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NI FEATURE: THE EDITORIAL DEBATE II-- PROS AND CONS
Year : 2019  |  Volume : 67  |  Issue : 2  |  Page : 393-394

Can cognitive decline be the nemesis of motor improvement secondary to deep brain stimulation?


Department of Neurological Surgery, Center for Neuromodulation, Neuroscience Research Institute, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA

Date of Web Publication13-May-2019

Correspondence Address:
Dr. Milind Deogaonkar
Center for Neuromodulation, 480 Medical Center Drive, Columbus, Ohio, 43210
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.258016

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How to cite this article:
Deogaonkar M. Can cognitive decline be the nemesis of motor improvement secondary to deep brain stimulation?. Neurol India 2019;67:393-4

How to cite this URL:
Deogaonkar M. Can cognitive decline be the nemesis of motor improvement secondary to deep brain stimulation?. Neurol India [serial online] 2019 [cited 2019 Jul 20];67:393-4. Available from: http://www.neurologyindia.com/text.asp?2019/67/2/393/258016




In this issue of the journal, Krishnan et al., discuss the results of their study about predictors of dementia-free survival after deep brain stimulation (DBS) in Parkinson's disease (PD). They conclude that an older age, a longer disease duration, a past history of depression or psychosis, freezing of gait in the OFF phase, worse activities of daily living (ADL) scores in the ON phase, a lower levodopa response of the Unified Parkinson's Disease Rating Scale (UPDRS) III axial subscores, and a poor performance in the Addenbrooke's Cognitive Examination and Wisconsin Card Sorting Test (WCST) were associated with shorter dementia-free survival. Among these, only freezing of gait and poor performance in WCST were independent predictors.[1]

DBS is an accepted therapy for treating motor symptoms of PD. It is considered as an intervention for alleviation of motor symptoms of PD in patients where medical therapy is maximized and not any more effective.[2] The goal of DBS implantation is to achieve maximal benefit (e.g., symptom relief) for the patient while avoiding or minimizing the likelihood of adverse effects.

After achieving an excellent motor control with DBS, the early onset of dementia results in failure of the intervention to achieve its stated goal of quality of life improvement. There are many studies that have looked into factors responsible for the early cognitive decline after DBS. In my view, the dementia-free survival after DBS depends on a host of factors that can be preoperative, intraoperative, or postoperative.

Pre-operative factors

As the study rightly points out, an older age, a longer disease duration, the past history of depression or psychosis, the freezing of gait in the OFF phase, worse ADL scores in the ON phase, a lower levodopa response of the UPDRS III axial subscores, and a poor performance in the Addenbrooke's Cognitive Examination and WCST are associated with early onset of dementia.

In addition, some imaging correlates like a smaller volume of left nucleus accumbens and larger volumes of lateral ventricles correlate with an early cognitive decline after DBS.[3] Multiple white matter lesions are also associated with an early cognitive decline after DBS.[4]

In a study at our institution, our team identified key factors like an age of ≥70 years, on anticoagulation therapy, behavioral problems unrelated to motor disease, cognitive impairment, requiring/receiving treatment for cardiopulmonary disease or other major systematic disease, frequent falls, poor social support, and need for bilateral treatment of motor disease symptoms, which were associated with a difficult postoperative course.

In the preoperative cognitive testing, global cognitive scores do not predict postoperative cognitive decline.[5] As this study points out, more focused tests like WCST are better predictors of cognitive decline. Early decline in verbal fluency after DBS is also not a predictor of early onset of postoperative cognitive decline.[6]

Intraoperative factors

Any surgery performed in patients with vulnerable cognition could result in failure due to the persistent postoperative cognitive decline. DBS surgery is not any different. Still there are certain factors that can increase the risk of cognitive decline. The electrode trajectory through or close to the caudate head can increase the risk of postoperative cognitive decline.[7] Multiple microelectrode penetrations through the same trajectory will cause increased disruption, thereby increasing that risk further. Bilateral subthalamic nucleus (STN) targets in patients with mild cognitive impairment will increase the risk of cognitive decline.[8]

Though some studies indicate that there is no difference in the early onset of dementia after STN or globus pallidus internus (GPi) DBS,[9],[10] in practice, we do see the procedure of STN DBS as being more likely to bring about an early cognitive decline.

Any intraparenchymal bleeding during surgery or a large pneumocephalus secondary to cerebral atrophy[11],[12] could also lead to an early cognitive decline.

Postoperative factors

Anterior STN is limbic. Anteriorly or very medially placed leads will cause cognitive and behavioral issues. Use of contacts close to the substantia nigra at the bottom of the STN will also cause behavioral changes.


  Conclusions Top


In conclusion, it is important to judge the cognitive reserve of patient before surgery and wisely choose a potential candidate for DBS with realistic expectations. I think the authors in the article by Krishnan et al.,[1] 'Predictors of dementia-free survival after deep brain stimulation (DBS) in Parkinson's disease' do make that point with excellent data.



 
  References Top

1.
Krishnan S, Pisharady KK, Rajan R, Sarma SG, Sarma PS, Kishore A. Predictors of dementia-free survival after bilateral subthalamic deep brain stimulation for Parkinson's disease. Neurol India 2019;67:459-66.  Back to cited text no. 1
  [Full text]  
2.
Rezai AR, Machado AG, Deogaonkar M, Azmi H, Kubu C, Boulis NM. Surgery for movement disorders. Neurosurgery 2008;62(Suppl 2):809-38.  Back to cited text no. 2
    
3.
Planche V, Munsch F, Pereira B, de Schlichting E, Vidal T, Coste J, et al. Anatomical predictors of cognitive decline after subthalamic stimulation in Parkinson's disease. Brain Struct Funct 2018;223:3063-72.  Back to cited text no. 3
    
4.
Blume J, Lange M, Rothenfusser E, Doenitz C, Bogdahn U, Brawanski A, et al. The impact of white matter lesions on the cognitive outcome of subthalamic nucleus deep brain stimulation in Parkinson's disease. Clin Neurol Neurosurg 2017;159:87-92.  Back to cited text no. 4
    
5.
Floden D, Busch RM, Cooper SE, Kubu CS, Machado AG. Global cognitive scores do not predict outcome after subthalamic nucleus deep brain stimulation. Mov Disord 2015;30:1279-83.  Back to cited text no. 5
    
6.
Borden A, Wallon D, Lefaucheur R, Derrey S, Fetter D, Verin M, et al. Does early verbal fluency decline after STN implantation predict long-term cognitive outcome after STN-DBS in Parkinson's disease? J Neurol Sci 2014;346:299-302.  Back to cited text no. 6
    
7.
Witt K, Granert O, Daniels C, Volkmann J, Falk D, van Eimeren T, et al. Relation of lead trajectory and electrode position to neuropsychological outcomes of subthalamic neurostimulation in Parkinson's disease: Results from a randomized trial. Brain 2013;136:2109-19.  Back to cited text no. 7
    
8.
Kim HJ, Jeon BS, Paek SH, Lee KM, Kim JY, Lee JY, et al. Long-term cognitive outcome of bilateral subthalamic deep brain stimulation in Parkinson's disease. J Neurol 2014;261:1090-6.  Back to cited text no. 8
    
9.
Boel JA, Odekerken VJ, Schmand BA, Geurtsen GJ, Cath DC, Figee M, et al. Cognitive and psychiatric outcome 3 years after globus pallidus pars interna or subthalamic nucleus deep brain stimulation for Parkinson's disease. Parkinsonism Rel Dis 2016;33:90-5.  Back to cited text no. 9
    
10.
Ardouin C, Pillon B, Peiffer E, Bejjani P, Limousin P, Damier P, et al. Bilateral subthalamic or pallidal stimulation for Parkinson's disease affects neither memory nor executive functions: A consecutive series of 62 patients. Ann Neurol 1999;46:217-23.  Back to cited text no. 10
    
11.
Azmi H, Machado A, Deogaonkar M, Rezai A. Intracranial air correlates with preoperative cerebral atrophy and stereotactic error during bilateral STN DBS surgery for Parkinson's disease. Stereotac Funct Neurosurg 2011;89:246-52.  Back to cited text no. 11
    
12.
Muthuraman M, Deuschl G, Koirala N, Riedel C, Volkmann J, Groppa S. Effects of DBS in parkinsonian patients depend on the structural integrity of frontal cortex. Sci Rep 2017;7:43571.  Back to cited text no. 12
    




 

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