Mirogabalin‐Induced Asterixis

A 90-year-old man presented with a 3-week history of bilateral hand weakness, gait disturbance, somnolence, and recurrent falls. His past medical history included lumbar spinal stenosis, for which he had been receiving mirogabalin 20 mg/day and duloxetine 40 mg/day for 5 years, with a baseline serum creatinine level of 0.88 mg/dL and no dose adjustments during the follow-up period. Additional comorbidities included diabetes mellitus, hypertension, myocardial infarction, and prostate cancer. There was no documented history of antiepileptic drug, antipsychotic, opioid, or immunosuppressant use, nor any history of hypoxic events. On examination, his Glasgow Coma Scale score was E4V4M6. Physical examination revealed pitting edema in the lower extremities. Neurological examination demonstrated asterixis in both upper and lower extremities (Video S1). Laboratory findings showed a serum creatinine of 1.57 mg/dL and creatinine clearance of 24 mL/min. Other laboratory examination revealed normal liver function tests, thyroid function test, serum ammonia, electrolytes, and blood glucose levels. Given these findings, mirogabalin-induced asterixis secondary to renal impairment was suspected, and the medication was discontinued. Eleven days following discontinuation, the patient's symptoms resolved (Video S1). The suspected adverse event and the decision to discontinue mirogabalin were explained to the patient and his family, and informed consent for the management plan was obtained. Mirogabalin is a voltage-gated calcium channel α2δ subunit ligand, similar to gabapentin and pregabalin. Gabapentin and pregabalin may induce asterixis [1, 2]. This adverse effect has been associated with elevated serum concentrations in the setting of renal insufficiency. Although the precise mechanism remains unclear, gabapentinoid-associated asterixis or negative myoclonus has been hypothesized to involve altered neuronal excitability and drug accumulation in the setting of renal impairment [1, 2]. This case suggests that it may similarly cause this phenomenon. To our knowledge, mirogabalin-induced asterixis has not been previously reported. Therefore, particular caution is warranted when prescribing mirogabalin in patients with renal dysfunction. The author has nothing to report. The author has nothing to report. This study was performed in accordance with the principles stated in the Declaration of Helsinki. Written informed consent was obtained from the patient. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions. Video S1: At presentation, the patient exhibited asterixis in the upper and lower extremities. Asterixis resolved on follow-up 11 days after discontinuation of mirogabalin. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

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Journal
Neurology and Clinical Neuroscience
Published
2026-02-17
DOI
https://doi.org/10.1002/ncn3.70087
Primary Topic
Glycogen Storage Diseases and Myoclonus
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article
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article

Mirogabalin‐Induced Asterixis

Tatsuya Ueno
Neurology and Clinical Neuroscience
Glycogen Storage Diseases and Myoclonus
article

Mirogabalin‐Induced Asterixis

Tatsuya Ueno
article en

Abstract

A 90-year-old man presented with a 3-week history of bilateral hand weakness, gait disturbance, somnolence, and recurrent falls. His past medical history included lumbar spinal stenosis, for which he had been receiving mirogabalin 20 mg/day and duloxetine 40 mg/day for 5 years, with a baseline serum creatinine level of 0.88 mg/dL and no dose adjustments during the follow-up period. Additional comorbidities included diabetes mellitus, hypertension, myocardial infarction, and prostate cancer. There was no documented history of antiepileptic drug, antipsychotic, opioid, or immunosuppressant use, nor any history of hypoxic events. On examination, his Glasgow Coma Scale score was E4V4M6. Physical examination revealed pitting edema in the lower extremities. Neurological examination demonstrated asterixis in both upper and lower extremities (Video S1). Laboratory findings showed a serum creatinine of 1.57 mg/dL and creatinine clearance of 24 mL/min. Other laboratory examination revealed normal liver function tests, thyroid function test, serum ammonia, electrolytes, and blood glucose levels. Given these findings, mirogabalin-induced asterixis secondary to renal impairment was suspected, and the medication was discontinued. Eleven days following discontinuation, the patient's symptoms resolved (Video S1). The suspected adverse event and the decision to discontinue mirogabalin were explained to the patient and his family, and informed consent for the management plan was obtained. Mirogabalin is a voltage-gated calcium channel α2δ subunit ligand, similar to gabapentin and pregabalin. Gabapentin and pregabalin may induce asterixis [1, 2]. This adverse effect has been associated with elevated serum concentrations in the setting of renal insufficiency. Although the precise mechanism remains unclear, gabapentinoid-associated asterixis or negative myoclonus has been hypothesized to involve altered neuronal excitability and drug accumulation in the setting of renal impairment [1, 2]. This case suggests that it may similarly cause this phenomenon. To our knowledge, mirogabalin-induced asterixis has not been previously reported. Therefore, particular caution is warranted when prescribing mirogabalin in patients with renal dysfunction. The author has nothing to report. The author has nothing to report. This study was performed in accordance with the principles stated in the Declaration of Helsinki. Written informed consent was obtained from the patient. The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions. Video S1: At presentation, the patient exhibited asterixis in the upper and lower extremities. Asterixis resolved on follow-up 11 days after discontinuation of mirogabalin. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

Neurology and Clinical NeuroscienceVol. 14(2)
Aomori Prefectural Central Hospital (JP)
Good health and well-being
Openalex Percentile: Top 54%
Glycogen Storage Diseases and Myoclonus
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