Review Article

Journal of Geriatric Psychiatry

and Neurology
A Systematic Review and Comparison 1-16
ª The Author(s) 2020
Article reuse guidelines:
of Neurocognitive Features of Late-Life sagepub.com/journals-permissions
DOI: 10.1177/0891988720944251
Attention-Deficit/Hyperactivity Disorder journals.sagepub.com/home/jgp

and Dementia With Lewy Bodies

Jennifer L. Prentice, PhD1 , Morgan J. Schaeffer, BSc1,

Alexandra K. Wall, MSc1 , and Brandy L. Callahan, PhD1,2,3

Abstract
Objective: Attention-deficit/hyperactivity disorder (ADHD) in adulthood and dementia with Lewy bodies (DLB) share many
cognitive and noncognitive similarities. The overlapping features between both disorders complicate differential diagnosis. The
aim of the current systematic review was to compare patterns of neuropsychological profiles in older adults with ADHD and DLB.
Method: Of the 1989 ADHD-related articles and 1332 DLB-related articles screened, 3 ADHD and 25 DLB articles were
retained for qualitative synthesis and review. Results: A synthesis of individual study findings revealed isolated working memory
deficits for late-life ADHD, and performance deficits in areas of attention, memory, language, and visuoperceptual abilities for
DLB. Results were limited by small samples and absence of data in some cognitive domains. Conclusion: These initial findings
support potentially unique neurocognitive profiles for ADHD in later life and DLB that would enable practitioners to differentially
diagnose and appropriately treat older adults presenting with these phenotypically similar disorders.

Keywords
attention-deficit/hyperactivity disorder, dementia with Lewy bodies, cognition, neuropsychology

Introduction a neurodegenerative disorder affecting the dopaminergic sys-

Attention-deficit/hyperactivity disorder (ADHD) is generally
considered a disorder of childhood, but there is growing rec-
ognition that symptoms can persist well into adulthood and late
life.1-3 Evidence suggests that behavioral (hyperactive) symp-
toms wane with age and give way to predominantly cognitive
(inattentive) symptoms,1,2,4,5 which may manifest as absent-
mindedness and forgetfulness.6 In older adults, these symptoms
can be misrecognized as signs of early dementia and contribute
to misdiagnosis.7-9 This is an issue which has received increas-
ing attention from scientists8-11 as well as the lay public,
recently receiving coverage in the New York Times (ADHD
Lasts a Lifetime, September 2015)12 and the Wall Street Jour-
nal (An Unexpected New Diagnosis in Older Adults: ADHD,
February 2020).13 Authors have specifically highlighted the
need to improve clinicians’ ability “to assess the significance
of ADHD symptoms in the context of late-life cognitive
impairments”10 and “distinguish it from aspects of age-
related cognitive decline.”14 This is particularly important con-
sidering the progressive aging worldwide population,15 which
will include a substantial number of individuals with persistent
ADHD symptoms from childhood.16
One important late-life condition from which ADHD must be
distinguished is early-stage dementia with Lewy bodies (DLB),
tem.17 Both ADHD and DLB share many cognitive and non-
cognitive similarities, including deficits in attention and
executive functions18,19 and fluctuations in cognition,17,20 as
well as similarly elevated rates of depression (44% in ADHD21
and 34% in DLB22). Furthermore, certain disturbances associ-
ated with ADHD are among the cardinal diagnostic features of
DLB, 17 including variable attention 20 and sleep distur-
bances.23,24 These overlapping features between both disorders
may cause confusion when older adults present to their practi-
tioner with concerns about possible dementia, and the cognitive
and behavioral traits associated with late-life ADHD may be
mistaken for early signs of DLB. Indeed, surveys of clinicians
1
Department of Psychology, University of Calgary, Alberta, Canada
2
Hotchkiss Brain Institute, Calgary, Alberta, Canada
3
Mathison Centre for Mental Health Research & Education, Calgary, Alberta,
Canada
Received 3/26/2020. Received revised 5/22/2020. Accepted 6/07/2020.
Corresponding Author:
Brandy L. Callahan, Department of Psychology, University of Calgary, 2500
University Dr. NW, Calgary, Alberta, Canada T2N1N4.
Email: brandy.callahan@ucalgary.ca
2 Journal of Geriatric Psychiatry and Neurology XX(X)
reveal that most do not feel confident recognizing adult ADHD
in older adults.10 Despite 3% to 4% prevalence in seniors,3,4,25
up to 40% of clinicians say they have never encountered ADHD
in older adults in their practice,10 suggesting some cases go
unrecognized and potentially misdiagnosed as other late-life
disorders (eg, DLB).
Some authors have argued that it should be relatively easy to
distinguish ADHD from early dementia when considering
symptom onset8,9 or performance on ADHD rating scales.8
However, these may not always be reliable indicators of diag-
nosis in adults with ADHD, particularly for individuals in later
life. First, onset of ADHD symptoms can sometimes occur dur-
ing adulthood,26 and late-onset trajectories may be particularly
difficult to distinguish from neurodegenerative etiologies.
Furthermore, there are anecdotal reports of worsening of cogni-
tive symptoms of ADHD (eg, forgetfulness) coinciding with
stressful life events that may occur in late life, such as retirement
or the death of a spouse, which may mimic de novo impairments
attributable to a neurodegenerative process; similar symptom
worsening due to late-life stressors has been documented in
other primary psychiatric illnesses, for example, the study by
Moos et al.27 In DLB, disease onset is not straightforward. Early
symptoms often begin decades before a formal DLB diagnosis
and include a variety of onset patterns that may not clearly
indicate DLB,28 potentially contributing to misdiagnosis with
late-life ADHD. There is also reason to doubt the utility of
ADHD rating scales as a supportive feature for differential diag-
nosis in adults. Specifically, performance on ADHD ratings
scales may not perfectly align with current formal diagnostic
criteria,5 and most screening instruments have yet to be vali-
dated in cohorts of older adults. Many items on ADHD rating
scales could plausibly be endorsed by individuals with early-
stage DLB, including difficulty organizing tasks or difficulty
focusing attention.
Thus, the clinical presentations of ADHD and DLB include
many overlapping features that can contribute to diagnostic con-
fusion, and symptom onset or ADHD rating scales may not
always reliably distinguish between both syndromes. Experts
have recommended that neuropsychological testing may aid in
the differential diagnosis9 in addition to a thorough evaluation of
an individual’s history, medical chart review, current symptoms,
and impact on functioning. Cognitive assessment alone is not
sufficient to diagnose either disorder, and in fact the utility of
neuropsychological evaluation in the diagnosis of adult ADHD
is disputed.29 However, establishing a patient’s cognitive profile
can be very helpful to differentiate a neurodegenerative disorder
(eg, DLB) from a non-neurodegenerative, potentially treatable
cause (eg, ADHD), usually by ruling in features that are charac-
teristic of a dementing disease.30,31 Assessment, and establish-
ing subsequent neurocognitive profiles, enhance diagnostic
precision by allowing practitioners to identify clinically mean-
ingful cognitive change, the presence or absence of dysfunction,
as well as to predict functional outcomes.32
Currently, neuropsychological testing is not straightforward in
light of limited existing knowledge regarding the cognitive profile
of ADHD in adults above age 40: the vast majority of
neuropsychological studies on “adult ADHD” (recently reviewed
by LeRoy et al33) are primarily focused on participants in their 20s
or 30s. Furthermore, a perusal of the separate literatures on each
disorder individually suggests that adult ADHD and DLB may
include similar types of cognitive deficits (eg, deficits in attention
and executive functions). However, a systematic comparison of
patterns of performance relative to age-expected performance has
never been undertaken and it is possible that certain domains of
cognition are more informative than others for guiding the differ-
ential diagnosis. This cognitive comparison in conjunction with
each disorder’s unique and overlapping clinical features will serve
to provide diagnostic clarity in older adults. As such, the purpose of
this review is to compare and contrast the neuropsychological
profiles of ADHD and DLB in adults aged 40 in an attempt to
quantify the extent of their overlapping cognitive features and
identify possible characteristics to assist with differential diagnosis
in older adults. Because cognitive comparisons between demented
(ie, DLB) and nondemented participants (ie, ADHD) may be con-
sidered unfair given that the dementia process results in much more
severe cognitive and functional impairment, we specifically aimed
to examine the overall profile (ie, cognitive strengths and weak-
nesses) of both disorders relative to age-expected performance.
This has been undertaken in several other studies comparing profile
patterns of cognitive performance between demented and nonde-
mented adults, for example, studies by Kontaxopoulou et al34 and
McLaughlin et al.35 Furthermore, a comparison of expected per-
formance to age-matched controls is typically used in clinical prac-
tice to differentiate among disorders. Therefore, our
methodological approach offers ecological validity.
Method
The present systematic review was predetermined and follows
the Preferred Reporting Items for Systematic Reviews and
Meta-Analyses (PRISMA) statement36 in the report of its find-
ings. Since the goal of the review was to compare and contrast
the neuropsychological profile literature on ADHD and DLB
rather than to compare interventions on a specific outcome, a
Patients, Interventions, Comparison, Outcomes (PICO) state-
ment was not applicable and was not employed in the reporting
template.
Search Strategy
The systematic review search was conducted across 3 databases:
EMBASE (Excerpta Medica Database), PyscINFO, and Med-
line. Search terms were limited to human studies, in English
only, with no limits on the time period. The search included
eligible studies up to August 2018 and was separated by the 2
topics of interest, ADHD and DLB.
The ADHD search strategy used the Boolean term “or” to
explode (search by subject heading) and map (search by key-
word) variations on the MeSH headings “attention deficit hyper-
activity disorder” and “ADHD”; and variations on the headings
“neuropsychology,” “cognition,” and “neuropsychological
Prentice et al
assessment.” The 2 searches were then combined using the Boo-
lean term “and” to produce the final search results.
The DLB search strategy followed a similar protocol by
exploding and mapping variations on the MeSH headings
“dementia with Lewy bodies” and “DLB”; and variations on
the headings “neuropsychology,” “cognition,” and
“neuropsychological assessment.” The 2 searches were then
combined using the Boolean term “and” to produce the final
search results for the DLB literature.
Since the goal of the review was to capture as many studies as
possible for the purpose of contrasting and comparing the neu-
ropsychological profiles of ADHD and DLB in older adults, the
search terms did not focus on a specific study design. However,
reviews, meta-analyses, qualitative studies, and case studies
were excluded as they did not constitute individual empirical
studies or were deemed to carry too high a risk of bias due to lack
of quantitative methodology or a small sample size. For a step-
by-step outline of each database’s search strategy by topic, please
see Appendix A in the included Supplementary Online Material.
Following the completion of the search, the ADHD and
DLB results were extracted to 2 individual data sets and dupli-
cates were removed. All screening and data extraction proce-
dures were conducted and are reported separately for each of
the 2 data sets. Screening of all articles was conducted by the
first and last authors independently. Interrater agreement was
calculated separately for the inclusion screening of the ADHD
and DLB data sets.
Study Selection
Study selection was carried out in a 2-step process by first
reviewing the titles of the studies and then, if deemed relevant,
the abstract of the study before a full-text review of the final list.
The 2 raters conducted the reviews for study inclusion indepen-
dently. Disagreements on inclusion were resolved by consensus.
Inclusion criteria for the ADHD literature were the following:
(1) Participants must be human and 40 years of age or older; (2)
Participants must be formally diagnosed with ADHD based on
the Diagnostic and Statistical Manual of Mental Disorders
(Third Edition, Fourth Edition, or Fifth Edition) criteria,37-41
including structured diagnostic interviews based on these man-
uals (ie, no symptom-only screening procedures); (3) The study
must include a pure ADHD group (ie, studies including only
participants with comorbid disorders were excluded); (4) The
study must include at least one clinical cognitive measure (ie,
experimental measures were not considered); (5) ADHD data
must be reported in comparison to a control group, or report
standardized scores calculated using normative data; (6) Neuro-
cognitive measures must not be used exclusively for correla-
tional purposes or as predictors of a noncognitive outcome
(eg, cognition as a predictor of functional independence); (7)
Participants are generally considered representative of broader
real-world samples (eg, samples consisting exclusively of prison
inmates were excluded).
The DLB inclusion criteria followed a similar template with
specific changes relevant to the DLB topic: (1) Participants
3
must be human and 40 years of age or older; (2) A formal
diagnosis of DLB must be a part of the study, using any version
of the McKeith criteria17 or adjusted criteria if studying a pro-
dromal/mild cognitive impairment phase; (3) Studies were
excluded if the sample included participants with comorbid
neurodegenerative disorders (eg, DLB with comorbid Alzhei-
mer disease); some studies reported depressive symptomatol-
ogy in their DLB samples and those studies were retained; (4)
Studies that included participants with Parkinson disease were
excluded; (5) The study must include a clinical cognitive mea-
sure (ie, experimental measures were excluded); (6) DLB data
must be reported in comparison to a control group, or report
standardized scores calculated using normative data; (7) The
neurocognitive measures are not used exclusively for correla-
tional purposes or as predictors of a noncognitive outcome (eg,
cognition as a predictor of survival); (8) Participants are gen-
erally considered representative of broader real-world samples
(eg, samples consisting exclusively of veterans were excluded).
These criteria were chosen to limit the included literature to
clinically relevant findings, since the goal of the systematic
review was to inform clinical decision-making. Only studies
that provided confirmation of a formal diagnosis were included
since screening and symptom-based assessment may not pro-
vide a pure or reliable ADHD or DLB study group. Comorbid-
ity exclusions were chosen to limit the impact of similar but
unrelated disorders on the cognitive findings. Similarly, studies
were only included if participants were 40 years of age or older
since DLB is a neurodegenerative disease that typically pre-
sents in older adults, and adolescent or younger adults with
ADHD were not considered fair comparison groups.
Data Extraction and Synthesis
Figures 1 and 2 show the PRISMA flow diagrams for the
ADHD and DLB search processes, respectively. The initial
search, after removing duplicates, yielded 1989 ADHD-
related articles and 1332 DLB-related articles for screening.
Following the screening process, 3 ADHD and 25 DLB articles
were included in the final synthesis. A data extraction form was
developed to categorize the literature according to author, year
of publication, sample size, age and sex of participants, educa-
tion of participants, type of neuropsychological measure(s)
used in the study, the diagnostic criteria employed, and the
main findings from the study separated into areas of interest
(memory, attention, language, visuoperceptual, and executive
functions). The same coding template was used for data extrac-
tion for ADHD and DLB studies. The data extraction was
completed and verified by 4 research assistants.
Methodological Quality
Given the broad range of study designs included in the systema-
tic review, it was difficult to create a unified quality assessment
procedure for comparing different types of studies. Although
critical appraisal tools exist for specific study designs,42 no cri-
teria have been offered for all study types captured in the present
4 Journal of Geriatric Psychiatry and Neurology XX(X)

Identification
Records identified through
database searching
(n = 2039)

Records after duplicates removed

(n =1989)
Screening

Records screened Records excluded

(n = 1989) (n = 1886)
Eligibility

Full-text articles
assessed for eligibility
(n = 103)
Full-text articles
excluded
(n = 100)
Included

Studies included in
synthesis
(n = 3)

Figure 1. Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) flow diagram for the attention-deficit/hyperactivity
disorder (ADHD) literature search.

review nor has there been a process proposed to adequately
compare quality ratings across different study types when they
are part of the same review. Yet, the use of multiple types of
studies in systematic reviews in health care has been increas-
ingly recognized as an important tool in accommodating com-
plex research questions and has been deemed appropriate as long
as the inclusion criteria are well specified.43 Consequently, we
were not able to systematically assess the quality of individual
studies included in the systematic review, as such an assessment
would not allow to meaningfully compare and contrast the full
list of included studies. However, we attempted to address study
quality by highlighting studies that we considered to be exemp-
lary of stringent reporting and methodological standards. The
annotations included in the reference list highlight examples of
such rigorous articles.
Results
Study Characteristics
Given the high number of original article abstracts that were
screened and the low number of included articles from the
original pool, there was substantial imbalance in the marginal
totals (ie, cell sizes) when calculating interrater agreement
using the k coefficient. The calculation resulted in a high
(95%) agreement rate, but a low k coefficient (.62). This has
been referred to as the k paradox44 and typically requires a
different interrater statistic to be employed. Gwet’s AC145 has
been proposed to solve this problem by correcting for chance
agreement like k does, but also taking into account potential
low marginal totals. Consequently, Gwet’s AC1 was run to
determine whether there was agreement between the 2 raters’
categorization of the ADHD articles as well as the DLB arti-
cles. There was high agreement between the 2 raters, Gwet’s
AC1 ¼ .96, standard error (SE) ¼ .01 (95% CI, 0.95-0.97) and
Gwet’s AC1 ¼ .93, SE ¼ .01 (95% CI, 0.92-0.95) for the
ADHD articles and DLB articles, respectively.
Tables S1 and S2 in the Supplementary Online Material pro-
vide a summary of the ADHD and DLB study characteristics.
All 3 ADHD studies had cross-sectional designs and included
age-matched control groups. Sample sizes ranged from 23 to 60
and involved a total of 127 participants. Participants ranged in
age from an average of 44 to 68 years old. There was a relatively
Prentice et al 5

Records identified through database

Identification
searching
(n = 1556)

Records after duplicates removed

(n =1332)
Screening

Records screened Records excluded

(n = 1332) (n = 1212)
Eligibility

Full-text articles
assessed for eligibility
(n = 120)
Full-text articles
excluded
(n = 95)
Included

Studies included in
synthesis
(n = 25)

Figure 2. Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) flow diagram for the dementia with Lewy bodies
(DLB) literature search.

equal distribution of males and females across the studies (aver-
age percent female was 48%-56%). The average level of educa-
tion reported in 2 of the 3 studies for the ADHD groups was 9
years. All studies were conducted in the United States.
Of the 25 DLB studies included, 19 were cross-sectional, 3
were cohort studies, and 3 were case–control studies. Nineteen
studies included an age-matched control group, while 2 included
a control group younger than the DLB group46,47 and 1 included
an older control group.48 Three studies did not include a control
group, but standardized cognitive scores using published nor-
mative data. 49-51 Sample sizes ranged from 10 to 87 and
involved a total of 701 participants. Participants ranged in age
from an average of 66 to 82 years old. The distribution of males
and females varied widely across studies, ranging from 16% to
80% female. The average level of education across studies that
reported it (22/25) was 11 years. Notably, there was an over-
representation of very mild DLB samples in the reviewed liter-
ature. Of the 25 included studies, 1 included a prodromal (ie, not
demented) sample of DLB52 and 13 included very mild DLB,
as reflected by Mini-Mental Status Examination (MMSE)53
and Montreal Cognitive Assessment (MoCA) 54 scores
20.46-48,51,55-63 Three studies did not report mean MMSE/
MoCA scores and 2 did not use these measures, making it dif-
ficult to ascertain the severity level of the samples included in
those studies. The largely mild severity of DLB in the surveyed
samples is consistent with the goal of this review, given that
diagnostic confusion between DLB and ADHD is more likely
in the prodromal or mild stages of DLB. It is at these low severity
stages when clinical and behavioral features are less likely to be
prominent and an understanding of a cognitive profile may be
more helpful compared to moderate or severe DLB.
Cognitive Domains
Table 1 summarizes performance in attention and processing
speed, visuoperceptual abilities, memory, language, and exec-
utive functions in both late-life ADHD and DLB.
Attention and Processing Speed
Attention-deficit/hyperactivity disorder. Performance in older adults
with ADHD was consistent on measures of attention and
6 Journal of Geriatric Psychiatry and Neurology XX(X)

Table 1. Summary of Performance in Main Cognitive Areas in Late-Life ADHD and DLB.

Cognitive Domains Late-life ADHD DLB

Attention and processing speed

Selective attention Normal in 1/1 study Consistently impaired
Impaired in 4/4 studies
Divided attention Normal in 1/1 study NA
Sustained attention Normal in 1/1 study Consistently impaired
Impaired in 3/3 studies
Shifting attention Normal in 1/1 study NA
Simple verbal attention/concentration Normal in 1/1 study Generally impaired
Impaired in 10/14 studies
Psychomotor speed Normal in 1/1 study Consistently impaired
Impaired in 11/12 studies
Psychomotor speed errors NA Mixed
Impaired in 1/2 studies
Processing speed Generally preserved Consistently impaired
Impaired in 1/2 studiesa Impaired in 5/5 studies
Visuoperceptual abilities
Spatial perception NA Consistently impaired
Impaired in 7/8 studies
Object perception NA Consistently impaired
Impaired in 5/7 studies
Memory
Immediate verbal recall NA Generally impaired
Impaired in 9/11 studies
Delayed verbal recall Normal in 1/1 study Generally impaired
Impaired in 15/17 studies
Verbal recognition NA Consistently impaired
Impaired in 6/6 studies
Immediate visual recall NA Mixed
Impaired in 1/2 studies
Delayed visual recall NA Generally impaired
Impaired in 2/3 studies
Visual recognition NA Consistently impaired
Impaired in 4/4 studies
Prospective memory NA Impaired in 1/1 studies
Language
Semantic fluency Normal in 2/2 studies Consistently impaired
Impaired in 15/15 studies
Phonemic fluency Normal in 2/2 studies Consistently impaired
Impaired in 17/17 studies
Confrontation naming NA Consistently impaired
Impaired in 13/14 studies
Executive functions
Inhibitory control Generally preserved Impaired in 1/3 studies Mixed
Impaired in 3/5 studies
Cognitive flexibility Mixed Generally impaired
Impaired in 1/2 studies Impaired in 11/13 studies
Working memory Consistently impaired Generally impaired
Impaired in 2/2 studies Impaired in 7/10 studies
Planning Normal in 1/1 study Consistently impaired
Impaired in 15/16 studies
Abstraction Normal in 1/1 study Generally impaired
Impaired in 4/6 studies
Abbreviations: ADHD, attention-deficit/hyperactivity disorder; DLB, dementia with Lewy bodies; NA, not available.
a
Impaired performance found on only 1 of 4 individual tests.

processing speed. Selective, divided, shifting, and sustained
attention appeared to be normal,64,65 and processing speed was
normal on most individual measures.65,66
Regarding individual attention task performance, selective
and divided attention on the Test of Everyday Attention was
reported as average, with superior sustained attention perfor-
mance on the Continuous Performance Test.64 Simple verbal
attention and psychomotor speed as measured by Digit Span
Forward and Trail Making Test A65 were reported as normal.
Processing speed performance on the color-naming condition of
Prentice et al
the Stroop task was generally normal,65,66 while speed on word
reading was normal in one study,65 but impaired in another.66
Dementia with Lewy bodies. Qualitative synthesis of evidence for
attentional performance in DLB was extracted from 19 studies,
as 6 did not include attention tasks. A preponderance of the
reviewed data showed that compared to healthy controls, atten-
tional performance in individuals with DLB was globally
impaired. Normal performance was reported by a minority of
studies and only in simple verbal attention/concentration49-51,67
and psychomotor speed error.59
With regard to specific domains, all studies that measured it
reported impairment in selective attention, typically measured
using the Picture Completion Task,50,67-69 and impairment in
sustained attention (no consistent measure).59,68,69 Simple ver-
bal attention/concentration, typically measured by the Digit
Span forward and combined tasks, was reported as impaired
by the majority of studies.46,47,52,55,57,59,60,68,70,71
Other subdomains of attention that were reported as consis-
tently impaired were psychomotor speed, typically measured by
the Trail Making Test A,47-49,51,52,55,58-61,72 and processing
speed (no consistent measure).49,52,57,60,61 In a study differentiat-
ing between mild and very mild DLB,55 impairment of psycho-
motor speed only appeared at the mild symptom level, whereas
very mild DLB was normal relative to age-matched controls. The
finding may have implications for interpretation of neuropsycho-
logical attentional task data based on DLB severity.
Comparison and Integration of Findings
Overall, findings on attentional performance appear to be dif-
ferent between ADHD and DLB. Attention-deficit/hyperactiv-
ity disorder participants demonstrate largely normal
performance across attention and processing speed domains.
On the other hand, DLB participants demonstrate severe and
widespread attentional impairment, affecting selective, divided,
sustained, and simple verbal attention, as well as processing and
psychomotor speed, with consistency in results across most
reviewed studies.
Visuoperceptual Functions
Attention-deficit/hyperactivity disorder. Visuoperceptual functions
were not evaluated in any of the retained ADHD studies.
Dementia with Lewy bodies. Visuoperceptual functions were assessed
in 11 of the 25 retained DLB studies,46-48,52,57,60-62,68,73,74 typi-
cally using Judgement of Line Orientation or subtests of the
Visual Object and Space Perception Battery (VOSP). All these
studies found some extent of visuoperceptual impairment in
DLB relative to controls, with the most consistently impaired
tasks being the “shape detection screen,” “incomplete letters,”
and “number location” subtests of the VOSP.
Comparison and integration of findings. Dementia with Lewy bod-
ies participants are consistently impaired on tasks of
7
visuoperceptual abilities such as detecting shapes and identify-
ing the position of items in space. This cognitive domain has
never been assessed in late-life ADHD.
Memory
Attention-deficit/hyperactivity disorder. The majority of the evi-
dence regarding episodic memory performance in late life
ADHD comes from a single small (n ¼ 23) population–based
study65 which found normal verbal memory performance rela-
tive to healthy controls on total and delayed word list recall.
There are currently no data regarding visual episodic memory
or prospective memory in late life ADHD.
Dementia with Lewy bodies. Performance on measures of
episodic memory was overall reported as impaired in DLB.
Twenty-one studies examined verbal episodic memory with
tests including word list learning,47-49,57,59 memory for a short
story,48-50,60,62,63,67,68 a selective reminding task,52,55,56,61,73 a
recognition memory test,51,67,68,74 the CERAD Verbal Memory
Test, the California Verbal Learning Test, a Word and Story
Recall Test, and the memory subtests of the Cambridge
Cognition Examination,69 the Dementia Rating Scale-2,71 and
the Montreal Cognitive Assessment.70 Only 2 of the 21 studies
reported normal immediate and delayed recall in patients
with DLB compared to controls, 49,59 although learning
processes were found to be impaired (>3 SD below normal) in
one.49 The remaining 19 studies reported impairments in one
or more aspects of verbal episodic memory including
free recall,47,50-52,55-57,60-63,67,68,70,73 cued recall,55,56,61,73
recognition,55,60,62,67,68,74 and retention.48 Overall, verbal
memory appears to be impaired in patients with DLB.
Eleven of the 21 studies also examined visual episodic mem-
ory in patients with DLB using tests such as recognition mem-
ory,74 delayed matching to sample,52,61 the Benton Visual
Retention Task, 49,73 the Rey-Osterrieth Complex Figure
Task,49,51,57,59 the Visual Association Task,47 and the Visual
Reproduction subtest of the Wechsler Memory Scale–
Revised.50,67 Of these 11 studies, 2 reported normal visual epi-
sodic memory performance.59,67 The remaining 9 reported
impairments in one or more aspects of visual memory including
recall,47,49,57 recognition,52,61,73,74 and reproduction.50,51,57,73
In sum, performance on measures of visual episodic memory
is generally impaired in patients with DLB.
One study also examined prospective memory in patients
with DLB using the Event-Based Prospective Memory Test and
the Time-Based Prospective Memory Test.57 Patients with
dementia with Lewy bodies were impaired on both event- and
time-based prospective memory compared to healthy controls.
Comparison and integration of findings. Verbal, visual, and pro-
spective memory performance is generally impaired in DLB.
However, no firm conclusions can be drawn regarding simila-
rities between ADHD and DLB patients on measures of episodic
memory, as only one study has examined memory performance
8 Journal of Geriatric Psychiatry and Neurology XX(X)
in late-life ADHD, and only included a single verbal memory
construct.
Language
Attention-deficit/hyperactivity disorder. Two studies to date have
explored language performance in adults with ADHD older than
age 40, both of which included verbal fluency as the only mea-
sure of language. A population-based study65 comparing 23
individuals with late-life ADHD to 208 healthy controls found
no differences in performance on tasks of phonemic (letter) or
semantic (category) fluency. Thorell et al66 also found no dif-
ferences in phonemic or semantic fluency between 44 individ-
uals with late-life ADHD recruited from an outpatient clinic and
58 healthy age-matched controls. In this study, person-oriented
analyses conducted against available normative data indicated
that 3 individuals with ADHD (6.8%) had a mild deficit (equiv-
alent to 1 SD) in phonemic fluency, and 5 (11.4%) a mild
deficit in semantic fluency. None exhibited severe deficits in
either domain of verbal fluency.
Dementia with Lewy bodies. Individuals with DLB exhibit
consistently impaired performance on language measures. In
total, 17 studies to date have examined language abilities in
DLB, all of which include at least one measure of verbal flu-
ency. Verbal fluency was assessed using both phonemic (letter)
and semantic (category) fluency tasks. Of these studies, 14
compared performance to a healthy control group and found
that individuals with DLB had significantly worse perfor-
mance, on both phonemic47-52,55,58-61,67,73,74 and semantic
fluency.47,51,52,55,57-62,67,68,73,74 In studies reporting standar-
dized scores calculated using published normative data, verbal
fluency performance in DLB was poor but not frankly impaired.
Phonemic fluency was reported to be in the low-average range in
one study49 and the borderline impairment range in 2 others,50,51
while semantic fluency was reported to be in the borderline
impairment range.51 Thus, overall results point to weaknesses
in language fluency in individuals with DLB.
Confrontation naming has also been examined in individuals
with DLB. Of the 12 studies that have looked at DLB perfor-
mance on such tasks, 10 have found significantly impaired per-
formance relative to healthy controls.48,52,55,57,60-62,68,73,74
Performance was otherwise borderline impaired 49 or low
average.50 The only report in the literature that contradicts these
findings is a study by Smits et al,47 which found no deficits in
DLB compared to controls on the naming portion of the Visual
Association Test. However, this study did find deficits on
another task of confrontation naming (the item naming portion
of Arizona Battery for Communication Disorders).
Thus, every study to date that has explored language perfor-
mance in participants with DLB has found some degree of
impairment spanning phonemic fluency, semantic fluency, and
confrontation naming. These studies include both clinical and
population-based samples and range in size from 10 to 70 DLB
participants. The consistent results between studies despite the
diversity in design, sample size, and study population lend
confidence to the finding that individuals with DLB have con-
sistent impairments in the domain of language.
Comparison and integration of findings. Although individuals with
DLB exhibit consistent and pervasive deficits in language abil-
ities, individuals with late-life ADHD do not appear to show
impairment in this domain. However, data on language abilities
in late-life ADHD come exclusively from 2 studies, both of
which only covered phonemic and semantic verbal fluency.
The majority of studies on cognition in late-life ADHD have
not included measures of language, and no studies to date have
examined confrontation naming.
Executive Functions
Attention-deficit/hyperactivity disorder. In late-life ADHD, perfor-
mance on measures of executive functioning is overall mixed.
The majority of evidence comes from 2 conflicting articles, one
small (n ¼ 23) population-based study65 which reported grossly
normal executive functioning, and a relatively larger (n ¼ 44)
clinic-based study66 which found widespread executive impair-
ments relative to age-matched controls. A third study (n ¼ 60)64
included only one measure of inhibitory control, and thus did not
contribute substantially to understanding executive perfor-
mance as a whole in late-life ADHD.
With regard to performance on individual executive tasks, 2
of 3 studies reported normal inhibitory control on a Matching
Familiar Figures task64 and on the Stroop Color-Word Interfer-
ence Test,65 while the third found large inhibition differences on
the Stroop relative to age-matched controls.66 Working memory
performance, measured using the Backwards Digit Span65,66 or
Sequencing subtests66 of the Wechsler Adult Intelligence Scale,
was grossly impaired, though in one study effect sizes were
small and primarily explained by depressive symptoms.65
Mixed performance was also apparent on cognitive flexibility
tasks, with normal performance on Trail Making Test B65 but
impaired performance on the Stroop Color-Word switching con-
dition.66 Planning abilities were measured in one study66 using
the Tower subtest of the Delis-Kaplan Executive Function Sys-
tem and were normal. Performance on Raven’s Coloured Pro-
gressive Matrices, used to measure abstract reasoning, was also
normal.65
Despite significant differences between the ADHD and con-
trol groups in Thorell and colleagues’ study,66 it is worth noting
that performance on all measures generally remained within
normal limits at the group level (ie, average group scaled scores
varied between 8.3 and 10.9 on executive tasks), and 20% of
individual participants in person-oriented analyses did not have
any objective deficit (ie, age-adjusted scaled scores 8, or
0.67 SD).
Dementia with Lewy bodies. Executive functions were assessed in
22 of the 25 retained DLB studies.46-51,55-63,67-71,73,75 On the
whole, most aspects of executive functioning were impaired in
DLB. Inhibitory control, which was always tested using a ver-
sion of the Stroop Color-Word Interference Test, was impaired
Prentice et al
in 355,57,67 of 5 studies that assessed it.55,57,58,67,68 Working
memory was typically assessed using the Backwards Digit Span
or Arithmetic subtests of the Wechsler Adult Intelligence Scale
and was impaired46,47,52,55,67,68 or borderline impaired50 in 7 of
the 10 studies that included these measures.46,47,49-52,55,59,67,68
Cognitive flexibility, usually assessed using Trail Making Test
B or the Wisconsin Card-Sorting Task, was impaired in 11
studies47-49,52,55-57,60,61,67,71 and normal in only 2.58,59 Planning
abilities were assessed using visuoconstruction tasks such as
Block Design, Clock Drawing, or the Rey-Osterrieth
Complex Figure copy trial. These were impaired in nearly all
studies, 48,50-52,55,57,60-62,67,70,71,73,75 with one exception.59
Abstract thinking and conceptualization abilities were variable.
Two49,67 of 3 studies49,67,73 found normal performance on the
Similarities subtest of the Wechsler Adult Intelligence Scale.
Studies using abstraction subscales of the Cambridge Cognition
Examination,69 Mattis Dementia Rating Scale,71 or Montreal
Cognitive Assessment70 reported impairments relative to controls.
Comparison and integration of findings. Overall, both ADHD and
DLB participants demonstrate executive difficulties in later life.
These impairments appear more severe and widespread in DLB,
affecting inhibitory control, cognitive flexibility, working mem-
ory, planning, and abstraction. In contrast, deficits in ADHD
may be relatively isolated to working memory, though more
research is certainly needed to extend these findings beyond the
few existing studies.
Studies of prodromal or mild DLB only. To infer the extent to
which global severity of cognitive decline may have influ-
enced domain-specific impairments in DLB, we reconsid-
ered the above findings including only studies with a
prodromal or mild DLB group (group MMSE or MoCA
20). Results reflected those of the broader review (ie,
broadly impaired attention, 46,47,50-52,55,57-61 visuoperceptual
functioning,46-48,52,57,60-62 verbal memory,47,48,51,52,55-57,60-62,76
visual memory,47,51,52,57,61 language,47,48,51,52,55,57-62 and execu-
tive functions48,51,52,55,57,60-62,70). With the exception of visuo-
perceptual functioning which was grossly normal, these results
also held when considering only the prodromal (ie, nondemen-
ted) DLB sample studied by Kemp and colleagues,52 in which
participants had a mean MMSE score of 27.36, comparable to
MMSE scores of ADHD participants reported in both studies
that included a measure of global cognition (mean ¼ 27.3965
and mean ¼ 28.4766).
Discussion
The primary objective of this systematic review was to
systematically compare and contrast patterns of neuropsycho-
logical performance of DLB and late-life ADHD, relative to
their age-matched healthy counterparts, in order to assist with
differential diagnosis and treatment planning. Unfortunately,
the lack of late-life ADHD studies severely limits the general-
izability of the findings and prohibits robust and reliable com-
parisons of cognitive features in some domains (ie, memory,
9
visuoperceptual abilities, and some language subdomains). Our
review identified only 3 suitable articles on late-life ADHD,
each with relatively small sample sizes (127 late-life ADHD
participants in the 3 studies combined). We recognize that no
firm conclusions can be drawn from such a limited number of
studies, and the findings presented in this review should be
considered as preliminary.
One important goal was to identify and summarize overlap-
ping areas of cognitive impairment between late-life ADHD and
DLB that may contribute to misdiagnosis between these syn-
dromes. Working memory was the only cognitive domain iden-
tified in the review in which individuals with late-life ADHD
and DLB demonstrated impairment. Both groups performed
significantly worse than healthy age-matched controls on tasks
of working memory, usually the Backwards Digit Span or Arith-
metic subtests of the Wechsler Adult Intelligence Scale. How-
ever, studies interpreting performance against published
normative data, rather than a control group, find that working
memory performance rather falls within average or low-average
ranges in ADHD66 and DLB.49-51 The use of published norma-
tive data, rather than a locally recruited control sample, is known
to underestimate the severity of cognitive impairment in
adults77,78 which may account for the discrepancies in perfor-
mance when using these different benchmarks. Thus, while
results from this literature review globally suggest working
memory weaknesses in both ADHD and DLB, these weaknesses
may be relatively mild in nature at the group level.
Initial results synthesized in this review suggest that perfor-
mance in the domains of attention and language may be differ-
entially affected in late-life ADHD and DLB and thus
potentially informative in the neuropsychological profiling pro-
cess, if additional studies of late-life ADHD cohorts corroborate
these findings. Attentional abilities (measured using tests such
as digit span and Trail Making Test A) and language abilities
(assessed through phonemic or semantic verbal fluency) were
preserved in both late-life ADHD studies that addressed these
skills, whereas participants with DLB were consistently
impaired. Tasks assessing planning (eg, Block Design; Rey
Complex Figure copy) and cognitive flexibility (eg, Trails B,
Wisconsin Card-Sorting Task) were impaired in nearly all DLB
samples, but unfortunately these specific subdomains of execu-
tive function were never assessed in more than one study of late-
life ADHD and thus no strong conclusions can be drawn about
whether these may serve as useful measures to assist in cognitive
profiling. Conclusive information on memory and visuopercep-
tual abilities that may differentiate late-life ADHD from DLB is
also lacking.
These behavioral characteristics are somewhat contrary to
conceptualizations of ADHD as a disorder primarily affecting
attention, for example, Barkley79 and Fuermaier et al80 and to
findings of largely impaired verbal fluency in adult ADHD.80
Intact performance on these measures may be attributable to an
attenuation of cognitive impairments with age in ADHD.81,82 It
may also be a reflection of the recognized heterogeneity in adult
ADHD: at the individual level, patients with ADHD may be
impaired on one cognitive measure within a domain while others
10
show deficits in another, resulting in overall attenuated findings
at the group level.80 While only 2 ADHD studies in this
review65,66 examined planning and abstraction skills with D-
KEFS Towers and Raven’s Coloured Progressive Matrices,
their findings of intact performance generally align with obser-
vations of mild to no planning impairments in young and
middle-aged adults with ADHD.83,84
The above findings are rather challenging to reconcile with
the neuroimaging literature in adult ADHD and DLB. Perfor-
mance on tasks of digit span, Trail Making Test A, and fluency is
thought to rely heavily on prefrontal brain circuits.85-87 Adults
with ADHD typically show reduced integrity of these regions88
despite normal behavioral performance in both studies included
in our review that used these tasks. In contrast, while frontal-
lobe structures are generally intact in DLB,89 these patients
obtained grossly impaired performance on frontally mediated
tasks in this review. Intact performance in ADHD participants
may be understood by aging brains “catching up” on earlier lags
in frontal-lobe brain maturation.81,82 Conversely, impaired Trail
Making Test A performance in DLB may be confounded by the
visuoperceptual nature of this task,90 as visual impairments are
well recognized in DLB and reflect reduced structural integrity
of parieto-occipital brain regions.89 Performance on verbal flu-
ency tasks may also be impacted by the integrity of temporal
lobe networks, which is affected in DLB relative to age-matched
controls.89 We remain cautious in these interpretations because
no studies have investigated the neuroimaging substrates of
cognitive performance in late-life ADHD specifically, and it is
reasonable to suspect that ADHD-related brain changes may
interact uniquely with age-related brain changes.
All in all, 3 small studies of late-life ADHD have found
evidence of mild working memory impairments and otherwise
grossly normal attention and executive functioning; 2 of these
studies additionally reported normal language skills. These abil-
ities were impaired in the vast majority of 25 retained DLB
studies, even when disease severity was considered mild or pro-
dromal. We propose that these cognitive features should be
investigated in other late-life ADHD cohorts to determine
whether they may be useful in distinguishing ADHD from DLB.
Some authors have called for the inclusion of neuropsychologi-
cal assessment as an objective measure of dysfunction in the
diagnostic criteria for ADHD91 and specifically to improve dif-
ferential diagnosis between late-life ADHD and neurodegenera-
tive disorders.9 On the other hand, this call has been contested by
other researchers, who contend that there is insufficient evi-
dence for the utility of neuropsychological testing in the evalua-
tion of individuals with ADHD.29,92 The contention is largely
based on a lack of demonstrated content validity and ecological
validity of neuropsychological test items for ADHD. Indeed,
neuropsychological profiles of ADHD in children and younger
adults have had mixed success in differentiating individuals
with ADHD from healthy controls,93-96 and formal tests of cog-
nitive abilities do not align well with the day-to-day difficulties
caused by ADHD symptoms.97-99 Given that ADHD is a clinical
diagnosis that relies on establishing lifetime symptoms and
functional impairment, diagnostic interviews that incorporate
Journal of Geriatric Psychiatry and Neurology XX(X)
collateral information about onset, severity, and chronicity of
symptoms and impairments may be better able to facilitate a
differential diagnosis from DLB than a neuropsychological
assessment. Thus, clinicians should not rely exclusively on neu-
ropsychological assessment in the differential diagnosis of
ADHD and DLB, but the results of the review tentatively sug-
gest that it may be useful to optimize diagnostic specificity (ie,
ruling out ADHD in older adults for whom performance is
grossly impaired). However, our results first need broader repli-
cation and would be strengthened by the use of longitudinal
study designs to determine age-specific changes in different
cognitive domains.
Research Gaps and Future Directions
Our review identified several gaps in the existing research liter-
ature. Most notable is the scarcity of studies investigating the
neuropsychological profile or cognitive domains of late-life
ADHD, with only 3 studies identified by this review. Of these
studies, only one assessed memory (verbal memory only65), 2
assessed one specific performance area of language (verbal flu-
ency65,66) and none evaluated visuoperceptual abilities. A con-
siderable body of literature exists examining memory and
language deficits in DLB, but to fully appreciate the extent of
overlapping and unique cognitive features between DLB and
ADHD, an important next step is to evaluate these neurocogni-
tive constructs in late-life ADHD. More comprehensive neurop-
sychological examination (ie, homogeneity of tasks, assessment
of cognitive domains, and subdomains) is also required in order
to draw meaningful comparisons between the disorders. For
example, the DLB studies only included measures of planning
that simultaneously involved a visuoconstruction component,
which is problematic because visuoperceptual abilities are
severely affected in DLB as demonstrated by the studies
included in this review. The interaction between multiple com-
peting cognitive domains therefore makes it difficult to accu-
rately isolate planning from visuoperceptual abilities, and future
studies should employ alternative measures of planning such as
the Towers of London or Hanoi to ensure a more accurate assess-
ment. Similarly, more research is needed on divided or shifting
attention in individuals with DLB since no studies report data in
these areas.
The dearth of late-life ADHD studies posed a significant
challenge to the current review’s purpose, as we were unable
to quantify the extent of cognitive performance overlap in sev-
eral domains. A more thorough investigation, such as the inclu-
sion of a confrontation naming test in the evaluation of language,
would permit a systematic comparison of the larger neuropsy-
chological domain. Overall, neuropsychological investigations
of late-life ADHD were severely underrepresented relative to
DLB, potentially because ADHD is generally considered a psy-
chiatric disorder of childhood and adolescence.
An important observed trend in the DLB literature was that
most studies did not assess the role of disease severity in cogni-
tive performance. Only one study differentiated between parti-
cipants with mild or very mild disease severity.55 Given that the
Prentice et al
authors found attentional performance to be impacted in the
mild group only, it would be highly beneficial to address neu-
rocognitive performance as a function of severity in DLB to
elucidate the trajectory of impairment as the disease progresses,
particularly as the potential for misdiagnosis with ADHD
depends on disease stage (ie, most likely in the earliest stages
of DLB). Our review captured a considerable number of mild
DLB samples, making its results applicable to clinical consid-
erations, but the overall sample size of existing studies was still
relatively low. Consequently, additional research focusing on
the mild stages of DLB would be particularly useful in informing
differential diagnosis protocols and guidelines. Unique neuro-
cognitive considerations/profiles based on symptom severity
may improve earlier identification and intervention, but also
allow for a clearer understanding of the overlapping and unique
features of late-life ADHD and very mild, mild, moderate, and
severe DLB.
An additional gap identified by the review was the lack of
measurement consistency among studies. The reviewed studies
used different measures to assess the same constructs (eg,
attention assessed using either time or errors on Trail Making
Test A), or a combination of tests measuring different con-
structs (eg, attention assessed using combined forward and
backward digit span). This posed a challenge to the synthesis
and aggregation of the methods and ultimately findings of this
review, as slightly different areas of cognition are involved in
each of these tests but were synthesized to represent the same
cognitive domain. The field would benefit from moving toward
the use of more standardized research instrument batteries.
Clinical scientists in the field of Alzheimer disease research
have already taken a step in this direction by creating the Uni-
form Data Set, a systematic neuropsychological testing proce-
dure to characterize cognition in Alzheimer disease and mild
cognitive impairment.100 Developing a similar standardized
uniform battery for studies assessing adult ADHD or DLB
would enable neuropsychologists to directly compare and con-
trast the neurocognitive findings across multiple studies.
Lastly, related to the gap of standardization, several of the
reviewed studies did not provide normative data to characterize
performance. Rather, performance was compared to a control
group, which was in some cases not perfectly age-matched.
While it is commonly agreed that worse performance by pro-
bands relative to a healthy control group indicates impairment, a
significant group difference does not indicate the degree of
impairment (eg, mild vs moderate). The use of normative data
can thus provide a helpful interpretive benchmark in this regard,
though in some cases may underestimate the severity of cogni-
tive impairment, as mentioned above.77,78
Limitations
Despite the methodological rigor and scientific novelty of the
study, the present review had several limitations, the most
important of which was the severely limited number of late-
life ADHD articles suitable for inclusion in our review. In addi-
tion, participants in the extracted ADHD articles, ranging from
11
44 to 68 years old, were considerably younger than those in the
DLB studies, ranging from 66 to 82 years old. A concern might
therefore be that discrepancies in their neurocognitive profiles
are the result of age-related change rather than differences in
disease processes. We attempted to mitigate this issue by explor-
ing deviations from age expected performance in each group: in
both the ADHD and DLB study collections, participants’ cog-
nitive scores were assessed against those of similar-aged healthy
controls, and the extent of deviation was the outcome of interest.
Thus, the neuropsychological profiles emerging from this
review take into account age-related changes in cognition by
using similar-aged peers as a control benchmark in each indi-
vidual study. A related issue concerns the fact that cognitive
comparisons between demented (ie, DLB) and nondemented
participants (ie, ADHD) may not be considered fair, regardless
of age matching, because global severity of cognitive decline
may have influenced domain-specific impairments (ie, the DLB
“profile” may have been reflective of more severe cognitive
impairment overall). However, as noted in our results, the
majority of the DLB samples were of mild severity; thus, the
influence of this potential confound is somewhat mitigated.
Furthermore, similar profile comparisons between older nonde-
mented and demented adults (ie, patients not matched on global
cognition) have been undertaken in many previous studies, for
example, Kontaxopoulou et al34 and McLaughlin et al,35 and
have been informative in determining distinct patterns of neu-
ropsychological performance across disorders despite global
cognitive differences between groups. Nonetheless, direct com-
parisons of ADHD and DLB participants, matched on age and
global cognition, tested on the same neuropsychological tests
within the same study, will ultimately be necessary to draw
robust conclusions about cognitive comparisons between these
disorders.
Only one of the studies included in the review reported using
neuropathologic or biomarker validation for the diagnosis of
DLB.56 This is considered a limitation given that extant data
highlight varying degrees of specificity and sensitivity of clin-
ical criteria for DLB depending on which revision is used.101
Results from this single study are consistent with those from the
broader review (ie, impaired verbal memory and cognitive flex-
ibility), but additional work describing the cognitive features of
DLB using biomarker-corroborated diagnoses will be helpful to
ensure that findings are truly reflective of a Lewy Body disease
process.
An alternative interpretation of our data must also be consid-
ered. Epidemiological research suggests that adults with ADHD
are more likely to be diagnosed with basal ganglia disorders in
later life, including DLB,102-104 and that persons with Lewy
body diseases are more likely to retrospectively report features
of ADHD earlier in life than persons with Alzheimer type
dementia,105,106 suggesting that ADHD and DLB may be dis-
tinct phenotypes along a disease continuum resulting from a
single etiology (eg, synucleinopathy). It may be the case that
ADHD and DLB are part of the same neuropathological pro-
cesses that result in changes at different times on the disease
continuum, similar to amnestic mild cognitive impairment
12
(aMCI) and Alzheimer disease, or to nonamnestic MCI and
frontotemporal dementia.107 For example, the neuropsycholo-
gical profile of aMCI is characterized by isolated deficiencies in
memory with preserved function whereas the progression to
Alzheimer disease features memory impairments with addi-
tional impairment in semantic networks and executive function.
Unfortunately, an empirical answer to this question is beyond
the scope of this review and can only be answered through pro-
spective follow-up of adults with ADHD into late adulthood.
Since our goal was to survey the literature and identify knowl-
edge gaps, rather than experimentally control factors of influ-
ences, the findings cannot clarify whether ADHD and DLB are
the same or different disease processes. This will be an area for
future longitudinal work.
Our search was limited to articles in English and did not
include sources that were not peer-reviewed. Therefore, we may
have missed relevant studies in other languages and in the gray
literature. Given that the retained studies were methodologically
diverse, and the primary goal was to assess the current state of
the literature on the neuropsychological profiles of late-life
ADHD and DLB, we did not carry out a meta-analysis which
would have allowed to draw statistical conclusions. The low
number of studies in the ADHD domain also precluded large-
sample statistical analyses and remains a significant barrier
toward drawing robust conclusions from these data. Future stud-
ies are encouraged to explore neurocognitive bases of late-life
ADHD in order to evaluate the research question statistically.
Lastly, the entire methodological process inherent to a systema-
tic review is subjective, which can introduce bias during study
selection and screening. We attempted to reduce this bias by
employing multiple raters in the process and establishing high
interrater reliability.
Conclusion
This systematic review was an important first step toward quan-
tifying the overlapping and unique cognitive features of late-life
ADHD and DLB. Results should be considered preliminary in
light of the severely limited number of late-life ADHD studies
but tentatively suggest performance differences in areas of
attention and language that may assist with diagnostic clarity.
Future suggested research directions include direct comparisons
of well-matched ADHD and DLB participants in subsequent
neuropsychological studies.
Authors’ Note
All procedures performed in studies involving human participants
were in accordance with the ethical standards of the institutional
and/or national research committee and with the 1964 Helsinki
declaration and its later amendments or comparable ethical standards.
The systematic search and review of retrospective studies did not
require formal consent.
Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to
the research, authorship, and/or publication of this article.
Journal of Geriatric Psychiatry and Neurology XX(X)
Funding
The author(s) disclosed receipt of the following financial support for
the research,authorship, and/or publication of this article: This study
was supported by the Canada Research Chair to BLC.
ORCID iDs
Jennifer L. Prentice https://orcid.org/0000-0002-5073-7815
Alexandra K. Wall https://orcid.org/0000-0003-1764-2774
Brandy L. Callahan https://orcid.org/0000-0001-5617-2379
Supplemental Material
Supplemental material for this article is available online.
References
*Indicates studies included in the literature review
1. Asherson P, Buitelaar J, Faraone SV, Rohde LA. Adult attention-
deficit hyperactivity disorder: key conceptual issues. Lancet Psy-
chiatry. 2016;3(6):568-578. doi:10.1016/S2215-0366(16)30032-3
2. Volkow ND, Swanson JM. Adult attention deficit-hyperactivity
disorder. N Engl J Med. 2013;369(20):1935-1944. doi:10.1056/
NEJMcp1212625
3. Faraone SV, Asherson P, Banaschewski T, et al. Attention-deficit/
hyperactivity disorder. Nat Rev Dis Primers. 2015;1:15020. doi:
10.1038/nrdp.2015.20
4. Kooij JJS, Michielsen M, Kruithof H, Bijlenga D. ADHD in old
age: a review of the literature and proposal for assessment and
treatment. Expert Rev Neurother. 2016;16(12):1371-1381. doi:10
.1080/14737175.2016.1204914
5. Callahan BL, Plamondon A. Examining the validity of the ADHD
concept in adults and older adults. CNS Spectr. 2019;24(5):
518-525. doi:10.1017/S1092852918001190
6. Rosler M, Casas M, Konofal E, Buitelaar J. Attention deficit
hyperactivity disorder in adults. World J Biol Psychiatry. 2010;
11(5):684-698. doi:10.3109/15622975.2010.483249
7. Callahan BL, Bierstone D, Stuss DT, Black SE. Adult ADHD:
risk factor for dementia or phenotypic mimic? Front Aging Neu-
rosci. 2017;9:1-15.
8. Pollack J. Distinguishing between adult ADHD and mild cogni-
tive impairment. Curr Psychiatr. 2012;(8):48-50.
9. Goodman DW, Mitchell S, Rhodewalt L, Surman CBH. Clinical
presentation, diagnosis and treatment of attention-deficit hyper-
activity disorder (ADHD) in older adults: a review of the evi-
dence and its implications for clinical care. Drugs Aging. 2016;
33(1):27-36. doi:10.1007/s40266-015-0327-0
10. Fischer BL, Gunter-Hunt G, Steinhafel CH, Howell T. The iden-
tification and assessment of late-life ADHD in memory clinics.
J Atten Disord. 2012;16(4):333-338. doi:10.1177/10870547113
98886
11. Ivanchak N, Fletcher K, Jicha GA. Attention-deficit/hyperactivity
disorder in older adults: prevalence and possible connections to
mild cognitive impairment. Curr Psychiatry Rep. 2012;14(5):
552-560. doi:10.1007/s11920-012-0305-8
12. Berck J. Is it old age, or A.D.H.D.? New York Times. September
28, 2015:D6. Accessed February 26, 2020. https://well.blogs.
nytimes.com/2015/09/28/is-it-alzheimers-or-a-d-h-d/
Prentice et al
13. Reddy S. An unexpected new diagnosis in older adults: ADHD.
Wall Str J. 2020. Accessed February 24, 2020. https://www.wsj.
com/articles/an-unexpected -new-diagnosis-in-older-adults-adhd-
11582558978
14. Hampton T. ADHD in older adults: is it on your radar? Med Page
Today. 2017. Accessed May 7, 2018. https://www.medpagetoday
.com/resource-centers/adult-adhd/adhd-older-adults-your-radar/
1597
15. Centers for Disease Control and Prevention. Trends in aging—
United States and worldwide. MMWR Morb Mortal Wkly Rep.
2003;52(6):101-104, 106. Accessed October 22, 2018. http://
www.ncbi.nlm.nih.gov/pubmed/12645839
16. Semeijn EJ, Comijs HC, De vet HCW, et al. Lifetime stability of
ADHD symptoms in older adults. Atten Defic Hyperact Disord.
2016;8(1):13-20. doi:10.1007/s12402-015-0178-x
17. McKeith IG, Boeve BF, Dickson DW, et al. Diagnosis and man-
agement of dementia with Lewy bodies: fourth consensus report
of the DLB Consortium. Neurology. 2017;89(1):88-100. doi:10
.1212/WNL.0000000000004058
18. Woods SP, Lovejoy DW, Ball JD. Neuropsychological character-
istics of adults with ADHD: a comprehensive review of initial
studies. Clin Neuropsychol. 2002;16(1):12-34. doi:10.1076/clin
.16.1.12.8336
19. Donaghy PC, McKeith IG. The clinical characteristics of demen-
tia with Lewy bodies and a consideration of prodromal diagnosis.
Alzheimers Res Ther. 2014;6(4):46. doi:10.1186/alzrt274
20. Bush G. Attention-deficit/hyperactivity disorder and attention
networks. Neuropsychopharmacology. 2010;35(1):278-300. doi:
10.1038/npp.2009.120
21. Michielsen M, Comijs HC, Semeijn EJ, Beekman ATF, Deeg
DJH, Sandra Kooij JJ. The comorbidity of anxiety and depressive
symptoms in older adults with attention-deficit/hyperactivity dis-
order: a longitudinal study. J Affect Disord. 2013;148(2-3):
220-227. doi:10.1016/j.jad.2012.11.063
22. Auning E, Rongve A, Fladby T, et al. Early and presenting symp-
toms of dementia with Lewy bodies. Dement Geriatr Cogn Dis-
ord. 2011;32(3):202-208. doi:10.1159/000333072
23. Snitselaar MA, Smits MG, Spijker J. Prevalence of restless legs
syndrome in adult ADHD and its subtypes. Behav Sleep Med.
2016;14(5):480-488. doi:10.1080/15402002.2015.1018386
24. Cortese S, Konofal E, Lecendreux M, et al. Restless legs syn-
drome and attention-deficit/hyperactivity disorder: a review of
the literature. Sleep. 2005;28(8):1007-1013. doi:10.1093/sleep/
28.8.1007
25. Michielsen M, Semeijn E, Comijs HC, et al. Prevalence of
attention-deficit hyperactivity disorder in older adults in the Neth-
erlands. Br J Psychiatry. 2012;201(4):298-305. doi:10.1192/bjp
.bp.111.101196
26. Caye A, Sibley MH, Swanson JM, Rohde LA. Late-onset ADHD:
understanding the evidence and building theoretical frameworks.
Curr Psychiatry Rep. 2017;19(12):106. doi:10.1007/s11920-017
-0858-7
27. Moos RH, Schutte KK, Brennan PL, Moos BS. The interplay
between life stressors and depressive symptoms among older
adults. J Gerontol B Psychol Sci Soc Sci. 2005;60(4):P199-
P206. doi:10.1093/geronb/60.4.p199
13
28. Fujishiro H, Iseki E, Nakamura S, et al. Dementia with Lewy
bodies: early diagnostic challenges. Psychogeriatrics. 2013;
13(2):128-138. doi:10.1111/psyg.12005
29. Barkley RA. Neuropsychological testing is not useful in the diag-
nosis of ADHD: stop it (or prove it)! ADHD Rep. 2019;27(2):1-8.
doi:10.1521/adhd.2019.27.2.1
30. Burrell JR, Piguet O. Lifting the veil: how to use clinical neurop-
sychology to assess dementia. J Neurol Neurosurg Psychiatry.
2015;86(11):1216-1224. doi:10.1136/jnnp-2013-307483
31. Smith GE, Bondi MW. Mild cognitive impairment. In: Smith GE,
Bondi MW, eds. Mild Cognitive Impairment and Dementia: Def-
initions, Diagnosis and Treatment. Oxford University Press;
2013:69-133.
32. Braun M, Tupper D, Kaufmann P, et al. Neuropsychological
assessment: a valuable tool in the diagnosis and management of
neurological, neurodevelopmental, medical and psychiatric dis-
orders. Cogn Behav Neurol. 2011;24(3):107-114. doi:10.1097/
WNN.0b013e3182351289
33. LeRoy A, Jacova C, Young C. Neuropsychological performance
patterns of adult ADHD subtypes. J Atten Disord. 2018:10870
5471877392. doi:10.1177/1087054718773927
34. Kontaxopoulou D, Beratis IN, Fragkiadaki S, et al. Exploring the
profile of incidental memory in patients with amnestic mild cog-
nitive impairment and mild Alzheimer’s disease. J Alzheimers
Dis. 2018;65(2):617-627. doi:10.3233/JAD-180328
35. McLaughlin PM, Wright MJ, LaRocca M, et al. The “Alzheimer’s
type” profile of semantic clustering in amnestic mild cognitive
impairment. J Int Neuropsychol Soc. 2014;20(4):402-412. doi:10
.1017/S135561771400006X
36. Moher D, Liberati A, Tetzlaff J, Altman DG, PRISMA Group.
Preferred reporting items for systematic reviews and meta-analy-
ses: the PRISMA statement. Ann Intern Med. 2009;151(4):
264-269. doi:10.7326/0003-4819-151-4-200908180-00135.
37. American Psychiatric Association. Diagnostic and Statistical
Manual of Mental Disorders (DSM-5®). American Psychiatric
Publication; 2013.
38. American Psychiatric Association. Diagnostic and Statistical
Manual of Mental Disorders, Third Edition. American Psychia-
tric Publishing; 1980.
39. American Psychiatric Association. Diagnostic and Statistical
Manual of Mental Disorders, Third Edition—Revised. American
Psychiatric Publishing; 1987.
40. American Psychiatric Association. Diagnostic and Statistical
Manual of Mental Disorders, Fourth Edition. American Psychia-
tric Publishing; 1994.
41. American Psychiatric Association. Diagnostic and Statistical
Manual of Mental Disorders, Fourth Edition—Text Revision.
American Psychiatric Publishing; 2000.
42. CEBM. Centre for evidence-based medicine critical appraisal
tools. 2018. Accessed November 4, 2018. https://www.cebm.
net/2014/06/critical-appraisal/
43. Peinemann F, Tushabe DA, Kleijnen J. Using multiple types of
studies in systematic reviews of health care interventions—a sys-
tematic review. Briel M, ed. PLoS One. 2013;8(12):e85035. doi:
10.1371/journal.pone.0085035
14
44. Cicchetti D V, Feinstein AR. High agreement but low kappa: II.
resolving the paradoxes. J Clin Epidemiol. 1990;43(6):551-558.
doi:10.1016/0895-4356(90)90159-m
45. Gwet KL. Computing inter-rater reliability and its variance in the
presence of high agreement. Br J Math Stat Psychol. 2008;61(1):
29-48. doi:10.1348/000711006X126600
*46. Oishi Y, Imamura T, Shimomura T, Suzuki K. Visual texture
agnosia in dementia with Lewy bodies and Alzheimer’s disease.
Cortex. 2018;103:277-290. doi:10.1016/j.cortex.2018.03.018
*47. Smits LL, van Harten AC, Pijnenburg YAL, et al. Trajectories of
cognitive decline in different types of dementia. Psychol Med.
2015;45(05):1051-1059. doi:10.1017/S0033291714002153
*48. Ferman TJ, Smith GE, Boeve BF, et al. Neuropsychological
differentiation of dementia with Lewy bodies from normal aging
and Alzheimer’s disease. Clin Neuropsychol. 2006;20(4):
623-636. doi:10.1080/13854040500376831 Note: This study
employs a rigorous, large sample for increased power.
*49. Aldridge GM, Birnschein A, Denburg NL, Narayanan NS. Par-
kinson’s disease dementia and dementia with Lewy bodies have
similar neuropsychological profiles. Front Neurol. 2018;9(3):
1-8. doi:10.3389/fneur.2018.00123
*50. Ferman TJ, Boeve BF, Smith GE, et al. Dementia with Lewy
bodies may present as dementia and REM sleep behavior dis-
order without parkinsonism or hallucinations. J Int Neuropsy-
chol Soc. 2002;8(7):907-914. doi:10.1017/s1355617702870047
*51. Westervelt HJ, Bruce JM, Faust MA. Distinguishing Alzhei-
mer’s disease and dementia with Lewy bodies using cognitive
and olfactory measures. Neuropsychology. 2016;30(3):304-311.
doi:10.1037/neu0000230
*52. Kemp J, Philippi N, Phillipps C, et al. Cognitive profile in pro-
dromal dementia with Lewy bodies. Alzheimers Res Ther. 2017;
9(1):19. doi:10.1186/s13195-017-0242. -1
53. Folstein MF, Folstein SE, McHugh PR. “Mini mental state” a
practical method for grading the cognitive state of patients for
the clinician. J Psychiatr Res. 1975;12(3):189-198.
54. Nasreddine ZS, Phillips NA, Bédirian V, et al. The Montreal
Cognitive Assessment, MoCA: a brief screening tool for mild
cognitive impairment. J Am Geriatr Soc. 2005;53(4):695-699.
doi:10.1111/j.1532-5415.2005.53221.x
*55. Petrova M, Pavlova R, Zhelev Y, Mehrabian S, Raycheva M,
Traykov L. Investigation of neuropsychological characteristics
of very mild and mild dementia with Lewy bodies. J Clin Exp
Neuropsychol. 2016;38(3):354-360. doi:10.1080/13803395.
2015.1117058 Note: This paper demonstrates the utility of
differentiating impairment across levels of severity of DLB.
*56. Salmon DP, Heindel WC, Hamilton JM, et al. Recognition mem-
ory span in autopsy-confirmed dementia with Lewy bodies and
Alzheimer’s disease. Neuropsychologia. 2015;75:548-555. doi:
10.1016/j.neuropsychologia.2015.07.014
*57. Xu Y, Chen K, Zhao Q, Guo Q. Comparing the neuropsycholo-
gical profiles of mild dementia with Lewy bodies and mild Alz-
heimer’s disease. Psychogeriatrics. 2018;18(1):64-71. doi:10
.1111/psyg.12293
*58. Bailon O, Roussel M, Boucart M, Krystkowiak P, Godefroy O.
Psychomotor slowing in mild cognitive impairment, Alzhei-
mer’s disease and Lewy body dementia: mechanisms and
Journal of Geriatric Psychiatry and Neurology XX(X)
diagnostic value. Dement Geriatr Cogn Disord. 2010;29(5):
388-396. doi:10.1159/000305095
*59. Bussè C, Anselmi P, Pompanin S, et al. Specific verbal memory
measures may distinguish Alzheimer’s disease from dementia
with Lewy bodies. J Alzheimers Dis. 2017;59(3):1009-1015.
doi:10.3233/JAD-170154
*60. Crowell TA, Luis CA, Cox DE, Mullan M. Neuropsychological
comparison of Alzheimer’s disease and dementia with Lewy
bodies. Dement Geriatr Cogn Disord. 2007;23(2):120-125.
doi:10.1159/000097791
*61. Heitz C, Noblet V, Phillipps C, et al. Cognitive and affective
theory of mind in dementia with Lewy bodies and Alzheimer’s
disease. Alzheimers Res Ther. 2016;8(1):1-15. doi:10.1186/
s13195-016-0179-9
*62. Mitolo M, Hamilton JM, Landy KM, et al. Visual perceptual
organization ability in autopsy-verified dementia with Lewy
bodies and Alzheimer’s disease. J Int Neuropsychol Soc. 2018;
22(6):609-619. doi:10.1017/S1355617716000436
*63. Perri R, Fadda L, Caltagirone C, Carlesimo GA. Word list and
story recall elicit different patterns of memory deficit in patients
with Alzheimer’s disease, frontotemporal dementia, subcortical
ischemic vascular disease, and Lewy body dementia. J Alzhei-
mers Dis. 2013;37(1):99-107. doi:10.3233/JAD-130347
*64. Bramham J, Murphy DGM, Xenitidis K, Asherson P, Hopkin G,
Young S. Adults with attention deficit hyperactivity disorder: an
investigation of age-related differences in behavioural symp-
toms, neuropsychological function and co-morbidity. Psychol
Med. 2012;42(10):2225-2234. doi:10.1017/
S0033291712000219
*65. Semeijn EJ, Korten NCM, Comijs HC, et al. No lower cognitive
functioning in older adults with attention-deficit/hyperactivity
disorder. Int Psychogeriatr. 2015:27(9):1-10. doi:10.1017/
S1041610215000010 Note: Comprehensive study that
recruited an ADHD sample that is older than 65 years old,
which is an important knowledge gap in the literature.
*66. Thorell LB, Holst Y, Chistiansen H, Kooij JJS, Bijlenga D, Sjö-
wall D. Neuropsychological deficits in adults age 60 and above
with attention deficit hyperactivity disorder. Eur Psychiatry.
2017;45:90-96. doi:10.1016/j.eurpsy.2017.06.005
*67. Downes JJ, Priestley NM, Doran M, Ferran J, Ghadiali E,
Cooper P. Intellectual, mnemonic, and frontal functions in
dementia with Lewy bodies: a comparison with early and
advanced Parkinson’s disease. Behav Neurol. 1999;11(3):
173-183. doi:10.1155/1999/851860
*68. Calderon J, Perry RJ, Erzinclioglu SW, Berrios GE, Dening TR,
Hodges JR. Perception, attention, and working memory are dis-
proportionately impaired in dementia with Lewy bodies com-
pared with Alzheimer’s disease. J Neurol Neurosurg
Psychiatry. 2001;70(2):157-164. doi:10.1136/jnnp.70.2.157
*69. Mosimann UP, Mather G, Wesnes KA, O’Brien JT, Burn DJ,
McKeith IG. Visual perception in Parkinson disease dementia
and dementia with Lewy bodies. Neurology. 2004;63(11):
2091-2096. doi:10.1212/01.WNL.0000145764.70698.4E
*70. Wang CSM, Pai MC, Chen PL, Hou NT, Chien PF, Huang YC.
Montreal Cognitive Assessment and Mini-Mental State Exam-
ination performance in patients with mild-to-moderate dementia
Prentice et al
with Lewy bodies, Alzheimer’s disease, and normal participants
in Taiwan. Int Psychogeriatrics. 2013;25(11):1839-1848. doi:10
.1017/S1041610213001245
*71. Varanese S, Perfetti B, Monaco D, et al. Fluctuating cognition
and different cognitive and behavioural profiles in Parkinson’s
disease with dementia: comparison of dementia with Lewy bod-
ies and Alzheimer’s disease. J Neurol. 2010;257(6):1004-1011.
doi:10.1007/s00415-010-5453-3
*72. Cormack F, Gray A, Ballard C, Tovée MJ. A failure of ‘pop-out’
in visual search tasks in dementia with Lewy bodies as compared
to Alzheimer’s and Parkinson’s disease. Int J Geriatr Psychia-
try. 2004;19(8):763-772. doi:10.1002/gps.1159
*73. Nervi A, Reitz C, Tang M-X, et al. Comparison of clinical man-
ifestations in Alzheimer disease and dementia with Lewy bodies.
Arch Neurol. 2008;65(12):1634-1639. doi:10.1001/archneur.65.
12.1634. Note: Large sample study with a comprehensive
assesment battery, allowing for nuanced evaluation of con-
structs of interest.
*74. Lambon Ralph MA, Powell J, Howard D, Whitworth AB, Gar-
rard P, Hodges JR. Semantic memory is impaired in both demen-
tia with Lewy bodies and dementia of Alzheimer’s type: a
comparative neuropsychological study and literature review. J
Neurol Neurosurg Psychiatry. 2001;70(2):149-156. Accessed
January 29, 2019. http://www.ncbi.nlm.nih.gov/pubmed/
11160461
*75. Ota K, Murayama N, Kasanuki K, et al. Visuoperceptual assess-
ments for differentiating dementia with Lewy bodies and Alz-
heimer’s disease: illusory contours and other
neuropsychological examinations. Arch Clin Neuropsychol.
2015;30(3):256-263. doi:10.1093/arclin/acv016
76. Serra L, Giulietti G, Cercignani M, et al. Mild cognitive impair-
ment: same identity for different entities. J Alzheimers Dis. 2013;
33(4):1157-1165. doi:10.3233/JAD-2012-121663
77. Arsenault-Lapierre G, Whitehead V, Belleville S, Massoud F,
Bergman H, Chertkow H. Mild cognitive impairment subcate-
gories depend on the source of norms. J Clin Exp Neuropsychol.
2011;33(5):596-603. doi:10.1080/13803395.2010.547459
78. Harrison AG, Armstrong IT, Harrison LE, Lange RT, Iverson GL.
Comparing Canadian and American normative scores on the
Wechsler Adult Intelligence Scale Fourth Edition. Arch Clin Neu-
ropsychol. 2014;29(8):737-746. doi:10.1093/arclin/acu048
79. Barkley RA. Behavioral inhibition, sustained attention, and exec-
utive functions: constructing a unifying theory of ADHD. Psychol
Bull. 1997;121(1):65-94. doi:10.1037/0033-2909.121.1.65
80. Fuermaier ABM, Fricke JA, de Vries SM, Tucha L, Tucha O.
Neuropsychological assessment of adults with ADHD: a Delphi
consensus study. Appl Neuropsychol Adult. 2019;26(4):340-354.
doi:10.1080/23279095.2018.1429441
81. Seidman LJ, Biederman J, Weber W, Hatch M, Faraone S V.
Neuropsychological function in adults with attention-deficit
hyperactivity disorder. Biol Psychiatry. 1998;44(4):260-268.
doi:10.1016/S0006-3223%2897%2900392-2
82. Schoechlin C, Engel RR. Neuropsychological performance in
adult attention-deficit hyperactivity disorder: meta-analysis of
empirical data. Arch Clin Neuropsychol. 2005;20(6):727-744.
doi:10.1016/j.acn.2005.04.005
15
83. Holst Y, Thorell LB. Neuropsychological functioning in adults
with ADHD and adults with other psychiatric disorders: the issue
of specificity. J Atten Disord. 2017;21(2):137-148. doi:10.1177/
1087054713506264
84. Boyer BE, Geurts HM, Van der Oord S. Planning skills of ado-
lescents with ADHD. J Atten Disord. 2018;22(1):46-57. doi:10
.1177/1087054714538658
85. Stuss D. Functions of the frontal lobes: relation to executive func-
tions. J Int Neuropsychol Soc. 2011;17(05):759-765. doi:10.1017/
S1355617711000695
86. Aleman A, van’t Wout M. Repetitive transcranial magnetic sti-
mulation over the right dorsolateral prefrontal cortex disrupts
digit span task performance. Neuropsychobiology. 2008;57(1-2):
44-48. doi:10.1159/000129666
87. Alvarez JA, Emory E. Executive function and the frontal lobes: a
meta-analytic review. Neuropsychol Rev. 2006;16(1):17-42. doi:
10.1007/s11065-006-9002-x
88. Kasparek T, Theiner P, Filova A. Neurobiology of ADHD from
childhood to adulthood. J Atten Disord. 2015;19(11):931-943.
doi:10.1177/1087054713505322
89. Mak E, Su L, Williams GB, O’Brien JT. Neuroimaging charac-
teristics of dementia with Lewy bodies. Alzheimers Res Ther.
2014;6(2):18. doi:10.1186/alzrt248
90. Sánchez-Cubillo I, Periáñez JA, Adrover-Roig D, et al. Construct
validity of the trail making test: role of task-switching, working
memory, inhibition/interference control, and visuomotor abilities.
J Int Neuropsychol Soc. 2009;15(03):438. doi:10.1017/
S1355617709090626
91. Gualtieri CT, Johnson LG. ADHD: is objective diagnosis possi-
ble? Psychiatry (Edgmont). 2005;2(11):44-53. Accessed February
7, 2019. http://www.ncbi.nlm.nih.gov/pubmed/21120096
92. Barkley RA, Eme R. Is neuropsychological testing useful for any
reason in the evaluation of ADHD? a rejoinder to Mapou. ADHD
Rep. 2019;27(5):1-8. doi:10.1521/adhd.2019.27.5.1
93. Bahcivan Saydam R, Ayvasik HB, Alyanak B. Executive func-
tioning in subtypes of attention deficit hyperactivity disorder.
Noro Psikiyatr Ars. 2015;52(4):386-392. doi:10.5152/npa.2015
.8712
94. Lawrence V, Houghton S, Douglas G, Durkin K, Whiting K,
Tannock R. Executive function and ADHD: a comparison of
children’s performance during neuropsychological testing and
real-world activities. J Atten Disord. 2004;7(3):137-149. doi:10
.1177/108705470400700302
95. Berlin L, Bohlin G, Nyberg L, Janols LO. How well do measures
of inhibition and other executive functions discriminate between
children with ADHD and controls? Child Neuropsychol. 2004;
10(1):1-13. doi:10.1076/chin.10.1.1.26243
96. Boonstra AM, Oosterlaan J, Sergeant JA, Buitelaar JK. Executive
functioning in adult ADHD: a meta-analytic review. Psychol
Med. 2005;35(8):1097-1108. Accessed June 5, 2017. http://
www.ncbi.nlm.nih.gov/pubmed/16116936
97. Barkley RA, Murphy KR. The nature of executive function (EF)
deficits in daily life activities in adults with ADHD and their
relationship to performance on EF tests. J Psychopathol Behav
Assess. 2011;33(2):137-158. doi:10.1007/s10862-011-9217-x
16
98. Biederman J, Petty CR, Fried R, et al. Discordance between
psychometric testing and questionnaire-based definitions of
executive function deficits in individuals with ADHD. J Atten
Disord. 2008;12(1):92-102. doi:10.1177/1087054707305111
99. Barkley RA, Murphy KR. Impairment in occupational function-
ing and adult ADHD: the predictive utility of executive function
(EF) ratings versus EF tests. Arch Clin Neuropsychol. 2010;25(3):
157-173. doi:10.1093/arclin/acq014
100. Morris JC, Weintraub S, Chui HC, et al. The uniform data set
(UDS): clinical and cognitive variables and descriptive data from
Alzheimer Disease Centers. Alzheimer Dis Assoc Disord. 2006;
20(4):210-216. doi:10.1097/01.wad.0000213865.09806.92
101. Yamada M, Komatsu J, Nakamura K, et al. Diagnostic criteria
for dementia with Lewy bodies: updates and future directions.
J Mov Disord. 2020;13(1):1-10. doi:10.14802/jmd.19052
102. Curtin K, Fleckenstein AE, Keeshin BR, et al. Increased risk of
diseases of the basal ganglia and cerebellum in patients with a
history of attention-deficit/hyperactivity disorder. Neuropsycho-
pharmacology. 2018;43(13):2548-2555. doi:10.1038/s41386-
018-0207-5
Journal of Geriatric Psychiatry and Neurology XX(X)
103. Fluegge K, Fluegge K. Antecedent ADHD, dementia, and
metabolic dysregulation: a U.S. based cohort analysis.
Neurochem Int. 2018;112:255-258. doi:10.1016/j.neuint.2017
.08.005
104. Tzeng NS, Chung CH, Lin FH, et al. Risk of dementia in adults
with ADHD: a nationwide, population-based cohort study in
Taiwan. J Atten Disord. 2019;23(9):995-1006. doi:10.1177/
1087054717714057
105. Golimstok A, Rojas JI, Romano M, Zurru MC, Doctorovich D,
Cristiano E. Previous adult attention-deficit and hyperactivity
disorder symptoms and risk of dementia with Lewy bodies: a
case–control study. 2011;18(1):78-84. doi:10.1111/j.1468-1331.
2010.03064.x
106. Walitza S, Melfsen S, Herhaus G, et al. Association of Parkin-
son’s disease with symptoms of attention deficit hyperactivity
disorder in childhood. J Neural Transm. 2007;(suppl 72):
311-315. doi:10.1007/978-3-211-73574-9_38
107. Petersen RC. Mild cognitive impairment as a diagnostic entity.
J Intern Med. 2004;256(3):183-194. doi:10.1111/j.1365-2796.
2004.01388.x