Cognitive Impairment and

Dementia in Parkinson
Disease
a,b, c,d
Jennifer G. Goldman, MD, MS *, Erica Sieg, PsyD

KEYWORDS
 Biomarker  Dementia  Diagnostic criteria  Executive function  Memory
 Mild cognitive impairment  Neuropsychological assessment

KEY POINTS
 Cognitive impairment in Parkinson disease (PD) is heterogeneous in its symptoms,
severity, and progression and can occur from early to advanced stages of the disease.
 Evaluation of cognitive impairment in PD includes the clinician’s assessment, patient and
informant report, and frequently more formalized neuropsychological testing of specific
cognitive domains.
 Optimal management of PD cognitive impairment encompasses a multidisciplinary
approach using pharmacologic, nonpharmacologic, and psychosocial strategies to
address patient and care partner needs.

INTRODUCTION

Cognitive impairment is a frequent nonmotor symptom in Parkinson disease (PD),

often associated with poor outcomes and reduced quality of life.1–3 Cognitive impair-
ment in PD can be heterogeneous in its symptoms, severity, and progression, ranging
from subtle changes to mild cognitive impairment (PD-MCI) to more severe deficits as
in dementia (PDD), and can be present from early on to more advanced stages of the
disease. The cognitive symptoms experienced in PD may reflect neurochemical
changes in dopaminergic, cholinergic, noradrenergic, serotonergic, and other neuro-
transmitter systems as well as pathologic changes such as Lewy bodies, Lewy

This article was to appear in Clinics in Geriatric Medicine, Volume 36, Issue 1, February 2020.
a
Parkinson’s Disease and Movement Disorders, Shirley Ryan AbilityLab, 355 East Erie Street,
Chicago, IL 60611, USA; b Departments of Physical Medicine and Rehabilitation and Neurology,
Northwestern University Feinberg School of Medicine, 710 North Lake Shore Drive, Chicago, IL
60611, USA; c Neuropsychology, Department of Psychiatry and Behavioral Sciences, North-
western University Feinberg School of Medicine, 710 North Lake Shore Drive, Chicago, IL 60611,
USA; d Department of Neurology, Northwestern University Feinberg School of Medicine, 710
North Lake Shore Drive, Chicago, IL 60611, USA
* Corresponding author.
E-mail address: jgoldman02@sralab.org

Clin Geriatr Med 36 (2020) 365–377

https://doi.org/10.1016/j.cger.2020.01.001 geriatric.theclinics.com
0749-0690/20/ª 2020 Elsevier Inc. All rights reserved.
366 Goldman & Sieg

neurites, and coexistent Alzheimers pathology (amyloid and tau) and cerebrovascular
disease. To date, medications have been geared to symptomatic treatment, albeit
with modest effects, and the field awaits successful disease-modifying or curative
treatments. Management of cognitive impairment in PD encompasses many different
components including appropriate diagnosis, counseling, and prognostication; incor-
porating pharmacologic, nonpharmacologic, and psychosocial strategies; and
addressing the needs of the person living with PD and their care partners. This review
covers key points regarding the phenotype, diagnosis, evaluations, and management
of PD cognitive impairment.

CHARACTERISTICS AND FREQUENCY

Cognitive impairment in PD demonstrates a broad range of severity, rate of progres-

sion, and affected cognitive domains.4 Phenotypic severity ranges from subtle
changes such as bradyphrenia, slower processing, or subjective cognitive complaints
without objective evidence of cognitive dysfunction to PD-MCI, in which cognitive def-
icits greater than typical for normal aging are evident on standardized neuropsycho-
logical testing and reflect a decline from prior functioning but do not significantly
interfere with daily functioning and to PDD, in which more severe cognitive deficits
occur, affect more than one domain, and significantly interfere with activities of daily
living. The frequency of subjective complaints is not well defined in PD, but self-
reported difficulties in cognition or memory in PD may also be associated with depres-
sion and anxiety.5,6 Subjective cognitive complaints should be monitored as they may
herald cognitive decline and are often accompanied, although not always, with objec-
tive changes.7–9 The frequency of MCI in newly diagnosed patients with PD is about
15% to 25%.10–15 In prevalent cases of patients with PD (ie, not newly diagnosed)
MCI occurs in 20% to 60%, mean 26%.4,16 MCI in PD increases the risk of conversion
to dementia 6-fold, and point prevalence estimates of PDD are about 30% to
40%.17,18 Although progression to dementia is not inevitable, it develops in up to
80% of patients with longer PD durations, particularly after 15 to 20 years.17,19–21
Risk factors for PDD include advanced age, older age of disease onset, predominant
gait dysfunction, hallucinations, baseline cognitive impairment or PD-MCI, and limited
cognitive reserve.17,19,20 PDD is often accompanied by behavioral features such as
apathy, mood disorders, excessive daytime sleepiness, and psychosis.17
A desire to improve long-term outcomes by delivering therapeutic interventions
earlier in the clinical course or to those at highest risk of dementia has led to a major
research focus on PD-MCI.22 Although not all individuals with PD-MCI go on to
develop PDD, many do, and some even decline more rapidly. Therefore, identifying
patients with PD-MCI has importance for clinical care, management, and potential
intervention trials.23 The International Parkinson and Movement Disorder Society
(MDS) developed diagnostic criteria for evaluating PD-MCI.24 PD-MCI criteria include
2 levels of comprehensiveness: level I based on an abbreviated assessment (limited
battery or scale of global cognitive abilities) and level II based on comprehensive neu-
ropsychological evaluation permitting MCI subtyping.23,25 The MDS PD-MCI Valida-
tion Study Group demonstrated that PD-MCI, when assessed using level II
evaluation, independently increased the hazard of PDD 3.46 (95% confidence interval
0.37–2.11) after accounting for various other effects (age, sex, years of education,
depression, severity of PD motor signs).23 However, access to resources, time,
cost, or a patient’s ability to cooperate with longer neuropsychological assessments
may preclude level II comprehensive assessment for some patients. Alternatively,
PD-MCI can be evaluated with a level I screening or limited assessment. Several
 Cognitive Impairment and Dementia 367

measures of global cognitive abilities have been studied in PD-MCI, although they vary
in their sensitivity and specificity in detecting PD-MCI.24,26,27 In another study, the
MDS PD-MCI Validation Study Group determined that level I PD-MCI, assessed by
a limited neuropsychological battery, also independently contributes to the hazard
of developing PDD, and level I and level II PD-MCI classifications have similar discrim-
inative ability with respect to time to PDD.28
Regarding the underpinnings of cognitive impairment in PD and PDD, dopamine
depletion in the nigrostriatal pathways has been implicated in impaired working mem-
ory, planning/sequencing, task switching, response inhibition, memory recall, verbal
fluency, and psychomotor speed.4 However, impairments in amnestic memory, lan-
guage (particularly semantic aspects including action verb naming), and visuospatial
impairment, with the latter two showing high sensitivity in detecting transition to
PDD,10,29 implicate other neurotransmitter systems including acetylcholine (particularly
in PDD neuropathology studies), noradrenaline, and serotonin. The “dual syndrome
hypothesis” has been proposed to explain differences in cognitive phenotype and pro-
gression in PD: (1) in some, there is greater frontal-striatal network dysfunction, modu-
lated by dopamine, lending to deficits in attention, working memory, planning, and
response inhibition; this can be present early on in the disease or in some, remain the
predominant features with little progression over time; and (2) greater posterior cortical
degeneration, associated with greater cholinergic loss, wherever present, lending to de-
mentia; in some, greater memory, language, and visuospatial impairment predominate
and may confer a higher risk of developing dementia.30
Of note, although not covered here, whether PDD and dementia with Lewy bodies
(DLB) are the same or distinct entities based on the presence of cognitive impairments
in prodromal and preclinical PD and overlapping clinical manifestations of motor and
cognitive symptoms for DLB has been debated, although the “1-year rule” has been
retained in recently updated DLB criteria.31–33 In addition, supporting a DLB and
PDD continuous spectrum, neuropsychological testing shows no significant differ-
ences in performance (both PDD and DLB showed severe deficits in executive func-
tioning, visual-spatial processing, and verbal learning), with neuropsychological
performance not able to reliably account for relative timing of motor diagnosis versus
diagnosis of dementia.
Neuropathology studies support the dual hypothesis for cognitive impairment in PD.
One postmortem study showed only 38% of patients with PDD had “pure” or exclusive
Lewy body pathology, but 59% presented with combined Lewy body and beta-
amyloid plaques and 3% showed Lewy bodies, beta-amyloid plaques, and neurofibril-
lary tangles.21,34 A significant positive relationship between cortical beta-amyloid
deposition and cognitive impairment exists, and 30% of nondemented PD cases
show beta amyloid accumulation.21,35,36
These multiple overlapping pathologies, however, occur in a complex framework of
multiple neurotransmitter deficiencies and presence of genetic risk factors for demen-
tia such as alpha-synuclein duplication/triplication mutations, the apolipoprotein E
epsilon 4 allele, the glucocerebrosidase gene, and microtubule-associated protein
tau H1 haplotype.21,37–39 The multiple overlapping pathologies, neurotransmitter defi-
ciencies, and genotypes all likely contribute to the heterogeneity of cognitive deficits
presentation in PD and PDD.

CLINICAL ASSESSMENT OF COGNITION IN PARKINSON DISEASE

Clinical evaluation of cognition in PD begins with routine inquiry, whether informal

with questions and “bedside” testing in the clinic or more formalized with global
368 Goldman & Sieg

screening, rating scales, or neuropsychological testing. Cognitive decline can be re-

ported by either the patient or informant or observed by the clinician.24 It is important
to understand whether cognitive symptoms represent a change from the patient’s
premorbid level, whether by inquiry (eg, is this a new symptom or has the person
had trouble in this area before?) or more formal assessment of premorbid intelligence
such as the Wechsler Test of Adult Reading or National Adult Reading Test. Eliciting
corroborating information and examples of the cognitive changes from an informant
can be helpful. One should note that mismatches between patient and informant
report can occur, with different estimations of cognitive impairment and contribu-
tions to everyday tasks; one may need to consider the cognitive functioning of infor-
mants as well.40 “Bedside” tests such as global cognitive screening scales (Montreal
Cognitive Assessment [MoCA], Mini-Mental Status- Examination [MMSE], Scales for
Outcomes in Parkinson’s Disease-Cognition, and Parkinson’s Disease-Cognitive
Rating Scale) or variations on delayed recall, phonemic and semantic fluency, clock
drawing, and others may be used. Neuropsychological evaluation, however, remains
the gold standard for formalized cognitive assessment, as discussed later. For the
diagnosis of PD-MCI and PDD, assessment of functional impairment as related to
cognitive symptoms constitutes an essential component with significant interference
of cognitive deficits, with functional independence being a hallmark of dementia.
Several scales assess functional impairment in PD, including the Penn Daily Activ-
ities Questionnaire patient and informant versions, the Parkinson’s Disease-
Cognitive Functional Rating Scale, Functional Assessment Questionnaire, and the
pill questionnaire.41–44
Other contributors to cognitive changes in PD should be considered and
assessed where appropriate. These include comorbid medical and neurologic
issues such as cerebrovascular disease, B12 deficiency, thyroid dysfunction, auto-
immune disease, head injury, subdural hematoma, and impaired vision or hearing,
among others. When there are acute cognitive changes, excluding infections
(urinary tract infection, pneumonia), metabolic abnormalities, subdural hematoma,
or acute medical reasons and certain medications (increased PD medication doses;
use of anticholinergics, amantadine, and dopamine agonists; use of overactive
bladder medications, pain medications, or other central nervous system–acting
agents) should occur and may reveal the reason for the abrupt mental status
change. It is important to inquire about mood (depression, anxiety), sleep disorders,
fatigue, psychosis, and orthostatic hypotension in PD, as these features frequently
overlap in PD and can be associated with cognitive impairment. Depression has
been associated with cognitive impairment and may share linked inflammatory-
immune responses45; higher anxiety scores have been associated with poorer
set-shifting in PD46; and apathy and executive dysfunction have common clinical
features and neural substrates.47 Orthostatic hypotension and cognitive impairment
in PD are interrelated on multiple levels, for example, acute and chronic effects of
cerebral hypoperfusion, associations between white matter hyperintensities and
postural drops in blood pressure, and underlying synuclein and neurochemical al-
terations in the locus ceruleus.48 To date, biomarkers such as neuroimaging (struc-
tural and functional MRI; nuclear medicine imaging assessing glucose metabolism
and blood flow, cholinergic deficits, and amyloid deposition), electroencephalo-
gram, and cerebrospinal fluid assessing amyloid-beta, tau, phosphor-tau, and syn-
uclein levels, plasma for homocysteine, epidermal growth factor, brain-derived
neurotrophic factor, and others play a role in research regarding PD cognitive
impairment but have not yet been incorporated into clinical or diagnostic evaluation
of PD cognitive impairment.49–51
 Cognitive Impairment and Dementia 369

NEUROPSYCHOLOGICAL ASSESSMENT OF COGNITION IN PARKINSON DISEASE

Many longitudinal studies focused on PD cognition, to date, provide data over a rela-
tively short period of time (4–5 years), focus on change in global cognitive state using
the MMSE, or have highly varied use of neuropsychological tests across studies
(Table 1).52 Medium-to-strong effect sizes can only be found in studies with follow-
up intervals of 4 years or longer.52 In addition, a lack of consensus regarding neuro-
psychological tests exists with respect to use of composite versus individual tests
or subtest scores and the interpretation of meaningful change, test score abnormal-
ities, and cognitive phenotyping.22,52 These aspects emphasize the need for the
assessment of larger PD cohorts over longer periods of time, with comprehensive,
agreed-upon neuropsychological batteries interpreted in a standardized manner.22,52
Although not a substitute for comprehensive neuropsychological testing, the MDS
Task Force in their rating scale review recommends 3 global screening scales for use
with PD: (1) MoCA, (2) Mattis Dementia Rating Scale Second Edition, and (3) the Par-
kinson’s Disease-Cognitive Rating Scale.27 Neuropsychological assessments are
discussed in detail later; however, caveats exist for normative limitations of screening
instrument’s cutoff scores for cognitive impairment applied to international/multicultural
populations, and using neuropsychological assessment to detect PD compared with
published norms only, rather than site-specific healthy controls.53,54 A PD-specific
cognitive battery with accurate normative data appropriate for multisite international
studies, sensitive to cognitive decline and response to therapeutic intervention, requires
additional research beyond several that have been proposed.53,55

DEEP BRAIN STIMULATION, COGNITION, AND NEUROPSYCHOLOGICAL

ASSESSMENT

Deep brain stimulation (DBS) is a relatively safe, effective treatment of some PD motor
symptoms and treatment-related complications and is often associated with quality-
of-life gains.56 Most DBS centers require neuropsychological evaluations before (and
less often, after) surgery to provide information to make reasonable risk-benefit as-
sessments regarding surgery.56,57
Adverse events (AE) in DBS are usually related to the procedure, device, or stimu-
lation or are unrelated (such as medications or disease progression).56 Regarding
cognitive or neurobehavioral changes, clinicians may underestimate symptomatic
AEs, interrater reliability may be poor, and AE rates tend to increase as a function of
length of follow-up in a progressive condition such as PD.56,58 Neuropsychologists
must consider the extent a patient’s demographics, disease, and neuropsychological
characteristics resemble those enrolled in DBS clinical trials, as these tend to have
greater homogeneity than generally found in clinical practices.56,59 As such, in clinical
practice, there may be different rates, magnitude, or severity of AEs (or possibly pos-
itive outcomes).56
Presently, regarding cognitive outcomes of DBS, literature indicates a minority of
patients (10%–15%) may experience declines on multiple cognitive measures (verbal
fluency being most common). Typically mild cognitive changes do not preclude, but
rather attenuate, quality-of-life gains and serious adverse events occur in only less
than 1% to 2% of patients.56 However, those with MCI before DBS may experience
greater development of dementia, which may possibly reflect disease progression,
but this is not yet clear. PD-MCI as an overall construct may not affect cognitive out-
comes, but MCI affecting specific domains (which potentially indicates greater extra-
striatal neuropathology) including attention, executive functions, visual spatial, and
memory impairments before DBS may confer cognitive decrements after DBS,
370 Goldman & Sieg
Table 1
Cognitive domains affected in Parkinson disease, their neuroanatomical correlates, and
potential neuropsychological tests for evaluation
Cognitive Neuroanatomical Correlates of
Domains Cognitive Dysfunction
Wakefulness, State-Dependent Networks
Arousal,  Midbrain neurotransmitter
Attentional/ projection networks
Executive Thalamus & Basal Ganglia
Frontal Networks
 Dorsolateral frontal cortex
 Ventromedial frontal cortex
 Subcortical white matter
projections between frontal
lobes and other cortical areas
Speech & Language Left Perisylvian Language Area
 Broca’s
 Wernicke’s
 Anterior temporal
 Angular gyrus
Visuospatial Parietal lobe (spatial distribution
of attention, right hemisphere)
Occipito-temporal (object
perception/recognition)
Memory Limbic Memory System
 Hippocampus
 Entorhinal and
parahippocampal cortices
 Amygdala
 Thalamic and hypothalamic
nuclei
Examples of Neuropsychological
Tests for Assessing the Cognitive
Domains
Orientation
 WMS-III Orientation
Attention/Working Memory
Processing Speed
 WAIS-IV Digit Span, Letter
Number Sequencing
 Trail Making Test A
 Stroop Test
Executive Attention
 Trail Making Test B
 Luria’s 3-step hand sequence
Concept Formation
 WAIS-IV Similarities, Matrix
Reasoning
 Wisconsin Card Sorting Test
(WCST)
 Booklet Category Test (BCT)
 Tower of London (TOL)
Verbal Fluency (FAS & Animals)
Boston Naming Test (BNT)
Neuropsychological Assessment
Battery (NAB) Naming Test
Aphasia Batteries
 Western Aphasia Battery (WAB)
 Boston Diagnostic Aphasia
Examination (BDAE)
Tests of Spatial Perception
 Target cancellation
 Line bisection
 Judgment of Line Orientation
Tests of Object Perception
 Visual Object and Space
Perception (VOSP) Battery
 Facial Recognition Test
Tests of Constructions
 WAIS-IV Block Design,
 Visual puzzles
 Figure copy tests
 Rey Auditory Verbal Learning
Test (RAVLT)
 Hopkins Verbal Learning Test
(HVLT)
 California Verbal Learning Test
(CVLT)
 WMS-IV Logical Memory
 Rey Osterrieth Complex
Figure Test (RCFT)
 Brief Visual Memory Test (BVMT)
 WMS-IV Designs and Visual
Reproduction
(continued on next page)
 Cognitive Impairment and Dementia 371

Table 1
(continued )
Examples of Neuropsychological
Cognitive Neuroanatomical Correlates of Tests for Assessing the Cognitive
Domains Cognitive Dysfunction Domains
Motor Primary and Supplementary Motor  Grooved Pegboard
Areas  Finger Tapping Test
Basal Ganglia  Hand Dynamometer/Grip
Strength
Psychological Anxiety/Depression Mood Anxiety/Depression
Functioning Disturbance:  Beck Depression Inventory-2nd
and Behavioral  Mesial-Frontal Networks (limbic Ed (BDI-II)
Status system, anterior cingulate,  State Trait Anxiety Inventory-
frontal lobes) 2nd Ed (STAI-II)
Behavioral Disturbance: Parkinson’s Specific:
 Orbital frontal cortex; right  Parkinson’s Disease
cerebral hemisphere Questionnaire-39
(disinhibition, socially Behavioral Disturbance
inappropriate behavior,  Frontal Systems Behavioral
anosognosia) Rating Scale (FrSB)
 Basal ganglia and dorsolateral  Behavior Rating Inventory of
frontal cortex (apathy, lack of Executive Functions (BRIEF)
initiation)  Neuropsychiatric Inventory
Questionnaire (NPI-Q)

although inconsistently so.56,60 Contraindications for DBS generally exist for those
with marked cognitive or behavioral impairments, and it is important to discuss these
issues and functional independence following DBS.56,61 Greater research is needed to
evaluate the impact of neurobehavioral criteria on DBS outcomes.56 Psychological as-
pects such as coping mechanisms and expectations seem to affect patient satisfac-
tion and quality of life regardless of actual motor or cognitive outcomes. In addition,
preoperative psychoeducation tends to enhance postsurgical patient satisfaction.56

CLINICAL MANAGEMENT OF PARKINSON DISEASE COGNITIVE IMPAIRMENT

Management of PD cognitive impairment encompasses pharmacologic, nonpharmaco-

logic, and psychosocial strategies (Table 2). As described earlier, management begins
with assessing the presence, extent, and impact of cognitive issues as well as investi-
gating any contributors such as comorbid conditions, certain medications, and any
modifiable risk factors. Subsequently, clinicians can counsel patients, caregivers, and
families and devise a management plan. Treatment trials for PD cognitive impairment
include those for PDD and more recently, PD-MCI.62,63 Many of the trials have studied
drugs developed for Alzheimer disease (cholinesterase inhibitors and memantine), and
only rivastigmine has been approved by the US Food and Drug Administration for treat-
ment of PDD. Side effects with cholinesterase inhibitors that may have particular
relevance in PD include nausea and gastrointestinal problems (decreased with trans-
dermal rivastigmine formulation), tremor and parkinsonism, and bradycardia and syn-
cope. Studies of memantine and PDD have yielded mixed results. More recently for
PDD, DBS of the nucleus basalis of Meynert has been explored, given this target’s
widespread cholinergic projections innervating the neocortex and hippocampus;
although the procedure and low-frequency stimulation were well tolerated in 6 patients
with PDD, there were no changes in cognitive measures at 6 weeks.64 Several
 372
Goldman & Sieg
Table 2
Double-blind, placebo controlled randomized trials for PD-MCI and PDD published in past 5 years

Sample Size Follow-up

Author Diagnosis Drug (Randomized) Primary Outcome Period Results
Mamikonyan et al,74 2015 PD-MCI Rivastigmine, 9.5 mg/ 28 ADCS-CGIC 24 wk No significant difference
24 h patch daily between groups on primary
outcome
Weintraub et al,75 2016 PD-MCI Rasagiline 151 SCOPA-Cog 24 wk No significant difference
1 mg daily between groups on primary
outcome but improved
motor symptoms
Hinson et al,76 2017 PD-MCI Atomoxetine 30 Global statistical test 10 wk No significant difference
80 mg daily (attention, working memory, between groups on primary
processing speed, set outcome but improved
shifting) subjective measures of
attention and impulsivity
Gratwicke et al,64 2018 PDD DBS of nucleus 6 California Verbal Learning 6 wk, cross- No significant difference
basalis of Meynert Test-II, Wechsler Adult over between groups on primary
Intelligence Scale-III digit (active vs outcome
span, verbal fluency, Posner sham
covert attention test, simple stimulation)
and choice reaction times

Abbreviations: ADCS-CGIC, Alzheimer’s Disease Cooperative Study–Clinical Global Impression of Change; AE, adverse event; DBS, deep brain stimulation;
PDDSCOPA-Cog, Scales for Outcomes of Parkinson’s Disease-Cognition.
 Cognitive Impairment and Dementia 373

randomized controlled trial studies on PD-MCI have studied MAO-B inhibitors, cholin-
esterase inhibitors, or atomoxetine, although without significant effects on cognitive
outcomes. Physical exercise and cognitive training as well as brain stimulation tech-
niques (eg, transcranial magnetic stimulation) represent potential treatment avenues
for PD cognitive impairment with a growing number of research studies and clinical trials
in PD with executive dysfunction or PD-MCI.65–68 Modifiable risk factors should be
addressed where possible. In a systematic review and meta-analysis, 9 modifiable
risk factors that increased the risk of PD cognitive impairment were identified, that is,
disease-related symptoms (postural instability gait disorder, hallucinations, orthostatic
hypotension), other comorbidities (cerebrovascular disease, diabetes mellitus, obesity,
cardiac disease), and lifestyle factors (alcohol consumption and smoking).69 Physical
activity was a protective factor in the systematic review, and some features were asso-
ciated with specific cognitive domains (eg, depression with attention, verbal learning,
visual learning; hypertension with verbal learning and verbal fluency; and education
with attention, executive function, verbal learning, and verbal fluency).
In addition, management of PD cognitive impairment includes discussions and
monitoring regarding work, driving, and home safety. Driving performance in PD
has been associated with disease severity, specific motor symptoms (axial rigidity,
postural instability), and performance on neuropsychological measures (Rey
Osterreith Complex Figure, Trails B, Hopkins Verbal List Learning Test—delayed
recall), which may be useful in distinguishing safe from unsafe drivers.70 Assess-
ments of driving abilities, with road tests or simulations, may be helpful. Addressing
the psychosocial aspects for someone with PD and their care partner and family fac-
ing cognitive changes are paramount. Caregiver burden and stress can be high in
advanced PD and with associated motor and nonmotor complications, including
cognitive decline and dementia.71 One qualitative study that explored the subjective
impact of PD cognitive impairment (normal cognition, PD-MCI, and PDD) on care
partners identified 4 main themes: threats to identity and role, predeath grief and
feelings of loss in carers, success and challenges to coping in people with PD,
and problem-focused coping and finding meaning in caring.72 For the carers, cogni-
tive impairment had a greater emotional impact than the physical symptoms of PD.
Advanced care planning and palliative care may complement the multidisciplinary
care of the advanced PD patient and with cognitive decline and dementia.73

SUMMARY

Cognitive impairment in PD represents a growing area of interest in the multidisciplinary

care of people with PD across all stages of the disease, from early, de novo stages to
advanced disease. Studies highlight the broad spectrum of PD cognitive impairment,
whether PD-MCI or PDD, as well as the variability in progression over time. Comprehen-
sive assessments including neuropsychological testing remain important methods for
understanding a patient’s cognitive profile and management needs. Greater consensus
regarding cognitive evaluations, determining impairment, and assessing functional
abilities in the context of cognitive impairment is still needed. Furthermore, effective
symptomatic, as well as disease-modifying, therapies, whether pharmacologic or non-
pharmacologic, remain unmet challenges for PD cognitive impairment.

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