Effect of Anxiety
Disorder on Impairment
The effect of anxiety disorder on recovery from
impairment following stroke was examined in 142
patients with acute stroke who had follow-up eval-
uations. Anxiety disorder significantly interacted
with depression to influence the severity and
course of depression, outcome of activities of daily
living, and social functioning. Anxiety disorder,
however, did not affect cognitive impairment,
which was influenced only by major depression.
These data suggest that the existence of anxiety
disorders plays an important role in the prognosis
of patients with poststroke depression. These data
also suggest that depression and anxiety disorder
may have different mechanisms.
(The Journal of Neuropsychiatry and Clinical
Neurosciences 1998; 10:3440)
34
and Recovery From
Stroke
Kengo Shimoda, M.D.
Robert G. Robinson, M.D.
T he relationship between anxiety disorder and de-
pressive disorder has been a topic of great interest
in psychiatry. Comorbidity of anxiety and depressive
disorders has been shown to influence many clinical as-
pects of these disorders, including onset, duration, re-
sponse to treatment, and severity, when compared with
each condition alone.14 Thus, the comorbid condition
appears to have important implications for both long-
term outcome and response to treatment.
During the past few years, we have been examining
the clinical and neuropathological correlates of anxiety
disorder following acute stroke.5,6 These studies have
identified the frequent comorbidity of depressive dis-
orders and anxiety disorders in patients with acute
stroke. Comorbid major depression and generalized
anxiety disorder were associated with left frontal corti-
cal lesions.5 Similarly, anxiety disorder, but not comor-
bid anxiety and depression, was associated with in-
creased frequency of alcohol abuse and right
hemisphere lesions.6 These data, as well as other similar
findings, suggest that comorbid anxiety and depression
may have a different etiological basis than depression
alone or anxiety without depressive disorder.
Previous studies have shown that poststroke depres-
sive disorders influence the cognitive7,8 and physical9
Received March 6, 1996; revised August 20, 1996; accepted September
26, 1996. From the Department of Psychiatry, University of Iowa Col-
lege of Medicine, Iowa City, Iowa; and Department of Neuropsychi-
atry, Nippon Medical School, Tokyo, Japan. Address correspondence
to Dr. Robinson, Department of Psychiatry, University of Iowa Hos-
pitals and Clinics, 200 Hawkins Drive #2887 JPP, Iowa City, IA 52242-
1057.
Copyright q 1998 American Psychiatric Press, Inc.
VOLUME 10 NUMBER 1 WINTER 1998

consequences of stroke. Major depressive disorder is as-
sociated with a significantly greater degree of cognitive
impairment than can be explained by the presence of
the lesion alone.10,11 Parikh et al.,9 as well as Sinyor et
al.,12 demonstrated that physical and language recovery
from stroke were adversely affected by the existence of
depressive disorder. We have not, however, previously
examined the influence of comorbid anxiety and de-
pressive disorder on cognitive or physical recovery from
stroke or the longitudinal course of depression. There-
fore, the present study examined the hypothesis that the
comorbid existence of anxiety and depressive disorder
would be associated with a greater degree of impair-
ment in cognitive function and a poorer recovery from
depression and physical impairment than would de-
pressive disorder without comorbid anxiety disorder.
METHODS
Patient Population
A consecutive series of 142 patients who were admitted
to University of Maryland Hospital, Baltimore, MD,
with a diagnosis of either acute intracerebral hemor-
rhage or acute cerebral infarction and who were seen in
the follow-up clinic were examined for psychiatric dis-
order after providing informed consent. Patients were
excluded only if they were unable to undergo a verbal
interview. Nearly one-third of patients admitted with
acute stroke were unable to complete an interview be-
cause of decreased level of consciousness or aphasia
with impaired comprehension. Of these 142 patients,
110 patients (77.5%) were examined at either 3-month
or 6-month follow-up (short-term follow-up), and 102 pa-
tients (71.8%) were examined at either 12-month or 24-
month follow-up (long-term follow-up). Patients were lost
to follow-up due to mortality (15%) or failure to show
up for appointments (10%).
Psychiatric and Neurological Evaluations
After obtaining informed consent, we examined the pa-
tients by using a structured mental status examination,
the Present State Examination13 (PSE). We made diag-
noses of major depression (MDD) or generalized anxiety
disorder (GAD) by using the symptoms elicited on the
PSE and the DSM-IV14 symptom criteria for major de-
pressive disorder and generalized anxiety disorder. The
diagnostic criteria for GAD were slightly modified from
DSM-IV criteria as follows: patients had to acknowledge
the presence of worry or anxious foreboding, and du-
ration criteria were excluded. In addition, the severity
of depression was measured with the Hamilton Rating
Scale for Depression15 (Ham-D). Cognitive functioning
JOURNAL OF NEUROPSYCHIATRY
SHIMODA AND ROBINSON
was evaluated with the Mini-Mental State Examina-
tion16 (MMSE). Scores range from 0 to 30, with lower
scores indicating greater impairment. Activities of daily
living were quantified by use of the Johns Hopkins
Functioning Inventory17 (JHFI). Scores range from 0 to
27, with higher scores indicating greater impairment.
Social functioning was assessed by use of the Social
Functioning Exam18 (SFE). Scores range from 0.00 to
1.00, with higher scores indicating greater perception of
impaired social function.
Lesion Location
Computed tomography scans were obtained from 73
(51.4%) of the patients included in the study and were
evaluated by a neurologist who was blind to the psy-
chiatric findings. All CT scans had consistent 10-mm
slice thickness and consistent angle to the canthomeatal
line. Methods for determining lesion location (lesion
volume, interrater reliability, cortical-subcortical loca-
tion) have been described in a previous report.5
Statistical Analysis
A 222 design was used in this study. Analysis of vari-
ance (ANOVA) and repeated-measures ANOVA were
performed to analyze the relation between dependent
variables such as MMSE scores and each of the depen-
dent variables such as the existence of depression or
GAD. If the ANOVA was significant, each group was
compared by using post hoc planned tests (Scheffe). Chi-
square tests were performed to analyze frequency dis-
tributions. Yates correction was used to adjust for ex-
pected cell sizes below 5, and two-tailed P-values were
used.
RESULTS
Background Characteristics
Subjects were divided into four groups: control
(n4100), generalized anxiety disorder only (n415), ma-
jor depressive disorder only (n49), and MDD plus GAD
(n418).
The background characteristics of these groups are
shown in Table 1. There were significantly more female
patients in the MDD and MDD plus GAD groups than
in the non-MDD groups (v2412.9, df43, P40.049);.
CT Findings
Of the 142 patients in this study, 48 had single lesions
restricted to cortical or subcortical structures as assessed
by CT scan. In all cases, brain lesions were found by a
neurologist to be compatible with findings on neuro-
logic examination. Cortical lesions were found in 13 of
35
ANXIETY DISORDER AND STROKE

27 patients (48.1%) in the control group, 0 of 4 patients
(0%) in the MDD-only group, and 4 of 5 patients (80%)
in the MDD plus GAD group. These were statistically
significant intergroup differences in the frequency of
cortical lesions (v247.4, df42, P40.03).
patients than for patients with MDD only or control sub-
jects, but there were no significant differences among the
groups at long-term follow-up (initial: F448.4, df42,86,
P,0.0001; long-term follow-up: F41.6, df42,86,
P.0.1).

Relationship to Diagnostic Outcome
We next examined diagnostic outcome among groups.
There were significant intergroup differences in the fre-
quency of major depression at short-term follow-up
(control: 5 of 73; MDD only: 0 of 8; MDD`GAD: 9 of
14; v2424.7, df42, P,0.0001). Most patients with MDD
plus GAD remained depressed at short-term follow-up,
whereas none of the MDD-alone patients remained de-
pressed (MDD only vs. MDD`GAD, v246.3, P40.02).
There were no significant intergroup differences, how-
ever, in the persistence of major depression at long-term
follow-up (control: 12 of 78; MDD only: 1 of 4;
MDD`GAD: 0 of 9; v243.2, df42, P.0.1).
We also examined changes in the severity of depres-
sion (Ham-D scores) during the follow-up evaluation. A
one-way ANOVA of Ham-D scores for the patients with
3- to 6-month follow-up showed that patients who had
MDD plus GAD in-hospital had significantly higher de-
pression scale scores at both time evaluations than did
patients with MDD only or control subjects (initial:
F487.8, df42,86, P,0.0001; short-term follow-up:
F415.4, df42,86, P,0.0001). Post hoc test (Scheffe)
demonstrated that patients with MDD plus GAD had
significantly higher depression scale scores at both time
evaluations than did patients with MDD only (initial:
P,0.001; short-term follow-up: P,0.05). In contrast,
one-way ANOVA of Ham-D scores for the patients with
12- to 24-month follow-up showed significantly higher
in-hospital depression scores for the MDD plus GAD
Effect of MDD and GAD on Impairment and Recovery
We found that non-MDD patients tended to be older
than patients with MDD (non-MDD, 59.2512.4, vs.
MDD, 54.0513.0: t41.93, df4140, P40.056), and non-
GAD patients tended to have larger lesion volumes than
patients with GAD (non-GAD, 7.457.3, vs. GAD,
3.452.8: t41.97, df465, P40.054). Values are reported
as means and standard deviations.
For the purpose of excluding factors other than MDD
or GAD that were known to effect stroke outcome, the
following analyses were done, using patients who were
matched for age (52 years), education (52 years), and
lesion volume (52% of total brain volume).
Relationship to Cognitive Impairment and Recovery: In
short-term follow-up, repeated-measures ANOVA of
MMSE scores (factor 1: presence or absence of MDD;
factor 2: presence or absence of GAD) showed signifi-
cant effects for MDD (F421.7, df41,56, P,0.0001) and
time (F47.23, df41,56, P40.009), but no significant ef-
fect for an MDD2time interaction and no significant
effect for GAD (Table 2). A two-way ANOVA at each
time showed a significant effect for MDD at both initial
and short-term follow-up (initial: F429.68, df41,56,
P,0.0001; short-term: F48.04, df41,56, P40.006), but
no effect for GAD and no MDD2GAD interaction. Sim-
ilarly, in long-term follow-up, repeated-measures
ANOVA of MMSE scores showed a significant effect of
MDD2time interaction (F46.57, df41,58, P,0.01), but

TABLE 1. Demographics of sample

Non-MDD MDD
Characteristic Control GAD only MDD only MDD~GAD
n 100 15 9 18
Age (years, mean5SD) 59.5512.2 56.9514.0 53.6512.7 54.2514.2
Education (years, mean5SD) 9.354.1 9.654.7 7.853.8 9.453.2
Sex (% female)a 37.0 33.3 77.8 72.2
Race (% black) 67.0 60.0 77.8 55.6
Marital status (% married) 49.0 60.0 11.1 50.0
Alcohol abuse (% positive) 6.0 13.3 11.1 16.7
Socioeconomic status (% class IV-V) 26.0 26.7 88.9 83.3
Family psychiatric history (% positive) 6.0 0.0 11.1 11.1
Past psychiatric history (% positive) 11.0 20.0 44.4 22.2
Medication
Antidepressants (% positive) 5.0 0.0 22.2 11.1
Other psychotropics (% positive) 0.0 0.0 0.0 0.0

Note: MDD4major depressive disorder; GAD4generalized anxiety disorder.

Significant differences between 4 groups (v2412.9, df43, P40.049).
a

36 VOLUME 10 NUMBER 1 WINTER 1998

 SHIMODA AND ROBINSON

not of GAD or other interaction. A two-way ANOVA at
each time showed a significant effect of MDD at initial
evaluation (F45.16, df41,58, P40.03), but not at long-
term follow-up (F40.10, df41,58, P40.8). In contrast,
there was no significant effect of GAD, and there were
no significant interaction effects at either time.
Relationship to Physical Impairment and Recovery: Re-
peated-measures ANOVA of JHFI scores for the patients
with 3- to 6-month follow-up showed a significant effect
for MDD (F48.78, df41,57, P40.004) and time
(F425.60, df41,57, P,0.0001), but no significant effect
for GAD or MDD2GAD interaction (Table 3). A two-
way ANOVA at each time showed no significant effect
at the initial evaluation. In contrast, however, patients
with major depression had significantly lower JHFI
scores at short-term follow-up than those who were not
depressed (MDD: F416.27, df41,57, P40.0002).
Repeated-measures ANOVA of JHFI scores for pa-
tients with 12- to 24-month follow-up showed signifi-
cant effects for MDD (F44.50, df41,55, P40.04) and
MDD2GAD interaction (F45.63, df41,55, P40.02),
but no significant effect for GAD or other interaction. A
two-way ANOVA at each time showed significant ef-
fects for MDD and an interaction with GAD at long-term
follow-up (MDD: F45.94, df41,55, P40.02;

TABLE 2. Mini-Mental State Examination scores at short-term and long-term follow-ups

Two-Way Analysis of Variance
Follow-up and Mean%SD MDD GAD Interaction
Time of Test Control GAD only MDD only MDD~GAD F P F P F P
(n436) (n49) (n46) (n49)
Short-term FU
Initial 26.153.5 24.754.1 18.553.4 18.355.6 29.68 0.0001 0.37 0.54 0.23 0.63
Short terma,b 26.455.3 26.353.8 21.754.1 21.756.2 8.04 0.006 0.001 0.98 0.001 0.98
(n445) (n47) (n43) (n47)
Long-term FU
Initial 25.453.6 24.753.4 22.0510.4 20.156.9 5.16 0.03 0.54 0.47 0.10 0.75
Long termc,d 25.653.6 24.955.2 25.755.1 24.455.3 0.10 0.92 0.36 0.55 0.03 0.87

Note: MDD4major depressive disorder; GAD4generalized anxiety disorder; FU4follow-up.

Repeated-measures analysis of variance:
a
Significant effect for MDD (F421.73, P,0.0001).
b
Significant effect for time (F47.23, P40.009).
c
Significant effect for time (F47.47, P40.008).
d
Significant effect for MDD(time (F46.57, P,0.01).

TABLE 3. Johns Hopkins Functioning Inventory scores at short-term and long-term follow-ups
Two-Way Analysis of Variance
Follow-up and Mean % SD MDD GAD Interaction
Time of Test Control GAD only MDD only MDD~GAD F P F P F P
(n436) (n49) (n46) (n410)
Short-term FU
Initial 5.854.4 6.254.4 6.855.5 9.856.6 2.23 0.14 1.21 0.28 0.64 0.43
Short terma,b 1.852.2 4.556.9 4.554.9 6.654.6 16.27 0.0002 0.25 0.62 2.25 0.14
(n445) (n46) (n43) (n45)
Long-term FU
Initial 5.253.7 4.855.2 4.353.5 10.054.5 1.61 0.21 2.46 0.12 3.29 0.08
Long termc,d,e 1.752.8 0.751.2 2.052.6 6.254.5 5.94 0.02 1.76 0.19 4.74 0.03

Note: MDD4major depressive disorder; GAD4generalized anxiety disorder; FU4follow-up.

Repeated-measures analysis of variance:
a
Significant effect for MDD (F48.78, P40.004).
b
Significant effect for time (F425.60, P40.009).
c
Significant effect for MDD (F44.50, P40.04).
d
Significant effect for MDD2GAD (F45.63, P40.02).
e
Significant effect for time (F47.47, P40.008).

JOURNAL OF NEUROPSYCHIATRY 37
ANXIETY DISORDER AND STROKE

MDD2GAD: F44.45, df41,40, P40.04). Thus, patients
who had both MDD and GAD in-hospital were more
impaired in their activities of daily living at long-term
follow-up than were control patients or patients with
GAD alone.
Relationship to Social Functioning: Repeated-measures
ANOVA of SFE scores for the patients with 3- to 6-
month follow-up showed significant effects for MDD
(F428.43, df41,54, P,0.0001), GAD (F416.93, df41,54,
P,0.0001), GAD2time interaction (GAD2time:
F44.88, df41,54, P40.03) and MDD2GAD2time
interaction (MDD2GAD2time: F46.56, df41,54,
P,0.01), but no significant effect for MDD2GAD
interaction (Table 4). A two-way ANOVA at each time
showed a significant effect for MDD at both times (ini-
tial: F413.48, df41,54, P,0.001; short-term: F421.52,
df41,54, P,0.0001). There were significant effects for
GAD and interaction with MDD at short-term follow-
up (GAD: F425.90, df41,54, P,0.0001; MDD2GAD:
F412.06, df41,54, P,0.001).
Repeated-measures ANOVA of SFE scores for pa-
tients with 12- to 24-month follow-up showed signifi-
cant effects for MDD (F411.65, df41,56, P,0.001),
GAD2time (F45.79, df41,56, P40.02), and
MDD2GAD2time interaction (F45.20, df41,56,
P40.03). A two-way ANOVA at each time showed a
significant effect for MDD at initial evaluation (F412.20,
df41,56, P40.0009). In contrast, there were significant
effects for GAD (F46.80, df41,56, P,0.01) and
MDD2GAD interaction (F46.46, df41,56, P,0.01) at
long-term follow-up, but not at initial evaluation. Thus,
patients with MDD plus GAD in the hospital were more
socially impaired at long-term follow-up than control
patients or patients with MDD alone.
DISCUSSION
The present study was undertaken to evaluate the effect
of comorbid anxiety disorder and depressive disorder
on impairment following acute stroke. Our findings
demonstrated for the first time that anxiety disorder fol-
lowing stroke influenced the severity and course of re-
covery from stroke. Anxiety disorder interacted with de-
pression to influence the degree of impairment in
activities of daily living and the course of recovery in
social functioning at long-term follow-up. On the other
hand, depression, but not an interaction with GAD, ex-
plained our previously demonstrated finding that de-
pression affects cognitive function following acute
stroke.7,11
Before further discussing these findings, we should
address several methodological limitations. First, cog-
nitive function was evaluated by using only the brief,
language-dominated MMSE. Because of the limited
number of cognitive functions evaluated by MMSE, we
were unable to determine whether there may have been
a subtle effect of GAD on cognitive function. This will
require a study using a more detailed neuropsycholog-
ical assessment.11 Second, patients with severe compre-
hension deficits were excluded, and the population of
this study was predominantly black and of lower socio-
economic status. Therefore, the results of this study may

TABLE 4. Social Functioning Exam scores at short-term and long-term follow-ups

Two-Way Analysis of Variance
Follow-up and Mean%SD MDD GAD Interaction
Time of Test Control GAD only MDD only MDD~GAD F P F P F P
(n436) (n48) (n46) (n48)
Short-term FU
Initial 0.1250.08 0.1750.08 0.2450.15 0.2850.11 13.48 0.0006 2.53 0.12 0.02 0.88
Short terma,b,c,d 0.1750.09 0.1650.09 0.3750.10 21.52 0.0001 25.90 0.0001 12.06 0.001
(n445) (n47) (n43) (n45)
Long-term FU
Initial 0.1750.09 0.1750.08 0.3450.25 0.2950.13 12.20 0.0009 0.42 0.52 0.64 0.43
Long terme,f,g 0.1550.14 0.1550.08 0.0950.06 0.3750.16 2.30 0.14 6.80 0.01 6.46 0.14

Note: MDD4major depressive disorder; GAD4generalized anxiety disorder; FU4follow-up.

Repeated-measures analysis of variance:
a
Significant effect for MDD (F428.43, P,0.0001).
b
Significant effect for AD (F416.93, P,0.0001).
c
Significant effect for GAD2time (F44.88, P40.03).
d
Significant effect for MDD2GAD2time (F46.56, P,0.01).
e
Significant effect for MDD (F411.65, P,0.001).
f
Significant effect for GAD2time (F45.79, P40.02).
g
Significant effect for MDD2GAD2time (F45.20, P40.03).

38 VOLUME 10 NUMBER 1 WINTER 1998


not apply to a more general population of poststroke
patients. Another limitation was the potential effect of
medications on cognitive function or recovery. Benzo-
diazepines or other sleeping medications are commonly
prescribed in this population and may contribute to cog-
nitive impairment or slower speed of recovery. When
we examined the frequency of various psychotropic
medications at the in-hospital evaluation, we did not
find significant differences in the frequency of antide-
pressant medications among groups, and we did not
find any patients who were treated with other psycho-
tropics such as benzodiazepines (Table 1). However, we
did not examine the frequency of medication use at fol-
low-up. Thus, there may have been medication effects
that were missed. Another limitation is that the number
of follow-up patients who were initially diagnosed with
GAD only or MDD only was small. Thus, the power of
our analysis was limited, and some significant effect of
GAD may have been masked by this. In addition, mor-
tality or failure to comply with follow-up evaluation led
to some attrition at each follow-up (24% at short-term
and 29% at long-term follow-up). About 20% of this
study population died within the 2-year follow-up pe-
riod.19
The most surprising finding in this study was that
neither GAD nor an interaction of GAD with MDD in-
fluenced cognitive impairment either in-hospital or dur-
ing follow-up. The failure of GAD to worsen the im-
pairment did not support our original hypothesis. This
finding also suggests that the mechanism of cognitive
impairment associated with depression is not altered by
comorbid anxiety disorder, implying perhaps the inde-
pendence of anxiety and depressive disorders. This find-
ing also supports our group designation of MDD plus
GAD. It might be argued, however, that these are not
comorbid disorders but rather are a type of anxious
depression. This issue will require further research.
Perhaps the most significant finding was that patients
with MDD plus GAD had greater impairment in activ-
ities of daily living at long-term follow-up than did pa-
tients with MDD alone, and the course of recovery in
social functioning was significantly worse in patients
with GAD plus MDD compared with control subjects or
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JOURNAL OF NEUROPSYCHIATRY
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