A3 Musculoskeletal Pain

Topic

Musculoskeletal pain originates primarily from elevated tissue pressure: when pressure on the tissue surrounding nociceptors increases, these nociceptors are activated and generate the signal for musculoskeletal pain.

In addition to elevated tissue pressure, mechanical deformation of nociceptors directly activates them, generating musculoskeletal pain even when tissue pressure has not increased.

When inflammation is present in the tissue, the activation threshold of nociceptors is lowered: pressure or deformation stimuli that were previously insufficient to activate them now do so; thus, inflammation amplifies the musculoskeletal pain caused by elevated tissue pressure and mechanical deformation of the nociceptors.

Alongside these three peripheral mechanisms, central sensitization further amplifies musculoskeletal pain. Within the central nervous system, neurons receiving signals from nociceptors become progressively more sensitive to those signals, such that a constant peripheral input produces an increasingly intense perception of musculoskeletal pain.

Once generated, musculoskeletal pain inhibits muscle activation: it reduces the signal the nervous system sends to the muscle to contract, and this inhibition diminishes the muscle's capacity to generate force and torque, resulting in muscle weakness.

In addition to inhibiting muscle activation, musculoskeletal pain alters the motor controller that regulates movement: it modifies the controller's proportional term—which corrects movement based on the deviation from the expected trajectory—and also modifies the derivative term, which corrects movement based on the rate at which that error changes. By altering both terms, musculoskeletal pain causes the motor controller to produce compensatory movement patterns that avoid loading the painful area. These compensatory movement patterns redistribute mechanical load to other structures and reduce the use of muscles affected by musculoskeletal pain, thereby perpetuating and maintaining the previously described muscle weakness. In turn, this same muscle weakness forces neighboring structures to withstand greater tissue pressure and increased mechanical deformation of nociceptors than they would under normal conditions, thus reinforcing the peripheral mechanisms that generate musculoskeletal pain and closing the weakness-pain-compensation cycle.

ID:503