ReviewPain and therapy2026
Shared Mechanisms and Integrated Management of Post-Stroke Pain and Depression: A Comprehensive Review.
Review in Pain and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Current Progress of Mechanisms Underlying Post-Stroke Depression and Music Therapy.Chinese journal of integrative medicine · 2026Review
- Impact of Glycemic Trajectory and Variability on Ischemic Stroke Prognosis and Exploration of Its Mechanisms: A Comprehensive Review.Healthcare (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Post-stroke pain (PSP) and post-stroke depression (PSD) represent two major neuropsychiatric complications that frequently co-occur, with comorbidity rates ranging from 34 to 65.6%. Despite their high prevalence and profound impact on functional recovery and quality of life, the shared mechanisms and optimal management of this complex comorbidity remain poorly understood. We conducted a systematic review of clinical and preclinical evidence to explore the epidemiological characteristics, diagnostic challenges, neurobiological underpinnings, and therapeutic strategies for comorbid PSP and PSD. Special emphasis was placed on neuroinflammatory cascades, glial cell dysfunction, monoaminergic system dysregulation, and maladaptive neural circuit remodeling. We found PSP and PSD exhibit overlapping pathophysiological mechanisms, including microglial activation, astrocytic reactivity, pro-inflammatory cytokine release (e.g., TNF-α, IL-1β, IL-6), and dysregulation of cortico-limbic circuits involving the anterior cingulate cortex, amygdala, and ventral tegmental area. Pharmacotherapies such as serotonin-norepinephrine reuptake inhibitors (SNRIs) and NMDA receptor antagonists (e.g., ketamine), as well as neuromodulation approaches (e.g., repetitive transcranial magnetic stimulation [rTMS], transcranial direct current stimulation [tDCS]), demonstrate efficacy in both conditions, likely through anti-inflammatory and neural circuit-modulating effects. We speculate that the comorbidity of PSP and PSD is underpinned by convergent neuroimmune and neural circuit mechanisms. Targeting these shared pathways-such as with cytokine inhibitors, glial modulators, and circuit-specific neuromodulation-holds promise for developing integrated, mechanism-based therapies. Future research should prioritize multimodal treatment strategies tailored to the neurobiological signatures of this debilitating post-stroke syndrome. Infographic available for this article.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.