Gray matter atrophy and white matter lesions burden in delayed cognitive decline following carbon monoxide poisoning.

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.

Carbon monoxide poisoning with hippocampi lesions on MRI: cases report and literature review.

BACKGROUND: Carbon monoxide (CO) poisoning is now one of the leading causes of poisoning-related mortality worldwide. The central nervous system is the most vulnerable structure in acute CO poisoning. MRI is of great significance in the diagnosis and prognosis of CO toxic encephalopathy. The imaging features of CO poisoning are diverse. We report atypical hippocampal lesions observed on MRI in four patients after acute CO exposure. CASE PRESENTATIONS: We report four patients who presented to the emergency department with loss of consciousness. The diagnosis of CO poisoning was confirmed on the basis of their detailed history, physical examination and laboratory tests. Brain MRI in all of these patients revealed abnormal signal intensity in hippocampi bilaterally. They all received hyperbaric oxygen therapy. The prognosis of all four patients was poor. CONCLUSION: Hippocampi, as a relatively rare lesion on MRI of CO poisoning, is of important significance both in the early and delayed stages of acute CO poisoning. In this article, we summarize the case reports of hippocampal lesions on MRI in patients with CO poisoning in recent years, in order to provide reference for the diagnosis and prognosis of CO poisoning.

A Graph Theory Study of Resting-State Functional MRI Connectivity in Children With Carbon Monoxide Poisoning.

BACKGROUND: The effect of carbon monoxide (CO) poisoning on the topology of brain functional networks is unclear, especially in children whose brains are still developing. PURPOSE: To investigate the topological alterations of the whole-brain functional connectome in children with CO poisoning and characterize its relationship with disease severity. STUDY TYPE: Cross-sectional and prospective study. SUBJECTS: A total of 26 patients with CO poisoning and 26 healthy controls. FIELD STRENGTH/SEQUENCE: A 3.0 T MRI system/echo planar imaging (EPI) and 3D brain volume imaging (BRAVO) sequences. ASSESSMENT: We used the network-based statistics (NBS) method to explore between-group differences in functional connectivity strength and a graph-theoretical-based analytic method to explore the topology of brain networks. STATISTICAL TESTS: Student's t-test, chi-square test, NBS, Pearson correlation coefficient, and false discovery rate correction. The statistical significance threshold was set at P < 0.05. RESULTS: The case group's brain functional network topology was impaired in comparison to the control group (reduced global efficiency and small-worldness, increased characteristic path length). According to node and edge analyses, the case group showed topologically damaged regions in the frontal lobe and basal ganglia, as well as neuronal circuits with weaker connections. Also, there was a significant correlation between the patients' coma time and the degree (r = -0.4564), efficiency (r = -0.4625), and characteristic path length (r = 0.4383) of the nodes in the left orbital inferior frontal gyrus. Carbon monoxide hemoglobin content (COHb) concentration and right rolandic operculum node characteristic path length (r = -0.3894) were significantly correlated. The node efficiency and node degree of the right middle frontal gyrus (r = 0.4447 and 0.4539) and right pallidum (r = 0.4136 and 0.4501) significantly correlated with the MMSE score. DATA CONCLUSION: The brain network topology of CO poisoned children is damaged, which is manifested by reduced network integration and may lead to a series of clinical symptoms in patients. EVIDENCE LEVEL: 2. TECHNICAL EFFICACY: Stage 2.

Two similar carbon monoxide poisoning cases with different outcomes: evidence from longitudinal fMRI.

Prognosis after carbon monoxide (CO) poisoning is difficult to assess using structural images. Functional connectivity provided by functional magnetic resonance imaging (fMRI) may explain the mechanism of differential prognosis. We report here two cases of carbon monoxide poisoning with simultaneous coma. They were nearly normal on days 7-8, but diagnosed with delayed neurological sequelae (DNS) with cognitive and motor impairments on days 22-29. Similar Methylprednisolone pulse therapy and hyperbaric oxygen therapy were given to them. The movement disorder of case 1 improved slightly during the recovery stage, while the movement disorder of case 2 worsened significantly. In case 1, the function of supplementary motor area decreased first and then increased, and the function of pallidum increased first and then decreased. Case 2 showed a reduction in the supplementary motor area and small changes in the pallidum after DNS, but both were reduced during recovery stage. The cognitive ability of case 1 remained poor, while that of case 2 improved during the recovery stage. FMRI showed damage to the right and bilateral hippocampus in case 1 and partial damage to the left hippocampus in case 2. Taken together, fMRI can be a useful method to study functional connectivity abnormalities corresponding to different prognoses.

Early gray matter atrophy and neurological deficits in patients with carbon monoxide poisoning.

PURPOSE: To investigate early neurological deficits-related change patterns in gray matter (GM) volume in patients with carbon monoxide poisoning (COP) and GM volume differences between patients with and without delayed neurological sequelae (DNS) and those with and without T2 hyperintense lesions after COP. METHODS: Forty-one COP patients (24 patients with DNS) and 36 sex- and age-matched healthy controls (HC) were enrolled in this study. The neurological assessments were administered within 24 h after MRI scans. Voxel-based morphometry analysis was used to detect regional GM volume change. RESULTS: The COP group had statistically significant GM atrophy in the bilateral prefrontal and temporal lobes, anterior cingulate (ACC), thalamus, posterior cerebellum, and right hippocampus compared to the HC group. Atrophy in the left medial orbital superior frontal gyrus (SFG), bilateral ACC, and bilateral thalamus were related to lower Mini-Mental State Examination (MMSE) scores and higher Unified Parkinson's Disease Rating Scale subsection III and neuro-psychiatric inventory scores. Atrophy in the hippocampus and posterior cerebellum were also related to decrease MMSE scores. The DNS subgroup had greater GM atrophy in the limbic system than the non-DNS subgroup. Compared to the subgroup without T2 hyperintense lesions, greater GM atrophy in the limbic system, motor and visual cortex, and default network was observed in the subgroup with T2 hyperintense lesions. CONCLUSION: GM atrophy in the medial orbital SFG, ACC, thalamus, hippocampus, and posterior cerebellum is associated with early neurological deficits in patients with COP. Greater atrophy occurred in patients with DNS and those with T2 hyperintense lesions.

Development of a Nomogram Based on Diffusion-Weighted Imaging and Clinical Information to Predict Delayed Encephalopathy after Acute Carbon Monoxide Poisoning.

BACKGROUND: Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a severe complication that can arise from acute carbon monoxide poisoning (ACOP). This study aims to identify the independent risk factors associated with DEACMP and to develop a nomogram to predict the probability of developing DEACMP. METHODS: The data of patients diagnosed with ACOP between September 2015 and June 2021 were analyzed retrospectively. The patients were divided into the two groups: the DEACMP group and the non-DEACMP group. Univariate analysis and multivariate logistic regression analysis were conducted to identify the independent risk factors for DEACMP. Subsequently, a nomogram was constructed to predict the probability of DEACMP. RESULTS: The study included 122 patients, out of whom 30 (24.6%) developed DEACMP. The multivariate logistic regression analysis revealed that acute high-signal lesions on diffusion-weighted imaging (DWI), duration of carbon monoxide (CO) exposure, and Glasgow Coma Scale (GCS) score were independent risk factors for DEACMP (Odds Ratio = 6.230, 1.323, 0.714, p < 0.05). Based on these indicators, a predictive nomogram was constructed. CONCLUSIONS: This study constructed a nomogram for predicting DEACMP using high-signal lesions on DWI and clinical indicators. The nomogram may serve as a dependable tool to differentiate high-risk patients and enable the provision of personalized treatment to lower the incidence of DEACMP.

[Research progress on head imaging features of carbon monoxide poisoning and delayed encephalopathy].

Acute carbon monoxide poisoning and its delayed encephalopathy have obvious damage to the central nervous system. There are different neuroimaging changes in different stages of the disease, and they are relatively specific. This article reviews the clinical research progress on the imaging changes of carbon monoxide poisoning and delayed encephalopathy, including computed tomography (CT) , conventional magnetic resonance imaging (MRI) , diffusion weighted imaging (DWI) , diffusion tensor imaging (DTI) , diffusion kurtosis imaging (DKI) , magnetic resonance spectroscopy (MRS) and other imaging changes reflecting the function and metabolic state of the brain tissue.

Neurological sequelae in acute carbon monoxide poisoning: A prospective observational study with MRI data.

OBJECTIVES: Acute carbon monoxide (CO) poisoning survivors may experience persistent neurological sequelae (PNS) and delayed neurological sequelae (DNS). This study evaluated the clinical features, laboratory results, acute brain lesions (ABLs) on diffusion-weighted imaging (DWI) at presentation, and long-term outcomes and explored differences between patients with PNS and DNS. METHODS: The study included 443 patients who had experienced CO poisoning, underwent DWI and completed 1-year follow-ups. The demographics, comorbidities, symptomatology, laboratory results, ABLs on DWI at presentation, and long-term outcomes were compared between patients with PNS and those with DNS. RESULTS: The 42 (9.5%) and 96 (21.7%) patients with PNS and DNS, respectively, showed no significant differences in demographics, duration of CO exposure, initial conscious level, symptomatology, and laboratory results. ABLs on DWI were observed in 33 patients (33/42) with PNS and 62 patients (62/96) with DNS. The most common region of ABLs was the globus pallidus (60.6% and 56.6% in PNS and DNS, respectively). The proportion of ABLs present and lesion distribution did not differ significantly between the two groups. At 1 year, a significantly higher proportion of patients in the PNS group showed a good outcome (defined as modified Rankin Scale [mRS] scores of 0-2, 81%) compared with the DNS group (81% vs. 56.3%, p = .047). CONCLUSION: Demographics, clinical features, laboratory results, and acute brain lesions on MRI at presentation did not differ between the PNS and DNS groups. However, the long-term outcome of PNS was better than that of DNS.

Predicting scale of delayed neuropsychiatric sequelae in patients with acute carbon monoxide poisoning: A retrospective study.

OBJECTIVE: To establish and validate a predictive formula for calculating the possibility of developing delayed neurological sequelae (DNS) after acute carbon monoxide (CO) poisoning to facilitate better decision-making about treatment strategies. METHODS: This study retrospectively enrolled 605 consecutive patients who had been newly diagnosed with CO poisoning from the Central Hospital of Enshi Prefecture between January 1, 2015 and December 31, 2020. The cohort was randomly divided into two subgroups: the development cohort (n = 104) and validation cohort (n = 44). Univariate analysis and backward elimination of multivariate logistic regression were used to identify predictive factors, and a predictive formula was established. The performance was assessed using the area under the curve (AUC), the mean AUC of five-fold cross-validation, and calibration plots. RESULTS: The formula included four commonly available predictors: initial GCS score, duration of exposure, CK, and abnormal findings on MRI. We next created a formula to calculate the risk score for developing DNS: Risk score = -4.54 + 3.35 * (Abnormal findings on MRI = yes) - 0.51 * (Initial GCS score) + 0.65 * (Duration of exposure) + 0.01 * (CK). Then, the probability of developing DNS could be calculated: Probability of DNS = 1/(1 + e Risk score). The model revealed good discrimination with AUC, and mean AUC of fivefold cross-validation in two cohort, and the calibration plots showed good calibration. CONCLUSIONS: This study established a prediction predictive formula for predicting developing of DNS, which could facilitate better decision-making about treatment strategies.

The diagnostic value of neurogranin in patients with carbon monoxide poisoning: Can it show early neurological damage?

BACKGROUND AND AIM: Carbon monoxide poisoning is a toxicological emergency that causes neurological complications. High serum neurogranin can be detected in acute or chronic conditions where brain tissue is damaged. This study aimed to investigate the diagnostic value of serum neurogranin level and its role in demonstrating neurological damage in patients admitted to the emergency department with carbon monoxide poisoning. MATERIALS AND METHODS: The study was conducted prospectively on patients with carbon monoxide poisoning (patient group) and healthy volunteers (control group). Demographic characteristics and serum neurogranin level of all participants and symptoms at admission, neurological examination findings, laboratory results, and Diffusion-Weighted Magnetic Resonance Imaging results of the patient group were recorded. We used an independent sample t-test to compare neurogranin levels and bivariate correlation analysis to compare the relationship between serum neurogranin levels and data belonging to the patient group. RESULTS: Sixty eight participants (patient group, n = 36; control group, n = 32) were included in the study. Serum neurogranin level was significantly higher in patients with carbon monoxide poisoning (0.31 ± 0.16 ng/ml) compared to control group (0.22 ± 0.10 ng/ml) (p = 0.015). The mean Glasgow Coma Scale of the patients with carbon monoxide poisoning was 14.59 ± 0.23, and of Diffusion Weighted Magnetic Resonance Imaging results were completely normal in 94.4% (n = 34). There was no correlation between serum neurogranin level and Diffusion Weighted Magnetic Resonance Imaging results (r = -0.011; p = 0.953). CONCLUSION: Serum neurogranin level may be a new diagnostic biomarker in patients admitted to the emergency department with carbon monoxide poisoning. The high serum neurogranin levels detected in patients with normal diffusion-weighted imaging after carbon monoxide poisoning suggest that there is neurological damage in these patients, even if imaging methods cannot detect it.

Hyperbaric oxygen therapy mobilized circulating stem cells and improved delayed encephalopathy after acute carbon monoxide poisoning with up-regulation of brain-derived neurotrophic factor.

Background Delayed encephalopathy (DE) is the most severe complication after acute carbon monoxide (CO) poisoning, which seriously affects the outcome of patients and leads to a high disability rate. Prior studies have shown that hyperbaric oxygen (HBO2) therapy is therapeutic for DE due to reducing immune-mediated neuropathology and thus improving cognitive performance. Methods In our present perspective study, five DE patients were treated regularly with HBO2 therapy. The mini-mental state examination (MMSE) and Barthel index (BI) were intermittently collected during their hospitalization for mental and physical status evaluation, the peripheral bloods were serially sampled to determine the concentration changes of circulating stem cells, as well as corresponding BDNF and neural markers. Results MMSE and BI showed series of improvements after multiple HBO2 therapies. The CD34+/CD90+ and CD34+/CD133+ dual positive cells, which were categorized as circulating stem cells, were observed an overall up-regulation since the beginning of the DE onset upon the application of HBO2 therapy. Characteristic neurotrophin BDNF, neural markers such as nestin and synaptophysin (SYP) were also up-regulated after exposure of HBO2. Conclusion The application of HBO2 therapy is of significance in improving the cognition of DE patients, along with mobilized circulating stem cells. We primarily infer that the CD34+/CD90+ and CD34+/CD133+ cells were mobilized by HBO2 exposure and have played a positive role in cognition improvement on DE patients by up-regulation of BDNF, nestin and SYP. The altering amount of circulating stem cells mobilized in peripheral blood could be a potential marker on predicting the outcome of DE.

Predictive factors for acute brain lesions on magnetic resonance imaging in acute carbon monoxide poisoning.

BACKGROUND: Acute brain lesions on diffusion-weighted-magnetic resonance imaging (MRI) after acute carbon monoxide (CO) poisoning were associated with delayed neurological sequelae. This study was conducted to identify the risk factors associated with acute brain lesions on MRI after acute CO poisoning and to help select patients who need acute-phase brain MRI after acute CO poisoning in the emergency department (ED). METHODS: This retrospective observational study included 103 adult patients who were hospitalized at a tertiary-care hospital between November 2016 and September 2019 and underwent brain MRI because of acute CO poisoning. Multivariable logistic regression analysis was applied to identify predictive factors for acute brain lesions on MRI after acute CO poisoning. RESULTS: Multivariable logistic regression analysis showed that Glasgow Coma Scale (GCS) score of <9 at ED presentation (odds ratio [OR] 17.749, 95% confidence interval [CI] 3.098-101.690, P = 0.001) and the initial troponin-I level at presentation in the ED (OR 13.657, 95% CI 1.415-131.834, P = 0.024) were predictive factors for acute brain lesions on MRI in acute CO poisoning. The receiver operating characteristics curve for initial troponin-I showed an area under the curve of 0.761 (95% CI 0.638-0.883, P < 0.001) and the optimal cutoff value was 0.105 ng/mL. CONCLUSIONS: Acute-phase brain MRI in acute CO poisoning can be considered for patients who present at the ED with a GCS score <9 or troponin-I level >0.105 ng/mL.

Usefulness of N-terminal pro-B-type natriuretic peptide (NT-ProBNP) as a marker for cardiotoxicity and comparison with echocardiography in paediatric carbon monoxide poisoning.

OBJECTIVES: To demonstrate the usefulness of N-Terminal Pro-B-Type natriuretic peptide (NT-proBNP) as an early biomarker of carbon monoxide-induced myocardial injury in children. It also aimed to identify the correlation between NT-proBNP and left ventricular systolic dysfunction findings shown by echocardiography. METHODS: Prospective, observational study conducted at a paediatric emergency department between October 2017 and April 2019 which involved children aged 0-17 years. The patients were divided into three groups based on severity; mild, moderate and severe groups. The patient characteristics, carboxyhaemoglobin, CK-MB Mass (CKMB-M), troponin-T, and NT-proBNP levels were measured, and echocardiography was performed and left ventricular ejection fraction was measured. RESULTS: Sixty-nine patients and 60 healthy controls were included. Male gender, younger age, higher carboxyhaemoglobin levels, and altered mental status were found as independent predictors of carbon monoxide-induced myocardial injury. If the cut-off value for NT-proBNP level is >480 pg/ml, the sensitivity-specificity for decreased left ventricular ejection fraction, which is the strongest carbon monoxide-induced myocardial injury sign, were 100-96%, respectively. A high negative correlation was found between NT-proBNP levels and left ventricular ejection fraction (r = -0.769, p < 0.01) in the carbon monoxide poisoning group, and there was a positive correlation between the carboxyhaemoglobin and NT-proBNP levels (r = 0.583, p < 0.01). CONCLUSION: Echocardiography is an ideal tool and very sensitive, but its routine use is limited due to its non-availability. An increased level of NT-proBNP (>480pg/ml) may be useful as an ideal biomarker for early detection of carbon monoxide-induced myocardial injury sign and reduced left ventricular ejection fraction which is the most crucial point in making a decision on hyperbaric oxygen therapy.

Gray matter nuclei damage in acute carbon monoxide intoxication assessed in vivo using diffusion tensor MR imaging.

OBJECTIVE: To observe the structural changes of gray matter nuclei in patients with acute carbon monoxide intoxication by diffusion tensor imaging (DTI), quantify the degree of deep gray matter damage in the brain by adopting imaging technology and research the characteristics of the damage and its pertinence with memory and cognitive impairment. METHODS: Twenty-five patients with acute carbon monoxide intoxication and 25 healthy volunteers matched in sex and age were examined by routine head MRI and diffusion tensor imaging (DTI). Bilateral hippocampus, dater nucleus, thalamus, amygdala, globus pallidus and putamen were taken as regions of interest. The mean diffusion coefficient (MD), anisotropic fraction (FA) and appearance of deep gray matter nucleus in patients with acute carbon monoxide intoxication were analyzed. It found that the change of diffusion coefficient (ADC) and its clinical correlation with cognitive impairment were generated by carbon monoxide intoxication. RESULTS: Compared with the healthy control group, the FA values of bilateral globus pallidus, hippocampus, dater nucleus and putamen decreased, while the FA values of amygdala and thalamus had no statistical significance; the MD values and ADC values of hippocampus, globus pallidus and putamen increased, while the MD and ADC values of dater nucleus, thalamus and amygdala had no statistical significance, either. CONCLUSION: DTI is capable of sensitively reflecting the damage of gray matter nuclei caused by acute carbon monoxide intoxication and quantifying the degree of hypoxic brain damage in a certain extent, and may be related 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.

Evaluation of changes in magnetic resonance diffusion tensor imaging after treatment of delayed encephalopathy due to carbon monoxide poisoning.

Diffusion tensor imaging of the brain tissue microstructure was performed to predict or diagnose the pathophysiological mechanism underlying delayed encephalopathy after carbon monoxide poisoning and the treatment effect was analyzed. The changes in the diffusion parameters (average diffusion coefficient and fractional anisotropy) in adult patients after hyperbaric oxygen therapy of delayed encephalopathy after carbon monoxide poisoning were not significant differences of the two lateral ventricles or anterior or posterior limb of the internal capsule. In the group exposed to hyperbaric oxygen therapy, the fractional anisotropy values of the white matter in the ventricles of the brain and anterior and posterior limbs of the internal capsule were higher than those recorded before therapy, while the average diffusion coefficient values were significantly lower. These finding provide important monitoring indicators for clinicians.

[Imaging diagnosis of 95 cases of moderate and severe acute carbon monoxide poisoning].

Objective: To explore the difference of radiological imaging features of delayed encephalopathy after carbon monoxide poisoning (DECMP) and acute carbon monoxide poisoning (ACMP) , and the correlation between the imaging findings and clinical prognosis of the disease. Methods: The correlation between imaging findings and clinical manifestations and prognosis of 95 patients with moderate and severe acute carbon monoxide poisoning were retrospectively analyzed. In the above 95 cases, there were 62 cases of ACMP and 33 cases of DEACMP. All patients underwent conventional CT, MRI and magnetic resonance diffusion tensor imaging (DTI) . Circular regions of interest (ROI) measurement was used for analysis of average diffusion coefficient (ADC) value and fractional anisotropy (FA) value of the MRI and DTI imaging manifestations in different brain regions. Results: The main clinical manifestation of moderate acute carbon monoxide poisoning was consciousness disorder and fatigue; Severe poisoning patients showed deep coma as the main clinical manifestations; The most prominent clinical manifestations of DEACMP were mental disorders and neurological impairment in the extrapyramidal system. A total of 95 cases with moderate or severe CO poisoning showed unilateral or bilateral cerebral cortex, bilateral basal ganglia (white ball) , cerebral white matter around bilateral ventricles or bilateral centrum semiovale, around bilateral ventricles cerebral white matter around bilateral ventricles and bilateral centrum semiovale, cerebral cortex and subcortical involvement. CT showed normal or low density shadow.MRI showed that the lesion T(1)WI presented slightly low or equal signal, T(2)WI and FLAIR sequences showed equal, a slightly higher or high signal; DWI sequence showed slightly higher or high signal. ADC value and FA value in different brain white matter regions of DEACMP group was significantly lower than those of ACMP group (P<0.05) , especially for those around semi oval center and lateral ventricles of the brain white matter (P<0.01) ; The ADC values increased significantly, FA value decreased significantly in the nerve nucleus (P<0.05) , especially for ADC values in globus pallidus (P<0.01) . Conclusion: DTI can evaluate the brain tissue damage in patients with DEACMP more early and more accurately.

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.