Background and Objectives: Botulinum neurotoxin A (BoNT-A) is the fi rst line treatment for cervical dystonia (CD). Three different preparations are available: abobotulinumtoxinA, onabotulinumtoxinA, and incobotulinumtoxinA. However, potencies between these preparations vary and the products are therefore not easily interchangeable. Methods: We retrospectively compared the treatment plans and outcome of 51 patients with CD who were treated either with abobotulinumtoxinA (n = 19), onabotulinumtoxinA (n = 20), or incobotulinumtoxinA (n = 12). Results: There were no differences between the three treatment groups in respect to time of fi rst improvement of symptoms (TIS), duration of symptom relieve (DSR), or maximum benefi t (MaxB). However, the total units used for treatment in the abobotulinumtoxineA group was signifi cantly higher than in both other groups, thus resulting in a conversion ratio of 4:1for abobotulinumtoxinA to onabotulinumtoxinA and a conversion ratio of 4.3:1 for abobotulinumtoxinA to incobotulinumtoxinA. Conclusion: In clinical practice, the conversion ratio between abototulinumtoxinA and onabotulinumtoxineA might be higher than previously indicated by prospective studies or in mouse assays. Consequently, lager studies are needed to determine the conversion ratio of the different preparations available as well as the optimization of doses and selection of preparation, therefore resulting in improved cost-effectiveness of different treatment options in clinical practice.

Objective: Striatal dopamine dysfunction caused by cortical abnormalities is a leading hypothesis of schizophrenia. Although prefrontal cortical pathology is negatively correlated with striatal dopamine synthesis, the relationship between structural frontostriatal connectivity and striatal dopamine synthesis has not been proved in patients with schizophrenia with different treatment response. We therefore investigated the relationship between frontostriatal connectivity and striatal dopamine synthesis in treatment-responsive schizophrenia (non-TRS) and compared them to treatment-resistant schizophrenia (TRS) and healthy controls (HC). Methods: Twenty-four patients with schizophrenia and twelve HC underwent [18F] DOPA PET scans to measure dopamine synthesis capacity (the influx rate constant Kicer) and diffusion 3T MRI to measure structural connectivity (fractional anisotropy, FA). Connectivity was assessed in 2 major frontostriatal tracts. Associations between Kicer and FA in each group were evaluated using Spearman’s rho correlation coefficients. Results: Non-TRS showed a negative correlation (r=-0.629, p=0.028) between connectivity of dorsolateral prefrontal cortex-associative striatum (DLPFC-AST) and dopamine synthesis capacity of associative striatum but this was not evident in TRS (r=-0.07, p=0.829) and HC (r=-0.277, p=0.384). Conclusion Our findings are consistent with the hypothesis of dysregulation of the striatal dopaminergic system being related to prefrontal cortex pathology localized to connectivity of DLPFC-AST in non-TRS, and also extend the hypothesis to suggest that different mechanisms underlie the pathophysiology of non-TRS and TRS.