Assessment of Pain 2
By Prof.Tissa Wijeratne, Dr. Ranjith Pallegama
and Dr. Dilani Wijeratne
Measurement of Neuropathic Pain
In recent years several screening tools that can help in identifying neuropathic pain have been introduced. These tools are based on verbal description of pain with or without limited bedside examination of the patient. The Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) scale and DN4 questionnaire (Douleur Neuropathique en 4 Questions) use an interview (questions) on symptom items and physical tests (pinprick and touch hypoesthesia) and demonstrate higher sensitivity and specificity than the screening tools with only interview questions. The Neuropathic Pain Questionnaire (NPQ) consists of 12 items (10 related to sensory responses or sensations and 2 related to affect). The NPQ demonstrated 66% sensitivity and 74% specificity compared to clinical examination that confirmed the diagnosis of neuropathic pain in a study of validation. The tool ID-Pain* has five sensory descriptor items and one item relating to joint pain. In the validation study 22% of the nociceptive group, 39% of the neuropathic and nociceptive group and 58% of the neuropathic group scored above 3, the recommended cut off score for neuropathic pain. Pain-DETECT is an easy to use self-report questionnaire with nine items (seven sensory descriptor items and two items relating to radiating and temporal characteristics of the individual pain pattern. Pain-DETECT demonstrated 83% sensitivity and 80% specificity in the validation study.
These instruments should not be used alone in determining the presence of neuropathic pain during routine clinical management. At the bed side examination, it is important to make sure that the abnormal sensory findings are neuroanatomically logical, i.e. those are compatible with a definite lesion site. Location, quality, and intensity of pain should be assessed. Accurate assessment requires a clear understanding of the possible types of negative (e.g. sensory loss) and positive (e.g. pain and paresthesias) symptoms and signs.
Neuropathic pain can be spontaneous (present without any precipitating or on-going cause being apparent) or elicited by a stimulus (evoked pain). Spontaneous pain is often described as a constant burning sensation, but may also be intermittent or paroxysmal, and includes dysesthesias as well. Paresthesias may also be present. Evoked pain (e.g. hyperalgesia, hyperpathia and allodynia by clinical examination) are elicited by mechanical, thermal, or chemical stimuli.
In patients with suspected neuropathic pain, the neurological examination should also include a thorough assessment of motor, sensory, and autonomic phenomena in order to identify all signs of neurological dysfunction. Sensory disorders should be recorded in detail, preferably on body sensory maps which provides valuable information. Tactile sense is best assessed with a piece of cotton wool, pinprick sense with a wooden tooth pick, thermal sense with warm and cold objects (e.g. metal rollers), and vibration sense with a 128-Hz tuning fork.
Autonomic dysfunction is more difficult to detect but careful inspection may reveal sweating, color and temperature asymmetries as well as skin and nail dystrophy.
Quantitative Sensory Testing (QST) analyses perception in response to external stimuli of controlled intensity. Detection and pain thresholds are determined by applying stimuli to the skin in an ascending and descending order of magnitude. Mechanical sensitivity for tactile stimuli is measured with filaments that produce graded pressures, such as the von Frey hairs, pinprick sensation with weighted needles, and vibration sensitivity with an electronic vibrameter. Thermal perception and thermal pain are measured using a thermode, or other device that operates on the thermoelectric effect.
QST has been used for the early diagnosis and follow-up of small-fiber neuropathy, and has proved useful in the early diagnosis of diabetic neuropathy. QST is also suitable for quantifying mechanical and thermal allodynia and hyperalgesia in painful neuropathic syndromes, and has been used in pharmacological trials to assess treatment efficacy on evoked pains. QST may show abnormal findings in non-neuropathic pain states such as rheumatoid arthritis and inflammatory arthromyalgias.
Large-size, non-nociceptive afferent nerve fibers have a lower electrical threshold than small-size, nociceptive afferents. Unless special techniques are used, i.e. experimental blocks or stimulation of special organs (cornea, tooth pulp), electrical stimuli also excite large afferents, thus hindering nociceptive signals. Hence standard neurophysiological responses to electrical stimuli, such as nerve conduction studies (NCS), can identify, locate, and quantify damage along the peripheral or central sensory pathways, but they do not assess the function of nociceptive pathway.
Researchers have tried numerous techniques for selectively activating pain afferents. One of the preferred approaches uses laser stimulators to deliver radiant-heat pulses that selectively excite the free nerve endings (Aδ and C) in the superficial skin layers. Late laser evoked potentials (Late-LEPs) are amongst the neurophysiological tools for assessing nociceptive pathway function and are diagnostically useful in peripheral and central neuropathic pain. In clinical practice, their main limitation is that they are currently available in too few centers. Ultralate LEPs (related to C-fiber activation) are technically more difficult to record, and few studies have assessed their usefulness in patients with neuropathic pain.
Contact Heat-Evoked Potentials are a recent development that still needs clinical validation. Painful neuropathies typically and preferentially involve small nerve fibers.
Nerve biopsy may be unrewarding in the early detection of small fiber neuropathy because small-fiber assessment is difficult and requires electron microscopy. Punch skin biopsy can quantify Aδ and C nerve fibers by measuring the density of Intra-Epidermal Nerve Fibers (IENF). IENF loss has been shown in various neuropathies characterized by small-fiber axonal loss. Punch skin biopsy is easy to do, minimally invasive, and optimal for follow-up. Despite these advantages, it is of no value in central pain and demyelinating neuropathy.
It is indeed very rare to have a test available that will make the diagnosis. It is really important to go through a careful and meticulous physical examination to identify the possible cause for the pain. (The clinical history will often generate a differential diagnosis; a detailed physical examination will often help us to select the most appropriate primary diagnosis, while tests/investigations may help to confirm this diagnosis on occasions.)
Assessment of vital signs, findings on inspection (posture, guarding, color and skin changes indicative of sympathetic dysfunction or herpes zoster eruption, swelling, atrophy) findings on palpation (warmth, edema, tenderness etc.), detailed muscular skeletal examination and detailed neurological examination may provide important clues to the underlying cause of the pain.
You may need to perform radiographic investigations from plain X- ray films to CT or MRI images in some of the pain patients. It is important to look for the clinical correlation and abnormal findings in imaging results. One of the basic principal in clinical medicine is to “not to treat X- rays or MRI films”.
Some patients may need nerve conduction studies and electromyography, and Somatosensory-Evoked Potential Testing in the process of assessment of their pain.
Assessment of pain can be an intensive process. On the basis of a solid knowledge of anatomy, physiology, and a systematic approach to the pain patient will help us to understand the etiology and pathophysiology of pain. Good assessment of pain is the foundation of management of pain
Aminoff JM, Boller F, Swaab FD. Pain: Handbook of Clinical neurology. Elsevier; 2006.
Ballantyne JC. The Massachusetts General Hospital handbook of Pain Management. Third Edition. Lippincott Williams & Wilkins; 2002.
Baron R, Binder A, Wasner G. Neuropathic pain: diagnosis, pathophysiological mechanisms and treatment. Lancet Neurol. 2010; 9: 807–19.
Baron R. Mechanisms of disease: neuropathic pain—a clinical perspective. Nat Clin Pract Neurol. 2006; 2: 95– 106.
Bennet MI, et al. Using screening tools to identify neuropathic pain. Pain. 2007; 127: 199-203.
Caterina MJ, Julius D. The vanilloid receptor: a molecular gateway to the pain pathway. Annu Rev Neurosci. 2001; 24: 487–517.
Cruccu G, Aminoff MJ, Curio G, Guerit JM, Kakigi R, et al. Recommendations for the clinical use of somatosensory-evoked potentials. Clin Neurophysiol. 2008; 119: 1705–1719.
Cruccu G, Anand P, Attal N, Garcia-Larrea L, Haanpa¨a¨ M, et al. EFNS guidelines on neuropathic pain assessment. Eur J Neurol. 2004; 11: 153–162.
Cruccu G, Truini A. Tools for Assessing Neuropathic Pain. 2009; PLoS Med 6(4):e1000045.doi:10.1371 /journal.pmed. 1000045.
Dworkin RH, O’Connor AB, et al. Recommendation for the Pharmacological Management of Neuropathic Pain: An overview and Literature Update. Mayo clin Proc. 2010; 85(3)(suppli): S3-S14.
England JD, Gronseth GS, Franklin G, Carter GT, Kinsella LJ, et al. Evaluation of distal symmetric polyneuropathy: The role of autonomic testing, nerve biopsy, and skin biopsy (an evidence-based review). Muscle Nerve. 2009; 39: 106–115.
Freynhagen R, To¨ lle TR, Baron R. Pain DETECT – ein Palmtopbasiertes Verfahren fur Versorgungsforschung, Qualita¨tsmanagement und Screening bei chronischen Schmerzen. Akt. Neurol. 2005; 34: 641.
Garcia-Larrea L, Convers P, Magnin M, Andre´- Obadia N, Peyron R, et al. Laser-evoked potential abnormalities in central pain patients: The influence of spontaneous and provoked pain. Brain . 2002; 125: 2766– 2781.
Granovsky Y, Matre D, Sokolik A, Lorenz J, Casey KL. Thermoreceptive innervation of human glabrous and hairy skin: A contact heat evoked potential analysis. Pain. 2005; 115: 238–247.
Hamilton ME, Gershwin ME. The Pain Management Handbook. Humana Press; 1998.
Hansson P. Neuropathic pain: clinical characteristics and diagnostic workup. Eur J Pain. 2002; 6 (suppl A): 47–50.
Koltzenburg M, Mc Mahon SB. Textbook of Pain. 5th Edition. Elsevier; 2006.
Krause SJ, Backonja MM. Development of a Neuropathic Pain Questionnaire. Clin J Pain. 2003; 19: 306–14.
Lauria G, Cornblath DR, Johansson O, Mc Arthur JC, Mellgren SI, et al. EFNS guidelines on the use of skin biopsy in thediagnosis of peripheral neuropathy. Eur J Neurol . 2005; 12: 747–758.
Nystrom B, Hagbarth KE. Microelectrode recordings from transected nerves in amputees with phantom limb pain. Neurosci Lett. 1981; 27: 211–16.
Orstavik K, Jorum E. Microneurographic findings of relevance to pain in patients with erythromelalgia and patients with diabetic neuropathy. Neurosci Lett. 2010; 470: 108–04.
Orstavik K, Namer B, Schmidt R, Schmelz M, Hilliges M, Weidner C. Abnormal function of C-fibers in patients with diabetic neuropathy. J Neurosci. 2006; 26: 11287–94.
Orstavik K, Weidner C, Schmidt R, et al. Pathological C-fibers in patients with a chronic painful condition. Brain. 2003; 126: 567–78.
Portenoy R. For the ID Pain Steering Committee. Development and testing of a neuropathic pain screening questionnaire: ID Pain. Curr Med Res Opin. 2006; 22: 1555–65.
Treede RD, Lorenz J, Baumga¨ rtner U. Clinical usefulness of laser-evoked potentials. Neurophysiol Clin. 2003; 33: 303–314.405–410.
Sri Lanka Association for the Study of Pain
The Sri Lankan Chapter of the International Association for the Study of Pain
© January 2014. Sri Lanka Association for the Study of Pain (SLASP). All Rights Reserved.
For Comments email@example.com