Wallerian degeneration of bilateral cerebral peduncles after acute carbon monoxide poisoning

BMC Neurology - Tập 20 - Trang 1-6 - 2020
Sui-yi Xu1,2, Chang-xin Li1, Le-yi Li3, Yu Song3, Yi Sui4
1Department of Neurology, The First Hospital of Shanxi Medical University, Taiyuan, China
2Department of Neurology, the First Affiliated Hospital of Shenzhen University, Health Science Center, Shenzhen Second People’s Hospital, Shenzhen, China
3Department of Radiology, Liaoning Jinqiu Hospital, Liaoning Provincial Geriatric Hospital, Shenyang, China
4Department of Neurology and Neuroscience, Shenyang First People’s Hospital, Shenyang Brain Hospital, Shenyang Brain Institute, Shenyang Medical College, Shenyang, China

Tóm tắt

Cases of Wallerian degeneration of bilateral cerebral peduncles after acute carbon monoxide poisoning have not yet been reported. To date, most of the delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) lesions captured in magnetic resonance imaging (MRI) has been located in the subcortical white matter and basal ganglia. Here we report two cases of DEACMP with abnormalities in the bilateral cerebral peduncles. The etiology of abnormalities, which were strictly confined to the bilateral cerebral peduncles, was Wallerian degeneration secondary to upstream nerve axonal damage, making this the first report on such bilateral cerebral peduncle abnormalities after DEACMP. In this report, we present two cases of DEACMP with abnormal signals in the bilateral cerebral peduncles captured during brain MRIs. Case 1 was of a 68-year-old man who presented with paroxysmal disturbance of the consciousness, left limb weakness for 16 days, and lagging responses for 2 days. Case 2 was of a 55-year-old man who was unconscious for 6 h. In addition to the above mentioned characteristics on the brain MRIs, the electroencephalography of case 1 indicated that his forehead scans had a mixture of wide sharp, sharp, and three-phase waves. Brain diffusion tensor imaging of case 2 further proved that the bilateral cerebral anomalies represented Wallerian degeneration secondary to upstream axonal damage. After the definitive diagnosis, the patients returned to the local hospital for hyperbaric oxygen therapy. Wallerian degeneration of the bilateral cerebral peduncles after acute carbon monoxide poisoning has never been reported before. The abnormal signals in the bilateral cerebral peduncles captured during brain MRIs indicated Wallerian degeneration secondary to upstream axonal damage; thus, these two cases may further our understanding of DEACMP imaging.

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