Pain measures can be divided into the recording of spontaneous pain and recording of evoked pains to different stimuli. For this purpose, visual analog scaling as well as multidimensional descriptor (e.g. the McGill Pain Questionnaire) and cross-modality matching scales have been used. Specific measures may be important in assessment in different pain conditions. For example, in neuropathic pain allodynia, wind up-like pain, after sensations, pain radiations, and area of hypersensitivity (e.g. allodynia) may be relevant. Recording of pain intensity is still the most frequently assessed dimension of therapeutic outcome. The visual analog scale (VAS), verbal category scales, and numerical rating scales are the
Table 11.3 Stimulus and response measures in neuropathic pain patients.
Stimulus modality Threshold Summation Stimulus response Area of abnormality
Touch von Frey hair Thermal
Mechanical pressure Capsaicin Electrical stimuli
Detection Touch-evoked allodynia + Detection Repetitive stimulation + Pain
Detection Pain Pain Pain
Repetitive stimulation Repetitive stimulation Repetitive stimulation
most commonly used scales. An example of a numerical rating scale is the 11-point Likert rating scale, whereby the subject is asked to rate his pain by giving a number between 0 (no pain) and 10 (most intense pain). Another widely used category scale is the four-point intensity scale (none, mild, moderate, and severe pain). However, this scale usually does not have sufficient levels to describe the effects of treatment accurately. Improved category scales with more descriptors are available. Pain intensity does fluctuate over time in many clinical pain conditions. In these cases, it may be necessary to rate the percentage of time that the patient's pain falls within certain intensity categories. A slightly different approach has been taken in the Brief Pain Inventory (BPI) of Wisconsin, which involves measurement of the pain intensity when it is at its worst, when it is at its least, and the average pain intensity.
A unidimensional recording of pain intensity or pain relief may overlook other important aspects of a therapeutic outcome, such as functional improvement or improvement in quality of life. Certain therapies which reduce pain intensity may be associated with side effects that diminished quality of life. If pain intensity or relief measures are used in isolation in this situation, then a falsely optimistic view of the effect of that therapy may be formed by the clinician.
In neuropathic pain, it is not sufficient to record one single pain condition; the various other neuropathic phenomena such as paroxysms, spontaneous ongoing pain, wind up-like pain, touch-evoked pain, and cold allodynia are equally important. Each pain component in a particular neuropathic pain condition may have its own magnitude and each may be influenced separately by a particular drug.
Whereas pain intensity scales focus on the present pain experience, pain relief scores rely on the patient's memory of pain. Since patients tend to overestimate their past pain, the use of pain relief scores may lead to an over-estimation of the effects of the treatment, certainly in cases of prolonged follow up. On the other hand, it has been suggested that pain relief category scales are more sensitive to small reductions in pain. A neuropathic pain scale (NPS) and the LANSS pain scale have been recently introduced and validated.63'64 It seems to be possible, at least to some degree, to identify patients in whom neuropathic mechanisms dominate their pain.65,66
An increasing number of clinical trials include measures of quality of life in the evaluation of the treatment of chronic pain. These measures have become an important indicator of treatment success. Among the measures of quality of life, the Sickness Impact Profile (SIP), the SIP Roland, the West Haven-Yale Multidimensional Pain Inventory, the Nottingham Health Profile, and the SF-36 have been validated (for further details of pain measures, see Chapter 3, Selecting and applying pain measures in the Practice and Procedures volume of this series).
Specific treatments have been designed and tried for different pain conditions, including neuropathic pain. They will be described in detail in other chapters. These treatments, which currently include tricyclic antidepressants, sodium channel blockers (such as carbama-zepine and lamotrigine), gabapentin and pregabalin, opioids, and N-methyl-D-aspartic acid (NMDA) channel blockers have specific targets for their mode of action. It has been suggested that this may help to unravel the mechanisms of neuropathic pain based on the specific action of these drugs. Previous studies have shown that such drugs may have an action not only on pain intensity, but also on specific aspects of pain, such as evoked pain. Studies have shown that in patients with neuropathic pain due to nerve injury and amputation, NMDA receptor antagonists can block both pain and evoked pain produced by touch stimuli, indicating that these phenomena are probably produced by the same mechanism, i.e. a central sensitization mediated by excess activity at NMDA receptor channels. An additional example would be the joint blockade of pain by sodium channel-blocking agents and NMDA receptor-blocking drugs, suggesting that at least two different mechanisms may operate in concert.
The introduction of the concept of number needed to treat (NNT) from systematic reviews has made it possible to compare the efficacy (NNT) and side-effect profile (NNH; number needed to harm) for a particular therapy in different pain conditions80 and thus to determine whether a drug with a known mechanism of action is effective in specific neuropathic pain conditions. In theory, this could enable the determination of the pain mechanisms involved for certain types of neuropathic pains. The same principle could also be applied using separate drugs for the same pathological condition to determine whether distinct or identical mechanisms may be in operation.6[I], 7[I] For example, a sodium channel blocker and an NMDA receptor antagonist modulate spontaneous pain, wind up-like pain, and touch-evoked pain in a different way in individual neuropathic pain patients which proposed that separate molecular mechanisms are involved in individual patients.25[II]
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