The anterior cruciate ligament (ACL) is a commonly injured ligament of the lower extremity, with over 200,000 tears occurring annually.1 ACL injuries frequently occur in sports that require extensive cutting and pivoting,2 with a significant number of injuries affecting basketball and soccer athletes.3 Sport-related knee injuries involving ligaments, such as ACL tears, are also associated with early onset knee osteoarthritis (KOA).4 Osteoarthritis (OA) is a degenerative joint disease distinguished by the deterioration of articular cartilage, hypertrophy of bone, and presence of subchondral sclerosis that commonly affects the knee.5 Interestingly, the incidence of OA in basketball and soccer athletes is higher than in the average population and is frequently diagnosed 4–5 years earlier.6–8 More specifically, the development of KOA after ACL reconstruction (ACLR) occurs in approximately 11%, 20%, and 52% of individuals within 5, 10, and 20 years of their ACLR, respectively.9 The ACL injury mechanism is also responsible for creating acute bone marrow lesions,10 which may play a major role in the development of early KOA symptoms in individuals with a history of ACLR.
Individuals post-ACLR may also exhibit psychological impairments such as pain catastrophizing and avoidance behaviors.11 Pain catastrophizing is a cognitive–affective response to anticipated or actual pain and has three primary components: rumination (i.e., “I keep thinking about how much it hurts”), magnification (i.e., “I become afraid the pain will get worse”), and helplessness (i.e., “It’s terrible, and I think it’s never going to get better”).12,13 Although pain catastrophizing may be considered a natural psychological response after ACL injury,14 it can negatively influence significant outcomes, such as pain intensity and self-reported function, for patients after ACLR.14,15 Similarly, previous research shows that over 35% of individuals with KOA exhibit high levels of catastrophizing and consequently demonstrate increased pain, physical disability, and psychological disability.16–21 Therefore, the exploration of theoretical models that explain the development and consequences of psychological impairments in individuals with ACLR may help clinicians better understand the impact of cognitive and affective factors on postinjury outcomes. This knowledge may ultimately help to identify potential intervention strategies to mitigate maladaptive psychological responses and improve patient outcomes after ACLR.
We believe that the neuromatrix theory of pain and the transactional theory of stress and coping explain the development and consequences of psychological impairments in individuals with ACLR and early KOA symptoms. The neuromatrix theory of pain describes pain as a multidimensional experience generated by various influences as opposed to solely being influenced by sensory input.22 The transactional theory of stress and coping describes the role of appraisal on individual-environment transactions and the subsequent coping strategies commonly employed in response to stress.23 This narrative review highlights how these theories explain the development of pain catastrophizing experienced with ACLR and early KOA symptoms. This is important because this will allow clinicians to assess pain and symptoms from a multifactorial perspective and implement appropriate psychological intervention strategies. Therefore, the purpose of this review was to examine and integrate the neuromatrix theory of pain and the transactional theory of stress and coping to improve understanding of the development and effects of pain catastrophizing in individuals with ACLR and early KOA symptoms. In addition to theoretical discussion, recommendations for clinical practice are provided.
Defining the Neuromatrix Theory of Pain
Traditionally, pain has been depicted as a sensation produced solely by injury, inflammation, or tissue pathology.24 Pain was thought to be detected by nociceptors that cause pain signals to be sent to the central nervous system where they would be received and registered.24 Later, the gate control theory of pain was developed, which advanced our understanding of pain processing by introducing the spinal cord and brain as critical and active components in pain processing as opposed to passive transmission stations.25 However, a recently proposed pain model, the neuromatrix theory of pain, has shown that fear and anxiety may influence the experience of pain.22,26 The neuromatrix theory of pain portrays pain as a multidimensional experience generated by various influences, such as cognitive and affective events.22
To better depict the neuromatrix theory of pain, four components of a novel conceptual nervous system were proposed, including the body-self neuromatrix, production of a neurosignature pattern, conversion of neurosignatures into awareness, and stimulation of the action neuromatrix.22 The basis of this theory starts in the body-self neuromatrix, which is a large neural network throughout the brain that is responsible for the generation of neural patterns and the processing of sensory, cognitive, and motivational information that dictates perception and action.22 Because of the interdependent perceptual relationships between cells, tissues, body, self, and society, these factors may also influence common psychosocial responses examined after injury.27 Furthermore, it is proposed that the neuromatrix is composed of genetically programmed neurons that leave a specific mark on all nerve impulse patterns that pass through it, which produces a unique “neurosignature” pattern.22 This neurosignature is left on all neural impulses that travel through the neuromatrix, but may be modified and marked with subsignatures created from sensory input.22 The continuous flow of the neurosignature from the body-self neuromatrix is sent to areas of the brain that transform the signal to a changing sense of awareness. It is theorized that the change of the neurosignature to awareness leads to stimulation of an action-oriented neuromatrix, which in turn, activates neurons within the spinal cord to produce muscle movement and, ultimately, action.22
A unique component of the neuromatrix theory of pain when compared with traditional models of pain is that it includes multiple determinants of pain.22 Although the theory proposes that the neurosignature for pain experience is genetically determined and influenced by sensory input, it is also proposed that this neurosignature pattern may be impacted by cognitive and affective factors, such as psychological stress.22 This is further supported by the concept of phantom limb pain and the experience of pain in the absence of a limb or after destruction of its sensory roots.28 The stress experience may also negatively affect systems that aid in regulating stress and may ultimately lead to an increase in pain sensitivity, the development of pain conditions, and resistance to many common treatment methods that attempt to treat sensory-based pain.22 Therefore, psychological impairments, such as pain catastrophizing, may have the ability to impact an individual’s neurosignature pattern and exacerbate the pain experience.
Applying the Neuromatrix Theory of Pain to ACLR and KOA
Pain catastrophizing may influence the neurosignature of individuals with ACLR and alter their pain experience despite adequate physiological and structural healing after surgery. Previous research has found increased levels of pain catastrophizing to be strongly associated with higher levels of knee pain during activity after ACLR.15 As proposed in the neuromatrix theory of pain, it is possible that pain catastrophizing negatively affects regulatory systems, which results in the increased sensitivity to pain observed in this population during physical activity.
Higher levels of pain catastrophizing have also been associated with a heightened perception of pain.29 Functional magnetic resonance imaging of the brain in individuals with a history of ACLR showed increased activation of the secondary somatosensory cortex during completion of a knee flexion–extension task.30 The posterior region of the secondary somatosensory cortex is responsible for the processing of painful stimuli31; however, the study participants did not report experiencing any physical pain while completing the movement task. This observed brain activity in the absence of a painful stimuli exemplifies the ability of potential cognitive and affective factors to influence an individual’s neurosignature and alter their pain experience. Additional functional magnetic resonance imaging studies have found that individuals with ACLR, OA, and chronic musculoskeletal conditions were unable to suppress the default mode network (DMN) during a picture imagination task.32,33 The DMN is a brain network that is most active at rest and is strongly associated with rumination,34 a primary component of pain catastrophizing. It was proposed that, although patients with a history of ACLR are structurally healed, they may be continuously processing, or ruminating, over the memory of their painful ACL injury.32 Additional functional magnetic resonance imaging research has identified functional connectivity changes and spatial reorganization of the DMN in patients with chronic back pain and OA.35 Furthermore, it was found that the reorganization of DMN spatial properties was different between conditions, which was suggested to be due to the different emotional, attentional, and cognitive abnormalities associated with different clinical chronic pain conditions.35 These ideas and evidence further support the neuromatrix theory of pain and the notion that psychological stress and affective factors experienced after ACLR or in the presence of KOA, such as pain catastrophizing, may play a prominent role in pain perception and processing in the absence of a painful sensory stimulus.
In addition to psychological impairments influencing neurosignature patterns, the damage that occurs to the mechanoreceptors in the ACL at the time of the initial injury may also affect the neurosignature. The altered somatosensory feedback that occurs because of ACL injury may change the signal being sent from the neurosignature to the brain and, ultimately, modify perceptions of the body,36 and even behavioral patterns for individuals with ACLR. Furthermore, given the ability for neurosignature patterns and resulting actions to continue without ongoing sensory input,37 altered neurosignature patterns may linger despite physiological healing after ACLR. Long-term modifications to these patterns, which influence awareness and action, may contribute to behavioral changes examined in individuals with ACLR. This may include decreased knee function,38 reduced levels of physical activity,39 or the development of psychological impairments, such as pain catastrophizing, which may lead to disuse or disability.26
Defining the Transactional Theory of Stress and Coping
The transactional theory of stress and coping is based on the appraisal of transactions (e.g., events) between an individual and their environment.23 Incorporated in this theory are the individual’s values and beliefs, as well as environmental factors, such as demands being placed on the individual and the available resources to respond to these demands.23 Cognitive appraisal is the subjective interpretation of an individual’s situation and may be further categorized into primary and secondary appraisal. Primary appraisal identifies how significant an individual/environmental transaction is to the individual’s well-being and may be defined as benign-positive, irrelevant, or stressful.23 Benign-positive transactions result in a positive effect on well-being, while irrelevant transactions have no significance on an individual’s well-being.23 However, it is suggested that a stressful transaction may result in the appraisal of substantial harm and/or loss, threatened harm and/or loss, or challenge, which may elicit negative emotions.40 In the event of a stressful transaction, secondary appraisal occurs during which the individual assesses situational factors and coping resources before initiating coping strategies.23 From this process, an individual can establish what they can do to manage the initial stressor and subsequent distress.
Coping is considered a process-oriented task that requires purposeful actions.23,41 Two primary forms of coping incorporated in this theory include problem-focused coping and emotion-focused coping. Problem-focused coping strategies try to directly manage the stressor, whereas emotion-focused coping strategies aim to regulate emotions resulting from the stressful situation.23 Once coping strategies are initiated and new environmental information is present, cognitive reappraisal occurs. Through reappraisal, an individual is able to reevaluate and identify whether the coping strategy employed was successful or if the transaction has become irrelevant or benign-positive instead of stressful.23 If the utilized coping strategy is considered sufficient, positive emotions will be produced; however, if the coping strategy is considered insufficient, the individual will be in distress, which will lead to the consideration of other coping strategies.23
Applying the Transactional Theory of Stress and Coping to ACLR and KOA
The rumination and magnification associated with pain catastrophizing may negatively influence an individual’s primary appraisal of pain and therefore cause an individual who experiences pain catastrophizing to interpret the painful stimulus as threatening.42 This catastrophic thinking and threatening interpretation of pain may then lead to a maladaptive recovery process consisting of fear of movement/reinjury, avoidance behaviors, and ultimately, disuse or disability.43 Despite suggested evidence that exercise produces a pain-reducing effect similar to nonsteroidal anti-inflammatory medications,44 previous research has identified that in patients with KOA, specifically those with higher levels of pain catastrophizing, an increased amount of daily physical activity is associated with increases in knee pain.45 The presence of pain catastrophizing and increased amount of pain sensitivity may worsen avoidance behaviors, increase disability, and negatively influence health-related quality of life in individuals with KOA. Although previous research has identified that individuals with a history of ACLR spend less time engaging in moderate to vigorous physical activity when compared with their peers,39 additional research is needed to identify whether pain catastrophizing plays a role in this lifestyle modification after ACLR.
Additionally, the helplessness component of pain catastrophizing may affect an individual’s secondary appraisal and lead to an inability to cope with pain.42 Helplessness is the sense of being unable to act or react to a negative situation. It has been hypothesized that the pain, swelling, and loss of mechanoreception that occurs after ACL injury and ACLR lead to changes in neural activity.46 These physiological changes may subsequently initiate feelings of uncontrollability and thus lead to learned helplessness when patients are unable to complete specific tasks.46 Poor psychological responses, such as pain catastrophizing, may further worsen neural responses and create a negative cyclical pattern that decreases postsurgical outcomes and quality of life in this population.46 Previous research has identified that higher pain catastrophizing scores are associated with greater pain intensity and depressive symptoms 2 weeks after ACLR, which increases the risk of decreased physical activity participation.47,48 Given the risk of depression also associated with KOA and that physical activity engagement is encouraged to combat the pain and disability commonly experienced with this condition,49,50 it is essential that pain catastrophizing be assessed and addressed throughout the ACLR rehabilitation process to reduce potential long-term consequences of ACLR that may lead to the development of KOA.
Assessment of Pain Catastrophizing
Pain catastrophizing plays a prominent role in a variety of clinical pain-related outcomes such as clinical pain severity, pain-related activity interference, disability, depression, and alterations in social-support networks.13 Therefore, timely assessment and intervention to address pain catastrophizing is critical to mitigate the potential consequences of this impairment. Pain catastrophizing is assessed most effectively with the pain catastrophizing scale (PCS), a patient-reported outcome designed to measure an individual’s perceptions of their pain experience. The 13-item questionnaire includes three subscales, which examine the primary components of pain catastrophizing: rumination, helplessness, and magnification. The PCS total score ranges from 0 to 52, where higher scores indicate greater pain catastrophizing; however, individuals who score between the 50th and 75th percentiles are considered at moderate risk for the development of chronic pain, and individuals who score above the 75th percentile are considered at high risk for the development of chronic pain.12 As a measure of pain catastrophizing in KOA patients specifically, the PCS has high internal consistency (Cronbach’s α = .94), construct validity, and structural validity.51 The PCS can be completed by a patient and scored by a clinician in less than 5 min, which makes it easily implementable in clinical practice. Furthermore, given that reductions in catastrophizing have been shown to prospectively predict reductions in pain and disability,52 use of the PCS by clinicians would allow for early identification of patients who may be at-risk for poor rehabilitative outcomes and allow for the introduction of intervention strategies to address pain catastrophizing into the rehabilitation program. However, it is important to note that the PCS has yet to be validated for the ACLR population. Development and use of a new questionnaire to assess pain catastrophizing in a high functioning, physically active population with a history of ACLR may be warranted.
Interventions to Address Pain Catastrophizing
Similar to what has been identified for other pathologic populations,27 rehabilitation for individuals with ACLR or KOA who experience pain catastrophizing should consist of a multidimensional approach that goes beyond the tissue level of treatment by also addressing patient perceptions. Additionally, given that pain catastrophizing is multifaceted and includes magnification, rumination, and helplessness, intervention strategies that target these dimensions may be most beneficial. If catastrophizing is viewed as an appraisal process, education-based programs, such as pain neuroscience education (PNE), may allow individuals experiencing pain catastrophizing to reappraise their pain and view it as less threatening.53 PNE incorporates educating the patient on the biological and physiological processes that may occur during a painful experience.54 The primary goal of PNE is to educate individuals on how their nervous system and psychosocial responses determine their pain experience.54 PNE can be used proactively for patients experiencing acute pain, or as an intervention for patients experiencing chronic pain.55 Specifically, PNE has demonstrated efficacy in pain reduction, improvement of patient pain knowledge, improvement in function and disability, reduction in psychosocial impairments, and movement enhancement in individuals with chronic musculoskeletal disorders.55 Recent qualitative research examining the use of PNE in the treatment of KOA suggests that the use of high-quality content PNE throughout prescribed KOA exercise may lead to positive changes in patient beliefs and behaviors.56 Therefore, PNE may demonstrate not only cellular and tissue-level improvements, but may also lead to improvements in the body-self connection (e.g., perceived ability) and the self-society connection (e.g., perception of self in the context of others) to promote a multidimensional treatment approach as proposed in the perceptual interdependence framework.27 However, the effectiveness of PNE on pain catastrophizing after ACL injury and reconstruction has yet to be explored. Future research should utilize PNE to identify its effect on pain reappraisal among patients with a history of ACLR and who have KOA.
If an individual’s appraisal process of catastrophizing results in increased attention or perceptions of pain, which is associated with higher levels of pain catastrophizing,29 intervention strategies that incorporate distraction mechanisms may be able to divert a patient’s attentional focus away from catastrophic thinking and the perceived painful stimulus. However, the type of distraction is important, as previous research has demonstrated that the attention to pain should be considered from a motivational perspective and that the competing stimulus should be adequately engaging.57–59 Therefore, due to the motivational aspect of many interactive games, virtual reality (VR) may be considered a viable intervention strategy to address pain.60–62 VR is a computer-based technology that generates a simulated environment for user interaction, which can range from nonimmersive to fully immersive.63,64 Fully immersive systems utilize an artificial three-dimensional simulated environment with increased incorporation of multisensory experiences using equipment such as a head-worn apparatus that covers the eyes and hand-held controllers.65–67 It is proposed that the increased engagement of multimodal stimuli (i.e., visual, auditory, tactile, and olfactory) with VR increases sensory distraction and thus decreases activity in the body-self neuromatrix,63 a primary component of the neuromatrix theory of pain. Therefore, while using VR, the user’s ability to process and perceive painful stimuli is limited, ultimately creating a “VR analgesia” effect. This analgesic effect has helped establish VR technology as a critical multidisciplinary tool for pain management that is effective in providing short-term pain relief in patients with both acute and chronic pain.68,69 Previous research has exhibited significant reductions in low back pain through the integration of 15-min VR sessions into a 3-day/week traditional therapeutic exercise program.70 Therefore, the ability to complete a shorter length of intervention and the possibility to combine VR experiences with a physical agent modality, such as heat, ice, or transcutaneous electrical nerve stimulation, which are frequently used in the treatment of musculoskeletal conditions, also makes VR a realistic addition to a multitude of orthopedic rehabilitation programs. Furthermore, access to cost-effective VR technology, such as Google Cardboard™, which averages $15, may establish VR as a potential nonpharmacological pain management technique that can be easily and affordably implemented in the outpatient rehabilitation setting.
Utilization of these educational and distraction-based intervention strategies throughout the ACLR rehabilitation process may help to address predetermined beliefs about pain. Through the transactional theory of stress and coping, this approach could ultimately lead to changes in appraisal and pain perception in this population. Furthermore, the use of PNE techniques may help patients better understand how neuroplastic changes and psychological responses influence the pain experience after injury. Better understanding of these concepts may lead to improved clinical outcomes that are commonly affected by pain catastrophizing, such as knee function.
Limitations of Presented Theories
These theories are not without limitations. Although the neuromatrix theory of pain is useful to understand the affective aspects of pain, the theory does not directly address the physical aspects of pain that may occur in the presence of tissue damage. Furthermore, this theory does not specifically identify how appraisal and coping strategies may influence the neurosignature and its subsequent output. Given that stressful transactions commonly lead to negative emotions and that the neurosignature pattern may be influenced by affective factors, primary appraisal may play a large role in altering the neurosignature pattern and therefore influence the resultant awareness and action in the neuromatrix theory of pain. Furthermore, an individual’s coping strategies may also positively or negatively influence psychological responses that act on the neurosignature and therefore impact an individual’s pain experience.
A limitation of the transactional theory of stress and coping regarding a better understanding of pain catastrophizing in individuals with ACLR and KOA is that it does not consider any of the central nervous system and neural alterations frequently associated with pain catastrophizing. It is also possible that the genetically determined neurosignature conceptualized in the neuromatrix theory of pain influences and modifies how an individual appraises, reappraises, and copes with pain. Integration of the proposed ideas may better explain how individual appraisal-specific factors (e.g., values and beliefs) could interact with predetermined genetic components or neural changes and how these factors may influence the appraisal of pain and coping in individuals with ACLR and early KOA symptoms.
Conclusions
The neuromatrix theory of pain and the transactional theory of stress and coping may be valuable in better understanding the development and effects of pain catastrophizing in individuals with a history of ACLR and who may be at risk for the development of early KOA symptoms. Clinicians should use these theories to guide the assessment of pain catastrophizing throughout the rehabilitation process to identify individuals who may be at-risk for experiencing long-term consequences of pain catastrophizing, such as depression and decreased quality of life. Furthermore, implementation of intervention strategies may improve an individual’s primary appraisal of pain, improve outcomes for individuals after ACLR, and reduce the risk of KOA.
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