LAUSR

Pisa syndrome (PS) describes a postural abnormality characterized by lateral trunk flexion greater than 10° in the upright position that reverts in the supine position or with passive mobilization [1]. PS was initially described as truncal dystonia in patients using typical neuroleptics [2], but it can be triggered by other drugs such as cholinergic agents or dopamine agonists. PS can also occur in neurodegenerative disorders such as Parkinson’s disease (PD) [3]. Even though basal ganglia abnormalities associated with asymmetric paraspinal dystonia appear to be necessary for PS, other factors such as vestibular imbalance, proprioceptive disintegration, and myopathy could also play a role [4, 5]. Pisa syndrome can be reversible in early phases when a triggering factor is identified and discontinued. Otherwise, PS can become chronic, severe, and treatment resistant. In these cases, botulinum neurotoxin (BoNT) injections and deep brain stimulation (DBS) of subthalamic (STN) or pedunculopontine nuclei (PPN) have been reported with overall disappointing results [6, 7]. We present a patient with PD and bilateral STN–DBS who developed PS that responded to contralateral voltage reduction. A 62-year-old right-handed man with 20 years of leftsided predominant, levodopa-responsive PD underwent bilateral STN–DBS after five years of worsening fluctuations including axial dyskinesia. No dystonia was evidenced during initial monopolar review. Appendicular symptoms improved after surgery but postural instability remained an issue requiring low-frequency stimulation. Additionally, the patient developed right foot dystonia requiring BoNT injections nine months after surgery. Seven years after STN–DBS, he developed PS with right-sided truncal deviation.