Osteoarthritis (OA) is the most common form of arthritis worldwide. The leading cause of disability associated with OA is mainly due to pain, which is the primary symptom of the disease. The pain experience in knee OA in particular is well-recognized as it typically transits from intermittent weight-bearing pain to a more persistent, chronic pain. The nature of the pain experience in OA is often complex. The etiology of pain in OA is recognized to be multi factorial, with both intra-articular and extra-articular risk factors. (Neogi, T. 2013). Nonetheless, greater insights are needed into pain mechanisms in OA to enable rational mechanism-based management of pain.
Unlike many other pain conditions in which the underlying injury typically heals or resolves, OA is a degenerative disease that does not resolve. Thus, OA is typically accompanied by chronic pain and the impact of this ongoing chronic pain i) plays an important nociceptive role, ii) represents maladaptive pain, or iii) reflects other aspects of the pain experience is not clear (kittelson et.al.,2014).
Due to the complex, multidimensional nature of pain in OA, the underlying etiology of the pain is multifactorial; therefore it is important that the patient should be considered in a biopsychosocial framework as is the case with Mr. M.
The process of pain is a complex phenomenon. It is an unpleasant sensation which is experienced differently by different individuals either in similar or different clinical contexts. The International Association for the Study of Pain defines it as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage”.
It is caused by the irritation of the pain receptors which are found in the skin, joints and other internal organs which are sensitive to mechanical, chemical or thermal stimuli. What is more interesting about pain is, it can also occur without any tissue damage or any apparent visible reason. This type of pain is referred to as psychogenic pain.(Sweiboda et.al.,2013)
Under normal circumstances, pain is considered as a warning sign that something is wrong. Pain usually plays a protective role, it signals the individual to withdraw from the threat, rest to allow tissue healing, or seek help, etc. However, once its warning role is over, persistent pain which leads to chronic pain, and is considered as maladaptive (kittelson et.al, 2014).
However the experience of pain depends on several factors like strength of the stimulus, individual susceptibility and individual resistance to pain. The operation of noxious stimulus to the pain receptors results in the processing of an electrical signal. This impulse is conducted by nerve fibers into the spinal cord and then to the brain. At this point, there is a realization that something hurts us, which is perceived as pain. Pain is not only somatic in nature, associated with the condition of the body, but also it is a multidimensional phenomenon.
Therefore, in addition to the physiological process of pain, its subjective perception is also important, which is decided by the central nervous system. (Sweiboda et.al. 2013)
Pain can be mainly classified in to three types i) Acute pain – pain which is less than three months of duration , ii) Chronic pain – Pain which lasts longer than three months duration and iii) Survived pain – occurs as a result of improper management of acute pain. (Sweiboda et.al. 2013).
Acute pain is self limited and serves a useful biological purpose which is usually associated with skeletal muscle spasm and sympathetic nervous system activation, provoked by a specific disease or injury. Chronic pain, in contrast, may be considered as a disease state. It is pain that exists beyond the normal healing time, if related with a disease or injury. Chronic pain may arise from psychological states, serves no biologic purpose, and has no specific end-point. Persistent pain associated with injuries or diseases (arthritis in case of Mr. M) can result from changes in the properties of peripheral nerves. This can occur through damage to the nerve fibres, leading to increased spontaneous firing or alterations in their conduction or neurotransmitter
Properties. (Sweiboda et.al. 2013).
Two different types of peripheral nociceptor neurons detect pain which are C-fiber nociceptors with slowly conducting unmyelinated axons, and A-delta nociceptors with thinly myelinated axons. Nociceptors become sensitized during inflammation; nociceptors discharge spontaneously, and produce ongoing pain. Prolonged firing of C-fiber nociceptors causes release of glutamate which acts on N-methyl-D-aspartate (NMDA) receptors in the spinal cord. Activation of NMDA receptors causes the spinal cord neuron to become more responsive to all of its inputs, resulting in central sensitization (Bennet, G J. 2000).
The activity- related symptoms appear to be of nociceptive nature during the general progression of OA from the early stages to a more persistent constant pain. Due to the tissue injury or inflammation there will be a decrease in the excitation threshold and an increase in responsiveness to peripheral sensitization. The noxious mechanical stimuli then produce some exaggerated responses known as primary hyperalgesia. A very normal stimulus such as a normal range of motion of the joint could initiate a pain response which is known as allodynia. (Neogi, T. 2013).
There are certain changes that occur in the central nervous system due to the activation of nociceptors after a tissue injury or inflammation. There are also changes that happen to dorsal horn transmission neuron receptors, which lead the transmission neurons to become hyper responsive to central sensitization, with reduction in the threshold for mechanically induced pain and an expansion of the receptive field of dorsal horn neurons. Radiating pain in OA is mainly caused due to this process (Neogi, T. 2013).
In the case of Mr. M, the activation threshold of nociceptors is decreased such that normally innocuous stimuli now cause pain which leads to allodynia. As a result of this, the stimulus–response curves are shifted to the left, where a noxious stimulus causes more pain than normal, a condition called hyperalgesia (Bennet, G J. 2000). Central sensitization is maintained by low-level noxious and non-nociceptive input from the periphery, once it is established. These changes in the central nervous system are mainly responsible for the increased sensitivity to mechanical stimuli that develop outside the area of the injury which is known as secondary hyperalgesia. (Neogi, T. 2013). Due to the presence of inflammation, nociceptors acquire new characteristics and become sensitized. They begin to discharge spontaneously. This spontaneous, or ongoing, discharge is at least partly responsible for the ongoing pain (Bennet, G J. 2000).
A progressive increase in discharges of dorsal horn neurons in response to repetitive afferent stimulation thought to reflect central sensitization is increased in the case of Mr. M as compared to people without knee OA (Neogi, T. 2013).
Mr. M is a fifty eight year old male patient with three year long history of unilateral Osteoarthritis knee (OA). Please refer to the appendix for the detailed information about the patient.
There are several aspects of Mr. M’s subjective assessment that needs to be taken into consideration. The long history of Mr. M’s knee OA is associated with persistent pain. Pain lasting for more than three months with an element of central sensitization as in the case of Mr. M, can be defined as chronic pain (Crofford, L.J. 2015).
Mr. M was presented with a high level of distress and anxiety during his first visit to the clinic. Cognitive and emotional factors have a vital role in pain perception (Crofford, L.J. 2015).
Patients with long-term chronic pain could develop anxiety and depression as a result of the activities in the ascending and descending pathways are altered by negative emotions among many other factors unrelated to the pain stimulus itself (Crofford, L.J. 2015). Patients who report knee OA with generalized knee pain with radiation had more persistent and severe pain, and higher anxiety levels (Lluch, et.al 2014) as it was in the case of Mr. M. Further evidence suggests that, poor mental health is linked to OA pain and pain flares and this precedes reporting of worse OA related pain and OA pain flares(Lim & Doherty, 2011).
Substantial occupational joint loading (kneeling, squatting, lifting heavy objects) could have had a greater impact on the lead up to the development of OA knee in case of Mr. M with a possibility of increased pain severity (Allen, et.al 2012). As per evidences there is a strong connection between engaged in work with knee OA with lower extremity joint loading and pain severity (Allen et.al. 2012). Prolonged squatting which Mr. M confirmed that he used to do on a regular basis could be viewed as one of the risk factors that would have lead to the development of knee OA in his case (Lim & Doherty, 2011). Pain catastrophization was evident in the case of Mr. M, he also reported about his sleep disturbances due to pain. Evidence suggests a stronger association between pain catastrophization, sleep disturbances and central sensitization, with poor sleep and higher catastrophization leading to the greatest level of central sensitization (Campbell et.al. 2015) which could most probably be the case with Mr. M.
Mr. M was asked about his expectation during the subjective examination and he said he wants to be pain free and avoid undergoing surgery as his doctor suggested. There were also a lot of catastrophic thoughts and anxiety surrounding his future with pain was evident throughout the subjective examination as he thinks that he will never recover from the chronic pain, he is already not doing the work he should be doing because of the fear of pain and he is worried about how long it will continue like this? as he cannot afford to let it continue for a long time as he needs to take care of his farm and business.
Fear avoidance model (FAM) play an important part in the journey to recovery for Mr. M and it was incorporated into the management of Mr. M. The fear-avoidance model of chronic pain emphasizes the role of fear-avoidance in the development of pain problems. FAM is a prevailing cognitive behavioral model of chronic pain. The FAM states that negative appraisal of acute pain evoke pain-related fear leading to avoidance and/or escape behaviors (Wong et.al. 2014). While avoidance behaviors such as limping and resting can be adaptive for reducing pain during the acute phase, prolonged engagement in avoidance behaviors is detrimental physically as well as psychologically. Physically it leads to loss of range of motion, mobility, muscle strength and fitness. Psychologically, avoidance behaviors may facilitate depression and loss of self-esteem, which may then amplify disability (Wong et.al. 2014). In the case of Mr. M, the key issue underpinning the FAM is that negative or catastrophic thinking influences avoidance behavior and subsequently amplifies disability (Wong et.al. 2014).
After the subjective examination and looking at the investigation reports it was concluded that Mr. M was suffering from knee OA with chronic pain and Central sensitization. However, objective examination too has been performed and confirmed the findings of the subjective examination and other investigation reports. There is a need of holistic assessment and individualized management plan in the case of Mr. M (Lim & Doherty, 2011).The use of both pharmacological and non-pharmacological treatments should be given equal importance (Lim & Doherty, 2011). Non-pharmacological management was ignored all these years in the case of Mr. M.
The clinical practice guidelines suggest that management plan for OA should consists of patient information, prescription of exercise (both local strengthening and general aerobic fitness), consideration of paracetamol as first-line oral analgesic, non steroidal anti-inflammatory drugs (NSAIDs), use of intra-articular corticosteroid for marked pain resistant to other measures; and consideration of surgery for marked pain and disability that interferes with quality of life and which is resistant to other conservative measures. Any management plan needs to be reassessed and potentially modified according to the response obtained from the patient (Lim & Doherty, 2011). In the case of Mr. M some key aspects of guidelines were ignored also Mr. M clearly didn’t want to undergo surgery but his doctor did not suggest him any other options other than that which increased Mr. M’s worries and anxiety.
(Gifford,1998) proposed the mature organism model (MOM) which was developed as a teaching tool to help clinicians and patients reach a broader understanding of pain, in a bio- psycho-social context and hence manage it better. A key feature of the model is the placement of pain and patient’s reaction to it in the broad discipline of stress biology. That is, the pain sensation should be seen as a perceptual component of the stress response whose chief adaptive purpose is to alter patient’s behaviour in order to enhance the processes of recovery. Incorporating this model into Mr. M’s management plan would bring a positive change in his recovery.
The unhelpful or maladaptive thoughts and feelings OF Mr. M may have occur not only as a result of ongoing pain and the increasing loss of function, but also due to the evident aspects such as mismanagement by his doctor over a long period of time (Gifford, 1998). Maladaptive CNS / brain outputs are thought to be produced as a result of the ongoing unpleasantness and general negative psychological and physiological aspects associated with ongoing pain (Gifford, 1998). People who are in pain, without an adequate understanding or explanation of their pain, may well focus on it to an unwarranted degree and thus habitually maintains open pain ‘gates’ which would otherwise be held closed. Thus focusing, repeating and giving attention to an experience can promote learning and altered CNS/brain processing (Gifford, 1998).
CNS/brain output systems govern tissue health, control recovery and maintain homoeostasis, in the case of Mr. M, it must be fully appreciated that negative psychological states limit the efficiency of CNS/brain output systems. On the other hand it is becoming evident that positive psychological states combined with healthy lifestyles and behaviour has the opposite effect (Gifford, 1998). Education about pain that includes modifying ‘abnormal structure/mechanics’ related beliefs about pain is essential along with the explanation of occurrence of altered sensitivity state as a result of altered information processing throughout the system, and not just because of damaged and degenerating tissues. This helps Mr. M accept the concept that “hurt does not necessarily equate with harm”. which leads on to the positive message that carefully graded increases in physical activity mean stronger and healthier tissues for his successful rehabilitation (Gifford, 1998). Whereas, continued focus on a tissue as the pain source strengthens fear of movement and activity, makes constantly vigilant for pain and the desire for expensive passive therapeutic interventions which are yet to convincingly demonstrate its efficacy (Gifford, 1998) .