scholarly journals 18F-Flutemetamol PET post-stroke - a seven year follow-up study

2019 ◽  
Author(s):  
Guri Hagberg ◽  
Hege Ihle-Hansen ◽  
Brynjar Fure ◽  
Bente Thommessen ◽  
Håkon Ihle-Hansen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Status ◽  
Cortical Atrophy ◽  
Csf Biomarkers ◽  
Stroke Survivors ◽  
Amyloid Β Peptide ◽  
Post Stroke ◽  
Amyloid Pathology ◽  
One Year

Abstract Background: Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol (18F-Flut) positron emission tomography (PET), is common in 7-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ₄₂) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods: 208 patients with first-ever stroke or TIA without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or none. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ₄₂ levels were assessed using linear regression. Results: In all, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ₄₂ levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18F-Flut-PET SUVr in this cohort.Conclusions: Amyloid binding were not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed amyloid did not correlate with other measures related to neurodegeneration and cognition. Therefore amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.

scholarly journals No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven year follow-up study

2020 ◽  
Author(s):  
Guri Hagberg ◽  
Hege Ihle-Hansen ◽  
Brynjar Fure ◽  
Bente Thommessen ◽  
Håkon Ihle-Hansen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Status ◽  
Cortical Atrophy ◽  
Csf Biomarkers ◽  
Stroke Survivors ◽  
Amyloid Β Peptide ◽  
Post Stroke ◽  
Amyloid Pathology ◽  
One Year

Abstract Background Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol ( 18 F-Flut) positron emission tomography (PET), is common in 7-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18 F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ 42 ) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods 208 patients with first-ever stroke or TIA without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or none. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18 F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18 F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ 42 levels were assessed using linear regression. Results In all, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ 42 levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18 F-Flut-PET SUVr in this cohort. Conclusions Amyloid binding were not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed amyloid did not correlate with other measures related to neurodegeneration and cognition. Therefore amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.

scholarly journals No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven year follow-up study

2020 ◽  
Author(s):  
Guri Hagberg ◽  
Hege Ihle-Hansen ◽  
Brynjar Fure ◽  
Bente Thommessen ◽  
Håkon Ihle-Hansen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Status ◽  
Amyloid Deposition ◽  
Cortical Atrophy ◽  
Csf Biomarkers ◽  
Stroke Survivors ◽  
Post Stroke ◽  
Amyloid Pathology ◽  
One Year

Abstract Background: Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol (18F-Flut) positron emission tomography (PET), is common in 7-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ₄₂) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods: 208 patients with first-ever stroke or transient Ischemic Attack (TIA) without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or normal. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ₄₂ levels were assessed using linear regression. Results: In total, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ₄₂ levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18F-Flut-PET SUVr in this cohort.Conclusions: Amyloid binding was not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed, cortical amyloid deposition did not correlate with other measures related to neurodegeneration or cognition. Therefore amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.Trial registration: Clinicaltrials.gov (NCT00506818)

scholarly journals No evidence for amyloid pathology as a key mediator of neurodegeneration post-stroke - a seven-year follow-up study

2020 ◽  
Author(s):  
Guri Hagberg ◽  
Hege Ihle-Hansen ◽  
Brynjar Fure ◽  
Bente Thommessen ◽  
Håkon Ihle-Hansen ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Amyloid Deposition ◽  
Trial Registration ◽  
Cortical Atrophy ◽  
Csf Biomarkers ◽  
Stroke Survivors ◽  
Post Stroke ◽  
Amyloid Pathology ◽  
One Year

Abstract Background: Cognitive impairment (CI) with mixed vascular and neurodegenerative pathologies after stroke is common. The role of amyloid pathology in post-stroke CI is unclear. We hypothesize that amyloid deposition, measured with Flutemetamol (18F-Flut) positron emission tomography (PET), is common in seven-year stroke survivors diagnosed with CI and, further, that quantitatively assessed 18F-Flut-PET uptake after seven years correlates with amyloid-β peptide (Aβ₄₂) levels in cerebrospinal fluid (CSF) at one year, and with measures of neurodegeneration and cognition at seven years post-stroke. Methods: 208 patients with first-ever stroke or transient Ischemic Attack (TIA) without pre-existing CI were included during 2007 and 2008. At one- and seven-years post-stroke, cognitive status was assessed, and categorized into dementia, mild cognitive impairment or normal. Etiologic sub-classification was based on magnetic resonance imaging (MRI) findings, CSF biomarkers and clinical cognitive profile. At seven years, patients were offered 18F-Flut-PET, and amyloid-positivity was assessed visually and semi-quantitatively. The associations between 18F-Flut-PET standardized uptake value ratios (SUVr) and measures of neurodegeneration (medial temporal lobe atrophy (MTLA), global cortical atrophy (GCA)) and cognition (Mini-Mental State Exam (MMSE), Trail-making test A (TMT-A)) and CSF Aβ₄₂ levels were assessed using linear regression. Results: In total, 111 patients completed 7-year follow-up, and 26 patients agreed to PET imaging, of whom 13 had CSF biomarkers from one year. Thirteen out of 26 patients were diagnosed with CI seven years post-stroke, but only one had visually assessed amyloid positivity. CSF Aβ₄₂ levels at one year, MTA grade, GCA scale, MMSE score or TMT-A at seven years did not correlate with 18F-Flut-PET SUVr in this cohort.Conclusions: Amyloid binding was not common in 7-year stroke survivors diagnosed with CI. Quantitatively assessed, cortical amyloid deposition did not correlate with other measures related to neurodegeneration or cognition. Therefore, amyloid pathology may not be a key mediator of neurodegeneration seven years post-stroke.Trial registration: Clinicaltrials.gov (NCT00506818). July 23, 2007. Inclusion from February 2007, randomization and intervention from May 2007 and trial registration in July 2007.

Abstract T P42: Patients With a Clinical Diagnosis of Non-disabling Stroke, and a Normal MRI are Clinically Indistinguishable From Patients With a MRI Lesion at 1 Year Post Stroke

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Stephen Makin ◽  
Martin Dennis ◽  
Joanna M Wardlaw
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Assessment ◽  
Expert Panel ◽  
Recurrent Stroke ◽  
Final Diagnosis ◽  
Cognitively Impaired ◽  
Post Stroke ◽  
Mild Stroke ◽  
One Year

Background: Up to one third of patients with a clinically apparent mild stroke and no other apparent cause of their symptoms have a normal MRI. We examined disability, recurrent stroke, and cognitive impairment at one year compared to patient with an MRI-DWI lesion. Methods: We recruited consecutive patients with a non-disabling ischaemic stroke, and performed clinical assessment and MRI (with DWI) . An expert panel reviewed all cases, we included patients with a final diagnosis of stroke and excluded patients with another diagnosis. At one year post stroke we recorded modified Rankin scale (mRs), stroke and TIA recurrence, Addenbrookes Cognitive Assessment Revised (ACE-R) and the Beck Depression index (BDI) and performed another MRI. Non-attenders were assessed by telephone or post. We defined cognitive impairment as ACE-R of <88, and depression as a BDI of >9. Results: Almost one third (75/264) (median NIHSS=2) of patients had a no relevant lesion on MRI DWI. There was no difference in age, sex, symptoms, or risk factors in patients with and without a lesion, 197 had MRI at 1 year (all had clinical follow-up). Of 75 with no lesion, 41% were mRs ≥2, 13% had recurrent stroke or TIA, 36% were cognitively impaired and 46% had depression. This was not significantly different from the patients with a lesion. Of the 197 who had a follow-up MRI 50 patients with no initial lesion had follow-up MRI and one had a new lesion, (versus 20/147 patients with a lesion) (p=0.016). Conclusions: Patients with a clinical stroke and no other obvious cause for their symptoms are clinically indistinguishable from patients with the same NIHSS who have a lesion on DWI-MRI, in terms of recurrence, disability, or cognitive impairment. Suggesting that these patients have had a stroke that does not appear on MRI. The presence of an initial lesion increases the liklihood of a lesion on 1 year MRI, however without a difference in clinical stroke this is of doubtful significance.

Remission of poststroke cognitive impairment no dementia: Clinical and imaging correlates

2011 ◽  
Vol 26 (S2) ◽  
pp. 1179-1179
Author(s):  
Y.K. Chen ◽  
E. Lee ◽  
G.S. Ungvari ◽  
J.Y. Lu ◽  
W.C.W. Chu ◽  
...  
Keyword(s):  
Logistic Regression ◽  
Cognitive Impairment ◽  
Hippocampal Volume ◽  
Cognitive Status ◽  
Cerebral Microbleeds ◽  
Younger Age ◽  
One Year ◽  
Cognitively Intact ◽  
Cognitive Impairment No Dementia

IntroductionCerebral microbleeds (CMBs) may contribute to cognitive deficits in stroke. Cognitive impairment that does not meet the criteria for dementia (cognitive impairment no dementia [CIND]) is common in stroke, and patients with such impairment can revert to normal cognition.ObjectiveTo investigate the association of CMBs and remission of poststroke CIND.AimTo understand the evolution of poststroke cognitive impairment no dementia (CIND) is bi-directional.Methods143 patients with CIND at three months after stroke were recruited and followed up for one year. Remission of CIND was defined as a conversion of cognitive status from CIND to cognitively intact at follow-up. MRI variables in terms of infarction, cerebral microbleeds (CMBs), and white matter hyperintensities (WMHs) and hippocampal volume were analyzed. Logistic regression was performed to find the predictors of the remission of poststroke CIND.Results30 (21.0%) out of the 143 patients converted to cognitive intact at follow-up. In univariate comparisons, subjects with remission of CIND had younger age (67.1 ± 9.5 vs.73.6 ± 7.6 years, p < 0.001) and higher education years (5.1 ± 4.0 vs.3.6 ± 4.0, p = 0.039). They also had lower WMHs volume (8.2 ± 8.2 vs. 18.6 ± 19.7 cm3, p < 0.001), lower frequency of CMBs (10.0% vs. 31.0%, p = 0.021) and lower volume of the lateral ventricle (33.3 ± 16.5 vs.42.6 ± 19.4 cm3, p = 0.017). In logistic regression, age (odds ratio [OR] = 0.913, 95%C.I. = 0.866–0.962, p = 0.001) and absence of CMBs (OR = 4.292, 95%C.I. = 1.174–15.625, p = 0.028) were significant predictors of remission of CIND.ConclusionsYounger age and absence of CMBs predict the remission of poststroke CIND.

scholarly journals Role of caregiver factors in outpatient medical follow-up post-stroke: observational study in Singapore

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Shilpa Tyagi ◽  
Gerald Choon-Huat Koh ◽  
Nan Luo ◽  
Kelvin Bryan Tan ◽  
Helen Hoenig ◽  
...  
Keyword(s):  
Observational Study ◽  
Management Strategies ◽  
Stroke Survivor ◽  
Stroke Survivors ◽  
Post Stroke ◽  
Memory Problems ◽  
Healthcare Needs ◽  
Stroke Study

Abstract Background Outpatient medical follow-up post-stroke is not only crucial for secondary prevention but is also associated with a reduced risk of rehospitalization. However, being voluntary and non-urgent, it is potentially determined by both healthcare needs and the socio-demographic context of stroke survivor-caregiver dyads. Therefore, we aimed to examine the role of caregiver factors in outpatient medical follow-up (primary care (PC) and specialist outpatient care (SOC)) post-stroke. Method Stroke survivors and caregivers from the Singapore Stroke Study, a prospective, yearlong, observational study, contributed to the study sample. Participants were interviewed 3-monthly for data collection. Counts of PC and SOC visits were extracted from the National Claims Database. Poisson modelling was used to explore the association of caregiver (and patient) factors with PC/SOC visits over 0–3 months (early) and 4–12 months (late) post-stroke. Results For the current analysis, 256 stroke survivors and caregivers were included. While caregiver-reported memory problems of a stroke survivor (IRR: 0.954; 95% CI: 0.919, 0.990) and caregiver burden (IRR: 0.976; 95% CI: 0.959, 0.993) were significantly associated with lower early post-stroke PC visits, co-residing caregiver (IRR: 1.576; 95% CI: 1.040, 2.389) and negative care management strategies (IRR: 1.033; 95% CI: 1.005, 1.061) were significantly associated with higher late post-stroke SOC visits. Conclusion We demonstrated that the association of caregiver factors with outpatient medical follow-up varied by the type of service (i.e., PC versus SOC) and temporally. Our results support family-centred care provision by family physicians viewing caregivers not only as facilitators of care in the community but also as active members of the care team and as clients requiring care and regular assessments.

scholarly journals COGNITIVE IMPAIRMENT, THEIR DYNAMICS AND STRUCTURE IN THE ACUTE AND RECOVERY PERIODS OF STROKE, DEPENDING ON ARTERIAL HYPERTENSION SEVERITY AND DURATION

2018 ◽  
Vol 13 (3-4) ◽  
pp. 22-27
Author(s):  
T.M. Cherenko ◽  
Yu.L. Heletyuk
Keyword(s):  
Blood Pressure ◽  
Cognitive Impairment ◽  
Arterial Hypertension ◽  
Blood Pressure Monitoring ◽  
Cognitive Status ◽  
Neurological Deficits ◽  
Stroke Patients ◽  
Mean Values ◽  
Post Stroke ◽  
The Mean

Relevance. Cognitive impairment is common in the post-stroke period. Different characteristics of arterial hypertension (AH), namely its severity, duration and variability of blood pressure, can affect the development of cognitive impairment in stroke patients. Objective: to investigate cognitive impairment, their dynamics and structure in acute and recovering stroke periods, depending on the arterial hypertension severity and duration. Materials and methods. 150 patients with a primary ischemic stroke and history of hypertension: 74 (49,3 %) women and 76 (50,7 %) men, the mean age (67,4±0,7) years have been examined. Neurological deficits was evaluated by the NIHSS scale. The cognitive status was evaluated by the MMSE scale at the end of an acute period of 21 days and 1 year. Diagnosis of hypertension was based on the clinical and instrumental examination results and medical documents. Daily blood pressure monitoring was using on admission and every 4 hours during 6 days of acute stroke stage. Mean SBP, mean DBP, maximum SBP and DBP, standard deviation (SD) of SBP and DBP were studied. Results. By the mean score on the MMSE scale, there are differences in patients during acute post-stroke period, depending on the severity of hypertension: 27,2±0,6 points in the case of hypertension stage 1, 24,3±0,6 in the case of hypertension stage 2 and 20,7±0,8 in case of AH stage 3, (p=0.001). By this indicator, patients with different AH duration were different: 26,4±0,9 points; 25,1±0,5 points; 20,5±0,7 points, respectively. The significance of these differences by the mean values of MMSE score was obtained in patients with a duration of AH less than 5 years and more than 10 years, as well as when comparing the group of "6-10 years" and "over 10 years" (p=0,001). Significant differences in the structure of cognitive deficits severity, depending on the hypertension stage and its duration, were observed only in patients with moderate and severe stroke (p=0,006). Cognitive deterioration a year after a stroke was observed in 40 (31,5 %) patients. They have significantly higher mean values SD 1-3, SD 1-6, SBP on the first day after a stroke, and duration of hypertension. Conclusions. The relationship between the degree of intellectual decline and the duration of hypertension (r=0,592, p=0,001), severity of hypertension (r=0,459, p=0,001) was found. The severity of the neurological deficiency affects the structure of cognitive impairment at discharge in patients with different severity and duration of hypertension, and higher mean values of the variability of blood pressure from 1 to 6 days, SBP on the first day after stroke and higher duration of hypertension in the history is associated with a negative dynamics of cognitive impairment in stroke patients in a year after stroke.

scholarly journals Anticholinergics and Benzodiazepines on Cognitive Impairment among Elderly with Alzheimer’s Disease: a One year Follow-Up Study

2019 ◽  
Author(s):  
Rewadee Jenraumjit ◽  
Surarong Chinwong ◽  
Dujrudee Chinwong ◽  
Tipaporn Kanjanarach ◽  
Thanat Kshetradat ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Psychological Symptoms ◽  
Esterase Inhibitors ◽  
One Year ◽  
State Examination ◽  
Harmful Effects

Abstract Objective Age-associated decline in central cholinergic activity makes older adults susceptible to harmful effects of anticholinergics (ACs). Evidence exists of an association between effects of AC medications on cognition. This retrospective cohort study examines how ACs affect cognition among older adults with Alzheimer’s disease (AD) who received acetylcholine esterase inhibitors (AChEIs) over the course of 12 months. Results A total of 133 (80% women, mean age 78.38 years, SD 7.4) were recruited. No difference in sex, age and comorbid diseases was observed between participants who took ACs, Benzodiazepines (BZDs) and AChEIs. The most common prescribed ACs was quetiapine, being used for behavioral and psychological symptoms (BPSD). Multilevel analysis showed that the change of mental state examination scores were significantly predicted in the group using ACs (t (169), -2.52, p = .020) but not with the groups using BZD (t (162), 0.84, p = .440). Evidence showed that older adults with Alzheimer’s disease and exposed to ACs exhibited lower global cognitive scores than those without AC exposure. Using ACs could be a trade-off between controlling BPSD and aggravating cognitive impairment. Highlighting the awareness of the potential anticholinergic effect is important and may be the best policy.

scholarly journals Association among depression, cognitive impairment and executive dysfunction after stroke

2012 ◽  
Vol 6 (3) ◽  
pp. 152-157 ◽  
Author(s):  
Luisa Terroni ◽  
Matildes F.M. Sobreiro ◽  
Adriana B. Conforto ◽  
Carla C. Adda ◽  
Valeri D. Guajardo ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Neuropsychological Tests ◽  
Executive Dysfunction ◽  
Stroke Survivors ◽  
Stroke Patients ◽  
Adequate Treatment ◽  
Post Stroke ◽  
Quantitative Studies ◽  
Post Stroke Depression ◽  
The Relationship

ABSTRACT The relationship between depression and cognitive impairment, frequent after stroke, is complex and has not been sufficiently elucidated. Objective: To review the relationship between post-stroke depression and cognitive impairment. Methods: We performed a PubMed database search spanning the last ten years, using the terms post-stroke depression, cognitive dysfunction, cognitive impairment and neuropsychological tests. Our target studies were original quantitative studies that investigated the relationship between post-stroke depression (PSD) and cognitive impairment in stroke patients. Articles published in English, Spanish, Italian and Portuguese were considered. Selection criteria were the use of neuropsychological tests to assess cognitive function, and of either instruments to diagnose major depression, or scales to assess depressive symptoms, within the first three months after stroke. Results: Six original quantitative studies fulfilled the criteria. The prevalence of PSD within the first three months after stroke ranged from 22% to 31%. Incidence ranged from 25% to 27% and was evaluated in only two studies. PSD was associated with increased cognitive impairment. Cognitive impairment was reported in 35.2% to 87% of the patients. Post-stroke cognitive deficits were reported mostly in executive function, memory, language, and speed of processing. Conclusion: Executive dysfunction and depression occur in stroke survivors, are frequently coexistent, and also associated with worse stroke prognosis. Healthcare professionals need to address and provide adequate treatment for depression and executive dysfunctions in stroke patients early in the first three months after stroke. Future studies should evaluate the efficacy of programs evaluating the early detection and treatment of PSD and executive dysfunction in stroke survivors.

Sign in / Sign up

Export Citation Format

Share Document