Massive subdural hematoma misdiagnosed as delayed encephalopathy of carbon monoxide poisoning: a case report and literature review

Subdural hematoma is often secondary to brain trauma and other diseases.The onset is hidden and the condition is critical.Timely detection and early treatment are particularly important.The patient denied a history of trauma,but had a history of consciousness loss after charcoal burning.The clinical symptoms were progressive cognitive impairment.The initial diagnosis was delayed encephalopathy caused by carbon monoxide poisoning.However,computed tomography(CT)scan of the brain showed a large area of subdural hematoma on the left side and the formation of a cerebral hernia,which was life-threatening.The patienfs symptoms gradually improved after an emergency operation.

Multimodality evoked potentials in patients with delayed encephalopathy after acute carbon monoxide poisoning

Objective： To evaluate the diagnostic and prognostic values in patients with delayed encephalopathy after acute carbon monoxide poisoning. Methods： The tibial nerve somatosensory evoked potentials （SEPs）, vision evoked potentials （VEPs）, and brain stem audition evoked potentials（BAEPs） were performed in 32 healthy adults and 43 patients with delayed encephalopathy after acute carbon monoxide poisoning. Results： This paper indicated abnormalities of tibial nerve SEPs in 31 patients （31/43, 72.1%）, VEPs in 17 patients （17/28, 60.7%）, and BAEPs in 14, patients （14/43, 32.6%）. These results showed that the greatest diagnostic value was SEPs, followed by VEPs and, BAEPs with the lowest sensitivity. Conclusion： Multimodality evoked potentials （EPs） can be used for evaluating the diagnostic and prognostic values in cases of delayed encephalopathy after acute carbon monoxide poisoning.

Spectrum of delayed post-hypoxic leukoencephalopathy syndrome:A systematic review

BACKGROUND Delayed post hypoxic leukoencephalopathy syndrome(DPHLS),also known as Grinker’s myelinopathy,is a rare but significant neurological condition that manifests days to weeks after a hypoxic event.Characterized by delayed onset of neurological and cognitive deficits,DPHLS presents substantial diagnostic and therapeutic challenges.AIM To consolidate current knowledge on pathophysiology,clinical features,diagnostic approaches,and management strategies for DPHLS,providing a comprehensive overview and highlighting gaps for future research.METHODS Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes guidelines,we systematically searched PubMed,ScienceDirect and Hinari databases using terms related to delayed post-hypoxic leukoencephalopathy.Inclusion criteria were original research articles,case reports,and case series involving human subjects with detailed clinical,neuroimaging,or pathological data on DPHLS.Data were extracted on study characteristics,participant demographics,clinical features,neuroimaging findings,pathological findings,treatment,and outcomes.The quality assessment was performed using the Joanna Briggs Institute critical appraisal checklist.RESULTS A total of 73 cases were reviewed.Common comorbidities included schizoaffective disorder,bipolar disorder,hypertension,and substance use disorder.The primary causes of hypoxia were benzodiazepine overdose,opioid overdose,polysubstance overdose,and carbon monoxide(CO)poisoning.Symptoms frequently include decreased level of consciousness,psychomotor agitation,cognitive decline,parkinsonism,and encephalopathy.Neuroimaging commonly revealed diffuse T2 hyperintensities in cerebral white matter,sometimes involving the basal ganglia and the globus pallidus.Magnetic resonance spectroscopy often showed decreased N-acetylaspartate,elevated choline,choline-to-creatinine ratio,and normal or elevated lactate.Treatment is often supportive,including amantadine,an antioxidant cocktail,and steroids.Hyperbaric oxygen therapy may be beneficial in those with CO poisoning.Parkinsonism was often treated with levodopa.Most of the patients had substantial recovery over the course of months and many cases had some residual neurocognitive deficits.CONCLUSION DPHLS remains a complex and multifaceted condition with various etiologies and clinical manifestations.Early recognition and appropriate management are crucial to improving patient outcomes.Future research should focus on standardizing diagnostic criteria,using advanced imaging techniques,and exploring therapeutic interventions to improve understanding and treatment of DPHLS.Conducting prospective cohort studies and developing biomarkers for early diagnosis and monitoring will be essential to advance patient care.

Hippocampus hypoxia-inducible factor-1 alpha and heme oxygenase-1 expression in the delayed encephalopathy after acute carbon monoxide poisoning rat model

Objective To research the expression of hypoxia-inducible factor-1 alpha(HIF-1α)and heme oxygenase-1(HO-1)in hippocampus of rats with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)and its functions.Methods One hundred and fiftysix rats were selected and randomly divided into

Digit and letter alexia in carbon monoxide poisoning

This study examined a 24-year-old patient with delayed encephalopathy, who was admitted to hospital with complaints of headache and visual impairment 1 week after acute carbon monoxide poisoning. The results of a visual field assessment, electroencephalography and head magnetic resonance imaging indicated damage to the cerebral cortex. After a 2-week treatment period, the patient had recovered from the visual impairment, but exhibited digit- and letter-reading difficulty. The Chinese aphasia battery and the number and letter battery supplement were conducted. The results revealed that the patient exhibited digit and letter alexia, while the ability to read Chinese characters was preserved. In contrast, the patient exhibited a deficit in Chinese character writing, while number and letter writing remained intact. Following treatment, reading and writing ability was improved and electroencephalographic abnormalities were ameliorated. Overall, our experimental findings demonstrated that delayed encephalopathy following acute carbon monoxide poisoning was characterized by digit and letter alexia.