Validation of the short-form McGill pain questionnaire-2 in younger and older people with cancer pain.

UNLABELLED: Pain is among the most common symptoms of cancer. Because cancer can occur at any age, it is imperative that pain assessment tools are valid for use across the adult lifespan. The Short-Form McGill Pain Questionnaire-2 (SF-MPQ-2) is a valid and reliable tool for the assessment of the multidimensional qualities of pain in people with chronic nonmalignant pain, but its psychometric properties in people with cancer pain and in older versus younger people require investigation. This study evaluated age differences in the validity, reliability, and use of the SF-MPQ-2 in 244 people with advanced cancer and pain. We confirmed the previously reported 4-factor solution in older (≥ 60 years) and younger (<60 years) patients. Internal consistency reliability and convergent validity were similar across age groups, although the SF-MPQ-2 sensory subscales were correlated with mental health quality of life in older, but not younger, patients. Older and younger patients selected the same words with the same intensity to describe their pain. The most commonly selected words in both age groups were aching, tiring-exhausting, sharp, and dull. These results demonstrate that the SF-MPQ-2 is appropriate for use across the adult lifespan in people with cancer pain. PERSPECTIVE: This study demonstrated that the SF-MPQ-2 is valid for use in older and younger people with advanced cancer and pain. This measure could improve cancer pain assessment across the adult lifespan, which may lead to improved pain management.

Pain.

Pain has many valuable functions. It often signals injury or disease, generates a wide range of adaptive behaviors, and promotes healing through rest. Despite these beneficial aspects of pain, there are negative features that challenge our understanding of the puzzle of pain, including persistent phantom limb pain after amputation or total spinal cord transection. Pain is a personal, subjective experience influenced by cultural learning, the meaning of the situation, attention, and other psychological variables. Pain processes do not begin with the stimulation of receptors. Rather, injury or disease produces neural signals that enter an active nervous system that (in the adult organism) is the substrate of past experience, culture, and a host of other environmental and personal factors. These brain processes actively participate in the selection, abstraction, and synthesis of information from the total sensory input. Pain is not simply the end product of a linear sensory transmission system; it is a dynamic process that involves continuous interactions among complex ascending and descending systems. The neuromatrix theory guides us away from the Cartesian concept of pain as a sensation produced by injury, inflammation, or other tissue pathology and toward the concept of pain as a multidimensional experience produced by multiple influences. These influences range from the existing synaptic architecture of the neuromatrix-which is determined by genetic and sensory factors-to influences from within the body and from other areas in the brain. Genetic influences on synaptic architecture may determine-or predispose toward-the development of chronic pain syndromes. WIREs Cogn Sci 2013, 4:1-15. doi: 10.1002/wcs.1201 For further resources related to this article, please visit the WIREs website.

Development and initial validation of an expanded and revised version of the Short-form McGill Pain Questionnaire (SF-MPQ-2).

The objective of the present research was to develop a single measure of the major symptoms of both neuropathic and non-neuropathic pain that can be used in studies of epidemiology, natural history, pathophysiologic mechanisms, and treatment response. We expanded and revised the Short-form McGill Pain Questionnaire (SF-MPQ) pain descriptors by adding symptoms relevant to neuropathic pain and by modifying the response format to a 0-10 numerical rating scale to provide increased responsiveness in longitudinal studies and clinical trials. The reliability, validity, and subscale structure of the revised SF-MPQ (SF-MPQ-2) were examined in responses from 882 individuals with diverse chronic pain syndromes and in 226 patients with painful diabetic peripheral neuropathy who participated in a randomized clinical trial. The data suggest that the SF-MPQ-2 has excellent reliability and validity, and the results of both exploratory and confirmatory factor analyses provided support for four readily interpretable subscales-continuous pain, intermittent pain, predominantly neuropathic pain, and affective descriptors. These results provide a basis for use of the SF-MPQ-2 in future clinical research, including clinical trials of treatments for neuropathic and non-neuropathic pain conditions.

Inflammation-susceptible Lewis rats show less sensitivity than resistant Fischer rats in the formalin inflammatory pain test and with repeated thermal testing.

Comparisons between Lewis and Fischer inbred strains of rats are used frequently to study the effect of inherent differences in function of the hypothalamic-pituitary-adrenal axis on pain-relevant traits, including differential susceptibility to chronic inflammatory disease and differential responsiveness to analgesic drugs. Increasing use of genetic models including transgenic knockout mice and inbred strains of rodents has raised our awareness of, and the importance of, thorough characterization (or phenotyping) of the strains of rodents being compared. Furthermore, genetic variability in analgesic sensitivity is correlated with, and may be caused by, genetically determined baseline sensitivity. Thus in this study, baseline inflammatory and thermal nociceptive sensitivities were measured in awake male and female Lewis and Fischer rats to examine whether the results could explain relevant strain differences reported in the literature. The effect of maternal separation was also examined and no effect was found on nociceptive sensitivity, corticosterone responses, or the development of adjuvant-induced arthritis, a model of rheumatoid arthritis. Lewis rats and female rats were more sensitive to thermal nociception in the tail withdrawal test (mean of 3 trials) than Fischer rats and male rats, respectively. Unexpectedly, the more inflammation-susceptible Lewis rats were less sensitive in the formalin inflammatory nociception test, and showed a significant decrease in sensitivity with repeated thermal nociceptive testing, whereas Fischer rats did not. These results affect the interpretation of previously observed results. Further study of the underlying mechanisms and the relevance to differential susceptibility to chronic inflammation is warranted.

The McGill pain questionnaire: from description to measurement.

On the language of pain. By Ronald Melzack, Warren S. Torgerson. Anesthesiology 1971; 34:50-9. Reprinted with permission. The purpose of this study was to develop new approaches to the problem of describing and measuring pain in human subjects. Words used to describe pain were brought together and categorized, and an attempt was made to scale them on a common intensity dimension. The data show that: 1) there are many words in the English language to describe the varieties of pain experience; 2) there is a high level of agreement that the words fall into classes and subclasses that represent particular dimensions or properties of pain experience; 3) substantial portions of the words have approximately the same relative positions on a common intensity scale for people who have widely divergent backgrounds. The word lists provide a basis for a questionnaire to study the effects of anesthetic and analgesic agents on the experience of pain.

Evolution of the neuromatrix theory of pain. The Prithvi Raj Lecture: presented at the third World Congress of World Institute of Pain, Barcelona 2004.

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. Acute pains evoked by brief noxious 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 discernable injury or pathology, remain a mystery. Furthermore, chronic psychological or physical stress is often associated with chronic pain, but the relationship is poorly understood. The neuromatrix theory of pain provides a new conceptual framework to examine these problems. It proposes that the output patterns of the body-self neuromatrix activate perceptual, homeostatic, and behavioral programs after injury, pathology, or chronic stress. 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.

The psychological assessment of candidates for spinal cord stimulation for chronic pain management.

It is known that, in spite of meeting appropriate clinical criteria for spinal cord stimulation (SCS) and having undergone flawless procedures, a significant number of patients who fail the therapy continues to exist. It is the purpose of this article to focus on the development of psychosocial indicators of success for SCS, if any. Referring to specialist literature authors present a review of what is known, what is not known, and what remains controversial on this topic. After reading this article we hope the reader will understand the importance of a psychological evaluation as part of the development of standards for identifying appropriate patients for this therapy. To improve treatment outcomes of SCS, seems to be essential to perform psychosocial evaluations on all persons clinically indicated for SCS to exclude those patients, who most probably, on a psychosocial level, will fail the procedure. To maximize treatment efficacy, authors believe spinal cord stimulation for chronic pain control must be part of a comprehensive program. An accurate preoperative psychosocial assessment and a course of psychological assistance both before and after therapy seems to be crucial for improving outcomes.

Age-related differences in the qualities but not the intensity of chronic pain.

Age differences in the experience of chronic pain remain unclear. A serious barrier to progress in the field of pain and aging arises from the lack of data regarding the psychometric properties of pain scales for use with the elderly. The present study was designed to assess age differences in pain intensity and quality and to compare the psychometric properties of the McGill Pain Questionnaire (MPQ) in young and elderly chronic pain patients. Young (n=139, mean age=42.93+/-9.41 years) and elderly (n=139, mean age=70.12+/-7.51 years) pain center patients, matched on primary diagnosis or pain location, duration, and sex, completed the MPQ, numeric ratings (0-10) of pain intensity, a Pain Map, and the Hospital Anxiety and Depression Scale (HADS). A Pain Management Index (PMI) score was calculated for each patient. Age differences on the measure of pain qualities were found. The elderly group had significantly lower MPQ total and sensory scores and chose fewer words than the young group. However, there were no significant differences between the groups on numeric ratings of highest, usual, and lowest pain intensity. Similarly, there were no age differences on PMI, Pain Map, or the HADS Depression or Anxiety Subscales. Finally, the latent structure, internal consistency, and pattern of subscale correlations of the MPQ were very similar in the young and elderly groups. Possible explanations for the discrepancy in the pattern of age differences on measures of pain intensity and quality are explored. The implications of this pattern of age differences for basic pain mechanisms and pain management should be given serious empirical attention.

The role of corticotropin-releasing factor in pain and analgesia.

Corticotropin-releasing factor (CRF) is a peptide that is released from the hypothalamus and in widespread areas of the brain following exposure to stressors. It is considered to be a mediator of many of the effects of stress, and its analgesic properties have been demonstrated in many studies. However, for primarily methodological reasons, the effects of CRF in the central nervous system have been neglected whereas the peripheral effects of CRF have been overemphasized. We present evidence that: (1) CRF can act at all levels of the neuraxis to produce analgesia; (2) the release of beta-endorphin does not explain the analgesia following intravenous or intracranial CRF administration; (3) inflammation must be present for local CRF to evoke analgesia and (4) the analgesic effects of CRF show specificity for prolonged pain. These findings suggest that CRF may have a significant role in chronic pain syndromes associated with hypothalamic-pituitary-adrenal axis abnormalities. Furthermore, CRF may represent a new class of analgesics that merits further study. Implications for the relationship between stress and pain are discussed.

From the gate to the neuromatrix.

The gate control theory's most important contribution to understanding pain was its emphasis on central neural mechanisms. The theory forced the medical and biological sciences to accept the brain as an active system that filters, selects and modulates inputs. The dorsal horns, too, were not merely passive transmission stations but sites at which dynamic activities (inhibition, excitation and modulation) occurred. The great challenge ahead of us is to understand brain function. I have therefore proposed that the brain possesses a neural network--the body-self neuromatrix--which integrates multiple inputs to produce the output pattern that evokes pain. The body-self neuromatrix comprises a widely distributed neural network that includes parallel somatosensory, limbic and thalamocortical components that subserve the sensory-discriminative. affective-motivational and evaluative-cognitive dimensions of pain experience. The synaptic architecture of the neuromatrix is determined by genetic and sensory influences. The 'neurosignature' output of the neuromatrix--patterns of nerve impulses of varying temporal and spatial dimensions--is produced by neural programs genetically build into the neuromatrix and determines the particular qualities and other properties of the pain experience and behavior. Multiple inputs that act on the neuromatrix programs and contribute to the output neurosignature include. (1) sensory inputs (cutaneous, visceral and other somatic receptors); (2) visual and other sensory inputs that influence the cognitive interpretation of the situation; (3) phasic and tonic cognitive and emotional inputs from other areas of the brain; (4) intrinsic neural inhibitory modulation inherent in all brain function; (5) the activity of the body's stress-regulation systems, including cytokines as well as the endocrine, autonomic, immune and opioid systems. We have traveled a long way from the psychophysical concept that seeks a simple one-to-one relationship between injury and pain. We now have a theoretical framework in which a genetically determined template for the body-self is modulated by the powerful stress system and the cognitive functions of the brain, in addition to the traditional sensory inputs.

The formalin test: a validation of the weighted-scores method of behavioural pain rating.

The formalin test was developed using an ordinal scale of weighted scores to rate the intensity of pain-related behaviours in animals. However, no studies have been carried out to establish the ordinal relationship of the behavioural categories used to generate the weighted pain intensity scores. The purpose of the present study was to evaluate the validity of the weighted-scores technique by assessing the ordinality of the behavioural categories associated with the specific category weights. The amount of time spent in each of 4 behavioural categories was measured as a function of the concentration of the formalin solution injected into the hindpaw of rats, and as a function of the dose of systemic morphine given to rats injected with a concentrated (5.0%) solution of formalin. The ordinal nature of the category weights was supported when the data were subjected to a polychotomous logistic regression for fitting an ordinal model.

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

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 neural mechanisms, such as nociceptor sensitization and neuroma formation, contribute to these pathological pain processes, recent evidence indicates that changes in central neural function may also play a significant role. In this review, we examine the clinical and experimental evidence which points to a contribution of central neural 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.

Temporal processes of formalin pain: differential role of the cingulum bundle, fornix pathway and medial bulboreticular formation.

Subcutaneous injection of formalin produces a characteristic biphasic pain response. An early phase develops in the first 5 min after injection; the pain then decreases for 10-15 min, followed by a gradual rise to a stable plateau that lasts about 1 h. Rats were injected with 1 microliter of 2% lidocaine or saline into the anterior cingulum bundle at 0 (immediately), 10 or 30 min prior to formalin injection, or 10, 20 or 30 min after formalin injection, and tested for analgesia in the late phase of the formalin test, 30-70 min after formalin injection. A time-dependent increase in analgesia was obtained when lidocaine was injected into the cingulum at periods ranging from 10 to 30 min after formalin injection, reflecting an anaesthetic duration of less than 20 min. When lidocaine was injected 0 or 10 min prior to formalin injection, a time-dependent increase in analgesia in the late phase was again observed. In these groups, lidocaine should have blocked cingulum activity during the early but not the late phase. The role of the fornix pathway and the medial bulboreticular formation in mediating formalin pain was also examined. Lidocaine produced analgesia in the late phase when injected into the fornix prior to formalin injection but had no effect when administered after it. In contrast, when lidocaine was injected into the medial bulboreticular formation it produced analgesia in the late phase when administered after formalin injection, but not prior to it. Taken together, these results suggest that the late pain response to formalin is in part dependent upon plasticity in the central nervous system which occurs during the transient early phase.

Analgesia produced by lidocaine microinjection into the dentate gyrus.

The local anesthetic lidocaine was injected into the dentate gyrus (DG) of alert, unrestrained rats 10 min prior to investigation within the formalin test. Regional anesthesia of the DG resulted in a reduction of pain scores when administered contralateral to the site of subcutaneous formalin injection. The analgesic effect was evident 30-50 min after central infusion. These results provide evidence of the involvement of the hippocampal formation (HF) in pain perception.

Pain 'memories' in phantom limbs: review and clinical observations.

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.

Comparisons between patients' and nurses' assessment of pain and medication efficacy in severe burn injuries.

In order to provide burn patients with adequate pain relief, the nurses must be able to accurately evaluate the patients' pain levels and to assess whether sufficient analgesia is achieved or not. The present study examined this issue by comparing the pain ratings in 42 patients hospitalized for burn injuries and 42 nurses. The patient and the attending nurse were asked to rate, independently of each other, the intensity of the pain felt by the patient during a therapeutic procedure and at rest. When analgesic medication was given prior to the procedure, both the patients and the nurses were asked to estimate the degree of pain relief. All ratings were obtained using visual analogue and verbal scales. The results revealed significant but small correlations between the nurses' and patients' ratings. Frequently, the nurses underestimated or overestimated the patients' pain. Discrepancies were also observed in the evaluation of pain medication efficacy, the nurses showing a tendency to overestimate the degree of pain relief. The accuracy of the nurses' perception did not vary as a function of the patients' age, socioeconomic status or burn severity. However, the number of years of experience in burn-nursing had a significant influence on the nurses' estimation of the patients' pain during therapeutic procedures. Theoretical and clinical implications of these results are discussed with a particular emphasis on the need to implement systematic procedures to assess pain and success of analgesia. Additional recommendations to optimize pain management in burn patients are also made.