Handbook of Neuropathic Pain Management Guidelines 2nd Edition

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A Summary of Recommendations Issued by the Multidisciplinary Panel on Neuropathic Pain (MPNP)

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Table of Contents
Introduction to neuropathic pain . . . . . . . . . . . . . . . . . . . . . . . . . . . . ......................................... 2 Introduction to the Multidisciplinary Panel on Neuropathic Pain (MPNP) ............. 4 MPNP members . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ......................................... 5 Overview of contents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ......................................... 6 Diagnosis and assessment of pain severity . . . . . . . . . . . . . . . ......................................... 7 Drugs used in the treatment of neuropathic pain . . . . . . ......................................... 9 Drug options and dosages . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....................................... 10 Side effect profiles and management tips . . . . . . . . . . ....................................... 12 Recommendations for postherpetic neuralgia . . . . . . . . . . . . ....................................... 14 Recommendations for idiopathic trigeminal neuralgia ..................................... 16 Recommendations for painful diabetic peripheral neuropathy ........................ 18 Recommendations for neuropathic pain associated with peripheral nerve entrapment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....................................... 20 Recommendations for central post-stroke pain . . . . . . . . . . ....................................... 22 Recommendations for neuropathic cancer pain . . . . . . . . ....................................... 24 Recommendations for neuropathic pain due to spinal cord pathologies ................. 26 Recommendations for complex regional pain syndrome .................................. 28 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....................................... 30

Handbook of Neuropathic Pain Management Guidelines – 2nd Edition

1

Introduction to neuropathic pain
Neuropathic pain
europathic pain covers a diverse group of pain conditions characterized by a primary lesion or dysfunction of the sensory nervous system. It is particularly challenging for clinicians to manage because of its chronicity and severity, poor responsiveness to traditional pain therapies, and wide individual variations in pain responsiveness.1,2 Unfortunately, neuropathic pain conditions are likely to increase as populations age and age-related disorders, such as herpes zoster, diabetes mellitus, cerebrovascular accidents, Parkinson’s disease and cancer, rise in prevalence.3 Medical treatment of neuropathic pain remains unsatisfactory for a substantial proportion of patients, and with the rising rates of disorders known to incite neuropathic pain syndromes, it is vital to improve patient outcomes with existing treatment options and continue to pursue new therapeutic strategies.

N

What is the difference between neuropathic pain and nociceptive pain?
There are two types of pain: nociceptive pain and neuropathic pain. Nociceptive pain serves as a warning of ongoing tissue damage due to injury or disease (eg, a wound, thermal insult or inflammation).3 It comprises somatic pain (in skin, muscles, joints, bone) and visceral pain (in an organ or its covering), and is an acute, self-limiting symptom. In contrast, neuropathic pain is initiated by injury or dysfunction of the peripheral or central nervous system, resulting in a delayed chronic response to damage that is no longer acute, but which continues to evoke pain.3

What causes neuropathic pain?
This disorder can be caused by injury to neuronal cell bodies in the peripheral or central nervous system via compression, transection, infiltration, ischaemia or metabolic injury, or any combination of these effects. Examples of peripheral neuropathic pain conditions include diabetic peripheral neuropathy, postherpetic neuralgia, tumour infiltration neuropathy, phantom limb pain, complex regional pain syndrome and trigeminal neuralgia. Central neuropathic pain conditions include multiple sclerosis, spinal cord injury, central post-stroke pain and Parkinson’s disease. Although the underlying neuronal mechanisms of neuropathic pain are not completely understood, various distinct pathophysiological mechanisms appear to be involved, resulting in both peripheral and central sensitization.4 Nerve lesions can trigger molecular changes in nociceptive neurons, making them abnormally sensitive and evoking pathological spontaneous activity. Inflammation in the damaged nerve trunk can induce ectopic nociceptor activity, causing spontaneous pain. This hyperactivity in nociceptors can induce

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Handbook of Neuropathic Pain Management Guidelines – 2nd Edition

shooting. cold. heat. so that input from mechanoreceptive A fibres is perceived as pain. electric shock-like. crushing. or vise-like. numbness. searing or scalding. May be mechanical. and the somatosensory system should be performed. light touch) when applied to the affected area. The pain may be continuous or paroxysmal in presentation. temporal variations in pain intensity and functional impact. pressure. Other common symptoms include3: • Allodynia – Pain due to nonnoxious stimuli (clothing. In addition. tingling. The sensory examination should include assessment of responses to touch. cold. amputated limb) or where there is no current injury • Referred pain – Occurs in a region remote from the source How to assess a patient for neuropathic pain Neuropathic pain should be suspected in patients who present with pain that they describe in any of the following terms: burning. Clinical evaluation should include a history to assess pain intensity. vibration and temporal summation in the area of maximal pain. Examples of screening tools include ID Pain and painDETECT. electric. A physical examination of gross motor function. pinprick. neuroplastic changes in the central pain modulatory systems can lead to further hyperexcitability. stabbing. sensory descriptions of the pain quality.What are the symptoms of neuropathic pain? Neuropathic pain is commonly described as burning. deep tendon reflexes. tingling and shooting in nature.4 . dynamic or thermal • Anaesthesia – Loss of normal sensation to the affected region • Dysaesthesia – Spontaneous or evoked unpleasant abnormal sensations • Hyperalgesia – Exaggerated response to a mildly noxious stimulus applied to the affected region • Hyperpathia – Delayed and explosive response to a noxious stimulus applied to the affected region • Hypoaesthesia – Reduction of normal sensation to the affected region • Paraesthesias – Nonpainful spontaneous abnormal sensations • Phantom pain – Pain from a specific site that no longer exists (eg.2 Patient-completed neuropathic pain screening tools can assist primary care physicians in differentiating between nociceptive and neuropathic pain. Handbook of Neuropathic Pain Management Guidelines – 2nd Edition 3 Neuropathic pain secondary changes in processing neurons in the spinal cord and brain.

Hong Kong physicians lacked local guidelines for managing neuropathic pain. geriatric medicine. Therefore. 4 Handbook of Neuropathic Pain Management Guidelines – 2nd Edition . For some time. anaesthesiology and orthopaedics. management and treatment of these conditions in Hong Kong. and to contribute to better diagnosis. It aims to act as an information source for medical professionals on the treatment and management of neuropathic pain and provide evidence-based resources on neuropathic pain. the MPNP has endeavoured to improve the understanding and general awareness of neuropathic pain syndromes.Introduction to the Multidisciplinary Panel on Neuropathic Pain (MPNP) T The MPNP he Multidisciplinary Panel on Neuropathic Pain (MPNP) comprises local thought leaders dedicated to improving the awareness and understanding of neuropathic pain in Hong Kong. and were potentially unaware of the most appropriate referral pathways and treatments. neurosurgery. The panel includes specialists from a range of disciplines involved in treating neuropathic pain: neurology.

and Adjunct Associate Professor. FRCP(Edin). Hong Kong SAR Chief of Service. Hong Kong SAR Dr Joseph MK LaM MBChB. Integrated Medical Services. FRCP(Lond). FFPMANZCA. The Chinese University of Hong Kong. FCSHK. Department of Orthopaedic Surgery. Consultant and Head. Department of Medicine and Therapeutics. The Chinese University of Hong Kong. Alice Ho Miu Ling Nethersole Hospital and North District Hospital. Prince of Wales Hospital. MRCP. MHA Dr Vincent MoK MBBS. Tak Hong TSoi and Vincent MoK. FRCS(Edin). L-R (seated): Chun Por Wong. Division of Neurology. DipPainMgt(HKCA). FRCP(Edin). FANZCA. Department of Anaesthesiology and Operating Theatre Services. Hong Kong SAR Professor and Head. MS. Josephine WY iP and Phoon Ping CHen . Hong Kong SAR Dr steven ho shan Wong MBBS. FHKAM(Med) Associate Professor and Chief. FRCP(Glas). Hong Kong SAR Professor Lawrence Ks Wong MBBS. FHKAM(Med). FHKAM(Ana). DipPainMgt Consultant Anaesthesiologist and Head of Pain Management Team. Queen Mary Hospital. FHKAM(Med). Joseph MK LaM. Department of Surgery. Prince of Wales Hospital. Queen Elizabeth Hospital. FRCP Hospital Chief Executive. FRCP(Lond). FRCS(Edin). The Chinese University of Hong Kong. FRCP(Edin). MD(CUHK) Consultant and Chief of Service. FANZCA.MPNP members Current members Dr Phoon Ping Chen MBBS. FHKAM(Ortho). Division of Hand and Foot Surgery. DipPainMgt(HKCA) Past members Dr Tsun Woon Lee MBBS. MRCP. FHKAM(Surg) Dr Chun Por Wong MBBS. FHKAM(Ana). DipHandSurg (FESSH) Dr Tak hong TsoI MBBS. FHKAM (Ana). Pok Oi Hospital. FHKCP. Hong Kong SAR 5 Handbook of Neuropathic Pain Management Guidelines – 2nd Edition The MPNP L-R (standing): Steven Ho Shan Wong. MD. FRCP(Glas). Hong Kong SAR Neurologist and Consultant Physician. The Chinese University of Hong Kong. Department of Medicine and Therapeutics. Pamela Youde Nethersole Eastern Hospital. Department of Anaesthesiology and Operating Services. Department of Medicine. FHKCA. The University of Hong Kong. Department of Geriatrics. Division of Neurology. Hong Kong SAR Associate Professor and Honorary Associate Consultant. FFPMANZCA. FANZCA. Division of Neurosurgery. FHKCP Honorary Consultant and Honorary Clinical Associate Professor. Prince of Wales Hospital. Ruttonjee and Tang Shiu Kin Hospitals. FHKAM (Med). Hong Kong SAR Dr Josephine WY IP MBBS.

As new research and clinical experience broadens medical knowledge. It is hoped that this concise guide will assist Hong Kong physicians in their daily management of patients suffering from neuropathic pain conditions. the diagnosis and management of neuropathic pain will undoubtedly change. and notes on the most common side effects associated with neuropathic pain medications. Particular emphasis is paid to details of appropriate treatment options. The contents include simple tools to assist in the diagnosis and evaluation of neuropathic pain. Full prescribing information should always be consulted before initiating therapy. For full details. It is important to note that not all drugs mentioned are licensed for use in neuropathic pain conditions. and is not meant as a comprehensive guide to the complete multidisciplinary management of patients with these conditions. which are available on the MPNP Web site (www.Overview of contents ince its inception in 2001.org). The largest section of the handbook is devoted to reproducing the treatment algorithms recommended by the MPNP for the management of neuropathic pain conditions. The MPNP cannot be held liable for any consequence arising from inappropriate application of the information provided in this handbook. the MPNP has published recommendations on a variety of neuropathic pain conditions. summary tables of dosage and administration details of many of the drugs used for neuropathic pain. which are endorsed by the Hong Kong Pain Society and are updated regularly. 6 Handbook of Neuropathic Pain Management Guidelines – 2nd Edition . The booklet is provided as a convenient summary of the medical management options in neuropathic pain conditions. physicians are encouraged to consult the original versions of the MPNP recommendations. thus ultimately helping to improve the quality of life of patients with these disabling conditions. This booklet summarizes these recommendations. S Overview Disclaimer Every effort has been made to ensure that the information contained in this handbook is accurate at the time of publication.neuropainhk.

can assist primary care physicians in differentiating nociceptive from neuropathic pain.6 Handbook of Neuropathic Pain Management Guidelines – 2nd Edition 7 Assessment of neuropathic pain . and can be used to monitor the effectiveness of therapy. Screening Questionnaire5. The Chinese version has recently been validated. and facilitate earlier and more appropriate treatment.Diagnosis and assessment of pain severity T he following patient-completed screening questionnaire. The two other items can help patients describe the extent and severity of pain. called ID Pain.

Assessment of neuropathic pain 8 Handbook of Neuropathic Pain Management Guidelines – 2nd Edition .

Anticonvulsants Anticonvulsants act as membrane-stabilizing agents by altering abnormal sodium channel function and calcium channel activity. The local anaesthetic mexiletine is structurally similar to lignocaine. is thought to relieve neuropathic pain by increasing NA and 5-HT activity in the central nervous system. sodium channel effects and N-methyl D-aspartate (NMDA) receptor antagonism. which has a membrane-stabilizing effect and disrupts transmission of pain signals. The assumed analgesic mechanism of action of these drugs is acute inhibition of sodium channels. The alpha-2-delta (A2D) ligands gabapentin and pregabalin may have a number of actions. Opioids relieve neuropathic pain in some patients. however. pain relief appears to be only moderate and treatment-limiting side effects are common. on average. Antidepressants Tricyclic antidepressants (TCAs) enhance the descending pain inhibitory system by preventing cellular reuptake of noradrenaline (NA) and serotonin (5-HT). it appears that reduced sensitivity to systemic opioids is present. Other possible mechanisms of action include α–adrenergic blockade. but binding to the α2-d subunit of the voltage-gated calcium channel appears to play a significant role in their antineuropathic activity. thus reducing the potential for transmission of abnormal pain signals. necessitating the use of higher doses. orally active and has antiarrythmic activity. The topical application of local anaesthetics (eg. Local anaesthetics The local anaesthetic lignocaine is used systemically and topically in neuropathic pain. Handbook of Neuropathic Pain Management Guidelines – 2nd Edition 9 Drugs for neuropathic pain Drugs used in the treatment of neuropathic pain . 5% lignocaine patch. The molecular mechanisms of opioid action in neuropathic pain are not yet fully understood. EMLA) may be useful for patients who have small areas of hyperaesthesia. a 5-HT and NA reuptake inhibitor (SNRI). Duloxetine. Opioids Despite the initial belief that neuropathic pain was opioid-resistant.

then increase by 50–100 mg every wk Increase by 10 to 25 mg weekly Recommended for starting dosage Dose titration (if necessary) Gabapentin* 300 mg at bedtime on Day 1.and second-line drugs mentioned in the treatment algorithms included in this booklet. tinnitus. Drug anticonvulsants Pregabalin* PHN (1st line) DPN (1st line) TN (2nd line) PHN (1st line) DPN (1st line) TN (2nd line) TN (1st line) PHN (2nd line) TN (2nd line) 150 mg/day as 75 mg bid Increase to 300 mg daily after 3–7 days.Drug options and dosages Drugs for neuropathic pain This table covers most of the first. dizziness. under occlusive dressing if possible 10 Handbook of Neuropathic Pain Management Guidelines – 2nd Edition . convulsions Increase by 50 mg every 2 to 3 days prn None needed – Mexiletine 5% lignocaine patch EMLA® PHN (1st line) PHN (1st line) 150 mg daily to 200 mg bid Apply patch for a maximum of 12 h tid. methadone. then by 150 mg/d every 3–7 days as tolerated Increase by 300 mg tid every 1–7 days as tolerated 100 mg every 3–7 days Increase to 50 mg/day for 2 wks. slurring of speech. diplopia. 300 mg tid on Day 3 100 mg bid 25 mg/day for 2 weeks Carbamazepine† Lamotrigine antidepressants Amitriptyline PHN (1st line) DPN (1st line) TN (2nd line) PHN (1st line) DPN (1st line) TN (2nd line) DPN (1st line) PHN (2nd line) 10–25 mg daily at bedtime Nortriptyline. oxycodone. perioral numbness. levorphanol Tramadol Local anaesthetics IV lignocaine 10–25 mg at bedtime Increase by 25 mg daily every 3–7 days as tolerated – After 1–2 wks. desipramine Duloxetine opioids Morphine. but does not represent an exhaustive list of treatment options. 300 mg bid on Day 2. Full prescribing information should be consulted before initiating therapy. eg. convert total daily dosage to long-acting opioid analgesic and continue short-acting medication as needed Increase by 50–100 mg daily in divided doses every 3–7 days as tolerated 60 mg/day 10–15 mg morphine q4h or as needed (equianalgesic dosages should be used for other opioid analgesics) 50 mg daily or bid DPN (2nd line) 5 mg/kg over 30–60 min Titrated based on symptoms of cyclic antidepressant toxicity.

Moulin DE. intravenous. 2008. The Merck Manual for Healthcare Professionals.600 mg/day 200–400 mg/day Up to 75 mg daily 150 mg daily 60 mg/day No maximum dosage with careful titration 400 mg daily (100 mg qid). September 2007. May 2007. Cahill CM. Leicestershire Medicines Strategy Group. Available at: http://www.B. 300 mg daily in patients >75 years 4 wks – 1.pdf. TN.html#CACIDGIH. Assessing and Treating Neuropathic Pain.600 mg daily (1.175:265-275.200 mg tid) 3–8 wks for titration plus 2 wks at maximum tolerated dosage 8-12 wks 12 wks (including titration period) 3 months at maximum tolerated dosage 6–8 wks with at least 2 wks at maximum tolerated dosage – 4–6 wks 1. CMaJ 2006. There is no evidence that paracetamol and NSAIDs are effective for the treatment of neuropathic pain. eutectic mixture of local anesthetics. –. EMLA. 2008. Watson CPN.Maximum dosage Duration of adequate trial 600 mg daily (200 mg tid or 300 mg bid) 4 wks wks. Neuropathic pain: a practical guide for the clinician. Accessed April 18. Available at: http://www. Guideline for treating patients with neuropathic pain. IV. postherpetic neuralgia. Accessed April 18.200 mg/day 3 patches daily for no more than 12 h in 24 h – – 2–4 wks – Handbook of Neuropathic Pain Management Guidelines – 2nd Edition 11 Drugs for neuropathic pain .lmsg. DPN. 2008.com/pain_mgmt/printversion/ama_painmgmt_m9. Module 9. weeks. Neurological Disorders. Pain. Accessed April 18. Available at: http://www. Sources: American Medical Association. amacmeonline.pdf. diabetic polyneuropathy. † Carbamazepine is licensed in Hong Kong for the treatment of trigeminal neuralgia and diabetic polyneuropathy. information unavailable/incomplete. 3.uk/ Guidelines/pdfdocs/NeuropathicPainGuideline200711. Gilron I. trigeminal neuralgia N.merck. * Pregabalin and gabapentin are licensed in Hong Kong for the treatment of neuropathic pain.com/mmpe/sec16/ ch209/ch209a. PHN.nhs.

unsteady gait. tiredness. change in hot or cold sensation 12 Handbook of Neuropathic Pain Management Guidelines – 2nd Edition . insomnia or drowsiness. somnolence. drowsiness. GI distress. constipation. serious AEs: hyponatraemia. constipation. urinary retention. The list is not exhaustive and full prescribing information should be consulted before initiating any therapy. slurred speech. dry mouth. nausea & vomiting. trembling. euphoric mood. dry mouth. risk of serotonergic syndrome if combined with SSRIs Mexiletine 5% lignocaine patch EMLA ® Mild localized skin reactions around application site Pale skin. change in sensorium. agitation. increased sweating. headache. vomiting. aplastic anaemia. palpitations. tremor. insomnia. constipation. peripheral oedema. fatigue opioids Morphine. nausea/vomiting. a change in personality. somnolence. dizziness. lightheadedness. ataxia. somnolence. methadone. vomiting. postural hypotension. blurred vision. dizziness. blurred vision. ataxia. arthralgia. constipation. emotional lability Lightheadedness. diplopia. Drug anticonvulsants Pregabalin Gabapentin Carbamazepine Dizziness. increased appetite. disturbed vision. nausea. dry mouth. balance disorder Sedation. sedation. dizziness. memory impairment. inco-ordination. oxycodone. cardiotoxicity. depression. nausea. dizziness. back pain antidepressants Amitriptyline Dry mouth. risk of seizures/ epilepsy. ataxia. sweating. dizziness. burning. blurred vision. insomnia. disturbed attention. nervousness. nausea. nystagmus. redness or swelling at the application site. weight gain. respiratory depression Dizziness. agranulocytosis. sedation. levorphanol Tramadol Local anaesthetics IV lignocaine Tremor.Side effect profiles and management tips Drugs for neuropathic pain This table summarizes some of the more commonly encountered adverse effects associated with neuropathic pain treatments. GI distress. decreased appetite. Stevens-Johnson syndrome* Potential adverse effects Lamotrigine Skin rash (potentially severe). irritability. desipramine Duloxetine Nausea. proarrhythmia. constipation. gait abnormalities. painful menses. nystagmus. hallucinations. diarrhoea. impaired haemodynamics Constipation. tremor. drowsiness Nortriptyline. nausea/vomiting.

Module 9. et al. contraindicated in porphyria. monoamine oxidase. Gilron I. O’Connor AB. Dworkin RH.com/ pain_mgmt/printversion/ama_painmgmt_m9. Leicestershire Medicines Strategy Group. September 2007. Accessed April 18. CMaJ 2006. administer with food or prescribe antacids to reduce GI AEs.merck. most cases of rash occur within first 8 weeks CI. Accessed April 18.nhs. –. Accessed April 18. Moulin DE. Watson CPN. may be poorly tolerated by the elderly. Pharmacologic management of neuropathic pain.Comments Dose adjustment needed in renal dysfunction Dose adjustment needed in renal dysfunction Monitor CBC. Backonja M. adverse effects. complete blood count. Cahill CM. Pain 2007.175:265-275. apply to affected area – Handbook of Neuropathic Pain Management Guidelines – 2nd Edition 13 Drugs for neuropathic pain . Guideline for treating patients with neuropathic pain. Available at: http://www. contraindicated.pdf. Pain. monitor and adjust dose to prevent QTc prolongation. MAO. AEs. patients should seek immediate medical assistance if fever. sore throat. eutectic mixture of local anesthetics. IV. use with caution in epileptic patients Decrease the infusion rate or discontinue treatment if signs of toxicity Consider cardiac evaluation before initiating therapy in patients with a significant heart disorder. EMLA. has a narrow therapeutic index Only apply to healed intact skin. Neurological Disorders. 2008. 2008. Assessing and Treating Neuropathic Pain. AV. Available at: http://www. monitor blood pressure. pdf.html#CACIDGIH. atrioventricular. CI in patients with glaucoma and those taking MAO inhibitors Nortriptyline causes less sedation and anticholinergic effects than amitriptyline. 2008. selective serotonin reuptake inhibitor.com/mmpe/ sec16/ch209/ch209a. Available at: http://www. CI in patients with glaucoma and those taking MAO inhibitors – Coadminister pre-emptive stool softeners and antiemetics Initiate therapy at low dose and titrate as tolerated. information unavailable/incomplete * Genetic susceptibility for Stevens-Johnson syndrome (HLA-B1502) should be assessed in Asian patients before commencing treatment with carbamazepine. rash or mouth ulcers. gastrointestinal. Sources: American Medical Association.lmsg. Evidence-based recommendations. CBC.amacmeonline.132:237-251. GI. bruising/bleeding develop Very slow dose titration minimizes risk of rash. SSRI.uk/Guidelines/pdfdocs/NeuropathicPainGuideline200711. titrate dose slowly. May 2007. liver enzymes and sodium levels for 1 year. Give dose at bedtime to minimize effect of sedation. The Merck Manual for Healthcare Professionals. Neuropathic pain: a practical guide for the clinician. AV block or with concomitant MAO inhibitors. intravenous.

N-methyl D-aspartate The A2D ligands are pregabalin and gabapentin * Genetic susceptibility for Stevens-Johnson syndrome (HLA-B1502) should be assessed in Asian patients before commencing treatment with carbamazepine. 14 Postherpetic neuralgia . eutectic mixture of local anaesthetics.Recommendations for postherpetic neuralgia7 Postherpetic neuralgia TCA. tricyclic antidepressant. EMLA. NMDA. Postherpetic neuralgia is a neuropathic pain syndrome that occurs following acute herpes zoster infection or shingles. A2D. transcutaneous electrical nerve stimulation. alpha-2-delta. TENS.

26 A multidisciplinary approach to managing these difficult-to-treat patients may be necessary. or in cases where TCAs are not tolerated or are contraindicated.8-13 In some practices.18 This can be first-line treatment if antidepressants and anticonvulsants are contraindicated.21 intrathecal steroids. such as NMDA receptor antagonists. • Consider tramadol19 or opioids20 if antidepressants and anticonvulsants are ineffective or are contraindicated.24 or combination therapy. such as a lignocaine patch14-16 or EMLA cream. • Carbamazepine is commonly used. • Add a topical local anaesthetic. • Consider transcutaneous electrical nerve stimulation (TENS) as adjunctive therapy.23.25.• Start low-dose amitriptyline or nortriptyline therapy (10 to 25 mg at night) and titrate weekly up to the maximum tolerated dose or a maximum of 150 mg. Postherpetic neuralgia 15 Postherpetic neuralgia . • For patients older than 60 years. consider referring the patient to a pain medicine specialist for alternative therapies. but there is little evidence to support its use.17.22 intravenous adenosine 5’-triphosphate (ATP). pregabalin and gabapentin are considered first-line therapy. • If adequate pain control is not achieved after 8 weeks. the A2D ligands pregabalin or gabapentin may be used.

alpha-2-delta. PRGR. percutaneous retro-Gasserian glycerol rhizotomy The A2D ligands are pregabalin and gabapentin * Genetic susceptibility for Stevens-Johnson syndrome (HLA-B1502) should be assessed in Asian patients before commencing treatment with carbamazepine. PRFR.Recommendations for idiopathic trigeminal neuralgia27 Diabetic neuropathy A2D. percutaneous radiofrequency rhizotomy. balloon compression rhizotomy. BCR. The second or third division of the trigeminal nerve is affected in most trigeminal neuralgia patients. 16 Painful diabetic peripheral neuropathy .

The second-line drugs include pregabalin.• The primary care physician should try carbamazepine first. one or two second-line drugs may be tried. an operation or interventional treatment should be considered.38-40 • If treatment is not successful following a trial of two or three medications for an adequate period (3 to 6 months). – In general. • Peripheral trigeminal nerve block is a useful adjunctive therapy.45 Painful diabetic peripheral neuropathy 17 Diabetic neuropathy .29-31 gabapentin.36 lamotrigine33 and antidepressant agents.43 – Gamma knife radiosurgery (GKR) should be reserved for patients who have failed both surgical and percutaneous procedures.37 • For chronic. microvascular decompression should be recommended.34.35 baclofen. for patients younger than 70 years who have a low surgical risk and prefer to preserve trigeminal nerve function. balloon compression rhizotomy (BCR) should be considered over PRFR. and may be used while pharmacotherapy is being optimized.33 clonazepam. intractable pain.11-13. Patients should be allowed to consider all of the available options.28 • If the response is not satisfactory or the patient cannot tolerate treatment.33 sodium valproate.42 – In cases involving the ophthalmic division or all three divisions. • Selecting a procedure is both difficult and controversial. a patient should be referred to a multidisciplinary pain management centre.32 phenytoin.44.41 – Percutaneous radiofrequency rhizotomy (PRFR) can be considered for patients who have failed medical treatment and suffer from intractable TN.

A2D. SNRI. NMDA. PENS. tricyclic antidepressant. percutaneous electrical nerve stimulation. 18 Idiopathic trigeminal neuralgia . alpha-2-delta. N-methyl-D-aspartate.Recommendations for painful diabetic peripheral neuropathy46 TCA. Diabetic neuropathy may lead to foot ulceration and even the need for amputation. transcutaneous electrical nerve stimulation. serotonin–norepinephrine reuptake inhibitor The A2D ligands are pregabalin and gabapentin Trigeminal neuralgia Approximately 20 to 40% of diabetic patients develop some sort of neuropathy. TENS.

desipramine) should be considered first-line therapies. • For acute pain. However. such as spinal cord stimulation. TCAs are contraindicated in patients with cardiac and hepatic disease.53 • Pain management programmes and behavioural therapy can also be used with pharmacological approaches to teach patients how to live with pain. if necessary. TCAs (eg. • For chronic pain. may be considered as a last option. but these can be minimized by starting with a low dose at night and increasing gradually.28-31.28 Pain relief may not be apparent for up to 3 weeks. 2 to 3 months with two to three different agents) should be referred to a multidisciplinary pain clinic for further therapeutic initiatives.48-50 • Tramadol may be an effective alternative for some patients. warm baths or elastic stockings may also help to relieve leg pain. carbamazepine or phenytoin. Some patients cannot tolerate the side effects of TCAs. • Physical stimulation. or as an add-on therapy to A2D ligands.47 In addition. Idiopathic trigeminal neuralgia 19 Trigeminal neuralgia . imipramine and desipramine are less sedating than amitriptyline. nortriptyline. More invasive stimulatory interventions. • If TCAs are contraindicated . Regular walking. pregabalin and gabapentin) should be considered as first-line treatment options due to their efficacy and safety. start with simple analgesics and progress to TCAs or other adjuvant analgesics. such as TENS52 and acupuncture. may counteract painful sensations. SNRIs should also be considered as an alternate first-line choice. acupuncture and topical treatments should be used with caution in the lower leg in patients with diabetes.51 • Patients remaining refractory to a reasonable trial of pharmacotherapy (eg. as these may aggravate the skin and lead to infection. Nortriptyline. A2D ligands are generally associated with fewer side effects compared with TCAs. the side effects can be further minimized by slow dosage titration. amitriptyline.• A2D ligands (eg. ineffective and/or not well tolerated. Also.

PENS. 20 Neuropathic pain associated with peripheral nerve entrapment .Peripheral nerve entrapment Recommendations for neuropathic pain associated with peripheral nerve entrapment54 Cervical radiculopathy Conservative treatment • Cervical collar • Oral NSAIDs • Physiotherapy/neck care exercises • Anticonvulsants or antidepressants • Epidural corticosteroid injection • Anterior discectomy with spinal fusion • Microforaminotomy • Cervical arthroplasty Lumbar radiculopathy • • • • • Lumbar corset Oral NSAIDs Physiotherapy PENS/TENS Anticonvulsants or antidepressants • Epidural corticosteroid injection • Chemonucleolysis • Discectomy • Microdiscectomy • Percutaneous discectomy • Lumbar foraminotomy • Lumbar spinal fusion Carpal tunnel syndrome • Physiotherapy • Wrist splinting • Oral steroids and local steroid injections • Diuretics Cubital tunnel syndrome • Educate patient on how to avoid provoking symptoms • Conservative treatment does not have a great role in management surgical interventions • Carpal tunnel release (open or endoscopic) • Simple neurolysis • Anterior transposition of ulnar nerve • Medial epicondylectomy of distal humerus • Cubital tunnel release (open or endoscopic) NSAIDS. percutaneous electrical nerve stimulation. transcutaneous electrical nerve stimulation Carpal tunnel syndrome results from compression of the median nerve at the carpal tunnel. TENS. nonsteroidal anti-inflammatory drugs.

Local steroid injection may be superior to oral corticosteroids.55 Carpal tunnel syndrome • Conservative strategies that may be of benefit include good ergonomics.62 • NSAIDs. postural training and activity modification. anterior transposition of the ulnar nerve or medial epicondylectomy of the distal humerus. rest at intervals and minimizing hand or wrist movements.63. splinting of the wrist in a neutral position. Pregabalin has demonstrated some benefit in cervical radiculopathy.58-60 • Gabapentin was effective in patients with chronic radiculopathy (L4-5 and/or L5-S1 bulging and/or protrusion).Cervical radiculopathy • Surgery (eg.61 Pregabalin as monotherapy or add-on therapy improved patientreported clinical outcomes in painful lumbar or cervical radiculopathy. Neuropathic pain associated with peripheral nerve entrapment 21 Peripheral nerve entrapment • Mild cases may improve without treatment. mobility must be maintained. or may benefit from short-term use of a cervical collar.56 • Oral NSAIDs57 and physiotherapy may be beneficial. decompression via an anterior cervical approach with spinal fusion or a posterior approach with laminectomy) is indicated for more severe cases or when other treatments have failed. or motor involvement or severe numbness is present.55 . Cubital tunnel syndrome • Frequently requires a release operation. neck-care exercises. Acupuncture and ultrasound may also reduce pain. Epidural corticosteroids and percutaneous or transcutaneous electrical nerve stimulation may give short-term relief. diuretics and oral corticosteroids are options for mild-to-moderate carpal tunnel syndrome.64 • Carpal tunnel release surgery (open or endoscopic) is indicated when conservative therapy has failed. Lumbar radiculopathy • Bed rest is not recommended. nonsteroidal anti-inflammatory drugs (NSAIDs). and intermittent cervical traction. such as simple neurolysis.

Recommendations for central post-stroke pain65 Central post-stroke pain A2D. tricyclic antidepressant. alpha-2-delta. Central post-stroke pain . central post-stroke pain The A2D ligands are pregabalin and gabapentin CPSP is characterized by constant or intermittent pain following a stroke. Around 8% of stroke patients will develop CPSP. CPSP. TCA.

66 • Lamotrigine may be used as a second-line agent or an alternative first-line treatment to TCAs.69 • Intravenous lignocaine may provide pain relief in some patients with CPSP. but may be associated with morbidity and mortality.75. To minimize side effects. spinal cord stimulation and stereotactic mesencephalic tractotomy may be beneficial.67 • Central pain appears to be poorly responsive. but not totally unresponsive. to opioids. another A2D ligand. Motor cortex stimulation.76 Central post-stroke pain 23 Central post-stroke pain • Gabapentin. is approved for the treatment of neuropathic pain and may be effective in treating CPSP. • Intrathecal baclofen may be effective in some patients with CPSP. • Surgical interventions can be considered for patients unresponsive to pharmacological therapy.71 • Mexiletine may be used as an adjunct to TCAs when patients do not respond to TCAs alone. commence at a low dose and titrate to a higher maintenance dose.73.74 but should only be considered after the failure of other pharmacologic therapies.• TCAs such as amitriptyline or nortriptyline should be considered as first-line therapy for central post-stroke pain (CPSP).72 • Patients remaining refractory to a reasonable trial of pharmacotherapy should be referred to a multidisciplinary pain clinic for further therapeutic initiatives. including CPSP.68 .70. • The A2D ligand pregabalin is a first-line treatment option as it has been shown to significantly reduce pain and improve health status in patients with central pain.

TCA. alpha-2-delta. CPSP. tricyclic antidepressant.Recommendations for neuropathic cancer pain77 Neuropathic cancer pain A2D. central post-stroke pain The A2D ligands are pregabalin and gabapentin 24 Neuropathic cancer pain .

certain interventional techniques for neuropathic pain should only be considered when pharmacologic interventions have failed.78 For example. radiation therapy or chemotherapy.87 • Patients with postsurgical neuropathic pain may also benefit from topical capsaicin cream when appropriate. radiotherapy can relieve neuropathic pain due to tumour-induced neural compression or irritation.81 Anticonvulsants should be initiated at a low dose and slowly titrated until the patient achieves adequate pain relief or side effects develop. but because of its adverse effects should be limited to experienced teams.80 Pregabalin after epidural anaesthesia significantly improved visual analogue scale (VAS) and quality-of-life scores in chronic cancer patients.86.84 Antidepressants may be given together with anticonvulsants when there is unsatisfactory response to either medication.• For neuropathic pain caused by direct tumour involvement. first-line management is oncologic treatment and may include surgery. spinal cord compression) should be managed appropriately.82 • Interventional therapy may also be effective for neuropathic cancer pain.88 However.87 . • Anticonvulsants should be considered if neuropathic pain is unresponsive to conventional analgesics. Neuropathic pain specifically due to cancer treatment may be treated with gabapentin.83.85 • Other adjunctive therapies include systemic lignocaine.82 • Antidepressants such as TCAs or selective serotonin reuptake inhibitors are alternative options for management of neuropathic pain.89 Neuropathic cancer pain 25 Neuropathic cancer pain • Systemic ketamine may be effective. are poorly tolerated or inappropriate.79 • Correctable causes of neuropathic pain (eg.

TCA. tricyclic antidepressant The A2D ligands are pregabalin and gabapentin Spinal cord pathology Pain develops in around 60 to 70% of patients with spinal cord injury. 26 Neuropathic pain due to spinal cord pathologies . alpha-2-delta.Recommendations for neuropathic pain due to spinal cord pathologies90 A2D. and about one third will report severe pain.

103 • Patients who respond poorly to oral. such as intrathecal drug administration. antineoplastic treatment may reduce tumour size and provide pain relief. then maintained at a dose of 5. if possible.102.93. incontinence). maintain treatment for 48 hours if initiated between 3 and 8 hours after injury. TCAs may also be considered as a first-line management option despite limited evidence.28 Patients may also be given other anticonvulsants or opioids to improve pain control. neurostimulation (eg.94 • A2D ligands (eg.4 mg/kg/h. surgery for certain structural abnormalities) and other neurological sequelae (eg. motor deficits. • Spinal cord injury (SCI) causing compression should be treated within 8 hours of compression.104-114 • A multidisciplinary approach should be taken to rehabilitation. If initiated within 3 hours. transdermal or intravenous analgesics may be considered for invasive procedures. spinal cord stimulation.91 Many patients achieve significant pain relief from physical therapy. pregabalin.96-100 • Intravenous ketamine may be used as third-line therapy. but requires meticulous monitoring for side effects. electroacupuncture) and dorsal root entry zone lesioning (DREZotomy).• Treatment of neuropathic pain due to spinal cord lesions includes primary treatment of the underlying cause (eg.96 Alternatively.94 Neuropathic pain due to spinal cord pathologies 27 Spinal cord pathology . treatment should be maintained for 24 hours.100.93. If neuropathic pain is due to direct compression by tumour. gabapentin) may be used in conjunction with physical and psychological therapy as first-line treatments for neuropathic pain due to spinal cord lesions.95.92 • There is very little evidence that NSAIDs have benefit for pain due to spinal cord lesions.91 Methylprednisolone may be given as a 30 mg/kg-bolus dose.

116 28 Complex regional pain syndrome . CRPS. The efficacy of sympathetic blocks in the treatment of CRPS is still poorly defined.Complex regional pain syndrome Recommendations for complex regional pain syndrome115 *Primarily diagnostic and/or to facilitate physical rehabilitation. nonsteroidal anti-inflammatory drug. TENS. complex regional pain syndrome. NSAID. tricyclic antidepressant. TCA. transcutaneous electrical nerve stimulation Adapted from treatment algorithm proposed by the International Coalition on Neuropathic Pain.

amitriptyline)120. and reduce depression and dependence on health care.125. • Whenever appropriate.66. • For patients with sympathetic maintained pain (SMP). pain relief may not be apparent for 3 weeks at the maximum tolerated dosage.123 Slow dosage titration (up to 8 weeks) is necessary to minimize side effects of both TCAs and anticonvulsants. pregabalin).122. especially for at-risk patients. Neurostimulation of the spinal cord or peripheral nerves may be effective. a trial of combined TCA and anticonvulsant may be effective.118. anti-inflammatory medications are useful in the acute phase following injury to minimize pain and swelling. sympathetic blocks provide effective pain relief to facilitate physical rehabilitation.117 • Psychological support and cognitive behavioural management programmes can help patients manage their pain. but this should only be used for shortterm treatment.116 • Rescue therapy with opioids may be necessary. Destructive or ablative surgery is not recommended127 and only has a limited role in providing relief for patients with a short life expectancy.121 or anticonvulsants (eg. This will improve pain control and mobility. gabapentin. invasive procedures can be considered.126 but may not improve long-term prognosis.• An early programme of physical and occupational therapy. • When the response to TCAs and anticonvulsants is unsatisfactory. is essential to treat the secondary complications of CRPS. such as decreased joint and tendon movement.119 • Primary pain management should include tricyclic antidepressants ([TCAs] eg. Complex regional pain syndrome 29 Complex regional pain syndrome • Patient outcomes are improved if treatment is started at an early stage: patients should be referred as soon as possible to pain specialists or physicians with experience in managing complex regional pain syndrome (CRPS).117 .124 • For patients remaining refractory to trials of pharmacotherapy and physiotherapy.

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