Etifoxine – a unique anxiolytic

Prescribing drugs for anxiety disorders is one of a psychiatrist’s most common tasks.

This is a summary of a longer, CPD accredited article available on www.medicalacademic.co.za

NXIETY DISORDERS ARE the most prevalent psychiatric disorders and are associated with a high burden of illness. Anxiety is an emotional experience that is characterised by a state of arousal and the expectation of danger. Anxiety and adjustment disorders are frequently comorbid with other medical conditions. It has an adaptive role, preparing the body to deal with future threatening stimuli arising from the environment.

Nevertheless, processing of such aversive information by the brain, particularly by the amygdala circuits, is associated with a negative subjective state. When excessive, a pathological anxious condition may be diagnosed. In DSM-5, these states include panic disorder, generalised anxiety disorder, separation anxiety disorder, specific phobias, social anxiety disorder and adjustment disorder with anxiety.

A

GABA A R

Brain imaging studies have demonstrated that prolonged dysregulation of brain networks involving cortical and specific subcortical areas (amygdala, hippocampus, thalamus, prefrontal, and cingulate cortex) contributes to the expression of anxiety symptoms. In particular, reduced inhibitory GABAergic transmission in the CNS has been shown to be critical for the manifestation of anxiety. In this respect, the structure and function of the GABA A receptor have been under intense scrutiny.

GABA A R is a heteropentamer made of five subunits delimiting a chloride/ bicarbonate-permeable channel. It is activated by at least two molecules of γ-aminobutyric acid (GABA), an amino acid neurotransmitter synthesised from glutamate in neurons expressing glutamate decarboxylase enzymes (i.e. GABAergic neurons). As for many ligand-gated receptor-channels the apparent affinity of GABA A Rs for GABA varies from low to high micromolar range. This parameter strongly depends on the subunit composition and, more specifically, on α-β subunit dimers forming together the agonist binding site for GABA. The anxiolytic effect of drugs binding to the GABA A receptor is attributed to the facilitation of chloride channel opening, thereby amplifying neuronal inhibition in response to GABA. Over the last halfcentury, numerous GABA A receptor ligands have been developed as therapeutic agents, including anxiolytics, hypnotics, muscle relaxants, and antiepileptics.

References available on request.

Story BRAND

SAFETY OF ETIFOXINE

Over the 30 years since etifoxine was first licensed, drug safety monitoring has confirmed the low risk of drug dependence or withdrawal symptoms following treatment cessation. The few reported

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adverse events mostly concern skin and subcutaneous tissue disorders, which generally resolve with treatment discontinuation.

CONCLUSION

Clinical studies have demonstrated the efficacy of etifoxine in the symptomatic treatment of anxiety, particularly in patients with ADWA, with daily doses of 150-200mg. The tolerability profile of etifoxine is better than that of BZDs, notably because of a lack of effect on memory and vigilance. In addition, treatment cessation does not induce drug dependence, withdrawal, or rebound anxiety. The anxiolytic efficacy of etifoxine, its good tolerability and the absence of drug dependence is strong arguments in favour of using etifoxine in the management of ADWA.