Pain

Cursory Statistics for Neuromusculoskeletal Pain

Upper extremity chronic pain is a dynamic condition with a multifactorial etiology and a poorly understood pathogenic mechanism. The most prevalent form of upper extremity pain is chronic shoulder and neck pain (cSNP), which affects 10-36% of the population at some point. cSNP can persist in the presence or absence of nociception and can arise from psychosocial factors along with neuroendocrine impairment, repetitive movement, forceful manipulation, constrained or contorted postures, and tissue and nervous system plasticity. Sensitization linked with chronic pain can cause patients to experience a degree of pain exceeding the observed pathology, meaning that for the nearly 25% suffering from cSNP, common therapeutic strategies may not be adequate. These observations help explain the nearly 50% of patients who experience a relapse following therapy.

Cause and Treatment of Neuromusculoskeletal Pain

cSNP is an interplay between peripheral and central neural pathways characterized by an increase in nociceptor sensitization to noxious stimuli, spontaneous neural discharges, neural inflammation, and sympathetic nervous system participation. Common treatment options include analgesic drugs, non-medication interventions such as physical therapy and behavioral modifications, electrotherapy, corticosteroid injections, and surgery. An interdisciplinary effort is often required to facilitate positive patient outcomes, for example, incorporating neural blockade with physical therapy or cognitive therapy. However, pain management is usually limited to the suppression of a single component found within the complex pain mechanism. An example is neural blockade, which interrupts afferent nociceptive activity, and although acutely effective, does not address the underlying causes of pain.

Although upper extremity pain is outlined in great detail, a wide-array of pain conditions demonstrate similar characteristics regarding how pain signals are initiated, transmitted, sustained, intensified, and treated.

Pain Pathway and Design of Treatments to Intervene Along Pathways

The pain pathway is divided into two pathways: the ascending and descending pathways. The ascending pathway involves the transmission of pain signal from the site of pain along neurons to the spinal cord and brain. The descending pathway is the transmission of a signal from the brain that either heightens or suppresses pain sensation. The ascending pathway involves the release of neurotransmitters (Substance P and glutamate) that, in turn, activate post-synaptic nerve cells. Pro-inflammatory cytokines activate nociceptors to release substance P and glutamate. Pain treatments commonly used to control or mitigate the ascending pain pathway include opioids, anti-inflammatory agents, and local anesthetics to interrupt nociception. Additionally, GABA neurotransmitters deactivate post-synaptic medications; therefore, medications like Lyrica and GABApentin are prescribed to suppress the ascending pathway. However, these treatments do not address the underlying cause of nociception.

The descending pain pathway involves the transmission of a signal from the brain that modulates the release of a neurotransmitter capable of affecting the activation of the post-synaptic nerve cell. Accordingly, medications like opioids, alpha-2 agonists, centrally acting analgesics, and anti-inflammatory agents are used to modulate chemical signals from the brain to mask pain sensation. Once again, failing to address cause of nociception, or in the case of the descending pathway, potential neuroplastic involvement.

Proper Treatment of Pain Requires a Comprehensive Approach

The cause of pain can be multifaceted and complicated, preventing the development and integration of an appropriate treatment strategy. However, there are basic elements, such as the reduction of pro-inflammatory cytokines and an increase in tissue regeneration components, that will certainly provide an effective therapeutic solution for a wide-array of pain-related conditions.


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