Tardive dystonia and dyskinesia

Authors

Keywords:

tardive dystonia, tardive dyskinesia, clinics, treatment

Abstract

Tardive dyskinesias are so named because they occur late (months or years) after treatment with neuroleptics. They can occur during the course of treatment, but also when the dosage is reduced or the treatment is stopped. They persist for at least one month after stopping the medication that caused the syndrome. Pathogenesis is associated with dopaminergic overactivity, activation of dopamine D2 receptors, and loss of GABA-ergic activity in the subthalamic nucleus. Clinically, dyskinesias manifest as restless movements of the tongue or tic-like movements of the face and clenching of the teeth. Mouth movements are stereotyped and rhythmic, grunting or moaning may be added due to involvement of the upper respiratory tract. Typical orobuccolingual dyskinesia resembles continuous chewing, with the tongue periodically darting out of the mouth. Late dystonia most often manifests as craniocervical dystonia affecting the lower part of the face (mouth, cheeks, tongue, and neck), blepharospasm, and cervical dystonia in various combinations. Dysphagia with swallowing disorder often occurs. Late movements are characterized by a diverse mixture of orofacial or other localized dystonia, athetosis, chorea, myoclonus, tics, facial grimacing, and stereotypies.
Treatment initially involves slow and gradual tapering of neuroleptic therapy, if possible. Clonazepam, valproates, vigabatrin, and baclofen can be used, but they are less effective. Tetrabenazine is administered in increasing doses of 25 mg daily until an effect is obtained. Valbenazine and deutetrabenazine are selective vesicular monoamine transporter type 2 (VMAT2) inhibitors that are effective and have fewer side effects. In isolated cases there has been a positive result from the administration of propranolol, clonidine, levetiracetam, amantadine, nifedipine, verapamil, opiates and lithium. Anticholinergic drugs affect dystonia but worsen tardive choreic dyskinesias and do not affect akathisia. Botulinum toxin primarily affects dystonias. Different movements are affected by different medications. The prognosis is different, ranging from spontaneous disappearance of dyskinesias up to 2 years after stopping treatment in 30% of patients to irreversible forms. Dystonic movements are often permanent.
In conclusion, the use of atypical neuroleptics, the careful assessment of the need for treatment with them and the approval of the modern group of selective inhibitors of the vesicular monoamine transporter type 2 (VMAT2) for the treatment of the late syndrome give hope for a better prognosis of the late syndrome.

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Published

30.10.2023

How to Cite

Milanov, I. (2023). Tardive dystonia and dyskinesia. Movement Disorders, 20(1), 9–18. Retrieved from https://multiplesclerosis-bg.com/journal/index.php/md/article/view/73