TY - JOUR
T1 - Stroke-Induced Central Pain
T2 - Overview of the Mechanisms, Management, and Emerging Targets of Central Post-Stroke Pain
AU - Mohanan, Anugeetha Thacheril
AU - Nithya, Sermugapandian
AU - Nomier, Yousra
AU - Hassan, Dalin A.
AU - Jali, Abdulmajeed M.
AU - Qadri, Marwa
AU - Machanchery, Shamna
N1 - Publisher Copyright:
© 2023 by the authors.
PY - 2023/8/4
Y1 - 2023/8/4
N2 - The incidence of stroke plays the foremost role in the genesis of central neuropathic pain. Central post-stroke pain (CPSP) is a central pain arising from a vascular lesion in the central nervous system that elicits somatosensory deficits, often contralateral to stroke lesions. It is expressed as continuous or intermittent pain accompanied by sensory abnormalities like dysesthesia and allodynia. CPSP remains de-emphasized due to the variation in onset and diversity in symptoms, besides the difficulty of distinguishing it from other post-stroke pains, often referred to as a diagnosis of exclusion. Spinothalamic dysfunction, disinhibition of the medial thalamus, and neuronal hyperexcitability combined with deafferentation in thalamocortical regions are the mechanisms underlying central pain, which play a significant role in the pathogenesis of CPSP. The treatment regimen for CPSP seems to be perplexed in nature; however, based on available studies, amitriptyline and lamotrigine are denoted as first-line medications and non-pharmacological choices may be accounted for cases intractable to pharmacotherapy. This review attempts to provide an overview of the mechanisms, existing management approaches, and emerging targets of CPSP. A profound understanding of CPSP aids in optimizing the quality of life among stroke sufferers and facilitates further research to develop newer therapeutic agents for managing CPSP.
AB - The incidence of stroke plays the foremost role in the genesis of central neuropathic pain. Central post-stroke pain (CPSP) is a central pain arising from a vascular lesion in the central nervous system that elicits somatosensory deficits, often contralateral to stroke lesions. It is expressed as continuous or intermittent pain accompanied by sensory abnormalities like dysesthesia and allodynia. CPSP remains de-emphasized due to the variation in onset and diversity in symptoms, besides the difficulty of distinguishing it from other post-stroke pains, often referred to as a diagnosis of exclusion. Spinothalamic dysfunction, disinhibition of the medial thalamus, and neuronal hyperexcitability combined with deafferentation in thalamocortical regions are the mechanisms underlying central pain, which play a significant role in the pathogenesis of CPSP. The treatment regimen for CPSP seems to be perplexed in nature; however, based on available studies, amitriptyline and lamotrigine are denoted as first-line medications and non-pharmacological choices may be accounted for cases intractable to pharmacotherapy. This review attempts to provide an overview of the mechanisms, existing management approaches, and emerging targets of CPSP. A profound understanding of CPSP aids in optimizing the quality of life among stroke sufferers and facilitates further research to develop newer therapeutic agents for managing CPSP.
KW - central post-stroke pain (CPSP)
KW - disinhibition
KW - dysesthesia
KW - neuronal hyperexcitability
KW - neuropathic pain
KW - pharmacotherapy
KW - somatosensory deficits
KW - spinothalamic dysfunction
KW - stroke
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UR - https://www.mendeley.com/catalogue/22e09b50-94b2-3f55-adca-a18441922173/
U2 - 10.3390/ph16081103
DO - 10.3390/ph16081103
M3 - Review article
C2 - 37631018
AN - SCOPUS:85168908254
SN - 1424-8247
VL - 16
JO - Pharmaceuticals
JF - Pharmaceuticals
IS - 8
M1 - 1103
ER -