| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Stroke. 2001;32:113.)
© 2001 American Heart Association, Inc.
Original Contributions |
From the Department of Psychiatry, The University of Iowa College of Medicine, Iowa City.
Correspondence to Eran Chemerinski, MD, Psychiatry Research/MEB, The University of Iowa, Iowa City, IA 52242. E-mail eran-chemerinski{at}uiowa.edu
| Abstract |
|---|
|
|
|---|
MethodsOn the basis of a semistructured psychiatric examination and DSM-IV diagnostic criteria, a consecutive series of patients with poststroke major or minor depression (n=55) were selected. Their impairment in ADL function was assessed by means of the Johns Hopkins Functioning Examination during acute hospitalization and either 3 or 6 months later.
ResultsPatients whose mood improved at follow-up (n=21) had significantly greater recovery in ADL functions at follow-up than patients whose mood did not improve (n=34). There were no differences in demographic variables, lesion characteristics, and neurological symptoms between the two groups. Furthermore, patients with either major or minor depression at the initial evaluation showed the same amount of recovery in ADL function if they improved at follow-up.
ConclusionsOur findings suggest that remission of poststroke depression over the first few months after stroke is associated with greater recovery in ADL function than continued depression. Early effective treatment of depression may have a positive effect on the rehabilitation outcome of stroke patients.
Key Words: cerebrovascular disorders depression physical function
| Introduction |
|---|
|
|
|---|
Depression is probably the most frequent emotional disorder that occurs after stroke. Numerous studies have reported frequencies for major depression ranging from 10% to 25%2 3 4 and for minor depression ranging from 10% to 40%.5 6
Several studies have shown that depression has a negative impact on recovery of ADL function in stroke patients. Kotilla et al,7 for example, reported poor outcome at 3 months and 1 year after stroke in patients with "inadequate emotional reactions." However, there was no assessment of reliability or validity of these emotional reactions. Feibel and Springer8 reported that depressed patients at 6 months after stroke had greater difficulties in returning to their prior social activities compared with nondepressed patients. Also, Sinyor et al9 reported worse physical therapy outcome at 6 weeks after stroke in depressed patients compared with nondepressed patients. These studies, however, did not assess depression by means of standardized diagnostic criteria and did not examine the influence of lesion side, volume, or location on outcome. In a study of patients with and without depression during the immediate period after stroke but with similar impairment in ADL scores, we found, 2 years later, that the depressed patients had significantly less recovery in their ADL functions than the nondepressed patients.10 The recovery curves for ADL function were not significantly different between patients with major depression versus those with minor depression,10 suggesting that both moderate and severe forms of depression lead to impaired recovery in ADL functions. Morris et al,11 who used an abbreviated version of the Barthel index, also reported that at 15 months after stroke, patients with major depression and those with minor depression had significantly greater physical disability than nondepressed patients.
Although it has been recognized that depression is associated with impaired recovery in ADL functions, it is unclear whether treatment of depression will improve recovery. Two studies have shown greater improvement in ADL scores in poststroke depressed patients who had a positive dexamethasone suppression test when they were treated in a double-blind study with the antidepressant trazodone over 6 weeks12 or in an open-label study with fluoxetine or nortriptyline.13 On the other hand, in 2 prior double-blind treatment trials, we failed to show any significant improvement in ADL among patients treated with nortriptyline compared with placebo.14 15
In this study, we used standardized diagnostic criteria and a structured interview to diagnose patients with in-hospital poststroke depression. At 3- or 6-month follow-up, we divided these patients into those with and those without mood improvement and examined their functional recovery. We hypothesized that there would be greater recovery in ADL functions among depressed patients with remission of their depression compared with depressed patients without mood recovery over the follow-up period.
| Subjects and Methods |
|---|
|
|
|---|
Psychiatric Examination
After obtaining informed consent, patients were
evaluated by a psychiatrist who used a modified version of the
semistructured interview, the Present State Examination
(PSE).17 A diagnosis of
"depression due to stroke with a major depressivelike episode" or
minor depression (based on research criteria) according to
DSM-IV18 criteria was made
by means of symptoms elicited from the PSE, which had been modified to
include all the appropriate DSM-IV symptoms. When patients were
examined before the 2-week-duration criteria were met, they were
required to have the symptoms present since the onset of the
stroke. The Hamilton Depression Scale (HDS, 17
items)19 was used to measure
the severity of depressive symptoms. In this scale, scores range from 0
to 52, with higher scores indicating more severe depressive symptoms.
Functional physical impairment was assessed by means of the Johns
Hopkins Functioning Inventory
(JHFI).20 The JHFI is a
10-item questionnaire that evaluates the patients degree of
independence in ADL including walking, dressing, eating, comprehension
of spoken and written language, writing, performing routine tasks,
finding ones way around, expressing needs, and maintaining sphincter
control. Scores may range from 0 to 27, with higher scores indicating
more severe impairment. Patients cognitive functioning was assessed
by means of the Mini-Mental State Examination
(MMSE),21 in which scores
range from 0 to 30, with lower scores indicating greater impairment.
The reliability and validity of these instruments in a population of
stroke patients have been demonstrated in prior
publications.22
Neuroimaging
A neurologist who was blind to the psychiatric
findings evaluated the computed tomography scans obtained as part of
the patients clinical care and transferred them onto standardized
templates by using the method of
Damasio.23 Lesion volume
(expressed as a percentage of total brain volume) was calculated from
the ratio of the largest cross-sectional area of the lesion on any CT
scan slice to the cross-sectional area of whole brain on the slice
passing through the body of the lateral ventricle. We have demonstrated
the reliability of these measurements as well as their utility in
stroke patients in a prior
publication.24
Statistical Analyses
Statistical analyses were performed by mean
and standard deviation, Students
t test, and ANOVA for the
parametric data and intergroup comparisons. Frequency
distributions were analyzed by means of
2
tests.
| Results |
|---|
|
|
|---|
An initial analysis of our total group of patients showed a positive correlation between changes in HDS scores (ie, follow-upinitial HDS scores) and changes in JHFI scores (ie, follow-upinitial JHFI scores) [F=10.4; df=1; 169, P=0.001, r=0.241]. Thus, greater improvement in mood was associated with more improvement in ADL function.
To examine our hypothesis that in poststroke depressed
patients, remission of depression is associated with greater recovery
in ADL function, we selected from our total population of patients only
those (n=74) who had an in-hospital diagnosis of major or minor
depression according to DSM-IV symptom criteria, by using the symptoms
elicited from the PSE. We then divided them on the basis of whether or
not their mood improved over the 3- or 6-month follow-up. Remission of
depression was defined as a >50% reduction in HDS scores and no
longer meeting criteria for either major or minor depression.
Nonremission of depression was defined as a
50% reduction in HDS
scores at follow-up. Because poststroke depressed patients with mood
improvement at the 3- or 6-month follow-up had lower (ie, less
impaired) initial JHFI scores than the nonimproved patients, we matched
patients having either major or minor depression whose depression had
remitted at the 3- or 6-month follow-up (n=21) with patients whose
depression had not remitted (n=34), based on comparable initial JHFI
scores (ie, +0.3). In-hospital JHFI scores were 8.3±5.9 for the
mood-improved patients and 8.0±5.0 for the nonimproved group, whereas
at the 3- or 6-month follow-up, the JHFI scores were 3.3±2.9 and
5.8±4.0, respectively. ANOVA revealed a significant group-by-time
interaction [F=5.37;
df=1; 53,
P=0.015]. Depressed patients
with remission at follow-up showed significantly greater recovery than
the nonremitted group at the 3- or 6- month follow-up
(Figure
).
|
In our previous 2-year follow-up study of ADL recovery among patients with and without depression,10 a factor analysis of items in the JHFI revealed 3 distinct factors: factor 1 included 6 "motor" items such as ability to walk, dress, eat, write, find ones way around a familiar setting, and perform routine tasks; factor 2 included 3 language items, including the comprehension of spoken and written language and the ability to express ones needs; and factor 3 included only sphincter control.
A repeated-measures ANOVA for each factor revealed a significant group (ie, remission versus nonremission)-by-time interaction for factor 1 [F=4.93; df=1; 41, P=0.03] but not for factor 2 [F=0.22; df=1; 42, P=0.6] or 3 [F=0.48; df=1; 42, P=0.49].
Depressed patients with remission at the 3- or 6-month follow-up had an in-hospital HDS of 14.4±5.5, whereas patients without remission had an in-hospital HDS of 12.3±5.7. At the 3- or 6-month follow-up, the HDS scores were 3.8±2.9 and 13.0±6.3, respectively. ANOVA revealed a significant group-by-time interaction [F=69.2; df=1; 53, P=0.0001]. Obviously, the remitted group showed lower HDS than the nonremitted group over the 3- or 6-month follow-up.
There were no significant differences between the two groups
in age, race, handedness, marital status, years of education, time
since stroke, socioeconomic status, personal or family history of
depression, history of alcohol abuse, or use of antidepressants. There
was, however, a significant difference in sex. There was a
significantly higher percentage of women in the nonremission group
(68%) compared with the remission group (33%)
(
2=6.2
df=1,
P=0.01)
(Table 1
). When we reanalyzed the data by using only
male patients, however, we continued to show a time-by-group
interaction [F=6.95;
df=1; 23,
P=0.014], indicating that the
improved recovery in remitted patients was not due to male-female
differences in ADL recovery.
|
Moreover, there were no significant differences in MMSE
scores; side, volume, or location (ie, cortical or subcortical) of
lesion; initial neurological deficits (motor, sensory, visual fields
deficits, dysarthria, aphasia, apraxia, or neglect); or the percentage
of patients assigned to a physical rehabilitation therapy program
(Table 2
).
|
Comparison Between Patients With Major
Depression and Those With Minor Depression
To detect any differences in the association of
remission of depression and ADL improvement between major or minor
depression, patients whose depression remitted over the 3- or 6-months
follow-up who could be matched for initial JHFI score (±0.10 were
divided into a major depressed/remission group (n=9) and a minor
depressed/remission group (n=9).
In the hospital, JHFI scores were 7.4±3.5 for the remitted major depression patients and 7.5±5.2 for the remitted minor depression group, whereas, at the 3- or 6-month follow-up, the JHFI scores were 3.7±2.9 and 2.4±2.4, respectively. ANOVA did not reveal any significant group-by-time interaction between the two groups.
Patients with remitted major depression had an in-hospital HDS of 16.6±4.5, whereas patients with remitted minor depression had an in-hospital HDS of 12±6.5. At the 3- or 6-month follow-up, the HDS scores were 5.5±2.8 and 2.1±2.4, respectively. ANOVA did not reveal any significant group-by-time interaction between the two groups.
There were no significant differences between the two groups in age, sex, race, handedness, marital status, years of education, time since stroke, socioeconomic status, personal or family history of depression, history of alcohol abuse, or use of antidepressants. Moreover, there were no significant differences in MMSE scores; side, volume, or location (ie, cortical or subcortical) of lesion; initial neurological deficits (motor, sensory, visual fields deficits, dysarthria, aphasia, apraxia, or neglect); or access to a physical rehabilitation therapy program between the two groups.
| Discussion |
|---|
|
|
|---|
Before further discussion of our results, it is important to acknowledge the methodological limitations of the study. First, the use of patients from 2 demographically distinct patient populations may have led to greater generalizability of findings or could have led to findings influenced by cohort effects. Second, our patients were predominantly of lower socioeconomic class. It is uncertain whether these findings pertain to other populations of stroke patients. Our measure of ADL function was the JHFI rather than a more commonly used instrument such as the Functional Independence Measure25 or the Barthel scale.26 These latter instruments use a wider range of scores and may be more sensitive to change. Thus, our finding that language function (ie, factor 2 of JHFI) did not change may have been related to the instrument we used.
Finally, although there were no significant differences in the frequency of antidepressant use among groups, some depressions were treated, but the vast majority spontaneously improved. There may be differences in ADL recovery between treated and spontaneously remitted depressions.
The major question raised by this study is why remission of either major or minor depression led to improved recovery in ADL over the first few months after stroke. One might speculate that the mechanisms of depression (eg, neurotransmitter depletion leading through some pathophysiology to the clinical manifestations of decreased concentration and energy) may have led to poor recovery. On the other hand, the fact that both major and minor depression showed an equal degree of recovery might lead to an alternate speculation that the effect of depression on physical impairment may be mediated by psychological rather than physiological mechanisms. For example, depressed patients may be hopeless about the future and thus may be less psychologically motivated to put any effort into rehabilitation or recovery. This could lead to slowed recovery in the depressed patients. This speculation that psychological rather than physiological mechanisms led to improved ADL recovery is also supported by our recent finding that recovery in cognitive function among patients who responded to treatment of poststroke depression occurred in patients with major but not minor depression.27 This finding related to cognitive recovery contrasts with our current findings but indicates that all poststroke recovery is not facilitated by any improvement in depression. Cognitive recovery appears to be aligned with the mechanism of major depression, whereas physical recovery appears to be aligned more broadly with an improvement in depression, thus suggesting perhaps a psychologically mediated mechanism. Whatever the explanation, the fact that remission of depression improves recovery from stroke impairments emphasizes the importance of recognizing and treating depression in patients with acute stroke.
| Acknowledgments |
|---|
Received June 23, 2000; revision received August 31, 2000; accepted September 7, 2000.
| References |
|---|
|
|
|---|
2.
House A, Dennis M,
Warlow C, Hawton K, Molyneux K. Mood disorders after stroke and their
relation to lesion location: a CT scan study.
Brain. 1990;113:11131130.
3.
Astrom M, Adolfsson
R, Asplund K. Major depression in stroke patients: a 3-year
longitudinal study. Stroke. 1993;24:976982.
4.
Gainotti G, Azzoni
A, Marra C, Frequency, phenomenology and anatomical-clinical correlates
of major post-stroke depression. Br J
Psychiatry. 1999;175:163167.
5. Morris PLP, Robinson RG, Raphael B. Prevalence and course of depressive disorders in hospitalized stroke patients. Int J Psychiatry Med. 1990;20:349364.[Medline] [Order article via Infotrieve]
6.
Eastwood MR, Rifat
SL, Nobbs H, Ruderman J. Mood disorder following cerebrovascular
accident. Br J Psychiatry. 1989;154:195200.
7.
Kotilla M, Waltimo
O, Niemim L, Laaksonen R, Lempinen M. The profile of recovery from
stroke in factors influencing outcome.
Stroke. 1984;15:10391044.
8. Feibel JH, Springer CJ. Depression and failure to resume social activities after stroke. Arch Phys Med Rehabil. 1982;63:276278.[Medline] [Order article via Infotrieve]
9. Sinyor D, Amato P, Kaloupek P. Post-stroke depression: relationship to functional impairment, coping strategies, and rehabilitation outcome. Stroke. 1986;17:112117.
10.
Parikh RM,
Robinson RG, Lipsey JR, Starkstein SE, Fedoroff JP, Price TR. The
impact of post-stroke depression on recovery in activities of daily
living over two year follow-up. Arch
Neurol. 1990;47:785789.
11. Morris PLP, Raphael B, Robinson RG. Clinical depression impairs recovery from stroke. Med J Aust. 1992;157:239242.[Medline] [Order article via Infotrieve]
12.
Reding MJ, Orto
LA, Winter SW, Fortuna IM, DiPonte P, McDowell FH. Antidepressant
therapy after stroke: a double-blind trial.
Arch Neurol. 1986;43:763765.
13. Gonzalez-Torrecillas JL, Mendlewicz J, Lobo A. Effects of early treatment of poststroke depression on neuropsychological rehabilitation. Int Psychogeriatr. 1995;7:547560.[Medline] [Order article via Infotrieve]
14. Lipsey JR, Robinson RG, Pearlson GD, Rao K, Price TR. Nortriptyline treatment of post-stroke depression: a double-blind study. Lancet. 1984;1:297300.[Medline] [Order article via Infotrieve]
15.
Robinson RG,
Schultz SK, Castillo C, Kopel T, Kosier T. Nortriptyline versus
fluoxetine in the treatment of depression and in short term recovery
after sroke: a placebo controlled, double-blind study.
Am J Psychiatry. 2000;157:351359.
16.
DeRenzi E,
Vignolo LA. The Token Test: a sensitive test to detect
disturbances in aphasics.
Brain. 1962;85:665678.
17. Wing JK, Cooper JE, Sartorius N. The Measurement and Classification of Psychiatric Symptoms: An Instructional Manual for the PSE and CATEGO Programs. New York, NY: Cambridge University Press; 1974.
18. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders - DSM-IV. 4th ed. Washington, DC: American Psychiatric Press, Inc; 1994.
19. Hamilton MA. A rating scale for depression. J Neurol Neurosurg Psychiatry. 1960;23:5662.
20. Robinson RG, Szetela B. Mood change following left hemispheric brain injury. Ann Neurol. 1981;9:447453.[Medline] [Order article via Infotrieve]
21. Folstein MF, Folstein SE, McHugh PR. Mini-Mental State: a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12:189198.[Medline] [Order article via Infotrieve]
22. Robinson RG. The Clinical Neuropsychiatry of Stroke. Cambridge, UK: Cambridge University Press; 1998.
23. Damasio H, Damasio A. Lesion Analysis in Neuropsychology. New York, NY: Oxford University Press; 1989.
24.
Starkstein SE,
Robinson RG, Price TR. Comparison of patients with and without
post-stroke major depression matched for size and location of lesion.
Arch Gen Psychiatry. 1988;45:247252.
25. Ottenbacher KJ, Mann WC, Granger CV, Tomita M, Hurren D, Charvat B. Inter-rater agreement and stability of functional assessment in the community-based elderly. Arch Phys Med Rehabil. 1994;75:12971301.[Medline] [Order article via Infotrieve]
26. Mahoney FI, Barthel DW. Functional evaluation: Barthel index. Md Med J. 1965;14:6165.
27.
Kimura M,
Robinson RG, Kosier T. Treatment of cognitive impairment after
poststroke depression. Stroke. 2000;31:14821486.
This article has been cited by other articles:
![]() |
C. L. Watkins and B. French Psychological Intervention Poststroke: Ready for Action? Stroke, September 1, 2009; 40(9): 2951 - 2952. [Full Text] [PDF] |
||||
![]() |
J. I. Cameron, C. Tsoi, and A. Marsella Optimizing Stroke Systems of Care by Enhancing Transitions Across Care Environments Stroke, September 1, 2008; 39(9): 2637 - 2643. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. G. Robinson, R. E. Jorge, and K. Clarence-Smith Double-Blind Randomized Treatment of Poststroke Depression Using Nefiracetam J Neuropsychiatry Clin Neurosci, May 1, 2008; 20(2): 178 - 184. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Nuyen, P. M. Spreeuwenberg, P. P. Groenewegen, G. A.M. van den Bos, and F. G. Schellevis Impact of Preexisting Depression on Length of Stay and Discharge Destination Among Patients Hospitalized for Acute Stroke: Linked Register-Based Study Stroke, January 1, 2008; 39(1): 132 - 138. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. L. Watkins, M. F. Auton, C. F. Deans, H. A. Dickinson, C. I.A. Jack, C. E. Lightbody, C. J. Sutton, M. D. van den Broek, and M. J. Leathley Motivational Interviewing Early After Acute Stroke: A Randomized, Controlled Trial Stroke, March 1, 2007; 38(3): 1004 - 1009. [Abstract] [Full Text] [PDF] |
||||
![]() |
I. G.L. van de Port, G. Kwakkel, I. van Wijk, and E. Lindeman Susceptibility to Deterioration of Mobility Long-Term After Stroke: A Prospective Cohort Study Stroke, January 1, 2006; 37(1): 167 - 171. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. G. Sugden and J. A. Bourgeois Drs. Sugden and Bourgeois Reply Psychosomatics, February 1, 2005; 46(1): 93 - 94. [Full Text] |
||||
![]() |
S. G. Sugden and J. A. Bourgeois Modafinil Monotherapy in Poststroke Depression Psychosomatics, February 1, 2004; 45(1): 80 - 81. [Full Text] [PDF] |
||||
![]() |
D. Long and J. Young Dexamphetamine treatment in stroke QJM, September 1, 2003; 96(9): 673 - 685. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Bogousslavsky William Feinberg Lecture 2002: Emotions, Mood, and Behavior After Stroke Stroke, April 1, 2003; 34(4): 1046 - 1050. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Berg, H. Palomaki, M. Lehtihalmes, J. Lonnqvist, and M. Kaste Poststroke Depression: An 18-Month Follow-Up Stroke, January 1, 2003; 34(1): 138 - 143. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2001 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |