Akathisia

Stewart A Factor DO (

Dr. Factor of the Emory University School of Medicine received honorariums from Adamas, Auspex/Teva, Avanir, Biogen, Chelsea, Lundbeck, Merz, Neurocrine, and UCB for consulting work; research grants from Auspex/Teva, Cynapsus, Genzyme, Ipsen, Solstice, US World Meds, Vaccinex, and Voyager as a site investigator; and educational grants from Allergan and Medtronics.

)
Joseph Jankovic MD, editor. (

Dr. Jankovic, Director of the Parkinson's Disease Center and Movement Disorders Clinic at Baylor College of Medicine, has received research and/or training grants from Adamas, Allergan, Biotie, Civitas/Acorda, Hoffmann-La Roche, Medtronic, Merz, Neurocrine , Nuvelution, Pfizer, Prothena, Psyadon, Revance, and Teva; and has served as a consultant or as an advisory committee member for Adamas, Allergan, Merz, Prothena, Revance, and Teva.

)
Originally released December 16, 1994; last updated February 21, 2018; expires February 21, 2021

Overview

Akathisia is the abnormal state of motor restlessness that is most commonly caused by neuroleptic therapy. It can be an acute side effect that improves with withdrawal of medication, or it can be tardive that worsens with drug withdrawal. Literature demonstrates that it occurs with atypical antipsychotics although perhaps less commonly than is seen with typical agents. This is a matter to be debated. It can also be caused by antidepressants. The treatment is different for acute and tardive forms. For acute withdrawal of the causative agent followed by use of propranolol, mirtazapine and trazodone may be used if necessary. These agents can be helpful, but other drugs for tardive dyskinesia may also be tried.

Key points

 

• Akathisia is a sensorimotor syndrome.

 

• Motor symptoms appear to be in response to sensory symptoms and are stereotyped and suppressible, and they decrease with distraction.

 

• Sensory symptoms are urges or other uncomfortable phenomena that improve with movement.

 

• Akathisia occurs acutely or subacutely with dopamine receptor-blocker therapy and improves with removing the drug, or it is chronic or tardive after chronic therapy with dopamine receptor-blocking agents and worsens with removing the drug.

 

• Mechanisms relate to impact of dopamine, serotonin, and noradrenergic systems on the somatosensory system in the brain.

 

• There should be a high index of suspicion as akathisia is frequently underrecognized.

 

• Akathisia is a complication of all atypical antipsychotics.

 

• First-line therapies include propranolol, mirtazapine, or trazodone.

Historical note and terminology

The term “akathisia” is from the Greek “inability to sit,” but it generally refers to an aversion to being still that is relieved by movement. The term was first used medically by Haskovec (Haskovec 1901) who thought the symptoms were the result of psychological disorders (Adler et al 2005). A Czech neuropsychiatrist and a former student of Charcot, Haskovec obviously described this phenomenon in the pre-antipsychotic era (Mohr and Volavka 2002). Akathisia was recognized as a complication of parkinsonism during the epidemic of encephalitis lethargica in the 1920s, and later, Parkinson disease. Dopamine receptor-blocking drugs for the treatment of psychosis were developed during the 1940s, and akathisia was recognized as a side effect of promethazine in 1947 (Adler et al 2005). Tardive akathisia, occurring after chronic neuroleptic therapy and remaining and worsening after withdrawal of the drug, was first reported in 1960 (Kruse 1960) but was not labeled “chronic akathisia” until 1983 (Braude and Barnes 1983). Akathisia is one of the most troublesome aspects of tardive dyskinesia (Waln and Jankovic 2013a; Frei et al 2018; Savitt and Jankovic 2018).

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