As described in last month’s newsletter, acute tissue injury involves an orchestrated influx of inflammatory cells and resident stem cells in a series of events to restore tissue homeostasis. However excessive (prolonged or chornic) activation of these mediators leads to fibrosis and neurodegenerative dysfunction resulting in long-term ‘pain states’. In this issue, I will discuss science of acute to chronic injury as well as how we perceive and interpret pain. My goal is to educate you on the differences and to give hope to pain relief in order to return to the activities that you love.
Approximately 80% of physician visits (I would say 99% for PT) are for pain-related complaints and approximately 20% of the adult population lives with ‘severe chronic pain’. That said the high prevalence of reported pain in the developed world has large scale impacts on social, economic, and medical systems. As pain is a subjective com-plaint, individuals should not compare their own perception of pain to that of someone else. Likewise as a provider I cannot rate your pain or compare you pain to someone else. Here in lies not only the physical but the psychological concepts of pain perception and interpretation. This is referred to as the ‘biopsycolsocial model’ of pain. As both acute and chronic pain is influenced by and interacts with physical, emotional, psychological, and social factors. This framework is frequently applied in clinical practice.
Acute injury and pain is most often summarized by a specific mechanism of injury; i.e. sprain, strain, fracture, or even surgical intervention. Pain sensation varies according to the intensity, quality, and duration of stimulus. Acute injury involves an insulting stimulus followed by tissue inflammation, and remodeling. Pro-inflammatory biomarkers are released in response to tissue injury (cell death). These cells that function to clean up and repair damaged tissue also stimulate sensory nerves which send signals to both the spinal cord and brain to create a heightened awareness to limit further injury. These pain receptors (aka nociceptors) are present in the skin, muscle, joints, and viscera. The density of nociceptors allows for the differentiation of sensory information. Nocioceptors respond to: single or combinations of stimuli – mechanical, temperature, and chemical – and in situations of trauma a combination of substances create the ‘inflammatory cocktail’
In cases where we haven’t allowed our injured tissue to fully recover, usually by overtraining or inadequate recovery time tissue remodeling is disorganized and can become sensitized creating a lowered threshold for activation. This by creating a lowered threshold our pain receptors can be activated by a stimulus that is normally harmless; such as pain with the light touch of clothing. In those with chronic pain conditions alterations in neural connectivity, and morphological, and biochemical changes in the brain’s ‘pain matrix’ have been reported. In a normal environment where the body is able to maintain homeostasis the pain matrix of the brain can amplify or attenuate noxious stimuli. However consequence prolonged peripheral sensitization can result in hypersensitivity of the central nervous system may that no longer directly reflects a painful stimulus; this is referred to as Central Sensitization. Now we can see how an acute injury that’s left untreated can lead to dysfunctional tissue repair at the local level and over time can lead to neural changes in the spine and brain’s perception of pain.
Case Example: Ordinary ankle sprain → continue training w/ pain → change in stride length and foot strike → altered muscle activation along the kinetic chain from foot to spine → increased lumbar paraspinal tone → lower back pain, hypersensitivity → changes in perception of back, hip, and leg pain facilitating a feedback loop of dysfunction
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