Dementia and survival in Parkinson disease

Section of Geriatric Psychiatry, Stavanger University Hospital, Arm Hansen v 20, N-4095 Stavanger, Norway.
Neurology (Impact Factor: 8.29). 04/2008; 70(13):1017-22. DOI: 10.1212/01.wnl.0000306632.43729.24
Source: PubMed


The risk for dementia in Parkinson disease (PD) is high, with important clinical consequences for patients with PD. However, the absolute risk of dementia and how it affects survival in PD are not known. Such questions are important for patients, their families, and service providers but require long-term studies.
This study is a prospective longitudinal cohort study with patients from a prevalence study of PD in Norway. Patients were reassessed 4, 8, 9, 10, 11, and 12 years after prevalence day. A dementia diagnosis according to Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised, criteria was based on a semistructured caregiver interview, cognitive rating scales, and neuropsychological tests. Progression from PD to PD with dementia and death was modeled using a continuous-time three-state irreversible Markov model.
A total of 233 PD patients were included, and 140 patients (60%, 95% CI 54% to 66%) had developed dementia by the end of the study period. The cumulative incidence of dementia steadily increases with age and duration of PD and, conditional on survival, increases to 80% to 90% by age 90 years. Women live with PD longer than men and spend more years with dementia. At age 70 years, a man with PD but no dementia has a life expectancy of 8 years, of which 5 years would be expected to be dementia free and 3 years would be expected to be with dementia.
Dementia is a key part of survival in Parkinson disease and must be planned for in services for this condition.

34 Reads
  • Source
    • "Prospective studies suggest that a considerable percentage of PD patients without cognitive impairment develop MCI just a few years after diagnosis (Broeders et al., 2013; Hobson & Meara, 2015). Following the onset of MCI, PD patients have a higher risk of developing dementia (Aarsland, Andersen, Larsen, Lolk, & Kragh-Sørensen, 2003; Buter et al., 2008; Janvin, Aarsland, & Larsen, 2005; Reid, Hely, Morris, Loy, & Halliday, 2011; Williams-Gray et al., 2013). These findings indicate that the course of PD involves continuum that goes from normal cognition to MCI to dementia. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Several studies have recently shown that basal ganglia (BG) deterioration leads to distinctive impairments in the domains of syntax, action verbs, and action semantics. In particular, such disruptions have been repeatedly observed in Parkinson's disease (PD) patients. However, it remains unclear whether these deficits are language-specific and whether they are equally dissociable from other reported disturbances -viz., processing of object semantics. To address these issues, we administered linguistic, semantic, and executive function (EFs) tasks to two groups of non-demented PD patients, with and without mild cognitive impairment (PD-MCI and PD-nMCI, respectively). We compared these two groups with each other and with matched samples of healthy controls. Our results showed that PD patients exhibited linguistic and semantic deficits even in the absence of MCI. However, not all domains were equally related to EFs and MCI across samples. Whereas EFs predicted disturbances of syntax and object semantics in both PD-nMCI and PD-MCI, they had no impact on action-verb and action-semantic impairments in either group. Critically, patients showed disruptions of action-verb production and action semantics in the absence of MCI and without any executive influence, suggesting a sui generis deficit present since early stages of the disease. These findings indicate that varied language domains are differentially related to the BG, contradicting popular approaches to neurolinguistics. Copyright © 2015 Elsevier Ltd. All rights reserved.
    Cortex 06/2015; 69. DOI:10.1016/j.cortex.2015.05.022 · 5.13 Impact Factor
  • Source
    • "A recent study documented that 70% of EPD patients showed normal cognitive performance (Elgh et al., 2009) and what deficits they do have tend to be mild (Lees and Smith, 1983; Owen, 2004). In contrast, prevalence of dementia in PD patients surviving past 90 years of age is over 80% (Buter et al., 2008). It is therefore more likely that performance of EPD patients on tasks of emotion recognition reflects the specific integrity of these emotion-related processes. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Parkinson’s disease (PD) is traditionally regarded as a neurodegenerative movement disorder, however, nigrostriatal dopaminergic degeneration is also thought to disrupt non-motor loops connecting basal ganglia to areas in frontal cortex involved in cognition and emotion processing. PD patients are impaired on tests of emotion recognition, but it is difficult to disentangle this deficit from the more general cognitive dysfunction that frequently accompanies disease progression. Testing for emotion recognition deficits early in the disease course, prior to cognitive decline, better assesses the sensitivity of these non-motor corticobasal ganglia-thalamocortical loops involved in emotion processing to early degenerative change in basal ganglia circuits. In addition, contrasting this with a group of healthy aging individuals demonstrates changes in emotion processing specific to the degeneration of basal ganglia circuitry in PD. Early PD patients (EPD) were recruited from a randomized clinical trial testing the safety and tolerability of deep brain stimulation of the subthalamic nucleus (STN-DBS) in early-staged PD. EPD patients were previously randomized to receive optimal drug therapy only (ODT), or drug therapy plus STN-DBS (ODT+DBS). Matched healthy elderly controls (HEC) and young controls (HYC) also participated in this study. Participants completed two control tasks and three emotion recognition tests that varied in stimulus domain. EPD patients were impaired on all emotion recognition tasks compared to HEC. Neither therapy type (ODT or ODT+DBS) nor therapy state (ON/OFF) altered emotion recognition performance in this study. Finally, HEC were impaired on vocal emotion recognition relative to HYC, suggesting a decline related to healthy aging. This study supports the existence of impaired emotion recognition early in the PD course, implicating an early disruption of fronto-striatal loops mediating emotional function.
    Frontiers in Aging Neuroscience 12/2014; 6(349). DOI:10.3389/fnagi.2014.00349 · 4.00 Impact Factor
  • Source
    • "In PD, the cognitive deficits are usually restricted to disturbances in executive functioning and visuospatial tasks. In up to 60% of these PD patients, the cognitive decline evolves into dementia, called Parkinson's disease related dementia (PDD) [1]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Dysfunction of the cholinergic neurotransmitter system is present in Parkinson's disease, Parkinson's disease related dementia and dementia with Lewy bodies, and is thought to contribute to cognitive deficits in these patients. In vivo imaging of the cholinergic system in these diseases may be of value to monitor central cholinergic disturbances and to select cases in which treatment with cholinesterase inhibitors could be beneficial. The muscarinic receptor tracer [(123)I]iododexetimide, predominantly reflecting M1 receptor binding, may be an appropriate tool for imaging of the cholinergic system by means of SPECT. In this study, we used [(123)I]iododexetimide to study the effects of a 6-hydroxydopamine lesion (an animal model of Parkinson's disease) on the muscarinic receptor availability in the rat brain. Rats (n=5) were injected in vivo at 10-13days after a confirmed unilateral 6-hydroxydopamine lesion. Muscarinic receptor availability was measured bilaterally in multiple brain areas on storage phosphor images by region of interest analysis. Autoradiography revealed a consistent and statistically significant lower [(123)I]iododexetimide binding in all examined neocortical areas on the ipsilateral side of the lesion as compared to the contralateral side. In hippocampal and subcortical areas, such asymmetry was not detected. This study suggests that evaluation of muscarinic receptor availability in dopamine depleted brains using [(123)I]iododexetimide is feasible. We conclude that 6-hydroxydopamine lesions induce a decrease of neocortical muscarinic receptor availability. We hypothesize that this arises from down regulation of muscarinic postsynaptic M1 receptors due to hyperactivation of the cortical cholinergic system in response to dopamine depletion. In rats, dopamine depletion provokes a decrease in neocortical muscarinic receptor availability, which is evaluable by [(123)I]iododexetimide imaging. This study may further underline the role of a dysregulated muscarinic system in patients with Lewy body disorders.
    Nuclear Medicine and Biology 01/2014; 41(1):90-95. DOI:10.1016/j.nucmedbio.2013.10.003 · 2.41 Impact Factor
Show more

Similar Publications