ORIGINAL ARTICLE
Characteristics and correlates of poststroke depression: An Indian study
Amlan Kusum Jana, Suddhendu Chakraborty1, Samir Kumar Praharaj2
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Department of Psychiatry, KPC Medical College and Hospital, Kolkata, 1Department of Psychiatry, Bongaon J R Dhar Sub
Divisional Hospital, Bongaon, West Bengal, 2Department of Psychiatry, Kasturba Medical College, Manipal, Karnataka, India
ABSTRACT
Background: Post stroke depression adversely affects long term outcome of stroke and increases mortality risk. Few
studies have looked into the comprehensive picture of post stroke depression in past.
Aim: The current study aimed to look into the phenomenology, characteristic features and various correlates of post
stroke depression.
Method: 142 consecutive stroke patients aged 60 years or above, fulfilling the inclusion criteria were assessed.
Sociodemographic and clinical data were gathered using a specially designed pro-forma. Depression, apathy and
psychosis were assessed by Post stroke depression rating scale, Apathy Evaluation Scale, and Brief Psychiatric Rating
Scale respectively. Groups (with or without major depression) were compared using Mann-Whitney U, chi square or
Fisher’s exact test. One way ANOVA was conducted to see the relations of lesion location and laterality with various
clinical parameters. Kaplan-Meier survival analysis was done to see the time to develop depression. The effect sizes
were reported as r and partial eta squared.
Results: Guilt was significantly higher (p<.05) with lesions in parietal lobe and remaining of middle cerebral artery
territory. Catastrophic reaction (p<.05) and emotional dyscontrol (p<.05) were higher for diffuse lesions, periventricular
lesions and lesions in frontal/occipital lobe. BPRS score, but not apathy, had a significant positive correlation with
depression (Pearson’s r=.692). Mean time to develop depression after stroke was 28.34 (95% CI 22.37 to 34.31) months.
Conclusions: Post stroke depression consists of various clinically important sub-components whose occurrence varies
with different lesion locations. Post stroke depression is discriminable from apathy but is related to psychosis.
Key words: Apathy, depression, stroke
INTRODUCTION
Stroke is a devastating neurological disorder with both
neurological and psychiatric complications. From aphasia,
hemiparesis, or other neurodeficits to depression, psychosis,
Address for correspondence: Dr. Suddhendu Chakraborty,
Department of Psychiatry, Bongaon J R Dhar Sub Divisional
Hospital, Bongaon ‑ 743 235, 24 Paraganas (North),
West Bengal, India.
E‑mail: dr.suddhendu.chakraborty@gmail.com
or apathy, burden of stroke can be quite heavy. Poststroke
depression especially worsens the overall outcome of
stroke. Patients with poststroke depression show far
less recovery from functional impairments compared to
nondepressed patients with stroke and are 3.4 times more
likely to die during the first 10 years after stroke.[1] The role of
depression in poststroke mortality has been re‑emphasized
in a meta‑analysis.[2] Opposing theories exist to explain the
relation between stroke and depression. Some propose
a biological mechanism behind depression, according
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DOI:
10.4103/psychiatry.IndianJPsychiatry_421_19
How to cite this article: Jana AK, Chakraborty S, Praharaj SK.
Characteristics and correlates of poststroke depression: An
Indian study. Indian J Psychiatry 2019;61:605-11.
© 2019 Indian Journal of Psychiatry | Published by Wolters Kluwer - Medknow
605
Jana, et al.: Characteristics of poststroke depression
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to which vascular insults directly affect neural circuits
regulating mood.[3,4] Inflammatory process, genetic and
epigenetic variations, white matter disease, cerebrovascular
dysregulation, altered neuroplasticity, and changes in
glutamate transmission have all been thought to be giving
rise to various psychiatric disorders after stroke.[5] Others
propose psychosocial mechanism which takes the social and
psychological stressors associated with stroke as the causes
behind depression.[6,7] However, current understanding
endorses a bidirectional relation between physical and
psychiatric illnesses.[8,9] There has been controversy
regarding phenomenology of poststroke depression as
well. Catastrophic reactions, hyperemotionality, and diurnal
mood variations have been proposed to be more consistently
associated with poststroke depression compared to
endogenous depression.[5] However, as these features
are widely seen in other neurological conditions without
depression, question remains about their specificity for
poststroke depression.[10] Researches have been carried out
to find an association between specific location of stroke
and subsequent development of depression. Robinson and
Szetela[11] in their landmark research had shown a significant
inverse correlation between the severity of poststroke
depression and the distance of the anterior border of the
lesion from the frontal pole. Since then, there have been a
number of researches looking for an association of specific
lesion location and depression though reaching a consensus
has not yet been possible.
At this juncture, a study of poststroke depression, looking
for the phenomenology, and the clinical and anatomical
correlates was felt necessary. There have been very few
studies in this field from South Asian countries, and the
single study from India[12] had a small sample size and had
assessed depression through an instrument which was
not specific for poststroke depression. The current study
attempted to overcome these methodological flaws and
present a holistic picture of poststroke depression.
MATERIALS AND METHODS
Participants
This was a cross‑sectional study carried out in the outpatient
clinic of the department of neurology in a tertiary hospital.
The hospital is situated in the southern part of Kolkata, India,
with a wide catchment area. Ethical clearance was obtained
from the institutional ethical committee before conducting
the study. The sample consisted of 142 consecutive patients,
giving written informed consent, diagnosed with stroke,
and fulfilling the study criteria. Inclusion criteria included
patients diagnosed with stroke by qualified neurologist(s)
and patients aged over 60 years. Patients with a past history
of psychiatric disorder, substance use (except nicotine),
family history of psychiatric disorder, poor cognitive
function so as to lead to unreliable psychiatric assessment
(Hindi Mental Status Examination score ≤23), and history of
606
stressful life events (excepting current illness) since the onset
of stroke or in the past 6 months (whichever is earlier) were
excluded from the study. Since the study was conducted in
the outpatient clinic, all those stroke patients who were
admitted to the hospital were automatically excluded.
Assessment
All the assessments were made by a single clinician. The
assessments were done before looking into neuroimaging or
other investigation findings. Sociodemographic and clinical
data were gathered using a pro forma specially designed
for the study which included all the relevant parameters as
described in literature including age, sex, marital status,
family type, monthly income, education, residence, current
and past employment status, and past medical history among
others. The details of stroke, which were filled up after the
clinical assessments, included location of lesion, number,
type (ischemia/hemorrhage), and the exact date of the event.
Poststroke depression was assessed by the Poststroke
Depression Rating Scale (PSDRS).[13] It consists of
10 sections. The first nine sections include depressed
mood, guilt feelings, suicidality, vegetative (sleep and
appetite) disorders, apathy/abulia/indifference, anxiety,
catastrophic reactions, difficulty in emotional control, and
anhedonia. The last section detects diurnal mood variation.
Each section has a score range of 0–5 with a higher score
meaning worse psychopathology. The assessment consists
of a semi‑structured interview that follows for each section.
In determining the total score, all the scores of the sections
are summed up excluding the last section which does not
denote depression severity.[14] Hence, the PSDRS score
ranges from 0 to 45. This scale is specifically designed
to detect poststroke depression, emphasizing on those
symptoms such as catastrophic reaction and emotional
dyscontrol which are common in poststroke depression but
not in functional depression. Besides, it is the only scale to
provide a holistic picture of poststroke depression, beyond
just depressive symptoms.
Apathy was separately assessed by the clinician‑rated
version of the Apathy Evaluation Scale.[15] It is an
18‑item scale with each item generating a score from 1
(“not at all characteristic”) to 4 (“a lot characteristic) on a
Likert scale. The maximum total score is thus 72. This is a
widely used scale for assessing apathy, especially in patients
with neurological illnesses.
For screening of cognitive impairment, the Hindi Mental
Status Examination[16] was used as all the participants in the
study could speak and understand Hindi. This is a modified
version of the Mini Mental Status Examination (MMSE).[17] In
this scale the main advantage over MMSE is that it can be
used in illiterate persons as well. The maximum score is 30,
and the cutoff for cognitive dysfunction is 23.
Indian Journal of Psychiatry Volume 61, Issue 6, November-December 2019
Jana, et al.: Characteristics of poststroke depression
To screen stressful live events, the Presumptive Stressful Life
Events Scale[18] was used which is an Indian adaptation of the
Social Readjustment Rating Questionnaire.[19] A total of 51
life events are included in the scale which are subclassified
according to whether they are personal or impersonal (not
dependent on the individual’s action) and according to
whether they are desirable, undesirable, or ambiguous.
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Psychosis was assessed by the Brief Psychiatric Rating
Scale (BPRS).[20] The Global Assessment of Functioning
(GAF)[21] scale was employed to assess patients’ functioning
in the past 1 month. Patients were also assessed by the
Diagnostic and Statistical Manual of Mental Disorders, 4th
Edition (DSM‑IV)[22] to detect whether or not they had major
depression.
Windows (SPSS Inc., Chicago, Ill, USA). One‑way analysis
of variance (ANOVA) was conducted to see the relations of
lesion laterality (left‑hemispheric lesion, right‑hemispheric
lesion, and bilateral lesion) as well as lesion location with
various clinical profiles including apathy, scores in the
subscales of PSDRS, BPRS score, and GAF score. Lesion
location was divided into four subgroups according to
predominant source of blood supply: Area A (74 patients):
basal ganglia (supplied mainly by the middle cerebral artery
[MCA]); Area B (28 patients): parietal lobe and rest of the
MCA territory; Area C (23 patients): brain stem, cerebellum,
and thalamus (supplied mainly by the posterior cerebral,
vertebral, and basilar arteries); and Area D (17 patients): the
remaining locations including diffuse lesions, periventricular
region, frontal lobe, occipital lobe, and other locations.
Statistical analysis
The collected data were statistically analyzed using the
Statistical Package for the Social Sciences (SPSS) 16.0 for
According to the DSM‑IV, patients were grouped as with or
without major depression. The groups were compared using
the Mann–Whitney U‑test for continuous variables and the
Table 1: Group differences in clinical and demographic profile
Age, mean (SD)
Years of education, mean (SD)
Time since stroke (months), mean (SD)
GAF, mean (SD)
AES (C), mean (SD)
BPRS, mean (SD)
Sex (male), n (%)
Marital status (married), n (%)
Family type (nonnuclear), n (%)
Lesion location, n (%)
Basal ganglia
Parietal lobe + MCA territory
Brain stem + cerebellum + thalamus
Others
Lesion laterality (n=141), n (%)
Left
Right
Bilateral
Current lesion number, n (%)
1
2
Multiple
Lesion type (ischemia), n (%)
Religion (Hindu), n (%)
Income (middle), n (%)
Occupation, n (%)
Employed
Unemployed
Others
Residence, n (%)
Urban
Rural
Semi‑urban
Family diagnosis (n=40), n (%)
Medical
Stroke/related
Family history (absent), n (%)
Past medical history (absent), n (%)
With major depression (n=55)
Without major depression (n=87)
P
67.42 (7.073)
9.16 (5.711)
14.75 (10.261)
71.42 (6.682)
34.11 (8.728)
15.91 (5.093)
30 (54.54)
51 (92.73)
45 (81.82)
68.02 (7.251)
9.71 (5.521)
13.94 (8.677)
74.74 (6.355)
34.89 (9.257)
12.47 (4.948)
48 (55.17)
83 (95.40)
59 (67.82)
0.591
0.619
0.766
0.007
0.753
0.000*
0.942
0.501
0.066
26 (47.27)
13 (23.64)
8 (14.54)
8 (14.54)
48 (55.17)
15 (17.24)
15 (17.24)
9 (10.34)
0.626
23 (42.59)
18 (33.33)
13 (24.07)
44 (50.57)
33 (37.93)
10 (11.49)
0.144
40 (72.73)
3 (5.45)
12 (21.82)
40 (72.73)
41 (74.54)
32 (58.18)
70 (80.46)
6 (6.89)
11 (12.64)
68 (78.16)
72 (82.76)
56 (64.37)
0.334†
4 (7.27)
19 (34.54)
32 (58.18)
5 (5.75)
30 (34.48)
52 (59.77)
0.961†
9 (16.36)
33 (60.00)
13 (23.64)
16 (18.39)
59 (67.82)
12 (13.79)
0.325
12 (75.00)
4 (25.00)
39 (70.91)
43 (78.18)
15 (62.50)
9 (37.50)
63 (72.41)
68 (78.16)
0.408
0.460
0.237
0.459
0.846
0.998
Fischer’s exact test conducted for these variables; *P<0.001. MCA – Middle cerebral artery; AES (C) – Apathy Evaluation Scale (clinician version); GAF – Global
Assessment of Functioning Scale; BPRS – Brief Psychiatric Rating Scale; SD – Standard deviation
†
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Jana, et al.: Characteristics of poststroke depression
Chi‑square test or Fisher’s exact test (whichever is applicable)
for categorical variables. Finally, Kaplan–Meier survival
analysis was done to see the time to develop depression after
stroke. The effect sizes were reported as r (calculated from
z value of the Mann–Whitney U‑test) and partial eta squared.
The level of significance was set at P < 0.05 (two‑tailed).
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RESULTS
Group comparison
As shown in Table 1, patients with major depression had
lower mean age, years of education, GAF score, and apathy
and higher mean time since stroke, but the differences
did not reach statistical significance. However, depressed
patients had a significantly higher BPRS score (P < 0.001;
r = 0.34) compared to their nondepressed counterparts.
In the distribution of sex, marital status, family type (nuclear vs.
nonnuclear), lesion location, laterality (right/left hemispheric
or bilateral), number (one/two/multiple) and type (ischemia
vs. hemorrhage), religion (Hindu vs. Muslim and others),
income (middle vs. low), occupation (employed, unemployed,
and others including students and homemakers), residence
(urban, rural, and semi‑urban), family history (present vs.
absent), past medical history (present vs. absent), and family
diagnoses (medical vs. stroke/related history), patients with
major depression were comparable to those without.
Relations of lesion laterality with other clinical
parameters
One‑way ANOVA [Table 2] between various clinical
parameters and lesion laterality did not show
left‑hemispheric lesions to be associated with a higher value
of guilt in PSDRS, but the association was not statistically
significant. Likewise, for the subscale of anxiety in the
PSDRS, left‑hemispheric lesions showed a higher value
compared to right‑hemispheric or bilateral lesion, but the
difference failed to reach statistical significance.
Relations of lesion location with other clinical parameters
One‑way ANOVA [Table 3] showed significant group differences
in apathy (P = 0.036; df: 3, 138) where patients with lesions in
Area C (brain stem, cerebellum, and thalamus) had the highest
value among different lesion locations. For the subscale of
guilt in the PSDRS, Area B, i.e., parietal lobe and the remaining
MCA territory lesions, produced a significantly higher (P =
0.025; df: 3, 138) score compared to other locations. BPRS
score (P = 0.001; df: 3, 138; partial eta squared = 0.112),
catastrophic reaction (P = 0.039; df: 3, 138), and emotional
dyscontrol (P = 0.013; df: 3, 138) were significantly higher
in patients with lesions in Area D (diffuse lesions, frontal
lobe, occipital lobe, periventricular region, etc.) compared to
other lesion location areas. Area D also registered a higher
value than other areas, for total PSDRS score (P = 0.070; df:
3, 138) and the subscale of sleep (P = 0.089; df: 3, 138). The
differences, however, did not reach statistical significance.
Similarly, a higher mean suicidality score (another subscale of
PSDRS) was seen with lesions in Area B which failed to achieve
statistical significance (P = 0.057; df: 3, 138).
Other findings
Poststroke depression total score was not significantly
correlated with age, years of education, time since stroke,
or apathy. However, a significant positive correlation
(P < 0.001) was seen with BPRS (Pearson’s r = 0.692). This
significance was maintained (P < 0.001) even when partial
correlation between them was calculated after age, years of
education, time since stroke, and apathy were controlled
(Pearson’s r = 0.731).
The prevalence of poststroke depression (major) in
the current study was 38.73% (55 patients out of 142).
Table 2: Relation of lesion laterality with various clinical profiles
Laterality, mean (SD)
PSDRS total
PSDRS mood
PSDRS guilt
PSDRS suicidality
PSDRS sleep
PSDRS appetite
PSDRS apathy‑indifference
PSDRS anxiety
PSDRS catastrophic reaction
PSDRS emotional dyscontrol
PSDRS anhedonia
PSDRS diurnal variation
GAF
AES (C)
BPRS
Time since stroke (months)
ANOVA
Left (n=67)
Right (n=51)
Bilateral (n=23)
F
P
18.10 (5.745)
2.12 (0.616)
1.48 (0.841)
0.99 (0.639)
1.43 (0.633)
1.04 (0.614)
2.76 (1.615)
2.34 (1.175)
1.04 (0.638)
1.15 (0.530)
3.75 (1.119)
1.78 (0.850)
73.67 (6.609)
35.18 (9.326)
14.24 (5.027)
14.57 (11.187)
16.90 (5.766)
1.98 (0.616)
1.12 (0.739)
0.98 (0.678)
1.31 (0.616)
0.96 (0.599)
2.75 (1.468)
1.94 (1.333)
1.06 (0.858)
1.16 (0.612)
3.65 (1.110)
1.69 (0.860)
73.94 (6.373)
33.35 (8.054)
13.10 (5.711)
13.04 (7.403)
16.39 (4.755)
1.91 (0.733)
1.39 (0.839)
1.09 (0.668)
1.35 (0.647)
0.91 (0.417)
2.83 (1.497)
1.74 (0.810)
0.78 (0.422)
1.04 (0.475)
3.35 (1.613)
1.87 (0.757)
72.52 (6.625)
35.65 (10.421)
13.78 (4.843)
15.74 (6.635)
1.102
1.200
2.694
0.241
0.546
0.562
0.022
2.928
1.419
0.377
0.931
0.405
0.387
0.772
0.682
0.722
0.335
0.304
0.055
0.787
0.580
0.571
0.978
0.057
0.245
0.687
0.397
0.668
0.680
0.464
0.507
0.488
PSDRS – Poststroke Depression Rating Scale; AES (C) – Apathy Evaluation Scale (clinician version); GAF – Global Assessment of Functioning Scale; BPRS –
Brief Psychiatric Rating Scale; ANOVA – Analysis of variance; SD – Standard deviation
608
Indian Journal of Psychiatry Volume 61, Issue 6, November-December 2019
Jana, et al.: Characteristics of poststroke depression
Table 3: Relation of lesion location with various clinical profiles
Lesion location, mean (SD)
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Age (years)
Years of education
Time since stroke (months)
GAF
AES (C)
BPRS
PSDRS total
PSDRS mood
PSDRS guilt
PSDRS suicidality
PSDRS sleep
PSDRS appetite
PSDRS apathy
PSDRS anxiety
PSDRS catastrophic reaction
PSDRS emotional dyscontrol
PSDRS anhedonia
PSDRS diurnal variation
ANOVA
Area A (n=74)
Area B (n=28)
Area C (n=23)
Area D (n=17)
F
P
68.46 (7.753)
9.64 (5.877)
13.31 (8.158)
74.42 (6.857)
32.85 (8.551)
12.70 (4.742)
16.84 (5.075)
2.00 (0.549)
1.24 (0.824)
0.88 (0.618)
1.27 (0.556)
0.97 (0.596)
2.74 (1.481)
2.04 (1.091)
0.95 (0.639)
1.05 (0.402)
3.69 (1.146)
1.74 (0.812)
66.79 (6.641)
8.86 (5.407)
15.62 (10.171)
73.32 (7.318)
34.50 (10.423)
15.64 (4.490)
19.25 (6.108)
2.21 (0.833)
1.75 (1.076)
1.25 (0.752)
1.57 (0.690)
1.07 (0.604)
3.07 (1.609)
2.18 (1.188)
1.11 (0.832)
1.14 (0.591)
3.89 (1.315)
1.64 (0.826)
67.35 (7.030)
9.70 (5.764)
14.23 (12.356)
72.57 (5.017)
38.70 (7.945)
12.48 (5.125)
16.09 (6.338)
1.91 (0.733)
1.13 (0.757)
1.04 (0.638)
1.39 (0.656)
0.87 (0.548)
2.52 (1.620)
1.83 (1.114)
0.87 (0.626)
1.09 (0.515)
3.43 (1.273)
1.91 (0.793)
67.12 (5.566)
9.71 (4.593)
15.71 (7.389)
70.65 (6.133)
36.71 (8.498)
17.35 (6.623)
19.53 (6.663)
2.24 (.831)
1.53 (.624)
1.18 (.728)
1.59 (.795)
1.18 (.529)
2.71 (1.532)
2.71 (1.687)
1.47 (1.007)
1.53 (.874)
3.41 (1.228)
1.76 (1.033)
0.473
0.153
0.547
1.689
2.925
5.827
2.403
1.410
3.214
2.573
2.214
1.097
0.578
1.948
2.875
3.729
0.862
0.443
0.702
0.928
0.651
0.172
0.036*
0.001*
0.070
0.242
0.025*
0.057
0.089
0.353
0.631
0.125
0.039*
0.013*
0.462
0.723
*P<0.05. Area A – Basal ganglia; Area B – Parietal lobe and rest of the MCA territory; Area – Brain stem, cerebellum, and thalamus; Area D – Others (diffuse lesions,
frontal lobe, occipital lobe, periventricular region, etc.). PSDRS – Poststroke Depression Rating Scale; AES (C) – Apathy Evaluation Scale (clinician version);
GAF – Global Assessment of Functioning Scale; BPRS – Brief Psychiatric Rating Scale; ANOVA – Analysis of variance; SD – Standard deviation
with current or past substance use and stressful life events
(excepting the current stroke) in a relevant time period.
Hence, the depression seen in the study population was
biologically and/or psychosocially related to stroke only,
and the confounding variables were taken care of. The
sample size was robust, and the instrument for detecting
depression was specific for poststroke depression only.
Figure 1: Kaplan–Meyer survival analysis showing time
to depression after stroke. Mean survival time – 28.34
(95% confidence interval: 22.37–34.31) months
Kaplan–Meier survival analysis showed [Figure 1] mean time
to develop depression (as diagnosed by the DSM‑IV) after
stroke was 28.34 (95% confidence interval: 22.37–34.31)
months.
DISCUSSION
A major strength of the current study lied in elimination
of rater bias. The rater was blind to investigation reports
(including neuroimaging findings) or current treatment
regimen as ratings were done before looking into them.
Sample selection was another area of strength. All the
predisposing factors for depression, apart from the stroke
itself, were eliminated by excluding patients with a past
history or family history of psychiatric illness and patients
The highlight of the current study finding is that though the
depression score (PSDRS total) was not significantly different
across lesion locations and did not change significantly
according to lesion laterality, its components did. Guilt,
catastrophic reaction, and emotional dyscontrol significantly
varied across lesion locations. Again guilt and anxiety, though
not statistically significant, did vary according to lesion
laterality. These findings probably justified the selection
of PSDRS over the other rating scales to detect functional
depression. It produces a comprehensive picture of poststroke
depression beyond the depressive symptoms. It also helped
in looking into the relation of symptoms more specific to
poststroke depression (as compared to functional depression,
e.g., catastrophic reaction), with lesion location and laterality.
Guilt and anxiety were more (though not statistically
significant) in left‑hemispheric lesions. Left‑hemispheric
lesions have been reported to be more consistently
associated with depression,[23] though the importance of
laterality is diluted with passage of time after stroke. By
3–6 months poststroke, proximity to the frontal lobe in
both hemispheres influences the occurrence of poststroke
depression.[24] Guilt also showed significantly different
values across lesion locations with the highest mean value
for lesions in the parietal lobe and the remaining of the MCA
territory. However, relations of components of poststroke
Indian Journal of Psychiatry Volume 61, Issue 6, November-December 2019
609
Jana, et al.: Characteristics of poststroke depression
depression‑like guilt with lesion laterality or location have
not been reported previously.
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Apathy, abulia, and indifference, as a subscale of PSDRS,
did not produce significantly different values across lesion
locations, but a composite measure of apathy through
the Apathy Evaluation Scale showed the highest value for
lesions in the thalamus, cerebellum, or brain stem. Apathy
is more commonly seen in lesions of cortico-subcortical
circuits[25] and basal ganglia which lead to dysfunctions of
frontal subcortical system.[26] However association of apathy
with thalamic lesions has also been seen.[27-29]
Catastrophic reaction and emotional dyscontrol had
significantly higher mean values for diffuse lesions,
periventricular lesions, and lesions in the frontal and
occipital lobes. This was in comparison with lesions
in the parietal lobe, basal ganglia, cerebellum, brain
stem, and thalamus. The current study population had a
disproportionately little number of patients with lesion in
the frontal and occipital lobes, and the group with lesions in
Area D (the “others” group) which included these locations
contained only 17 patients. Hence, this particular finding
should be cautiously generalized.
Depression, as assessed by total score of PSDRS, did not
have any significant correlation with apathy. Apathy has
been reported to be related to but discriminable from
depression.[15] The current finding thus is in accordance
with that. However, poststroke depression was significantly
positively correlated with psychosis (BPRS score), and the
significance was maintained in partial correlation between
them after the possible confounding variables were
controlled. This was reflected in comparison of groups as
well. Patients with depression (diagnosed by the DSM‑IV)
had a significantly higher BPRS score than those without.
This relation between poststroke depression and psychosis
has not been reported in the past. Poststroke depression and
psychosis are two distinguishable entities, but BPRS might
not be the best instrument to detect poststroke psychosis.
Probably, this finding should encourage researchers to
device an instrument to specifically detect poststroke
psychosis.
The prevalence of major depression (as per the DSM‑IV)
was seen to be 38.73% which falls in the range described
in literature.[10] Mean time to develop major depression
was 28.34 months. This is longer than what is described
in literature so far,[30] which reports the peak prevalence
of depression to be around 3–6 months following stroke,
declining by about 50% in 1 year time. However, in the
current study, survival analysis was done only for major
depression (as per the DSM‑IV) and not minor depression or
dysthymia which also are common after stroke. This might
explain the longer mean time to develop depression.
610
CONCLUSION
It can be said that poststroke depression consists of various
clinically important subcomponents apart from depressed
mood, and their occurrence varies according to lesion
locations. Poststroke depression is discriminable from
apathy but is related to poststroke psychosis.
The current study had certain limitations. First, the
cross‑sectional design failed to detect the relation of stroke
and depression over a longer time period. It also could
not throw any light on the course and long term outcome
of poststroke depression. Second, since the study was
hospital based, many patients in community who were not
obtaining the services of this hospital were missed. Finally,
to eliminate confounding variables for depression, patients
with a past or family history of depression and patients with
current or past substance use were excluded from the study.
This elimination was achieved against a cost as it made the
current study unable to detect the association between
these factors and poststroke depression. In the future,
community‑based prospective studies from these parts of
the world might shed more light in this interesting field.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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