![]() ![]() 5 Sixty days later (in January 2013), the patient underwent another neuropsychological evaluation. 3,4 Considering the time elapsed since poisoning and in absence of a specific treatment, doctors began a therapeutic trial with citicoline at 1 g/day. The possible diagnosis of dementia-like symptoms due to delayed encephalopathy secondary to CO poisoning was confirmed based on similar images in the literature. These findings were more noticeable in the frontal and parietal areas even without gadolinium contrast ( Fig. Brain magnetic resonance imaging (MRI) revealed T2-weighted and FLAIR signal intensity, as well as bilaterally symmetric restricted diffusion which was partially confluent in the periventricular white matter. Electroencephalography (EEG) showed normal alpha rhythm with bilateral, polymorphic, and intermittent theta wave activity. Cytological and chemical studies of cerebrospinal fluid (CSF) yielded normal findings. All laboratory analyses showed normal results, and the VDRL and HIV tests were both negative. The examination detected no focal signs, myoclonias, or movement disorders. The patient's score on the Mini-Mental State Examination (MMSE) was 19/30 and his score on Addenbrooke's Cognitive Examination (ACE) was 61/100. Constructional apraxia was confirmed and he scored only 2 points on the clock-drawing test. ![]() He demonstrated altered function when performing the Luria test (fist, edge, and palm) with signs of frontal release and compromised episodic memory, but with preserved long-term memory. At 53 days after symptom onset, the patient was admitted to our hospital awake, showing disorientation, labile attention, and significant impairment of executive functions. General examinations ruled out infectious or vascular aetiology, and the patient was transferred to our centre to complete the study. He was readmitted to the local hospital, and a brain CT performed at that time yielded normal results. After that initial month, his wife noticed changes in his behaviour: he was apathetic, disoriented, confused, and had difficulty completing professional and other daily tasks. The patient returned to work with no incidents for the following 30 days. He was admitted to a provincial hospital due to confusional state after 24 hours in observation without hyperbaric oxygen treatment, he was discharged with no neurological disorders. On 16 September 2012, after having consumed alcohol, the patient fell asleep near a lit heater and was exposed to carbon monoxide for 14 hours. Our patient is a 52-year-old man (a right-handed married freelance worker) with a long history of alcohol and tobacco dependence. We report the case of a patient who presented this entity, which is characterised by pronounced cognitive impairment. Its main symptoms are cognitive impairment, parkinsonism, ataxia, and/or behavioural disorder. Delayed-onset encephalopathy secondary to carbon monoxide poisoning (CO) is a serious although infrequent complication that manifests within the first and the sixth week after poisoning. ![]()
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