Catastrophic thinking is a new puzzle piece in understanding anterior knee pain

Issue: February 2014

ByVicente Sanchis-Alfonso, MD, PhD

Editor’s note: Members of the Patellofemoral Foundation review and add clinical perspective to recently published studies on the causes, prevention and treatment of patellofemoral disorders. The twice monthly blogs are edited by John Fulkerson, MD, and can be found on www.healio.com/orthopaedics. To read all the Patellofemoral Update blogs, click here.

Anterior knee pain is one of the most common reasons to consult an orthopaedic surgeon who specializes in the knee. Despite the high frequency of anterior knee pain, its etiopathogeny is not well known and myths about the condition are widespread. One myth is the patient with anterior knee pain as a patient with peculiar psychological traits responsible for the genesis of pain.

Many patients with anterior knee pain (AKP) have insubstantial clinical and radiologic findings. However, their pain and disability are important. If we add in the allodynia and hyperalgesia that many patients have, then we could be led to believe that the problem is psychological. This is not true. Patients with AKP have a high incidence of anxiety, depression, kinesophobia (the belief that movement will create additional injury or re-injury and pain) and catastrophizing (the belief that pain will get worse and one is helpless to deal with it). However, it is also true that these psychological disorders are the result of the pain severity but not the cause of the pain and disability.

Psychological factors

We must remember there are biomechanical and neuroanatomic explanations for the pain. Nevertheless, it is also true that psychological factors play an important role as pain modulators. Even in cases with clear structural findings, psychological factors influence and modify pain sensation as well as subsequent impairment and, therefore, can be barriers to recovery.

Our findings suggest that certain psychological factors may predispose patients with AKP to adverse pain-related and functional outcomes following physiotherapy or surgical treatment. That is, psychological factors could be the cause for persistent unexplained pain and poor function after a correct treatment. Along with patients’ beliefs and cognition about pain, we must not forget the beliefs and cognition of the physicians who treat the patients. The treating physician could influence the course of the illness by reinforcing or modifying the patients’ beliefs and cognition about pain.

Cognitive-behavioral model of pain

Our findings are in agreement with the cognitive-behavioral model of pain which suggest that negative appraisals of pain (e.g., catastrophic thinking) will influence the intensity and persistence of pain. Pain catastrophizing is a multidimensional construct with elements of magnification (i.e., heightened perception of pain), rumination (i.e., excessive focus on pain), and helplessness (i.e., beliefs that the control of pain is beyond one’s ability). Each element has an adverse impact on pain experience. The term “catastrophizing” was first coined by Ellis in 1962 to describe the process where anxious patients dwell on the most extreme negative consequences conceivable.

It is interesting to note that catastrophizing significantly predicts the degree of pain and disability the AKP patient has in a specific moment in time. It has been shown in patients with AKP that catastrophizing itself can explain 37% of the pain variance and catastrophizing together with depression can explain 56% of the variance of the disability. This confirms what has been shown in other musculoskeletal conditions with chronic pain. The association between catastrophizing and the development of chronic pain and AKP, which is a paradigm of chronic pain, is not an exception. The correlation between pain and disability is only moderate in patients with AKP. Pain by itself is not a variable that could fully explain the different degrees of disability these patients have.

Psychological factors influence in the degree of disability. Among all the psychological factors we analyzed, the most relevant one from a clinical standpoint is catastrophizing, which was related to the pain as well as to the disability that patients with AKP have. For this reason, we routinely perform the Pain Catastrophizing Scale on a patient with AKP at the first office visit. Given the importance that catastrophizing has as a barrier in the recovery from pain and disability, it should be included in the therapeutic targets to complement and to improve the results of conventional treatments (physical therapy and/or surgery).

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Gender differences

It is well-known that AKP occurs more frequently in women than men. Men and women respond differently to painful stimulus, with a greater susceptibility toward pain in women. Moreover, there is also a greater risk to develop painful symptoms in women. Biological factors (sexual hormones and endogenous opioids) and psychosocial factors (pain coping strategies, social stereotype and stressful situations at an early stage of life) could be responsible for the differences between men and women.

Catastrophizing could be another factor to explain the differences between men and women since women catastrophize more than men. Also catastrophizing could partly explain the racial differences in pain tolerance. However in our research, gender differences were not predictors of change in pain and disability after treatment for patients with AKP.

Pain modulation

Catastrophizing is not only responsible for the chronification of pain due to a psychological mechanism, but also could influence the neurophysiology of pain modulation. In a functional MRI study, Gracely and colleagues showed that for patients with chronic pain catastrophizing, ideas were associated with a higher degree of brain activity not only in the pain regions but also in the cortical regions associated with attention, anticipation of pain and emotional aspects of pain.

Edward and colleagues found that for healthy subjects whose pain was caused by a heat stimulus, a high level of catastrophizing showed longer and more intense pain. This indicates that catastrophizing could play a role as a facilitator of the pain perception process. Moreover, high levels of pain catastrophizing have been associated with poorer response to opioids. It also has been suggested that pain catastrophizing may interfere with descending pain-inhibitory systems and may facilitate neuroplastic changes in the spinal cord during repeated painful stimulation, subsequently promoting sensitization in the central nervous system.

Clinical implications

There is controversy about whether catastrophizing is a stable construct, like a personality trait that predisposes a patient with AKP to the chronification of pain and disability, or whether it is a dynamic attribute that can be modified. If the first premise is correct, then catastrophizing could be an obstacle to recovery.

We believe, as well as other authors, that the second premise is correct since we have observed that catastrophizing is reduced when patients feel a reduction of pain after a classic biomedical treatment. We have observed that changes in catastrophizing are the most powerful predictors of the changes in the degree of post-treatment pain. We found the reduction of catastrophizing explains by itself the 48% of the variance of the changes in the degree of pain. The reduction of catastrophizing and anxiety would explain 56% of the variance in disability. This finding is clinically relevant because it contradicts the belief that patients with AKP are patients with pre-existing psychological problems frequently responsible for pain. We believe nothing is farther from the truth.

Pain is a multidimensional phenomenon composed by sensitive, cognitive-evaluative and affective-motivational domains. Catastrophizing modulates the perception of pain and this relation seems to be bidirectional in a dynamic manner. Our results suggest that patients with AKP tend to catastrophize when pain is more intense. Conversely, some studies have shown in other chronic pain conditions that as catastrophizing is primarily decreased, pain sensation and function improve. However, what we do not know is if this pain reduction is a consequence of the reduction of catastrophizing or if the catastrophizing decreases because the pain is reduced because of physical therapy or surgery.

Further studies are necessary to demonstrate if a cognitive-behavioral treatment to reduce catastrophizing could reduce pain for patients with AKP. Our study group is now in this phase. Cognitive behavioral interventions designed to reduce pain catastrophizing are effective for patients medically treated for arthritis. It is interesting to note that similar results have been observed between lumbar fusion and cognitive behavioral interventions for patients with lumbar pain.

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Conclusion

Currently, the etiopathogeny of AKP is not yet well known. To be able to correctly understand chronic pain, and AKP should not be an exception, we must not only consider anatomic, biological and biomechanical factors, but also psychological and social factors. This approach is known as the “biopsychosocial model” in contrast to the classic “biomedical model” that correlates the pain with the tissue damage and/or structural changes only.

The biopsychosocial model is widely used in the management of back pain, and it is perfectly applicable to patients with AKP. Anterior knee pain, along with lumbar pain, has a low correlation between symptoms and abnormal findings in imaging studies. Both entities also have a tendency to become chronic and patients develop severe disability. Chronic pain and disability in patients with AKP would be justified by the conjunction of biomechanical factors, anatomic factors, biological factors, social environment, psychologic distress, attitudes and beliefs, such as catastrophyzing. The clinical interest of addressing the whole picture is to identify the potentially modifiable factors to achieve better outcomes.

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For more information:
Julio Doménech, MD, PhD, is associate professor of orthopaedic surgery, Faculty of Medicine, at University Cardenal Herrera, Valencia, Spain; email: julio.domenech@uch.ceu.es.
Erik Montesinos-Berry, MD, is consultant orthopaedic surgeon, Agoriaz Medical Center, Rue de la Saletta 10, 1632 Riaz, Switzerland; email: erik.montesinos@gmail.com.
Vicente Sanchis-Alfonso, MD, PhD, is consultant orthopaedic surgeon at Hospital Nisa 9 de Octubre, Valencia, Spain. He is also member of the International Patellofemoral Study Group. He can be reached at Valle de la Ballestera # 59, 46015, Valencia, Spain; email: vicente.sanchis.alfonso@gmail.com.

Disclosure: Doménech, Montesinos-Berry and Sanchis-Alfonso have no relevant financial disclosures.