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 p
ositive AChR-Ab. Because of this clinical observation, we gave 150 mg/kg GB
P to rats with experimental autoimmune myasthenia gravis (EAMG). Repetitive
nerve stimulation at 3-Hz was performed, and the 5th/1st amplitude ratio w
as used to calculate the decremental response. In all EAMG rats, GBP induce
d a transient, abnormal decrement (7-20%) 90 to 240 min after administratio
n, No decrement was induced by GBP in normal rats. Thus, GBP aggravates the
decrement in EAMG, The mechanism involved in the hitherto unreported possi
ble unmasking of myasthenia gravis (MG) by GBP is unknown, Gabapentin shoul
d be used with caution in this disease. (C) 2000 John Wiley & Sons, Inc.