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Research Progress on the Mechanisms of Central Post-Stroke Pain: A Review

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Abstract

Central Post-Stroke Pain (CPSP) is a primary sequelae of stroke that can develop in the body part corresponding to the cerebrovascular lesion after stroke, most typically after ischemic stroke but also after hemorrhagic stroke. The pathogenesis of CPSP is currently unknown, and research into its mechanism is ongoing. To summarize current research on the CPSP mechanism and provide guidance for future studies. Use “central post-stroke pain,” “stroke AND thalamic pain,” “stroke AND neuropathic pain,” “post-stroke thalamic pain” as the search term. The search was conducted in the PubMed and China National Knowledge Infrastructure databases, summarizing and classifying the retrieved mechanism studies. The mechanistic studies on CPSP are extensive, and we categorized the included mechanistic studies and summarized them in terms of relevant pathway studies, relevant signals and receptors, relevant neural tissues, and described endoplasmic reticulum stress and other relevant studies, as well as summarized the mechanisms of acupuncture treatment. Studies have shown that the pathogenesis of CPSP involves the entire spinal-thalamo-cortical pathway and that multiple substances in the nervous system are involved in the formation and development of CPSP. Among them, the relevant receptors and signals are the hotspot of research, and the discovery and exploration of different receptors and signals have provided a wide range of therapeutic ideas for CPSP. As a very effective treatment, acupuncture is less studied regarding the analgesic mechanism of CPSP, and further experimental studies are still needed.

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Data availability is not applicable to this article as no new data were created or analyzed in this study

Abbreviations

ACC:

Anterior cingulate cortex

ACCGABA→Glu :

Anterior cingulate cortex GABA-containing neurons to glutamatergic neurons

ATP:

Adenosine triphosphate

BCAO:

Bilateral carotid artery occlusion

BDNF:

Brain-derived neurotrophic factor

CFA:

Complete Freund’s adjuvant

CPSP:

Central post-stroke pain

CXCR4:

C-X-C motif chemokine receptor 4

DHA:

Docosahexaenoic acid

EA:

Electroacupuncture

EETs:

Epoxyeicosatrienoic acids

EPA:

Eicosapentaenoic acid

ER:

Endoplasmic reticulum

GABA:

Gamma-aminobutyric acid

GABAaR:

Gamma-aminobutyric acid a receptor

GRP40:

Free fatty acid receptor 1 (FFA1)

HCN:

Hyperpolarization-activated cyclic nucleotide-gated

HIF-1α:

Hypoxia-inducible factor 1α

I/R:

Ischemia/reperfusion

IL-1β:

Interleukin-1β

ITAB:

Intra-thalamic autologous blood

ITC:

Intra-thalamic collagenase

LPA:

Lysophosphatidic acid receptors

MD:

Medial dorsal thalamus

MED1:

Mediator complex subunit 1

MT:

Medial thalamus

NLRP3:

NLR pyrin domain-containing 3

NOS:

Nitric oxide synthase

PEALut:

N-palmitoylethanolamide and luteolin

PFC:

Prefrontal cortex

PFGlu :

Parafascicular thalamic nucleus

PIT:

Photochemically induced thrombosis

POGlu :

Posterior thalamic nucleus

PUFA:

Polyunsaturated fatty acid

PWT:

Paw retraction threshold

S1Glu :

Primary somatosensory cortex glutamatergic neurons

SDF1:

Stromal cell-derived factor 1

sEH:

Soluble epoxide hydrolase

STT:

Spinal thalamic tract

TH:

Thalamic hemorrhage

THS:

Thalamic hemorrhagic stroke

TNF-α:

Tumor necrosis factor-α

TrkB:

Tropomyosin receptor kinase B

TRN:

Thalamic reticular nucleus

TSPO:

Translocator protein

UPR:

Unfolded protein response

VB:

Ventrobasal thalamus

VPL:

Ventral posterolateral

VPM:

Ventral posteromedial

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YC: collected and summarized the literatures and wrote the first draft of this review. JH and YC: were involved in the collection and arrangement of the literatures. BW: reviewed and revised the paper. All authors contributed to the final version of the manuscript.

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Correspondence to Bangqi Wu.

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Cheng, Y., Wu, B., Huang, J. et al. Research Progress on the Mechanisms of Central Post-Stroke Pain: A Review. Cell Mol Neurobiol 43, 3083–3098 (2023). https://doi.org/10.1007/s10571-023-01360-6

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