Delayed encephalopathy after carbon monoxide intoxication: case report
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LETTER TO THE EDITOR
Delayed encephalopathy after carbon monoxide intoxication: case report Zerrin Yıldırım1,2 · Yavuz Altunkaynak3 · Sevim Baybaş3 Received: 31 August 2019 / Accepted: 9 October 2019 © Belgian Neurological Society 2019
Dear Editor, Carbon monoxide (CO) intoxication is an important cause of emergency unit admissions and one of the leading causes of toxic deaths [1]. The syndrome has two temporally divided different clinical manifestations: acute intoxication and delayed encephalopathy. In the acute intoxication, headache, nausea, vomiting, dyspnea, fatigue and clouded consciousness with varying severity may be observed in the first 24–48 h. Delayed encephalopathy occurs in a period of 2–40 days in some of the patients who showed clinical improvement after the acute period and clinically characterized by a subacute course of cognitive impairment with varying severity, Parkinson’s-like motoric impairment, incontinence and psychosis [2]. The temporal gap between the two manifestations is called “lucid interval”. Ischemic changes, demyelination and abnormal inflammatory responses play a role in the pathophysiology of the disease [3]. Hyperbaric oxygen and corticosteroid therapy may be used for the treatment [2]. A 71-year-old right-handed man, who did not have any medical history, was admitted to the hospital with a 1-month history of progressive amnesia, loss of behavioral spontaneity, unsteady gait and urinary incontinence. On admission, he was awake and cooperative. Apathy, hypomimia and decreased spontaneous speech were readily observable during the examination. Temporal and spatial orientation
* Zerrin Yıldırım [email protected] 1
Department of Neuroscience, Aziz Sancar Institute of Experimental Medicine, Istanbul University, Istanbul, Turkey
2
Department of Neurology, Bagcilar Education and Research Hospital, Istanbul, Turkey
3
Department of Neurology, Bakirkoy Prof. Dr. Mazhar Osman Mental Health and Neurological Diseases Education And Research Hospital, Istanbul, Turkey
was markedly impaired. Attention deficits were prominent. Resistance to interference and ability to inhibit inappropriate responses were significantly impaired in Stroop test and Go-no-go test and he was visibly distractable. Mini Mental State Examination (MMSE) score was 12/30. His gait was slow with short steps. Bilateral symmetric bradykinesia and mild rigidity were detected. Routine laboratory investigations including hemogram, biochemistry, thyroid function tests, liver function tests, ferritin, folate, vitamin B12, hepatitis markers, syphilis markers, anti-HIV, chest X-ray and electrocardiography were normal. Arterial blood gases and serum lactate levels were normal. Serum ammonia level was normal. Brain magnetic resonance imaging (MRI) showed conflating hyperintensities in the anterior peri and paraventricular white matter in T2, FLAIR and diffusion-weighted sequences in white matter with normal ADC values (Fig. 1). Electroencephalography revealed mild diffuse slowing in both hemispheres (6–7 Hz)
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