Ifeanyi Igboaka

Chronic back pain is a common medical condition that affects millions of patients throughout a variety of age ranges. Common causes of back pain include nonspecific pain or muscle strain, herniated disk, spondylolysis, scoliosis, and Scheuermann’s kyphosis (1). With chronic back pain, along with other chronic disease states, the debilitating side effects of these conditions can make daily activities very difficult to complete. Excitatory neurotransmitters, such as dopamine, can play a part in how well one can tolerate back pain. The midbrain dopamine center comprises a key network for reward, salience, motivation, and mood (6). Evidence from various clinical and preclinical settings points to the midbrain dopamine circuit as an important modulator of pain perception and pain-induced anxiety and depression (6).

Patients dealing with low back pain all have various profiles that play into the tolerance of their pain, how long flare-ups last, and the specific area of their pain. Most chronic low back pain includes elements of nociceptive pain, neuropathic pain, and nonorganic pain (2). One element that’s a key factor in regards to the intensity of chronic back pain is the amount of dopamine circulating in the body. Research on pain areas using functional magnetic resonance imaging (fMRI) and positron emission tomography has shown that the dopamine system contributes to the pathology of chronic low back pain (2). Dopamine regulation involves a complex number of systems and dysfunction of these systems can cause a variety of health issues long term. The mesolimbic system, a neural circuit, delivers dopamine from the ventral tegmental area to neural structures such as the nucleus accumbens, prefrontal cortex, anterior cingulate cortex, and amygdala (4). Chronic pain patients suffer from low dopamine production and delivery in this system(4).

Dopamine in the nucleus accumbens is critical for reward and motivation, including the reward from pain relief, thus targeting reward/motivation circuits could be used for pain modulation (5). In healthcare, there are a multitude of treatments that are used to help alleviate chronic low back pain. Treatment needs and considerations vary between each patient, but treatment options can include medications such as tylenol, ibuprofen, opioid analgesics, and non-pharmacological treatments such as ice packs and exercise. Dopamine regulation can affect how well cellular receptors respond to pain treatment. Crucially, activity-reducing mutations in dopamine-clearing genes, such as COMT (catechol-O-methyltransferase), also appear to modify pain sensitivity by changing functional responses of μ-opioid receptors in the nucleus accumbens and other pain modulating circuits (3). Such maladaptation may ultimately impact pain tolerance and affective states (3). Dopamine regulation plays a key factor in how each individual tolerates pain. Thankfully, an abundance of treatment options are available to help patients improve the quality of their lives.

Reviewed by: Ishtiak Ahmed Chowdhury (Scientific Writing Team Lead)

Sources:

  1. Bernstein RM, Cozen H. Evaluation of back pain in children and adolescents. Am Fam Physician. 2007 Dec 1;76(11):1669-76. PMID: 18092709.
  • Shin-ichi Konno, Miho Sekiguchi, Association between brain and low back pain, Journal of Orthopaedic Science, Volume 23, Issue 1, 2018, Pages 3-7, ISSN 0949-2658
  • Serafini, R. A., Pryce, K. D., & Zachariou, V. (2020). The Mesolimbic Dopamine System in Chronic Pain and Associated Affective Comorbidities. Biological psychiatry87(1), 64–73
  • Yang S, Boudier-Revéret M, Choo YJ, Chang MC. Association between Chronic Pain and Alterations in the Mesolimbic Dopaminergic System. Brain Sciences. 2020; 10(10):701
  • Li C, Liu S, Lu X, Tao F. Role of Descending Dopaminergic Pathways in Pain Modulation. Curr Neuropharmacol. 2019;17(12):1176-1182. doi: 10.2174/1570159X17666190430102531
  • Mitsi, Vasiliki, and Venetia Zachariou. “Modulation of pain, nociception, and analgesia by the brain reward center.” Neuroscience vol. 338 (2016): 81-92. doi:10.1016/j.neuroscience.2016.05.017
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