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Decrease in Blood Cortisol Corresponds to Weight Gain following Deep Brain Stimulation of the Subthalamic Nucleus in Parkinson’s Disease

months (p = 0.001). WG was associated with changes of ghrelin and leptin levels at 3 and 6 months. The authors concluded that STN DBS may temporarily dysregulate the hypothalamic secretion of NPY and ghrelin, whereas the WG may be related to an increased production of ghrelin and leptin. These observations bear remarkable similarities to our earlier study, in which we assessed anthropometric and hormonal profiles in 27 PD patients on the day of surgery and at 2, 4, 6 and 12 months on STN DBS [5] . Our patients’ weight continuously increased throughout the study, with the mean body weight change with regard to baseline being +4.16 8 3.5 kg (p ! 0.001) at 6 months and +5.18 8 5.8 kg (p ! 0.001) at 12 months. Furthermore, in both studies, leptin and ghrelin levels correlated with body WG, corresponding to the known roles of the adipocytederived leptin and the orexigenic hormone ghrelin. Curiously enough, Markaki et al. [4] do not pay much attention to their own finding of markedly decreased cortisol levels following STN DBS. Nevertheless, this result is in surprisingly precise agreement with our observation, probably shedding more light on the mechanisms of WG in PD following STN DBS ( table 1 ). At 3 months after STN DBS, Markaki et al. [4] noticed a significant decrease in blood cortisol (–23.8%, p = 0.027). In our study, cortisol levels decreased at 2 months, (–23.9%, p ! 0.002), still remaining significantly reduced compared to baseline at 12 months after DBS implantation (–22.9%, p = 0.008) [5] . These results seem to indicate the involvement of hypothalamic-pituitaryadrenal axis in the mechanisms of WG after STN DBS. It can be hypothesized that STN DBS acts on adjacent nerve fibers and structures including hypothalamic nuclei, where it suppresses secretion of corticotropin-releasing factor with a subsequent decrease in the production of cortisol. Since the level of corticotropin-releasing factor is low, its catabolic effect is mitigated; therefore, the homeostatic balance shifts towards predominance in It has repeatedly been shown that patients with Parkinson’s disease (PD) gain body weight under treatment with deep brain stimulation of the subthalamic nucleus (STN DBS) [1–3] . However, the mechanisms underlying this weight gain (WG) remain unclear. We, therefore, read with great interest the recently published article ‘The role of ghrelin, neuropeptide Y and leptin peptides in weight gain after deep brain stimulation for Parkinson’s disease’ by Markaki et al. [4] . The authors performed body composition measurements and blood sampling before, and 3 and 6 months after STN DBS in 23 PD patients, looking for relations between WG and changes in blood levels of the metabolic hormones ghrelin, neuropeptide Y (NPY) and leptin. A significant WG (3.09 8 5 kg, mean 8 SD, p = 0.007) was observed 3 months after surgery, with no further increase at 6 months. Also the circulating levels of NPY increased significantly (p = 0.05) at 3 months, while the increase of ghrelin was significant only at 6 Received: April 27, 2012 Accepted: July 5, 2012 Published online: October 17, 2012