Pain can be managed with medications, physical therapies and modalities, behavioral interventions and counseling, and more invasive intrathecal, electric stimulation, and surgical approaches. The aims are to eliminate pain or at least make discomfort tolerable and to restore physical and social functioning. People with chronic debilitating pain are sometimes best managed as inpatients, especially if they need to be withdrawn from high doses of narcotic analgesics and have poor exercise toler-
Table 8-8. Stages of Reflex Sympathetic Dystrophy
Stage 1 Develops in first month; Edema, burning, warm and dry or cold and lasts 3-6 months sweaty skin
Stage 2 Follows stage 1; Atrophic skin, osteoporosis, spreading lasts 3-6 months pain, joint fibrosis, muscle wasting
Stage 3 Duration varies Resolving pain, contractures, cool skin, atrophy ance. Outpatient chronic pain management programs include a team that can carry out behavioral modification, relaxation, and cognitive, physical, and occupational therapies to increase activity and reduce pain behavior. In addition, the team may adjust medications, deal with mood disorders, and provide education. Claims about the efficacy of pain treatments that have not been subjected to a clinical trial must be considered in relation to the nonspecific placebo effects provided by the team's interest, attention, and overall approach to the patient. Hands-on therapies such as soft tissue manipulations and ultrasound are less likely to affect neuropathic compared with muscu-loskeletal sources of pain. However, nocicep-tive pain from muscles and joints commonly accompanies neurologic diseases, causes disability, and degrades quality of life, and can exacerbate neuropathic sources of pain.
The dimensions of pain that are unique to individuals include quality, intensity, duration, course, personal meaning, and impact on function and roles. Their measure poses challenges. Subjective personal assessements of pain are used most often. These measures are supported by scales of motor performance, ADLs, work history, mood, and quality of life. Clinicians most often record the frequency of pain-related behaviors and employ visual analog scales for pain, verbal pain rating scales, the McGill Pain Questionnaire,95 the Minnesota Multiphasic Personality Inventory, and the Sickness Index Profile (see Chapter 7).
Remarkably few placebo-controlled, randomized clinical trials with more than 20 subjects who had a similar etiology or type of chronic central pain have been reported. Table 8-9 includes a few of the better studies. Most drug trials that show a benefit reveal this for some pain sensations more than others, such as diminishing cold-induced allodynia or hy-peralgesia, or the drug helps at-level pain more than below-level pain after a SCI. For peripheral neuropathies such as diabetes mellitus that cause pain, the tricyclics, anticonvulsant sodium channel blockers, and NMDA antagonist dextromethorphan, followed by gabapentin, tramadol, SSRIs, and capsaicin seem most efficacious.96 Although some animal studies do not point to an increase in GABA with the use of gabapentin, magnetic resonance spectroscopy in healthy persons reveals that GABA levels rise approximately 50%
by 6 hours after a dose and levels rise by over 25% after 4 weeks of the anticonvulsants top-iramate, lamotrignine, or gabapentin.97
For postherpetic neuralgia, clinical trials show that lidocaine patches, gabapentin, and tricyclics work best. For HIV-associated distal sensory neuropathy, tricyclics and lamotrigine were shown in controlled trials not to be useful. Unfortunately, the efficacy of the drugs used to treat neuropathic pain is low. The clinician will have to treat from 3 to 6 patients with any one drug to see a partial benefit in 1
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