SREE CHITRA TIRUNAL INSTITUTE FOR MEDICAL SCIENCES AND …dspace.sctimst.ac.in/jspui/bitstream/123456789/2625/1/... · 2017. 1. 24. · 1 SREE CHITRA TIRUNAL INSTITUTE FOR MEDICAL

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SREE CHITRA TIRUNAL INSTITUTE FOR MEDICAL SCIENCES AND TECHNOLOGY

THIRUVANANTHAPURAM, KERALA

VALIDATION OF MALAYALAM VERSION OF MONTREAL COGNITIVE ASSESSMENT FOR KERALITE PATIENTS WITH PARKINSON’S DISEASE Thesis submitted in partial fulfilment of the rules and regulations

for DM degree Examination

By

Dr. Radhamani M Resident in Neurology

Month and year of submission: May 2015

DEPARTMENT OF NEUROLOGY Jan 2012 – May 2015

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DECLARATION

I, Dr. RADHAMANI M., hereby declare that this project was

undertaken by me under the supervision of the faculty, Department of

Neurology, Sree Chitra Tirunal Institute for Medical Sciences and

Technology.

Thiruvananthapuram Dr.RADHAMANI M. Date: 01-05-2015 DM Neurology resident

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Forwarded

The candidate, Dr. RADHAMANI M. has carried out the project under

my guidance.

Thiruvananthapuram Dr.SYAM K.

Date: 01-05-2015 Associate Professor

Department of Neurology

SCTIMST

Thiruvananthapuram

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Forwarded

The candidate Dr. RADHAMANI M., has carried out the minimum

required project.

Thiruvananthapuram PROF. Dr. MURALIDHARAN NAIR Date: 01-05-2015 Prof & HOD Department of Neurology

SCTIMST Thiruvananthapuram

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ACKNOWLEDGEMENT

I take this opportunity to express my sincere gratitude to Dr. Syam K, Associate

Professor of Neurology and Movement Disorders expert, SCTIMST, my guide for the study,

for his expert guidance, constant review, kind help and keen interest at each and every step

during the completion of the study.

I am indebted to Dr. Asha Kishore, Professor of Neurology and Movement

Disorders expert,SCTIMST for her guidance, encouragement and support during the period

of the study.

I thank Dr. Muralidharan Nair, Professor and Head, Department of Neurology for

his guidance, encouragement and valuable suggestions during the period of the study.

I am thankful to Ms. Sunitha J., Neuropsychologist ,department of Neurology,

SCTIMST, for her valuable input and assistance to the study.

I am indebted to Dr.Ramshekhar Menon, Assistant Professor, Department of

Neurology, for his guidance and support during the period of the study.

I express my sincere thanks to Dr. Sankara Sarma, Professor, Achutha Menon

Centre for Health Science Studies, for helping me with the statistical analysis of this study.

I express my heartfelt gratitude to Mr. Gangadhara Sarma, clinical psychologist

and social worker, Comprehensive Centre for Movement Diosrders, SCTIMST, for the

assistance in translation and for his sincere efforts and constant assistance during the entire

course of the study.

I extend my gratitude to all my patients who participated in this study.

Dr Radhamani M

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INDEX

1 Introduction 1

2 Review of literature 4

3 Objectives 30

4 Materials and Methods of the study 31

5 Statistical Analysis 36

6 Results 37

7 Discussion 51

8 Conclusion 55

9 Bibliography 57

10 Annexure 71

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INTRODUCTION

Parkinson’s disease (PD), the second most common

neurodegenerative disorder was initially known as a ‘motor” disorder

characterized by tremor, bradykinesia, rigidity and postural abnormalities. It

is now known that nonmotor manifestations are very common in PD, and

contribute to disability and impaired quality of life in patients.1,2 ,3,4

Cognitive impairment is one among the important non-motor manifestations

of PD . Non-motor manifestations, including cognitive dysfunction

dominate the clinical picture in the later stages of the disease. 1,2 Cognitive

dysfunction is an important non-motor manifestation, 5,6 with significant

impacts on functioning, quality of life and caregiver burden.7,8,9,10 The

spectrum of cognitive dysfunction range from mild cognitive impairment

(PD-MCI) to PD dementia (PDD). Cognitive dysfunction increases the risk

of nursing home placement and contribute to personal and socioeconomic

burden in patients with Parkinson’s disease 11,12 PD-MCI is common and

appears to place patients at risk of progressing to dementia.13 Dementia

occurs upto 83% of patients with PD over 20 years. 14 Even mild cognitive

deficits in PD are associated with functional impairment15,16 and worse

QOL.17,18

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Early identification is very important to start early interventions to

improve functioning and quality of life . Brief and sensitive

neuropsychological tests are required to administer in these patients for

early identification of the cognitive decline . Cognitive domains affected in

PD are attention , working memory, executive function, language, memory

and visuospatial function. 5,6,13 Validated neuropsychological tests sensitive

for detection of cognitive dysfunction in these domains are available in

English and other languages . Tests requiring long time are difficult to use

in PD patients in the clinic . Many short neuropsychological tests have

been developed and validated in PD patients . The Montreal Cognitive

Assessment was designed by by Nasreddine et al.19 as a brief screening

tool for MCI and has become an increasingly popular screening tool for

cognitive dysfunction not only in PD but also in the setting of Alzheimer

disease,stroke,vascular dementia, traumatic brain injury, and frontotemporal

dementia . This screening tool tests Short-term memory , visuospatial

function, executive function , attention ,concentration and working memory,

language and orientation in 10 minutes time. 19

The usefulness of MoCA as a suitable, accurate, and brief test for

screening all levels of cognition in PD has also been established. 20 In the

present study, we aimed to create a cross cultural adaptation of MoCA

(MoCA- Malayalam - “MoCA-M”) , and test its metric properties and

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reliability for use in Malayalam-speaking patients with PD. We hope that

MoCA-M will be a novel screening tool useful for detecting cognitive

impairment in its early stage itself, for use in Keralite population.

Review of Literature

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REVIEW OF LITERATURE

Parkinson’s disease is the second most common neurodegenerative

disorder with increased prevalence in males and age more than 60 years and

is a common cause of disability. PD was initially described by Dr James

Parkinson in “An essay of the shaking palsy”.21 The description of the

disorder was similar to how we describe it today, as a progressive disease

due to probable degenerative pathology in the central nervous system. The

main symptoms were characterized by resting tremor, flexed posture and

shuffling gait. The intellect and senses were described as being intact in the

initial description; cognitive dysfunction not considered as part of disease

till 1960s. There have been many diagnostic criteria proposed for the

clinical diagnosis; the United Kingdom Parkinson’s Disease Society Brain

Bank (UKPDSBB) criteria22 is the most widely used one and is well

validated.


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UK PARKINSON’S DISEASE SOCIETY BRAIN BANK CLINICAL

DIAGNOSTIC CRITERIA

1. Diagnosis of Parkinsonian Syndrome

Bradykinesia

At least one of the following

1. Muscular rigidity

2. 4-6 Hz rest tremor

3. postural instability not caused by primary visual, vestibular,

cerebellar, or proprioceptive dysfunction

2. Exclusion criteria for Parkinson’s disease

• History of repeated strokes with stepwise progression of

parkinsonian features

• History of repeated head injury

• History of definite encephalitis

• Oculogyric crises

• Neuroleptic treatment at onset of symptoms

• More than one affected relative


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• Sustained remission

• Strictly unilateral features after 3 years

• Supranuclear gaze palsy

• Cerebellar signs

• Early severe autonomic involvement

• Early severe dementia with disturbances of memory, language, and

praxis

• Babinski sign

• Presence of cerebral tumor or communication hydrocephalus on

imaging study

• Negative response to large doses of levodopa in absence of

malabsorption

MPTP exposure

3. Supportive prospective positive criteria for Parkinson’s disease

Three or more required for diagnosis of definite Parkinson’s disease

in combination with step one

• Unilateral onset


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• Rest tremor present

• Progressive disorder

• Persistent asymmetry affecting side of onset most

• Excellent response (70-100%) to levodopa

• Severe levodopa-induced chorea

• Levodopa response for 5 years or more

• Clinical course of ten years or more

Prevalence of PD

The prevalence of PD in people over 65 years of age is around 1-2%

and increases from 0.6% in the ages 65-69 to 2.8% in the ages 85-

89years.23,24 The cumulative incidence ( the life time risk) of PD up to 89

years of age is close to 3%.24 The mean age at symptom onset is in the late

60’s and population based studies report age at diagnosis to around 70 years

of age.25

Non motor symptoms of PD

PD is classically considered as a motor disorder but a diverse range

of nonmotor symptoms (NMS) including cognitive dysfunction occur in the

majority and dominate the clinical picture in the later stages of the


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disease.1,2 The nonmotor symptoms(NMS) of PD are increasingly

recognized as being critical to identify and treat because of their impact on

quality of life in PD perhaps having an even greater impact than motor

symptoms.4,26 The most commonly described primary NMS of PD are

autonomic dysfunction, cognitive abnormalities, sleep disorders, mood

disorders, pain, and sensory disorders.27 Non-motor symptoms in PD

include neuropsychiatric symptoms with depression, apathy, hallucinations,

cognitive impairment and dementia, sleep disorders with restless legs,

REMsleep behavior disorder, excessive daytime somnolence, vivid

dreaming and insomnia, autonomic symptoms with bladder disturbances,

orthostatic hypotension and sweating, sensory symptoms with olfactory

disturbance, pain and visual dysfunction and gastrointestinal symptoms with

constipation.4,27 There are also NMS in PD that are secondary to

treatment, such as impulse control disorders and psychosis. 27 Recent studies

shows that NMS may be present in the early PD 28 or may be the presenting

symptom in some patients. 29 NMS are missed in 50% of patients with PD

in routine consultations.28

Cognitive dysfunction in PD

Patients with PD have an almost six fold increased risk of

developing dementia compared with age-matched individuals

without PD.30 Cognitive dysfunction in PD may present in varying degrees.


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Occurrence is common even among patients with mild motor symptoms,

and includes difficulties such as bradyphrenia, or slowing of thinking, and

executive dysfunction, such as impairment of planning and goal-directed

behaviors.27 Subtle cognitive impairment is common in early disease and

one study has reported that over a third of patients have deficits at the time

of their diagnosis.31 Cognitive dysfunction is an important non-motor

manifestation,5,6 with significant impacts on functioning, quality of life and

caregiver burden.7,8,9,10

Although the cognitive deficits in PD have traditionally been

classified as being ‘‘subcortical’’ in nature, a range of cognitive domains

are impaired in PD patients without dementia. The spectrum of cognitive

dysfunction range from mild cognitive impairment (PD-MCI) to PD

dementia (PDD). Cognitive dysfunction in PD not only increases the risk of

nursing home placement, but also contribute to a more malignant course of

illness, and exacerbate personal and socioeconomic burden.11,12 PD-MCI is

common and appears to place patients at risk of progression to dementia;

13even mild cognitive deficits in PD are associated with functional

impairment 14,15 and worse QOL.17,18


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Pathogenesis of cognitive decline in PD

PD is characterized by a progressive widespread diffusion of the Lewy

body neuropathology from subcortical to cortical structures, therefore at

different disease stages, PD patients present different loads of Lewy body

neuropathology and different involvements of subcortical and cortical

structures.32 PD is associated with cortical Lewy pathology including limbic

and neocortical regions33 and AD related changes, including the

hippocampus suggesting that both PD and AD pathologies contribute to

cognitive decline in PD.34 Lewy bodies and neuronal loss in the substantia

nigra occurs concurrently with accumulation of α-synuclein deposition in

cholinergic neurons of the BF. 32 Loss of midbrain dopaminergic neurons of

the substantia nigra pars compacta, results in striatal dopaminergic

denervation.32 Cholinergic projection losses that vary from 5% to 25% in

PD subjects both with and without dementia.35,36

Pathogenesis of cognitive dysfunction in PD is heterogeneous and

may differ between individuals and between subtypes. Clinicopathological

studies showed brainstem predominant LB disease in majority and less

frequent brainstem-limbic forms(33%) and neocortical type of LB disease

in PD-MCI.37 Multiple pathogenic substrates in PDD include dysfunctions

of the subcortico-cortical networks 38,39 resulting from neuronal loss and

atrophy in amygdala and limbic areas,40 cholinergic deficits in cortex 41,42


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and thalamus associated with neuronal loss in the nucleus basalis of

Meynert (NBM) and decreased nicotinic acetylcholine receptors.43,44 The

number of LBs in the frontal cortex or of LB densities in the limbic cortex

may be a better predictor of dementia in PD.45

Cognitive deficits in early PD are associated with impaired

nigrostriatal dopaminergic function, which results in abnormal processing in

the frontostriatal circuit with reduced prefrontal and parietal metabolism.46

Parkinson’s disease -mild cognitive impairment (PD-MCI )

PD-MCI is thought to be common in non-demented PD patients and

is associated with increasing age, disease duration and disease severity.

PD-MCI is thought to predict the development of PD-D.13,47 The concept of

PD-MCI is now well supported by a number of studies showing an

association between electrophysiological, imaging, biochemical and

neuropathological variables and cognitive impairment in PD patients

without dementia.48-58. The QEEG measures of background rhythm

frequency and relative power in the theta band are potential predictive

biomarkers for dementia incidence in PD and EEG measures have potential

use as biomarkers in the study of both early and late cognitive deterioration

in PD.48 SPECT studies done in PD patients with normal cognition had

limited areas of hypometabolism in the frontal and occipital cortices and in


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the PDMCI patients, there were extensive areas of hypometabolism in the

posterior cortical regions, including the temporo-parieto-occipital junction,

medial parietal, and inferior temporal cortices suggest that posterior cortical

dysfunction is the primary neuroimaging feature of PD patients at risk for

dementia.50,51

In noncomplicated PD, structural neuroimaging (cranial computed

tomography and MRI) may be normal or show mild diffuse brain atrophy

and temporal lobe changes in early PD . Hippocampal atrophy and lateral

ventricular enlargement are structural biomarkers for PD-MCI . Marked

gray matter atrophy occurs in PDD, whereas far fewer extensive changes are

evident in PD-MCI.52 Studies on cerebrospinal fluid (CSF) biomarkers

suggest that CSF Aβ-42, and tau predict cognitive decline in PD. 55,56

Prevalence of PD-MCI

The studies done so far indicate that 18.9% -38.2 % of non-demented

PD patients have PD-MCI.47,59-65. In nondemented PD patients mean

prevalence was 27%; range, 19%–38% and is associated with the

subsequent development of PD Dementia(PDD) .The frequency of MCI

increases with age and with duration and severity of PD.13 Studies on newly

diagnosed PD patients also have shown significant cognitive decline over


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years.66,67 Nonamnestic, single-domain impairment (i.e., any single

nonmemory domain) is the most common subtype of PD-MCI.13

Figure1.Flowchart for the diagnosis of mild cognitive impairment and its

subtypes


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Risk factors for PD-MCI

Different studies showed that increasing age, male gender, lower

levels of education,later onset of disease, greater PD severity and longer

disease duration are associated with PD-MCI.68,69

Patterns of cognitive deficit in PD-MCI

Cognitive domains typically affected in PD include executive

function, attention, processing speed, visuospatial, learning and memory.68

PD-MCI may affect a range of cognitive domains, but single domain

impairment is more common than multiple domains and within a single

domain, nonamnestic impairment is more common than isolated amnestic

deficits. 13 In the nonamnestic single domain , high proportion of

visuospatial and executive function deficits observed such as problem

solving and working memory. Attentional-executive dysfunction is common

in most PD patients without dementia and up to half of these may also

experience visuospatial and free recall memory problems.68

Definition of PD MCI

PD MCI denotes cognitive decline that is not normal for age but with

essentially normal functional activities (fail to meet the criteria for PD-D)

and could be present even at the time of diagnosis of PD and prior to


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initiation of dopaminergic therapy. This operational definition was

uniformly followed in the longitudinal 47,54 and cross-sectional 56-61 studies

done so far, but there was no uniformity in the number of impaired

cognitive tests required in each domain, the number of involved domains

and the degree of involvement in each domain, to be classified as PD-MCI .

The need for formal diagnostic criteria for PD-MCI has been highlighted13

and the Movement disorder Society (MDS) commissioned a task force to

review the available literature on PD-MCI and formulate a diagnostic

criteria. The MDS task force diagnostic criteria have been published

recently.70 The MDS Task Force diagnostic criteria include (1)

characterization of the clinical syndrome and (2) methods for its diagnosis.

PD-MCI Criteria

The diagnosis of PDMCI needs satisfaction of the inclusion and

exclusion criteria specified; two levels of diagnostic categories and various

subtypes of PD-MCI have been defined. PD-MCI is a syndrome defined by

clinical, cognitive,and functional criteria.70 The MDS Task Force criteria

are rooted in the MCI criteria previously described, but modified to address

issues relatively specific to PD. The criteria were also designed to be

consistent with the MDS proposed PDD criteria and thereby allow

transitions between categories of normal cognition, MCI, and dementia.71


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I. Inclusion criteria

1. Diagnosis of Parkinson’s disease as based on the UK PD Brain Bank

Criteria17

2. Gradual decline, in the context of established PD, in cognitive ability

reported by either the patient or informant, or observed by the

clinician

3. Cognitive deficits on either formal neuropsychological testing or a

scale of global cognitive abilities (detailed in section III)

4. Cognitive deficits are not sufficient to interfere significantly with

functional independence, although subtle difficulties on complex

functional tasks may be present.

II. Exclusion criteria

1. Diagnosis of PD dementia based on MDS Task Force proposed

criteria57

2. Other primary explanations for cognitive impairment (e.g.,

delirium,stroke, major depression, metabolic abnormalities, adverse

effects of medication,or head trauma)


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3. Other PD-associated comorbid conditions (e.g., motor impairment or

severe anxiety, depression, excessive daytime sleepiness, or

psychosis)that, in the opinion of the clinician, significantly influence

cognitive testing

III. Specific guidelines for PD-MCI level I and level II

categories

A . Level I (abbreviated assessment)

1. Impairment on a scale of global cognitive abilities validated for use in

PD or

2. Impairment on at least two tests, when a limited battery of

neuropsychological tests is performed (i.e., the battery includes less

than two tests within each of the five cognitive domains, or less than

five cognitive domains are assessed)

[scales of global cognitive abilities validated in PD are –MoCA,

SCOPA-COG(Scales for Outcomes of Parkinson’s disease–Cognition) ,

PD-CRS(Parkinson’s Disease-Cognitive Rating scale), MDRS(Mattis

Dementia Rating Scale)]


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B. Level II (comprehensive assessment)

1. Neuropsychological testing that includes two tests within each of the

five cognitive domains (i.e., attention and working memory, executive,

language, memory, and visuospatial)

2. Impairment on at least two neuropsychological tests, represented by

either two impaired tests in one cognitive domain or one impaired

test in two different cognitive domains

3. Impairment on neuropsychological tests may be demonstrated by:

Performance approximately 1 to 2 SDs below appropriate

norms or

Significant decline demonstrated on serial cognitive testing or

Significant decline from estimated premorbid levels

IV. Subtype classification for PD-MCI (optional, requires two

tests for each of the five cognitive domains assessed and is

strongly suggested for research purposes) a

a Subtype classifications are applicable only to those PD-MCI who have had at least two

tests within each of the five cognitive domains administered.


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1. PD-MCI single-domain—abnormalities on two tests within a single

cognitive domain (specify the domain), with other domains

unimpaired or

2. PD-MCI multiple-domain—abnormalities on at least one test in two

or more cognitive domains (specify the domains)

Neuropsychological tests for the five cognitive domains

Attention and working memory

WAIS-IV (or earlier version) Letter Number Sequencing,

WAIS-IV Coding (or earlier version) or other substitution task,

written or oral

Trail Making Test,

Digit span backward or digit ordering,

Stroop color-word test.

Executive function

Wisconsin Card Sorting Test (CST), or modified CST(Nelson’s

modification)

Tower of London test–Drexel version, or Stockings of Cambridge

(CANTAB)


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Verbal fluency test, such as letter fluency (COWAT or similar tests),

Category fluency (animals, supermarket, or similar), or alternating

fluency tasks(if a well-standardized version is used).

10 points Clock Drawing Test

Language

WAIS-IV (or earlier version) Similarities

Confrontation naming task, such as Boston Naming Test (or short-

form validated in PD) or Graded Naming Test

Memory

Word list learning test with delayed recall and recognition conditions,

such as Rey’s Auditory Verbal Learning Test, California Verbal

Learning Test, Hopkins Verbal Learning Test, and Selective

Reminding Test

Prose recall test with a delayed recall condition, such as Wechsler

Memory Scale-IV Logical Memory subtest (or earlier version) or

River mead Behavioural Memory Test, paragraph recall subtest

Brief Visuospatial Memory Test–Revised (BVMT-R)


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Visuospatial function

Benton’s Judgment of Line Orientation

Hooper Visual Organization Test

Clock copying (e.g., Royall’s CLOX)

The level I category allows for the diagnosis of PDMCI based on an

abbreviated cognitive assessment, because comprehensive testing may not

always be practical or available. Level I criteria provide less diagnostic

certainty than level II . When a limited battery of neuropsychological tests is

performed, impairment must be present on at least two tests to diagnose PD-

MCI by level I criteria. Level I criteria do not allow complete sub typing of

PD-MCI.

For the diagnosis of PD-MCI by level II criteria and PD-MCI sub

typing, the task force recommends formal, comprehensive

neuropsychological testing that includes at least two tests for each of the

five cognitive domains previously listed. Impairment should be present on at

least two tests, either within a single cognitive domain or across different

cognitive domains.


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Risk of progression to PDD

Mild cognitive impairment in Parkinson's disease is an important

predictor for the progression to PDD. Longitudinal studies on non-

demented PD patients show that 20-60% develop PD dementia over 2-5

years.54,72-77 Information on the conversion of PD-MCI to PDD is

scanty.47,54,59 Around 60% of PDMCI are converted to PD-D over 4 years,

compared to 20% of PD patients with normal cognition.47 Cognitive decline

correlating with the neuropathologic stage of PD demonstrated in a

clinicopathological study also support PDMCI as a risk factor for PD-D.78,79

It has been shown that majority of PD patients develop dementia over

time.80,81 The cumulative prevalence of PDD for patients surviving more

than 10 years is at least 75%.80,81 The point prevalence of PD-MCI13,72 and

PD-D6 are similar. Thus, PDMCI precedes PDD and majority of PD-MCI

are converted to PDD over time.13

PDD

Diagnosis of PD dementia must be based on the presence of deficits

in at least two of the four core cognitive domains (attention, memory,

executive and visuo-spatial functions) as shown in clinical and cognitive

examination, and be severe enough to affect normal functioning. The


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Movement Disorder Society (MDS) Task Force defined the clinical

diagnostic criteria for PD-D.71

Features of dementia associated with Parkinson’s disease

I. Core features

1. Diagnosis of Parkinson’s disease according to Queen Square Brain

Bank criteria.

2. A dementia syndrome with insidious onset and slow progression,

developing within the context of established Parkinson’s disease and

diagnosed by history, clinical, and mental examination , defined as :

Impairment in more than one cognitive domain

Representing a decline from premorbid level

Deficits severe enough to impair daily life (social, occupational, or

personal care), independent of the impairment ascribable to motor

or autonomic symptoms.

II. Associated clinical features

1. Cognitive features

• Attention: Impaired. Impairment in spontaneous and focused

attention, poor performance in attentional tasks; performance may

fluctuate during the day and from day to day.


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• Executive functions: Impaired. Impairment in tasks requiring

initiation, planning, concept formation, rule finding, set shifting or set

maintenance; impaired mental speed (bradyphrenia)

• Visuo-spatial functions: Impaired. Impairment in tasks requiring

visual-spatial orientation, perception, or construction

• Memory: Impaired. Impairment in free recall of recent events or in

tasks requiring learning new material, memory usually improves with

cueing, recognition is usually better than free recall

• Language: Core functions largely preserved. Word finding difficulties

and impaired comprehension of complex sentences may be present

2. Behavioral features:

• Apathy: decreased spontaneity; loss of motivation, interest, and

effortful behavior

• Changes in personality and mood including depressive features and

anxiety

• Hallucinations: mostly visual, usually complex, formed visions of

people, animals or objects

• Delusions: usually paranoid, such as infidelity, or phantom boarder

(unwelcome guests living in the home) delusions

• Excessive daytime sleepiness


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Based on these features clinical diagnostic criteria for probable and

possible PD-D are described .

Scientific and clinical significance of identifying PD-MCI

As discussed above, PD-MCI is common and precede PD-D. Most

PD patients develop dementia,80-83 the impact of which is substantial. PD-D

has major consequences for psychiatric morbidity,84 functioning,15,85,86

caregiver burden,87,88 nursing home placement9 and mortality.89,90 . Even

mild cognitive deficits affect functioning and quality of life in PD.15-18 Early

identification is very important and help early interventions to improve

functioning and QOL as well as drug development and other measures

aimed to delay the development of PDD. This has got public health

importance, considering the commonness of PD.91 Early recognition of

cognitive impairment could offer a window for novel therapeutic

interventions, aiming to alter the course of this natural history.

Tools for Assessment of Cognition in PD

There are a number of issues that are not fully resolved in the

cognitive testing in PD, including the ideal cut-off scores, number of tests to

be done in each domain, number of tests/domains to be involved to classify

as PD-MCI, the potential non-linear nature of cognitive decline in PD, and

the issue of whether different cognitive domains decline at same or different


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rates.13 Assessment of cognition in PD can be complicated by disease- or

medication-related effects, such as bradykinesia, fatigue, sleepiness, and

mood disorders, which can adversely affect test results regardless of

cognitive abilities.13 The recently published MDS PD-MCI diagnostic

criteria70 specifies two levels of diagnosis; level I is the “abbreviated

assessment” and level II, “Comprehensive assessment”.

Level I requires impairment on a scale of global cognitive abilities

validated for use in PD or impairment on a limited battery of

neuropsychological tests . Level II requires testing with at least two

cognitive tests, assessing each of the five cognitive domains (Attention and

working memory, executive function, language, memory and visuospatial

function). As each of the recommended tests take 5-15 minutes13 a

minimum of 1- 1 ½ hours may be required for the individual patient. This

has practical challenges; hence the level I testing may be more suitable in

the clinic settings and require only impairment in a scale of global cognitive

abilities validated for use in PD or a limited battery of cognitive tests.

Neuropsychological Scales for Assessing Global Cognitive Abilities

validated for use in PD are Montreal Cognitive Assessment (MoCA);

Parkinson’s Disease-Cognitive Rating scale (PD-CRS); Scales for

Outcomes of Parkinson’s disease–Cognition(SCOPA-COG) and Mattis

Dementia Rating Scale(MDRS) . Based on the Movement disorder Task


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Force’s evaluation criteria the Montreal Cognitive Assessment (MoCA),

appeared to be the most suitable measure and recommended consideration

of the MoCA as a minimum cognitive screening measure in clinical trials of

PD.13,70

The Montreal Cognitive Assessment (MoCA)

The MoCA was designed by by Nasreddine et al.19 in English

language as a brief screening tool for MCI and has become an increasingly

popular screening tool for identifying cognitive impairment . As it is brief

(can be administered in around 10 minutes)13 and can be easily administered

even by non-specialist staff it has become very useful and common

screening test. MoCA covers a range of executive functions and addresses

frontal functions better than the widely used Mini-Mental Status

Examination (MMSE).92 The MoCA is divided into 7 subscores :

visuospatial/executive(5 points); naming (3 points); memory(5points for

delayed recall); attention (6 points);language (3 points); abstraction (2

points); and orientation (6 points). One point is added if the subject has < 12

years of education.19 MoCA has high sensitivity and specificity for MCI and

has good test-retest reliability, internal consistency and content validity 92. It

has been studied in patients with MCI , Alzheimers disease (AD), Vascular

Cognitive Impairment, post stroke ,PD, Huntington’s disease , Epilepsy

,traumatic brain injury, Frontotemporal dementia,multiple sclerosis and


35

tumors of brain and found to be a useful screening tool in all these

conditions. 93,94

The usefulness of MoCA as a suitable, accurate and brief test for

screening all levels of cognition in PD, has been demonstrated.20,95 MoCA

doesn’t have the pronounced ceiling effect seen with MMSE and is a more

sensitive tool to identify early cognitive impairment in PD, especially PD-

MCI.20,96It has also been found that approximately half of the patients with

normal MMSE have cognitive impairment based on MoCA.97 Based on

these findings, the MDS task force has recommended MoCA as a

neuropsychological scale to test the global cognitive abilities in PD,13,70 to

make a “level I” diagnosis of PD-MCI. The optimal MoCA screening cut-

off values for PD-D and PD- MCI have recently been defined as 21/30

and 26/30 respectively.95 The scale was originally designed in English and

cross-cultural adaptation and validation was done for use in 43 other

languages.93

Addenbrooke’s Cognitive Examination

The Addenbrooke’s Cognitive Examination (ACE),a global cognition

screening battery, is a reliable and sensitive tool consists of six components

evaluating separate cognitive domains.98 A maximum score of 100 is

weighted as orientation(10) , attention(8) , memory(35) , verbal fluency(14)


36

, language(28) , and visuospatial ability(5) . Scores for each of the six

domains can be calculated separately and their sum gives the composite

score on the ACE. The MMSE score can also be calculated from this . The

ACE can be administered in 15 to 20 minutes.98 Addenbrookes Cognitive

Examination is validated for dementia evaluation in PD, with a cut-off

score of 83 points.99 It is adapted into Malayalam and validated for use

in our population and normative data for different ages and educational

levels are available.100,101

Mini Mental Status Examination

The Mini Mental Status Examination (MMSE) (Folstein et al., 1975),

is a widely used cognition screening test in many parts of the world ,

modified and adapted into many local languages. Malayalam version of

MMSE with normative scores are published earlier.101 MMSE is being used

for long time for testing cognition in PD . But it is less sensitive for the

detection of cognitive impairment seen in early PD.96 It shows a ceiling

effect in patients and normal controls.97 Studies in patients with PD showed

that approximately half of patients with a normal MMSE score have

cognitive impairment by testing with MoCA.97

Aims & Objectives

37

Aims and objectives of the study

1. Cross-cultural adaptation of Montreal Cognitive assessment (MoCA)

scale into the regional language (Malayalam)

2. Study the validity and reliability of Montreal Cognitive assessment-

Malayalam (MoCA-M) for cognitive assessment in Parkinson’s

disease patients .

Materials and Methods

38

Materials and Methods of the study

Cross-cultural adaptation of MoCA to Malayalam (MoCA-M)

MoCA is copyright protected cognitive assessment tool required

written permission of the copyright holder for translation and use for

research purpose. We contacted the copyright holder and obtained

permission for translation (to Malayalam) and use for this project. The

copyright holders have also provided guidelines for translation of MoCA to

Malayalam. The English version was used as a base for translation. The 5-

word recall and sentence repetition items was adapted to the language and

culture, based on the guidelines provided. In order to ensure accurate

translation of the test and instructions, a back translation (from Malayalam

to English) was done and compared with the original English version. The

translation and back-translation was done independently by two bilingual

experts, who are clinical psychologists well versed with similar tasks and

consensus was obtained. The final version was discussed and approved

within an internal committee consisting of the bilingual experts as well as

the investigators.


39

Validation of Montreal Cognitive assessment-Malayalam

(MoCA-M)

Study design and setting

The study was a hospital based cross-sectional study. The subjects

were selected from among the patients attending the movement disorder

clinic of our tertiary care University hospital (Sree Chitra Tirunal Institute

for Medical Sciences and Technology, Thiruvananthapuram).

Study period:

The study was conducted over a period of 18 months from January

2013 to June 2014.

Methods

For validation, the test (MoCA-M) was administered to 100

consecutive patients with Parkinson’s disease, attending the Movement

Disorders clinic of SCTIMST and satisfying the entry criteria, and 100

normal controls. The controls were selected from the hospital staff, friends

and relatives of hospital staff and visitors of the in-patients in the hospital

who agreed to participate.


40

Ethical considerations:

Written informed consent was obtained from all the subjects

participating in the study. The study was approved by the Institutional

Ethics Committee. (SCT/IEC/438/DECEMBER-2012)

Inclusion criteria (for PD patients):

1. Diagnosis of PD, as per standard diagnostic criteria (United Kingdom

Parkinson’s Disease Society Brain Bank Diagnostic Criteria)22

2. Ability to read, understand and write Malayalam well.

3. Ability to provide written informed consent.

Inclusion criteria (for Controls)

1. No known neurological disorders.

2. Normal neurologic examination (except for assessment of higher

functions)

3. Age, gender and level of education matched with patients.

4. Ability to read, understand and write Malayalam well.

5. Ability to provide written informed consent.


41

Exclusion criteria (for PD patients and Controls)

1. Clinically significant depression (Beck’s Depression Inventory

(BDI) Score ≥20) 102

2. Any significant neurological, psychiatric or medical co-morbidity

interfering with cognitive testing or affecting cognitive functions in

the judgement of the investigators.

The Malayalam version of MoCA(MoCA-M) was applied to

consecutive patients with PD diagnosed using the United Kingdom

Parkinson’s Disease Society Brain Bank Diagnostic Criteria , attending the

Movement Disorders clinic of our hospital having atleast 10 years of formal

education and able to read , write and understand Malayalam. MoCA-M was

also applied to age and education -matched healthy controls without any

neurological disorders . All the patients underwent a formal neurological

examination including assessment using Unified Parkinson’s Disease rating

Scale (UPDRS I-IV)103 The UPDRS part III (motor examination) was done

in the “off” state in patients having motor fluctuations. The severity of

motor symptoms of PD was assessed by the Hoehn and Yahr stage. The age

of onset of motor symptoms of PD, duration of motor symptoms and details

of ongoing treatment was collected by directly interviewing the patients /


42

caregivers and by review of hospital files. The controls also underwent a

neurological examination to ensure that they have no neurological disorders.

The neuropsychologic evaluation was done in the “On” (well

medicated) state with the help of the qualified Neuropsychologist, attached

to the Movement Disorders Program of the Institute. All the subjects (PD

patients and controls) were undergone neuropsychological assessment using

the MoCA-M, Addenbrooke’s Cognitive Examination –Malayalam (ACE-

M)100 , and Beck depression inventory(BDI) . Those with clinically

significant depression (Beck’s Depression Inventory score >20)102 or any

significant neurological, psychiatric, or medical co-morbidity affecting

cognitive functions or interfering with cognitive testing in the judgment of

the investigators were excluded.

The ACE has several advantages (The MMSE is also included in it, is

validated for use in Parkinson’s disease,98 adaptation is available for use in

Malayalam speaking population100 and cut-off scores are well defined in our

population, adjusted for age and level of education.101 The normative data

for each of the individual domains of ACE also has been published101

making it ideal as a standard for validating the new scale. The Malayalam

version of ACE (M-ACE)100 was used for the study. A subgroup of subjects

were re-examined using the MoCA-M after an interval of 2 weeks to

determine the test-retest reliability.

Statistical Analysis

43

Statistical analysis

Cronbach’s alpha was calculated to assess the internal

consistency of MoCA-M. Pearson correlation coefficient was used to the

assess test-retest reliability as well as to assess the relationship between

MoCA-M scores and the performance in other cognitive tests. The data were

analyzed using statistics software (Statistical Package for the Social

Sciences (SPSS) Inc, Illinois, Chicago) with guidance from the Medical

Statistics expert of the institute.

Results

44

Results

Baseline clinical characteristics

There were 100 patients with PD and 100 healthy controls. Mean age

of patient group was 57.8(± 9.3) years ,range 35-78 years . In the control

group mean age was 58.94(±8.42),range 39-85 years .

The mean years of education was 12.19(±3.46) in patient group, and

13.6(±3.20)in the control group .

Table 1 Demographic data of patients and controls

Patient Control P value

Age (years) 57.8(± 9.3) 58.94(±8.42) 0.38

Education (years) 12.19(±3.46) 12.2 (±1.97) 0.98

Age and education were similar in the patient and control groups and

there was no statistically significant difference .

In the patient group 71% were men and 29% were women and in the control

group 53% were men and 47% were women.

Results

45

Figure 2. Sex distribution

The mean duration of motor symptoms was 6.58 (±4.04) years ,

range from 2-18 years. The mean age of onset of symptoms was

52.42(±10.02) years range from 30-76 years . The mean Levodopa

equivalent dose (LEDD) was 615(±295.51)mg .

The severity of motor symptoms according to Hoehn and Yahr (H

and Y) stage was as follows: Stage 1- 7% (7patients), stage2−44%

(44patients), stage 3−43% (43patients), stage 4−6% (6 patients). Majority

of the patients were in stages 2 and 3.

0%

20%

40%

60%

80%

100%

Patients Controls

71

53

29

47

male female

Results

46

Figure 3 Number of patients distributed in various H&Y stages

7

44 43

6

00

5

10

15

20

25

30

35

40

45

50

H&Ystage

1 2 3 4 5

Results

47

Neuropsychology Test Results:

Patients

The mean MoCA score was 24.41( ±4.04) ranging from 8-30 in

patients with PD. ACE mean score was 83.99(±9.99)ranging from 49-99 .

MMSE mean score was 28.55±1.73 ranging from 21-30 .

Controls

The mean MoCA score was 27.78±1.67ranging from 23-30 in

normal controls. ACE mean score was 91.56±4.98 ranging from 80-99 .

MMSE mean score was 29.220±0.98 ranging from 23-30 .

Table 2.Mean scores in cognitive testing in patients

No of

patients

Minimum

score

Maximum

score

Mean

score

Std dev

MoCA 100 8 30 24.4 4.04

ACE 100 49 99 83.99 9.99

MMSE 100 21 30 28.55 1.73

Results

48

Table 3. Mean scores in cognitive testing in patients

No of

controls

Minimum

score

Maximum

score

Mean

score

Std dev

MoCA 100 23 30 27.78 1.67

ACE 100 80 99 91.56 4.98

MMSE 100 23 30 29.22 0.98

The mean MoCA-M, MMSE, and ACE scores of the patients and

healthy controls are shown in Table 4. The scores in all the three tests

differed significantly between patients and normal controls .

Table 4. The MoCA-M, MMSE, and ACE scores of patients and healthy

controls

Patients Healthy controls P value

MoCA-M 24.41 ±4.04 27.78±1.67 <0.001

MMSE 28.55±1.73 29.220±0.98 0.003

ACE 83.99±9.99 91.56±4.98 <0.001

Results

49

Mean BDI score was 3.9(±4.84) , range from 0-20 in the patient

group . In the control group mean score was 3(±4.5) ranging from 4-12 .

There was no significant difference between patient and control group.

Table 5. BDI scores of patients and controls

Mean Std dev Range

Patient 3.9 4.84 4-20

Control 3 4.4 0-12

There was no correlation between age and the scoring in cognitive

tests , in the patient group (pearson correlation R 0 .023 and p value 0.82) or

in the control group (R -.04 and p value 0.69) .

Table 6. Correlation of age and MoCA scores

Correlations

MoCA_TOTAL

Age (years) patient

Pearson Correlation .023

Sig. (2-tailed) .823

N 100

Age (years) control

Pearson Correlation -.040


N 100

Results

50

There was no significant difference in scores between males and

females in the patient group (p value 0.83) or the control group(p value

0.873).

Table 7. MoCA score in male and female in control group

GENDER Mean N Std. Deviation Median Minimum Maximum

male 27.76 53 1.55 28.00 25.0 30.0

female 27.81 47 1.81 28.00 23.0 30.0

Total 27.78 100 1.67 28.00 23.0 30.0

Table 8. MoCA score in male and female in patient group

GENDER Mean N Std. Deviation Median Minimum Maximum

male 24.47 71 3.57 26.00 14.0 30.0

female 24.28 29 5.07 26.00 8.0 29.0

Total 24.41 100 4.04 26.00 8.0 30.0

There was no correlation between duration of PD and the scoring in

cognitive testing in MoCA , R was .057 and p value is 0.57 . There was no

correlation between age onset of symptoms and scoring in cognitive testing

R -.012 and p value was .91. There was no correlation between LEDD and

MoCA scores , R -.053 p value was 0.60

Results

51

Table 9. Correlation of MoCA score with demographics of patients

Correlations

MoCA total

Duration in years



N 100

Age of onset years



N 100

Daily L-dopa dose



N 100

LEDD



N 100

The mean MoCA score in H&Y stage 1 was 23.71±7.36 , stage 2 was

24.34±3.65, stage3 was 24.28±3.95 and stage 4 was 26.67±2.34 . There was

no significant difference in the MoCA score in different H&Y stages and

the p value was 0.51 .

Results

52

Table 10. MoCA score in various H&Y stages in the off state of patients

H&Y stage off N Mean Std.

Deviation Median Minimum Maximum

1.0 7 23.71 7.36 27.00 8.0 29.0

2.0 44 24.34 3.65 26.00 14.0 28.0

3.0 43 24.28 3.95 26.00 14.0 30.0

4.0 6 26.67 2.34 26.50 24.0 30.0

Total 100 24.41 4.04 26.00 8.0 30.0

There was no correlation between H&Y stage of PD and the scoring

of cognitive testing in MoCA , MMSE or ACE .

Figure 4.Scoring in cognitive tests in each H&Y stages

0

10

20

30

40

50

60

70

80

90

100

1 2 3 4 5

MoCA30

MMSE30

ACE100

Results

53

Table 11. Scores in cognitive tests in each H&Y stage

1 2 3 4 P value

MoCA mean

score 23.71±7.36 24.34±3.65 24.28±3.95 26.67±2.34 0.59

ACE mean score 82.28±16.24 84.51±9.5 82.91±9.64 91.00±5.34 0.39

MMSE mean

score 28±3.10 28.69±1.53 28.40±1.76 29.33±0.81 0.62

Results did not show any significant difference in the test scores in

patients with various H&Y stages . There was no correlation between

H&Y stage and MoCA score .

Results

54

Validity and Reliability of MoCA-M

MoCA-M showed good internal consistency; the Cronbach’s alpha

for MoCA-M was 0.72 in patients with PD and 0.40 in controls.

There was also excellent test-retest reliability for the total score of

MoCA-M, as well as for the individual items.

Table 12. Test‑retest reliability of MoCA-M

Cognitive domains Pearson’s correlation coefficient P value

Visuo spatial/executive 0.87 <0.0001

Naming 0.63 <0.0001

Attention 0.96 <0.0001

Language 0.95 <0.0001

Abstraction 0.96 <0.0001

Delayed recall 0.96 <0.0001

Orientation 0.58 0.001

Total 0.97 <0.0001

The scores of MoCA,MMSE and ACE differed significantly

between patients and normal controls with a significant p value . There was

significant difference in the scores of MoCA-M and ACE between healthy

controls and patients and p value was <0.001. Though the difference in the

MMSE scores of controls and patients was less it was significant

statistically and the p value was 0.003 .

Results

55

Table 13. The MoCA-M, MMSE, and ACE scores of patients and healthy

controls

Patients Healthy controls P value

MoCA-M 24.41 ±4.04 27.78±1.67 <0.001

MMSE 28.55±1.73 29.220±0.98 0.003

ACE 83.99±9.99 91.56±4.98 <0.001

The MoCA-M scores correlated well with the MMSE (R = 0.67; P <

0.0001) and ACE (R=0.81;P<0.0001) scores in patients with PD .

Table 14.Correlation of MoCA scores with MMSE and ACE in patient

group

Correlations

MoCA_TOTAL ACE_TOTAL MMSE

MoCA_TOTAL

Pearson Correlation 1 .807** .670**

Sig. (2-tailed) .000 .000

N 100 100 100

ACE_TOTAL

Pearson Correlation .807** 1 .730**

Sig. (2-tailed) .000 .000

N 100 100 100

MMSE

Pearson Correlation .670** .730** 1

Sig. (2-tailed) .000 .000

N 100 100 100

**. Correlation is significant at the 0.01 level (2-tailed).

Results

56

The healthy controls showed good correlation of MoCA scores with

ACE (R = 0.49; P < 0.0001); however, correlation with MMSE scores (R =

0.23; P = 0.02) was weak.

Table 15. Correlation of MoCA scores with MMSE and ACE in control

group

Correlations

MoCA_TOTAL ACE_TOTAL MMSE

MoCA_TOTAL

Pearson Correlation 1 .489** .233*

P Value .000 .020

N 100 100 100

ACE_TOTAL

Pearson Correlation .489** 1 .229*

P Value .000 .022

N 100 100 100

MMSE

Pearson Correlation .233* .229* 1

P Value .020 .022

N 100 100 100

**. Correlation is significant at the 0.01 level (2-tailed). *. Correlation is significant at the 0.05 level (2-tailed).

Results

57

Table 16. Correlation of MoCA score with ACE and MMSE score of

patients and controls

ACE

patient

ACE

control

MMSE

score

patient

MMSE

score

control

MoCA

score

Pearson

correlation R 0.81 0.49 0.67 0.23

P value <0.0001 <0.0001 <0.0001 0.02

Discussion

58

Discussion

There is increasing evidence that dementia is common in advancing

PD, affecting up to 80% of patients followed long term.14 Recognition of

cognitive impairment at its initial stage will enable clinicians to educate

patients and family members about prognosis and to allow informed

decisions about the risks and benefits of therapeutic interventions. Screening

tests used in PD should be brief and sensitive for the type of cognitive

dysfunction seen in these patients as it is difficult to do long tests due to the

motor dysfunction . MoCA is well-recognized as a suitable sceening test for

cognition in PD94-97 as it is a brief test , has demonstrated good test–retest

and interrater reliabilities and high intraclass correlation coefficients in

patients with PD and has been translated to many languages.93,94 The

cognitive domains tested by MoCA include executive and visuospatial

function, memory, language, and attention. The

domains of executive and visuospatial function are known to be affected

relatively early in PD and hence MoCA could be a useful instrument to

screen for cognitive dysfunction in PD.

In this study we translated and adapted MoCA into our regional

language Malayalam and demonstrated the usefulness of the Malayalam

version of MoCA for screening cognitive functions in PD. We created

Discussion

59

MoCA-M (the test and instructions for testing have been posted at the

official website of MoCA93 and are available on line at www.mocatest.org)

by translating MoCA to Malayalam and cross-culturally adapting the

relevant items. We have changed the 5 words in the delayed recall item

relevant to our language and culture. Back translation of the test and

instructions was done by bilingual experts and compared with the original

English version, and consensus was obtained. The back translations were

accepted by the group who invented the original version of MoCA and hold

the copyright.

The mean duration of motor symptoms of PD in our patient group

was 6.58years . The mean age of patients was 57.8 years which was

comparable with the control group . The mean age of onset of symptoms

was 52.42(±10.02) years . Most of the patients were in the H and Y stage 2

or 3 and there was no patients in the stage 5 .There was no significant

relation between the H&Y stage and scoring in cognitive testing in our

study. Males were more in the patient group which was expected as PD is

more common in males.

The MoCA-M takes about10minutes to administer. MoCA-M was

compared with ACE for several reasons–it is a brief test battery

encompassing all the cognitive domains,98 its validity in PD has been

Discussion

60

demonstrated,99 its validated adaptation for Malayalam speaking population

is available 100 , and it also gives the MMSE score

MoCA-M showed good internal consistency, and the test-retest

reliability was excellent. We found that MoCA-M scores of patients

correlated well with their performance in ACE. The MoCA-M scores also

showed good correlation with MMSE scores in patients with PD. MoCA-M

is more brief and easy to administer compared to ACE . MoCA’s superiority

for testing cognition in PD, compared to MMSE has already been

demonstrated.65,96,97 The cognitive dysfunction in PD is characterized by a

frontal, attentional-executive dysfunction in most patients, in addition to

visuospatial defects and memory problems.66-69 The utility of MoCA for

screening cognition in PD and its superiority over MMSE are well described

96,97 and it tests frontal functions better than MMSE, in addition to testing

the other cognitive domains.

We also examined 100 age and education matched healthy volunteers

and demonstrated good correlation of MoCA-M scores with performance in

ACE. However, unlike the observation in patients with PD, correlation of

MMSE scores with MoCA–M scores of control group was weak. The

MMSE scores were significantly higher for healthy volunteers, and the poor

correlation between MoCA-M and MMSE scores in this group is

Discussion

61

attributable to the ceiling effect of MMSE,65,72 which is not observed for

MoCA.

We found that the performance of patients with PD in all the three

tests was significantly worse compared to controls. The MoCA-M mean

score in the patient group was 24.41(±4.04) versus 27.78(±1.67) in the

control group. The mean MoCA-M score of the patients was falling below

the cut-off levels defined for MCI, for the original version of MoCA19. The

ACE score was 83.99(±9.99) in the patient group and 91.56(±4.99) in the

control group . The significantly low MoCA-M and ACE scores in patients,

compared to controls is not surprising, considering the mean duration of PD

in our patient group; a considerable number of them are expected to have

MCI. MoCA-M is a cross-cultural adaptation of MoCA, its normative data

and cut-off scores for MCI in PD and PD-D need to be separately defined

by further studies .

In this study we have done cross cultural adaptation of MoCA into

Malayalam and demonstrated the reliability and validity of the Malayalam

version for screening cognition in patients with PD .

Conclusion

62

CONCLUSION

1. MoCA –M is a cross cultural adaptation of MoCA for use in

Malayalam speaking patients. MoCA’s validity for screening

cognition for patients with all stages of PD, is already well

established .

2. We showed that the MoCA –M had good test- retest reliability and

internal consistency, similar to the original version of MoCA.

3. The comparison of MoCA-M with other standard cognitive tests

used in patients with PD, showed good correlation .

4. MoCA-M scores differed significantly between patients with PD

and healthy volunteers , paralleling the observation in a more

elaborate and established cognitive testing instrument- the

Malayalam version of ACE.

5. MoCA-M is valid and reliable, similar to the original English

version, for screening for cognitive dysfunction in Malayalam

speaking PD patients.

Summary

63

SUMMARY

We created a cross-cultural adaptation of MoCA (MoCA-M) , for use

for cognitive screening in Malayalam speaking patients, especially with

PD. We have shown that it is a valid and reliable tool for the purpose.

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64

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Annexure

Abbreviations

ACE- Addenbrooke’s Cognitive Examination AD-Alzheimers isease BDI- Beck’s Depression Inventory H&Y stage- Hoehn and Yahr stage LEDD- Levodopa equivalent dose MCI- Mild cognitive impairment MDRS-Mattis Dementia Rating Scale MDS- Movement Disorder Society MMSE- Mini-Mental Status Examination MoCA- Montreal Cognitive Assessment MoCA-M- Montreal Cognitive assessment-Malayalam NMS- Nonmotor symptoms PD-Parkinson’sdisease PD-CRS-Parkinson’s Disease-Cognitive Rating scale PDD- Parkinson’s disease dementia QOL- Quality of life SCOPA-COG-Scales for Outcomes of Parkinson’s disease–Cognition UKPDSBB- United Kingdom Parkinson’s Disease Society Brain Bank criteria UPDRS- Unified Parkinson’s Disease rating Scale

PROFORMA- FOR NORMAL CONTROLS Validation of the Malayalam Version of the Montreal Cognitive Assessment (MoCA) Scale and a Prospective Evaluation of Mild

Cognitive Impairment in Parkinson’s disease Using the Malayalam version (“MoCA-M”).

Date of Evaluation: 1. Subject details and history:

Name: Age:

Gender:

Level of Education: Total number of years of formal education:

Marital status:

Address:

Telephone No:

Details of any medical illnesses:

2. Details of any Medications which the subject is taking

Present Medications Total Daily Dose Duration of Exposure Dosing Schedule

3. Clinical Examination:

4. Neuropsychological evaluation:

MoCA score: Total

ACE- Total score:

MMSE:

BDI score:

PROFORMA- FOR PD PATIENTS Validation of the Malayalam Version of the Montreal Cognitive

Assessment (MoCA-M) Scale and a Prospective Evaluation of Mild Cognitive Impairment in Parkinson’s disease Using Malayalam

version (MoCA-M). Date of Evaluation:

1. Patient’s details and history:

Name: Hospital no:

Age: Gender: Level of Education: Total number of years of formal education: Marital status: Address: Telephone No: Duration of disease: Age at onset: Type of Parkinson’s disease: Tremor Dominant / Rigid Bradykinetic / mixed Side of onset : Right/ Left / Can’t say Motor fluctuations: Yes/ No Duration of MF: Dyskinesia: Duration: Type: Other medical illnesses: Family History of PD: No of family members affected: Non-motor Symptoms: Sleep dysfunction: Description: Hallucinations: Description: Other psychotic features: Impulse control disorders: Memory dysfunction: Other Cognitive symptoms: Description: Urinary disturbances: Other autonomic symptoms: Constipation: Other GI symptoms: Any other non-motor symptoms: Description:

2. Details of Medications Present Medications Total Daily Dose Duration of Exposure Dosing Schedule LEDD: Past Medications: Dose Duration of Exposure Anticholinergics (Specify) Amantadine:

3. Clinical Examination: “On” “Off” UPDRS I : UPDRS II: UPDRS III: UPDRS IV A: UPDRS IV B: Hoehn & Yahr stage:

4. Neuropsychological evaluation: MoCA score: Total ACE- Total score: MMSE: BDI score:

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