Akathisia – Pathophysiology, Diagnosis and Management Strategies
In this video, Dr Sanil Rege discusses the following:
- Clinical features of akathisia
- Types of akathisia
- Differentiating akathisia from agitation and restless legs syndrome
- Clinical cases
- Medications (non-psychotropic) associated with akathisia
- Pathophysiology of akathisia
- Management algorithm for akathisia
What Is Akathisia?
- Akathisia is defined as subjective complaints of restlessness, often accompanied by observed excessive movements (e.g. fidgety movements of the legs, rocking from foot to foot, pacing, inability to sit or stand still), developing within a few weeks of starting or raising the dosage of a medication (such as a neuroleptic) or after reducing the dosage of a medication used to treat extrapyramidal symptoms. [DSM-5]
Pathophysiology of Akathisia:
- The pathophysiology of akathisia appears to be complex involving several neurotransmitters including dopamine, acetylcholine, y-aminobutyric acid (GABA), norepinephrine, serotonin, and neuropeptides.
- The neurotransmitters most specifically linked to akathisia are gamma-aminobutyric acid (GABA) and serotonin.
- GABA (mainly via GABAA receptor interactions) exerts an influence on dopamine-dependent signalling, thus, increasing or reducing locomotor activity Akathisia may result from efforts to compensate for dopaminergic underactivity in the nucleus accumbens
- Reduce dose
- Switch to low risk antipsychotic
- Adjunctive approaches:
- Propranolol 40-80 mg/day
- 5HT2A receptor antagonists (e.g. mirtazapine 15 mg PO daily, cyproheptadine 8-16 mg PO daily)
- Benzodiazepines (e.g. clonazepam 0.5-1 mg PO daily, diazepam 5-15 mg PO daily)
- Anticholinergics (e.g. benztropine 1-4 mg PO daily) should be used mainly for patients who have concurrent Parkinsonism
We cover an algorithm for the management of akathisia based on evidence-based guidelines.