Both peripheral and central mechanisms have been identified as contributing to endogenous analgesia during inflammation. These endogenous analgesic compounds include opioid peptides, endocannabinoids, somatostatin, and anti-inflammatory cytokines. The activation of peripheral nociceptive C and Aδ fibers of primary afferent neurons, Neurogenic pain/inflammation Neurogenic inflammation describes the inflammatory response observed following the release of proinflammatory mediators from peripheral terminals of activated primary (afferent) sensory neurons. Mechano-insensitive, but heat- and chemo-sensitive, C nociceptors are responsible for the neurogenic vasodilation in human skin. These sensory receptors ending in the dorsal horn of the spinal cord release neurotransmitters and neuromodulators in response to peripheral noxious stimuli. As a result of local depolarization, the nociceptive sensory neurons release proinflammatory mediators in the periphery, which produce vasodilatation and edema. They can recruit and activate immune cells as well as adaptive immune cells, which, together with the mediators released from the immune cells, participate in the phenomenon of neurogenic inflammation. Calcitonin gene-related peptides, substance P, and several other neuropeptides are the main mediators responsible for the sequence of pathogenic events leading to neurogenic inflammation (Mangus et al., 2022). The stimuli influencing Case study 3 Zain started a career life earlier than an average Canadian living in Calgary. At just 25 years of age, he competed in and won three different national championship slams in Rugby. In every state of the country, his story—much too high levels of commendations—is shared proudly in different youth boot camps of nearly every sports scouting event. The ‘Headbull,’ as he is proudly called, Zain had gained national prominence after signing for the Fluminense Rugby Team as an up-field attacker in 2013. With the demand of his role of play, he is expected to make aggressive over-the-top runs at a charging barrage of opponent lines. He is well known for his signature ‘bull-them-all’ runs executed as a daring charge through the opponent lines using the head and an overly flexed shoulder positioning. Not only has this move gained him prominence in the National Rugby League, but it has also won him numerous ‘Player of the Match’ and ‘Player of the Tournament” awards. Safe to say, Zain enjoyed an early rugby career in glitz, fame, and glamour. However, this would not last forever, at least not for the length of his playing career that abruptly ended in 2018—5 years after his debut as a senior rugby player. Zain’s injury woes all started in June 2017, when Zain was stretchered off the field of play for a tackle he received from an opposition defender. Although cleanly executed, the tackle appeared to have immobilized Zain. He had groaned in pain and immediately complained about a ‘painful tingling sensation running through the neck to the back.’ First aid assistance on the field could not help, and he was stretchered off for special medical care. He would return to open play 4 months later after missing 10 championship games. However, his posture had changed, he made fewer executions of his signature run, and most importantly he changed from an up-field attacking role to a wide-receiver role. This new role significantly influenced his style of play. However, 6 months after the first incident, Zain sustained another injury to the back causing him to limp off the
by several proinflammatory mediators such as histamine, serotonin, H+, and cytokines, gives rise to action potentials that are conducted to the dorsal horn of the spinal cord (Castroman et al., 2022). Subsequently, through several neuronal pathways, the nociceptive information can reach the higher brain centers, including the thalamus and cortex. neurogenic inflammation activate the transient receptor potential (TRP) ion channels and the purinergic (P2X) receptors, which play a crucial role in the development of inflammation and the perception of pain. Therefore, ligands to these receptors or drugs able to counteract proinflammatory molecules may represent promising avenues in the management of inflammatory pain. Recent evidence suggests that triggering the combined actions of neurons and immune/vascular cells in the central nervous system (CNS) may be associated with neuronal activity, exhibiting a profile similar to other neuroinflammatory states. The term “neurogenic neuroinflammation” was then proposed to define inflammatory responses triggered by neuronal activity in the CNS. It was postulated that neurogenic neuroinflammation might have useful effects associated with regeneration processes (Manchikanti et al., 2020). In this context, maladaptive responses may arise when neurogenic neuroinflammation persists or spreads, becoming markedly relevant in conditions such as pain or epilepsy. field of play. About 2 weeks later, he was diagnosed with fibromyalgia, chronic back pain, and hypertension. Physical examination and vitals Zain reported primary pains radiating from the neck to the lower back. A pain assessment was consulted to fully understand the level of sensation he had and the severity over different locations and ranges of movement. He self-reported his pains on a 10-point scale by life impacts starting from muscle and skeletal pains to soft tissue pains. The Fluminense medical team documented his report as follows: ● Upper back pains: life impact rank 8 out of 10. A year before the first incidence, he had experienced radiating upper back pain and was relieved by opioids. ● Bilateral hip pains: life impact rank 7 out of 10. ● Lumbar pains: life rank of 8.5 out of 10. ● Radiological examinations suggest progressive degeneration of the sacroiliac joints and a moderate multilevel fate arthropathy. On lumber epidural, the pain was significantly reduced, and Lidocaine patches also helped. ● Shifting musculoskeletal pains: life impact of 8 out of 10 with pain sensations radiating from the gluteals to the deltoids. Pain complication report On further questioning, the medical team identified some lifestyle problems that might have negatively impacted Zain’s fibromyalgia and his road to recovery: ● Smoking: Zain’s smoking habit is well known. Over the past 2 years, he had reportedly consumed tobacco at levels more than the average Norway smoker. ● Insomnia: with a poor sleep habit, Zain has developed insomnia for ‘the longest of times he could remember.” ● Sedentary lifestyle: With the exemption of his rugby career, Zain lived a largely sedentary lifestyle, rarely going out and walking less than 5,000 steps on most days.
Book Code: PYCA2725
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