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MOCA VERSUS MMSE IN ASSESSING COGNITION IN PD

A Comparison of the Mini Mental


State Exam to the Montreal
Cognitive Assessment in
Identifying Cognitive Decits in
Parkinsons Disease
Cindy Zadikoff, MD,1,2 Susan H. Fox, MD, PhD,2
David F. Tang-Wai, MDCM FRCPC,2
Teri Thomsen, MD,2 Rob M.A. de Bie, MD, PhD,2,3
Pettarusup Wadia, MD,2
Janis Miyasaki, MD Med FRCPC,2
Sarah Duff-Canning, PhD., C Psych,2
Anthony E. Lang, MD,2
and Connie Marras, MD, PhD2*
1

Department of Neurology, Northwestern University,


Parkinsons Disease and Movement Disorders Center,
Chicago, Illinois; 2Division of Neurology, Toronto Western
Hospital, University of Toronto, Toronto, Ontario, Canada;
3
Department of Neurology, Academic Medical Center,
Amsterdam, The Netherlands
Abstract: Dementia is an important and increasingly recognized problem in Parkinsons disease (PD). The mini-mental state examination (MMSE) often fails to detect early
cognitive decline. The Montreal cognitive assessment
(MoCA) is a brief tool developed to detect mild cognitive
impairment that assesses a broader range of domains frequently affected in PD. The scores on the MMSE and the
MoCA were compared in 88 patients with PD. A pronounced ceiling effect was observed with the MMSE but not
with the MoCA. The range and standard deviation of scores
was larger with the MoCA(730, 4.26) than with the
MMSE(16 30, 2.55). The percentage of subjects scoring
below a cutoff of 26/30 (used by others to detect mild
cognitive impairment) was higher on the MoCA (32%) than
on the MMSE (11%)(P < 0.000002). Compared to the
MMSE, the MoCA may be a more sensitive tool to identify
early cognitive impairment in PD. 2007 Movement Disorder Society
Key words: Parkinsons disease; dementia; mild cognitive
impairment; MMSE; MoCA.

Depending on the method of ascertainment of cases,


20 80% of patients with Parkinsons disease (PD) will

*Correspondence to: Dr. Connie Marras, Toronto Western Hospital,


Morton and Gloria Shulman Movement Disorders Center, McL-7, 399
Bathurst St., Toronto, Ontario, Canada M5T 2S8.
E-mail: connie.marras@utoronto.ca
Received 6 June 2007; Revised 7 August 2007; Accepted 12 October
2007
Published online 28 November 2007 in Wiley InterScience (www.
interscience.wiley.com). DOI: 10.1002/mds.21837

297

develop dementia (PDD) over time.1,2 Recognition of


cognitive impairment in PD is important as it is associated with shorter life expectancy,3 contributes signicantly towards caregiver distress,4 and is associated with
increased adverse affects from antiparkinsonian medications.5 Moreover, dementia itself is an absolute contraindication to deep brain stimulation (DBS),6 a surgical
procedure used to ameliorate the motor symptoms in
patients with PD. Therefore, early recognition of these
decits is important so as to direct appropriate treatment
decisions and to reduce morbidity.
Neuropsychological testing is the gold standard for assessing cognition but it is time consuming and many clinicians lack easy and timely access to such assessments. The
use of a rapid and easily applied screening test sensitive to
cognitive impairment in PD is a more practical approach as
it can guide clinical decision making and triage referral to
neuropsychological testing. The mini-mental state examination (MMSE) is widely used because it is quick and easy
to administer in a clinical setting.7 However, it is insensitive
to mild cognitive impairment. Moreover, it lacks adequate
sampling of executive functions and therefore may not
detect cognitive decits common to PD, especially in the
early stages of the disease.8 11
The Montreal Cognitive Assessment (MoCA) is a brief
30-point screening instrument that was developed and validated to identify patients with mild cognitive impairment
(MCI), a clinical state that often progresses to dementia.12
Compared to the MMSE, the MoCA has a sensitivity of
90% compared to 18% in detecting MCI. In addition, the
MoCA uses more numerous and demanding tasks to assess
executive function, higher level language abilities, memory,
and complex visuospatial processing. For example, the
MoCA utilizes more words for learning and employs a
longer interval in assessing delayed recall. The cognitive
prole of PDD is qualitatively similar to PD but with more
severe and extensive decits including impairments in attention, learning and memory, and visuospatial functions.
Thus, the MoCA may be more sensitive than the MMSE to
early stages of dementia characteristic of PDD.
The objective of this study was to compare MMSE to
MoCA scores in patients with idiopathic PD. This rst
step was to determine whether the MoCA is a more
sensitive screening tool than the MMSE for identifying
cognitive decits in patients with PD. Secondary objectives were to (1) determine the range of MoCA scores
exhibited by patients with idiopathic PD, and (2) assess
the correlation between the UPDRS Part I item 1 scores
(subjective assessment of cognitive decits from the
patient and caregivers point of view) and the scores
obtained on the MMSE and MoCA.

Movement Disorders, Vol. 23, No. 2, 2008

298

C. ZADIKOFF ET AL.

TABLE 1. Number of subjects with scores above and below


the 26-point cutoff on each test
MMSE 26
MMSE 26
Total

MoCA 26

MoCA 26

Total

50
0
50

28
10
38

78
10
88

DESIGN/METHODS
Inclusion Criteria
Patients with idiopathic PD of at least 5 years duration
presenting for routine follow-up at the Toronto Western
Hospital Movement Disorders Center were asked to
participate.
Exclusion Criteria
Signs or symptoms atypical for idiopathic PD or signicant depression (score 2 on the UPDRS I (Q1.3)).
Data Collection
All patients were in the ON state at the time of
assessment. Items common to both tests were asked only
once using a combined version of the MMSE and
MoCA, and the sequence of items similar in both tests
was alternated from subject to subject to avoid order
effects when comparing the MMSE to MoCA scores.
The primary outcome measure was the proportion of
patients with a score less than 26 on either test. A score
of less than 26 on the MMSE has been used in other
studies as a cutoff providing evidence for cognitive impairment.11,12 A cutoff of 26 in the MoCA was chosen as
this was found to be the score optimizing sensitivity and
specicity in the original study assessing MCI.12
Sample Size Calculation and Analysis
Assuming a frequency of MCI of 40%, a sample size of
198 subjects would provide 80% power for a two-tailed
P-value at a signicant level of 0.05 to detect a 10%
difference in the proportion of subjects screening positive
between the two tests. Proportions were compared using
chi-square tests. Correlations were tested using Spearman
correlation coefcients due to the ordinal nature of the
UPDRS scores. Continuous data are expressed as means
and standard deviation. One point was added to an individuals score if s/he had twelve years or fewer of formal
education, for a total maximum of 30 points.
RESULTS
The study was terminated early due to resource limitations. Eighty-eight subjects (26 F, 62 M) participated. The
mean age of the sample was 65 (/10) years, mean

Movement Disorders, Vol. 23, No. 2, 2008

disease duration 9.5 (/5) years, mean UPDRS III 20.7


(/11.6), and mean levodopa equivalent dose 1,242 mg
(/2,943). Thirty eight subjects (43%) did not complete
high school, 7 subjects (8%) completed high school, and 43
subjects (48%) had a university degree. After adjusting for
education, more subjects had a score of less than 26 on the
MoCA (43%) than on the MMSE (11%) (2 22.5, P
0.000002). No subject with a score greater than 25 on the
MoCA scored less than 26 on the MMSE while 36% of
those who scored greater than 25 on the MMSE had a score
less than 26 on the MoCA (P 0.0001) (Table 1). The
range and standard deviation of scores was larger with the
MoCA (730,4.26) than with the MMSE (16 30, 2.55).
There was a more pronounced ceiling effect of the MMSE
(27 subjects had a score of 30) than of the MoCA (4
subjects had a score of 30) (see Fig. 1). Both the MMSE and
the MoCA correlated with UPDRS I item 1, but the MMSE
slightly more so (Spearman correlation coefcients 0.34,
P 0.0013 vs. 0.26, P 0.0153). When MMSE and
MoCA scores on items assessing the same cognitive domain or function were compared, items assessing attention,
visuospatial function, executive function, naming, and repetition contributed to the lower MoCA scores. Recall scores
correlated with the order in which the items were given and
not with the specic test (MMSE or MoCA).
DISCUSSION
In this study we demonstrated that the MoCA, compared to the MMSE, is less prone to ceiling effects in PD
and classies more patients as having mild cognitive
impairment, as dened by a score less than 26. PD
patients commit more errors on the MoCA than on the
MMSE in domains typically affected in PDD such as
attention, executive function, and visuospatial processing. This suggests that the MoCA will be more sensitive
than the MMSE to early cognitive impairment in PD.

FIG. 1. Frequency of scores on the Montreal cognitive assessment and


the mini mental state exam.

GCH1 MUTATION IN A BRAZILIAN FAMILY WITH DRD


Two cognitive scales11,13 have been developed recently for use in PD, but each has its own limitations.
The rst, Cambridge Cognitive Assessment-Revised
(CAMCOG-R),11 takes at least 30 min to administer, and
the latter, SCales for Outcomes in PD-cognition
(SCOPA-COG),13 developed as a research tool, only
examines a narrow range of cognitive domains specic
to PD. Patients with PD can develop impairment in
multiple cognitive domains, including memory. Therefore, a need exists for a brief and simple tool that assesses multiple cognitive domains that can be administered in an outpatient clinical setting for both screening
and following patients longitudinally.
One limitation of this study is that while a score less than
26 has been used as a criterion for MCI in previous studies;
it is not known whether this is the correct cutoff to appropriately identify patients with early cognitive impairment in
the PD population. Secondly, because the gold standard,
neuropsychological testing, was not applied we cannot be
certain that the lower scores on the MoCA are detecting
meaningful cognitive differences. Furthermore, only longitudinal follow-up can determine whether or not MoCA
scores are better predictors of future cognitive decline.
Longitudinal studies validating the MoCA against a formal
neuropsychological battery in PD patients are underway so
that the true sensitivity and specicity of the MoCA for
detecting MCI can be determined and appropriate cutoff
scores can be assigned.
We believe that the MoCA provides considerably
more insight into the cognitive status of patients with PD
than other simple screening tools such as the MMSE and
pending the results of studies correlating the MoCA to
formal neuropsychological testing, that the MoCA would
be a better choice than the widely used MMSE as a
cognitive screening instrument.
Acknowledgments: Funding for this study was provided by
the University of Toronto Behavioral Neurology section to CZ.
The assistance of staff and patients in the Movement Disorder
Clinic is greatly appreciated.

299

5. Holroyd S, Currie L, Wooten GF. Prospective study of hallucinations and delusions in Parkinsons disease. J Neurol Neurosurg
Psychiatry 2001;70:734 738.
6. Defer GL, Widner H, Marie RM, et al. Core assessment program
for surgical interventional therapies in Parkinsons disease (CAPSIT-PD). Mov Disord 1999;14:572584.
7. Folstein M, Folstein S, McHugh P. mini mental statea practical method for grading the cognitive state of patients for clinicians. J Psychiatr Res 1975;12:189 198.
8. Wind AW, Schellevis FG, Van Staveren G, et al. Limitations of the
mini-mental state examination in diagnosing dementia in general
practice. Int J Geriatr Psychiatry 1997;12:101108.
9. Tombaugh TN, McIntyre NJ. The mini-mental state examination:
a comprehensive review. J Am Geriatr Soc 1992;40:922935.
10. Tang-Wai DF, Knopman DS, Geda YE, et al. Comparison of the
short test of mental status and the mini-mental state examination in
mild cognitive impairment. Arch Neurol 2003;60:17771781.
11. Athey RJ, Porter RW, Walker RW. Cognitive assessment of a
representative community population with Parkinsons disease
(PD) using the cambridge cognitive assessment-revised (CAMCOG-R). Age Ageing 2005;34:268 273.
12. Nasreddine ZS, Phillips NA, Bedirian V, et al. The montreal
cognitive assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc 2005;53:695 699.
13. Marinus J, Visser M, Verwey NA, et al. Assessment of cognition
in Parkinsons disease. Neurology 2003;61:12221228.

Novel GCH1 Mutation in a


Brazilian Family with DopaResponsive Dystonia
Sarah Teixeira Camargos, MD,1
Francisco Cardoso, MD,1 Parastoo Momeni, PhD,2,3
Juliana Gurgel Gianetti, MD,1 Andrew Lees, MD,4
John Hardy, PhD,2,5 and Andrew Singleton, PhD2*
1
Universidade Federal de Minas Gerais, Department of
Clinical and Neurological Sciences, Movement Disorders
Group, Brazil; 2Laboratory of Neurogenetics, National
Institutes on Aging, National Institutes of Health, Maryland,
USA; 3Department of Neurology, Texas Tech University
Health Sciences Center, Texas, USA; 4Reta Lila Weston
Institute of Neurological Studies, University College London,
London, United Kingdom; 5Department of Molecular
Neuroscience, Institute of Neurology, Queen Square, London,
United Kingdom

REFERENCES
1. Sutcliffe RL, Meara JR. Parkinsons disease epidemiology in the
Northampton District, England, 1992 Acta Neurol Scand 1995;92:
443 450.
2. Aarsland D, Andersen K, Larsen JP, et al. Risk of dementia in
Parkinsons diseasea community-based, prospective study. Neurology 2001;56:730 736.
3. Marder K, Leung D, Tang M, et al. Are demented patients with
Parkinsons disease accurately reected in prevalence surveys? A
survival analysis. Neurology 1991;41:1240 1243.
4. Aarsland D, Larsen JP, Karlsen K, et al. Mental symptoms in
Parkinsons disease are important contributors to caregiver distress. Int J Geriatr Psychiatry 1999;14:866 874.

Abstract: Dopa responsive Dystonia (DRD) was rst described in 1971 and typically begins at childhood with gait
dysfunction caused by foot dystonia progressing to affect

*Correspondence to: Andrew Singleton, Laboratory of Neurogenetics, National Institutes on Aging, National Institutes of Health, Bethesda, MD 20892. E-mail: singleta@mail.nih.gov
Received 3 May 2007; revised 17 July 2007; accepted 15 October
2007
Published online 28 November 2007 in Wiley InterScience (www.
interscience.wiley.com). DOI: 10.1002/mds.21842

Movement Disorders, Vol. 23, No. 2, 2008

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