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Review
. 2021 May 31;9(6):624.
doi: 10.3390/biomedicines9060624.

Neural Plasticity in the Brain during Neuropathic Pain

Affiliations
Review

Neural Plasticity in the Brain during Neuropathic Pain

Myeong Seong Bak et al. Biomedicines. .

Abstract

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.

Keywords: anterior cingulate cortex; basal ganglia; neural plasticity; neuropathic pain; periaqueductal grey; primary somatosensory cortex.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Neural plasticity in four brain areas during neuropathic pain. Arrows up (↑) and down (↓) indicate ‘increase’ and ‘decrease’, respectively.

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References

    1. Raja S.N., Carr D.B., Cohen M., Finnerup N.B., Flor H., Gibson S., Keefe F.J., Mogil J.S., Ringkamp M., Sluka K.A., et al. The revised International Association for the Study of Pain definition of pain: Concepts, challenges, and compromises. Pain. 2020;161:1976–1982. doi: 10.1097/j.pain.0000000000001939. - DOI - PMC - PubMed
    1. Jensen T.S., Baron R., Haanpää M., Kalso E., Loeser J.D., Rice A.S.C., Treede R.-D. A new definition of neuropathic pain. Pain. 2011;152:2204–2205. doi: 10.1016/j.pain.2011.06.017. - DOI - PubMed
    1. Argyriou A.A., Bruna J., Marmiroli P., Cavaletti G. Chemotherapy-induced peripheral neurotoxicity (CIPN): An update. Crit. Rev. Oncol. Hematol. 2012;82:51–77. doi: 10.1016/j.critrevonc.2011.04.012. - DOI - PubMed
    1. Campbell J.N., Meyer R.A. Mechanisms of neuropathic pain. Neuron. 2006;52:77–92. doi: 10.1016/j.neuron.2006.09.021. - DOI - PMC - PubMed
    1. Brown M.J., Asbury A.K. Diabetic neuropathy. Annal. Neurol. 1984;15:2–12. doi: 10.1002/ana.410150103. - DOI - PubMed

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