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558 - When Anticholinergics Add Up: Carbamazepine-Induced Toxicity in an Adult with Neuromyelitis Optica Spectrum Disorder (NMOSD)

Thursday, February 27, 2025

5:00 PM - 6:30 PM MST

Presenting Author(s)

JD

John DesRochers, BS

Medical Student (OMS-III)
Rowan-Virtua School of Osteopathic Medicine
Brick, New Jersey, United States

Co-Author(s)

Kelly Crawford, MD

Residency Program Director
Department of Physical Medicine and Rehabilitation Carolinas Rehabilitation/Carolinas Medical Center/Atrium Health
Charlotte, North Carolina, United States
ZS

Zachary Shumaker, MD

Resident Physician
Carolinas Rehabilitation
Charlotte, North Carolina, United States

Case Diagnosis: Anticholinergic toxicity secondary to carbamazepine utilized to treat upper extremity spasms in a patient with Neuromyelitis Optica Spectrum Disorder (NMOSD).

Case Description: 61-year-old female presented to the hospital with complaints of nausea, left-sided numbness, and left-sided weakness. CT imaging was acutely negative but revealed lesions in brain and spinal cord concerning for a demyelinating disorder. MRI confirmed demyelination and serum AQP4 IgG levels returned positive, diagnostic for NMOSD. Following transfer to inpatient rehabilitation, the patient developed severely painful bilateral upper extremity muscle spasms. Spasms persisted despite brief trials of methocarbamol and baclofen, necessitating carbamazepine initiation. The patient was also receiving meclizine 12.5 mg TID and, days prior, had received a scopolamine patch and a few doses of hydroxyzine. The patient became agitated, disoriented, and restless, with dilated pupils, hypertension, and urinary retention, indicative of anticholinergic toxicity. Improvement occurred with discontinuation of the anticholinergic medication and administration of IV lorazepam.

Discussions: Carbamazepine is a less frequently used anticonvulsant today; however, painful tonic spasms, common in NMOSD, are often resistant to typical antispasmodic agents, and carbamazepine is endorsed as the drug of choice. Only around 6% of carbamazepine toxicity is related to recommended therapeutic dosing, opposed to supratherapeutic. Additionally, anticholinergic toxicity from carbamazepine is exceedingly rare, with only a few case reports of urinary retention. Despite this, in the setting of recent meclizine, hydroxyzine, and scopolamine administration, anticholinergic toxicity was induced. These medications are among the many anticholinergic medications commonly used in neurorehabilitation.

Conclusions: Combinations of medications regularly prescribed in neurorehabilitation can lead to anticholinergic toxicity. This case serves as a cautionary tale for physiatrists to assess the cumulative anticholinergic burden of a patient’s medications before initiation of an additional pharmacologic, even if it has only mild anticholinergic activity.