Skip to main content
NCBI home page
NIHPA Author Manuscripts logoLink to NIHPA Author Manuscripts
. Author manuscript; available in PMC: 2022 May 1.
Published in final edited form as: Gen Hosp Psychiatry. 2021 Mar 8;70:98–102. doi: 10.1016/j.genhosppsych.2021.03.004

Relationship between NIH Stroke Symptoms and Post-traumatic Stress Disorder in Patients Evaluated for Transient Ischemic Attack/Stroke

Emily Pedowitz 1, Lilly Derby 2, Gaspar J Cruz 2, Alison Trainor 2, Donald Edmondson 2, Talea Cornelius 2
PMCID: PMC8127400  NIHMSID: NIHMS1685615  PMID: 33774490

Abstract

Objective.

Post-traumatic stress disorder (PTSD) can develop after a life-threatening medical event. According to the enduring somatic treat (EST) model, internal somatic cues (e.g., rapid heart rate) may contribute to symptoms of stroke/TIA-induced PTSD. To address this possibility, the present study tested the association of stroke-induced disability with PTSD symptoms in patients treated for stroke or transient ischemic attack (TIA).

Method.

Participants (n = 300) were drawn from an observational cohort study examining PTSD symptoms in patients admitted to the NewYork Presbyterian Hospital between 2015-2017 for a stroke/TIA. Patients self-reported acute stress symptoms in-person approximately 3 days post-stroke/TIA and PTSD symptoms via telephone one month later. Severity of stroke symptoms (i.e., stroke disability) was evaluated using the NIH Stroke Scale prior to hospital discharge.

Results.

Stroke disability had a significant, positive association with acute stress symptoms early post-stroke/TIA, B = 0.46, se = 0.15, p = .002, and with PTSD symptoms one month later, B = 0.56, se = 0.19, p = .003.

Conclusions.

Stroke disability is positively associated with both acute distress and PTSD symptoms one month later following a stroke/TIA, supporting the hypothesis that internal somatic symptoms contribute to the development stroke/TIA-induced PTSD symptoms.

Keywords: Post-traumatic stress disorder, ED threat perceptions, Stroke, Disability, Enduring somatic threat

1. Introduction

Post-Traumatic Stress Disorder (PTSD) has historically been associated with events such as combat or sexual assault. Increasingly, however, PTSD has been found to be a consequence of life-threatening medical events such as HIV (Sherr et al., 2011), cancer diagnosis (O’Connor et al., 2011), and acute coronary syndrome (Edmondson et al., 2012). Stroke patients also report symptoms of PTSD (Vilchinsky et al., 2017), particularly those patients who require intensive care (Tedstone & Tarrier, 2003). Meta-analytic reviews have estimated that 12-25% of stroke or transient ischemic attack (TIA) patients screen positive for PTSD in the first year after the event (Edmondson et al., 2013; Rutovic et al., 2019).

The leading theory explaining the development of PTSD after acute life-threatening medical events, the enduring somatic threat (EST) model, suggests that internal somatic reminders of ongoing risk for recurrent medical events are related to incident PTSD symptoms (Edmondson, 2014). Yet, research testing the association of somatic cues with stroke/TIA-induced PTSD remains sparse and inconclusive. Some studies have shown that individuals who experience a TIA, but no long-term disability, can still go on to develop stroke/TIA-induced PTSD (i.e., disability is not a necessary caus; Kiputh et al., 2014; Favrole et al., 2013; Merriman et al., 2007; Stein et al., 2018), and others have shown a positive relationship between stroke disability and PTSD symptoms. In one study, physical disability caused by stroke correlated with greater PTSD severity in 78 patients at 3 months after stroke (Wang et al., 2011), and, in another disability was associated with stroke-induced PTSD within 5 years of stroke onset (Goldfinger et al., 2014). Similarly, in patients with moyamoya disease (a cerebrovascular disease caused by blocked arteries in the basal ganglia), greater neurological disability was associated with higher PTSD scores (Liu et al., 2019). Further longitudinal research following patients from stroke onset to PTSD onset one month later is needed to clarify these associations. Our study addressed this gap by following patients from hospitalization through one month post-discharge in a large and diverse sample of patients assessed for stroke/TIA.

Understanding whether disability is a risk factor for PTSD following a stroke has important clinical and theoretical implications. Stroke/TIA-induced PTSD is associated with non-adherence to medications for secondary prevention in patients with cardiovascular disease (CVD) (Goldfinger et al., 2014), and may even increase secondary CVD risk directly (Edmondson et al., 2012). If stroke disability is a reliable risk factor for PTSD, clinicians could identify patients who are at high risk for developing PTSD and improve PTSD detection rates, allowing for swift interventions to improve mental health and promote adherence to medications and other recommended health behaviors. Elucidating the association (or lack thereof) of chronic somatic reminders of patients’ index stroke/TIA event (operationalized as stroke disability) with initial distress and subsequent PTSD symptoms adds to the empirical evidence base to aid theory refinement (Edmondson, 2014).

The goal of the present study was thus to estimate the association between stroke-induced disability and the development of stroke/TIA-induced PTSD symptoms one month later. Informed by EST (Edmondson, 2014), we hypothesized that greater disability secondary to stroke would be associated with greater stroke-related distress early post-stroke/TIA (i.e., acute stress symptoms) and risk for stroke/TIA-induced PTSD one month after hospital discharge.

2. Methods

2.1. Participants

Participants were enrolled as part of a larger observational cohort study on the association of stroke/TIA-induced PTSD with secondary CVD risk. Eligible patients were at least 18 years of age and presented to the NewYork Presbyterian Hospital (NYPH) ED with an admitting diagnosis of stroke/TIA as confirmed by a neurologist. Exclusion criteria were (1) non English or Spanish speaking, (2) terminal non-cardiovascular illness with a life expectancy of < 1 year, (3) severe mental illness requiring urgent psychiatric hospitalization/intervention, (4) alcohol or substance abuse, (5) severe stroke (NIH Stroke Scale >14) and/or significant cognitive impairment, and (6) lack of availability for 1 year follow-up. Study materials were available in both English and Spanish. Materials in Spanish were either translated internally via a certified translator or via the Columbia University Irving Medical Center’s Spanish Translation Center. The study and all associated materials was approved by the Institutional Review Board (AAAQ4612 M08Y03) at Columbia University Irving Medical Center. All participants provided written informed consent before completing study procedures.

2.2. Procedure

To identify eligible patients, bilingual research assistants (RAs) conferred with the caregiving ED physician and/or a clinical member of the NYPH Stroke Service. They obtained permission to approach patients to assess eligibility and interest in study participation. Interested participants provided written informed consent in the ED or during inpatient care. At that time, patients self-reported sociodemographic information, including age, race/ethnicity, gender, and education level. During inpatient assessments (on average 3 days later), patients reported early acute stress symptoms (a precursor to PTSD; Bryant et al., 2000), pre-existing PTSD symptoms (not due to the stroke/TIA), and depression symptoms. PTSD symptoms secondary to the stroke event were assessed during the one-month follow-up phone call. NIHSS scores were extracted from participants’ medical records.

2.3. Measures

Stroke/TIA-induced acute stress symptoms.

The Acute Stress Disorder Scale (ASDS) is a 14-item self-report inventory which indexes the early impact of a traumatic event on an individual (a pre-cursor to developing PTSD; Bryant et al., 2000). The ASDS is scored on a five-point scale, ranging from “not at all” (1) to “very much” (5), and all questions were answered in relation to “the stroke event that brought you to the hospital […].”

The PTSD Checklist for DSM-5 (PCL-5) is a psychometrically sound and widely used self-report scale for assessing PTSD in both clinical and research settings (Weathers et al., 2013). The 20 items correspond to DSM-5 criteria for PTSD, and assess the presence, frequency, and severity of PTSD symptoms on a five-point Likert scale ranging from “not at all” (0) to “extremely” (4). The scale results in a continuous symptom severity score (possible range: 0, 80). Patients were given the following prompt: “Many people feel distressed after experiencing a stroke/TIA event. Which of the following was the most distressing part of your stroke/TIA experience?” Possible answers were, “the stroke/TIA problem/symptoms experienced,” “the experience in the ED,” “the experience in the hospital,” and “the experience in the clinic.” After selecting the most distressing component, patients answered all PCL-5 items in relation to this response.

National Institutes of Health Stroke Scale.

The National Institutes of Health Stroke Scale (NIHSS) is a clinical stroke assessment tool used to evaluate the neurological status of stroke patients, to predict lesion size and impairment, and to predict clinical outcomes (Richardson et al., 2006; Smith et al., 2018). The scale is comprised of 11 items, each scoring a specific neurological ability from “normal function” (0) to “high impairment” (4). Questions included in the NIHSS assess level of consciousness, horizontal eye movement, patient vision, facial palsy, arm and leg motor (independently), limb ataxia, sensory, language skills, dysarthria (motor skill to produce speech), and extinction and inattention.

Items are summed to calculate a total NIHSS score (possible range 0, 42), which represents the severity of stroke disability due to an overall neurologic impairment (Harrison et al., 2013). Each patient’s medical provider completed the NIHSS on the patient while in the ED.

Covariates.

Covariates were selected a priori and for consistency with the larger parent cohort analyses. These included self-reported gender, age, race/ethnicity, pre-existing PTSD symptoms, and pre-existing depression symptoms (Weathers et al., 2013; Korenke et al., 2009).

Pre-existing PTSD symptoms.

At baseline only, participants completed the Life Events Checklist (LEC), a validated tool for assessing lifetime exposure to traumatic events (Gray et al., 2004). Participants who endorsed one or more lifetime trauma exposures completed the PCL-5 with reference to that trauma. Items were summed to create a continuous score.

Depression.

Depression symptoms during the inpatient stay were assessed using the Patient Health Questionnaire (PHQ-8), a validated tool for assessing severity of depression (Kroenke et al., 2009). Items were summed to create a continuous score.

2.4. Analytic Strategy

A multiple linear regression model was specified for each dependent variable: (1) continuous ASDS and (2) continuous PCL-5 at one month post-stroke. The focal independent variable was continuous NIHSS score. Covariates included age, race, ethnicity, gender, pre-existing PTSD symptoms, and pre-existing depression. Due to the non-normal distribution of ASDS and PCL scores, sensitivity analyses were conducted with natural log transformed variables as the dependent variables. The values presented are unstandardized regression coefficients, and alpha was set at .05, two-sided.

3. Results

Full data were available for N = 300 patients (out of 515). Of the 300 patients included in this study, 184 had a confirmed stroke. Those retained in the analysis had higher levels of acute stress symptoms, p = .022, and pre-existing PTSD symptoms, p = .016, as well as greater stroke-induced PTSD symptoms at one month, p = .031, but did not differ in terms of baseline depression, disability, or demographic covariates.

Mean age was 61.3 years (SD = 15), 20% were black, 47 % were Hispanic, 24% were non-Hispanic white, and 9% were other. Slightly more than half (56%) were female. Median stroke severity per the NIHSS was 2 (interquartile range 1, 4). Mean scores on the ASDS at 3 days were 33.35 (Median = 30.00), mean PCL-5 scores at one month were 11.93 (Median = 7.00), and 31 (10%) met the criteria for clinically significant PTSD at one month (scores ≥ 33).

ASDS.

Covariates significantly associated with acute stress disorder symptoms included age, B = −0.10, se = 0.03, p = .002, pre-existing PTSD symptoms, B = 0.39, se = 0.04, p < .001, and baseline depression, B = 0.79, se = 0.10, p < .001. Disability had a significant, positive association with acute stress symptoms, B = 0.46, se = 0.15, p = .002. Sensitivity analyses substituting the natural log of ASDS did not alter conclusions; neither did a post-hoc analysis conducted among the 184 patients with a confirmed stroke diagnosis, B = 0.30, 95% CI −0.01, 0.61, p = .060.

PCL at 1 month.

In Model 2, covariates significantly associated with PTSD symptoms at 1 month included age, B = −0.13, se = 0.04, p = .003, pre-existing PTSD symptoms, B = 0.32, se = 0.05, p < .001, and baseline depression, B = 0.65, se = 0.12, p < .001. Disability had a significant, positive association with PTSD symptoms at one month, B = 0.56, se = 0.19, p = .003. Sensitivity analyses substituting the natural log of PTSD symptoms did not alter conclusions; neither did a post-hoc analysis conducted among the 184 patients with a confirmed stroke diagnosis, B = 0.40, 95% CI −0.01, 0.81, p = .056.

4. Discussion

In this large observational cohort study of stroke/TIA patients, stroke-induced disability was positively associated with stroke/TIA-induced PTSD symptoms both early post-event and one month later. Our results have practical implications for medical practitioners, in that they suggest to clinicians and family members that patients with greater stroke disability may be at increased risk for PTSD following a stroke or TIA. By building on prior research and addressing limitations of these studies (e.g., small sample size, cross-sectional studies, studies that assess PTSD beyond the one month timeline for PTSD incidence), our results provide additional support for the EST model in that an internal somatic cue (i.e., stroke-induced disability) is associated with the development of stroke/TIA-induced PTSD symptoms one month later (Edmondson, 2014).

The EST model may be a potential explanation of stroke/TIA-induced PTSD, in that disability is associated with increased risk of developing PTSD symptoms secondary to a stroke, even while controlling for pre-existing psychological distress (i.e., depression and prior PTSD symptoms) (Edmondson, 2014; Meli et al., 2017). Critically, individuals who have greater stroke-induced disability experience more reminders of this traumatic event, and may therefore avoid reminders such as medications or activities that increase awareness of their ongoing somatic symptoms (e.g., avoiding physical activity; Goldfinger et al., 2014; Edmondson, 2014). Not only does avoidance of health promoting behaviors increase risk for morbidity and mortality, but anxiety and biological markers of stress (inflammation, blood pressure, etc.) may also increase patients’ risk (Chen et al., 2015; Gander & Känel, 2006; Känel et al., 2010).

Given the unique presentation of PTSD symptoms following acute medical events (compared to PTSD due to external events such as combat; El-Gabalawy et al., 2018), further research is needed to develop and refine effective treatments for PTSD secondary to stroke/TIA. Interventions should take a trauma-informed approach to patient care, combining psychological interventions with promotion of positive health behaviors, simultaneously appreciating the fact that these behaviors may increase psychological distress (El-Gabalawy et al., 2018). Such interventions must acknowledge that these patients face constant somatic reminders of their vulnerability and should work to increase acceptance of, and coping with, stroke-induced disability. Early interventions might also be considered, for example, by targeting modifiable environmental factors that increase distress in the hospital (e.g., Cornelius et al., 2018). Intervention targets may include increasing social connection and advocacy support, reducing overcrowding and hallway treatment, and improving patient-clinician communication (Edmondson et al., 2013; Goldfinger et al., 2014).

There were several limitations to this study. Individuals with severe stroke (NIHSS >14) were excluded to ensure participants were able to complete study procedures, but this exclusion criterion contributed to range restriction on the focal predictor. Indeed, the population studied in this paper had a median stroke severity score of 2.0, and so the true prevalence of PTSD symptoms in stroke survivors may have been underestimated. Our findings may not generalize to individuals with more severe stroke impact, or other patient populations. It is also important to note that data collected during in-patient assessment at baseline for pre-existing symptoms of PTSD and depression took place on average three days after admission to the ED. As such, patients’ responses to these questions may be biased due to the hospitalization. In addition, both acute stress symptoms and PTSD symptoms were self-reported, and clinical diagnostic interviews may have yielded lower estimates of PTSD burden in the sample (see Edmondson et al., 2012). Missing data may also contribute to an overestimation of PTSD in this sample, since those excluded from the analysis self-reported lower levels of distress. Critically, even low PTSD burden contributes to significant risk for event recurrence and mortality (Edmondson et al., 2012).

Data pertaining to other major medical conditions (e.g., cancer) were unavailable, which may have partially confounded the association of stroke disability with the development of PTSD symptoms secondary to a stroke/TIA. Data regarding treatment setting and procedures (e.g., length of stay, invasive treatment) were also unavailable and should be included in future research. Although our sample was among the largest to date to assess the development stroke/TIA-induced PTSD longitudinally, we did not a priori specify whether (or which) different types of stroke disability would differentially contribute to PTSD risk. This is an important avenue for future research, as is an assessment of the association of fluctuations in somatic symptoms and PTSD symptoms over time. Although patients may have a heightened awareness for internal somatic cues (e.g., heart rate) that contribute to subsequent feelings of threat and psychological outcomes, it is possible that the emotional response (e.g., feeling sad or distressed when unable to accomplish a task) is another mechanism underlying any association between somatic symptoms and PTSD.

5. Conclusion

In a large and diverse sample of stroke/TIA patients, the present study tested whether stroke disability is a risk factor for developing stroke/TIA-induced PTSD symptoms during the early days and months following stroke/TIA evaluation and treatment. Results confirmed a significant positive relationship between disability and PTSD symptoms, offering a potential screening and intervention target for evidence-based treatments to improve psychological well-being in patients, as well as offering support for a mechanistic theory of how internal somatic reminders of stroke (i.e., disability) contribute to the development of PTSD. Future research should seek to examine the circumstances and disabilities that are most likely to yield PTSD symptoms and develop interventions for patients that have experienced these common but traumatic events, to improve psychological, behavioral, and cardiovascular outcomes.

Table 1.

Demographic Characteristics of Participants

Participants (N=300) Frequency (%)
Demographic Characteristics (average age: 61.3 y)
  Gender
    Women 168 (44.0)
    Man 132 (56.0)
  Race
    White 71 (23.7)
    Black 61 (20.3)
    Other 27 (9.0)
  Ethnicity
    Hispanic or Latino 141 (47.0)
  English as first language
    Yes 183 (61.0)
    No 117 (39.0)
  Education
    Less than High School 41 (13.7)
    Some High School 28 (9.3)
    High School diploma 56 (18.7)
    Trade School 8 (2.7)
    Some College 43 (14.3)
    College Graduate 61 (20.3)
    Graduate School 60 (20.0)
    Declined to respond 3 (1.0)
  Overall PCL-5 Score at 1 month (imputed)
    Mean 11.9
    Median 7.0
    Standard Deviation 14.1
  PHQ Score at Baseline (imputed)
    Mean 6.1
    Median 4.0
    Standard Deviation 6.1
  Overall PCL-5 Score at Baseline (imputed)
    Mean 13.0
    Median 7.0
    Standard Deviation 15.7
  NIH Stroke Scale Score
    Median 2.0
    Interquartile Range 3.0
Open in a new tab

Acknowledgements:

EP led in the conception of the manuscript; EP and LD coordinated the design of the manuscript, data analysis and interpretation of data, and were primarily responsible for the writing and editing of the manuscript; AT and GC participated in the copy-editing and formatting of the manuscript; and were involved in the study protocol. DE participated in the conception and funding of this study and provided substantial comments of the manuscript. TC participated in the design of the manuscript, data analysis, data interpretation and oversaw writing of EP and LD. All authors read and approved the final version of the manuscript prior to submission.

Funding Sources: This work was supported by the National Heart, Lung, and Blood Institute [HL132347].

Footnotes

Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

References

  1. Ashbaugh AR, Houle-Johnson S, Herbert C, El-Hage W, & Brunet A (2016). Psychometric validation of the English and French versions of the Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5). PLoS One, 11(10), e0161645. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Breslau N, Davis GC, & Schultz LR (2003). Posttraumatic stress disorder and the incidence of nicotine, alcohol, and other drug disorders in persons who have experienced trauma. Archives of general psychiatry, 60(3), 289–294. 10.1001/archpsyc.60.3.289. [DOI] [PubMed] [Google Scholar]
  3. Carod-Artal J, Egido JA, González JL, & Varela de Seijas E (2000). Quality of life among stroke survivors evaluated 1 year after stroke: experience of a stroke unit. Stroke, 31(12), 2995–3000. [DOI] [PubMed] [Google Scholar]
  4. Chen M-H, Pan T-L, Li C-T, Lin W-C, Chen Y-S, Lee Y-C, … Tsai C-F (2015). Risk of stroke among patients with post-traumatic stress disorder: nationwide longitudinal study. The British Journal of Psychiatry, 206(4), 302–307. [DOI] [PubMed] [Google Scholar]
  5. Cornelius T, Agarwal S, Garcia O, Chaplin W, Edmondson D, & Chang BP (2018). Development and validation of a measure to assess patients’ threat perceptions in the emergency department. Academic Emergency Medicine, 25(10), 1098–1106. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Edmondson D (2014). An Enduring Somatic Threat Model of Posttraumatic Stress Disorder Due to Acute Life-Threatening Medical Events. Social and Personality Psychology Compass, 8(3), 118–134. 10.1111/spc3.12089 [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Edmondson D, Richardson S, Falzon L, Davidson KW, Mills MA, & Neria Y (2012). Posttraumatic stress disorder prevalence and risk of recurrence in acute coronary syndrome patients: a meta-analytic review. PloS one, 7(6), e38915. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Edmondson D, Shimbo D, Ye S, Wyer P, & Davidson KW (2013). The association of emergency department crowding during treatment for acute coronary syndrome with subsequent posttraumatic stress disorder symptoms. JAMA Internal Medicine, 173(6), 472–475. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. El-Gabalawy R, Mota N, Sommer JL, & Edmondson D (2018). Prevalence of illness-induced posttraumatic stress disorder in the United States. Psychosomatic Medicine, 80(8), 783–785. [DOI] [PubMed] [Google Scholar]
  10. Favrole P, Jehel L, Levy P, Descombes S, Muresan IP, Manifacier MJ, & Alamowitch S (2013). Frequency and predictors of post-traumatic stress disorder after stroke: a pilot study. Journal of the Neurological Sciences, 327(1-2), 35–40. [DOI] [PubMed] [Google Scholar]
  11. Ferro JM, Caeiro L, & Figueira ML (2016). Neuropsychiatric sequelae of stroke. Nature Reviews Neurology, 12(5), 269. [DOI] [PubMed] [Google Scholar]
  12. Gander ML, & Känel RV (2006). Myocardial infarction and post-traumatic stress disorder: frequency, outcome, and atherosclerotic mechanisms. European Journal of Cardiovascular Prevention & Rehabilitation, 13(2), 165–172. [DOI] [PubMed] [Google Scholar]
  13. Goldfinger JZ, Edmondson D, Kronish IM, Fei K, Balakrishnan R, Tuhrim S, & Horowitz CR (2014). Correlates of post-traumatic stress disorder in stroke survivors. Journal of Stroke and Cerebrovascular Diseases, 23(5), 1099–1105. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Gray MJ, Litz BT, Hsu JL, & Lombardo TW (2004). Psychometric properties of the life events checklist. Assessment, 11(4), 330–341. [DOI] [PubMed] [Google Scholar]
  15. Harrison JK, McArthur KS, & Quinn TJ (2013). Assessment scales in stroke: clinimetric and clinical considerations. Clinical interventions in aging, 8, 201. [DOI] [PMC free article] [PubMed] [Google Scholar]
  16. Kiphuth IC, Utz KS, Noble AJ, Köhrmann M, & Schenk T (2014). Increased prevalence of posttraumatic stress disorder in patients after transient ischemic attack. Stroke, 45(11), 3360–3366. [DOI] [PubMed] [Google Scholar]
  17. Kroenke K, Strine TW, Spitzer RL, Williams JB, Berry JT, & Mokdad AH (2009). The PHQ-8 as a measure of current depression in the general population. Journal of Affective Disorders, 114(1-3), 163–173. [DOI] [PubMed] [Google Scholar]
  18. Kronish IM, Edmondson D, Goldfinger JZ, Fei K, & Horowitz CR (2012). Posttraumatic stress disorder and adherence to medications in survivors of strokes and transient ischemic attacks. Stroke, 43(8), 2192–2197. 10.1161/STROKEAHA.112.655209 [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Liu C, Yi X, Li T, Xu L, Hu M, Zhang S, & Jiang R (2019). Associations of depression, anxiety and PTSD with neurological disability and cognitive impairment in survivors of moyamoya disease. Psychology, Health & Medicine, 24(1), 43–50. [DOI] [PubMed] [Google Scholar]
  20. Maher MJ, Rego SA, & Asnis GM (2006). Sleep disturbances in patients with post-traumatic stress disorder: epidemiology, impact and approaches to management. CNS drugs, 20(7), 567–590. 10.2165/00023210-200620070-00003 [DOI] [PubMed] [Google Scholar]
  21. Meli L, Alcántara C, Sumner JA, Swan B, Chang BP, & Edmondson D (2017). Enduring somatic threat perceptions and post-traumatic stress disorder symptoms in survivors of cardiac events. Journal of Health Psychology, 1359105317705982. [DOI] [PMC free article] [PubMed] [Google Scholar]
  22. Merriman C, Norman P, & Barton J (2007). Psychological correlates of PTSD symptoms following stroke. Psychology, Health & Medicine, 12(5), 592–602. [DOI] [PubMed] [Google Scholar]
  23. National Institute of Neurological Disorders and Stroke. (n.d.). Retrieved April 25, 2019, from https://www.ninds.nih.gov/
  24. O'Connor M, Christensen S, Jensen AB, Møller S, & Zachariae R (2011). How traumatic is breast cancer? Post-traumatic stress symptoms (PTSS) and risk factors for severe PTSS at 3 and 15 months after surgery in a nationwide cohort of Danish women treated for primary breast cancer. British Journal of Cancer, 104(3), 419–426. [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. Richardson J, Murray D, House KC, & Lowenkopf T (2006). Successful implementation of the National Institutes of Health Stroke Scale on a stroke/neurovascular unit. [DOI] [PubMed] [Google Scholar]
  26. Rutovic S, Kadojic D, Dikanovic M, Solic K, & Branko M Prevalence and correlates of post-traumatic stress disorder after ischaemic stroke. Acta Neurol Belg (2019). 10.1007/s13760-019-01200-9 [DOI] [PubMed] [Google Scholar]
  27. Sherr L, Nagra N, Kulubya G, Catalan J, Clucas C, & Harding R (2011). HIV infection associated post-traumatic stress disorder and post-traumatic growth–a systematic review. Psychology, Health & Medicine, 16(5), 612–629. [DOI] [PubMed] [Google Scholar]
  28. Smith EE, Kent DM, Bulsara KR, Leung LY, Lichtman JH, Reeves MJ, … & Zahuranec DB (2018). Accuracy of prediction instruments for diagnosing large vessel occlusion in individuals with suspected stroke: a systematic review for the 2018 guidelines for the early management of patients with acute ischemic stroke. Stroke, 49(3), e111–e122. [DOI] [PubMed] [Google Scholar]
  29. Stein LA, Goldmann E, Zamzam A, Luciano JM, Messé SR, Cucchiara B, … & Mullen MT (2018). Association between anxiety, depression, and post-traumatic stress disorder and outcomes after ischemic stroke. Frontiers in Neurology, 9, 890. [DOI] [PMC free article] [PubMed] [Google Scholar]
  30. Tedstone JE, & Tarrier N (2003). Posttraumatic stress disorder following medical illness and treatment. Clinical Psychology Review, 23(3), 409–448. [DOI] [PubMed] [Google Scholar]
  31. Vilchinsky N, Ginzburg K, Fait K, & Foa EB (2017). Cardiac-disease-induced PTSD (CDI-PTSD): A systematic review. Clinical Psychology Review. [DOI] [PubMed] [Google Scholar]
  32. von Känel R, Begré S, Abbas CC, Saner H, Gander ML, & Schmid JP (2010). Inflammatory biomarkers in patients with posttraumatic stress disorder caused by myocardial infarction and the role of depressive symptoms. Neuroimmunomodulation, 17(1), 39–46. [DOI] [PubMed] [Google Scholar]
  33. Wang X, Chung MC, Hyland ME, & Bahkeit M (2011). Posttraumatic stress disorder and psychiatric co-morbidity following stroke: the role of alexithymia. Psychiatry Research, 188(1), 51–57. [DOI] [PubMed] [Google Scholar]
  34. Weathers FW, Litz BT, Herman DS, Huska JA, & Keane TM (1993, October). The PTSD Checklist (PCL): Reliability, validity, and diagnostic utility. In annual convention of the international society for traumatic stress studies, San Antonio, TX: (Vol. 462). [Google Scholar]
  35. Weathers FW, Litz BT, Keane TM, Palmieri PA, Marx BP, & Schnurr PP (2013).The PTSD Checklist for DSM-5 (PCL-5). [Google Scholar]
  36. White JH, Attia J, Sturm J, Carter G, & Magin P (2014). Predictors of depression and anxiety in community dwelling stroke survivors: a cohort study. Disability and Rehabilitation, 36(23), 1975–1982. [DOI] [PubMed] [Google Scholar]
  37. Zen AL, Whooley MA, Zhao S, & Cohen BE (2012). Post-traumatic stress disorder is associated with poor health behaviors: findings from the heart and soul study. Health psychology: official journal of the Division of Health Psychology, American Psychological Association, 31(2), 194–201. 10.1037/a0025989 [DOI] [PMC free article] [PubMed] [Google Scholar]

RESOURCES