Axial truncal dystonia can present as either flexion or extension, often with a tendency toward lateral movement. Flexion dystonia is more common and may represent a clinical spectrum associated with parkinsonism. In contrast, extensor trunk dystonia is less frequent and exhibits a diverse range of causes. In this paper, we reviewed the literature on axial extensor trunk dystonia. We identified 11 studies involving 49 patients, of which only 10 had idiopathic trunk dystonia. Treatment with botulinum neurotoxin A (BoNT/A) emerged as the most effective therapy; however, many studies did not provide detailed descriptions of the treatment (4/11) and follow-up periods were not specified or short term (up to one–two years). We present four new, well-documented patients with the idiopathic form of extensor trunk dystonia who were treated with BoNT/A with moderate to significant effect according to Global Clinical Impression scale (GCI) and Burke-Fahn-Marsden (BFM) dystonia scale. These cases include long-term follow-up for three patients, all without any adverse events. While the diagnostic process and treatment can be challenging, we recommend using BoNT/A with adjusted doses tailored to the appropriate muscle groups as a first-line treatment.

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Introduction. Dopamine agonist withdrawal syndrome (DAWS) comprises a wide range of neuropsychiatric and autonomic symptoms that occur in temporal relation with the reduction or withdrawal of dopamine agonists (DAs) in a dose-dependent manner. This syndrome was described as an important complication in Parkinson’s disease (PD) and restless legs syndrome (RLS) treatment. State of the art. Dopamine agonist withdrawal syndrome affects even up to 24% of PD patients treated with DAs in whom the medication was tapered. Predominant symptoms include the following: anxiety, depression, irritability, panic attacks, sleep disorders, and suicidal thoughts along with autonomic problems such as fatigue, orthostatic hypotension, nausea, and vomiting. Dopamine agonist withdrawal syndrome remains a therapeutic challenge as it is refractory to levodopa (LD), other PD therapies, anti-depressants, and anti-psychotics. The therapy-resistant syndrome may be a pitfall for patients trapped between intolerable side effects of DAs (impulse control disorder [ICD]) and withdrawal symptoms. Clinical implications. Recognition of DAWS as a threatening condition is important for choosing the best treatment option for the patient. Due to the increasingly widespread use and efficacy of advanced therapies such as deep brain stimulation, enteral and subcutaneous LD, as well as apomorphine infusions, the risk of DAWS development should be considered. Dose reduction or discontinuation of DAs should be carefully planned and managed individually (personalized, based on main symptoms). Future directions. Further research should focus on the natural evolution, risk factors, and duration of DAWS. Development of new generation DAs, such as tavapadon, which may reduce the side effects of dopaminergic therapy, may set new standards for treatment. Guidelines on the taper velocity of DAs, risk factors, and management therapies are to be established to improve detection and treatment of DAWS. Keywords: Parkinson’s disease dopamine agonist dopamine agonist withdrawal syndrome ropinirole pramipexole deep brain stimulation depression irritability anxiety sleep disorders