The PMCS category nociceptive: inflammatory is described in terms of nociception and inflammation. Nociception is the ability to detect harm from stimuli in the nervous system. That harm can be actual or potential. When actual harm occurs, the detection or response at the neuronal level can occur based on pressure, temperature, and chemical factors.^12,13

Mechanical factors may be mediated secondary to pressure sensitivities based on increasing or prolonged tissue deformation. Chemical pain may involve inflammatory processes that cause a baseline level of irritation in the tissues. When chemical pain is present, there is a constant, unchanging level of irritation in the tissue. Chemical pain requires the use of chemicals such as medications to reduce the symptoms and presenting pathology. Medications during this stage can include anti-inflammatory medications, oral nonsteroidal medications, oral steroids, or potentially more invasive steroid injections into the tissue. Mechanical pain can be constant but can have varying intensities. Mechanical pain will alter and improve with changes in movements and positioning. Once the clinician performs a traditional mechanical repeated movement exam of the tissue in question, he or she will find that in a chemical pain state most movements will make the pain worse. A mechanical inflammatory pain mechanism will present with a preferred direction and signs of centralization or localization of symptoms. Mechanical pain may have a movement-based cause or solution to a pain problem, indicating the need to prescribe movements in a direction of preference and protective strategies in the direction of worsening. Patient education regarding the condition is important. How symptoms change location and improve will be imperative to the success of a mechanical pathology. This can determine success of the mechanical reduction, maintenance of the reduction, and prevention of a future reoccurrence. In order to differentiate chemical and mechanical nociceptive inflammatory pain, the clinician will need expertise in clinical reasoning, history-taking, and a mechanical examination.^11,12,13 When reflecting on directional preference and patient exercise, it is important to utilize appropriate clinical reasoning because the wrong direction can quickly worsen patient presentation.¹⁴

The PMCS category nociceptive: ischemia is described in target tissues as a result of mechanical and physiologic processes of both noninjured and injured tissues that stimulate high-threshold primary afferent C and A-δ fibers.^15,16 Ischemia can involve a deprivation of necessary circulation and potential hypoxia in the tissues. Ischemic tissue will require remodeling and the need to address the underlying cause or interruption of the current state of restricted blood flow or prolonged inactivity.¹⁵ Movement in an ischemic state involves proper patient education and is active care dosage and intensity dependent, especially when adaptive shortening is present. Typically, in this state the active care intently produces and increases the symptoms during the exercise in an effort to remodel the tissue to greater extensibility, strength, or restoration of functional ability. When ischemia is the dominating mechanism, the therapeutic intervention needs to be aggressive, or there is a risk that active care has no effect on the symptoms. In addition, patient education needs to support the intensity and expectation of pain with exercise. The practitioner should acknowledge pain and range of motion guidelines. The patient needs to understand that during healing times and early repair phases, tissues and symptoms may be more irritable. If movement is excessive for the tissue’s repair tolerance, then chemical inflammation may be triggered. If movement is too weak in remodeling, a weak scar may continue to be sensitized to movement. If movement does not occur frequently enough or with enough force, there may be no change in the tissues to introduce necessary healing. In the nociceptive ischemia pain mechanism, patient education is critical for rehabilitation success. The message with patient education and the ischemic pain mechanism should be that exercise that produces, or increases, pain but remains no worse as a result and there is no resulting change in range of motion is always good. This presentation is regardless of the various subclassification names that may have been given (dysfunction, tendinopathy, etc.).

The PMCS category peripheral neurogenic is related to the neural tissue outside the dorsal horn. This tissue terminates in nerve terminal branches. The resultant symptoms that occur are derived from alterations in nerve structure, function, conduction, and dynamics. These neural tissues can be related to the actual associated trauma or disease of the peripheral nerves, excessive pressure, tension, or associated entrapment of the container surrounding the nervous tissue.¹⁷ In the peripheral neurogenic pain mechanism, often the nerve is the victim, and the culprit is the adjacent connective tissue that surrounds and traps the nerve, resulting in neurogenic-type symptoms. In this type of neurogenic mechanical dysfunction, the focus of care is restoring the surrounding tissue balance to movement and using neurodynamic slider movements to encourage an enhanced relationship to movement locally with the associated nerve and surrounding tissue. The other type of neurogenic mechanical dysfunction involves the nerve as the victim and the culprit; the nerve itself needs to be remodeled to greater extensibility, loading properties, and functional ability. Please refer to Chapter 22 in for further review.¹⁸ Patient education in this mechanism is similar to the ischemic pain mechanism. There will be an emphasis on patient education, and the respective exercise should produce symptoms in order to drive remodeling of the nerve’s mobility and dynamics. The focus on neurodynamic exercise will be on increasing tension at multiple links that are involved in the extremity, especially the areas that have a symptom presentation. The practitioner should be able to direct the neurodynamic exercise movements by producing the symptoms in specific peripheral and cutaneous nerves.

The PMCS category central sensitization is related to heightened pain sensitivity and the altered cognition and interpretation of the nociceptive signal occurring in the CNS. The patient’s pain alarm system in the brain and spinal cord presents with an overprotective mode related to the altered cognitive processing. Altered processing may be related to cognitive domains such as negative and catastrophic words, thoughts, and beliefs related to the pain experience and the potential threat of the injury. In chronic musculoskeletal conditions, central mechanisms may dominate the maintenance of symptoms to a greater extent than peripheral nociception, especially if symptoms persist beyond normal connective tissue healing time frames.^16,17 It is unclear what physiologically manifests central sensitization or why some may be more prone to sensitization than others; however, research is emerging that may describe some genetic components that can be heightened by worries, stress, concerns, and beliefs.^19,20 The intervention for central sensitivity is highlighted by patient education regarding neurologic pain mechanisms. The positive focus regarding this condition will be on the need to correct and interpret the catastrophic thoughts. Patient education should promote confidence and competence in understanding the analysis of “movement safe pain” for correct interpretation of nociceptive signals. Patients must be held accountable to applying this education in their everyday life. Active care is focused on gradual exposure to fear avoidant movement, work or physical activities, functional or pleasurable life events and reestablishing the normal mode in the pain alarm system circuitry.