LETTER TO THE EDITOR Rasagiline and Pisa syndrome in Parkinson’s disease patients Paolo Solla • Antonino Cannas • Gianni Orofino • Francesco Marrosu Received: 21 October 2014 / Accepted: 27 November 2014 / Published online: 7 December 2014 Ó Springer-Verlag Italia 2014 Dear Editor, We read with interest the article written by Valentino et al. [1] about the insidious onset of Pisa syndrome in a patient with Parkinson’s disease during treatment with rasagiline, an inhibitor of monoamine oxidase type B (MAO-B). Although we are in agreement with the authors that a dopaminergic impairment seems to play a major role in the development of PS [2–4], we are not undoubtedly certain that only rasagiline might be con- sidered the unique iatrogenic factor favoring the onset of PS in this patient. To this regard, although the authors hypothesized that the drug alone was probably not sufficient to induce PS, they only considered a combination of other genetic and clinical PD characteristics as concomitant risk factors, ignoring the possible involvement of other iatrogenic agents. In fact, as suggested by the same authors, a close tem- poral relationship between rasagiline introduction and development of PS onset was not noted, with PS occurring nearly 1 year before the addition of rasagiline. Further- more, it should be highlighted that, at PS onset, the patient was taking other concomitant drugs such as pramipexole and levodopa, which are well-described iatrogenic factors [2–4]. Interestingly, also in two previous studies which repor- ted rasagiline as an iatrogenic factor favoring the onset of PS [3, 5], this drug was concomitant to pramipexole or levodopa treatment, and never in monotherapy. Moreover, in four of these five cases [5], rasagiline was introduced to manage motor worsening or wearing-off phenomena, while in the remaining case levodopa and pramipexole were added to improve motor impairment. Thus, no patient with PS has been described in mono- therapy with rasagiline to date. Moreover, although the authors reported that the postural bending observed com- pletely remitted 1-month after rasagiline withdrawal, it should be noted that the patient in Fig. 1b of [1] presented with a residual truncal deviation to the left, despite the EMG findings. Finally, because the clinical effect of rasagiline mainly relies on the MAO-B inhibition which can lead to the increase of extracellular dopamine levels in striatal syn- apses, we retain that PS in these patients could be determined by an unbalance between the overall dopa- minergic stimulation (comprehensive of dopamine ago- nists and levodopa in addition to rasagiline, and not determined by the only MAO-B inhibitor) and the disease progression characterized by the presence of motor worsening or wearing-off phenomena. With this regard, a reduction of dopaminergic treatment might represent a feasible strategy in the resolution of this postural disability. In conclusion, we agree with the authors about the importance of a rapid individuation of PS in PD, before it evolves in a chronic posture with irreversible changes. Acknowledgements Dr. Paolo Solla gratefully acknowledges Sardinia Regional Government for the financial support (P.O.R. Sardegna F.S.E. Operational Programme of the Autonomous Region of Sardinia, European Social Fund 2007–2013—Axis IV Human Resources, Objective l.3, Line of Activity l.3.1 ‘‘Avviso di chiamata per il finanziamento di Assegni di Ricerca’’). P. Solla (&) Á A. Cannas Á G. Orofino Á F. Marrosu Movement Disorders Center, Department of Neurology, Policlinico Universitario Monserrato, University of Cagliari, SS 554 Bivio per Sestu, Monserrato, Cagliari 09042, Italy e-mail: paosol29@yahoo.it 123 Neurol Sci (2015) 36:485–486 DOI 10.1007/s10072-014-2024-x