Why are you doing this research when the correct solution is to prevent depression by having EXACT 100% RECOVERY PROTOCOLS? Are you that blitheringly stupid along with your mentors and senior researchers?
You're smarter than me; send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? Your patients need an explanation of why you aren't trying to get survivors 100% recovered.
Why isn't your 'professional' solving stroke?
Laziness? Incompetence? Or just don't care? NO leadership? NO strategy? Not my job? Not my Problem!
Lesion-Network Mapping of Poststroke Depressive Symptoms: Evidence From Two Prospective Ischemic Stroke Cohorts
Abstract
BACKGROUND:
Poststroke depression affects up to one-third of stroke survivors, significantly impacting recovery and quality of life. However, its pathophysiology remains unclear.
METHODS:
We analyzed 2 independent, prospective ischemic stroke cohorts (PROSCIS-B [Prospective Cohort of Incident Stroke Berlin] and BAPTISe [Biomarkers and Perfusion-Training-Induced Changes After Stroke]; n=377) enrolled at the Charité Hospital, Germany, to identify brain regions and networks associated with depressive symptoms poststroke. Lesion-symptom mapping assessed associations between lesion location and depressive symptoms measured by the Center for Epidemiological Studies Depression Scale at 6 (BAPTISe) or 12 (PROSCIS-B) months poststroke. Lesion-network mapping evaluated lesion connectivity with brain networks. A mixed-effects model, including cohort as a random effect, assessed the relationship between network similarity (Pearson correlation) and Center for Epidemiological Studies Depression Scale scores. Dice coefficients (DC) quantified spatial overlap with canonical resting-state networks.
RESULTS:
Lesion-symptom mapping showed no significant associations between lesion location and depressive symptoms. In contrast, lesion-network mapping revealed that lesion connectivity to brain regions including the frontal pole, middle and inferior frontal gyri, inferior temporal gyrus, supramarginal gyrus, angular gyrus, frontal orbital cortex, and thalamus weakly correlated with Center for Epidemiological Studies Depression Scale scores (β, 11.4 [95%CI, 1.8–21.1]; P=0.02). These regions overlapped with the frontoparietal (DC=0.28), salience (DC=0.27), and default mode (DC=0.20) networks, as well as a published depression circuit (DC=0.43). However, these findings did not replicate across data sets.
CONCLUSIONS:
Lesion location alone was not associated with poststroke depression. However, connectivity-based analyses implicated disruption of large-scale brain networks in the development of depressive symptoms. The failure to validate this association across data sets underscores the need for further studies with more comparable patient populations—particularly in terms of stroke severity and harmonized assessment time-points—to confirm these findings and their clinical relevance.
REGISTRATION:
URL: https://www.clinicaltrials.gov; Unique identifier: NCT01363856. URL: https://www.clinicaltrials.gov; Unique identifier: NCT01954797.
Graphical Abstract
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