Posttraumatic Stress Symptoms After Stroke: The Effects of Anatomy and Coping Style.


Journal

Stroke
ISSN: 1524-4628
Titre abrégé: Stroke
Pays: United States
ID NLM: 0235266

Informations de publication

Date de publication:
06 2022
Historique:
pubmed: 11 3 2022
medline: 26 5 2022
entrez: 10 3 2022
Statut: ppublish

Résumé

Posttraumatic stress disorder (PTSD) can be triggered by life-threatening medical emergencies, such as stroke. Data suggest that up to 25% of stroke survivors will develop PTSD symptomatology, but little is known about predisposing factors. We sought to examine whether neuroimaging measures and coping styles are related to PTSD symptoms after stroke. Participants were survivors of first-ever, mild-moderate ischemic stroke, or transient ischemic attack from the TABASCO study (Tel Aviv Brain Acute Stroke Cohort). All participants underwent a 3T magnetic resonance imaging at baseline and were examined 6, 12, and 24 months thereafter, using neurological, neuropsychological, and functional evaluations. At baseline, coping styles were evaluated by a self-reported questionnaire. PTSD symptoms were assessed using the PTSD checklist. Data were available for 436 patients. Forty-eight participants (11%) developed probable PTSD (PTSD checklist ≥44) during the first year after the stroke/transient ischemic attack. Stroke was more likely to cause PTSD than transient ischemic attack. Stroke severity, larger white matter lesion volume, and worse hippocampal connectivity were associated with PTSD severity, while infarct volume or location was not. In a multivariate analysis, high-anxious and defensive coping styles were associated with a 6.66-fold higher risk of developing poststroke PTSD ([95% CI, 2.08-21.34]; In our cohort, PTSD was a common sequela among stroke survivors. We suggest that risk factors for PTSD development include stroke severity, white matter damage, and premorbid coping styles. Early identification of at-risk patients is key to effective treatment.

Sections du résumé

BACKGROUND
Posttraumatic stress disorder (PTSD) can be triggered by life-threatening medical emergencies, such as stroke. Data suggest that up to 25% of stroke survivors will develop PTSD symptomatology, but little is known about predisposing factors. We sought to examine whether neuroimaging measures and coping styles are related to PTSD symptoms after stroke.
METHODS
Participants were survivors of first-ever, mild-moderate ischemic stroke, or transient ischemic attack from the TABASCO study (Tel Aviv Brain Acute Stroke Cohort). All participants underwent a 3T magnetic resonance imaging at baseline and were examined 6, 12, and 24 months thereafter, using neurological, neuropsychological, and functional evaluations. At baseline, coping styles were evaluated by a self-reported questionnaire. PTSD symptoms were assessed using the PTSD checklist. Data were available for 436 patients.
RESULTS
Forty-eight participants (11%) developed probable PTSD (PTSD checklist ≥44) during the first year after the stroke/transient ischemic attack. Stroke was more likely to cause PTSD than transient ischemic attack. Stroke severity, larger white matter lesion volume, and worse hippocampal connectivity were associated with PTSD severity, while infarct volume or location was not. In a multivariate analysis, high-anxious and defensive coping styles were associated with a 6.66-fold higher risk of developing poststroke PTSD ([95% CI, 2.08-21.34];
CONCLUSIONS
In our cohort, PTSD was a common sequela among stroke survivors. We suggest that risk factors for PTSD development include stroke severity, white matter damage, and premorbid coping styles. Early identification of at-risk patients is key to effective treatment.

Identifiants

pubmed: 35264011
doi: 10.1161/STROKEAHA.121.036635
doi:

Types de publication

Journal Article Research Support, U.S. Gov't, Non-P.H.S. Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1924-1933

Auteurs

Einor Ben Assayag (E)

Departments of Neurology, Psychiatry and Radiology, Tel Aviv Sourasky Medical Center, Israel (E.B.A., O.T., S.S.-T., E.S., D.N., J.M., H.H.).
Faculty of Medicine (E.B.A., O.T., A.D.K., S.S.-T., D.N., H.H.), Tel Aviv University, Israel.

Oren Tene (O)

Departments of Neurology, Psychiatry and Radiology, Tel Aviv Sourasky Medical Center, Israel (E.B.A., O.T., S.S.-T., E.S., D.N., J.M., H.H.).
Faculty of Medicine (E.B.A., O.T., A.D.K., S.S.-T., D.N., H.H.), Tel Aviv University, Israel.

Amos D Korczyn (AD)

Faculty of Medicine (E.B.A., O.T., A.D.K., S.S.-T., D.N., H.H.), Tel Aviv University, Israel.

Zahava Solomon (Z)

Bob Shapell School of Social Work (Z.S.), Tel Aviv University, Israel.

Natan M Bornstein (NM)

Department of Neurology, Shaare Zedek Medical Center, Jerusalem, Israel (N.M.B.).

Shani Shenhar-Tsarfaty (S)

Departments of Neurology, Psychiatry and Radiology, Tel Aviv Sourasky Medical Center, Israel (E.B.A., O.T., S.S.-T., E.S., D.N., J.M., H.H.).
Faculty of Medicine (E.B.A., O.T., A.D.K., S.S.-T., D.N., H.H.), Tel Aviv University, Israel.

Estelle Seyman (E)

Departments of Neurology, Psychiatry and Radiology, Tel Aviv Sourasky Medical Center, Israel (E.B.A., O.T., S.S.-T., E.S., D.N., J.M., H.H.).

Dana Niry (D)

Departments of Neurology, Psychiatry and Radiology, Tel Aviv Sourasky Medical Center, Israel (E.B.A., O.T., S.S.-T., E.S., D.N., J.M., H.H.).
Faculty of Medicine (E.B.A., O.T., A.D.K., S.S.-T., D.N., H.H.), Tel Aviv University, Israel.

Jeremy Molad (J)

Departments of Neurology, Psychiatry and Radiology, Tel Aviv Sourasky Medical Center, Israel (E.B.A., O.T., S.S.-T., E.S., D.N., J.M., H.H.).

Hen Hallevi (H)

Departments of Neurology, Psychiatry and Radiology, Tel Aviv Sourasky Medical Center, Israel (E.B.A., O.T., S.S.-T., E.S., D.N., J.M., H.H.).
Faculty of Medicine (E.B.A., O.T., A.D.K., S.S.-T., D.N., H.H.), Tel Aviv University, Israel.

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