Premium
Gabapentin may be hazardous in myasthenia gravis
Author(s) -
Boneva Neli,
Brenner Talma,
Argov Zohar
Publication year - 2000
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/1097-4598(200008)23:8<1204::aid-mus7>3.0.co;2-h
Subject(s) - myasthenia gravis , pyridostigmine , medicine , gabapentin , neuromuscular junction , anesthesia , weakness , asymptomatic , acetylcholine receptor , pyridostigmine bromide , repetitive nerve stimulation , neuromuscular transmission , electromyography , surgery , receptor , pathology , psychology , alternative medicine , neuroscience , psychiatry
Abstract A patient with painful neuropathy developed ocular, facial, and masticatory weakness and fatigue after 3 months of gabapentin (GBP) treatment (400 mg/day). An elevated level of serum acetylcholine receptor antibodies (AChR‐Ab) was detected. The patient recovered following pyridostigmine therapy and withdrawal of GBP and, 2 years later, is practically asymptomatic despite positive AChR‐Ab. Because of this clinical observation, we gave 150 mg/kg GBP to rats with experimental autoimmune myasthenia gravis (EAMG). Repetitive nerve stimulation at 3‐Hz was performed, and the 5th/1st amplitude ratio was used to calculate the decremental response. In all EAMG rats, GBP induced a transient, abnormal decrement (7–20%) 90 to 240 min after administration. No decrement was induced by GBP in normal rats. Thus, GBP aggravates the decrement in EAMG. The mechanism involved in the hitherto unreported possible unmasking of myasthenia gravis (MG) by GBP is unknown. Gabapentin should be used with caution in this disease. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 1204–1208, 2000