Etifoxine for Pain Patients with Anxiety.
- Author:
Yun Mi CHOI
1
;
Kyung Hoon KIM
Author Information
- Publication Type:Review
- Keywords: Antianxiety drugs; Anticonvulsants; Anxiety; Etifoxine; Human translocator protein (18kDa); Gamma-aminobutyric (GABA) receptors; Mechanism of action; Nerve regeneration; Neuropathic pain; Neurosteroids
- MeSH: Amnesia, Anterograde; Anti-Anxiety Agents; Anticonvulsants; Anxiety Disorders; Anxiety*; Benzodiazepines; Flumazenil; Humans; Kidney; Liver; Mitochondrial Membranes; Nerve Regeneration; Neuralgia; Neurotransmitter Agents; Peripheral Nerves; Peripheral Nervous System; Psychomotor Performance; Receptors, GABA-A; Respiratory Insufficiency; Serotonin Uptake Inhibitors; Shock; Sleep Stages
- From:The Korean Journal of Pain 2015;28(1):4-10
- CountryRepublic of Korea
- Language:English
- Abstract: Etifoxine (etafenoxine, Stresam(R)) is a non-benzodiazepine anxiolytic with an anticonvulsant effect. It was developed in the 1960s for anxiety disorders and is currently being studied for its ability to promote peripheral nerve healing and to treat chemotherapy-induced pain. In addition to being mediated by GABA(A)alpha2 receptors like benzodiazepines, etifoxine appears to produce anxiolytic effects directly by binding to beta2 or beta3 subunits of the GABA(A) receptor complex. It also modulates GABA(A) receptors indirectly via stimulation of neurosteroid production after etifoxine binds to the 18 kDa translocator protein (TSPO) of the outer mitochondrial membrane in the central and peripheral nervous systems, previously known as the peripheral benzodiazepine receptor (PBR). Therefore, the effects of etifoxine are not completely reversed by the benzodiazepine antagonist flumazenil. Etifoxine is used for various emotional and bodily reactions followed by anxiety. It is contraindicated in situations such as shock, severely impaired liver or kidney function, and severe respiratory failure. The average dosage is 150 mg per day for no more than 12 weeks. The most common adverse effect is drowsiness at the initial stage. It does not usually cause any withdrawal syndromes. In conclusion, etifoxine shows less adverse effects of anterograde amnesia, sedation, impaired psychomotor performance, and withdrawal syndromes than those of benzodiazepines. It potentiates GABA(A) receptor-function by a direct allosteric effect and by an indirect mechanism involving the activation of TSPO. It seems promising that non-benzodiazepine anxiolytics including etifoxine will replenish shortcomings of benzodiazepines and selective serotonin reuptake inhibitors according to animated studies related to TSPO.
