Clinical Information

Gabapentin is an antiepileptic drug that is effective in treating seizures, neuropathies, and a variety of neurological and psychological maladies. Although designed as a gamma-aminobutyric acid (GABA) analogue, gabapentin does not bind to GABA receptors, nor does it affect the neuronal uptake or degradation of GABA. In fact, the precise mechanism by which it exerts its analgesic and anticonvulsant effects is unknown.

After oral administration and absorption, gabapentin circulates essentially unbound to serum proteins. In addition, gabapentin does not undergo hepatic metabolism, unlike most other antiepileptic drugs, and is eliminated almost entirely by renal excretion with a clearance that approximates the glomerular filtration rate. The elimination half-life is 5 to 7 hours in patients with normal kidney function.

Since gabapentin does not bind to serum proteins, it does not exhibit pharmacokinetic variability and interactions with other highly protein-bound medications (eg, phenytoin). In addition, the lack of hepatic metabolism eliminates the interactions with other hepatically cleared medications, which can induce/inhibit hepatic drug metabolizing enzyme systems (eg, cytochrome P450 enzymes). Therefore, gabapentin serum concentration is not changed following the addition or discontinuation of other common anticonvulsants (ie, phenobarbital, phenytoin, carbamazepine, or valproic acid), nor are their serum concentrations altered upon the addition or discontinuation of gabapentin.

In general, adverse effects with gabapentin are infrequent and usually resolve with continued treatment. The most common side effects include somnolence, dizziness, ataxia, and fatigue. Experience to date indicated that gabapentin is safe and relatively nontoxic.