Increased Prevalence of Posttraumatic Stress Disorder in

Patients After Transient Ischemic Attack

Ines C. Kiphuth, MD; Kathrin S. Utz, PhD; Adam J. Noble, PhD; Martin Köhrmann, MD;
Thomas Schenk, PhD

Background and Purpose—A transient ischemic attack (TIA) involves temporary neurological symptoms but leaves a
patient symptom-free. Patients are faced with an increased risk for future stroke, and the manifestation of the TIA itself
might be experienced as traumatizing. We aimed to investigate the prevalence of posttraumatic stress disorder (PTSD)
after TIA and its relation to patients’ psychosocial outcome.
Methods—Patients with TIA were prospectively studied, and 3 months after the diagnosis, PTSD, anxiety, depression,
quality of life, coping strategies, and medical knowledge were assessed via self-rating instruments.
Results—Of 211 patients with TIA, data of 108 patients were complete and only those are reported. Thirty-two (29.6%)
patients were classified as having PTSD. This rate is 10× as high as in the general German population. Patients with TIA
with PTSD were more likely to show signs of anxiety and depression. PTSD was associated with the use of maladaptive
coping strategies, subjectively rated high stroke risk, as well as with younger age. Finally, PTSD and anxiety were
associated with decreased mental quality of life.
Conclusions—The experience of TIA increases the risk for PTSD and associated anxiety, depression, and reduced mental
quality of life. Because a maladaptive coping style and a subjectively overestimated stroke risk seem to play a crucial role
in this adverse progression, the training of adaptive coping strategies and cautious briefing about the realistic stroke risk
associated with TIA might be a promising approach. Despite the great loss of patients to follow-up, the results indicate
that PTSD after TIA requires increased attention.   (Stroke. 2014;45:3360-3366.)
Key Words: anxiety ◼ depression ◼ ischemic attack, transient ◼ quality of life ◼ stress disorders, posttraumatic
Downloaded from http://ahajournals.org by on May 12, 2019

See related article, p 3182.
W ith an estimated lifetime prevalence of 5 per 1000 peo-
ple, transient ischemic attack (TIA) is one of the most
common neurological conditions.1 TIAs have been defined
as brief episodes of neurological dysfunction resulting from
focal cerebral ischemia not associated with permanent cere-
bral infarction.2 Symptoms may include the sudden onset of
numbness, weakness or paralysis, slurred speech, aphasia,
blurred vision, confusion, and severe headache. With ≈15%
of all ischemic strokes being preceded by a TIA,3 TIAs are
considered a warning event for a stroke.4,5 Therefore, guide-
lines recommend that suspected TIA patients are immediately
referred to rapid access clinics so secondary prevention treat-
ments can be commenced (eg, prescription of antiplatelet and
cholesterol-lowering medication) and those at highest risk of
stroke be identified.6
It is well known that even a mild stroke can cause clinical
levels of depression, anxiety, and posttraumatic stress disorder
(PTSD).7 In fact, in the case of subarachnoid hemorrhage, it
has been found that such psychosocial sequelae have a bigger
impact on survivors’ quality of life (QoL) than neurological
or neuropsychological disorders.8,9 Despite the often dramatic
and sudden onset of TIAs, their aftermath, and requisite treat-
ments, little is known about the psychosocial impact of expe-
riencing a TIA, including the information patients are given
about their health. Can such an experience cause chronic psy-
chosocial problems? Can the diagnosis of a TIA, with the asso-
ciated knowledge that the patient is of increased risk to have a
stroke in the future, reduce QoL, cause anxiety, depression, or
PTSD? Having answers to these questions is important so that
appropriate support can be offered to patients and families, not
least because disorders such as PTSD are associated with low
adherence to medication,10,11 which might in turn elevate a TIA
patient’s risk of experiencing further health events.
A recent systematic review found no study that focused exclu-
sively on the prevalence of PTSD after TIA.12 Instead, studies
have mixed stroke and TIA patients together.13–16 However, with a
mixed sample it is not clear what the critical factor for developing

Received December 11, 2013; final revision received July 4, 2014; accepted July 21, 2014.
From the Department of Neurology, Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany (I.C.K., K.S.U., M.K., T.S.); and Institute
of Psychology, Health and Society, University of Liverpool, Liverpool, United Kingdom (A.J.N.).
Guest Editor for this article was Eric E. Smith, MD, MPH.
The online-only Data Supplement is available with this article at http://stroke.ahajournals.org/lookup/suppl/doi:10.1161/STROKEAHA.
113.004459/-/DC1.
Correspondence to Kathrin S. Utz, PhD, Department of Neurology, University of Erlangen-Nuremberg, Schwabachanlage 6, 91054 Erlangen, Germany.
E-mail kathrin.utz@uk-erlangen.de
© 2014 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STROKEAHA.113.004459

3360

PTSD is. Is it the residual impairment (in the case of stroke)
or the traumatic experience of neurological symptoms during
the ictus (in the case of both stroke and TIA)? This can only be
determined in a TIA-only sample. Thus, the primary aim of our
study was to investigate how TIA on its own influences the preva-
lence of PTSD. Secondary aims were to explore the link between
PTSD, anxiety, depression, and QoL, and to identify potential
risk factors for PTSD, such as demographic variables, disposi-
tional coping style, and knowledge about the disorder. Therefore,
we prospectively investigated patients who were diagnosed with
a TIA and assessed their anxiety, depression levels, diagnosis of
PTSD, QoL, and coping style with standardized questionnaires.
Additionally, the patients’ clinical status was documented and
their knowledge about the disorder was assessed.
Methods
Patients
The charts of patients who were admitted between October 2010 and
December 2011 to the stroke unit of the Department of Neurology
of the University Hospital Erlangen because of a TIA were screened.
To ensure that we only included patients with reliable signs of a TIA,
we determined the ABCD2 score (a score that takes into account age,
blood pressure, clinical features, duration of symptoms, and diabetes
mellitus), which indicates the risk to suffer a stroke <2 days after a
TIA. We included patients with an ABCD2 score >3 (meaning a 4%
risk of having a future stroke) or patients with an ABCD2 score ≤3,
who also reported the experience of a hemiparesis, aphasia, or amau-
rosis fugax during the ictus. To exclude patients with mild stroke, all
patients received a brain scan, and only those patients without any sign
of brain lesion were included. Furthermore, only those patients were
included where the discharge letter from the responsible neurologist
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in our clinic stated that all symptoms related to the ictus had resolved.
During the study period, 243 patients were admitted to our clinic
because of suspected TIA, and 211 patients met our inclusion criteria
and received our questionnaires 3 months after the ictus via mail. In
the patient information form, it was stated that the purpose of the
study was to investigate whether psychological problems may fol-
low the experience of transient neurological symptoms. The protocol
was conducted in accordance with the Declaration of Helsinki II and
was approved by the ethics committee of the Friedrich-Alexander
University Erlangen-Nuremberg. All participants gave their written
informed consent before the investigation.
One hundred twenty-eight patients sent back the questionnaires.
A further exclusion criterion was applied here. In separate letters pa-
tients were sent forms of the modified Rankin Scale (indictating the
degree of disability or dependence in daily activities). On the first
form they were asked to estimate the degree of disability before the
TIA, on the second form they had to indicate their current status of
disability. Only patients with modified Rankin Scale scores between
0 and 2 on both forms were included. There was a minor worsening of
symptoms only in 3 patients (ie, score 0, pre-TIA; score 1, 3 months
post-TIA; see Table). Thus, we can exclude that our patients had de-
veloped disabilities because of TIA.
Of the 211 included patients, data of 108 patients were complete
and included in the analyses (Table), meaning a loss of 103 patients
for analysis. However, sex, age, and atrial fibrillation did not signifi-
cantly differ between patients whose data were included and patients
who did not respond or had incomplete data (all P>0.05).
Self-Rating Instruments
Patients were asked to fill in the following questionnaires.
Posttraumatic Stress Diagnostic Scale
The German version (Ehlers A et al, unpublished data) of the well-
established posttraumatic stress diagnostic scale17 was used to test if
Kiphuth et al   PTSD After TIA    3361
a participant warranted a diagnosis of full PTSD in relation to their
TIA according to criteria of the Diagnostic and Statistical Manual
of Mental Disorders, Fourth Edition. The posttraumatic stress di-
agnostic scale asks participants to rate their experience of the 17
PTSD symptoms in the past month and allows a symptom sever-
ity score, ranging from 0 to 51, to be calculated. To be classified
as having a diagnosis of PTSD, a participant’s answers needed to
show that they experienced intense fear, helplessness, or horror at
time of the event (criterion A); had persistently re-experienced the
event (criterion B intrusion); persistently avoided stimuli associated
with their TIA and showed a numbing of responsiveness (criterion
C); and had persistent symptoms of increased arousal (criterion D).
This symptom picture must have been present for ≥1 month (crite-
rion E) and caused them significant distress or impairment in social,
occupational, or other important areas of functioning (criterion F).
Psychometric evidence shows that the posttraumatic stress diagnos-
tic scale performs well in relation to standardized diagnostic inter-
view techniques. It has adequate diagnostic agreement compared
with interview (82%) and good sensitivity (0.89) and specificity
levels (0.75).18
Hospital Anxiety and Depression Scale
The degree of depression and anxiety during the preceding week was
assessed with the German version19 of the hospital anxiety and de-
pression scale.20 Separate anxiety and depression subscale scores can
be computed. When compared with diagnostic interview, an optimal
balance between sensitivity (0.80) and specificity (0.80) is achieved
most frequently when caseness is defined by a score of ≥8 on either
of its subscales.21 A score of 8 to 10 is been taken as indicating mild
to moderate distress, whereas a score ≥11 as indicating moderate to
severe distress.22
Short Form 36
Physical QoL and mental QoL were measured with the Short Form-
36 self-rating questionnaire and compared with the normative sample
described in the test manual.23
Brief COPE Inventory
The German adaptation24 of the brief COPE Inventory25 was applied
to assess patient’s disposition for using maladaptive coping strategies.
Studies having used this German adaptation showed its usefulness.
For example, higher scores in scales measuring burnout, depression,
and anxiety were correlated with higher scores in maladaptive coping
in German students.26 The occurrence of depression and PTSD after
spinal cord injury was mediated by maladaptive coping style.27 The
sum of maladaptive coping strategy scores (denial, substance use, be-
havioural disengagement, self-distraction, self-blame) was computed
as an indicator of maladaptive coping. The higher the maladaptive
coping test score, the more patients habitually use maladaptive cop-
ing strategies.
Medical Knowledge About TIAs
To measure the patients’ medical knowledge about TIAs, they had to
answer questions (see the online-only Data Supplement) dealing with
the risk to suffer a stroke in the future, the impact of lifestyle habits
and medication on this risk, and indicate whether they considered
themselves to be well informed on TIAs or not. They were also asked
to rate their personal risk for a further attack in percentage terms on
a visual scale. A score between 1 and 4, with 1 meaning no medical
knowledge about TIAs and 4 meaning very good medical knowledge
about TIAs, was computed.
Statistical Analyses
Descriptive statistical analyses were performed, and the prevalence
rates of PTSD and reduced QoL were determined and compared with
German normative samples.23,28 χ2 and Mann–Whitney U tests were
used to look for differences in the assessed variables between patients
 3362  Stroke  November 2014

Table.  Characteristics of Patients With Transient Ischemic Attack With and Without Posttraumatic Stress Disorder According to
the Posttraumatic Stress Diagnostic Scale
Patients Not Included
Because of Missing Data
Whole Sample (n=108) PTSD (n=32) No PTSD (n=76) Test (PTSD vs No PTSD) (n=103)
Male/female sex 59/49 17/15 42/34 χ2(1)=0.42; P=0.502 52/51
Age, y, median (IQR) 70 (17) 64.5 (22) 71 (14) U=951; z=−1.781; P=0.075 73.5 (18)
mRS pre-TIA, estimated 3 mo after the 0.5 (1) 1 (1) 0 (1) U=1176.5; z=−0.652; P=0.768 …
ictus, median (IQR)
mRS, 3 mo post-TIA, median (IQR) 1 (1) 1 (1) 1 (1) U=1128.5; z=−0.652; P=0.515 …
Atrial fibrillation, number of patients/% 19/17.6 3/9.4 16/21.1 χ (1)=2.118; P=0.117
2
24/23.3
PTSD severity score, median (IQR) 6 (12) 17.5 (12) 3 (7) U=79; z=−7.71; P<0.001 …
Anxiety test score, median (IQR)/% 4.5 (7)/19.4 9.5 (5)/43.8 3 (4)/9.2 U=316.5; z=−6.07; P<0.001 …
> cutoff
Depression test score, median (IQR)/% 4 (5)/9.3 6.5 (7)/12.5 2 (5)/7.9 U=608.5; z=−4.115; P<0.001 …
> cutoff
Mental QoL test score, median (IQR)/% 68 (32)/13.9 52 (20)/21.9 76 (28)/10.5 U=484; z=−4.935; P<0.001 …
<5% cutoff
Physical QoL test score, median 80 (45)/6.5 60 (40)/6.3 85 (44)/6.6 U=888; z=−2.219; P=0.02 …
(IQR)/% <5% cutoff
Maladaptive coping test score, 16 (7) 19 (7) 15 (5) U=660.5; z=−3.75; P<0.001 …
median (IQR)
Medical knowledge test score, 3 (1) 3 (1) 3 (1) U=1105; z=−0.789; P=0.43 …
median (IQR)
Perceived risk of a future stroke (%), 30 (40) 50 (25) 20 (35) U=645; z=−3.9; P<0.001 …
median (IQR)
The higher the maladaptive coping test score, the more the patients habitually use maladaptive coping strategies. IQR indicates interquartile range; mRS, modified
Rankin Scale; PTSD, posttraumatic stress disorder; QoL, quality of life; and TIA, transient ischemic attack.
Downloaded from http://ahajournals.org by on May 12, 2019

with and without PTSD. Nonparametric tests were chosen for this
purpose because of the different group sizes (n=33 versus 77).
Stepwise multiple regressions with backward elimination methods
were computed when the outcome variable was continuous, and lo-
gistic regression with backward elimination methods (likelihood ra-
tio test) was applied when the outcome variable was dichotomous.
The amount of variation in the dependent variable that is explained
by the logistic regression model was indicated via Cox and Snell R2
and Nagelgerke R2. Wald statistic was used to test the significance of
an independent variable’s contribution. IBM SPSS Statistics 19 was
used for analyses and α set at P=0.05.
Results
Prevalence of PTSD
Thirty-two of 108 patients (29.6%) were diagnosed with
PTSD according to the posttraumatic stress diagnostic scale.
The median symptom severity score of this group was 17.5
(interquartile range, 12). The prevalence found in our sample
was 10× higher than in the general German population, where
a prevalence of 2.9%28 was found with the same measure. This
difference is statistically significant, as indicated by the 95%
confidence interval of 26.06% to 37.94% of the prevalence of
our sample, which lies clearly above the 2.9% prevalence in
the general German population.
Reduced QoL
Fifteen of 108 patients with TIA (13.9%) showed significantly
reduced mental QoL, and physical QoL was reduced in 7
patients (6.5%) when compared with the age-matched 5% cut-
offs of the German normative sample.23 These differences are
statistically significant, as indicated by the 95% confidence
interval of 12.27% to 20.36% of the prevalence of our sample
for mental QoL and 5.77% to 8.22% of physical QoL, lying
clearly above the 5% cutoff of the general German population
for mental QoL and marginally for physical QoL.
Comparison Between Patients With Versus
Without PTSD
Patients diagnosed with PTSD and patients without PTSD did
not significantly differ according to age and sex (see Table).
Patients with a PTSD diagnosis scored significantly higher
in the depression, anxiety, and negative coping scales, esti-
mated their risk to suffer a stroke as higher, and showed sig-
nificantly reduced mental and physical QoL compared with
patients without PTSD. Note that the median anxiety score of
the PTSD group is almost identical with the cutoff point of 10.
Variables Associated With PTSD
We used a logistic regression model with the dichotomous
version of the PTSD variable (present/absent) as our depen-
dent variable and age, sex, maladaptive coping, and medi-
cal knowledge as independent variables. We did not include
depression and anxiety as independent variables because of the
significant content overlap between items for depression/anxi-
ety and PTSD. The full model was significant (χ2[4]=17.66;
P=0.001), indicating that the model distinguishes success-
fully between patients with and without PTSD. The model
explained between 15.1% (Cox and Snell R2) and 21.4%

(Nagelkerke R2) in the variance of PTSD occurrence and
correctly classified 75% of cases. Only maladaptive coping
strategies and age significantly contributed to the model with
maladaptive coping strategies as the strongest associated vari-
able (odds ratio, 1.2; 95% confidence interval, 1.07–1.32; B
[SE]=0.173 [0.054]; Wald[1]=10.297; P=0.001). This means
that the risk to develop PTSD is 1.2× higher for patients with
TIA using maladaptive coping strategies. In contrast, age
seems to act as a protective factor. With every additional year,
patients are 0.96× less likely to develop PTSD (odds ratio,
0.96; 95% confidence interval, 0.924–0.999; B [SE]=−0.04
[0.02]; Wald[1]=4.08; P=0.043). Figure 1 shows the box plot
for maladaptive coping scores of patients with/without PTSD.
We repeated the above-mentioned logistic regression but
replaced the independent variable medical knowledge (total
score of the medical knowledge scale) with the independent
variable perceived risk of a future stroke (subscore of the cor-
responding item in the medical knowledge scale). The full
model was again significant (χ2[4]=35.59; P<0.001), explain-
ing between 28.1% (Cox and Snell R2) and 39.9% (Nagelkerke
R2) in the variance of PTSD occurrence, and correctly clas-
sified 79.6% of cases. Maladaptive coping strategies, sub-
jectively rated stroke risk, and age significantly contributed
to the model with subjectively rated stroke risk as a signifi-
cantly associated variable (odds ratio, 1.06; 95% confidence
interval, 1.03–1.09; B [SE]=0.057 [0.015]; Wald[1]=13.61;
P<0.001). This means that patients who estimate their risk to
have a stroke as high are more likely to develop PTSD. Again,
maladaptive coping strategies (odds ratio, 1.2; 95% confi-
Downloaded from http://ahajournals.org by on May 12, 2019
dence interval, 1.07–1.34; B [SE]=0.18 [0.06]; Wald[1]=9.16;
P=0.002) and age (odds ratio, 0.95; 95% confidence interval,
0.91–0.99; B [SE]=−0.055 [0.022]; Wald[1]=6.168; P=0.013)
were also significantly associated with PTSD occurrence.
This link between perceived stroke risk and PTSD is also con-
firmed by an additional analysis where we split the sample of
patients into 2 groups according to whether their stroke risk
estimate was unrealistically high (risk >20%; n=61) or cor-
rect or too low (risk ≤20%; n=47). Only 14.9% of the correct/
low-risk patients were diagnosed with PTSD in contrast with
Figure 1. Box plot comparing the maladaptive coping score of
patients with and patients without posttraumatic stress disorder
(PTSD).
Kiphuth et al   PTSD After TIA    3363
a much higher 40.9% in the high-risk group. This difference
was significant (χ2[1]=8.67; P=0.003).
Variables Associated With QoL
Thirty-eight percent of variance in mental QoL was accounted
for (R2=0.385; F4, 107=16.141; P<0.001) in the stepwise multi-
ple regression with age, sex, PTSD severity score, and anxiety
as independent variables. We have not included the depression
score as independent variables in the model because mental
QoL includes depression as a component dimension. PTSD
symptom severity score (squared semipartial correlation
[sr2]=0.027; standardized β=−0.261; P=0.032) and anxiety
score (sr2=0.054; standardized β=−0.364; P=0.003) were sig-
nificantly associated variables. Age and sex were not predic-
tive for mental QoL. Figure 2 shows the box plot for PTSD
severity scores of patients with/without reduced mental QoL.
Sixteen percent of variance of physical QoL was accounted
for (R2=0.165; F5,107=4.02; P=0.002) in the linear regression
with age, sex, PTSD severity score, anxiety, and depression as
independent variables. Age emerged as the only variable sig-
nificantly associated with physical QoL (sr2=0.109; standard-
ized β=−0.346; P<0.001). This means the older the patients
the lower the physical QoL. Sex, anxiety, depression, and
PTSD severity were not predictive of physical QoL.
Discussion
To our knowledge, this is the first study investigating the
prevalence of PTSD in a TIA-only sample, which is essential
for disentangling the contribution of residual impairment after
stroke and other factors such as the traumatic experience of
the ictus for developing PTSD. Given that patients with TIA
experience only temporary neurological symptoms, which
completely recover without leaving brain lesions, the finding
of an increased prevalence of PTSD and poor psychosocial
outcome is remarkable and deserves increased attention and
prevention efforts. The fact that patients with TIA can also
develop PTSD supports the assumption that neither brain
damage nor physical or mental disability on its own explain
the association of neurological disorders with increased rates
Figure 2. Box plot comparing posttraumatic stress disorder
(PTSD) severity score of patients with normal and patients with
reduced mental quality of life (QoL).
 3364  Stroke  November 2014
of PTSD. Elevated prevalence of PTSD has previously been
found after cerebrovascular diseases, including subarach-
noid hemorrhage,8 spontaneous cervical artery dissection,29
or stroke.7 In line with those studies, we found a 10× higher
prevalence of PTSD in patients having experienced a TIA in
comparison with the general German population. Some stud-
ies have investigated the occurrence of PTSD in stroke/TIA
patients before. Kronish et al15 and Goldfinger et al14 reported
a PTSD prevalence of 18% in patients having experienced
a stroke or TIA in the previous 5 years. Patients with PTSD
had higher modified Rankin Scale scores, were younger, and
were more likely to be women and to show depressive symp-
toms compared with patients without PTSD.14,15 In a study by
Favrole et al,13 a PTSD prevalence of 25% (Impact of Events
Scale) or 10% (Interview) was observed 1 to 6 months after
the ictus in a mixed stroke and TIA sample. Furthermore, 40%
of the patients with PTSD were depressed. Sembi et al16 found
a prevalence between 7% (Penn Inventory of PTSD) and 21%
(Impact of Events Scale) 1 to 18 months after a first-ever
stroke or TIA using self-report measures.
Although TIA causes no brain lesion, metabolic changes
such as alterations of lactate/N-acetylaspartate ratio can occur
up to 3 days after TIA.30 Changes in N-acetylaspartate have
also been observed in patients with PTSD.31 Thus, we can-
not exclude that such metabolic processes play a role in the
development of PTSD after TIA. However, we assessed PTSD
3 months after TIA and metabolic changes were only assessed
<3 days after TIA.30 Furthermore, those studies only show cor-
relative associations between metabolic changes and TIA and
Downloaded from http://ahajournals.org by on May 12, 2019
metabolic changes and PTSD respectively; thus, the direction
of the associations is not clear.
Which other factors might be responsible for the devel-
opment of PTSD after TIA? It seems likely that the sudden
experience of the neurological symptoms itself is a major
factor in triggering PTSD in patients with TIA. In this vein,
Favrole et al13 showed that the risk to develop PTSD was
higher for stroke/TIA patients reporting strong peritraumatic
reactions. Furthermore, the fear that the experienced neuro-
logical symptoms might be precursors of a stroke leading to
more permanent deficits might also contribute to the devel-
opment of PTSD. This fear is partly justified,32 but it is pos-
sible that patients who overestimate this risk might be also at
higher risk of developing PTSD. Our findings provide sup-
port for this hypothesis. We found that the perceived risk of a
future stroke is significantly linked to PTSD. On the contrary,
knowledge about TIA and the associated stroke risk might be
a protective factor. However, we found no correlation between
the patient’s medical knowledge on TIAs and the likelihood
of developing PTSD. But, because we used a nonvalidated
measure for the assessment of the patients’ knowledge, further
research is needed to clarify this relationship. Furthermore,
the range of the factor medical knowledge score was rather
narrow, a fact that could be in part responsible for its insignifi-
cant association with our outcome measures.
Another potential factor for the development of PTSD after
TIA might be the experience of acute pain, such as severe
headache, which can occur during the attack. Acute pain was
shown before to predict PTSD symptoms.33–36 Pain may be a
sufficient but probably not necessary condition for the develop-
ment of PTSD. There are certainly cases of PTSD where pain
is involved (eg, subarachnoid hemorrhage), but there are also
cases where physical pain does not play a role (eg, PTSD in
relatives and friends of subarachnoid hemorrhage patients37).
In the context of our study, pain probably also plays a role, but
only a minor one because only 3 patients mentioned headache
as one of the TIA symptoms. Instead, PTSD was predicted
by a maladaptive coping style, a factor that has been shown
to be predictive for PTSD in patients with other cerebrovas-
cular diseases.8,29,38 This provides a possible starting point for
the prevention of PTSD in patients with TIA. The training
of adaptive coping strategies and cautious briefing about the
realistic stroke risk associated with TIA might reduce the risk
for developing PTSD after TIA. Such a prevention approach
may be of particular importance to younger patients who are
more likely to have PTSD (see the findings from this study,
but also Kronish et al15 [for patients with TIA] and Noble et
al8 [for patients with subarachnoid hemorrhage]). To ensure
that patients who are at increased risk of developing PTSD are
identified, collaboration with psychiatrists is important.
Interestingly, the presence of PTSD together with anxiety
was associated with reduced mental QoL. A relation between
anxiety and QoL has been reported before in stroke patients39
and between both anxiety and depression in a mixed stroke
and TIA sample.40 Moreover, a correlation between PTSD
and mental QoL was previously found in subarachnoidal
haemorrhage8 and spontaneous cervical artery dissection.29
Furthermore, Goldfinger et al14 observed decreased physical
and mental health in stroke/TIA patients with PTSD. Franzén-
Dahlin and Laska41 found a higher decrease in QoL in female
compared with male patients between 6 and 8 weeks after a
TIA. No such relation was found in a mixed TIA and stroke
sample,42 but given the delay of 15 years between ictus and
assessment in the study by van Wijk et al,42 it can be assumed
that adaptation had probably taken place.
Patients with TIA with PTSD had a lower mental QoL,
were more likely to have depression and anxiety, thereby
corroborating findings from previous studies in TIA/stroke
patients.16,42–44 The adverse psychosocial outcome in patients
with TIA with PTSD underlines once more that early preven-
tion, for example via briefing and coping training, is advisable.
With respect to physical QoL, a different pattern emerged. Age
rather than PTSD or depression was found to be significantly
associated with physical QoL in our sample. Older patients
had a more reduced physical QoL score. This finding is in line
with age differences reported in the test manual of the German
version of the Short Form 36.23
We acknowledge the following potential limitations to our
study: First, because of the cross-sectional design, we were
only able to detect a correlation between coping style and
PTSD. However, in a prospective study45 it has been shown
that habitual use of maladaptive coping strategies predicted
the occurrence of PTSD, indicating that maladaptive coping
style may be a cause rather than a consequence of PTSD. The
same may be true in our group of patients, but to confirm the
causal link between coping style and PTSD, an interventional
study is needed. It is also possible that coping style is an

enduring personality trait that is not amenable to coping train-
ing. Positive findings of studies on coping training in other
patient groups do, however, suggest otherwise.46–48 The cross-
sectional nature of our design also affects the interpretation
of the observed correlations between perceived stroke risk,
PTSD, depression, and anxiety. In all of these cases, it remains
unclear whether these variables act as causes, mediators, or
reflect consequences.
Second, with respect to the correlation between per-
ceived stroke risk and PTSD, a further limitation needs to
be acknowledged. The perceived stroke risk is a subjective
estimate by the patients. We do not know to what extent this
estimate is informed by objective clinical information and
reflects variations in objective stroke risk. Although it would
have been interesting to parcel out the objective stroke risk
and calculate the extent to which patients overestimate the
risk of a future stroke, such a calculation is fraud with dif-
ficulties. The available figures relate to the risk of patients
with TIA left untreated. But all the patients in our sample
received treatment that is known to reduce the risk on aver-
age by 80%.49 Furthermore, the timescale for the objective
stroke risk (typically the risk for a stroke within the next 90
days) differs from the timescale for the subjective estimate
(patients were asked to predict their risk for their remaining
lifetime). As a consequence, all we can say at the moment
is that the perceived risk of a future stroke is related to an
increased risk of developing PTSD; we cannot say to which
extent these concerns of having a stroke in future are unwar-
ranted or justified.
Downloaded from http://ahajournals.org by on May 12, 2019
Third, given the relative short time period between ictus
and PTSD assessment, we currently do not know whether the
high rate of PTSD in our sample will persist. However, studies
in patients with other neurological disorders such as stroke7
or subarachnoid hemorrhage8 have found an increased preva-
lence of PTSD 1 year after the ictus. No significant change
was found in a study with patients with subarachnoid hemor-
rhage8 when PTSD rates at 3 and 13 months post ictus were
compared.
Fourth, given the high number of patients who failed to
return or complete all forms, there is the possibility that our
sample is not fully representative of the eligible population of
patients with TIA. However, the reader should note that even
if we assumed the most extreme case, namely that PTSD did
not occur at all in the drop-out group, we still had a preva-
lence of 15.16% in the entire population, which amounts
to a 5-fold increase compared with the general population.
Conversely, it is also possible that patients with PTSD tended
to avoid to fill in questionnaires dealing with the traumatic
experience, and thus the prevalence of PTSD might in fact be
even higher. Under both assumptions, PTSD is significantly
elevated in patients after a TIA. Furthermore, the investigated
sample was on average 3 years younger than the patients who
were excluded. As we found age to be a protective factor,
we would expect the prevalence of PTSD to be lower in the
excluded population, but we would not expect that this reduc-
tion is substantial because the likelihood to develop PTSD is
reduced merely by 0.96× per additional year. Therefore, we
think that the central message of our study is still valid.
Kiphuth et al   PTSD After TIA    3365
Conclusions
The experience of a TIA, despite leaving patients symptom-
free, increases the risk of developing a PTSD and associated
depression, anxiety, and reduced QoL. Especially, patients using
maladaptive coping strategies and patients overestimating their
stroke risk are more likely to have PTSD after a TIA, a cycle
that may be broken by offering patients better risk counseling
and more adaptive strategies of coping with their experience of
a TIA. The great loss of patients to follow-up in our study does
not change the important conclusion that PTSD after TIA and
the associated psychosocial outcome is a serious concern.
Disclosures
None.
References
1. MacDonald BK, Cockerell OC, Sander JW, Shorvon SD. The incidence
and lifetime prevalence of neurological disorders in a prospective com-
munity-based study in the UK. Brain. 2000;123(pt 4):665–676.
2. Easton JD, Saver JL, Albers GW, Alberts MJ, Chaturvedi S, Feldmann
E, et al; American Heart Association; American Stroke Association
Stroke Council; Council on Cardiovascular Surgery and Anesthesia;
Council on Cardiovascular Radiology and Intervention; Council on
Cardiovascular Nursing; Interdisciplinary Council on Peripheral
Vascular Disease. Definition and evaluation of transient ischemic attack:
a scientific statement for healthcare professionals from the American
Heart Association/American Stroke Association Stroke Council; Council
on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular
Radiology and Intervention; Council on Cardiovascular Nursing; and the
Interdisciplinary Council on Peripheral Vascular Disease. The American
Academy of Neurology affirms the value of this statement as an educa-
tional tool for neurologists. Stroke. 2009;40:2276–2293.
3. Hankey GJ. Impact of treatment of people with transient ischemic attacks
on stroke incidence and public health. Cerebrovasc Dis. 1996;6(suppl
1):26–33.
4. Coull AJ, Lovett JK, Rothwell PM; Oxford Vascular Study. Population
based study of early risk of stroke after transient ischemic attack or
minor stroke: implications for public education and organisation of ser-
vices. BMJ. 2004;328:326.
5. Giles MF, Rothwell PM. Risk of stroke early after transient isch-
emic attack: a systematic review and meta-analysis. Lancet Neurol.
2007;6:1063–1072.
6. National Collaborating Center for Chronic Conditions (UK). Stroke:
National Clinical Guideline for Diagnosis and Initial Management
of Acute Stroke and Transient Ischemic Attack (TIA). London: Royal
College of Physicians (UK); 2008. http://www.ncbi.nlm.nih.gov/books/
NBK53295/. Accessed December 5, 2013.
7. Bruggimann L, Annoni JM, Staub F, von Steinbüchel N, Van der Linden
M, Bogousslavsky J. Chronic posttraumatic stress symptoms after non-
severe stroke. Neurology. 2006;66:513–516.
8. Noble AJ, Baisch S, Mendelow AD, Allen L, Kane P, Schenk T.
Posttraumatic stress disorder explains reduced quality of life in subarach-
noid hemorrhage patients in both the short and long term. Neurosurgery.
2008;63:1095–1104, discussion 1004.
9. Noble AJ, Schenk T. Which variables help explain the poor health-
related quality of life after subarachnoid hemorrhage? A meta-analysis.
Neurosurgery. 2010;66:772–783.
10. Cohen MA, Alfonso CA, Hoffman RG, Milau V, Carrera G. The impact
of PTSD on treatment adherence in persons with HIV infection. Gen
Hosp Psychiatry. 2001;23:294–296.
11. Shemesh E, Yehuda R, Milo O, Dinur I, Rudnick A, Vered Z, et al.
Posttraumatic stress, nonadherence, and adverse outcome in survivors of
a myocardial infarction. Psychosom Med. 2004;66:521–526.
12. Edmondson D, Richardson S, Fausett JK, Falzon L, Howard VJ, Kronish
IM. Prevalence of PTSD in Survivors of Stroke and Transient Ischemic
Attack: A Meta-Analytic Review. PLoS One. 2013;8:e66435.
13. Favrole P, Jehel L, Levy P, Descombes S, Muresan IP, Manifacier MJ,
et al. Frequency and predictors of post-traumatic stress disorder after
stroke: a pilot study. J Neurol Sci. 2013;327:35–40.
 3366  Stroke  November 2014
14. Goldfinger JZ, Edmondson D, Kronish IM, Fei K, Balakrishnan R,
Tuhrim S, et al. Correlates of post-traumatic stress disorder in stroke
survivors. J Stroke Cerebrovasc Dis. 2014;23:1099–1105.
15. Kronish IM, Edmondson D, Goldfinger JZ, Fei K, Horowitz CR.
Posttraumatic stress disorder and adherence to medications in sur-
vivors of strokes and transient ischemic attacks. Stroke. 2012;43:
2192–2197.
16. Sembi S, Tarrier N, O’Neill P, Burns A, Faragher B. Does post-traumatic
stress disorder occur after stroke: a preliminary study. Int J Geriatr
Psychiatry. 1998;13:315–322.
17. Foa EB. Post-Traumatic Stress Diagnostic Scale (PDS). Minneapolis,
MN: National Computer Systems; 1995.
18. Foa EB, Cashman L, Jaycox L, Perry K. The validation of a self-report
measure of posttraumatic stress disorder: The posttraumatic diagnostic
scale. Psychol Assess. 1997;9:445–451.
19. Hermann-Lingen C, Buss U, Snaith RP. Hads-d Hospital Anxiety and
Depression Scale—Deutsche Version. Bern: Hans Huber; 1995.
20. Zigmond AS, Snaith RP. The hospital anxiety and depression scale. Acta
Psychiatr Scand. 1983;67:361–370.
21. Bjelland I, Dahl AA, Haug TT, Neckelmann D. The validity of the
Hospital Anxiety and Depression Scale. An updated literature review. J
Psychosom Res. 2002;52:69–77.
22. Snaith AS, Zigmond RP. The Hospital Anxiety and Depression Scale
Manual. Windsor: NFER-Nelson; 1994.
23. Bullinger M, Kirchberger I. Sf-36 fragebogen zum gesundheitszustand.
Göttingen, Germany: Hogrefe; 1998.
24. Knoll N, Rieckmann N, Schwarzer R. Coping as a mediator between per-
sonality and stress outcomes: a longitudinal study with cataract surgery
patients. Eur J Personal. 2005;19:229–247.
25. Carver CS. You want to measure coping but your protocol’s too long:
consider the brief COPE. Int J Behav Med. 1997;4:92–100.
26. Prinz P, Hertrich K, Hirschfelder U, de Zwaan M. Burnout, depression
and depersonalisation–psychological factors and coping strategies in
dental and medical students. GMS Z Med Ausbild. 2012;29:Doc10.
27. Schönenberg M, Reimitz M, Jusyte A, Maier D, Badke A, Hautzinger M.
Depression, posttraumatic stress, and risk factors following spinal cord
injury. Int J Behav Med. 2012:1–8.
Downloaded from http://ahajournals.org by on May 12, 2019
28. Hauffa R, Rief W, Brähler E, Martin A, Mewes R, Glaesmer H. Lifetime
traumatic experiences and posttraumatic stress disorder in the German
population: results of a representative population survey. J Nerv Ment
Dis. 2011;199:934–939.
29. Speck V, Noble A, Kollmar R, Schenk T. Diagnosis of spontaneous cervi-
cal artery dissection may be associated with increased prevalence of post-
traumatic stress disorder. J Stroke Cerebrovasc Dis. 2014;23:335–342.
30. Bisschops RH, Kappelle LJ, Mali WP, van der Grond J. Hemodynamic
and metabolic changes in transient ischemic attack patients: a magnetic
resonance angiography and (1)H-magnetic resonance spectroscopy
study performed within 3 days of onset of a transient ischemic attack.
Stroke. 2002;33:110–115.
31. Hull AM. Neuroimaging findings in post-traumatic stress disorder.
Systematic review. Br J Psychiatry. 2002;181:102–110.
32. Dennis M, Bamford J, Sandercock P, Warlow C. Prognosis of transient
ischemic attacks in the Oxfordshire Community Stroke Project. Stroke.
1990;21:848–853.
33. Bryant RA, Creamer M, O’Donnell M, Silove D, McFarlane AC. A study
of the protective function of acute morphine administration on subse-
quent posttraumatic stress disorder. Biol Psychiatry. 2009;65:438–440.
34. McGhee LL, Slater TM, Garza TH, Fowler M, DeSocio PA, Maani CV.
The relationship of early pain scores and posttraumatic stress disorder in
burned soldiers. J Burn Care Res. 2011;32:46–51.
35. Schreiber S, Galai-Gat T. Uncontrolled pain following physical injury as
the core-trauma in post-traumatic stress disorder. Pain. 1993;54:107–110.
36. Wikman A, Messerli-Bürgy N, Molloy GJ, Randall G, Perkins-Porras
L, Steptoe A. Symptom experience during acute coronary syndrome
and the development of posttraumatic stress symptoms. J Behav Med.
2012;35:420–430.
37. Noble AJ, Schenk T. Posttraumatic stress disorder in the family and
friends of patients who have suffered spontaneous subarachnoid hemor-
rhage. J Neurosurg. 2008;109:1027–1033.
38. Bryant RA, Marosszeky JE, Crooks J, Baguley I, Gurka J. Coping style
and post-traumatic stress disorder following severe traumatic brain
injury. Brain Inj. 2000;14:175–180.
39. Sturm JW, Donnan GA, Dewey HM, Macdonell RA, Gilligan AK,
Srikanth V, et al. Quality of life after stroke: the North East Melbourne
Stroke Incidence Study (NEMESIS). Stroke. 2004;35:2340–2345.
40. Ahlsiö B, Britton M, Murray V, Theorell T. Disablement and quality of
life after stroke. Stroke. 1984;15:886–890.
41. Franzén-Dahlin Å, Laska AC. Gender differences in quality of life after
stroke and TIA: a cross-sectional survey of out-patients. J Clin Nurs.
2012;21:2386–2391.
42. van Wijk I, Gorter JW, Lindeman E, Kappelle LJ, van Gijn J,
Koudstaal PJ, et al. Mental status and health-related quality of life in
an elderly population 15 years after limited cerebral ischemia. J Neurol.
2007;254:1018–1025.
43. El Husseini N, Goldstein LB, Peterson ED, Zhao X, Pan W, Olson DM,
et al. Depression and antidepressant use after stroke and transient isch-
emic attack. Stroke. 2012;43:1609–1616.
44. Luijendijk HJ, Stricker BH, Wieberdink RG, Koudstaal PJ, Hofman A,
Breteler MM, et al. Transient ischemic attack and incident depression.
Stroke. 2011;42:1857–1861.
45. Gil S. Coping style in predicting posttraumatic stress disorder among
israeli students. Anxiety Stress Copin. 2005;18:351–359.
46. Chesney MA, Chambers DB, Taylor JM, Johnson LM, Folkman S.
Coping effectiveness training for men living with HIV: results from a
randomized clinical trial testing a group-based intervention. Psychosom
Med. 2003;65:1038–1046.
47. Keefe FJ, Blumenthal J, Baucom D, Affleck G, Waugh R, Caldwell DS,
et al. Effects of spouse-assisted coping skills training and exercise train-
ing in patients with osteoarthritic knee pain: a randomized controlled
study. Pain. 2004;110:539–549.
48. Kennedy P, Duff J, Evans M, Beedie A. Coping effectiveness training
reduces depression and anxiety following traumatic spinal cord injuries.
Br J Clin Psychol. 2003;42(pt 1):41–52.
49. Rothwell PM, Giles MF, Chandratheva A, Marquardt L, Geraghty O,
Redgrave JN, et al; Early use of Existing Preventive Strategies for Stroke
(EXPRESS) Study. Effect of urgent treatment of transient ischemic attack
and minor stroke on early recurrent stroke (EXPRESS study): a prospective
population-based sequential comparison. Lancet. 2007;370:1432–1442.