The past three decades have witnessed increasing interest in strategies to improve neurologic function after spinal cord injury. As progress is made in our understanding of the pathophysiologic events that occur after acute spinal cord injury, neuroprotective agents are being developed
Clinicians who treat acute spinal cord injuries should have a basic understanding of the pathophysiologic processes that are initiated after the spinal cord has been injured. A familiarity with the literature on which the current use of methylprednisolone is based is also essential.
Literature review.
Literature review of animal data on pathophysiologic mechanisms, and of both animal and human trials of neuroprotective agents.
The mechanical forces imparted to the spinal cord cause primary damage to the neural tissue, but a complex cascade of pathophysiologic processes that imperil adjacent, initially spared tissue to secondary damage rapidly follows this.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes . Attenuating this secondary damage with neuroprotective strategies requires an understanding of these pathophysiologic processes. Many researchers are investigating the role of such processes as ischemia, inflammation, ionic homeostasis and apoptotic cell death in the secondary injury cascade, with hopes of developing specific therapies to diminish their injurious effects. Beyond methylprednisolone, a number of other pharmacologic treatments have been investigated for the acute treatment of spinal cord injury, and even more are on the horizon as potential therapies.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
This review summarizes some of the important pathophysiologic processes involved in secondary damage after spinal cord injury and discusses a number of pharmacologic therapies that have either been studied or have future potential for this devastating injury.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
A 58-year-old obese white male presents to ED with chief complaint of fever, chills, pain, and swelling in the right great toe. He states the symptoms came on very suddenly and he cannot put any weight on his foot. Physical exam reveals exquisite pain on any attempt to assess the right first metatarsophalangeal (MTP) joint. Past medical history positive for hypertension and Type II diabetes mellitus. Current medications include hydrochlorothiazide 50 mg po q am, and metformin 500 mg po bid. CBC normal except for elevated sedimentation rate (ESR) of 33 mm/hr and C-reactive protein (CRP) 24 mg/L. Metabolic panel normal. Uric acid level 6.7 mg/dl.
Neurologic and Musculoskeletal Pathophysiologic Processes
Concerning the patient’s presenting symptoms, it is highly likely that he has gouty arthritis. Inflammatory reaction due to the deposition of monosodium urate (MSU) crystals into the joints causes this diagnosis type. Gouty arthritis commonly occurs in patients with hyperuricemia. Components of the innate immune system drive the inflammation induced by MSU (Wilson & Saseen, 2016). The innate immunity normally provides with the initial nonspecific immune response against the invading pathogens. The synovial phagocytic cells engulf the MSU crystals deposits, leading to an inflammatory process involving chemokines, lysosomal enzymes, and other mediators. The cytokines released within the joint produce signals to the brain. The brain then processes sickness-related symptoms such as fever.Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .
The key inflammatory mediators or players of the immune response involved in gouty arthritis’s pathophysiology include IL-1β. Interleukin 1 regulates cell proliferation, differentiation, and apoptosis. IL-1β is a pro-inflammatory cytokine, which signals other cell types to promote inflammation (Cleophas et al., 2017). IL-1β leads to the expression of a number of inflammatory mediators. Case Study Analysis On Neurologic and Musculoskeletal Pathophysiologic Processes .The inflammatory mediators are directly responsible for neutrophil influx into the patient’s first metatarsophalangeal (MTP) joint synovium. The entrance of neutrophils into the joint fluid is the hallmark of gouty arthritis. Over time, repeated flares of gouty arthritis are accompanied by inflammation can cause pathologic joint damage. Tophi emerge from the inflammation and repeated deposition of the MSU crysta
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