Chapter 13 Pain Management
Introduction
Even premature babies have a fully functioning pain system and using morphine for their pain has a significant effect on morbidity and mortality. Heel stab and circumcision studies have demonstrated that the experience of early pain has a profound impact on future pain response (Goldschneider 1998).
Pain as a symptom is defined by the International Association for the Study of Pain (IASP) as ‘an unpleasant and emotional experience associated with actual or potential tissue damage, or described in terms of such damage’ (Merskey 1979). This encourages us to view pain as a complex perceptual experience that involves sensory-discriminative, affective-motivational and cognitive-evaluative components and not merely sensory information (Melzack and Casey 1968).
Wall (1989) described pain as a ‘need state’ in the way that hunger is, rather than a pure nociceptive sensation. Hunger drives the urge to find food, with relief of hunger being related more to expectations of the effect of eating rather than directly related to actual blood sugar levels.
Similarly, pain drives the urge to:
1. Escape from its cause: verified by the involvement of the motor cortex and cerebellum in pain processing. Movement strongly influences these controls from both the periphery and the brain. Wall (1995) suggested that ‘the input may be better perceived in terms of the motor action which is appropriate, so that sensory and motor control are seen as two sides of the same coin’, and (Wall 1999a Epilogue) ‘pain is not just a sensation but … is an awareness of an action plan to be rid of it.’
2. Seek relief: this is supported by the fact that pain intensity is reduced in the presence of an intervention perceived as adequately effective in dealing with the cause, even if its actual therapeutic effect is zero (Wall 1999b). The placebo response can be powerful; the effect of sham surgery can last for 6 months or longer (Cobb et al 1959). Pain is the main driver for patients to present to health care establishments and the most frequent symptom encountered by health professionals.
Is the pain acute or chronic? Is there a difference?
Understanding pain as merely a signal of damage has hampered clinicians’ and patients’ views about how pain should be managed; clinicians and patients need to rethink what acute and chronic pain are. Moseley and colleagues have demonstrated that understanding what pain is has a significant real effect upon pain intensity and disability (Moseley et al, 2004).
Acute pain
Acute pain is defined as pain that occurs at the time and for a period following injury, disease process or acute ischaemia. Signals from damaged tissue are relayed to the central nervous system (CNS) via nociceptors and nociceptive neurons (Woolf and Ma 2004).
Upon reaching the CNS, nociceptive signals may be automatically modified by factors that demand attention. These include the perceived threat of the situation and injury, past experiences, genetic factors, environmental and cultural factors, expectations and beliefs (Moseley 2007). Nociceptive signal reduction can be such that major injuries can, for a period, be experienced as pain-free, allowing for defensive and escape behaviours (Fanselow and Sigmundi 1986, Wall 1999a Chapter 1). Some minor injuries though can seem disproportionately painful. The CNS, therefore, does not merely passively relay and receive information.
When acute conscious pain occurs it is also accompanied by widespread reactions: alertness, orientation, attention and exploration, changes to heart and breathing rates and blood pressure, sweating, slowing of gut motility and rising anxiety (Wall 1999a). This is not just to support ‘flight and fight’ but also to initiate seeking (appropriate) help. Acute pain then continues to quite a varying degree while the healing, autoimmune, ischaemic or infective inflammatory processes are on-going. Inflammatory processes or peripheral nerve damage produce further integration of the distinctive patterns of adaptive, neuronal changes in the CNS (Milan 1999). Changes in the thalamus and somatosensory cortex can lead to quite marked hypersensitivity, frequently mistaken for inflammation. Inflammation is usually fairly transitory, its limit for even major injuries being at most a week (Evans 1980). Such changes usually resolve when the nociceptive stimuli stop.
During this recovery period however, symptoms can still be aggravated by certain physical factors such as prolonged immobilisation at any stage, or over-use in the early stages. Emotional factors such as stress, anger, depression, anxiety and anticipation (Main et al 2008 Chapter 2) can also amplify symptoms; many areas of the brain involved in pain processing are also activated during the experience of emotions. Emotions of course will partly be driven by beliefs and expectations; something that physiotherapists can influence.
Chronic pain
Chronic pain is defined as pain that continues past the expected healing time or on-going pain (IASP 1994). An arbitrary time-frame of 3 months post onset/injury is a practical cut-off point for confirming the diagnosis of chronic pain since primary healing of all injury types will have been completed by then. Minor injuries (cuts, minor fractures, sprains) will have healed much faster and signs of chronicity can sometimes be picked up soon after injury:
• Mirror pains appearing on the contralateral limb.
• Sharp, shooting or stabbing pain.
• Feelings of swelling, stiffness, hot/cold.
• Feelings of ants crawling/water flowing/feels woody, etc.
• All movements hurt (not in normal distribution).
• Pain has a ‘mind of its own’.
Fifty per cent of those with chronic pain remember no causative factors as the brain has the ability to generate a perception of pain without a nociceptive input (Tracey 2005). Chronic pain is distinguished from acute pain by the involvement of the pain system producing on-going central sensitisation (Sterner and Gerdle 2004).
Some patients with central sensitisation pain can have on-going perceptual problems, e.g. a limb feeling swollen when it is not, or is difficult to determine where it is, including sense of left/right and problems with discrimination (Lotze and Moseley 2007; Moseley 2004). Since these features were not recognised in the past, patients may have been worried that their problem was more serious than their health professionals considered it to be.
Key risk factors for chronic pain disability
Most people who experience post injury pain have little hesitation in gradually reintroducing movements and activities. They may seek some reassurance or advice, but they generally manage recovery and rehabilitation instinctively and reasonably well. This is not always the case however, and until recently, the incidence of chronic pain disability was rising exponentially. Chronic pain and disability prevention is thus as important for acute pain as acute pain treatment. The importance of psychosocial factors in the development of these chronic problems has consistently been demonstrated (Shaw et al 2005) (Box 13.1).
Box 13.1 Early risk factors for chronic pain disability (adapted from Shaw et al 2005)
• Patients with increased pain affecting sleep despite analgesia
• Belief that pain is harmful or potentially disabling
• Fear avoidance behaviour from fear of pain or fear of harm/causing damage
• Catastrophising (thinking the worst)
• Low mood due to pain and the consequences of injury
• Expectation that passive treatments rather than active participation in therapy would help
• Patients not making expected improvements 2–4 weeks after treatment for an acute (LBP) problem
• Patients who have significant difficulty with ADL or work, for more than 4 weeks (there is evidence for this factor for LBP and whiplash-associated disorders, but look for it with any pain)
Assessment for pain: different presentations, pain syndromes
The IASP have produced referenced clinical updates on each of these pain syndromes (http://www.iasp-pain.org).
Neurogenic pain: slowly developing regional musculoskeletal or ‘neuralgia-like’ pains
These pains classically have no obvious causative injury. A period of unaccustomed work or activity may precede it, but recovery with paced activity would normally be expected to occur, but does not. A poor tolerance for static positions, for activity and/or stress of the body region, and reduced fitness of the whole body or body region ensues. Examples include syndromes such as repetitive strain disorder, epicondylitis, LBP and osteoarthritic pains which are becoming recognised as neurogenic pains and not tissue-based conditions (e.g. Laursen et al 2006). Comparing X-ray changes with normal subjects of similar ages shows little difference apart from pain hypersensitivity. Clear fMRI evidence is emerging of changes in the sensory cortex (Flor et al 1997). Neurogenic pain is not limited to the musculoskeletal system: some pelvic and bladder pains, chronic indigestion, irritable bowel and headaches are all now considered to be neurogenic pain. Such cases are often referred to non-pain specialists where focus on the painful tissues often leads to a poor outcome.
Neurogenic pain: chronic widespread pain and fibromyalgia syndrome (FMS)
FMS is a non-articular disorder of unclear aetiology characterised by widespread pain throughout the body. The commonly encountered features of FMS are listed in Box 13.2.
Box 13.2 Frequently reported features of fibromyalgia
• Widespread musculoskeletal pain, typically diffuse or multifocal
• Joints or limbs feel swollen
• Temporomandibular joint dysfunction
• Irritable bowel syndrome; bladder disturbances; dysmenorrhoea
• Fatigue, reduced energy and drive
• Disturbed sleep; non-restorative sleep
• Problems with concentration, attention, or memory
Recent FMS criteria proposed by the American College of Rheumatology (Wolfe 2010) introduced a ‘Widespread Pain Index’ and a ‘Symptom Severity Score.’ Clinical relevance however remains to be explored.
Neuropathic pain
This is spontaneous pain and hypersensitivity associated with primary injury or dysfunction of the nervous system following peripheral nerve or spinal cord trauma or where disease process has damaged peripheral nerves, e.g. shingles, diabetes, human immunodeficiency virus (HIV)/acquired immune deficiency syndrome, alcoholism, vasculitis and multiple sclerosis. Following stroke, spinal cord injury or syringomyelia, patients frequently develop neuropathic pain. Changes occur in peripheral afferents, causing ectopic discharges at the site of the injury, at any neuromas and at the dorsal root ganglion (Woolf 2004).
Self report questionnaires have been developed to evaluate the presence of neuropathic pain such as ‘painDETECT’ which was developed to assess the neuropathic components of LBP (Freynhagen et al 2006) and the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) (Bennett 2001).
Chronic regional pain syndrome (CRPS)
CRPS begins as rapidly escalating post-injury pain. Genetic factors have been identified that predispose to the development of CRPS. The extent of mechanical hyperalgesia in CRPS has been correlated to the extent of cortical reorganisation assessed on fMRI (Pleger et al 2006).
• CRPS type I: following minor injuries or fracture of a limb.
• CRPS type II: following injury to a major peripheral nerve.
Stiffness, on-going spasm and signs of developing CRPS emerge.
Recognition of early stage CRPS may follow the removal of a cast, e.g. post Colles fracture, where the patient holds the now healed wrist as if it is still fractured. The Budapest criteria can provide a helpful framework for defining a diagnosis of CRPS (Box 13.3).
Box 13.3 Budapest Clinical Diagnostic Criteria for CRPS (Harden et al 2010)
