Neuralgia and Neuropathy

Neuralgia and Neuropathy

Overview

Pathophysiology Signs of Neuralgia and Neuropathy Key Drivers Red Flags Treatment Recommendations Additional Considerations Supportive Programs Diet and Lifestyle Footnote References

Pathophysiology:


  • Neuralgia is defined as painful sensations arising from impaired or injured nerve structures. [1] Clinical presentations of neuralgia may feature [2]:
    • Hyperesthesia: Heightened sensitivity to nonpainful stimuli (e.g. light touch);
    • Hyperalgesia: Heightened sensitivity to painful stimuli (e.g. pinprick), or reduced threshold to feel pain; and
    • Allodynia: Pain provoked by a stimulus that is not normally painful.
  • Neuralgia is commonly associated with neuropathy, which describes disorders that share injury to the nervous system that encompasses nerve pathways involved in motor, sensory, and autonomic function. [3]
  • Various conditions may cause neuralgia and neuropathy due to their detrimental effects on nerve anatomy; associated with either nerve compression or damage to axon and myelin tissue. These include:
    • Metabolic conditions: Type 2 diabetes mellitus (T2D); malnutrition; vitamin B12 deficiency; thiamine deficiency; and Fabry’s disease. [4]
    • Inflammatory conditions: Autoimmune diseases (systemic vasculitides, systemic lupus erythematosus [SLE], Sjögren’s syndrome, Guillain–Barré syndrome etc.), acute inflammatory demyelinating polyneuropathy (classically presents with ascending weakness and numbness, although pain is also a common feature), chronic inflammatory demyelinating polyneuropathy, sarcoidosis and multiple sclerosis [MS]. [5]
    • Infectious illnesses: Post viral (brachial neuritis), human immunodeficiency virus/acquired immune deficiency syndrome [HIV/AIDS], shingles and postherpetic neuralgia (i.e. varicella-zoster virus), Lyme disease, leprosy and syphilis. [6]
    • Infiltrative causes: Amyloidosis, paraproteinemias (e.g. monoclonal gammopathy of uncertain significance [MGUS] associated neuropathy). [7]
    • Malignant causes: Neoplastic and paraneoplastic-carcinomatous infiltration of nerve/nerve root.
    • Drugs/toxicity: History of alcoholism, chemotherapeutic agents (paclitaxel, vincristine), isoniazid, metronidazole, or heavy metals (i.e. thallium and arsenic). [8]
    • Structural injury: Nerve entrapment or disc pathology (e.g. carpel tunnel syndrome, trigeminal neuralgia etc.). [9]
  • Proper clinical evaluation and monitoring is key to ensure appropriate management and reduce symptom progression.
    • In a study of 284 patients diagnosed with idiopathic neuropathy, 67.3% of patients were found to have underlying pathologies that were often treatable. [10]
  • In cases where neuralgia and neuropathy are associated with systemic disease, treatment outcomes are dependent on supporting the management of metabolic, inflammatory, infectious, oncological and neurotoxic drivers.

Signs of Neuralgia and Neuropathy

  • Pain described as burning, hot or cold, ‘icy hot,’ ‘pins and needles’, stinging, lancinating, sharp or shooting.
  • Symptom distribution in areas where socks or gloves are worn (i.e. generalised neuropathy) or numbness in a peripheral nerve territory (i.e. focal neuropathy).
  • Dysesthesias (i.e. abnormal sensations) without numbness (generalised small fibre neuropathy) or coexisting numbness, hyporeflexia, or weakness, usually worse distally (large fibre neuropathy).
  • Nerve root symptoms: Coexisting neck or low back pain that radiates along a specific dermatome (most common cause is structural compression).
  • Spinal cord symptoms: Coexisting spasticity with bowel or bladder involvement.

Key Drivers:

  • Diabetes/Hyperglycemia: Diabetes is the most common cause of neuropathy, occurring in up to 50% of patients. [13] In type 1 diabetes, increased blood glucose levels have been linked to the risk of neuropathy. [14] In T2D, other metabolic features including hyperlipidemia and obesity are important contributors to the risk of neuropathy and nerve damage. Specific pathogenic mechanisms, ultimately leading to mitochondrial injury and axon loss in both types of diabetes, include activation of the polyol pathway, formation of advanced glycation end products [AGEs], altered diacylglycerol/protein kinase activity, and oxidative stress. [15] Further, diabetic medication, metformin, is also associated with inducing vitamin B12 deficiency resulting in degeneration of the spinal cord and peripheral nerves. [16] Short-term treatment with metformin causes a decrease in serum folic acid and increase in homocysteine, which leads to peripheral neuropathy in T2D patients. [17]
  • Nerve compression: Peripheral nerves are vulnerable to compression at specific anatomic sites, which may result in neuropathic symptoms due to nerve impingement. The most common are median nerve compression at the wrist within the carpal tunnel (carpal tunnel syndrome), ulnar nerve compression at the elbow (cubital tunnel syndrome), and peroneal nerve compression over the lateral fibular head. [18]
  • Hypothyroidism: Neuromuscular dysfunction including neuropathy is strongly associated with hypothyroidism. [19] Decreases in thyroid hormones have been associated with primary axonal degeneration in the form of axonal shrinkage, disintegration of neurofilaments and neurotubules. Moreover, in hypothyroidism, fluid accumulation may also lead to compression of peripheral nerves. [20] Further, patients with T2D (a leading cause of neuropathy) are at a greater risk of developing subclinical hypothyroidism, highlighting the compounding effects of hypothyroid disease. [21]
  • Nutritional deficiency/excess: Peripheral polyneuropathy may also develop with deficiency of a number of vitamins and nutrients. [22] Deficiency of vitamin B12 results in severe combined degeneration of the spinal cord and peripheral nerves. Copper deficiency, often due to zinc overload, causes a similar syndrome. Vitamin E deficiency causes ataxia. Vitamin B1 (thiamine) deficiency may cause a severe sensorimotor axonal neuropathy in addition to the classic triad of Wernicke encephalopathy. Vitamin B6 (pyridoxine) is unique in that neuropathy may develop with either deficiency or overload. Excessive doses of B6 result in a sensory neuropathy that ranges in severity from mild distal numbness and tingling with modest exposure to severe sensory ataxia with higher doses. [23]
  • Autoimmune disease/Neuroinflammation: Autoimmune-meditated neuroinflammation (caused by MS, Guillain–Barré syndrome, SLE, Sjögren’s syndrome and paraneoplastic antibodies), or other causes of over active inflammatory processes (i.e. chronic inflammatory demyelinating polyradiculoneuropathy [CIDP], rheumatoid arthritis and vasculitis) often trigger chronic neuralgia and neuropathy symptoms. This occurs as a result of their perpetually degenerative effects on axonal or myelin nerve components. [24],[25] Emerging research suggests that chronic inflammation caused by these conditions compounds neuroinflammation originally triggered by nerve injury, resulting in a vicious cycle of impaired neuronal healing and chronic nerve damage. [26]
  • Chronic Infection: Infections such as HIV, herpes zoster, and Lyme disease (i.e. Borellia burgdorferi) may trigger neuralgia. [27] In HIV, demyelinating neuropathy may arise in both early and late stages of infection. In patients with a history of shingles (i.e. varicella-zoster virus), the virus usually remains latent in cranial or spinal ganglia after resolution of a systemic infection. Reactivation of the virus may be frequent in elderly and immunocompromised patients, causing a vesicular skin eruption accompanied by pruritus and dysesthesias. In Lyme disease, symptoms that arise as a result of advanced infectious sequelae can result in focal and multifocal peripheral or cranial neuropathies and sensory axonal polyneuropathy. Other infections including syphilis, leprosy and diphtheria are also associated with neuropathic inflammation. [28],[29]
  • Medication use: The most common category of drugs associated with neuropathy is antineoplastic agents resulting in chemotherapy-induced neuropathy (CIN). In some cases, the neuropathy progresses for weeks following discontinuation of exposure (hexane and cisplatin), and improvement often requires many months. [30] Medications associated with neuropathy symptoms include: Chemotherapeutics (paclitaxel, cisplatin, oxaliplatin, bortezomib, thalidomide), antimicrobial drugs (chloroquine, dapsone, isoniazid, metronidazole, nitrofurantoin), cardiac drugs (amiodarone, perhexiline, hydralazine) and other medications, including colchicine, gold salts, phenytoin and disulfiram. [31]
  • Toxicity: Toxins including alcohol, nitrous oxide (recreational drug use), lead, arsenic, mercury, organophosphate and solvents have been linked to polyneuropathy. [32] These are cited as rare causes of neuropathic symptoms, [33],[34] however may manifest in patients with a history of chronic exposure as a result of their degenerative neurotoxic and inflammatory effects.

Red Flags:

  • B12 malabsorption: Gastric acid is required to release vitamin B12 from proteins in food. Achlorhydria is prevalent among the elderly, in patients with a history of gastric surgery, and in individuals who regularly use pharmaceuticals that inhibit gastric acid production (proton pump inhibitors, histamine H2 receptor antagonists), contributing to a lack of vitamin B12 availability from the diet. [35] Educate the patient on appropriate methods to enhance digestive absorption and assess and manage vitamin B12 deficiency as required.
  • Coeliac disease: Vitamin B12 deficiency may be associated with mucosal damage caused by coeliac disease in response to gluten exposure, and is a differential diagnosis of neuropathy that may present concurrently. [36] If coeliac disease is suspected, refer patient for serologic testing including tissue transglutaminase (tTG) and deamidated gliadin peptide (DGP) antibody tests.
  • Diabetic complications: In diabetics, impaired sensory function due to losses in nerve function increases the risk of foot ulceration by sevenfold. [37] Abnormal results in monofilament testing and vibratory perception are the most helpful sign for the detection of large fibre neuropathy associated with sensory loss. [38] Refer patient to a General Practitioner for assessment where indicated, and ensure patient is able to access appropriate podiatry or wound care support. To support metabolic health, review the treatment protocol for Diabetes Type 1 and Type 2 to support the management of hyperglycaemia.
  • Neurological paraneoplastic syndromes: These form a group of conditions associated with an immunological response to the tumour, resulting in damage to the nervous system or muscle resulting from axonal degeneration or demyelination. The cancers most commonly implicated are those of the lung, pancreas, breast, prostate, ovary and lymphoma. [39] If the patient presents with signs of neuromuscular dysfunction and malignancy has not been screened as a differential, refer them for assessment by a General Practitioner.
  • Pernicious anaemia: Pernicious anaemia is an organ-specific autoimmune disorder in which the gastric mucosa is atrophic, with loss of parietal cells causing intrinsic factor (IF) deficiency. IF is required for absorption of vitamin B12 in the ileum. In the absence of IF, less than 1% of dietary vitamin B12 is absorbed. [40] If patient presents with chronic vitamin B12 deficiency without a clear probable cause, consider referral to screen for anti-parietal cell antibodies and support B12 repletion.
  • Restrictive diets: Patients adhering to restrictive diets, including vegans and vegetarians, are at an increased risk of vitamin B12 deficiency, as well as those with increased nutritional requirements, such as in pregnancy. [41] Dietary deficiency of vitamin B12 puts patients at a greater risk of developing neurological symptoms. Consider prescribing ongoing nutritional support alongside restrictive diets to ensure adequate vitamin B12 intake.
  • Spinal cord compression: Structural compression complicates approximately 5% of cancers and is most common in myeloma, prostate, breast and lung cancers that involve bone. Cord compression often results from posterior extension of a vertebral body mass, however intrathecal spinal cord metastases can cause similar signs and symptoms. Spinal cord compression initially presents 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. [42] Spinal cord compression is a medical emergency. If suspected, immediately refer the patient for assessment by an overseeing medical Practitioner/General Practitioner or call triple zero (000) in case of emergency.
  • Vitamin B1 deficiency: In patients with chronic alcoholism, or in patients who fail to follow the recommended nutritional supplementation following bariatric surgery, thiamine deficiency may manifest as axonal neuropathy. [43] Refer patient for pathology screening to assess serum thiamine level <20 ng/dL, and provide vitamin B1 supplementation to replete thiamine levels.

Treatment Recommendations

Core Recommendations

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 reduce chronic pain associated with neuralgia and neuropathy.

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 endogenous cannabinoid system (ECS) activity to down-regulate pain and inflammation. [44] PEA has also been shown to minimise pain amplification driven by glial cells, [45],[46] and desensitise transient receptor potential vanilloid type 1 (TRPV1) receptors to mitigate pain sensitivity. [47],[48]
    • Clinically, 600 mg/d of PEA has been shown to reduce neuropathic pain scores from 71% to 21% (p<0.05), [49] with numerous similar trials supporting the efficacy of 600 mg/d of PEA to reduce pain scores by >50% within four weeks. [50],[51]
    • In patients with traumatic and diabetic neuropathy, an eight-week regime that provided a loading dose of 1,062 mg/d of PEA for 10 days, followed by 708 mg/d for the remaining weeks improved pain scores (82% down to 58%); p<0.001), and decreased neuropathic symptoms, such as burning and numbness (5.20 ± 1.5 reduced to 3.8 ± 2.1; p<0.025). [52]
    • PEA can be safely co-prescribed alongside several pain medications classes, such as opioids, non-steroidal anti-inflammatories (NSAIDs), muscle relaxants and corticosteroids. [53],[54],[55],[56]
  • Saffron has been observed to reduce pain receptor sensitivity by blocking transient receptor potential ankyrin 1 (TRPA1). [57]
    • Saffron [58],[59] and its isolated constituent, safranal,[60] have been shown to decrease nerve inflammation by inhibiting microglial and astrocyte activation in models of nerve trauma and oxidative damage. [61],[62],[63] Through reducing glial activation, safranal was shown to improve neuropathic allodynia in vivo. [64]
  • Thiamine (vitamin B1) is a key nutrient required for healthy nerve cell function. [65]
    • In animals, thiamine supplementation following nerve injury was shown to reduce pain transmission. [66]
    • Thiamine promotes myelin synthesis surrounding axonal tissue to preserve nerve structures [67] by enhancing transketolase enzyme activity. [68]

Gamma-Aminobutyric Acid (GABA)

Dosage: Take 250 mg – 500 mg twice daily.

GABA functions as a primary inhibitory neurotransmitter in the central nervous system (CNS), reducing neuronal hyperexcitation that contributes to nerve pain.

Mechanism of Action/Clinical Research:

  • GABA regulates neuronal excitability via GABA receptor subunits, which are classified into three main groups (alpha, beta and gamma). [69]
  • 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. [70]
  • 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. [71]

PLUS

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 ECS-enhancing 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. [72]
  • Insufficient magnesium intake is associated with muscle tension, [73]which may exacerbate chronic nerve 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). [74]
  • Through enhancing ECS activity, PEA* reduces pain amplification driven by immune cells (i.e. microglial and astrocytes), [75],[76] and helps to downregulate TRPV1 nociceptor sensitivity. [77],[78]
    • In patients with chronic jaw pain associated with trigeminal neuralgia, one week of 900 mg/d of PEA followed another a second week of 600 mg/d of PEA significantly decreased pain intensity scores (reduced from 69.9% down to 7.6%) compared to ibuprofen (reduced from 68.4% down to 37.4%; p<0.0001). [79]
    • 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). [80]

Alpha Lipoic Acid for Antioxidant Support

Dosage: 1 tablet daily with food.

Alpha-lipoic acid (ALA) is an intracellular antioxidant that protects neuronal membranes from free radical damage, improving their structure and function. Lipoic acid also enhances glucose uptake, and supports the elimination of toxic heavy metals, all of which are relevant clinical drivers of neuropathy.

Mechanism of Action/Clinical Research:

  • In a randomised, placebo-controlled study, enhanced blood glucose clearance was demonstrated in 55 T2D patients receiving using oral doses of ALA over four weeks between 600 mg/d to 1800 mg/d. [81]
  • In a placebo-controlled trial conducted in 181 diabetic patients, a ≥50% reduction in neuropathic symptoms was achieved in 62% of patients receiving 600 mg/d of LA over five weeks. [82]
  • ALA can modify the chemical reactivity of heavy metals by forming stable complexes with them, thereby neutralising their reactive properties. In vitro studies indicate that ALA preferentially binds to copper, zinc, and lead. [83]

Lipids and Tocotrienols for Healthy Cell Membranes and Cognition

Dosage: Take 1 metric teaspoon (5.0 mL or by measuring cap) twice daily.

A combination of phospholipids and essential fatty acids to enhance neuronal membrane structures and support nerve regeneration, including myelin and axonal repair.

Mechanism of Action/Clinical Research:

  • Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are crucial to normal neurological function, with deficiency resulting in neuronal impairment. [84]
  • In animal models, administration of omega 3 fatty acids (EPA and DHA) has been found to prevent myelin and peripheral nerve degeneration. [85]
  • In vitro depletion of phospholipids within the mitochondria has been found to severely impair mitochondrial membrane potential, respiratory chain activity, [86] and adenosine triphosphate (ATP) production, impairing overall neuronal cell survival and growth. [87]
  • Tocotrienols (vitamin E) are potent antioxidants for lipid-rich tissue [88] found within the central nervous system and mitochondria, correcting redox imbalances that would otherwise promote deoxyribonucleic acid (DNA) damage within neuronal tissue and disrupt cellular homeostasis. [89]

If presenting with vitamin B12 deficiency:

B12/Folate (5-MTHF) for Cellular Health

Dosage: Take 1 capsule daily with food.

Vitamin B12 to replenish deficient levels in addition to nutritional cofactors to promote methylation. Vitamin B12 deficiency is associated with reduced methionine synthase reactions, [90] which may negatively impair methylation processes. The methylation of myelin sphingolipids via the S-adenosyl methionine pathway (involving methylcobalamin) [91] produces the major phospholipid component of membranes in neural tissues.

Mechanism of Action/Clinical Research:

  • In states of poor vitamin B12 absorption, oral vitamin B12 at a dose of 1,000 µg/d has been shown to be adequate in the repletion of vitamin B12 and may serve as an effective alternative to intramuscular B12 injections. [92]

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 your evening meal.

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

Mechanism of Action/Clinical Research:

  • Zizyphus activates glutamic acid decarboxylase, which catalyses GABA synthesis, while also sensitising GABA receptors by increasing their subunit expression, [93] 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. [94]
    • 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. [95]
  • 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). [96]
    • 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 anxiety and sleep quality. [97]
  • California poppy stimulates binding of the GABAαreceptor site, providing sedative effects. [98]

Additional Considerations:

To manage chronic and acute inflammation:

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

Dosage for adults: For the relief of pain, muscle aches and joint stiffness due to mild osteoarthritis: Take 3 capsules twice daily with food.For the relief of mild inflammation: Take 2 capsules daily with food.

A combination of herbs to reduce the production of inflammatory mediators at multiple points of the inflammatory cascade, while also decreasing oxidative stress and tissue damage in neuroinflammatory conditions.

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 (IL)-12. [99],[100]
  • Boswellic acid, acetyl-11-keto-beta-boswellic acid (AKBA), demonstrates anti-inflammatory actions via allosteric regulation of 5-LOX, resulting in LT inhibition. [101] Additionally, boswellia exerts anti-inflammatory activity further up the inflammatory cascade, inhibiting the activation of proinflammatory signalling pathway, nuclear factor kappa B (NFĸB). [102]
  • 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. [103]
    • 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. [104]

OR

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 nerve injury.

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. [105],[106]
  • Boswellia exerts anti-inflammatory activity further up the inflammatory cascade, inhibiting the activation of proinflammatory signalling pathway, NFĸB. [107]
  • The ginger constituents, gingerol and gingerdione, have been shown to down-regulate arachidonic acid metabolism via partial inhibition of 5-LOX. [108] Ginger also inhibits NFĸB activation via suppressing the phosphorylation of protein, inhibitor of ĸB (IĸB), thereby keeping NFĸB sequestered and reducing inflammation. [109]
  • Quercetin is an anti-inflammatory flavonol, found to suppress the production of the inflammatory cytokines IFN-γ and IL-2 that occurs following stimulation of T cell receptors. [110]

Specialised Pro-Resolving Mediators [*]

Specialised pro-resolving mediators (SPMs) to promote resolution of inflammation, reduce pain, encourage the clearance of pathogens and mitigate pathological inflammation, without immunosuppression. In doing so, SPMs address inflammation, which is a major contributor to neuroinflammation.

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 neutrophils (PMNs) and promote efferocytosis and tissue repair. [111]

  • If presenting with Diabetes or Hyperglycaemia - Refer to either Diabetes Type 1 protocol, Diabetes Type 2 protocol or the Metabolic Syndrome Protocol
  • If presenting with Hypothyroidism - Refer to Hypothyroidism protocol
  • If presenting with Autoimmune Disease - Refer to Autoimmune Disease protocol, or specific protocol for Autoimmune conditions.
  • If presenting with Chronic Infection - Refer to Shingles Protocol, Lyme-like illness Protocol, EBV Protocol, CMV Protocol or Chronic Infection Protocol

Supportive Programs

Managing toxicity associated with neuropathy, as well as reducing exposure to environmental toxins supports tissue regeneration and may mitigate chronic neuroinflammation. The Metagenics Clinical Detoxification Program is designed to reduce toxic burden, increase toxin resilience and improve the efficiency of waste elimination. Full instructions and food lists are available for free download.

Diet and Lifestyle Recommendations

Diet:

  • Nutritional effects of uncontrolled pain may include unstable blood glucose, anorexia (loss of appetite), muscle wasting and weakness.
  • To mitigate these effects, patients with chronic pain should aim to eat adequate protein and to limit refined carbohydrate (sugars and starches)-induced episodes of hypoglycemia. This approach is also desirable to promote strength, movement, energy, and mental function.
  • High-level evidence suggests that the Mediterranean diet is associated with a lower risk of disease development. [112]
  • The Mediterranean diet is inclusive of 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 and also provides a simple guide to moderate portion size and the overall balance of macronutrients.
  • Avoid low kilojoule diets, low carbohydrate diets or high energy foods that are nutritionally poor. Energy-dense foods, such as chocolate bars or caffeinated drinks, only offer a temporary energy boost that may worsen hypoglycaemia.
  • Opioids are also linked to causing a ‘sugar desire effect’ on opioid receptors. Consequently, the combination of severe chronic pain and opioid treatment can cause unstable glucose metabolism in patients, and a potent desire to ingest primarily sugars and starches, with little protein or fat intake.
  • Reduce alcohol intake: When consumed in excess, alcohol can exacerbate nerve damage to nerves associated with alcohol-induced vitamin B1 deficiency. [113]

Lifestyle:

  • Ensure adequate sleep, achieving approximately eight hours of sleep each night. [114]
  • Counseling should be initiated at the beginning of therapy to address any psychological issues exacerbating physiologic pain. [115]
  • Physical therapy i.e. massage, physiotherapy etc. should be considered, especially in cases of chronic neck and low back pain. [116]

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.

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