PAIN MANAGEMENT Medical Presentation

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Pain Management Introduction
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Pain is a multidimensional experience that has been defined as an unpleasant sensory and emotional experience As the definition implies, pain not only involves the sensation (location, duration, intensity, quality) but also has an emotional component (unpleasantness). Physiotherapy management of a person with pain, therefore, involves multiple interventions that include education, exercise, manual therapy and modalities such as electrical and thermal agents.
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THE PATIENT’S PAIN EXPERIENCE end-organ model or structure–pathology model Limitations: Firstly, the central nervous system modifies sensory input Secondly, persistent pain is frequently not stimulus-dependent, while much of the musculoskeletal examination is based on responses to stimuli. Finally, pain is ultimately an intensely subjective experience, which is intimately connected with personal meaning. Although it is acknowledged that an individual’s pain is influenced by, for instance, age, ethnicity, religion and gender, the focus here is on personal experience.
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COMING TO TERMS WITH PAIN AND DISABILITY Most people who experience pain first try to find a resolution. Unfortunately not all pain can be eliminated or even reduced, leading people with persistent pain to visit numerous health-care practitioners in search of a cure. Explanations should help the patient make sense of not only the nociceptive origins of their pain, but also reasons for its persistence. People with persistent pain find it difficult to maintain a sense of control, because long-term pain tends to fluctuate unpredictably. This makes it difficult to plan activities and set goals, both in the shorter and longer term. . An understanding of the physiology and psychology of persistent pain, combined with a belief in what the patient reports, can aid in the provision of realistic and empathetic explanations.
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PERSONAL AND SOCIAL CHANGES IN RESPONSE TO PAIN long-term pain can lead to a hardening of attitudes towards others, a reduction in empathy and lashing out at friends and relatives, fear about the future a cause of anxiety and distress, a loss of hope, low mood and tendency at lash out at those around them, Roles within the family also change, withdraw from interaction with others. aim to adjust overall wellbeing: Bodywork approaches such as yoga, qigong, Feldenkrais or Rolfing, having a (pain) diagnosis and a supportive environment, Visits to a familiar health-care practitioner over an extended period
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ADOPTING A ROLE IN THE HEALTH AND SOCIAL CARE SYSTEM Individuals with persistent pain often go through numerous health-care appointments with long waits in between and repeated disappointments. Building a relationship is therefore a key component of the consultation.
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CONCLUSION An understanding of subjective aspects of living and coping with pain can help clinicians to empathize and engage with their patients, and to find effective painmanagement strategies for them as individuals.
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EDUCATIONAL APPROACHES TO PAIN MANAGEMENT
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DELIVERY OF PATIENT EDUCATION Education can be delivered verbally to individuals or to groups of patients10–via written materials such as leaflets or information booklets, by material from the Internet including web pages, social media/ YouTube and smartphone apps, or by educational videos. Education can also be delivered at a societal level and mass media campaigns have been developed to educate the public about pain. Education for patients with musculoskeletal pain typically involves providing information on diagnosis, prognosisand management of their condition.
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CONTENT OF EDUCATION INTERVENTIONS FOR LOW BACK PAIN These approaches can be grouped into three broad categories: biomedical, biopsychosocial or pain neurophysiology education. Biomedical approaches to education focus on biomechanical properties of the spine and information is provided on ergonomics and advice on posture./back school Biopsychosocial educational approaches emphasize the importance of the relationship between thoughts and feelings to low back pain/ disability43 and advise patients to avoid bed rest44 and that a gradual return to activity is likely to increase the rate of their recovery./back book Pain neurophysiology education or pain biology education attempts to reconceptualize a patient’s understanding of their pain by emphasizing that pain does not reflect the extent of tissue damage, but is rather a protective output produced by the brain when sensory information is evaluated as threatening, dangerous or harmful.
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THE EFFECTIVENESS OF PATIENT EDUCATION FOR LOW BACK PAIN Much of the research on the effectiveness of patient education for musculoskeletal conditions has been conducted on patients with low back pain. The effectiveness of educational interventions is usually determined by their effects on pain, disability and return to work. Findings and conclusions are typically made from comparing the educational approach to waitlist, placebo or usual care assessed at short term, when the effects are presumed to be largest.
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Biomedical Education (Back Schools) Brox et al. and heymans et al. found conflicting evidence. Turner and Demoulin et al. concluded that biomedical education is not effective at reducing either pain intensity or disability for patients with chronic low back pain. Turner and Demoulin et al. concluded that biomedical education is not effective at reducing either pain intensity or disability for patients with chronic low back pain. Heymans et al. found conflicting evidence. The quality of the evidence for these conclusions was typically low to moderate.
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Biopsychosocial Education (Advice/ Brief Education) Brox et al. concluded that brief education is effective at reducing disability, whereas Engers et al. and Shaheed et al. concluded that it was not. Brox et al. and Shaheed et al. concluded that brief education was effective at reducing sick leave. Henrotin et al. concluded a biopsychosocial booklet alone was insufficient to produce effects . Engers et al.9 concluded that only education that lasted longer than 2.5 hours was effective, although there was no effect for patients with chronic low back pain. the quality of available evidence was ‘very low’.
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Pain Neurophysiology/Pain Biology Education Clarke et al. and Louw et al. concluded that pain neurophysiology education was effective at reducing pain intensity for patients with chronic low back pain or other chronic pain. Clarke et al. found evidence that these effects become larger over time. Louw et al. concluded that pain neurophysiology education decreased disability for patients with different chronic pain conditions whereas Clarke et al. did not reach the same conclusion for patients with chronic low back pain. The quality of the evidence included in these reviews typically ranged from moderate- to highquality studies.
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PATIENT EDUCATION AND MALADAPTIVE BELIEFS Pain, disability and return to work are important outcomes that reflect patients’ concerns61 and are included in the core outcomes for research on low back pain. Psychological theories suggest that underlying these outcomes are patient beliefs. Patient beliefs can therefore be considered to be the primary targets of patient education, and changes in these beliefs are likely to lead to improved patient outcomes.
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COMMON BELIEFS TARGETED BY PATIENT EDUCATION Suitable targets for education are beliefs about pain that have been shown to be associated with poor outcome, including catastrophic pain beliefs (a belief that the pain has a serious cause, that the pain will persist and the condition will inevitably deteriorate), fear-avoidance beliefs (when pain is experienced physical activities should be avoided and rest should be taken) and selfefficacy beliefs (the confidence that a patient has the ability to achieve outcomes that are important and desirable). Research that shows that these beliefs are associated with poor outcomes such as pain and disability was a major reason for the development of biopsychosocial education. Pain neurophysiology education focuses on identifying and changing a belief that hurt equals harm.
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PAIN NEUROPHYSIOLOGY EDUCATION In particular, pain neurophysiology has been found to decrease pain-related catastrophizing in people with chronic or subacute pain.
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PHYSICAL INTERVENTIONS OF PAIN MANAGEMENT AND POTENTIAL PROCESSES
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EXERCISe Exercise is a mainstay of physiotherapy interventions. There are numerous forms of exercise including stretching, strengthening, motor control, coordination, endurance and aerobic.
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Clinical Studies Further exercise can reduce the number of recurrences of low back pain. Lastly, using a large-population database those who are regularly physically active are less likely to develop chronic musculoskeletal pain conditions than those who are sedentary.
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Dosing Despite the strong evidence that exercise is effective, there are insufficient data to make recommendations regarding the frequency, duration and intensity of an effective exercise programme. for those with chronic pain, both strengthening and aerobic conditioning exercises are equally effective. in people with low back pain equivalent reductions in pain and disability and improvements in function and quality of life occurred when motor control exercises were compared with graded activity, or when motor control exercises were compared with general aerobic exercise. in fibromyalgia comparing muscle strengthening exercises to an aerobic exercise training programme produced similar reductions in pain and improvements in quality of life. in those with osteoarthritis aerobic exercise, strengthening exercises and aquatic exercises all reduce pain and improve function. complementary and alternative therapies that include exercise, such as yoga and tai chi, as well as lifestyle physical activity are also effective in people with a variety of pain conditions.
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Basic Mechanisms Although a significant amount of clinical literature supports the effectiveness of exercise for pain, few studies have addressed the underlying mechanisms.
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Central Mechanisms Endogenous opioids are produced in a wide range of tissue types, including the midbrain periaqueductal grey (PAG), rostral ventromedial medulla (RVM), spinal cord and muscle, and are key players in exercise-induced analgesia. serotonin is a major neurotransmitter found in endogenous inhibitory pathways including the PAG, RVM and spinal cord and plays a significant role in analgesia. In healthy human subjects there are increased serum levels of β-endorphin in response to aerobic exercise. exercise activates our central inhibitory pathways to produce analgesia through opioid and serotonergic mechanisms.
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Peripheral Mechanisms reducing nociceptor activity or enhancing endogenous inhibitory neuromodulators. Aerobic exercise running reduced the enhanced current densities of HVA and LVA calcium channels, suggesting reductions in nociceptor activity and thus it is possible that regular exercise reduces pain hypersensitivity by normalization of enhanced ion channel activity of nociceptors.
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TENS Transcutaneous electrical nerve stimulation (TENS) is the application of electrical stimulation to the skin for pain relief. TENS is generally applied at low frequencies (<10 Hz) or high frequencies (>50 Hz), at varying intensities. Electrodes can be placed to surround the site of pain, over a nerve or segmentally – not much research has been done to examine optimum electrode placement sites.
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Clinical Studies Systematic reviews show significant reductions in pain in individuals post-operatively, those with osteoarthritis and those with peripheral neuropathy. other systematic reviews similarly show TENS is ineffective or inconclusive for a variety of painful conditions including acute pain, osteoarthritis, low back pain and postoperative pain; this effect may be dependent on dosing of TENS. TENS has also been shown in individuals with postoperative pain, osteoarthritis and fibromyalgia to reduce pain with movement, but not pain at rest, suggesting that TENS is more effective for movement-related pain. TENS may be effective for other evoked pain like hyperalgesia and allodynia, in addition to movement pain. Indeed TENS reduces hyperalgesia in those with osteoarthritis and fibromyalgia, and allodynia in those with neuropathic pain. Low-frequency TENS activates mu-opioid receptors whereas highfrequency TENS activates delta-opioid receptors. As opioids can produce analgesic tolerance, repeated daily use of TENS at the same frequency and intensity (dose) in healthy controls can also induce analgesic tolerance. a cumulative effect of TENS (delivered two to five times per week) has been shown in individuals with chronic low back pain, osteoarthritis and neuropathic pain. TENS could normalize pain physiology (i.e. reduce central sensitization or increase central inhibition). individuals with fibromyalgia showed that TENS delivered to the neck or back increased pain thresholds outside the site of stimulation (leg) and increased central inhibition (central pain modulation).
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Dosing intensity of TENS is critically important to obtain a positive effect. stimulation amplitude must be of sufficient strength to produce an analgesic response. In healthy subjects, TENS delivered at a strong but comfortable intensity provided a significant analgesic effect, whereas TENS delivered at or below sensory threshold was ineffective. systematic reviews that consider dosing show that high intensities are associated with significant reductions in both post-operative and osteoarthritis pain while lower intensities are not effective.
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Basic Science Mechanisms At frequencies and intensities used clinically, TENS activates large-diameter afferent fibres. This afferent input is sent to the central nervous system to activate the descending inhibitory system to reduce hyperalgesia. Specifically, blockade of neuronal activity in the PAG, RVM and spinal cord inhibits the analgesic effects of TENS.
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In human subjects high-frequency TENS increases the concentration of β-endorphins in the bloodstream and cerebrospinal fluid, and methionine-enkephalin in the cerebrospinal fluid. The reduction in hyperalgesia by high-frequency TENS is prevented by blockade of δ-opioid receptors in the RVM or spinal cord, or synaptic transmission in the ventrolateral PAG. The reduction in hyperalgesia produced by high-frequency TENS is prevented by blockade of muscarinic receptors (M1, M3) in the spinal cord – muscarinic receptors are implicated in opioid analgesia in the spinal cord. High-frequency TENS also enhances release of the inhibitory neurotransmitter GABA in the spinal cord dorsal horn and the TENS antihyperalgesia is reduced by blockade of GABAA receptors in the spinal cord. However, blockade of serotonin or noradrenergic receptors in the spinal cord has no effect on the reversal of hyperalgesia produced by high-frequency TENS. Thus high-frequency TENS produces analgesia by activating endogenous inhibitory mechanisms in the central nervous system involving opioid, GABA and muscarinic receptors.
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Low-frequency TENS reduces hyperalgesia after joint inflammation and this reduction is prevented by blockade of µ-opioid receptors in the spinal cord or the RVM, or synaptic transmission in the ventrolateral PAG. The analgesia produced by low-frequency TENS is also reduced by blockade of GABAA, serotonin 5-HT2A and 5-ht3 and muscarinic m1 and m3 receptors in the spinal cord. Increases in blood flow occur with stronger low-frequency TENS at intensities that produce motor contraction (intensity greater than 25% above motor threshold). Thus, peripheral effects of TENS may involve opioid receptors and changes in sympathetic activity utilizing local α2anoradrenergic receptors.
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MANUAL THERAPY Manual therapy techniques may include traditional massage, soft tissue mobilization, joint mobilizations and manipulations, nerve or ‘neural’ mobilization procedures, joint stabilization exercises and self-mobilization exercises. Clinical evidence supports the use of massage and manipulations for a variety of pain conditions.
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Basic Science Mechanisms The basic science mechanisms underlying massage have included evidence aimed at deciphering which central pathways are activated. After delayed onset muscle soreness (DOMS) induced in otherwise healthy male subjects, 10 minutes of massage reduced excitatory signally at the level of the muscle (decreases in cytokines, heat shock protein phosphorylation and NFκB) and increased signalling proteins involved in tissue repair and metabolic control (MAP kinases, PGC-1). Joint manipulation and mobilization use similar multiple mechanisms to reduce pain that include effects peripherally at the site of application and in the central nervous system. Manipulation and mobilization clearly increase pain thresholds in healthy controls and increase pain-free range of motion of the upper limb tension test. Peripherally, in healthy human subjects, manipulation produces a short-lived (10–30 seconds) decrease in motoneuron excitability.
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In addition, evidence suggests that joint mobilization activates central inhibitory mechanisms to reduce central excitability and have a more widespread effect. In healthy controls there is a decrease in temporal summation, which is a measure of central excitability, following spinal manipulation, suggesting central mechanisms may play a role. In people with lateral epicondylalgia, joint mobilization of the cervical spine (grade III lateral glide of C5/6) increases pressure pain thresholds, pain-free range of motion for the upper limb tension test and painfree grip force. in people with knee osteoarthritis application of joint mobilization to the knee increases pressure pain thresholds at the knee (i.e. primary hyperalgesia) and the heel (i.e. secondary hyperalgesia). joint mobilizations not only have local effects but that the effects can be widespread, indicating reductions in central excitability. joint mobilizations reduce pain through effects in the central nervous system by activating descending inhibitory pathways from the RVM and dorsolateral pontine tegmentum (DLPT) that are non-opioid.