Anna Kufner, Ana Sofía Ríos, Benjamin Winter, Uchralt Temuulen, Ahmed Khalil, Ulrike Grittner, Johanna Schöner, Asli Akdeniz, Ulrike Lachmann, Golo Kronenberg, Arno Villringer, Karen Gertz, Matthias Endres
{"title":"纹状体卒中后的神经精神变化——来自观察性精神病后研究的结果。","authors":"Anna Kufner, Ana Sofía Ríos, Benjamin Winter, Uchralt Temuulen, Ahmed Khalil, Ulrike Grittner, Johanna Schöner, Asli Akdeniz, Ulrike Lachmann, Golo Kronenberg, Arno Villringer, Karen Gertz, Matthias Endres","doi":"10.1186/s42466-025-00390-3","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Ischemic stroke can lead to neuropsychiatric sequelae such as depression and post-traumatic stress disorder (PTSD), resulting in poorer functional outcomes. The POST-stroke PSYchological DIStress PostPsyDis; NCT01187342) study aimed to investigate whether ischemic lesions in the striatum increase the risk of depression and PTSD after stroke.</p><p><strong>Methods: </strong>This monocenter, observational, case-control study included 84 ischemic stroke patients with striatal (n = 54) and non-striatal ischemic brain lesions (n = 30). Primary study endpoints included symptoms of depression (assessed via the Geriatric Depression Scale; GDS-30) and PTSD (assessed via the Posttraumatic Symptom Scale; PTSS-10) 90 days post-stroke. A normative functional connectome was used to obtain a measure of striatal connectivity to the rest of the brain (\"striatal network\"). Network damage scores were used to estimate damage of each lesion to the striatal network.</p><p><strong>Results: </strong>Patients with striatal lesions had higher GDS-30 scores at 90 days post-stroke (median 5.6 vs. 3.0; Cohen's d = 0.39; p = 0.057), indicating a small to moderate effect. However, no meaningful group differences were observed in the incidence of depression or PTSD. In multivariable regression analyses, striatal infarction had an adjusted beta coefficient (β) of 1.9 (95%CI 0.19-3.7; p = 0.076) for GDS-10 and 1.8 (95%CI -1.9-5.5; p = 0.25) for PTSS-10 scores after 90 days. Only female sex was independently associated with PTSD severity (adjusted β = 5.1, 95% CI 1.3-8.8; p = 0.008). Analyzing lesion connectivity to the striatal network did not change these findings.</p><p><strong>Conclusions: </strong>Taken together, the PostPsyDis study suggests a high rate of psychiatric morbidity in stroke patients. Moreover, the study suggests increased neuropsychiatric symptoms in patients with striatal lesions. There is a clear need for larger studies to investigate the role of the striatum in post-stroke neuropsychiatric disorders.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov (NCT01187342) Registered 23 August 2009, https://clinicaltrials.gov/study/NCT01187342 .</p>","PeriodicalId":94156,"journal":{"name":"Neurological research and practice","volume":"7 1","pages":"32"},"PeriodicalIF":0.0000,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12067745/pdf/","citationCount":"0","resultStr":"{\"title\":\"Neuropsychiatric changes following striatal stroke- results from the observational PostPsyDis study.\",\"authors\":\"Anna Kufner, Ana Sofía Ríos, Benjamin Winter, Uchralt Temuulen, Ahmed Khalil, Ulrike Grittner, Johanna Schöner, Asli Akdeniz, Ulrike Lachmann, Golo Kronenberg, Arno Villringer, Karen Gertz, Matthias Endres\",\"doi\":\"10.1186/s42466-025-00390-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Ischemic stroke can lead to neuropsychiatric sequelae such as depression and post-traumatic stress disorder (PTSD), resulting in poorer functional outcomes. The POST-stroke PSYchological DIStress PostPsyDis; NCT01187342) study aimed to investigate whether ischemic lesions in the striatum increase the risk of depression and PTSD after stroke.</p><p><strong>Methods: </strong>This monocenter, observational, case-control study included 84 ischemic stroke patients with striatal (n = 54) and non-striatal ischemic brain lesions (n = 30). Primary study endpoints included symptoms of depression (assessed via the Geriatric Depression Scale; GDS-30) and PTSD (assessed via the Posttraumatic Symptom Scale; PTSS-10) 90 days post-stroke. A normative functional connectome was used to obtain a measure of striatal connectivity to the rest of the brain (\\\"striatal network\\\"). Network damage scores were used to estimate damage of each lesion to the striatal network.</p><p><strong>Results: </strong>Patients with striatal lesions had higher GDS-30 scores at 90 days post-stroke (median 5.6 vs. 3.0; Cohen's d = 0.39; p = 0.057), indicating a small to moderate effect. However, no meaningful group differences were observed in the incidence of depression or PTSD. In multivariable regression analyses, striatal infarction had an adjusted beta coefficient (β) of 1.9 (95%CI 0.19-3.7; p = 0.076) for GDS-10 and 1.8 (95%CI -1.9-5.5; p = 0.25) for PTSS-10 scores after 90 days. Only female sex was independently associated with PTSD severity (adjusted β = 5.1, 95% CI 1.3-8.8; p = 0.008). Analyzing lesion connectivity to the striatal network did not change these findings.</p><p><strong>Conclusions: </strong>Taken together, the PostPsyDis study suggests a high rate of psychiatric morbidity in stroke patients. Moreover, the study suggests increased neuropsychiatric symptoms in patients with striatal lesions. There is a clear need for larger studies to investigate the role of the striatum in post-stroke neuropsychiatric disorders.</p><p><strong>Trial registration: </strong>ClinicalTrials.gov (NCT01187342) Registered 23 August 2009, https://clinicaltrials.gov/study/NCT01187342 .</p>\",\"PeriodicalId\":94156,\"journal\":{\"name\":\"Neurological research and practice\",\"volume\":\"7 1\",\"pages\":\"32\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-05-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12067745/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neurological research and practice\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1186/s42466-025-00390-3\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurological research and practice","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1186/s42466-025-00390-3","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}
Neuropsychiatric changes following striatal stroke- results from the observational PostPsyDis study.
Background: Ischemic stroke can lead to neuropsychiatric sequelae such as depression and post-traumatic stress disorder (PTSD), resulting in poorer functional outcomes. The POST-stroke PSYchological DIStress PostPsyDis; NCT01187342) study aimed to investigate whether ischemic lesions in the striatum increase the risk of depression and PTSD after stroke.
Methods: This monocenter, observational, case-control study included 84 ischemic stroke patients with striatal (n = 54) and non-striatal ischemic brain lesions (n = 30). Primary study endpoints included symptoms of depression (assessed via the Geriatric Depression Scale; GDS-30) and PTSD (assessed via the Posttraumatic Symptom Scale; PTSS-10) 90 days post-stroke. A normative functional connectome was used to obtain a measure of striatal connectivity to the rest of the brain ("striatal network"). Network damage scores were used to estimate damage of each lesion to the striatal network.
Results: Patients with striatal lesions had higher GDS-30 scores at 90 days post-stroke (median 5.6 vs. 3.0; Cohen's d = 0.39; p = 0.057), indicating a small to moderate effect. However, no meaningful group differences were observed in the incidence of depression or PTSD. In multivariable regression analyses, striatal infarction had an adjusted beta coefficient (β) of 1.9 (95%CI 0.19-3.7; p = 0.076) for GDS-10 and 1.8 (95%CI -1.9-5.5; p = 0.25) for PTSS-10 scores after 90 days. Only female sex was independently associated with PTSD severity (adjusted β = 5.1, 95% CI 1.3-8.8; p = 0.008). Analyzing lesion connectivity to the striatal network did not change these findings.
Conclusions: Taken together, the PostPsyDis study suggests a high rate of psychiatric morbidity in stroke patients. Moreover, the study suggests increased neuropsychiatric symptoms in patients with striatal lesions. There is a clear need for larger studies to investigate the role of the striatum in post-stroke neuropsychiatric disorders.
Trial registration: ClinicalTrials.gov (NCT01187342) Registered 23 August 2009, https://clinicaltrials.gov/study/NCT01187342 .
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