Gabapentin is used for treatment of nerve pain in adults which is a result of herpes virus or shingles. It represents an analogue to GABA and is used for treatment of patients (mainly adults) that has partial seizures, or suffers from mixed seizure disorders. It is also used for treatment of refractory partial seizures in children. Thus gabapentin is an effective medication used to treat epilepsy. It is also well-known as anticonvulsant drug. Another sphere where gabapentin can be used is as tricyclic antidepressant.
Moreover, once labeled as antiepileptic drug, gabapentin proved to be effective in treatment of neurotic pain in clinical as well as in preclinical settings. It can be employed as an effective measure against any neuropathic conditions. It is considered to be effective in terms of pain relief. All other drugs of similar action have pretty many side-effects and should be prescribed very carefully, while gabapentin has relatively mild side-effects profile. According to statistics from the available trials, withdrawal of treatment was not common among the placebo groups. The most frequent side effects are dizziness, somnolence, headache, diarrhea, confusion and nausea (Baillie, 2007, p.34). However, there exists a possibility of increasing adverse effects in case of interactions with other agents.
In humans, gabapentin is effective in reducing neuropathic pain resulting from diabetes mellitus, cancer, postherpetic neuralgia and other pain syndromes. Baillie (2007) writes that “gabapentin is ineffective in acute post-operative pain following mastectomy and interestingly, the analgesic efficacy of this agent is dependent on the presence of some pathological state, such as nerve injury or inflammation” (p.33). Gabapentin is also effective with other antineuropathic and analgesic agents in some human volunteers.
The precise mechanisms of action for gabapentin as analgesic and antiepileptic measure are unknown. The main studies of this drug have been conducted on rats and mice. The results showed that gabapentin prevents pain-related responses of neuropathic pain in mice and rats and decreases pain-related responses after peripheral inflammation. However, it does not immediate pain-related behavior. The drug also exhibits antiseizure in mice and rats. However, these models have not been tested on humans and relevance of these results to humans is unknown (“Neurontin”, n.d.). As for humans, it is concluded that it prevents allodynia (behavior related to pain which is a response to a normally innocuous stimulus) and hyperalgesia (response to painful stimuli in excess of normal). Gabapentin is not appreciably metabolized in humans. Food has slight effect on gabapentin absorption.
As gabapentin was designed as an analogue to GABA, no evidence was found that could prove the direct interaction between the key receptors of in central pain transmission. Gabapentin does not directly interact with the glycine-NMDA complex. Baillie (2007) notes that “gabapentin exhibits a profound synergic anti-allodynic action with the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), suggesting that the two drugs do not act at the same time” (p. 34). Also there has been identified high-affinity binding site for gabapentin. In vitro studies discovered that gabapentin binds using the α2δ auxiliary subunit of voltage-activated calcium channels which is upregulated after nerve injury. Despite the fact that this binding demonstrated no therapeutic effect, this subunit has become a subject of new research and a basis for new drug development.
References
Baillie, K. (2006). The Mechanism of Action of Gabapentin in Neuropathic Pain. Current Opinion in Investigational Drugs, 7(1): 33-39. Retrieved from http://www.researchgate.net/publication/7346510_The_mechanism_of_action_of_gabapentin_in_neuropathic_pain
“Neurontin.” (n.d.). RxList. Retrieved from http://www.rxlist.com/neurontin-drug/clinical-pharmacology.htm
