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Dear Editor, We have read with interest comments by Solla et al. [1] regarding our Letter to the Editor published in NeurologicalSciences titled ‘‘Insidious onset of Pisa Syndrome afterrasagiline therapy in a patient with Parkinson’s Disease’’[2]. We thank the authors for their interest in our paper, but we think it is necessary to make some clarifications regarding the temporal relationship between the onset of Pisa Syndrome (PS) and rasagiline therapy. PS occurred in fact after and not before rasagiline treatment as stated by Solla et al. In particular, PS occurred after a time interval of 6–12 months and anyway after rasagiline was added to patient’s therapy. This long time interval is one of the elements that makes the case interesting (time period longer than previously described). Temporal relationship is fundamental for the interpretation of clinical and electrophysiological findings in our case. Rasagiline is an inhibitor of monoamine oxidase type B, and although different mechanisms of action have been advocated, its effect is primarily dopamine mediated [3]. This means that occurrence of Pisa syndrome in our case was likely related not only to the specific mechanisms of action of the drug but also to increased dopamine extracellular levels at the striatal synapses, and thus to the total dopamine agonism load. To conclude, though it is likely that concomitant use of other antiparkinsonian drugs could have contributed to the onset of PS in our patient, it is noteworthy that PS was not evident before rasagiline was started, it became evident after rasagiline was initiated, and it was not anymore evident after rasagiline was stopped.

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The effectiveness of cognitive rehabilitation (CR) in Parkinson’s disease (PD) is in its relative infancy, and nowadays there is insufficient information to support evidence-based clinical protocols. This study is aimed at testing a validated therapeutic strategy characterized by intensive computer-based attention-training program tailored to attention deficits. We further investigated the presence of synaptic plasticity by means of functional magnetic resonance imaging (fMRI). Using a randomized controlled study, we enrolled eight PD patients who underwent a CR program (Experimental group) and seven clinically/demographically-matched PD patients who underwent a placebo intervention (Control group). Brain activity was assessed using an 8-min resting state (RS) fMRI acquisition. Independent component analysis and statistical parametric mapping were used to assess the effect of CR on brain function. Significant effects were detected both at a phenotypic and at an intermediate phenotypic level. After CR, the Experimental group, in comparison with the Control group, showed a specific enhanced performance in cognitive performance as assessed by the SDMT and digit span forward. RS fMRI analysis for all networks revealed two significant groups (Experimental vs Control) × time (T0 vs T1) interaction effects on the analysis of the attention (superior parietal cortex) and central executive neural networks (dorsolateral prefrontal cortex). We demonstrated that intensive CR tailored for the impaired abilities impacts neural plasticity and improves some aspects of cognitive deficits of PD patients. The reported neurophysiological and behavioural effects corroborate the benefits of our therapeutic approach, which might have a reliable application in clinical management of cognitive deficits.