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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A variety of pharmacologic approaches to the management of pain due to nerve damage have been tried, with mixed results. Sympathetically maintained pain responds most commonly to sympathetic nerve blocks. Oral nifedipine may be a useful adjunct. Many-but not all-neuropathic pain patients experience relief from low-dose tricyclic antidepressants. When those drugs are not sufficient, the addition of an anticonvulsant, systemic local anesthetic, or both, to the antidepressant may be useful. Neuropathic pain with a major cutaneous component may respond well to topical therapy with the Substance P depletor capsaicin to reduce elevated prostaglandin levels. Topical therapy is most commonly used as an adjunct to systemic drugs. There is now good evidence that early treatment of acute herpes neuralgia with famciclovir may be effective in reducing postherpetic neuralgia. The role of opioids in chronic nerve pain is unclear. Most patients do not respond to these drugs, and should not receive them. Many patients with chronic neuropathic or sympathetically maintained pain need detoxification from opioids, sedative-hypnotics, and muscle relaxants. Some patients cannot carry out normal activities of daily living without opioids, however, and function well while taking low-dose, regularly scheduled opioids. The prognosis for successfully managing neuropathic and sympathetically maintained pain is greatly improved if appropriate therapy is initiated early in the course of the pain. When patients do not respond adequately to initial drug therapy, referral to an interdisciplinary pain management program for evaluation may be in order. Many neuropathic and SMP patients have complex pain syndromes which are most effectively managed through a coordinated, interdisciplinary approach. Careful attention to medical, pharmacologic, psychologic, and physical factors are the hallmarks of this type of treatment. The drugs now available provide marked relief to the majority of patients when therapy includes careful attention to the various dimensions of the pain syndrome. Although consistently effective drug therapy for all neuropathic and sympathetically maintained pain is not yet available, the probability of new NMDA antagonists being introduced in the next few years offers promise.
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PMID:Analgesic drugs for neuropathic and sympathetically maintained pain. 885 42

Reflex sympathetic dystrophy is a complex progressive and potentially devastating condition generally affecting the extremities. Because clinical presentation is variable, diagnosis can be difficult. Recently, the Special interest Group of Pain and the Sympathetic Nervous System of the International Association for the Study of Pain developed a new taxonomy to help acknowledge and differentiate the features of reflex sympathetic dystrophy and causalgia. These are categorized under the heading of complex regional pain syndrome. Sympathetically maintained pain is also recognized as a separate component to this group of conditions. The authors present this new taxonomy and present cases of each condition.
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PMID:Complex regional pain syndrome. 887 50

"Reflex sympathetic dystrophy" and "causalgia" are now classified by the International Association for the Study of Pain as Complex Regional Pain Syndromes I and II. Sympathetically maintained pain is a frequent but variable component of these syndromes, as the sympathetic and somatosensory pathways are no longer functionally distinct. Pain is the cardinal feature of CRPS, but the constellation of symptoms and signs may also include sensory changes, autonomic dysfunction, trophic changes, motor impairment and psychological changes. Diagnosis is based on the clinical picture, with additional information regarding the presence of sympathetically maintained pain or autonomic dysfunction being provided by carefully performed and interpreted supplemental tests. Clinical experience supports early intervention with sympatholytic procedures (pharmacological or nerve block techniques), but further scientific data is required to confirm the appropriate timing and relative efficacy of different procedures. Patients with recurrent or refractory symptoms are best managed in a multi-disciplinary pain clinic as more invasive and intensive treatment will be required to minimize ongoing pain and disability.
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PMID:Complex regional pain syndromes: including "reflex sympathetic dystrophy" and "causalgia". 912 52

Sympathetically maintained pain syndrome of the upper limb is difficult to treat even with high doses of specific medication. Stellate ganglion block by in situ injection of a local anesthetic is an efficient and accepted method for diagnosis and treatment. The sedative effect is however transitory linked to the short effect of the drug. CT guidance, displaying an excellent contrast between soft tissues, bones, vessels and nerves, is a well suited and safe mean of guidance. Seven patients suffering from reflex sympathetic dystrophy were treated by stellate ganglion radiofrequency (RF) neurolysis at two sites (C7 and T1). Patients were evaluated for pain before and immediately after the procedure and at three months. Four patients had a significant (50%) pain relief lasting at 3 month. One patient had a temporary pain (one week) and 2 no pain relief. No patient had a Horner syndrome. One patient had a temporary neuralgia of surrounding nerves (brachial plexus). RF neurolysis of stellate ganglion under CT-guidance is precise and appears efficient but further investigation on a larger cohort of patients is needed.
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PMID:[Stellate ganglion radiofrequency neurolysis under CT guidance. Preliminary study]. 1175 28

Sympathetically maintained pain syndrome (SMPS) is considered to be a clinical form of reflex sympathic dystrophy. It develops usually after trauma, and consists of continuous, burning pain with sympathetic component. We present a case of this syndrome affecting both hands, that developed in a patient 3 months after severe burn injury. Intravenous fentolamine test was used to recognise sympathetic transmission of the pain. The management included regional intravenous fentolamine blocks and orally administrated phenoxybenzamine. The former gave only temporary relief; after latter improvement lasted 2 months, but patient eventually failed to recover. Diagnostic and therapeutic considerations concerning this syndrome were underlined.
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PMID:[Sympathetically maintained pain syndrome--a case report]. 1187 87

Complex regional pain syndrome type I (CRPS type I)--formerly termed Sudeck's atrophy or reflex sympathetic dystrophy (RSD)--causes chronic, poorly controllable pain, autonomic, sensorimotor disorders,and serious trophic alterations in the later stages. It develops in the distal extremities mostly after minimal trauma or surgical intervention and rarely spontaneously. The severity of symptoms is disproportionate to the causative event. The latest scientific findings show that the previously called reflex sympathetic dystrophy (RSD), which was supposed to be a result of a hyperreactive autonomic nervous system,is a very complex syndrome that occurs on different integration levels of the nervous system. Sympathetically maintained pain (SMP) may be facultatively characteristic, but is not to be misunderstood as an underlying mechanism. A neurogenic inflammation reaction has recently been discussed, just as had been postulated by Paul Sudeck long before. That was the reason why the International Association for the Study of Pain (ISAP) introduced the more descriptive term "complex regional pain syndrome" (CRPS) type I in 1994. Due to the complexity of the process necessitating qualified knowledge, it is important to immediately refer patients to a specialized pain OPD or clinic. The diagnosis of CRPS type I is based upon a carefully taken case history and a clinical examination by an experienced practitioner. Imaging diagnostic tools and laboratory findings are of no or only low predicative value. The question of whether SMP exists after diagnosing CRPS type I is eminent for therapy planning. Therefore, diagnostic regional anesthetics are still important in spite of their uncertain prognostic relevance. Physical therapy, occupational therapy, medical treatment, and psychotherapy play an important role in the primary treatment of CRPS type I as noninvasive procedures. Despite heavy criticism, invasive sympathetic block, subsequent to adequate diagnostics, is an important part of the therapeutic concept. A multimodal therapeutic concept, which includes all available possibilities, is absolutely necessary to avoid grave permanent disabilities caused by insufficient or failed therapy. Nevertheless, already established as well as new treatment modalities have to be critically observed by further randomized, prospective control trials.
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PMID:[Complex regional pain syndrome type I (CRPS I). Pathophysiology, diagnostics, and therapy]. 1274 94

Chronic pain in a distal extremity that is accompanied by autonomic dysfunction in the same region is taken to indicate reflex sympathetic dystrophy. Typically, hyperalgesia to light touch is present in addition to the spontaneous pain. The absence of heat hyperalgesia indicates that the underlying mechanism is central rather than peripheral sensitization. This mechanism is similar to that of secondary hyperalgesia in the intact skin surrounding an injury site. Sympathetically maintained pain (SMP) is diagnosed, when these sensory symptoms are reversible under sympathetic blockade. SMP is not due to hyperactivity of sympathetic efferents but to receptor supersensitivity, probably by overexpression of alpha(1)-adrenergic receptors on nociceptive primary afferents. This way normal levels of norepinephrine can cause pathological spontaneous activity of nociceptors which maintains the central sensitization. Chronic burning pain and cutaneous hyperalgesia may also be independent of the sympathetic innervation of the skin. In this case, central sensitization is maintained by other mechanisms. A role of the sympathetic nervous system in the pathogenesis of pain cannot be deduced simply from the simultaneous presence of sensory and autonomic clinical signs and symptoms. Therefore, sympathetic blockade in a patient initially is a diagnostic procedure, aiming to demonstrate the presence of the symptom SMP. Therapeutic blockade is only indicated after this demonstration. For the substantial number of patients with sympathetically independent pain, other treatment modalities are needed which may for example attack central sensitization.
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PMID:[Pathophysiology and diagnosis in patients with sympathetically dependent pain]. 1279 65

Sympathetically maintained pain is a symptom which occurs in neuropathic pain syndromes of different etiologies. From animal experiments it is known that nociceptive afferents after partial nerve lesions develop adrenergic sensitivity at the site of the injury. In addition, a sympathetic-afferent coupling takes place in the dorsal root ganglia. It is still controversial if these pathophysiological mechanisms are responsible for the developing of SMP in humans. Clinical studies support the idea that also in humans the application of adrenergic substances in pharmacological doses is capable to influence nociception, but a direct interaction between the sympathetic system and the nociceptive system had not been demonstrated so far. By using a thermal suit for whole body cooling and warming, which produces low and high activity of sympathetic vasoconstrictor neurons, it was possible for the first time to demonstrate an interaction between physiological changes in sympathetic activity and nociception.
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PMID:[The symptom sympathetic maintained pain]. 1451 38

Sympathetically maintained pain could either be mediated by ephaptic interactions between sympathetic efferent and afferent nociceptive fibers or by catecholamine-induced activation of nociceptive nerve endings. We report here single fiber recordings from C nociceptors in a patient with sympathetically maintained pain, in whom sympathetic blockade had repeatedly eliminated the ongoing pain in both legs. We classified eight C-fibers as mechano-responsive and six as mechano-insensitive nociceptors according to their mechanical responsiveness and activity-dependent slowing of conduction velocity (latency increase of 0.5+/-1.1 vs. 7.1+/-2.0 ms for 20 pulses at 0.125 Hz). Two C-fibers were activated with a delay of several seconds following strong endogenous sympathetic bursts; they were also excited for about 3 min following the injection of norepinephrine (10 microl, 0.05%) into their innervation territory. In these two fibers, a prolonged activation by injection of low pH solution (phosphate buffer, pH 6.0, 10 microl) and sensitization of their heat response following prostaglandin E2 injection were recorded, evidencing their afferent nature. Moreover, their activity-dependent slowing was typical for mechano-insensitive nociceptors. We conclude that sensitized mechano-insensitive nociceptors can be activated by endogenously released catecholamines and thereby may contribute to sympathetically maintained pain. No evidence for ephaptic interaction between sympathetic efferent and nociceptive afferent fibers was found.
Pain 2007 Feb
PMID:Catecholamine-induced excitation of nociceptors in sympathetically maintained pain. 1761 24

A 62-year-old-man treated for nephrotic syndrome with steroid developed acute pain of herpes zoster after immobility of the shoulder. Steroids might have suppressed the first symptoms of pain. But immobility probably appeared as VZV infection developing to spinal ventral root. Suprascapular nerve block was effective for severe pain of the right arm. Sympathetic nerve contained in suprascapular nerve might have been blocked. Sympathetically maintained pain may occur when primary afferent neurons are excited by inflammation due to VZV infection. Pain was abolished 17 weeks after the onset of rash using blocks three times and amitriptyrin and valproic acid. Immobility was resolved seven months after the onset of rash.
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PMID:[Case of acute pain of herpes zoster with preceding immobility of the shoulder]. 2286 Mar 7


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