David Rosenblum, MD Garden City and Brooklyn Pain Physician, world renown for his work on the PainExam Podcast, PainExam Pain Management Board Review and NRAP Academy's Continuing Medical Education Programs discusses Central post-stroke pain (CPSP).

Central Post Stroke Pain is a debilitating condition that affects a significant number of stroke survivors. It is characterized by persistent neuropathic pain, often described as burning, shooting, or electric shock-like sensations, in the areas of the body affected by the stroke. CPSP can significantly impact a patient's quality of life and functional recovery, making it crucial for physicians to have a comprehensive understanding of its pathophysiology.

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Neuropathic Pain and Central Sensitization:CPSP is classified as a neuropathic pain syndrome, which means it arises from a dysfunction or damage to the nervous system. The exact pathophysiology of CPSP is complex and multifactorial, but it often involves the phenomenon of central sensitization. Central sensitization refers to the increased excitability and responsiveness of neurons within the central nervous system (CNS) in response to peripheral input.

Cortical Reorganization and Plasticity:

One key aspect of CPSP pathophysiology is cortical reorganization and plasticity. Following a stroke, the brain undergoes structural and functional changes as a result of the injury. This neuroplasticity, particularly in the somatosensory cortex, can contribute to the development of CPSP. Maladaptive plasticity may occur, leading to abnormal sensory processing and the generation of pain signals in response to non-painful stimuli.

Disrupted Pain Modulation Pathways:The pain perception and modulation pathways in the CNS play a crucial role in regulating pain signals. In CPSP, these pathways can be disrupted, leading to abnormal pain processing. Alterations in the descending inhibitory pathways, such as reduced inhibitory neurotransmitter release or impaired endogenous opioid system function, can result in increased pain sensitivity and the persistence of pain signals even after the resolution of the initial injury.

Inflammatory Processes and Neurotransmitter Imbalances:Inflammation within the CNS and imbalances in neurotransmitter systems also contribute to CPSP. Following a stroke, there is an inflammatory response that involves the release of pro-inflammatory cytokines and activation of immune cells. This inflammation can lead to sensitization of nociceptive neurons and exacerbate pain signaling. Additionally, imbalances in neurotransmitters, such as glutamate, serotonin, and norepinephrine, may disrupt the normal pain processing pathways, further amplifying pain perception.

Peripheral and Central Lesions:CPSP can arise from both peripheral and central lesions. Peripheral lesions, such as damage to the spinothalamic tract or thalamus, can directly affect the transmission of pain signals. Central lesions, on the other hand, involve damage to the somatosensory cortex, thalamus, or other brain regions involved in pain processing. Both types of lesions can contribute to the development of CPSP through various mechanisms, including altered neuronal activity, disrupted connectivity, and aberrant sensory processing.

The complex interplay of cortical reorganization, disrupted pain modulation pathways, inflammatory processes, and peripheral and central lesions contribute to the development and persistence of CPSP. Further research is needed to unravel the intricacies of CPSP's pathophysiology, leading to the development of targeted therapies to alleviate the burden of this debilitating condition.

References

Liampas, A., Velidakis, N., Georgiou, T. et al. Prevalence and Management Challenges in Central Post-Stroke Neuropathic Pain: A Systematic Review and Meta-analysis. Adv Ther 37, 3278–3291 (2020). https://doi.org/10.1007/s12325-020-01388-w

SYSTEMATIC REVIEW article Front. Neurol., 18 August 2021Sec. Stroke Volume 12 - 2021 | https://doi.org/10.3389/fneur.2021.678198