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LBP Sensory system Physiology of LBP Low back pain (LBP) is one of the most common musculo-skeletal conditions that affect 84% of adult (Balague, 2012).In chronic LBP, the pain in the low back (lumbar) lasts for 3 months as Sue (Mostagi, 2015). Nociceptors are the specialized peripheral- sensorial form of neurons, which mediates pain sensation and provoke Sue to the potentialstimuli(compressioninlumbar-segment)inherskin.Thisoccursby transduction of the damaging- stimuli into the form of electrical signals, which were then transmitted (relayed) up to the higher centers of brain (Douglas, 2012). Nociceptorsarethereceptorsthatconsistofpseudo-formunipolar-primary somato-sensory neurons having their neuronal bodies that are located in the DRG (dorsal-root ganglion) (Allegri, 2016). These are bifurcated axons; peripheral-nerve branch innervates skin (causes acute tenderness in Sue) while the central-nerve branch synapses with 2nd-order neurons that are located in the spinal cordsdorsal horn which transmits pain to the mesencephalon & thalamus, then to somato-sensory & anterior- form cingulated-cortex so as to enable discrimination between sensorial and affective- cognitive pain features respectively (Dubin, 2010). As the irritating stimulus of chronic stress persists in Sue, the peripheral as well ascentralsensitizationoccursthatconvertsacutetochronicpainwithcentral protrusions. This central sensitization increases the excitability of CNS neurons that transforms normal inputs into abnormal responses causing acute tenderness in Sue (Allegri,2016,Nijs,2014).Minoralterationsinposture,chronicstresswithrich 1
LBP innervationsofA-deltanerve-fibersinthebones,ligaments,vertebral-discs,and vertebral- bones result in chronification of LBP in Sue (Allegri, 2016). Pharmacological actions of NSAIDS NSAIDs are commonly used to treat pain in musculoskeletal problems (Lewis, 2013). Sue’s history suggests that she has long-term LBP along with stiffness, acute- tenderness and protrusions in lower-back (L3- L4). NSAIDs are used as the front-line agents for pain relief because of their rapid action with increased drug tolerance which is needed in Sue’s condition (Yacobi, 2013). NSAIDS exert itstherapeutic-actions both locally at peripheral-inflammatory areas as well as centrally by inhibiting the synthesis and release of prostaglandins; although there is an effect on leukotriene production. The principal mode of action of NSAIDs is at the molecular level comprising of the inhibition of cyclooxygenase (COX) which is an enzyme that takes part in the arachidonic-acidcascadethatsynthesizesinflammatory-mediatorsofthe prostaglandins. COX has 2 iso-forms as COX-1 and COX-2 in which COX-2is better in its actions than COX-1 (Fig: 1) (Kuritzky, 2012).In Sue, the therapeutic-effects of NSAIDs occurs because of the therapeutic inhibition of COX-2(Yacobi, 2013). COX-2 is the principle pathway along which the conversion of arachidonic- acid into inflammatory prostaglandins takes place in Sue (that produces pain). Therefore, interrupting this pathway; an action that is common in all NSAIDs (aspirin) is the basis for relief of pain in Sue (Kuritzky, 2012).COX-2 is commonly accepted as an ‘inducible enzyme’, i.e., COX-2 is inactive when the stimuli (as inflammation) are absent. Hence, NSAIDS are used at a low dose and at short- time for pain relief in Sue with chronic LBP. 2
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