Very few imaging studies have been carried out on patients with chronic nociceptive pain. Most of these studies did not assess clin- ical pain directly. Instead, they investigated responses to experimen- tal pain (painful heat or pressure) in patients with chronic nociceptive pain (Fig. 7-4).
In a study in patients with rheumatoid arthritis (RA), a classic model of chronic nociceptive pain, painful heat stimuli induced a decrease in rCBF in the PFC and ACC. Effective coping strategies in these patients have been proposed to explain these surprising obser- vations.42,43However, conflicting results were reported in a more recent study from the same group44assessing the patterns of brain activation in RA patients at rest, during acute spontaneous arthritis- related pain, and experimental heat pain. In this study, the authors reported a stronger signal in structures from the medial pain system (ACC, amygdala, and orbitofrontal cortex [OFC]) for arthritic pain than for evoked pain. The unpleasantness of pain was also closely correlated with the activation of these structures, but no major hypoactivation was described. These apparently conflicting results may be accounted for by the small number of patients (six) eval- uated in the first study.43
DLPF*** AAC*** LN* Th* Ins*** S 2*** Cer* OFC*** S 1***
Figure 7^4.Changes in brain activity associated with experimentally evoked pain in low back pain (LBP) and rheumatoid arthritis patients.The regions displaying an increase in rCBF or BOLD responses are indicated. ACC, anterior cingulate cortex; Cer, cerebellum; DLPF, dorsolateral prefrontal cortex; Ins, insula; LN, lentiform nucleus; OFC, orbitofrontal cortex; S1, primary somatosensory cortex; S2, secondary somatosensory cortex; Th, thalamus.The number of stars *, **, *** associated with each structure is a symbolic correlate of the number of
studies showing significant changes. (Adapted from references 44, 4649.)
49 II ASSESSMENT OF PAIN AND ITS TREAT MENT
Low back pain (LBP) is a highly prevalent condition and is the second most frequent symptom-related reason for which patients consult a physician.45It is frequently classified as a type of nocicep- tive pain, although its mechanisms are probably complex and remain poorly understood. It may be idiopathic or secondary to various conditions (e.g., fractures, inflammatory diseases, surgery). An elegant study showed a differential pattern of activation during two different components of spontaneous pain in LBP patients: ‘‘increasing’’ and ‘‘high constant" pain.46During an increase in spontaneous pain, an increase in the signal from the IC, S1, S2, mid-ACC, and cerebellum was detected. Changes in IC activity were found to be positively correlated with the increase in spontane- ous pain. In contrast, when pain remained at high constant levels, the activity of the medial PFC (including the rostral ACC) increased; this increase being directly correlated with pain intensity. Interes- tingly, these authors also described a decrease in cortical density in the same area of the dorsolateral PFC (DLPF) in LBP patients.47
In LBP patients, the application of a painful heat stimulus to the lower back induced a significantly stronger bilateral signal in the IC, S2, and ACC and a significantly stronger signal in the right DLPF than that observed in normal controls.
Other studies have evaluated brain processing in LBP patients during experimental pain distant from the lower back region. Derbyshire and colleagues48 compared responses to painful heat stimulation of the hand in LBP patients. Activation, mostly observed in the cerebellum, midbrain, thalamus, lentiform nucleus, PFC, midcingulate cortex, and IC, was similar in patients and con- trols. In another study, painful pressure stimuli applied to the thumb induced similar patterns of brain activation in patients with LBP (or fibromyalgia) and controls, but the intensity of the signals was greater in patients.49
These studies in patients with RA and LBP tend to confirm that the changes in brain activity associated with clinical nociceptive pain are different, at least quantitatively, from those induced by experimental pain. In particular, chronic clinical nociceptive/ inflammatory pain seems to be more specifically associated with changes in the medial pain system.
CONCLUSIONS
Modern functional imaging of the brain has helped to improve our understanding of the mechanisms of normal physiologic pain and, to a much lesser extent, of some specific clinical pain states. The available data tend to indicate that pathologic pain does not corre- spond simply to the abnormal activation of a single "pain matrix," but rather that different types of pain (e.g., neuropathic, nocicep- tive) and probably different pain symptoms (spontaneous continu- ous pain, allodynia) involve different brain mechanisms. These findings highlight the need for a more rational and pathophysiolo- gic classification of pain syndromes. Future studies should also help to define the place of functional neuroimaging in mechanism-based approaches to chronic pain.
R
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Chapter 8
POTENTIAL
DOCUMENTATION
TOOLS FOR
OPIOID
THERAPY
Howard S. Smith and Kenneth L. Kirsh
INTRODUCTION
The field of pain management is still relatively young compared with other medical specialties, but it has experienced a tremendous period of growth since the late 1980s. Realization has grown that chronic pain affects the lives of millions of people and that this issue must be addressed. Indeed, we see that issues with pain are the number-one reason that patients go to see their physicians. However, this increased recognition of the problem has been somewhat tempered by the souring of the regulatory climate and the growth of prescrip- tion drug abuse. Because of this, there has been a trend for clinicians to shy away from using high opioid doses or even utilizing this modality at all in the treatment of chronic pain (Box 81).
Despite these fears and concerns, the use of long-term opioid therapy (OT) to treat chronic nonmalignant pain is growing, based in part on evidence from clinical trials and a growing consensus among pain specialists. The appropriate use of these drugs requires skills in opioid prescribing, knowledge of addiction medicine principles, and a commitment to perform and document a comprehensive assessment repeatedly over time. Inadequate assess- ment can lead to undertreatment, compromise the effectiveness of therapy when implemented, and prevent an appropriate response when problematic drug-related behaviors occur.
There is a burgeoning interest in the development of tools that can be useful for screening patients up front to determine the relative risk for patients having problems with prescription drug abuse or misuse (Box 82). To date, a number of tools have arisen, including the Screening Tool for Addiction Risk (STAR), Drug Abuse Screening Test (DAST), Screener and Opioid Assessment for Patients with Pain (SOAPP), and the Opioid Risk Tool (ORT). The choice in tools for a more thorough ongoing assessment, however, has been somewhat more limited up until now and is the focus of the discussion.
Oversight by regulatory agencies, state medical boards, and various peer-review groups includes examination of appropriate medical care as well as proper documentation. As the old axiom states, ‘‘if it isn’t written, it didn’t happen.’’ In cases of OT for chronic pain, issues beyond typical office visit charting may deserve attention and documentation. Although there are no explicit requirements for what and how to document issues related to OT, it is belived by some that the use of specific tools and instru- ments in the chart on some or all visits may boost adherence to