Ronald Melzack

The McGill Pain Questionnaire: Major properties and scoring methods

Abstract The McGill Pain Questionnaire consists primarily of 3 major classes of word descriptors — sensory, affective and evaluative — that are used by patients to specify subjective pain experience. It also contains an intensity scale and other items to determine the properties of pain experience. The questionnaire was designed to provide quantitative measures of clinical pain that can be treated statistically. This paper describes the procedures for administration of the questionnaire and the various measures that can be derived from it. The 3 major measures are: (1) the pain rating index, based on two types of numerical values that can be assigned to each word descriptor, (2) the number of words chosen; and (3) the present pain intensity based on a 1–5 intensity scale. Correlation coefficients among these measures, based on data obtained with 297 patients suffering several kinds of pain, are presented. In addition, an experimental study which utilized the questionnaire is analyzed in order to describe the nature of the information that is obtained. The data, taken together, indicate that the McGill Pain Questionnaire provides quantitative information that can be treated statistically, and is sufficiently sensitive to detect differences among different methods to relieve pain.

The short-form McGill Pain Questionnaire

&NA; A short form of the McGill Pain Questionnaire (SF‐MPQ) has been developed. The main component of the SF‐MPQ consists of 15 descriptors (11 sensory; 4 affective) which are rated on an intensity scale as 0 = none, 1 = mild, 2 = moderate or 3 = severe. Three pain scores are derived from the sum of the intensity rank values of the words chosen for sensory, affective and total descriptors. The SF‐MPQ also includes the Present Pain Intensity (PPI) index of the standard MPQ and a visual analogue scale (VAS). The SF‐MPQ scores obtained from patients in post‐surgical and obstetrical wards and physiotherapy and dental departments were compared to the scores obtained with the standard MPQ. The correlations were consistently high and significant. The SF‐MPQ was also shown to be sufficiently sensitive to demonstrate differences due to treatment at statistical levels comparable to those obtained with the standard form. The SF‐MPQ shows promise as a useful tool in situations in which the standard MPQ takes too long to administer, yet qualitative information is desired and the PPI and VAS are inadequate.

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

&NA; Peripheral tissue damage or nerve injury often leads to pathological pain processes, such as spontaneous pain, hyperalgesia and allodynia, that persist for years or decades after all possible tissue healing has occurred. Although peripheral Neurol mechanisms, such as nociceptor sensitization and neuroma formation, contribute to these pathological pain processes, recent evidence indicates that changes in central Neurol function may also play a significant role. In this review, we examine the clinical and experimental evidence which points to a contribution of central Neurol plasticity to the development of pathological pain. We also assess the physiological, biochemical, cellular and molecular mechanisms that underlie plasticity induced in the central nervous system (CNS) in response to noxious peripheral stimulation. Finally, we examine theories which have been proposed to explain how injury or noxious stimulation lead to alterations in CNS function which influence subsequent pain experience.

Central nervous system plasticity in the tonic pain response to subcutaneous formalin injection.

Evidence is presented which suggests that central neural changes occur during the brief early phase after subcutaneous formalin injection that are essential for the expression of pain during the long-lasting (tonic) later phase. First, tonic pain responses to subcutaneous formalin injections are abolished only if the injected hindpaw is locally anesthetized at the time of injection as well as the time of testing (30-60 min later). Second, tonic formalin pain is substantially reduced by brief spinal anesthesia given 5 min before, but not 5 min after the formalin injection.

Trigger points and acupuncture points for pain: Correlations and implications

&NA; Trigger points associated with myofascial and visceral pains often lie within the areas of referred pain but many are located at a distance from them. Furthermore, brief, intense stimulation of trigger points frequently produces prolonged relief of pain. These properties of trigger points — their widespread distribution and the pain relief produced by stimulating them — resemble those of acupuncture points for the relief of pain. The purpose of this study was to determine the correlation between trigger points and acupuncture points for pain on the basis of two criteria: spatial distribution and the associated pain pattern. A remarkably high degree (71%) of correspondence was found. This close correlation suggests that trigger points and acupuncture points for pain, though discovered independently and labeled differently, represent the same phenomenon and can be explained in terms of the same underlying neural mechanisms. The mechanisms that play a role in the genesis of trigger points and possible underlying neural processes are discussed.

Pain – an overview

The neuromatrix theory of pain proposes that pain is a multidimensional experience produced by characteristic “neurosignature” patterns of nerve impulses generated by a widely distributed neural network – the “body‐self neuromatrix”– in the brain. These neurosignature patterns may be triggered by sensory inputs, but they may also be generated independently of them. Pains that are evoked by noxious sensory inputs have been meticulously investigated by neuroscientists, and their sensory transmission mechanisms are generally well understood. In contrast, chronic pain syndromes, which are often characterized by severe pain associated with little or no discernible injury or pathology, remain a mystery. The neuromatrix theory of pain, however, provides a new conceptual framework that is consistent with recent clinical evidence. It proposes that the output patterns of the neuromatrix activate perceptual, homeostatic and behavioral programs after injury or pathology, or as a result of multiple other inputs that act on the neuromatrix. Pain, then, is produced by the output of a widely distributed neural network in the brain rather than directly by sensory input evoked by injury, inflammation or other pathology. The neuromatrix, which is genetically determined and modified by sensory experience, is the primary mechanism that generates the neural pattern that produces pain. Its output pattern is determined by multiple influences, of which the somatic sensory input is only a part, that converge on the neuromatrix.

Prolonged relief of pain by brief, intense transcutaneous somatic stimulation.

Abstract The purpose of this study was to examine the effects of brief, intense transcutaneous electrical stimulations at trigger points or acupuncture points on severe clinical pain. The McGill Pain Questionnaire was used to measure the change in pain quality and intensity produced by stimulation. The data indicate that the procedure provides a powerful method for the control of some forms of severe pathological pain. The average pain decrease during stimulation sessions was 75% for pain due to peripheral nerve injury, 66% for phantom limb pain, 62% for shoulder‐arm pain, and 60% for low‐back pain. The duration of relief frequently outlasted the period of stimulation by several hours, occasionally for days or weeks. Different patterns of the amount and duration of pain relief were observed. Daily stimulation carried out at home by the patient sometimes provided gradually increasing relief over periods of weeks or months. Control experiments, which included two forms of placebo stimulation, showed that brief, intense electrical stimulation is significantly more effective than placebo contributions. Possible neural mechanisms that underlie these patterns of pain relief by brief, intense stimulation are discussed.

Pain ‘memories’ in phantom limbs: review and clinical observations

&NA; This paper reviews reports of phantom limb sensations which resemble somatosensory events experienced in the limb before amputation. It also presents descriptions of this phenomenon in 68 amputees who took part in a series of clinical studies. These somatosensory memories are predominantly replicas of distressing pre‐amputation lesions and pains which were experienced at or near the time of amputation, and are described as having the same qualities of sensation as the pre‐amputation pain. The patients who experience these pains emphasize that they are suffering real pain which they can describe in vivid detail, and insist that the experience is not merely a cognitive recollection of an earlier pain. Reports of somatosensory memories are less common when there has been a discontinuity, or a pain‐free interval, between the experience of pain and amputation. Among the somatosensory memories reported are cutaneous lesions, deep tissue injuries, bone and joint pain and painful pre‐amputation postures. The experience of somatosensory memories does not appear to be related to the duration of pre‐amputation pain, time since amputation, age, gender, prosthetic use, level of amputation, number of limbs amputated, or whether the amputation followed an accident or illness. The results suggest that somatosensory inputs of sufficient intensity and duration can produce lasting changes in central neural structures which combine with cognitive‐evaluative memories of the pre‐amputation pain to give rise to the unified experience of a past pain referred to the phantom limb. Implications for pre‐ and post‐operative pain control are discussed.

Chronic pain in elderly people.

Abstract Chronic pain in elderly people has only recently begun to receive serious empirical consideration. There is compelling evidence that a significant majority of the elderly experience pain which may interfere with normal functioning. Nonetheless, a significant proportion of these individuals do not receive adequate pain management. Three significant factors which may contribute to this are (1) lack of proper pain assessment; (2) potential risks of pharmacotherapy in the elderly; and (3) misconceptions regarding both the efficacy of non‐pharmacological pain management strategies and the attitudes of the elderly towards such treatments. In this review the most commonly used assessment instruments and patterns of age differences in the experience of chronic pain are described and evidence for the efficacy of psychological pain management strategies for this group is reviewed.

Central Neuroplasticity and Pathological Pain

Abstract: The traditional specificity theory of pain perception holds that pain involves a direct transmission system from somatic receptors to the brain. The amount of pain perceived, moreover, is assumed to be directly proportional to the extent of injury. Recent research, however, indicates far more complex mechanisms. Clinical and experimental evidence shows that noxious stimuli may sensitize central neural structures involved in pain perception. Salient clinical examples of these effects include amputees with pains in a phantom limb that are similar or identical to those felt in the limb before it was amputated, and patients after surgery who have benefited from preemptive analgesia which blocks the surgery‐induced afferent barrage and/or its central consequences. Experimental evidence of these changes is illustrated by the development of sensitization, wind‐up, or expansion of receptive fields of CNS neurons, as well as by the enhancement of flexion reflexes and the persistence of pain or hyperalgesia after inputs from injured tissues are blocked. It is clear from the material presented that the perception of pain does not simply involve a moment‐to‐moment analysis of afferent noxious input, but rather involves a dynamic process that is influenced by the effects of past experiences. Sensory stimuli act on neural systems that have been modified by past inputs, and the behavioral output is significantly influenced by the “memory” of these prior events. An increased understanding of the central changes induced by peripheral injury or noxious stimulation should lead to new and improved clinical treatment for the relief and prevention of pathological pain.