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Treating akathisia with pregabalin – A case report

Akathisia is a movement disorder characterized by a subjective experience of restlessness alongside an urge to move, generating repetitive movements1,2. Its clinical presentation can be confusing and vague, making the diagnosis often problematic and posing an important challenge in clinical practice1. This challenge stems not only from its symptoms and difficult treatment, but also from the association with aggression and violence, emergence and/or worsening of suicidal ideation, insomnia and exacerbation of the psychotic illness1,2. Akathisia is the most common movement disorder associated with psychotropic medication1, primarily antipsychotic drugs, but also occurs as a side effect of selective serotonin reuptake inhibitors2. Among antipsychotics, first generation agents have a higher risk of eliciting akathisia than second generation agents1. While neurobiological mechanisms underlying akathisia are still uncertain, dysfunctions of basal ganglia and striatal circuits have been commonly implicated in its development. Gamma-aminobutyric acid and serotonin are the neurotransmitters most specifically linked to this movement disorder. An imbalance between serotonergic/ noradrenergic and dopaminergic neurotransmitter systems has been classically considered as the origin of akathisia. Nonetheless, other theories have been proposed, such as an overstimulation of the locus ceruleus and D2/D3 receptor occupancy variations in the ventral striatum1. Akathisia is usually classified according to the symptom’s development timing. As such, and considering consensual scientific entities, there is acute akathisia, subacute/chronic akathisia, tardive akathisia and withdrawal akathisia. The first occurs within a few days to weeks of antipsychotic drug initiation or dosage increase. Chronic akathisia defines an akathisia that has been present for several months. As the name suggests, tardive akathisia arises late (1-3 months), happening not only during the course of neuroleptic treatment, but also after neuroleptic dosage reduction or discontinuation. Withdrawal akathisia happens within 2 weeks of neuroleptic dosage reduction or discontinuation, typically being selflimited and resolving in 6 weeks1. As previously stated, the treatment of akathisia can be difficult. Typically, two strategies are defended when dealing with this issue. The first is a change in medication, either reducing the dose of the culprit agent or switching to another agent. The second strategy lies with the addition of anti-akathisia pharmaceuticals. Many drugs have been proposed to this effect, including propranolol, mirtazapine, anticholinergics (Biperiden, Benztropine, Trihexyphenidyl), Mianserine, benzodiazepines, Cyproheptadine, Amantadine and Clonidine1. More recently, there has been a case report showing success of Pregabalin in the treatment of akathisia3,4. In this paper, we report one other case of akathisia that improved after the introduction of Pregabalin.