Pain is a feeling that is caused by provocative stimuli. It is interpreted by the brain after nociceptive stimulation at a peripheral site. Pain can either be classified according to the International Association For the study Of Pain or the Woolf classification. The IASP classification categorizes pain on the following characteristics: region of the body involved, the duration and pattern of pain, the intensity, timing and its etiology. (IASP, 2011) The Woolf classification categorizes pain as inflammatory, nociceptive or pathologic. (Woolf C., 2010)
The genesis of lower back pain and its perception occurs through the peripheral, transmission and integration stages. (Motoc D et al, 2010) The peripheral stage entails tissue damage that is caused by mechanical stimuli such as disc herniation and is thereafter followed by the release of pain releasing chemicals. The stimulus activates poly modal receptors that are innervated by type C fibers. In the transmission stage, the sensation is transmitted by substance P which is the main neurotransmitter in Type C fibers. The sensation is then transmitted to the dorsal horn of the spinal cord from the receptors and ascends to the sensory cortex of the brain via the ascending spinothalamic tracts (Motoc D et al, 2010). The integration stage takes place at the sensory cortex and the limbic system. It is at this level that the brain facilitates flexion responses, behavioral responses and pain learning and memory. It is the integration stage that makes Mrs. Pru go to the outpatient department to seek treatment and how he has modified his lifestyle to live with the back pain.
Reasons for Reduced Level of Nociception
Mrs.Pru has been on Vitamin D and over the counter calcium supplements. Recent studies have shown a direct correlation between hypovitaminosis D and progressive lower back pain. (Hoffmeister E 2016) Vitamin D is key to calcium metabolism and homeostasis. Vitamin D has the net effect of increasing intestinal absorption of calcium. Calcium is the active mineral in bones and is vital in osteogenesis. Hypovitaminosis D and low calcium levels in the body lead to weak vertebral bones that are prone to fractures. Fractures exacerbate bone pain. Both Vitamin D and calcium supplementation may alleviate the back pain from severe back pain to mild pain.
Hypothyroidism which refers to decreased thyroxin production by the thyroid gland causes muscle pain and stiffness. (Cannone J, 2011) Recent research has shown a relationship between hypothyroidism and fibromyalgia. Fibromyalgia presents as knee pain, back pain and neck pain. Mrs. Pru has been on levothyroxine sodium for the probable treatment of hypothyroidism meaning that the back pain in this particular case may be reduced.
Recent findings have shown an association between smoking and chronic low back pain. (Shiri et al, 2010) Smoking causes reduced circulating levels of estrogen in both men and women .Estrogen facilitates calcium mobilization into the bones. Thus, individuals who smoke have thinner bones because less calcium is directed to osteogenesis. In addition, smoking increases the risk of developing fractures. The fact that Mrs. Pru does not smoke reduces the severity of the lower back pain. The same studies have shown that the association is greater in adolescents than in adults.
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Moshumi, L. (2015, June 24). Study finds link between vitamin D deficiency and chronic low back pain. Retrieved from https://www.vitamindcouncil.org/study-finds-link-between-vitamin-d-deficiency-and-chronic-low-back-pain/
Motoc, D., Turtoi, N. C., Vasca, V., Vasca, E., & Schneider, F. (2010). PHYSIOLOGY OF PAIN – GENERAL MECHANISMS AND INDIVIDUAL DIFFERENCES. Jurnal Medical Aradean, 12(4), 22.
Nih.gov. (2016, May). Smoking and Bone Health | NIH Osteoporosis and Related Bone Diseases National Resource Center. Retrieved from https://www.bones.nih.gov/health-info/bone/osteoporosis/conditions-behaviors/bone-smoking
Shiri R , et al. (2010, January). The association between smoking and low back pain: a meta-analysis. – PubMed – NCBI. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/20102998
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