Translate this page into:
Basics of Chronic Pain Management
*Corresponding author: Vrishali Ramesh Ankalwar, Associate Professor, Department of Anaesthesia, Government Medical College, Nagpur, Maharashtra, India. vriankalwar@yahoo.com
-
Received: ,
Accepted: ,
How to cite this article: Ankalwar VR. Basics of Chronic Pain Management. Vidarbha J Intern Med 2022;32:120-8.
Abstract
Approximately one in ten people suffer from chronic pain globally with pain being the most common reason to seek medical help. Despite the long-term prevalence of pain, the practice of pain management and the scientific discipline of pain research are relatively new fields. To relieve suffering from chronic pain in the ‘fifth vital sign’ era to date remains a 21st-century dilemma for healthcare providers. In the current review article, numerous articles from various pain journals and books for chronic pain management using medical search engines such as PubMed, Scopus, and Google scholar have been reviewed in an attempt to shed light on the approach, evaluation, and management of chronic pain. Along with the same, recent advances in pharmacotherapy and interventional nerve blocks have been discussed in brief.
Keywords
Chronic non cancer pain
Pharmacotherapy
Nerve blocks
Cancer pain
INTRODUCTION
The International Association for Study of Pain defines pain as ‘An unpleasant sensory and/or emotional experience associated with, or resembling that associated with, actual or potential tissue damage.’ Even if the patient is experiencing pain in the absence of actual tissue damage, it should be accepted as pain. According to a global burden disease study, one in ten adults is diagnosed with chronic pain each year globally.[1]
PAIN PATHWAYS
(1) Transduction, (2) Transmission, (3) Perception, and (4) Modulation. These are the sequence of events that are involved in the neural processing of noxious stimuli [Figure 1].[2-6]
TYPES OF AFFERENT FIBERS THAT CARRY PAIN
A-Delta fibre– myelinated and fast, with a conduction velocity of 5–15 m/s, transmits sharp, localised, and fast pain
C-fibres – unmyelinated with slow conduction <2 m/s, carry dull, diffuse, aching, and delayed pain.
Gate control theory of pain
Melzak and Wall proposed historical ‘Gate control theory’ in 1965. It states that activating larger diameter A-beta fibres leads to inhibition of pain signals transmitted through smaller diameter A delta and C fibres. An inhibitory interneuron acts as physiological gate which is closed by stimulation of A beta fibres. For example, Spinal cord stimulator and TENS for myofascial pain.[6]
AUTONOMIC NERVOUS SYSTEM
Autonomic nervous system plays an important role in different types of pain. For example, pain signals from thoracic or abdominal viscera and intervertebral disc-or vertebral body are carried by different afferent sympathetic fibres.[1,2-4,7]
SOMATIC SYMPATHETIC COUPLING AND MECHANISM
Somatic and sympathetic nerves are well insulated with no crosstalks in between them. However, with pathological conditions such as peripheral nerve injury/neurolysis and complex regional pain syndrome (CRPS), there is a cross-connection between somatic and sympathetic signals. Sympathetic efferent fibres release catecholamines, which instead of acting on sympathetic receptors may stimulate the nociceptors and generate action which is carried by somatic nerves[2]
SYMPATHETIC BLOCKADE AND ITS SIGNIFICANCE IN PAIN MANAGEMENT
Sympathetic blockade results in interruption of transmission by both the efferent and afferent fibres. It does not result in sensory or motor loss as seen in the somatic blockade.[2]
Examples of sympathetic blockade at various levels:
Stellate ganglion and lumbar sympathetic blockade for CRPS of the upper and lower limbs
Splanchnic and celiac plexus block for the upper abdominal malignancy and chronic benign pain
Superior hypogastric plexus block: Cancer and non-cancer chronic pelvic pain.[8]
TYPES OF PAIN
Based on time
Based on mechanism
Nociceptive pain arises from actual or threatened damage to non-neural tissue. For example, acute trauma, postoperative pain, and sickle cell crisis
Neuropathic pain is caused by a lesion or disease of somatosensory nervous tissue. For example, post-herpetic neuralgia, trigeminal neuralgia, distal polyneuropathy, and CRPS type
Mixed pain is having both nociceptive and neuropathic components. For example, cancer pain and vascular pain syndromes
Non-inflammatory/non-nociceptive where the aetiology of the origin of the pain is still confusing. For example, fibromyalgia and irritable bowel syndrome.
ASSESSMENT AND DIAGNOSIS OF PAIN
Pain history
An effective history is vital in making a diagnosis of pain. A pain questionnaire should be based on the following aspects of pain.[9-18]
Onset, location, and radiation of pain
-
Character or description of pain:
Nociceptive pain – Dull aching, cramp, stabbing knife, shooting and throbbing
Neuropathic pain – current-like and tingling pain
Mixed–burning pain in the chest
Aggravating and relieving factors would explain the possible pathophysiological mechanism.
PAIN ASSESSMENT TOOLS[2,8,18]
Visual Analogue Scale (VAS): This is the most commonly used scale. In this, the patient is asked to place a marker on a 100 mm continuous line between no pain and the worst imaginable pain on every visit [Figure 2]
Numerical Rating Scale (NRS): The patient directly assigns a number between 0 (no pain) and 10 (the worst pain imaginable) [Figure 2]
-
Verbal Categorical Scale: The patient describes the severity of pain ranging from no pain to ‘mild,’ ‘moderate’ and ‘severe’ [Figure 2].
Mild pain: VAS or NRS of 0–3
Moderate pain: VAS or NRS of 4–7
Severe pain: VAS or NRS of 8–10 or even if the pain is moderate but the patient says I cannot bear it, it can be counted as severe pain.
The faces pain rating scale is used mainly for children and mentally impaired patients. The scale depicts six faces of facial features, each with a numeric value of 0–5, ranging from a smiling and happy face to a sad and teary face.
-
Comprehensive Pain assessment Questionnaires:
McGill pain questionnaires
Brief pain inventory
Oswestry pain questionnaire
Patient health questionnaire-9 scoring is to rule out depression.
CLINICAL EXAMINATION
General physical examination
Pain diagram
It is essential to draw a pain diagram for assessment of pain as it provides [Figure 3][8]
Visual confirmation of patient’s pain
It can be stored as a medical record
It helps to note the change in the area of pain especially if the patient’s pain keeps on changing with every visit.
NEUROLOGICAL EXAMINATION
It consists of an examination of all cranial nerves, spinal nerves, and autonomic nervous systems.
Musculoskeletal system examination
It includes:
Posture, muscle symmetry, and obvious muscle wasting: Muscle spasm occurs in spinal nerve compression in corresponding myotomes. Straightening of lumbar lordosis or canal stenosis occurs due to spasm of erector spinae muscle. For example, stooped gait or ‘shopping cart’ posture in lumbar canal stenosis
Range of motion of joints is noted.
-
Palpation: Done for soft tissues and bones in affected dermatomyotomes to map areas of pain
Oedema, clicks, and crepitus in joints
Cord like the feel of muscles that are in spasm can be palpated
Tenderness, for example, paraspinal tenderness may be felt in facet joint pain
The presence of trigger points like trapezius trigger points can cause pain and numbness of the arm or forearm and mimic pain caused by a cervical herniated disc.
SPINE EXAMINATION
It includes sensory and motor examination of spinal nerves.
Spine symmetry and kyphosis or scoliosis should be noted.
Spinal flexibility – Pain on certain movements of the spine could indicate possible diagnosis in spine pain patients like pain in the neck or back on forward bending will indicate discogenic pain. On the contrary; pain on backward bending will point toward facet arthritis or muscular spasm [Table 1].
Name of the tests | Analyse | Remarks |
---|---|---|
SLR or Lasegues test | Leg pain at an angle between 40 to70 will be positive | Positive means L4, L5, S1, and S2 are having pain on stretching the leg |
Reverse SLR | Anterior thigh pain on the stretch will be positive reverse SLR | Positive meaning L2, 3, 4 could be getting stretched causing pain |
Cross SLR | Positive leg pain on the affected side will indicate stretch of L4,5, S1nerveroots | More specific than SLR |
Fabre test for sacroiliac joint pain | Pain on the affected side will indicate strain of the SI joint capsule and ligaments | Not specific but hints at SI joint pathology |
Palpation
Spinous process tenderness might be present in discogenic pain, vertebral body fractures, or spine metastasis.
PHARMACOTHERAPY IN PAIN MANAGEMENT
The most common method of pain management is the use of drugs. Nociceptive pain responds well to simple analgesics such as anti-inflammatory agents, but neuropathic pain responds better to coanalgesics such as anticonvulsants and anti-depressants.[2,8]
Drugs should have
Rapid onset, long duration, and effective pain relief
Minimal side effects on long-term use
Easily self-administered.
WHO STEP LADDER
The World Health Organisation 1986 devised a step-wise approach popularly known as the ‘WHO step ladder’ approach for the management of chronic pain and cancer pain patients. In 2016, with the advent of newer modalities and interventions, this original analgesic ladder was upgraded to the current modified four-stepladder approach [Figure 4].[2]
Drugs used in pain management can be categorised under two broad headings: Analgesics and Coanalgesics.
Analgesics are anti-inflammatory, non-selective COX – inhibitors like NSAIDs, and selective COX-2 inhibitors. Acetaminophen/Paracetamol and Opioids
Coanalgesics or adjuvant group includes anticonvulsants, antidepressants, local anaesthetics, steroids, muscle relaxants, botulinum toxins, and NMDA receptor antagonists. Others such as Alpha 2, agonists, calcium channel blockers, vitamins, and nutritional supplements.
ANALGESICS
Anti-inflammatory, COX –inhibitors: NSAIDs, COX -2 inhibitors
Commonly used NSAIDs for pain management include Ibuprofen, Diclofenac sodium, Nimesulide, Ketoprofen, Naproxen, Piroxicam, and Mefenamic acid. COX-2 selective inhibitors such as etoricoxib and celecoxib have better gastrointestinal safety profiles and least effect on platelet function.[2,19,20]
These are useful in inflammatory conditions such as rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis where inflammation is the main pathology.
OPIOIDS
Opioids can be classified according to their receptor activity or duration of action (long acting and short acting) or their analgesic and ceiling effects (weak and strong opioids). Opioid receptors are G protein-coupled receptors. mu is the major receptor responsible for analgesia. Pure agonist like morphine is preferred in moderate-to-severe chronic pain like cancer pain. Opioids with agonist-antagonist have a ceiling effect for analgesia. Weak opioids are tramadol, tapentadol, and codeine. Strong opioids are morphine, fentanyl, and buprenorphine. Long-acting opioids are good to treat baseline pain whereas short-acting opioids are useful in breakthrough pain. If a trial of opioids is considered, then: [Table 2][8]
Drug | Route | Starting dose and frequency | Onset of action |
---|---|---|---|
Codeine | Oral | 30 mg 3–6 hrly | 30–45 min |
Morphine | Oral | 10 mg 3–6 hrly | 30–60 min |
Morphine Parenteral | SC/IM/IV | 5 mg 3–6 hrly | Subcutaneous10–30 min. |
IM 10–20 min; IV2–5 min | |||
Fentanyl Trandermal | Transdermal | 25 ug once in 3 days | 10–12 hrs |
Fentanyl Parenteral |
Transdermal | 50 ug 1–4 hrly | SC 10–20 min; IM 10–20 min IV 2–5 min |
Fentanyl Lozenges | Transmucosal (Lollipop) |
200 ug | 5–10 min |
Pentazocine | SC/IM/IV | 30 mg 3–6hrly |
SC 10–30 min; IM 10–20 min IV 2–10 min |
Buprenorphine (Transdermal) |
Transdermal | 5 mg once in 7 days | 12–24 h |
Buprenorphine Parenteral |
SC/IM/IV | 150 ug 8–12 hrly |
SC 10–30 min; IM 10–20 min IV 2–10 min |
Tramadol | Oral | 50 mg 6–8 hrs | 30–60 min |
Tramadol | SC/IM/IV | 50–100 mg 6–8 hrly |
10–30 mins |
Tapentadol | Oral | 50 mg, 100 mg OD to 4 times a day |
10–30 min |
The patient should be explained the benefits and risks of opioids use
The WHO analgesic ladder to be followed
Strong opioids like morphine should never be used as SOS drug
Side effects should be explained and majors to be taken to correct them if possible
For elders ‘start low and go slow’, instructions for follow-up and emergency should be provided.
The oral route is the preferred root of administration. Other routes are subcutaneous, IM, IV, transdermal patches, and intrathecal pumps.
Common side effects are nausea, vomiting, itching, drowsiness, euphoria, constipation, urinary retention, respiratory depression, tolerance, dependence, sexual dysfunction, etc.
COMMONLY USED ANTICONVULSANTS IN PAIN PRACTICE
These are mainly either sodium or calcium channel blockers which raise the threshold for nerve depolarisation and thus suppress abnormal neuronal discharge [Table 3].
Drug Name | Dose | Mechanism of Action | Side Effects |
---|---|---|---|
Gabapentin | Starting dose 100–300 HS. The usual dose is 900–3600 (max) mg in three divided doses |
Membrane stabiliser by binding at alpha2delta subunit of L type calcium channel. | Dizziness, somnolence, fatigue, Peripheral oedema |
Pregabalin | Starting dose 50 mg/day Max dose 300 mg/day |
Dizziness, somnolence, fatigue, peripheral oedema, ataxia | |
Carbamazepine | Starting dose 100 mg/day Max dose1800 mg/day |
Sodium channel blocker Inhibit pain via a central and peripheral mechanism |
Aplastic anaemia, Agranulocytosis, leukop enia, sedation, gait alteration. |
Oxcarbazepine | Starting dose 300 mg/day Max dose 1200– 2400 mg/day |
Maybe modulating voltage-activated calcium current | Risk of hyponatremia in first few months |
Topiramate | Starting dose 50 mg/day Max dose 200 mg/day |
Enhances action of GABA, Inhibit AMPA Type glutamate | Sedation, may predispose glaucoma and renal calculi |
Lamotrigine | Starting dose 20–50 mg/day Max dose 300–500 mg/day |
Prevent the release of glutamate | Rash |
COMMONLY USED ANTIDEPRESSANTS PAIN PRACTICE
These drugs have a direct analgesic effect at doses much lower than that required for antidepressant action with the added advantage of sedation, diminished anxiety, muscle relaxation, and a restored sleep cycle. These drugs act on descending inhibitory pain pathways. Depending on the mechanism of action antidepressants are-Tricyclic antidepressants, selective serotonin reuptake inhibitors, serotonin norepinephrine re-uptake inhibitors [Table 4].
Drug Name | Oral dose in mg/duration | Clinical consideration |
---|---|---|
Amitriptyline (TCA) | 10–25/12–24 h | Caution in elderly male Urinary retention |
Nortriptyline (TCA) | 10–25/12–24 h | Better tolerated than amitriptyline |
Duloxetine (SNRI) | 20–60/12–24 h | DOC IN diabetic peripheral neuropathy & fibromyalgia. |
Milnacipran (SNRI) | 50–100/12–24 h | FDA-approved drug for fibromyalgia |
Venlafaxine (SNRI) | 37.5–112.5/12–24 h | SNRI better tolerated |
Desipramine (TCA) | 10–25/24 h | Better tolerated TCA in elderly |
COMMONLY USED MUSCLE RELAXANTS IN PAIN PRACTICE
Muscle relaxants are used in addition to rest, physical therapy, and other measures to relieve discomfort. They are typically prescribed for short-term use to treat acute, painful musculoskeletal conditions [Table 5].
Drug Name | Dose (Max) Po Mg/Duration | Special Points |
---|---|---|
Baclofen | 5–10 (80)/8–24 h | Abrupt withdrawal may predispose to seizures, hallucinations and increased flexor spasm |
Tizanidine | 4–8 (36)/12–24 h | More effective in reducing muscle spasm but less consistent in decreasing muscle tone. Careful administration when used with other antihypertensive |
Diazepam | 2–4 (20)/12–24 h | Concomitant use of other centrally acting drugs may potentiate side effects |
Steroids
Glucocorticoids are extensively used in pain management for their anti-inflammatory and possibly analgesic actions. Although epidural and intra-articular steroids are frequently used in pain management, scope of oral steroid is limited. Particulate steroids are preferred over soluble preparations. Commonly used preparations are triamcinolone acetate and methylprednisolone.
NMDA receptor antagonist
NMDA receptors are involved in ‘windup’ phenomenon, modulation of pain pathway and hyperalgesia. Thus, inhibition of these can have potent analgesic effect. Ketamine is popular one but has no oral preparation. Parental ketamine is used in central conditions such as fibromyalgia, CRPS and opioid-induced hyperalgesia.
Alpha agonists
These drugs have sympatholytic effect and they also alter calcium and potassium conductance at spinal cord level. Commonly used is Clonidine (dose 0.1 mg/day orally). It is useful in sympathetically mediated neuropathic pain conditions like CRPS.
Local anaesthetics
Local anaesthetics drugs such as lignocaine and bupivacaine are used to block nerves as a diagnostic or therapeutic procedure. In central desensitisation procedure, it acts as a membrane stabiliser.
Botulinum toxin
Pain associated with spasticity, myofascial pain, cervical dystonia, and some headache well responds to therapeutic botox injection. It acts on the neuromuscular junction, analgesic action probably mediated by blockade of substance P, glutamate, and calcitonin gene-related peptide.
Topical agents
NSAIDs gel, Capsaicin gel, Lignocaine gel, and EMLA cream are found to be useful in pain management.
Interventional pain procedures
An interventional pain procedure is interruption of signals traveling along a nerve by injecting steroids or neurolytic agent on the nerve or using radio-frequency ablation of the nerve [Table 6].
Interventions | Indication | Special Points | Imaging Required |
---|---|---|---|
Trigger Point Injection | Muscle Spasm, | Lignocaine and normal saline injections of steroids may be added hydrodilatation of muscles |
Blind Or USG Guided |
Intraarticular Steroid Injections | Osteoarthritis | Repeated steroid injections may lead to damage to cartilage, osteopenia |
USG, fluoroscopic guided |
Intraarticular platelet-rich plasm (Prp) Injections |
Osteoarthritis | Promising results | Blind, USG or fluoroscopic guided |
Lumbar and steroid cervical injections |
Lumbar or cervical disc prolapse, nerve rootirritation, sciatica, lumbar canalstenosis |
Very effective in pain relief, can be repeated 3–4 times in a year risk of infection minimal | Mostly fluoroscopic guided recently USG guided |
Lumbar Transforaminal injections |
|||
Gasserian Neurolysis | Trigeminal Neuralgia | Radiofrequency ablation is preferred Effective In Primary Trigeminal Neuralgia Glycerol Phenol 6% p |
Fluoroscopic Or CT guided |
Thoracic Epidural Steroid Injection | Post-herpetic Neuralgia | Intercostal nerve block with steroid need to be combined in a thoracic dermatomal distribution |
Fluoroscopic guided |
Ulnar Nerve Or Median Nerve Hydrodilattion |
Cubital Tunnel or Carpal tunnel Syndrome |
Steroid injection or hydro dilatation |
USG guided |
Sympatholytic Blocks | |||
Stellate Ganglion Block | CRPS Hand Reynauld’s Disease Peripheral Vascular Disease | Steroid (Triamicinolone) is preferred Needs repetition 2-3 Times No Alcohol or Phenol Or Radiofrquency Ablation as it may lead permanent toHorner’s Syndrome |
Fluoroscopic Or USG guided USG guided blocks has better results |
Lumbar Sympathetic Blocks | Burgers’ Disease Pvd Diabetic Neuropathy Phantom Limb |
Steroid Injection Alcoho80% Phenol 6% Radiofrequency Ablation |
Fluoroscopy Guided USG Guided for Patient Who Cannot Lie Prone |
Splanchnic Nerve Blocks Celiac Plexus Block | Chronic Pancreatitis Upper GI Malignancy GB Malignancy Irritable Bowel Syndrome |
Steroid Injection Alcohol 80% PHENOL 6% Radiofrequency ablation |
Fluoroscopy guided CT guided |
Superior Hypogastric Plexus Block | Chronic Pelvic Pain Carcinoma Of Uterus, Bladder, Vagina, Cervix |
Alcohol 80% Phenol 6% Radiofrequency Ablation |
Fluoroscopy guided USG guided patients who cannot lie prone |
Ganglia Impar | Coccydynia Ca Anal Canal Ca Vagina | Steroid Alcohol 80% Phenol 6% Radiofrequency Ablation |
Fluoroscopy guided |
COMMONLY PERFORMED INTERVENTIONS FOR CHRONIC PAIN MANAGEMENT
Regenerative therapy
Is rapidly emerging with extensive biomedical research over the past decade.[2,8,12]
Platelet-rich plasma
Growth factor
Stem cells
Prolotherapy.
SPINAL CORD STIMULATOR
Spinal cord stimulation (SCS), also known as neurostimulation, utilises an implant and electrodes to deliver mild electrical pulses to the nerves around the spinal column usually the dorsal column of spinal cord, to stimulate the nerves and block or lessen pain signals that are being sent to the brain [Figure 5].[21,22]
The major benefit of SCS is that it provides targeted pain relief up to 60% with improved mobility, allowing the patients to return to their daily activities. It minimises the need for invasive surgeries to correct spinal conditions and majority of the times remains the last resort for treating chronic back pain.
CANCER PAIN MANAGEMENT: SPECIAL POINTS
Cancer pain affects more than 9 million people worldwide annually. An estimated one-third (24–60%) and two-thirds (62–86%) of cancer patients suffer from pain, with more than one-third having moderate-to-severe pain. Pharmacotherapy constitutes the mainstay of treatment and approach for pain management as per the WHO analgesic ladder. Indications for interventions are unacceptable side effects and well localised pain syndromes in which pain may get relieved by nerve blocks or a comprehensive trial of pharmacologic therapy fails to provide pain relief. Interventional techniques for pain management include [Figure 6][23-27]
Regional Infusions
Neuraxial analgesia (Intrathecal pump)
Neurodestructive procedures
Neuromodulation
Percutaneous vertebroplasty/kyphoplasty
Radiofrequency ablation.
CONCLUSION
Pain treatment goals should include improved functioning and pain reduction. Along with pharmacological treatment, non-pharmacological therapies including integrative medicine therapies such as yoga, physiotherapy, and acupressure which widen the horizon of pain medicine should be routinely considered.
Knowledge of interventional nerve blocks and recent advances such as regenerative therapies and spinal cord stimulators has revolutionised the management of pain in CNCP and cancer patients. Thus, adequate control of chronic pain can be achieved in nearly all patients in a way that adequately balances benefits and potential harms.
Declaration of patient consent
Patient’s consent not required as there are no patients in this study.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
- Available from: http://www.iasp.pain.org/taxonomy#pain [Last accessed on 2022 Jul 16]
- Painpathways In: Basics of Pain Mangement (2nd ed). CBS Publishers: New Delhi; 2019. p. :3-8.
- [Google Scholar]
- Ascending projection systems In: McMahon SB, Koltzenburg M, eds. Wall and Melzack's Textbook of Pain (5th ed). Elsevier Churchill Livingstone; 2006. p. :187-203.
- [CrossRef] [Google Scholar]
- Peripheral Pain Mechanisms and Nociceptor Sensitization In: Fishman SM, Ballantyne IC, Rathmell IP, eds. Bonica's Management of Pain (4th ed). Baltimore, MD: Lippincott, Williams and Wilkins; 2010. p. :24-34.
- [Google Scholar]
- Available from: https://www.physio-pedia.com/epidemiology_of_pain [Laast accessed on 2022 Jun 25]
- Functional neuroanatomy of the nociceptive system In: Fishman SM, Ballantyne IC, Rathmell JP, eds. Bonica's Management of Pain (4th ed). Baltimore, MD: Lippincott, Williams and Wilkins; 2010. p. :98-119.
- [Google Scholar]
- Handbook of Pain Management a Case based Approach. (1st ed). New Delhi: Jaypee Distributors; 2018.
- [CrossRef] [Google Scholar]
- Modulation of spinal nociceptive processing In: Fishman SM, Ballantyne IC, Rathmell JP, eds. Bonica's Management of Pain (4th ed). Baltimore, MD: Lippincott, Williams and Wilkins; 2010. p. :48-60.
- [Google Scholar]
- Part III: Pain terms, current list with definitions and note son usage In: Classification of Chronic Pain (2nd ed). Seattle: IASP Task Force on Taxonomy, IASP Press; 1994.
- [Google Scholar]
- The biopsychosocial approach to chronic pain: Scientific advances and future directions. Psychol Bull. 2007;133:581.
- [CrossRef] [PubMed] [Google Scholar]
- Clinical Methods in Pain Medicine New Delhi: CBS Publishers and Distributors; 2015. p. :2-17.
- [Google Scholar]
- Long-lasting analgesic effects of daily sessions of repetitive transcranial magnetic stimulation in central and peripheral neuropathic pain. J Neurol Neurosurg Psychiatry. 2005;76:833-8.
- [CrossRef] [PubMed] [Google Scholar]
- Identifying neuropathic pain among patients with chronic low back pain: Use of the Leeds assessment of neuropathic symptoms and signs pain scale. Reg Anesth Pain Med. 2005;30:422-8.
- [CrossRef] [PubMed] [Google Scholar]
- The S-LANSS score for identifying pain of predominantly neuropathic origin: validation for use in clinical and postal research. J Pain. 2005;6:119-58.
- [CrossRef] [PubMed] [Google Scholar]
- Peripheral mechanisms of cutaneous nociception In: McMahon SB, Koltzenburg M, eds. Wall and Melzack's Textbook of Pain (5th ed). London, United Kingdom: Elsevier, Churchill Livingston; 2006. p. :3-34.
- [CrossRef] [Google Scholar]
- Oxford Handbook of Pain Management. London: Correct Medicine Group; 2008:1-35.
- [CrossRef] [Google Scholar]
- Pain assessment in adult patients In: McMohan SB, Koltzenburg MZ, eds. Wall and Melzacks Textbook of Pain (5th ed). London: Elsevier; 2006. p. :291-304.
- [CrossRef] [Google Scholar]
- Regional Anesthesia and Pain Management (1st ed). Philadelphia, PA: Saunders; 2009. p. :103-22.
- [Google Scholar]
- A review of spinal cord stimulation systems for chronic pain. J Pain Res. 2016;9:481-92.
- [CrossRef] [PubMed] [Google Scholar]
- Predictors of spinal cord stimulation success. Neuromodulation. 2015;18:599-602.
- [CrossRef] [PubMed] [Google Scholar]
- Intrathecal pumps for managing the cancer pains. Am J Nurs. 2016;116:36-44.
- [CrossRef] [PubMed] [Google Scholar]
- Opioids in chronic non cancer pain: systematic review of efficacy and safety. Pain. 2004;112:372-80.
- [CrossRef] [PubMed] [Google Scholar]
- Cancer pain management continuum: A flexible approach. Clin J Pain. 2001;17:206-14.
- [CrossRef] [PubMed] [Google Scholar]
- Cancer pain In: Joshi MI, ed. Textbook of Pain Management (3rd ed). Hyderabad: Paras; 2014. p. :392-405.
- [Google Scholar]