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Table of Contents    
Year : 2019  |  Volume : 67  |  Issue : 2  |  Page : 395-396

Dementia in Parkinson's disease after subthalamic deep brain stimulation - Is it inevitable and predictable?

Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India

Date of Web Publication13-May-2019

Correspondence Address:
Dr. Dwarakanath Srinivas
National Institute of Mental Health and Neurosciences, Bangalore - 560 011, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.258018

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How to cite this article:
Srinivas D. Dementia in Parkinson's disease after subthalamic deep brain stimulation - Is it inevitable and predictable?. Neurol India 2019;67:395-6

How to cite this URL:
Srinivas D. Dementia in Parkinson's disease after subthalamic deep brain stimulation - Is it inevitable and predictable?. Neurol India [serial online] 2019 [cited 2020 Sep 27];67:395-6. Available from:

Krishnan et al.,[1] have presented an excellent article focusing on the predictors of dementia-free survival after bilateral subthalamic deep brain stimulation (STN-DBS) in Parkinson's disease (PD). In this analysis of 116 patients, with a 542-person year follow-up, operated with a mean duration of PD prior to undergoing surgery of 11.2 (±4.2) years, 30 patients developed dementia. The mean dementia-free survival after surgery was 8.7 years.

In the univariate analysis, the baseline factors of older age, longer disease duration, past history of depression or psychosis, freezing of gait in the OFF phase, worse activities of daily living (ADL) scores in the ON phase, lower levodopa response as assessed by the Unified Parkinson's Disease Rating Scale (UPDRS) III axial sub-scores, and a poor performances in the Addenbrooke's Cognitive Examination and Wisconsin Card Sorting Test (WCST) were associated with a shorter dementia-free survival. Among these, only freezing of gait and a poor performance in the WCST score were independent predictors

Dementia in PD, though classically absent at diagnosis, has been a major concern over the course of the disease. This parameter, along with the other non-motor symptoms, such as autonomic failure, hypersomnolence, imbalance, and drug-related neuropsychiatric disturbances are a major cause of morbidity and mortality in these patients. The Sydney multicentre study of PD by Hely et al.,[2] is an excellent review of the natural course of PD in a single cohort of 136 newly diagnosed patients with PD over a period of 20 years. Dementia was present in 83% of the patients (25/30) at 20 years. Approximately 50% of the 17 patients (8/17) who had undergone a post-mortem histopathological assessment had diffuse Levy body disease. Also, 70% of the patients were demented before they expired, prior to 20 years. The mean onset of dementia after the diagnosis had been established was 10.9 years, and once diagnosed, the median survival was 54 months. Another interesting fact was that the neurologists actually underestimated the prevalence of dementia in these patients, as the neuropsychological criteria were reached earlier than that assessed on the mini-mental scale examination (MMSE).

Hobson et al.,[3] in a community cohort of 86 patients, found the risk of developing dementia in 5.1% of the patients. An increasing age, the later age of onset of PD, the longer duration of PD symptoms, the presence of hallucinations, and the impairment of memory and language functions, were all predictive factors for the development of dementia. Zetusky et al.,[4] and Zankovic et al., in the Datatops cohort[5] opined that that different PD clinical phenotypes have different progress and prognosis. Patients with tremor predominant phenotypes had a milder disease course. Kempster et al.,[6] observed that younger patients with a more severe motor fluctuation showed a more rapid disease evolution than that seen in older patients with non-fluctuating motor symptoms.

While deep brain stimulation (DBS) has a maximal response on the cardinal symptoms of PD, namely, tremor, rigidity, bradykinesia and drug induced dyskinesias, whether or not DBS actually slows down the progression of the disease has been a matter of debate. Merola et al.,[7] in their study of 19 patients operated after an average duration of 22.84 years of PD, did not find evidence that DBS slows down the progress of dementia. In fact, 70% of the operated patients showed dementia, falls, dysphagia or urinary incontinence at 30 years after the disease onset. However, Fasano and colleagues[8] found a lower incidence of dementia and postural instability at 5 and 8 years after surgery. Moro et al.,[9] however, observed the progressive development of non-levodopa responsive symptoms over 5-6 years of evaluation. Also, several studies[10],[11],[12] have presented data that hypothesise that the age of surgery, the disease duration and the age at onset of PD, may play a significant role in determining the long-term outcome after the performance of STN DBS.

Some studies have been published with a long-term follow-up data of up to 10 years after surgery.[13],[14],[15] Their results indicated the persistent effect of stimulation on the core motor symptoms. An increase in the disability and cognitive impairment due to disease progression, however, persisted.

While ageing has been suggested as a prognostic factor for determining the neurosurgical outcome, studies addressing the issue of long-term clinical evolution in early versus late STN DBS are lacking. Janssen et al.,[16] analysed the motor and neuropsychological outcome after 10 years of STN DBS for PD. When they analysed the cognitive outcomes, mood and behaviour, they found that the relative scores on learning, recall and decrease in learning occurred between 5-10 years after surgery. The mini mental state examination (MMSE) and Beck depression inventory (BDI-II) scores were relatively stable after 10 years. Thus, they concluded that STN-DBS cannot prevent the cognitive decline that occurred along the course of the disease.

While there is no evidence to suggest that DBS in PD slows down the onset of the disease, there are many studies which have presented data to show that STN-DBS in PD does not alter the natural course of the disease. However, it is important to prognosticate the occurrence of dementia after STN-DBS in PD, as the patient can be counselled regarding the expectations and outcomes after surgery. It should be emphasised that STN DBS is, at best, performed for managing the cardinal symptoms of PD, while the course of the cognitive and non-motor symptoms will not be altered. In this aspect, this article by Krishan et al.,[1] helps us in developing better understanding of the long-term outcomes after STN-DBS and is an important addition to the literature.

  References Top

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]  
Hely MA, Reid WG, Adena MA, Halliday GM, Morris JG. The Sydney multicenter study of Parkinson's disease: The inevitability of dementia at 20 years. Mov Disord 2008; 23:837-44.  Back to cited text no. 2
Hobson P, Meara J. Risk and incidence of dementia in a cohort of older subjects with Parkinson's disease in the United Kingdom. Mov Disord 2004; 19:1043-9.  Back to cited text no. 3
Zetusky WJ, Jankovic J, Pirozzolo FJ. The heterogeneity of Parkinson's disease: Clinical and prognostic implications. Neurology 1985; 35:522-6.  Back to cited text no. 4
Jankovic J, McDermott M, Carter J, Gauthier S, Goetz C, Golbe L, et al. Variable expression of Parkinson's disease: A baseline analysis of the DATATOP cohort. The Parkinson study group. Neurology1990; 40:1529-34.  Back to cited text no. 5
Kempster PA, Williams DR, Selikhova M, Holton J, Revesz T, Lees AJ. Patterns of levodopa response in Parkinson's disease: A clinico-pathological study. Brain 2007; 130:2123-8.  Back to cited text no. 6
Merola A, Zibetti M, Angrisano S, Rizzi L, Ricchi V, Artusi CA, et al. Parkinson's disease progression at 30 years: A study of subthalamic deep brain-stimulated patients. Brain 2011; 134; 7:2074-84.  Back to cited text no. 7
Fasano A, Romito LM, Daniele A, Piano C, Zinno M, Bentivoglio AR, et al. Motor and cognitive outcome in patients with Parkinson's disease 8 years after subthalamic implants. Brain2010; 133:2664-76.  Back to cited text no. 8
Moro E, Lozano AM, Pollak P, Agid Y, Rehncrona S, Volkmann J, et al. Long-term results of a multicenter study on subthalamic and pallidal stimulation in Parkinson's disease. Mov Disord 2010; 25:578-86.  Back to cited text no. 9
Welter ML, Houeto JL, Tezenas du Montcel S, Mesnage V, Bonnet AM, Pillon B, et al. Clinical predictive factors of subthalamic stimulation in Parkinson's disease. Brain 2002; 125:575-83.  Back to cited text no. 10
Derost PP, Ouchchane L, Morand D, Ulla M, Llorca PM, Barget M, et al. Is DBS-STN appropriate to treat severe Parkinson disease in an elderly population? Neurology 2007; 68:1345-55.  Back to cited text no. 11
Russmann H, Ghika J, Villemure JG, Robert B, Bogousslavsky J, Burkhard PR, et al. Subthalamic nucleus deep brain stimulation in Parkinson disease patients over age 70 years. Neurology 2004; 63:1952-4.  Back to cited text no. 12
Zibetti M, Merola A, Rizzi L, Ricchi V, Angrisano S, Azzaro C, et al. Beyond nine years of continuous subthalamic nucleus deep brain stimulation in Parkinson's disease. Mov Disord 2011; 26:2327-34.  Back to cited text no. 13
Castrioto A, Lozano AM, Poon YY, Lang AE, Fallis M, Moro E. Ten-year outcome of sub- thalamic stimulation in Parkinson disease: A blinded evaluation. Arch Neurol 2011; 68:1550-56.  Back to cited text no. 14
Zangaglia R, Pasotti C, Mancini F, Servello D, Sinforiani E, Pacchetti C. Deep brain stimulation and cognition in Parkinson's disease: An eight-year follow-up study. Mov Disord 2012; 27:1192-94.  Back to cited text no. 15
Janssen ML, Duits AA, Turaihi AH, Ackermans L, Leentjens AF, Leentjes AF, et al. Subthalamic nucleus high-frequency stimulation for advanced Parkinson's disease: Motor and neuropsychological outcome after 10 years. Stereotact Funct Neurosurg 2014; 92:381-7.  Back to cited text no. 16


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