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

The purpose of this article has been to heighten awareness of the recognition, diagnosis, and therapy of the sympathetically maintained pain syndromes. Classification of RSD and causalgia as semantic subdivisions of SMP should be maintained until further laboratory and clinical analyses, with strict uniform diagnostic criteria, define similarities or differences in clinical behavior and therapeutic responses.
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PMID:Role of the sympathetic nervous system in painful nerve injury. 182 28

We present a woman who developed left arm sympathetically maintained pain (SMP, or "shoulder-hand syndrome") as a result of brachial plexus injury. After confirmatory diagnosis with both stellate local anesthetic block and intravenous phentolamine infusion, the patient had a cervical epidural catheter placed and a local anesthetic infusion started. After numerous unilateral blocks were obtained, a cervical epidurogram demonstrated a probable cervical midline epidural septum. Catheter placement was adjusted, and a successful chemical sympathectomy was performed for 6 days. This resulted in significant relief of the patient's shoulder pain as well as almost complete resolution of the patient's left arm SMP symptoms. This case represents, to our knowledge, the first documentation of the use of phentolamine for the diagnosis of SMP secondary to pathology at a site proximal to that of symptomatology, as well as the first documentation of presumptive cervical midline epidural septum.
J Pain Symptom Manage 1994 Apr
PMID:Probable cervical midline epidural septum complicating the treatment of a patient with upper extremity sympathetically maintained pain. 751 59

We have tested the effects of cutaneous application of noradrenaline in 35 patients presenting with neuropathic pain. Depending on the outcome of sympatholytic interventions the patients were considered to have sympathetically maintained pain (SMP; n = 25) or sympathetically independent pain (SIP; n = 10). Iontophoretic application or cutaneous injection of noradrenaline into symptomatic skin aggravated pain and mechanical or thermal hyperalgesia in 7/25 SMP patients. Results from differential nerve blocks suggested that noradrenaline-induced ongoing pain and heat hyperalgesia were signalled by unmyelinated afferents, while touch-evoked pain and cold hyperalgesia were signalled by myelinated afferents. In none of the remaining 18/25 SMP patients, 10 SIP patients or 18 normal subjects did application of noradrenaline result in any appreciable increase of pain. A follow-up of 12 patients (initially 9 SMP, 3 SIP) after 12-16 years showed that one individual (previously SMP) was healthy, while 3 patients still suffered from SMP and 8 from SIP. Of the 5 SMP patients who had noradrenaline-induced pain at the initial examination, only 1 SMP patient still responded to noradrenaline with pain and hyperalgesia. Three other patients had changed to SIP and 1 individual was healthy. None of these 4 and none of the 7 initially noradrenaline-unresponsive patients experienced pain to the noradrenaline challenge at follow-up. Thus, cutaneous noradrenaline application can aggravate the pain in some, but not all SMP patients. THe abnormal noradrenaline reaction can change over time as can the pain relieving effects of sympatholytic therapy.
Pain 1995 Oct
PMID:Noradrenaline-evoked pain in neuralgia. 857 78

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

A new classification system, termed complex regional pain syndromes types I and II, has been devised to replace the nomenclature of pain disorders previously termed reflex sympathetic dystrophy and causalgia. CRPS type I does not have identifiable major nerve injury, whereas CRPS type II has an identifiable major nerve injury. The classification is based on clinical symptoms and signs without incorporating any mechanistic connotations. These CRPS disorders may have SMP, SIP, or both.
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PMID:Classification of complex regional pain syndromes. New concepts. 927 37

Some humans with partial nerve injury present a syndrome of neuropathic sensory disorders which depend on the sympathetic activity (sympathetically-maintained pain, SMP). Several years ago we introduced a rat model for SMP, produced by tightly ligating 1/3-1/2 of the sciatic nerve, leading to a partial denervation of the hindpaw (Partial Sciatic Ligation, PSL model) [Seltzer, Z., Dubner, R. and Shir, Y., Pain, 43 (1990) 245-250]. After working with this model for several years we encountered difficulties in replicating it although rat strain, vendor, gender, age and weight, surgical approach and sensory testing procedures were not changed. We report here that this variability can be attributed, at least in part, to the diet the animals consumed. Rats fed perioperatively with soy-containing diets expressed significantly weaker neuropathic sensory disorders compared to rats fed on soy-free diets. We conclude that diet may greatly affect experimental outcome in the PSL model.
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PMID:Neuropathic pain following partial nerve injury in rats is suppressed by dietary soy. 948 75

The striking response of causalgia and reflex sympathetic dystrophy (RSD) to sympatholytic procedures together with signs of autonomic nervous system abnormalities suggest that the sympathetic efferent system can generate or enhance pain (sympathetically maintained pain, SMP). This concept is supported by human and animal experiments indicating that sympathetic activity and catecholamines can activate primary afferent nociceptors. Some clinical evidence, however, calls the SMP concept into question and alternative explanations have been advanced. In this review, we describe the clinical features of causalgia and RSD and the evidence for sympatholytic efficacy. The major barrier to proving the SMP concept is that all available sympatholytic procedures are problematic. We conclude that, although the weight of current evidence supports the SMP concept and its relevance to causalgia and RSD, it remains unproven by scientific criteria. More careful adherence to diagnostic criteria and well-controlled trials of sympatholysis are needed to finally settle the issue.
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PMID:Causalgia and reflex sympathetic dystrophy: does the sympathetic nervous system contribute to the generation of pain? 1036 21

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

Complex regional pain syndromes (CRPS, reflex sympathetic dystrophy, causalgia) are painful disorders that develop after trauma affecting a limb with (I) or without (II) nerve injury. Clinical features are pain, impairment of motor function, swelling and autonomic abnormalities (changes in sweating and blood flow). Autonomic abnormalities. The maximal skin temperature difference between the affected and unaffected extremity that occurs during a controlled thermoregulation can be used as a diagnostic tool. SMP. Sympathetic outflow to the painful extremity was experimentally activated. The intensity as well as area of spontaneous pain and mechanical hyperalgesia increased considerably in patients that had been classified as having SMP by positive sympathetic blocks. A pathological interaction between sympathetic vasoconstrictor and afferent neurons within the affected skin is the likely explanation for SMP in CRPS patients. Motor abnormalities. Kinematic analysis of target reaching as well as grip force analysis showed a pathological sensorimotor integration located in the parietal cortex. Furthermore, MEG studies demonstrated a continuous inhibition of the primary motor cortex. Neurogenic inflammation. Some features of acute CRPS (vasodilatation, swelling, pain) indicate a localized inflammatory process. Transcutaneous electrical stimulation of nociceptive C-fibre provoked protein extravasation into the interstitial fluid (microdialysis) only in CRPS patients and not in controls.
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PMID:Mechanistic and clinical aspects of complex regional pain syndrome (CRPS). 1546 53

Chronic pain, whether arising from viscera, bone, or any other tissue or structure, is, more often than commonly thought, the result of a mixture of pain mechanisms, and therefore there is no simple formula available to manage chronic complex pain states. Box 1 summarizes a pharmacological algorithm for difficult-to-treat chronic pain, which merely introduces the medication aspect of the treatment. In effect, any comprehensive algorithm should call for an interdisciplinary approach that would include rehabilitation, as well as psychosocial, and when indicated, interventional techniques. Box 1 Analgesic algorithm for difficult-to-treat pain syndromes. Pharmacological Interventions. Moderate to severe pain/functional impairment; pain with a score of >4 on the brief pain inventory. 1. Gabapentinoid (gabapentin, pregabalin)+/-Opioid/opioid rotation or 2. Antidepressant (TCA, duloxetine, venlafaxine)+/-Opioid/opioid rotation or 3. Gabapentinoid+antidepressant+Opioid/opioid rotation; in addition, may consider trials of one or more of the following adjuvants when clinically appropriate: Topical therapies for cutaneous allodynia/hyperalgesia. Anti-inflammatory drugs (corticosteroids for acute inflammatory neuropathic pain)IV bisphosphonates for cancer bone pain or CRPS/RSDNon-gabapentinoid AEDs such as carbamazepine or oxcarbazepine or lamotrigine+/-baclofen for intermittent lancinating pain due to cranial neuralgiasNMDA antagonists Mexiletine On a compassionate basis, according to the patient's clinical condition and pain mechanism, the physician may want to consider an empirical trial of one or more of the emergent topical, oral or parenteral/intrathecal therapies as discussed in the text. If SMP, consider topical clonidine and sympatholytic interventions; if clinically feasible, trials of topical therapies, eg, lidocaine 5% patch, may be considered for a variety of pain states and features.The major rationale for introducing adjuvants is to better balance efficacy and adverse effects. The following scenarios should prompt the use of adjuvants in clinical practice: The toxic limit of a primary analgesic has been reached. The therapeutic benefit of a primary analgesic has plateaued, eg, treatment has reached its true efficacy limit or pharmachodynamic tolerance has developed. The primary analgesic is contraindicated, eg, substance abuse, aberrant behavior, organ failure, allergy, and so forth. Subjective and qualitative symptoms demand broader coverage. Patients often convey that different medications will impart distinct analgesic benefits. Presence of disabling nonpainful complaints and need to manage symptoms such as insomnia, depression, anxiety, and fatigue that all cause worsening of the patient's quality of life and function. Physicians have also been drawn to the adjuvants secondary to new realities of clinical practice. Moreover, aversion to addiction and diversion remains a potent force that shapes prescribing profiles.
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PMID:Adjuvant analgesics. 1716 7


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