The practice and theoretical basis of pain measurement is reviewed and critically examined in the areas of animal research, human subjects laboratory investigation and clinical study. The advantages and limitations of both physiological and behavioral methods are discussed in each area, and subjective report procedures are evaluated in human laboratory and clinical areas. The need for procedures that bridge these areas is emphasized and specific issues are identified. Progress in the technology of pain measurement over recent decades is reviewed and directions for future work are suggested.

This paper advances a psychophysiological systems view of pain in which physical injury, or wounding, generates a complex stress response that extends beyond the nervous system and contributes to the experience of pain. Through a common chemical language comprising neurotransmitters, peptides, endocannabinoids, cytokines and hormones, an ensemble of interdependent nervous, endocrine, and immune processes operates in concert to cope with the injury. These processes act as a single agent and comprise a supersystem. Acute pain in its multiple dimensions, and the related symptoms that commonly occur with it, are products of the supersystem. Chronic pain can develop as a result of unusual stress. Social stressors can compound the stress resulting from a wound or act alone to dysregulate the supersystem. When the supersystem suffers dysregulation, health, function and sense of well-being suffer. Some chronic pain conditions are the product of supersystem dysregulation. Individuals vary and are vulnerable to dysregulation and dysfunction in particular organ systems due to the unique interactions of genetic, epigenetic and environmental factors, as well as the past experiences that characterize each person.Perspective-Acute tissue injury activates an ensemble of interdependent nervous, endocrine and immune processes that operate in concert and comprise a supersystem. Some chronic pain conditions result from supersystem dysregulation. Individuals vary and are vulnerable to dysregulation due to the unique interactions of genetic, epigenetic and environmental factors, and past experiences that characterize each person. This perspective can potentially assist clinicians in assessing and managing chronic pain patients.

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IntroductionDespite increased attention to the problem in recent decades, acute postoperative pain (POP) control remains an ongoing challenge 1,4,9 . Failure to control POP effectively increases cost of care and causes significant suffering. Widespread speculation based on emerging literature holds that inadequately controlled postoperative pain is one of the major risk factors for the development of chronic postoperative pain 3,5 .Progress in POP management depends on quality of POP assessment. Current pain assessment practices hinder progress in pain control because of three limitations. First, postoperative pain, like all pain, is complex and multidimensional 10 , and reducing it to a single number is a pragmatic over-simplification. Clinicians may sometimes reify the number and treat it rather than the person in pain. Second, the 11-point numerical rating scale (NRS) and the 101-point visual analog scale (VAS), while adequate for epidemiological purposes, are too imprecise to characterize individual patient POP meaningfully Donaldson 2 . Third, POP assessment methods typically ignore the self-limiting nature of acute pain and fail to determine the rate of POP resolution. Because acute pain is self-limiting, its chronological dimension merits inclusion in pain assessment.Measurement precision is a function of measurement error. All measurement involves some degree of error, and measures with less error are more precise than those with more error. Rating scale scores include error because they correspond imperfectly to the patient's true, underlying pain. The standard error of measurement (SEM) gauges a measurement tool's precision, indicating the typical error of measurement, the give-or-take amount by which a single score is likely to be off. Measurements with small SEMs are quite accurate and therefore reasonably precise, while measurements with large SEMs have poor accuracy and low precision. For a given measurement instrument, the SEM is the standard deviation of the measurement errors across individuals in a population. Improved precision is a fundamental goal of innovation in POP measurement.Resolution over time is a key feature of POP, and rate of pain resolution is a potentially important clinical outcome. Yet, conventional POP measurement practices focus on static Address Correspondence to: C. Richard Chapman, Ph.D., Professor and Director, Pain Research Center, University of Utah, Department of Anesthesiology, 615 Arapeen Dr, Suite 200, Salt Lake City, UT 84108, USA, crc20@utah.edu. The authors have no financial or other relationships that constitute a conflict of interest.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content...

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The initial development of PAIN OUT has been achieved. From 2013, it continues as a not-for-profit academic project, open to clinicians and researchers worldwide. The International Association for Study of Pain and PAIN OUT will work together to maintain, disseminate and develop the registry.

Pupillary response to noxious stimulation was investigated in men (n = 11) and women (n = 9). Subjects experienced repeated trials of noxious electrical fingertip stimulation at four intensities, ranging from faint to barely tolerable pain. Measures included pupil dilation response (PDR), pain report (PR), and brain evoked potentials (EPs). The PDR began at 0.33 s and peaked at 1.25 s after the stimulus. Multivariate mixed-effects analyses revealed that (a) the PDR increased significantly in peak amplitude as stimulus intensity increased, (b) EP peaks at 150 and 250 ms differed significantly in both amplitude and latency across stimulus intensity, and (c) PR increased significantly with increasing stimulus intensity. Men demonstrated a significantly greater EP peak amplitude and peak latency at 150 ms than did women. With sex and stimulus intensity effects partialled out, the EP peak latency at 150 ms significantly predicted PR, and EP peak amplitude at 150 ms significantly predicted the PDR peak amplitude.