Journal
BIOMEDICINES
Volume 9, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/biomedicines9060624
Keywords
neuropathic pain; neural plasticity; primary somatosensory cortex; anterior cingulate cortex; periaqueductal grey; basal ganglia
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Funding
- National Research Foundation of Korea (NRF) [NRF-2017M3A9E4057926]
- National Research Foundation of Korea [2017M3A9E4057926] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Neuropathic pain is a chronic pain caused by damage to the somatosensory nervous system, and it is essential to fully understand the pathological mechanisms in order to develop efficient therapeutic methods. Neural plasticity in the brain plays a critical role in the development and maintenance of neuropathic pain, and recent technological advances allow for more precise understanding and modulation of brain activity to reverse pain states.
Neuropathic pain is an intractable chronic pain, caused by damage to the somatosensory nervous system. To date, treatment for neuropathic pain has limited effects. For the development of efficient therapeutic methods, it is essential to fully understand the pathological mechanisms of neuropathic pain. Besides abnormal sensitization in the periphery and spinal cord, accumulating evidence suggests that neural plasticity in the brain is also critical for the development and maintenance of this pain. Recent technological advances in the measurement and manipulation of neuronal activity allow us to understand maladaptive plastic changes in the brain during neuropathic pain more precisely and modulate brain activity to reverse pain states at the preclinical and clinical levels. In this review paper, we discuss the current understanding of pathological neural plasticity in the four pain-related brain areas: the primary somatosensory cortex, the anterior cingulate cortex, the periaqueductal gray, and the basal ganglia. We also discuss potential treatments for neuropathic pain based on the modulation of neural plasticity in these brain areas.
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