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Comment & Response
August 2015

Subthalamic Nucleus Deep Brain Stimulation in Parkinson Disease

Author Affiliations
  • 1Movement Disorders Group, Department of Neurology, University of São Paulo, São Paulo, Brazil
  • 2Pain Center, Department of Neurology, University of São Paulo, São Paulo, Brazil
JAMA Neurol. 2015;72(8):948. doi:10.1001/jamaneurol.2015.0902

To the Editor We read with interest the article by Jung et al1 reporting the effects of subthalamic nucleus deep brain stimulation (STN DBS) on pain characteristics in patients with Parkinson disease (PD) after an 8-year follow-up. These findings provide new insights into the mechanisms by which DBS improves pain and its long-term effects.

Despite the beneficial long-term effects of STN DBS on pain in patients with PD, some considerations should be pointed out. Although the overall pain intensity improved, pain prevalence increased from 67% to 83%, and new-onset pain developed in most of the patients during the 8-year follow-up. Common reasons associated with chronic pain incidence in the general population (eg, diabetic neuropathy and osteoarthritis) were largely ignored in the article.1 Nevertheless, the number of patients reporting fluctuations in pain with motor symptoms (fluctuating pain) decreased significantly after surgery, suggesting that DBS could improve motor fluctuations and pain by different mechanisms.2 In addition, while dystonic pain responded well to DBS (usually presenting during off periods), other syndromes, such as neuropathic and musculoskeletal pain, did not seem to do so. The authors concluded that musculoskeletal pain does not respond to STN DBS.1 We found strikingly different data 1 year after DBS in a group of 41 patients with PD prospectively assessed for the effects of DBS in nonmotor symptoms.2 These differences probably resulted from a lack of validation and specificity of current classifications of pain in PD. There is currently no validated pain classification system for PD pain that takes into account the various aspects of pain,3 its impact on daily activities,4 the presence of neuropathic pain as it is presently defined,5 or standardized information on the presence of pain fluctuation according to motor symptom swings. Also, secondary hyperalgesia in areas of referred pain from myofascial trigger points are frequently overlooked2 and may lead to the overdiagnosis of central pain, which itself does not have formal diagnostic criteria or a validated definition.

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