in eight patients. The median NSE value was significantly higher in the DNS group than in the non-DNS group. There was a statistical difference between the non-DNS group and the DNS group in terms of CO exposure time, Glasgow Coma Scale (GCS), loss of consciousness, creatinine kinase, and troponin I. GCS and NSE were the early predictors of development of DNS. The area under the curve according to the receiver operating characteristic curves of GCS, serum NSE, and GCS combined with serum NSE were 0.922, 0.836, and 0.969, respectively. In conclusion, initial GCS and NSE served as early predictors of development of DNS. Also, NSE might be a useful additional parameter that could improve the prediction accuracy of initial GCS.

Paediatric emergency department-based carbon monoxide detector intervention: a randomised trial.

BACKGROUND: Although non-fire-related carbon monoxide (CO) poisoning is almost entirely preventable, over 400 people die and 20 000 people are injured each year in the USA from unintentional CO poisoning. Thus, there is a critical need for evidence-based interventions for preventing CO poisoning and increasing the proper use and installation of CO detectors. METHODS: A randomised, controlled trial (Project CODE, a Carbon Monoxide Detector Education intervention) with 2-week and 6-month follow-up home observations was conducted in 299 parents of children aged ≤18 years recruited in the emergency department of a level 1 paediatric trauma centre. The intervention group received an educational tool, a spiral-bound, laminated booklet that resembled a CO detector containing theory-based safety messages based on the precaution adoption process model, a plug-in CO detector and 9 V battery. The control group received a one page flyer on CO poisoning prevention. RESULTS: Although the difference was not statistically significant, mean CO knowledge score increased at a greater rate for the intervention group than the control group. Intervention group parents were more likely to exhibit 'safe' CO detector use than control group parents at the 2-week follow-up (RR: 2.75; 95% CI 2.06 to 3.69) and 6-month follow-up (RR: 2.78; 95% CI 2.06 to 3.76), after adjusting for self-reported CO detector use behaviour at enrolment and annual per capita income. CONCLUSIONS: An emergency department-delivered intervention containing a theory-based educational tool paired with a CO detector can be an effective method for increasing knowledge about CO poisoning, for prevention and for appropriate use of a CO detector. TRIAL REGISTRATION NUMBER: NCT00959478.

Neuropsychological Evaluation of Children and Adolescents With Acute Carbon Monoxide Poisoning.

OBJECTIVES: Carbon monoxide (CO) poisoning is a worldwide health problem. We have limited information regarding psychological adversities of CO poisoning in children and adolescents. The aim of this study was (1) to investigate the effects of severe CO poisoning on cognitive functions, mood, and behaviors in children and adolescents and (2) to identify factors related to occurrence of neuropsychological symptoms. METHODS: This study included pediatric patients, who were evaluated after CO poisoning at the Department of Child and Adolescent Psychiatry between January 2012 and April 2013. The patients were evaluated at 2 time points. The first evaluation was done when they were discharged from emergency department, and the second evaluation was done 1 month after CO poisoning. Turkish versions of internationally recognized tests were used to evaluate anxiety, depressive symptoms, attention, visual-spatial skills, memory, and behaviors of patients. RESULTS: Twenty-seven patients were analyzed. The mean age of the patients was 11.8 ± 2.7 years (range, 6-18 years). The mean carboxyhemoglobin level was 31.5% ± 7.8% (range, 19%-51%) dir. Delayed neurological sequel was observed in only 1 patient, who had headache and tinnitus. We found that carboxyhemoglobin level was not correlated with later neuropsychiatric test scores. However, we found a correlation between history of loss of consciousness and anxiety symptom level, hyperbaric oxygen (HBO) therapy session and behavioral problems, and time to HBO therapy and attention problems. CONCLUSIONS: We suggest that CO exposure duration, history of loss of consciousness, time to HBO therapy, and the number of HBO therapy session affect neuropsychological symptom levels and occurrence of attention and behavioral problems.

MRI and clinical manifestations of delayed encephalopathy after carbon monoxide poisoning.

To explore the relationship between the clinical manifestations and functional magnetic resonance images of delayed encephalopathy after carbon monoxide intoxication. Six patients received the MRI were diagnosed with delayed encephalopathy after carbon monoxide (CO) poisoning. Clinical manifestations were observed in each patient. MRI revealed multiple lesions. The majority of the lesions were located in the globus pallidus, sub cortical white matter, and basal ganglia. The cognitive injury, akinetic mutism, fecal and uroclepsia, forced crying, forced laughing and extra pyramidal syndromes such as chorea and parkinsonism were manifested in clinic. Cognitive impairment improved greatly while involuntary movements only improved slightly after several months. Meanwhile brain MRI suggested remarkable improvement. Neuroimaging directly correlated with the clinical manifestations.

Effect of free radical scavenger, edaravone, for patients with carbon monoxide poisoning.

OBJECTIVE: Chronic neurological symptoms after carbon monoxide (CO) poisoning are caused by various biological processes in the damaged brain, with free radicals playing roles as mediators in establishing pathological processes leading to chronic neurological symptoms under CO poisoning. This study aimed to clarify the effects of a free radical scavenger, edaravone, in patients with CO poisoning. METHODS: We retrospectively compared two groups comprising patients treated with hyperbaric oxygenation alone (Group A, n=25) or edaravone in addition to hyperbaric oxygenation (Group B, n=25). Edaravone was administrated intravenously at 30 mg every 12h for 7 days. Patient characteristics, general conditions on admission, and frequency of chronic neurological symptoms were compared between groups. Among patients showing chronic neurological symptoms, cognitive function and daily activity were also compared between groups. RESULTS: No significant differences in characteristics or general conditions on admission were identified between groups. In Group B, no patients presented with marked complications caused by edaravone. Although chronic persisting symptoms were less frequent in Group B (n=1, 0.04%) than in Group A (n=5, 20%), this difference was not significant. In the 11 patients showing chronic symptoms, scores for cognitive function and daily activity in the chronic phase were better in Group B than in Group A, but no significant differences were apparent. CONCLUSIONS: The present results suggest that edaravone represents a tolerable and feasible treatment for CO-poisoned patients. Further studies are needed to clarify whether edaravone can favorably influence chronic neurological symptoms caused by CO poisoning.

[Delayed neurological syndrome after CO intoxication of elderly female]. / Laattijdige neuropsychologisch syndroom na CO-intoxicatie bij een bejaarde vrouw.

This article discusses the case history of an 87-year old woman with loss of consciousness following accidental CO intoxication. A few weeks later, the patient's cognitive abilities progressively deteriorated. This is hence a case of Delayed Neurological Symptoms after CO intoxication. This condition occurs in 40% of patients with CO intoxication and manifests itself 3-240 days after apparent recovery. Symptoms can linger for a long time and are in some cases even permanent. Treatment of CO intoxication usually consists of administering normobaric oxygen and in certain cases hyperbaric oxygen. The role of treatment with hyberbaric oxygen in delayed neurological symptoms after CO intoxication remains controversial, however.