|Year : 2015 | Volume
| Issue : 2 | Page : 90-95
Study of cognitive profile in the elderly presenting with both depressive and cognitive symptoms
Shipra Singh, Sunitha Shanker, Alka A Subramanyam, Ravindra M Kamath
Department of Psychiatry, Topiwala National Medical College and BYL Nair Charitable Hospital, Mumbai, Maharashtra, India
|Date of Web Publication||18-Jan-2016|
OPD-13, Department of Psychiatry, Topiwala National Medical College and BYL Nair Charitable Hospital, Mumbai, Maharashtra
Source of Support: None, Conflict of Interest: None
Background: Elderly patients presenting with cognitive and depressive symptoms often create a diagnostic challenge between depression and the dementing process. Various screening and diagnostic instruments have been developed for differentiating the two, one of which is Addenbrooke's cognitive examination (ACE). However, results have not been consistent across various studies, and not much data is available in the Indian context.
Aims and Objectives: To study cognition in elderly patients presenting with both cognitive and depressive symptoms at the baseline and at 3 months follow-up after starting antidepressants, and to compare the two profiles.
Materials and Methods: It was a follow-up study with 70 participants who had presented with both depressive and cognitive symptoms. Tablet escitalopram was given and ACE was performed at the baseline and at 3 months after starting antidepressants. Improvement on ACE was present in 37 participants and absent in 33 participants. The cognitive profile of these two groups was subjected to statistical analysis. Wilcoxon signed-rank test was used to study the difference between the full and domain ACE scores between the preintervention phase and postintervention phase within each group.
Results: There is a significant difference between preintervention and postintervention full ACE scores and different domain scores in the depression group unlike in the MCI group.
Conclusion: Diagnostic tools such as ACE can be utilized for differentiating mood disorder with an actual dementing process. It also reveals the need for periodic assessments of such patients.
Keywords: Cognition, depression, mild cognitive impairment (MCI)
|How to cite this article:|
Singh S, Shanker S, Subramanyam AA, Kamath RM. Study of cognitive profile in the elderly presenting with both depressive and cognitive symptoms. J Geriatr Ment Health 2015;2:90-5
|How to cite this URL:|
Singh S, Shanker S, Subramanyam AA, Kamath RM. Study of cognitive profile in the elderly presenting with both depressive and cognitive symptoms. J Geriatr Ment Health [serial online] 2015 [cited 2020 Aug 9];2:90-5. Available from: http://www.jgmh.org/text.asp?2015/2/2/90/174274
| Introduction|| |
A national crisis in geriatric mental health care is imminent because of the anticipated growth of the geriatric population. A variety of old age-specific disorders and issues are coming into notice lately. 
Patients presenting with combinations of cognitive, affective, and behavioral problems pose a clinical conundrum; it is difficult to establish whether the cognitive impairment is secondary to an affective disorder or whether it is a more sinister, organic dementing process. Depressive symptoms are common in the elderly population without dementia. , Around two-third of depressed individuals present with significant cognitive underfunctioning, formerly known as depressive pseudodementia, "memory disorder in the context of depressive illness," or "the dementia syndrome of depression." Impaired ability to think, concentrate, or make decisions is a Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic criterion for major depressive episode. In clinical practice, this group remains difficult to identify. One of the major confounding factors is that many patients with organic dementia also have affective symptoms. ,
The differential diagnosis is especially difficult because these diseases greatly overlap in cognitive impairments. Mild Alzheimer's disease (AD) is characterized in the early stages by deficits in episodic memory,  with no apparent insufficiencies in tasks requiring learning and retention of either verbal or nonverbal information. , However, patients with severe depression also tend to perform poorly in both verbal and nonverbal memory tests. , To complicate matters even further, verbal episodic memory tasks such as recall tasks often fail to discriminate accurately severe depression patients from patients having mild dementia.  One important aspect of the clinical assessment of cognitive impairment in depression should be identifying cognitive screening instruments that differentiate the cognitive deficits most characteristic of depression from those that are most likely to reflect dementia spectrum. 
As far as progression of cognitive symptoms is concerned, major late-life depression does not progress to dementia in most cases. Instead, it is a stable disturbance that improves to a certain extent when the depressive symptoms are ameliorated. , However, older patients with major depression and a dementia syndrome that subsides after remission of depression are at a high risk of developing irreversible dementia. ,,,
One important aspect of the clinical assessment of cognitive impairment and depression in the elderly should be identifying cognitive screening instruments that differentiate the cognitive deficits most characteristic of depression from those that are most likely to reflect dementia. Unfortunately, there are few empirical data on screening measures that effectively discriminate between the cognitive presentations of AD and depression.  Several screening and diagnostic tests for dementia are available but their complexity and need for specialized test equipment put them beyond routine bedside use.
This concept has been understudied and Indian data in this context are not robust; therefore, this study aimed at examining the cognitive profile in patients having both cognitive and depressive symptoms at the time of presentation and after 3 months follow-up after intervention with the antidepressant, and comparing the two.
[TAG:2]MATERIALS AND METHODS [/TAG:2]
It was a follow-up study of 6 months duration conducted at the psychiatric outpatient department in a tertiary care hospital, after obtaining approval from the institutional ethics committee. A total of 74 participants were included in the study, who were more than 50 years of age, had depressive symptoms [geriatric depression scale (GDS)>5] as well as cognitive symptoms. Those participants having symptoms secondary to any organic condition, unstable medical or surgical illness, or any other psychiatric disorder (including bipolar disorder) and those who were lost to follow-up were excluded from the study. The participants were assessed using ACE at the baseline (at first visit) and after a period of 3 months during which they received treatment for the depressive symptoms.
The first phase of assessment was performed when the patients were recruited in the psychogeriatric clinic. Each patient was seen by the psychiatrist for a clinical diagnostic assessment to rule out the common causes for reversible cognitive deficits after which the all the necessary investigations were performed, along with the cognitive assessment. All the patients were prescribed tablet escitalopram in optimum doses. The second phase of assessment was conducted after 3 months of pharmacological intervention wherein two groups emerged, based on their cognitive assessment profile, as:
1. Whose cognitive deficits improved with pharmacological intervention for depressive symptoms (were considered as having depression) and
2. Those whose cognitive deficits did not improve after intervention and treatment of depression [were suspected of having mild cognitive impairment (MCI)].
These two groups were subjected to statistical analysis to check for differences between the cognitive scores within each group in the preintervention phase and postintervention phase.
Thus, in this study a total of 74 participants were included. They were divided into two groups based on the diagnosis made. In the depression group, there were 41 subjects and there were 33 subjects in the MCI group. In the postintervention phase of assessment, 37 subjects were followed up and assessed in the depression group and 33 were assessed in the MCI group. The tool used for cognitive assessment was:
Addenbrooke's cognitive examination (ACE)
It is a brief, 15-20-min test battery originally designed to detect and classify different kinds of dementia, particularly AD and frontotemporal dementia without the use of specialized test equipment.  The ACE-Revised (ACE-R) takes between 12 min and 20 min to administer and score in a clinical setting. It contains five subtests, each one representing one cognitive domain: Attention/orientation, memory, fluency, language, and visuospatial. The maximum score is 100, composed by the addition of the all subtests.
The scale has been normed with significant validity and reliability for the Indian population by Mathuranath et al.  The normative data were gathered specifically from South India; however, the authors have reported that the normative data can be generalized and used for the rest of India.
The sample under study and the score distribution was not normal and it was a nonparametric sample. Descriptive statistics in the form of mean and standard deviation was used for the age and years of education in each group. Mann-Whitney U test was performed to study the difference between the mean age and years of education between the groups, and Wilcoxon signed-rank test was performed to study the difference between the full and domain ACE scores between the preintervention phase and postintervention phase within each group.
| Results and discussion|| |
The demographic details of the participants are shown in [Table 1]. Mean age in the depression group was 71.43 years and in the MCI group, it was 69.70 years. The average year of education in the depression group was 7.92 years and in the MCI group, it was 7.89 years. [Table 1] also indicates no significant difference in the age (Z = 1.21, P = 0.229) and years of education (Z = 0.24, P = 0.812) between both the groups. This is a significant observation to note because the normative study of ACE in India found that education plays an important role in the response and scores of the patients tested. 
Considering the individual cognitive domains (as assessed by the ACE) affected in patients with depression and MCI prior to pharmacological intervention, not much difference was evident in the two groups [as shown in [Figure 1] and [Figure 2].
|Figure 1: Shows the distribution of cognitive defi cits (according to ACE) in patients with MCI prior to intervention|
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However, previous studies have shown a difference in the cognitive deficits between the two groups. Mild Alzheimer's or MCI presents mostly with problems in episodic memory, language, praxis, and gnostic processes, with preserved learning of verbal and nonverbal information. ,, On the other hand, in depression, the areas affected are those of speed processing, selective attention, response inhibition, and executive function. ,, Therefore, presentation of the cognitive symptoms in this study highlights the issue that both MCI and depression can present in a similar fashion, leading to further diagnostic dilemma.
The sample studied was nonparametric in nature; hence, Wilcoxon signed-rank test was used to study the difference between the two phases (prepharmacological intervention and postpharmacological intervention) in each group. The full and domain ACE normative scores for the Indian population that were used were as per the years of education obtained; hence, the cutoff for each participant differed based on his/her years of education obtained. Thus, instead of the mean, the median was calculated.
[Table 2] shows the difference between the preintervention and postintervention full ACE scores in the depression group. The preintervention assessment median ACE full score was 59 and the postintervention phase ACE score was 74. The significant difference between the scores (F = 5.30, P = .000), suggests that there was an increase in scores in the postintervention phase, indicating that with improvement in the depressive mood, cognitive deficits were significantly reduced.
|Table 2: Difference between the preintervention and postintervention full ACE scores in the depression group|
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[Table 3] shows the difference between the preintervention and postintervention full ACE scores in the MCI group. The preintervention assessment median ACE full score was 57 and the postintervention phase ACE score was 56. This shows that there was no significant increase in the postintervention phase (F = 1.66, P = 0.068), which signifies that those with MCI did not see a noteworthy improvement in their cognitive condition after an intervention for mood symptoms.
|Table 3: Difference between the preintervention and postintervention full ACE scores in the MCI group|
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Observation of the preintervention and postintervention ACE domain scores in the depression group clearly indicated that there was significant difference between preintervention and postintervention scores in all domains of the ACE that were tested [Table 4], suggesting that as there was improvement in the depressive mood, the cognitive deficits observed in each domain significantly reduced.
|Table 4: Difference between the preintervention and postintervention ACE domain scores in the depression group|
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Studying the preintervention and postintervention ACE domain scores in the MCI group indicates that there was no significant difference between the preintervention and postintervention scores in any of the domains of the ACE that were tested [Table 5].
|Table 5: Difference between the preintervention and postintervention ACE domain scores in the MCI group|
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The above results indicate that ACE is a useful instrument that can be employed to distinguish between those having a primary mood disorder in old age versus those who have cognitive deficits that are more significant than the mood state. The improvement in the full scaled scores and the domain scores in the depression group indicates that in those who have a primary mood disorder, the alleviation of the mood symptoms brings about a significant improvement in their cognitive condition. In clinical practice where the differential diagnosis of depressive mood conditions versus MCI or dementia is difficult, this is a noteworthy finding.
Alexopoulos reports that some elderly patients develop significant cognitive deficits during the depressive episodes that subside after remission of the depressive symptoms.  Reischies and Lee have also shown that cognitive deficits related to MCI or other primary cognitive disorders that evolve during the episode of depression in the elderly persist after the depressive symptoms have remitted. , We have seen similar results in our studies where there was a significant improvement in the cognitive variables after the intervention for depression.
In the depression group, the median scores indicate that the domains of attention, registration, recall, and verbal fluency have relatively more improvement than the other cognitive domains. Thus, largely the difference of improvement has been in the domains of attention, executive functions, and working memory. Previous studies have consistently shown that depressed individuals show deficits in making decisions, attention, executive function, and working memory. ,,,, Thus, with the improvement of the mood-related symptoms we have seen a significant rise in the scores in these domains further helping us to substantiate that the depressed group of elderly individuals were clearly distinguishable from those with primary MCI.
| Conclusion and implication|| |
It is evident that there was an improvement in cognition as observed in ACE scores after antidepressant intervention in the depression group but not in those having MCI. This highlights the need and importance for continuous periodic assessment in the elderly who present with a combination of behavioral, mood, and cognitive symptoms, which would allow us to see the symptoms that get filtered away with appropriate intervention, and then come to a specific conclusion about their primary condition. This will help us handle and resolve the difficulty that surrounds in making the fine distinction between primary depression that presents with significant cognitive impairment and primary MCI. However, a larger sample with longer follow-up and multiple assessments would yield better and generalizable results.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Jeste DV, Alexopoulos GS, Bartels SJ, Cummings JL, Gallo JJ, Gottlieb GL, et al
. Consensus statement on the upcoming crisis in geriatric mental health: Research agenda for the next 2 decades. Arch Gen Psychiatry 1999;56:848-53.
Copeland JR, Gurland BJ, Dewey ME, Kelleher MJ, Smith AM, Davidson IA. Is there more dementia, depression, and neurosis in New York? A comparative study of the elderly in New York and London using the computer diagnosis AGECAT. Br J Psychiatry 1987; 151:466-73.
Blazer D, Williams CD. Epidemiology of dysphoria and depression in an elderly population. Am J Psychiatry 1980;137:439-44.
Des Rosiers G. Primary or depressive dementia: Hedonic tone and memory. [Dissertation] UK: University of Cambridge; 1994.
Garcia CA, Reding MJ, Blass JP. Overdiagnosis of dementia. J Am Geriatr Soc 1981;29:407-10.
Grober E, Dickson D, Sliwinski MJ, Buschke H, Katz M, Crystal H, et al
. Memory and mental status correlates of modified Braak staging. Neurobiol Aging 1999;20:573-9.
Dudas RB, Clague F, Thompson SA, Graham KS, Hodges JR. Episodic and semantic memory in mild cognitive impairment. Neuropsychologia 2005;43:1266-76.
Perry RJ, Watson P, Hodges JR. The nature and staging of attention dysfunction in early (minimal and mild) Alzheimer′s disease: Relationship to episodic and semantic memory impairment. Neuropsychologia 2000;38:252-71.
Abas MA, Sahakian BJ, Levy R. Neuropsychological deficits and CT scan changes in elderly depressives. Psychol Med 1990;20:507-20.
Burt DB, Zembar MJ, Niederehe G. Depression and memory impairment: A meta-analysis of the association, its pattern, and specificity. Psychol Bull 1995;117:285-305.
O′Carroll RE, Conway S, Ryman A, Prentice N. Performance on the delayed word recall (DWR) fails to differentiate clearly between depression and Alzheimer′s disease. Psychol Med 1997;27:967-71.
Steffens DC, Potter GG. Geriatric depression and cognitive impairment. Psychol Med 2008;38:163-75.
Murphy CF, Alexopoulos GS. Attention network dysfunction and treatment response of geriatric depression. J Clin Exp Neuropsychol 2006;28:96-100.
Nakano Y, Baba H, Maeshima H, Kitajima A, Sakai Y, Baba K, et al
. Executive dysfunction in medicated, remitted state of major depression. J Affect Disord 2008;111:46-51.
Reynolds CF 3 rd
, Kupfer DJ, Hoch CC, Stack JA, Houck PR, Sewitch DE. Two-year follow-up of elderly patients with mixed depression and dementia. Clinical and electroencephalographic sleep findings. J Am Geriatr Soc 1986;34:793-9.
Kral VA, Emery OB. Long-term follow-up of depressive pseudodementia of the aged. Can J Psychiatry 1989;34:445-6.
Copeland JR, Davidson IA, Dewey ME, Gilmore C, Larkin BA, McWilliam C, et al
. Alzheimer′s disease, other dementias, depression and pseudodementia: Prevalence, incidence and three-year outcome in Liverpool. Br J Psychiatry 1992;161:230-9.
Alexopoulos GS, Meyers BS, Young RC, Mattis S, Kakuma T. The course of geriatric depression with "reversible dementia": A controlled study. Am J Psychiatry 1993;150:1693-9.
Mathuranath PS, Nestor PJ, Berrios GE, Rakowicz W, Hodges JR. A brief cognitive test battery to differentiate Alzheimer′s disease and frontotemporal dementia. Neurology 2000;55:1613-20.
Mathuranath PS, Cherian JP, Mathew R, George A, Alexander A, Sarma SP. Mini mental state examination and the Addenbrokke′s cognitive examination: Effect of education and norms for a multicultural population. Neurol India 2007;55:106-10.
Beats BC, Sahakian BJ, Levy R. Cognitive performance in tests sensitive to frontal lobe dysfunction in the elderly depressed. Psychol Med 1996;26:591-603.
Nebes RD, Butters MA, Mulsant BH, Pollock BG, Zmuda MD, Houck PR, et al
. Decreased working memory and processing speed mediate cognitive impairment in geriatric depression. Psychol Med 2000;30:679-91.
Austin MP, Mitchell P, Wilhelm K, Parker G, Hickie I, Brodaty H, et al
. Cognitive function in depression: A distinct pattern of frontal impairment in melancholia? Psychol Med 1999;29:73-85.
Alexopoulos GS. Depression in elderly. Lancet 2005;365:1961-70.
Reischies FM, Neu P. Comorbidity of mild cognitive disorder and depression - A neuropsychological analysis. Eur Arch Psychiatry Clin Neurosci 2000;250:186-93.
Lee JS, Potter GG, Wagner HR, Welsh-Bohmer KA, Steffens DC. Persistent mild cognitive impairment in geriatric depression. Int Psychogeriatr 2007;19:125-35.
Doumas M, Smolders C, Brunfaut E, Bouckaert F, Krampe RT. Dual task performance of working memory and postural control in major depressive disorder. Neuropsychology 2012;26:110-8.
Elderkin-Thompson V, Moody T, Knowlton B, Hellemann G, Kumar A. Explicit and implicit memory in late-life depression. Am J Geriatr Psychiatry 2011;19:249-55.
Marazziti D, Consoli G, Picchetti M, Carlini M, Faravelli L. Cognitive impairment in major depression. Eur J Pharmacol 2010;626:83-6.
Weiland-Fiedler P, Erickson K, Waldeck T, Luckenbaugh DA, Pike D, Bonne O, et al
. Evidence for continuing neuropsychological impairments in depression. J Affect Disord 2004;82:253-8.
[Figure 1], [Figure 2]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]