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Severe Cerebellar Atrophy Following Acetylsalicylate Poisoning: A Case Report

Mitsunori Morimatsu^1*, Takesuke Yamashita², Toyohisa Nabeyama³ and Koki Shimizu⁴

¹Department of Neurology, Tokuyama Medical Association Hospital, Shunan, Japan

²Department of Internal Medicine, Yamashita Internal Medicine Clinic, Shunan, Japan

³Department of Psychiatry, Izumihara Hospital, Shunan, Japan

⁴Department of Emergency Medicine, Tokuyama Central Hospital, Shunan, Japan

Received Date: Jan 10, 2024 / Published Date: Feb 12, 2024

Citation: Morimatsu M, Yamashita T, Nabeyama T, Shimizu K (2024) Severe Cerebellar Atrophy Following Acetylsalicylate Poisoning: A Case Report. J Alzheimers Dis Parkinsonism 14:589.DOI: 10.4172/2161-0460.1000589

Copyright: © 2024 Morimatsu M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Introduction: Acetylsalicylate is a common Over-The-Counter (OTC) drug that is used for suicide attempts. Acetylsalicylate toxicity ranges from mild to death, according to the amount that is taken and the response of the patient. In particular, toxicity may occur in a delayed manner, causing serious damage to the brain as a sequela.

Case presentation: A 43-year-old woman attempted suicide by overdosing with Bufferin^®. Due to frequent vomiting, she was transported to an emergency hospital in the morning. However, in the hospital, she became alert and looked well after intravenous infusions, and was transferred to a psychiatric hospital for observation. She vomited several times during the night and was transported to the emergency hospital the following morning due to obtunded consciousness. Due to hypoxemia, intra-tracheal intubation and respiratory control with a respirator were performed. Metabolic acidosis and acute rhabdomyolysis were successfully treated. However, support with a respirator and non-invasive positive pressure ventilation were necessary up to the 20th hospital day. Thereafter, she regained normal consciousness and intelligence. She subsequently presented with dysarthria and gait disturbance. Three years later, a detailed neurological examination revealed marked cerebellar ataxia and exclusive cerebellar atrophy on Magnetic Resonance Imaging (MRI) of the brain.

Conclusion: The exclusive cerebellar ataxia and atrophy on MRI associated with acetylsalicylate poisoning were probably induced by respiratory insufficiency secondary to Hypoxic-Ischemic Encephalopathy (HIE). However, salicylate toxicity and several other disorders may have contributed to the pathogenesis.

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