Pain Management

Pain Management

Overview

Pathophysiology Signs and Symptoms Key Drivers Red Flags Treatment Recommendations Additional Considerations Supportive Programs Diet and Lifestyle Clinical Assessment Footnote References

Pathophysiology

  • Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, and is a highly prevalent health issue. [1]
  • The sensation of pain, or pain signalling, begins when pain stimuli is sensed by peripheral nociceptors, which then transmits pain signals via the primary afferent neuron to the spinal cord. These signals are further conveyed through a synapse within second-order neurons, which transmits the signal onwards into the brain (Figure 1). [2]
  • The intensity of pain signals are subject to extensive modulation within the following tiers of the nervous system: [3]
    • Peripheral nerves: Pain sensitisation is associated with inflammation (i.e. increased capillary permeability, tissue oedema and release of inflammatory mediators), which activates nociceptors of primary afferent neurons. This generates action potentials transmitted by sensory neurons to the spinal cord. If inflammatory pain-provoking stimuli persists, the activation threshold of sensory neurons is reduced, resulting increased transmission of pain signals. [4]
    • The spinal cord: Several neurotransmitters are involved in pain processing at this level, including glycine and gamma-aminobutyric acid (GABA) [inhibitory] and glutamate (excitatory); neuropeptides, such as substance P and calcitonin gene-related peptide (CGRP); and endorphins. [5]
    • The brain: In chronic pain states, activated astrocytes and microglia release pro-inflammatory cytokines that intensify pain, this in turn may also alter re-uptake of glutamate and excitatory neurotransmitters increasing pain signalling. [6]
  • Sensitisation is a key feature of pain processing, where both the peripheral and central nervous system (CNS) rapidly adapts to the presence of pain. This process is called neuronal plasticity, which may lead to prolonged changes in the pathways involved in detecting and processing pain, resulting in chronic pain syndromes. [7]
  • Glutamate, acting via the N-methyl-d-aspartate (NMDA) receptor complex, plays a key role in central sensitisation. [8] In response to sustained pain, increased amounts of glutamate are released in the spinal cord, overcoming the inhibitory action of magnesium ions, resulting in activation of the NMDA receptor. This initiates a cascade of intracellular signaling events that lead to prolonged modifications of somatosensory processing, with amplification of pain responses and continued neuronal firing. [9]
  • Pain can be a presenting feature of a wide range of disorders. The first step in evaluation of a patient with pain should be to perform appropriate investigations required to define the underlying cause of the pain.

Figure 1: Pain signalling pathways involving the peripheral nervous system, the spinal cord and regions of the brain that link emotional, sensory and cognitive experiences of pain. [10]

Key: Ascending pathways: blue; Descending pathways: red.

Signs and Symptoms of Pain

Table 2: Classifications and Symptoms of Pain.

Type of pain

Features

Acute pain [12]
  • Acute pain tends to start out sharp or intense before gradually improving.
  • Common causes of acute pain include:
    • Broken bones
    • Surgery
    • Dental work
    • Labor and childbirth
    • Cuts and burns

Chronic pain [13]
  • Pain that lasts for more than six months, even after the original injury has healed is considered chronic, including:
    • Frequent headaches
    • Nerve damage-related pain
    • Lower back pain
    • Arthritis pain
    • Fibromyalgia pain

Visceral pain [14]
  • Visceral pain results from inflammation, injury or damage within internal organs.
  • Pain may be felt in the chest, abdomen, and pelvis.
  • Difficult to pinpoint the exact location of visceral pain, described as:
    • Pressure
    • Aching
    • Squeezing
    • Cramping
    • Examples include: gallstones, appendicitis, endometriosis or irritable bowel syndrome.

Referred pain [15]
  • Problems affecting the abdomen (e.g. gallstones), heart (e.g. angina, heart attack) and lungs (e.g. pneumonia) may cause shoulder pain.

Phantom pain [16]
  • Pain in a part of the body that has been removed (e.g. breast pain after mastectomy.
  • Pain typically lessens after the first year, however may remain longer in some individuals.

Non-specific pain symptoms [17]
  • Fatigue
  • Headache
  • Anxiety
  • Depression
    • Cognitive dysfunction

Specific pain sites: [18]

Bone pain
  • Tender area over bone
  • Possible pain on movement

Joint pain
  • Pain on range of motion, limited range of motion, and joint locking.
  • Arthralgia worsens with activity, and most commonly affects highly active, or load bearing joints.

Musculoskeletal pain [19]
  • Caused by chronic inflammation triggered by physical trauma or injury to tissue (i.e. bursitis, ligament damage, synovitis, joint trauma, tendonitis etc.)

Increased intracranial pressure
  • Headache, worse in the morning, associated with vomiting and occasionally delirium

Abdominal colic
  • Intermittent, severe, spasmodic, associated with nausea or vomiting

Liver capsule pain
  • Right upper quadrant abdominal pain, often associated with tender enlarged liver
  • Responds poorly to opioids

Neuropathic pain
  • Spontaneous pain
  • Light touch, pressure and temperature changes are painful; increased pain on pin-prick
  • Numbness, tingling or loss of temperature sensation
  • Skin feels abnormal

Ischaemic pain
  • Diffuse, severe, aching pain associated with evidence of poor perfusion
  • Responds poorly to opioids

Incident/Breakthrough pain
  • Episodic pain usually related to movement or bowel spasm, coughing, deep breathing etc.

Key Drivers:

  • Chronic inflammation: Chronic inflammation and immune activation characterised by prolonged and maladaptive production of inflammatory mediators, can perpetuate oxidative stress, [20] resulting in a proinflammatory environment that may contribute to elevated pain sensitivity. [21] This is a feature of many conditions associated with chronic pain, including autoimmune diseases (i.e. rheumatoid arthritis [RA], multiple sclerosis), chronic infections (i.e. chronic inflammatory response syndrome [CIRS] or Lyme-like illness), toxicity caused by environmental agents (i.e. heavy metal poisoning) and other conditions, including neuralgia, osteoarthritis, endometriosis and more.
  • Chronic stress: Chronic stress is associated with a proinflammatory state, marked by neuroinflammation and structural and functional changes within the CNS, which may influence pain sensitivity.[22] Increased activity of the HPA axis, leading to elevated catecholamines [23] and decreased GABA levels, [24] which can cause excessive activation of the pain response. Chronic pain is also strongly associated with limited physical function, work disability, and reduced quality of life that may further implicate chronic HPA activation due to stressful circumstances, resulting in greater pain sensitivity. [25] Chronic physiological stress may also be associated with insomnia, illicit drug use, stimulant substances (caffeine, nicotine), which again may perpetuate chronic HPA axis dysfunction-mediated inflammation.[26]
  • Poor diet: Emerging research indicates that poor nutritional intake (i.e. low fibre intake, caloric excess etc.) is associated with oxidative stress and tissue damage throughout the body. [27] These events activate toll-like receptors (TLRs), triggering a cascade of pro-inflammatory central immune signalling events, including microglial and astrocyte activation-associated CNS sensitisation [28] that have been linked to chronic pain conditions, including chronic back pain and fibromyalgia. Diet-induced neuroinflammation and chronic pain symptoms have been linked to elevated concentrations of blood glucose and low HDL cholesterol, supporting the importance of healthy diet to manage chronic pain. [29]
  • Magnesium deficiency: Inadequate intake of magnesium is associated with mechanisms that adversely affects pain sensitisation, including activation of the NMDA receptor, which increases nociceptive signalling. [30] Experimental models of induced magnesium deficiency indicate that magnesium depletion increases pain sensitivity and hyperalgesia that could be reversed by NMDA receptor antagonists, supporting the pain-reducing effects on magnesium to limit NMDA activation. [31]
  • Neuralgia, neuropathy and nerve compression: Patients that cite pain to feel like burning, hot or cold, ‘icy hot,’ ‘pins and needle’, stinging, lancinating, sharp or shooting indicates injury or damage sustained by nerve tissue. [32] This is a common cause of peripheral nerve sensitisation, and may present in addition to other pathophysiological causes of pain. This may present with dysesthesias (i.e. abnormal sensations) without numbness (generalised small fibre neuropathy) or coexisting numbness, hyperreflexia, or weakness, usually worse distally (large fibre neuropathy). Nerve root symptoms are also involved in the pathophysiology of pain. This commonly manifests as coexisting neck or low back pain that radiates along a specific dermatome (most common cause is structural compression). [33]
  • Cancer: Cancer pain may result as a primary effect of tumour growth or secondary to cancer treatments. Primary cancer pain is often associated with tumour growth, which compresses bones, nerves or other organs in the body. Pain may also be due to cytotoxic cancer treatments that cause nerve inflammation via chemotherapy-induced neuropathy [CIN] or due to pain and neuroinflammation at the site of injection. [34]
  • Opioid overuse/addiction: Opiate-induced hyperalgesia is broadly defined as a state of nociceptive sensitisation caused by over-exposure to both pharmaceutical and illicit opiates. [35] Mechanistic studies suggest that opioid-prolonged pain arises due to activation of spinal microglia and NOD-like receptor protein 3 inflammasome (NLRP3) that activates interleukin-1β, a cytokine described as the “gatekeeper of inflammation”. [36] Physical pain is a common precipitating factors that results in opioid addiction, resulting in a vicious cycle of chronic opiate use and reduced pain tolerance that often triggers relapse to addiction. [37]
  • Mechanical stress: Mechanical joint injury or overuse and dysplasia are the most prominent drivers in pain due to joint damage. [38] Chondrocytes within joints have several mechano-sensing mechanisms and can perceive loads above a defined threshold as injurious. Excess joint loading results in chronic cartilage catabolism and degeneration. This can occur when abnormal loads are sustained by a normal joint (e.g. increased mechanical stress due to obesity, repetitive occupational loads, or increased load due to structural joint malalignment). Mechanical stress also occurs when normal loads are experienced by a joint that has lost its mechano-protective mechanisms (i.e. loss of muscle support, joint destabilisation due to ligament damage, cartilage weakened by previous arthritis etc.). [39]
  • Obesity/Metabolic dysfunction: Obesity contributes to pain in conditions that affects the spine, knee, hip joints through mechanical overload, as well as poor joint muscle support as a result of sedentary behaviour. [40],[41] Excess adiposity is also associated with increased systemic inflammation driven in part by inflammatory cytokines that further compound inflammation and chronic pain states. [42] In patients who are overweight (i.e. body mass index [BMI] >25 kg/m 2) or obese (BMI>30 kg/m 2), a minimum weight loss target of 5% to 7.5% of body weight is recommended to improve pain in conditions such as osteoarthritis. [43]

Red Flags:

The Pain Management treatment protocol is a general resource designed to support the management of a wide range of pain conditions. As such, further red flags may arise depending on the type of pain, or in conditions where pain secondary to chronic inflammation (i.e. autoimmune disease). Refer to specific treatment protocol for additional red flag information.


  • Bone Fracture: Bone fracture caused by either major trauma or a minor trauma in vulnerable patients (i.e. elderly or osteoporotic patients) may manifest as acute pain and progress into chronic pain if left unmanaged. If the presenting pain complaint (i.e. lower back pain) is associated with an incident that may have resulted in bone trauma, in addition to other signs of inflammation, such as swelling, limited mobility or avoidance of particular movements, refer patient to their General Practitioner or to the emergency department for clinical investigations and X-rays to rule out bone fracture.
  • Malignancy: Cancer pain is often associated with tumour growth, which compresses bones, nerves or other organs in the body. Neuropathic pain may also be caused by spinal cord compression, which often results from posterior extension of a vertebral body mass. Intrathecal spinal cord metastases can cause similar signs and symptoms. This may present with back pain, particularly when coughing and lying flat. Subsequently, sensory changes develop in dermatomes below the level of compression and motor weakness distal to the block occurs. Advanced progression is associated with sphincter disturbance, causing urinary retention and bowel incontinence. [44] If suspected, immediately refer the patient for assessment by an overseeing medical Practitioner/General Practitioner or call Triple Zero (000) in case of emergency.

Treatment Recommendations

The Pain Management treatment protocol is a general resource designed to support the management of a wide range of pain conditions. For further condition-specific recommendations, refer to specific protocol/s.

Considerations for presenting with acute pain

High Potency Anti-inflammatory Herbs
Dosage: Take 1 tablet every 2 hours (up to 6 tablets daily).

Anti-inflammatory and analgesic herbs to reduce acute increases in inflammatory cytokines and oxidative stress markers associated with acute pain.

Mechanism of Action/Clinical Research:

  • Curcumin has broad anti-inflammatory effects, decreasing many inflammatory mediators including phospholipase, lipoxygenase (LOX), cyclooxygenase–2 (COX-2), leukotrienes (LTs), thromboxane, prostaglandins (PGs), nitric oxide (NO), collagenase, elastase, hyaluronidase, monocyte chemoattractant protein-1, interferon-inducible protein, TNF-α, and interleukin-12 (IL-12). [45], [46]
    • As an example of curcumin’s effects, 45 patients with RA were randomised into three equal groups to receive either BCM-95™ Turmeric (25 g/d), NSAID medication diclofenac sodium (50 mg/d), or a combination of both. BCM-95™ Turmeric was found to be as effective or superior to diclofenac sodium for reducing RA symptoms. [47]
  • Boswellia exerts anti-inflammatory activity further up the inflammatory cascade, inhibiting the activation of proinflammatory signalling pathway, nuclear factor kappa B (NFĸB). [48]
  • Ginger constituents, gingerol and gingerdione, have been shown to down-regulate arachidonic acid metabolism via partial inhibition of 5-LOX. [49] Ginger also inhibits NFĸB activation via suppressing the phosphorylation of protein, inhibitor of ĸB (IĸB), thereby keeping NFĸB sequestered and reducing inflammation. [50]
  • Quercetin is an anti-inflammatory flavonol, found to suppress the production of the inflammatory cytokines interferon gamma and IL-2. [51]

Highly Bioavailable PEA and Magnesium for Neuromuscular Support and Pain
Dosage: Add 1 level scoop (5 g) to 200 mL of water twice daily, with food.

A combination of PEA* and Magnesium bisglycinate with anti-inflammatory, glutamate-blocking and endocannabinoid-like actions to attenuate pain signaling.

Mechanism of Action/Clinical Research:

  • Magnesium has been found to block glutamate via inhibition of the N-methyl-D-aspartate (NMDA) receptor and reduce excitatory neurotransmission associated with pain signalling and increased pain sensitisation. [52]
  • Insufficient magnesium intake is associated with muscle tension, [53] which may exacerbate chronic pain.
  • 300 mg/d of magnesium bisglycinate over four weeks was shown to reduce muscle pain and reduce cramp intensity and frequency by 50% (p<0.05). [54]
  • Through enhancing endogenous cannabinoid system (ECS) activity, PEA reduces pain amplification driven by immune cells (i.e. microglial and astrocytes), [55],[56] and helps to downregulate TRPV1 nociceptor sensitivity. [57],[58]
    • In patients with chronic neuromuscular joint pain, one week of 900 mg/d of PEA followed another a second week of 600 mg/d of PEA decreased pain intensity scores (from 69.9% down to 7.6%) compared to ibuprofen (reduced from 68.4% down to 37.4%; p<0.0001). [59]
    • In patients experiencing lumbar pain due to nerve compression, 300 mg/d of PEA over three weeks reduced pain scores from 65% to 36%, while 600 mg/d of PEA reduced pain scores from 71% to 21% (p<0.05). [60]

Highly Bioavailable Palmitoylethanolamide (PEA), with Saffron and Thiamine for Nerve Pain

Dosage: Take 1 capsule twice daily.

Highly bioavailable PEA* in combination with saffron and vitamin B1 providing anti-inflammatory and endocannabinoid-like actions to address chronic pain, inflammatory nerve damage and pain hypersensitivity.

Mechanism of Action/Clinical Research:

  • PEA has been shown to promote the expression and activity of cannabinoid receptor 1 (CB1) and cannabinoid receptor 2 (CB2), thereby enhancing ECS activity to down-regulate pain and inflammation. [61] PEA has also been shown to minimise pain amplification driven by glial cells, [62],[63] and desensitise transient receptor potential vanilloid type 1 (TRPV1) receptors to mitigate pain sensitivity. [64],[65]
    • PEA can be safely co-prescribed alongside several pain medications classes, such as opioids, NSAIDs, muscle relaxants and corticosteroids. [66],[67],[68],[69]
    • Clinically, 600 mg/d of PEA has been shown to reduce chronic pain scores from 71% to 21% (p<0.05), [70] with numerous similar trials supporting the efficacy of 600 mg/d of PEA to reduce pain scores by >50% within four weeks. [71],[72]
  • Saffron has been observed to reduce pain receptor sensitivity by blocking transient receptor potential ankyrin 1 (TRPA1). [73]
    • Saffron [74],[75] and its isolated constituent, safranal, [76] have been shown to decrease nerve inflammation by inhibiting microglial and astrocyte activation in models of nerve trauma and oxidative damage. [77],[78],[79] Through reducing glial activation, safranal was shown to improve neuropathic allodynia in vivo. [80]
    • In patients with elevated inflammatory biomarkers (e.g. CRP >3 mg/L), 30 mg/d of saffron over 12 weeks has been shown to significantly reduce serum CRP and TNF-α, [81] to manage chronic inflammation.
  • Thiamine (vitamin B1) is a key nutrient required for healthy nerve cell function. [82]
    • In animals, thiamine supplementation following nerve injury was shown to reduce pain transmission. [83]
    • Thiamine promotes myelin synthesis surrounding axonal tissue to preserve nerve structures [84] by enhancing transketolase enzyme activity. [85]

Gamma-Aminobutyric Acid (GABA)

Dosage: Take 250 mg – 500 mg twice daily.

GABA functions as a primary inhibitory neurotransmitter in the CNS, reducing neuronal hyperexcitation that contributes to increased pain sensitivity.

Mechanism of Action/Clinical Research:

  • GABA plays a critical role in pain transmission. GABA neurons and receptors, found in supraspinal sites, regulate sensory information processing in the spinal cord, subsequently altering pain perception in response to painful stimuli. [86]
  • GABA regulates neuronal excitability via GABA receptor subunits, which are classified into three main groups (alpha, beta and gamma). [87]
  • An efficient efflux transport system enhances the passage of GABA across the blood brain barrier (BBB), which also acts as an efflux pump for the excitatory amino acids glutamate and aspartate, to reduce the brain interstitial fluid concentrations. [88]

OR

If presenting with chronic pain:

BCM-95™ Turmeric & Devil's Claw to Treat Chronic Inflammation

Dosage: Acute dose: 3 capsules twice daily, reducing to the maintenance dose of 1 capsule morning and two capsules evening, once symptoms have improved.

A combination of BCM-95™ turmeric, devil's claw and Jamaica dogwood to reduce the production of inflammatory mediators at multiple points of the inflammatory cascade, while also decreasing oxidative stress and tissue damage associated with chronic pain.

Mechanism of Action/Clinical Research:

  • Curcumin has broad anti-inflammatory effects, decreasing many inflammatory mediators including phospholipase, LOX, COX-2, LTs, thromboxane, PGs, NO, collagenase, elastase, hyaluronidase, monocyte chemoattractant protein-1, interferon-inducible protein, TNF-α, and IL-12. [89], [90]
    • As an example of curcumin’s effects, 45 patients with RA were randomised into three equal groups to receive either BCM-95™ Turmeric (25 g/d), NSAID medication diclofenac sodium (50 mg/d), or a combination of both. BCM-95™ Turmeric was found to be as effective or superior to diclofenac sodium for reducing RA symptoms.[91]
  • Boswellic acid, acetyl-11-keto-beta-boswellic acid (AKBA), demonstrates anti-inflammatory actions via allosteric regulation of 5-LOX, resulting in LT inhibition. [92] Additionally, boswellia exerts anti-inflammatory activity further up the inflammatory cascade, inhibiting the activation of proinflammatory signalling pathway, NFĸB. [93]
  • Devil’s claw provides significant analgesic effects by reducing pain sensations in the brain via increasing GABA levels and opioid activity, while also reducing glutamate signalling. [94]
    • An eight-week study involving 259 arthritis patients who were prescribed 1.4 g/d to 2.9 g/d of devil’s claw for eight weeks reported a significant reduction in pain, stiffness and function, as well as an increase in quality of life. Forty percent of participants also recorded significant improvements in pain, daily functioning and stiffness after just two weeks of treatment. [95]

Specialised Pro-Resolving Mediators[*]

SPMs to promote resolution of inflammation, reduce pain and encourage the clearance of pathogens. In doing so, SPMs actively reduce chronic inflammation, which is a major contributor of pain sensitivity affecting peripheral nerves and microglia.

Mechanism of Action/Clinical Research:

  • SPMs encourage resolution by regulating macrophage polarisation. SPMs trigger the switch from proinflammatory M1 macrophages to anti-inflammatory M2 macrophages, reducing inflammation and tissue damage, promoting resolution. Additionally, M2 macrophages have been shown to inhibit polymorphonuclear leukocytes and promote efferocytosis and tissue repair.[96]
  • This effect on macrophages also applies to microglia,[97]which are a key treatment target in chronic pain conditions.[98]

Additional Considerations

If presenting with insomnia due to pain:

California Poppy and Passionflower for Sleep

Dosage: For insomnia associated with pain, take 2 tablets once daily with an evening meal.

A blend of sedating herbs including zizyphus, passionflower and Californian poppy to modulate neurotransmitter pathways, including GABA and glutamate, monoamine and catecholamine activity (which support sleep quality), HPA function, formation of synaptic pathways, and brain plasticity.

Mechanism of Action:

  • Zizyphus activates glutamic acid decarboxylase, which catalyses GABA synthesis, while also sensitising GABA receptors by increasing their subunit expression, [99] thereby enhancing GABA neurotransmission to promote sleep maintenance.
  • Passionflower has been found to modulate the GABA system, demonstrating an affinity for both GABAα and GABAβ receptors, increasing its inhibitory effects. [100]
    • A study involving 154 participants who were prescribed 1,020 mg/d of dried passionflower extract for 12 weeks demonstrated improvement in sleep disturbances, including positive effects on sleep quality and maintenance. [101]
  • Lavender oil promotes a GABAergic response by blocking calcium ion channel activity within neurons and suppressing glutamate excitation, with inhibitory effects comparable to those seen in pregabalin (a pharmaceutical agent that mimics the effects of GABA). [102]
    • A double-blind, randomised, multi-centre trial involving 170 patients that were prescribed 80 mg/d of lavender oil for 12 weeks showed significant improvements in in anxiety and sleep quality. [103]
  • California poppy stimulates binding of the GABAαreceptor site, providing sedative effects. [104]

If vitamin D levels are <75 nmol/L:

Vitamin D3
Dosage: Take 1 capsule daily with food.

Vitamin D to modulate the immune response and regulate dysfunctional immune activity that may be involved in aberrant inflammation in patients with chronic pain.

Mechanism of Action/Clinical Research:

  • In 50,834 patients with arthritis, muscle pain and widespread chronic pain, vitamin D deficiency (<75 nmol/L) occurred at a significantly higher rate, suggesting that low 25(OH)D concentrations may be associated with chronic pain. [105]

Supportive Programs

The Metagenics Shake It Practitioner Weight Management Program is designed to help patients comfortably transition from a hypercaloric diet to a hypocaloric diet, facilitating sustainable weight loss while also improving insulin sensitivity and optimising metabolic function. This in turn can reduce systemic inflammation contributing to pain symptoms, as well as reducing loading weight on joint pain. [86] Full instructions and food lists are available for free download.

The Metagenics Clinical Detoxification Program is designed to reduce toxic burden, increase toxin resilience and improve the efficiency of waste elimination. In particular, the Gut Pathogen Elimination Detoxification stream may be used to address gut dysbiosis and intestinal permeability, whilst the Liver Chemical Clearance Program may support the elimination of toxic metals that may exacerbate chronic inflammation in pain conditions.

Diet and Lifestyle Recommendations


Diet:

  • In a large systematic review and meta-analysis examining the effects of nutritional interventions on non-cancer pain, researchers found that altering dietary intakes to either a plant-based, or Mediterranean-style diet may significantly lower pain scores (p<0.03). [107]
  • Current evidence suggests that the Mediterranean diet provides protection against several diseases associated with inflammation and immune activation.[108]
  • The Mediterranean diet is inclusive of a high intake of fruits and vegetables, lean protein, quality essential fatty acids, and wholegrains (limiting starchy grains and vegetables).
  • The Metagenics Wellness Diet reflects the wholefood principles of the Mediterranean diet also provides a simple guide to moderate portion size and the overall balance of macronutrients.
  • If the patient is overweight or obese, successful weight loss may be achieved using either a hypocaloric ketogenic-style diet or a low-fat diet outlined in the Metagenics Shake It Practitioner Weight Management Program:
    • Both dietary options feature adequate protein for satiety, increased thermogenesis (i.e. promoting fat burning) and to help maintain lean muscle mass.
  • Both of these diets emphasise the minimisation of refined starches, sugar, and saturated and trans-fatty acids, which are generally of poor nutritional value. Further, due to their inflammatory nature, these may cause an activation of the innate immune system by excessive production of proinflammatory cytokines. [109] This may negatively influence inflammation associated with pain conditions, and potentiate degenerative processes in afflicted tissues.

Lifestyle:

  • Exercise: Physical activity and exercise may also improve pain severity and physical function and enhance quality of life. [110] Land-based activities such as walking, gym work, exercise classes, yoga, pilates and tai-chi, or water-based activities such as hydrotherapy and swimming are suggested as gentle and achievable activities to support pain management. [111]
  • Therapies such as acupuncture and transcutaneous electrical nerve stimulation (TENS) may assist in the reduction of pain. [112]
  • Beyond physical treatments, optimising pain management may also involve therapies or supportive strategies that address mental, emotional, behavioral and occupational factors (Figure 2).
  • Psychological therapy is used to increase coping skills and improve quality of life when facing the challenges of living with chronic pain. [113]
    • There are a range of ways in which psychological therapies can be delivered, including individual one-to-one sessions, group sessions, multidisciplinary pain management programs, or web-based or telephone-based programs.
    • Acceptance and commitment therapy (ACT) is based on CBT principles but also uses components of mindfulness to improve psychological flexibility in the context of living with chronic pain. [114]
    • Relaxation techniques, such as biofeedback and mindfulness meditation with regular practice may further provide sustained benefit in chronic pain conditions. [115]

Clinical Assessment


Clinical Screening

Rationale

Mood and Stress Questionnaire

A questionnaire designed to help Practitioners establish levels of stress, anxiety and mood concerns, prioritised in relation to each other. Appropriate treatment strategies based on common response patterns under stress and neurotransmitter patterns.

Health Appraisal Questionnaire (HAQ)

The HAQ provides a comprehensive assessment of physical health, allowing Practitioners to gain insight into patient symptoms and evaluate overall health and wellbeing.

Metagenics Detoxification Questionnaire.

A questionnaire designed to help Practitioners establish levels of environmental toxin exposure and related symptoms. Appropriate treatment strategies based on exposure risk and detoxification capacity.

Footnote

*For formulations containing Palmitoylethanolamide (PEA) - This medicine is not to be used for more than 21 consecutive days, and may interact with other prescription analgesic medicines.

Figure 1: Pain signalling pathways involving the peripheral nervous system, the spinal cord and regions of the brain that link emotional, sensory and cognitive experiences of pain. [10]
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