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Sir, We thank Dr Morishita and colleagues (2014) for their interest and valuable contribution. Many studies report a slight decline in cognitive functioning after subthalamic nucleus (STN) stimulation for Parkinson’s disease (Parsons et al. , 2006; Witt et al. , 2008). The observed neuropsychological sequelae are likely caused by several independent factors: first, there is a patient-inherent risk profile including age, impaired attention, higher antiparkinsonian medication, higher scores on axial motor symptoms and a lower l-DOPA response before surgery (Smeding et al. , 2009; Daniels et al. , 2010). However, these patient-related factors explain only 23% of the variance of postoperative decline (Daniels et al. , 2010). In our study we found penetration of the caudate nucleus to be associated with an increased risk for a decline in global cognitive functioning and working memory abilities (Witt et al. , 2013). Furthermore, we were able to show that an additional factor is the placement of the stimulated electrode contact. We concluded, that besides the well-known inherent risk factors (age and disease progression), the electrodes track and the …

Reply: Cognitive declines after deep brain stimulation are likely to be attributable to more than caudate penetration and lead location