|
 |
|
| |
NEUROPATHIC PAIN
Chronic pain can develop after injury to any level of the nervous system, peripheral or central. A variety of specific syndromes have been identified. Their pathogeneses remain obscure and their incidence and prevalence are unknown but appear to be low relative to the injuries that precede them, except for root avulsion injuries and perhaps phantom limb pain. Two broad categories of nervous system damage appear to involve reorganization of central somatosensory processing: (1) deafferentation pains (those due to partial or complete interruption of peripheral or central afferent neural activity) and (2) sympathetic-mediated pains (those dependent on efferent sympathetic activity). Both syndromes are complex, and though presumably related pathogenetically, they diverge substantially. For example, a thalamic lesion that causes pain without autonomic or trophic changes and is unresponsive to manipulation of the sympathetic nervous system is clearly distinct from a lesion producing reflex sympathetic dystrophy, in which all of these characteristics may be present. Nevertheless, both are believed to involve reorganization of central pain pathways as the primary process related to pain perception. Another subgroup of neuropathic pains appears to involve predominantly peripheral processes (eg, nerve compression or neuroma formation). In addition to the measures described below, primary therapies directed at the peripheral focus (eg, decompression of nerve) sometimes may help these disorders.
Though deep aching may accompany nerve injury, these pain states tend to produce a spontaneous burning pain, often with a superimposed lancinating component. Other sensations (eg, hyperesthesia, hyperalgesia, allodynia [pain from a non-noxious stimulus], and hyperpathia [particularly unpleasant, exaggerated pain response]) may also occur.
Principles of Treatment
1. Accurate diagnosis is essential: In particular, deafferentation pain from peripheral nerve damage must be distinguished from other forms of neuropathic pain in which an ongoing, potentially treatable, pathologic process involves a peripheral nerve. For example, phantom limb pain must be distinguished from stump pain, since the latter suggests a different pathophysiology (neuroma). Additional evaluation (to rule out infection, hypertrophic scar, bone fragments) and unique treatments (injection or resection of the neuroma) may be indicated. Even central pains may be caused by a remediable process (eg, tumor or syrinx) and should be fully assessed. A practical aspect of diagnosis concerns the distinction between pains that may be ameliorated by manipulation of the sympathetic nervous system (eg, reflex sympathetic dystrophy) and those that are not. Initial management often depends on this categorization, as outlined below.
2. Mobilization of the painful part: Particularly in peripheral nerve lesions, the development of trophic changes, compounded by disuse atrophy and joint ankylosis, can be a devastating complication, ultimately increasing both pain and disability. Vigorous rehabilitative therapy should be given to maintain full motion at affected joints, improve muscle strength and tone, further desensitize the painful extremity by repeatedly stimulating it, and retain functional use of the limb as far as possible.
3. Constant consideration of psychologic factors, beginning at the start of therapy: Profound psychologic impairment may be present in these disorders. Anxiety and depression must be addressed directly and treated appropriately. Social isolation is common and reintegration into the family and society at large should be specific therapeutic goals. Loss of function beyond that explained by the neurologic deficit should be vigorously managed with psychologic and rehabilitative techniques (see below).
These treatment principles provide an environment in which drug and nondrug methods of pain control can be initiated; therapies applied without concern for diagnosis, rehabilitation, and psychosocial issues have a limited chance of success.
REFLEX SYMPATHETIC DYSTROPHY
This prototype of sympathetically mediated pain occurs following injury to bone and soft tissue. The diagnosis depends on pain associated with autonomic changes (eg, sweating or vasomotor abnormalities) and/or dystrophic changes (eg, skin or bone atrophy, hair loss, joint contractures). Radionuclide bone scan (increased uptake), x-rays of the extremity (bone loss), and thermography (decreased skin temperature) may be useful confirmatory tests, but none need be positive for the pain syndrome to exist.
Causalgia may be viewed as a subtype of reflex sympathetic dystrophy. In this syndrome, usually partial injury to a nerve trunk (typically the median nerve above the elbow or sciatic nerve above the knee) produces severe, burning pain in the extremity. The pain usually occurs immediately or soon after the injury and in time becomes associated with the autonomic and trophic changes described above.
Treatment
Combined with physical therapy, anesthetic or pharmacologic blockade of sympathetic nerve function is the most important modality. Sympathetic nerve block should be used. Transient relief after repeated temporary blocks suggests the need for surgical or chemical sympathectomy. Regional sympathetic blockade with IV guanethidine or reserpine is a specialized anesthetic technique that may be useful in selected patients. The sympatholytic drugs prazosin (1 to 8 mg/day orally in divided doses) and phenoxybenzamine (40 to 120 mg/day orally in divided doses) have been reported in uncontrolled series to be of benefit. Other suggested drugs include nifedipine (10 to 30 mg orally tid), corticosteroids (eg, prednisone 60 to 80 mg/day orally tapered over 2 to 4 wk), tricyclic antidepressants (see above), and anticonvulsants (see TABLE 119-5). Anecdotal reports in postherpetic neuralgia and other neuropathic pain states also suggest benefit from topical application of capsaicin cream 0.025% as well as selected neuroleptics (eg, fluphenazine 1 to 2 mg orally tid). Recently, the analgesic potential of local oral anesthetics (mexiletine 150 to 300 mg tid is preferred) has been explored and a trial in refractory neuropathic pain states is warranted. Chronic treatment with opioid analgesics is controversial, but may occasionally be useful in reliable patients; such therapy should be considered only after all other approaches have failed and if close physician follow-up is possible.
Physical therapy is essential during all phases of therapy. If myofascial trigger points are found, they should be injected. Transcutaneous electrical nerve stimulation (TENS) may be helpful, and a prolonged trial at multiple locations and stimulation parameters should be attempted. Alternative methods of nervous system stimulation (neuroaugmentation) include counterirritation (brisk rubbing of the affected part) and acupuncture. No studies have established that one form of neuroaugmentative therapy is superior to another or that patient response to other forms will be poor if one type is unsuccessful. Thus, treatment remains empiric.
Psychologic therapies are described below, under PSYCHOGENIC PAIN SYNDROMES.
Finally, a recent surgical innovation, the dorsal root entry zone lesion, can be considered for disabling pain unresponsive to conservative measures.
OTHER NEUROPATHIC SYNDROMES
The remaining deafferentation nerve injury syndromes are distinguished from those above by lack of observed long-term efficacy of sympathetic blockade. These include postherpetic neuralgia (see in Ch. 14), phantom limb pain, root avulsions, painful polyneuropathy, central pain syndromes (potentially caused by virtually any lesion at any level of the nervous system), and postsurgical pain syndromes, eg, postmastectomy syndrome, postthoracotomy syndrome, and stump pain.
Treatment
Drug treatment with tricyclic antidepressants, anticonvulsants, oral local anesthetics, and/or neuroleptics may be useful (see above). Diphenhydramine in relatively high doses (eg, 400 to 600 mg/day in divided doses), IV naloxone infusions, and both L-tryptophan (2 to 3 gm/day in divided doses) and 5-hydroxytryptophan (up to 800 mg/day in divided doses) have been anecdotally reported to be salutary in central pain states. All the other nondrug therapies described for reflex sympathetic dystrophy, above, may be tried, excluding those that block sympathetic nerve function.
Patients can exhibit profound functional and psychologic impairment. These lesions can produce severe pain, but there is wide individual variation in the ability to cope with this situation and continue a semblance of normal existence, especially in the face of repeated therapeutic failures. The development of abnormal illness behavior with prominent social withdrawal, familial disruption, and progressive inactivity is not inevitable, but patients who develop these aberrant behaviors begin to resemble those with no or insufficient explanation for pain; ie, those with the chronic nonmalignant pain syndrome (see below). The development of psychologic and social dysfunction must be recognized and treated. When this pattern is entrenched, patients may benefit from the comprehensive approach provided by a pain clinic.
Back
|
| |
