Pain Mechanism Classification System Overview and Focus on the Motor/Autonomic Mechanism

Pain Mechanism Classification System Overview and Focus on the Motor/Autonomic Mechanism

Annie O’Connor

Melissa C. Kolski

Pain Mechanism Classification System Allows for Central Nervous System Subgrouping

Chronic pain is a leading source of worldwide disability and a cause of staggering health care costs. Advances in imaging technology over the past decade have enabled the observation of brain properties in chronic pain conditions. Studies from various patient cohorts now show that chronic pain is not just correlated with nociceptive processes, but also associated with brain functional and anatomical changes.

Pain Mechanism Classification System Categories

Pain is a continuum with differing mechanisms and dimensions of pain. A problem occurs when isolated views of structure or patho-anatomy are considered in determining the diagnosis, staging the disorder, deciding appropriate treatment, and predicting outcomes.1 This may lead to overutilization of resources, improper diagnoses, ineffective interventions, and poor patient outcomes.2,3,4,5 In musculoskeletal pain conditions, goal setting and outcome measures play a critical role in allowing practitioners the evaluative tools to demonstrate change to patients and third party payers. Communication and appropriate patient education can be a critical intervention once mechanisms are identified as dominating.

In 1987, Gifford and Butler6 presented a pain mechanism classification system (PMCS) into clinical practice, differentiating six common pain mechanisms. At the Shirley Ryan AbilityLab (formerly the Rehabilitation Institute of Chicago), the use of this system in relation to patient outcomes and internal training programs has been investigated. Currently, the observed phenomenon of decreased health care resource utilization and better outcomes in patients who are seen by therapists trained in the classification system has been demonstrated in clinical practice.

PMCS has been introduced into the diagnostic process for pain practitioners.7,8,9,10 The clinical indicators of nociceptive, peripheral neuropathic, and central mechanisms have been used to classify patients’ reports of pain.9,10 Theoretical support exists for the PMCS; however, the empirical evidence to support the use of the system to facilitate consistency in decision-making is still in the process of validation.

The PMCS represents the pain continuum from peripheral mechanisms of mechanical nociception to central mechanisms within the limbic brain, including the amygdala, hippocampus, and frontal and somatosensory cortex regions. Six fundamental mechanisms make up the system.

The peripheral categories of the PMCS are as follows:

  • Nociceptive: inflammatory

  • Nociceptive: ischemia

  • Peripheral neurogenic

The central categories of the PMCS are as follows:

  • Central sensitization

  • Affective

  • Motor/autonomic

Patients can have multiple pain mechanisms that do not act in isolation, representing the continuum of pain that is seen along the journey of individuals with chronic pain. Each mechanism will have subtle differences but will also require different interventions. Different centers in the brain may be involved with each mechanism. Central sensitization, and affective and motor/autonomic mechanisms are all subcategories of central nervous system (CNS) mechanisms. Some individuals may see the categories as a progression of the continuum of pain; however, the question remains: “Which mechanism is dominating?” A patient can present with both a peripheral pain mechanism and a central mechanism with emotional, social, and psychological factors involved at the same time. This indicates the need for clinicians to identify how far into the pain mechanism continuum the patient has evolved and which way he or she is headed from mechanical to neurologic. Recommendations for patient education and active care interventions will depend on peripheral or centrally acting mechanisms (see patient education graph page 194 of book entitled “A World of Hurt: Guide to Classifying Pain”).11 This PMCS addresses multiple dimensions to pain and challenges clinicians to treat patients on the basis of the presenting mechanism. The patient’s pain experience may be multifaceted, and it is important for the clinician to acknowledge the mechanism that is dominating at the time that treatment is sought. Refer to the text A World of Hurt for examples of such treatment scenarios.11

The analogy of a pain alarm system can help the reader to differentiate the complexities of pain mechanism classification. The human body’s pain alarm system is similar to the electrical system in a lamp. The “Working Lamp Analogy” allows the individual and pain practitioner to identify a simplistic viewpoint of pain, as compared to what occurs during the process of repair during the breakdown of a lamp. When a patient experiences a symptom, this indicates a possible breakdown in the alarm system. When the body hurts, the question one must ask is, where is the mechanism breakdown in the pain alarm system, and what should the individual do? This question is similar to the question when a lamp doesn’t turn on: Where is the mechanism breakdown and what should you do? (Fig. 9.1).

Step 1: When the lamp doesn’t turn on, the easiest steps to begin with are to check the bulb, then check the switch on the wall. Comparatively, when the body hurts, the easiest first step is to check the local body tissues for nociceptive signs of chemical or mechanical inflammation or ischemia. This will present as the need to watch the amount of motion and the direction of motion that is occurring or the need for more motion.

Step 2: When the bulb and switch do not turn the lamp on, check the cord and the outlet. When the local body tissues have no signs of nociceptive inflammation or ischemia, check the peripheral nerve to that body part for the presence of being “trapped” or “tight.”

The peripheral nerve will conduct, or behave similarly to the lamp’s cord. The outlet is the connection to the lamp’s cord, analogous to the main circuitry in the house. The peripheral nerve (cord) connects to the central processing unit (outlet). The lamp’s cord may be crimped or has a weight/pressure on it, and the ability to move and conduct is impaired. The outlet provides further feedback to the CNS or the processing ability of the “lamp’s cord.”

Step 3: When the cord and outlet appear to be fine and the lamp continues to be ineffective, the next step is to check the circuit breaker and flip the circuit breaker switch. When the body’s peripheral nerve is not trapped or tight, the next step is to check the brain’s “Threat Center” for signs of central sensitivity. Central sensitivity can enhance the interpretation of the body’s nociceptive signal by the thalamus and amygdala, believing harm is occurring in the body. This can result in a lack of inhibition and increased sensitivity in the nervous system centrally.

Step 4: When there are no signs of fear-avoidance behavior toward work, or physical activity, and the circuit breaker is in working condition, but the lamp still remains dark, check the local electrical provider for power outages. The brain’s emotional and social centers have a potential for negative emotions, poor coping, and an affective pain mechanism.

Step 5: When the electricity provider reports there are no outages and the lamp still remains dark, check the central grid system to make sure the service provider, box, pole, and power lines are recognizing the correct house. If positive coping strategies exist, but the patient still presents with negative emotions and social dimensions to pain, consider reflection on the autonomic/motor pain mechanism. The motor autonomic pain mechanism, the brain’s virtual body, maps the ability to localize or recognize alterations or impairments in the actual body

Figure 9.1 Five steps to a pain-free life.

Nociceptive: Inflammatory

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

Nociceptive: Ischemia

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.).

Peripheral Neurogenic

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.

Central Sensitization

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.

Apr 17, 2020 | Posted by in PHYSICAL MEDICINE & REHABILITATION | Comments Off on Pain Mechanism Classification System Overview and Focus on the Motor/Autonomic Mechanism

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