Gabapentin enacarbil for antipsychotic induced akathisia in schizophrenia patients: a pilot open-labeled study

Abstract

Objective

Gabapentin and its prodrug are candidate therapeutic agents for akathisia. An open-label pilot study was conducted to investigate the therapeutic potential of gabapentin enacarbil (GE) for akathisia.

Methods

In an open-labeled investigator-initiated clinical trial, nine outpatients with antipsychotics-induced akathisia were administered GE (300 or 600 mg/day) over 2 weeks. The BARS global akathisia score was used to assess akathisia. The BPRS was used to assess psychiatric symptoms. The subjects were also systematically questioned regarding the adverse events described in an interview form following GE treatment. An intension-to-treat analysis including all patients enrolled in the present study was completed.

Results

One patient declined to participate further in the study on the third day after the start of treatment. Eight patients thus completed the entire trial (male: 2, female: 6, age [mean±SD]: 38.8±11.6 years). The average dosage of GE was 567 mg/day (300 mg/day [n=1], 600 mg/day [n=8]). The BARS global akathisia score significantly decreased after 1 and 2 weeks of treatment when compared to baseline (P=0.01 and P=0.01, respectively). There were no significant differences in BPRS score 1 or 2 weeks after the start of treatment. No serious adverse events occurred.

Conclusion

GE has therapeutic potential for antipsychotics-induced akathisia. No additional risk of GE use for the management of akathisia was indicated.

Keywords:

• clinical trial
• antipsychotic agents
• restless legs syndrome
• schizophrenia

Acknowledgments

We thank Editage (www.editage.jp) for English language editing.

Author contributions

All authors contributed to data analysis, drafting and revising the article, gave final approval of the version to be published, and agree to be accountable for all aspects of the work.

Disclosure

MT has received speaker’s honoraria from Mitsubishi Tanabe Pharma Corporation, Otsuka Pharmaceutical, Sumitomo Dainippon Pharma, Daiichi Sankyo Company, and Eisai. TK has received speaker’s honoraria from Otsuka Pharmaceutical, MSD, and Eisai. TS has received research grants from Eisai and MSD, and speaker’s honoraria from MSD, Takeda Pharmaceuticals, Pfizer, and Yoshitomi Pharmaceuticals. The authors report no other conflicts of interest in this work.