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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with reflex sympathetic dystrophy or causalgia characteristically have ongoing pain and pain to light touch (hyperalgesia). Some of these patients obtain relief of their pain following interruption of sympathetic function to the affected area and, therefore, have sympathetically maintained pain (SMP). Evidence suggests that the pain and hyperalgesia in SMP are related to activation of peripheral adrenergic receptors. We wished to determine the contribution of alpha 1- and alpha 2-adrenergic receptors in SMP and thus examined the effects of local application of adrenergic agents in patients with SMP. The alpha 2-adrenergic agonist clonidine, available as a transdermal patch, was delivered topically to the patients' hyperalgesic skin. In four patients with SMP, clonidine eliminated or substantially reduced hyperalgesia to mechanical and cold stimuli. In three of these patients the effects were confined to the skin region beneath the patch, suggesting a peripheral and not central effect. The relief of hyperalgesia was not due to a local anesthetic effect since touch thresholds were unaffected. Topical clonidine did not relieve hyperalgesia of similar severity for two other patients whose hyperalgesia and pain were unaffected by sympathetic ganglion blocks (i.e., diagnosed as having sympathetically independent pain). In two SMP patients, intradermal injection of norepinephrine or phenylephrine (a specific alpha 1-adrenergic agonist) at a site treated with clonidine evoked intense pain and rekindled the pre-clonidine hyperalgesia at that site. It is likely that clonidine locally blocks the release of norepinephrine via activation of alpha 2 receptors on the sympathetic terminals. This study suggests, therefore, that SMP is mediated via alpha 1-adrenergic receptors located in the affected tissue.
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PMID:Topical application of clonidine relieves hyperalgesia in patients with sympathetically maintained pain. 823 54

A syndrome of cold hyperalgesia associated with cold hypoaesthesia is described in 28 patients with peripheral polyneuropathy or mononeuropathy of various aetiologies. A mechanism of sensory disinhibition, where diminished cold-specific A delta input releases cold pain input carried by C nociceptors, is proposed to explain the hyperalgesia. In most patients, the symptomatic skin is abnormally cold. This is a likely consequence of vasospasm, due to sympathetic denervation supersensitivity, caused by dropout of sympathetic efferents as part of the small caliber nerve fibre insult. The term 'triple cold syndrome' is coined to describe this specific pathophysiological condition. Descriptively it is a mirror image of erythralgia, as described by Sir Thomas Lewis (1936) and updated by one of the present authors, a human condition also centred around anomalous primary nociceptor input, in which there is heat hyperalgesia and hot symptomatic skin due to C nociceptor sensitization and vasodilatation from antidromic discharge. Thus, like the latter condition, the triple cold syndrome emerges as an independent clinical entity with definable abnormal mechanisms which should be retrieved out of the all-embracing, descriptive, diagnostic category 'reflex sympathetic dystrophy--causalgia'.
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PMID:The triple cold syndrome. Cold hyperalgesia, cold hypoaesthesia and cold skin in peripheral nerve disease. 814 11

The identification of a neuropathic pain syndrome in a cancer patient requires a focused clinical evaluation based on knowledge of common neuropathic pain syndromes. If a tumor is directly involved in the etiology of the pain, oncologic treatment is an initial consideration and may include surgery, radiation, or chemotherapy. There is no single accepted algorithm for the analgesic treatment of neuropathic pain and a systematic approach utilizing therapeutic trials of specific agents at gradually increasing doses is warranted. A trial of opioids, perhaps in combination with an NSAID, is warranted. If the pain is relatively unresponsive to an opioid, a trial with an adjuvant analgesic is reasonable. For example, a tricyclic antidepressant might be selected early for patients with continuous dysesthesia, and early treatment with an anticonvulsant might be used if the pain is predominantly lancinating or paroxysmal. Other adjuvant analgesics can be selected if there is insufficient response to these agents. A trial of sympathetic blockade, pharmacologic, anesthetic or surgical, should be considered in patients with evidence of causalgia or reflex sympathetic dystrophy. Physiatric modalities such as massage, heat, or cold; counterstimulation or transcutaneous electrical nerve stimulation (TENS), and orthopedic interventions, such as braces and splints may be useful. Epidural injections or neurostimulation of the spinal cord or brain can be considered in selected cases where appropriate expertise is available. Treatment of neuropathic pain remains a challenge for both clinicians and patients. The complexity of syndromes and underlying etiologic mechanisms warrants further clinical trials to determine the best treatment modalities for individual pain syndromes.
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PMID:Neuropathic pain in cancer patients: mechanisms, syndromes, and clinical controversies. 926 40

In the literature there is no unanimity with respect to the diagnosis of reflex sympathetic dystrophy (RSD). Frequently, the diagnosis is established on mere clinical grounds. In our opinion, however, bone scintigraphy is of major importance for the diagnosis. Using this examination, true RSD can be clearly differentiated from other conditions which are incorrectly diagnosed and treated as RSD. If the bone scan is not suggestive of RSD, the clinical picture, radiological examination and vascular scan may lead to the correct diagnosis. This may be a pseudodystrophy, in which a hypovascularization is found right from the start, while in true RSD there is initially a hypervascularization. Other conditions which may be confused with RSD are causalgia, neurotic compulsive postures, hysterical conversion, malingering and even self-mutilation. In the spontaneous course of RSD three phases can be distinguished. Stage I is the warm or hypertrophic phase, stage II the cold or atrophic phase. Per definition the third phase corresponds to stabilization or, in rare instances, to healing. By means of the vascular scan the correct stage can be determined, and the results of treatment evaluated. Finally it should be noted that in children the condition is completely different from true RSD, as it concerns a pseudodystrophy or disuse-related dystrophy. This condition may also be seen in adults and adolescents, usually females. The bone scan is always negative. In this way bone scintigraphy constitutes the means to answer the question as to what RSD is and what it is not. An algorithm for the differential diagnosis is presented.
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PMID:What is reflex sympathetic dystrophy? 1042 3

Early diagnosis is a prerequisite for a successful treatment of complex regional pain syndrome (CRPS). In order to describe neurological symptoms which characterize CRPS, we evaluated 145 patients prospectively. Two-thirds of these were women, the mean age at time of investigation was 50.4 years. CRPS followed limb trauma, surgery and nerve lesion. Employing the current IASP criteria 122 patients were classified as CRPS I and 23 as CRPS II. All patients were assessed clinically pain was quantified using the McGill pain questionnaire, skin temperature was measured by an infrared thermometer and a subgroup of 57 patients was retested in order to determine thermal thresholds (QST). Of our patients 42% reported stressful life events in a close relationship to the onset of CRPS and 41% had a history of chronic pain before CRPS. The latter group of patients gave a higher rating of CRPS pain (P<0.05). The major symptoms were pain at rest in 77% and hyperalgesia in 94%. Typical pain was deep in the limb having a tearing character. Patients getting physical therapy had significantly less pain than those without (P<0.04). Autonomic signs were frequent (98%) and often changed with the duration of CRPS. Skin temperature was warmer in acute and colder in chronic stages (P<0.001). Likewise edema had a higher incidence in acute stages (P<0.001). We found no correlation between pain and autonomic dysfunction. Motor dysfunction (present in 97%) included weakness, tremor, exaggerated tendon reflexes, dystonia or myoclonic jerks. QST revealed increased warm perception thresholds (P<0.02) and decreased cold pain thresholds (P<0.03) of the affected limb. The detailed knowledge of clinical features of CRPS could help physicians early to recognize the disease and thus to improve therapy outcome.
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PMID:Neurological findings in complex regional pain syndromes--analysis of 145 cases. 1077 May 24

Based on bed-side neurological testing, it has recently been shown that 33% of chronic complex regional pain syndrome (CRPS) type I patients exhibit sensory impairments, which extend past the painful area of the affected limb in a hemisensory distribution (Pain, 80 (1999) 95). In the present study, the clinically observed changes in touch and temperature sensations on the side of the body ipsilateral to the affected limb were investigated quantitatively. Neurophysiological and psychological examinations were conducted to detect changes in the peripheral and central nervous system as well as psychopathological abnormalities. In 40 patients with CRPS, a bed-side neurological examination was performed. Quantitative sensory testing was conducted at five locations on each side of the body. The evaluation of touch thresholds was performed using von Frey filaments (n=40). To measure cool, warm and heat pain thresholds quantitatively, a thermal stimulator using a Peltier-element was used (n=28). With respect to clinical findings, the initiating trauma and severity of abnormalities on nerve conduction testing, three patients were diagnosed as having a reliable CRPS II (causalgia) and five patients a possible CRPS II. Thirty-two patients were diagnosed as having a CRPS I.On clinical examination, 15 patients revealed generalized sensory deficits on the side of the body ipsilateral to the affected limb (hemisensory deficit, n=12; sensory impairment in the upper quadrant of the body, n=3). Patients with these generalized sensory deficits had a significantly longer illness duration (P<0.05) and a significantly higher percentage of mechanical allodynia/hyperalgesia than patients with spatially restricted sensory deficits (n=25) (P<0.05). In patients with generalized sensory impairment, thresholds for touch, warm and cold sensations, and for heat pain were significantly increased at all five locations tested ipsilaterally compared with the contralateral body side, except for the cool threshold on the chest and the heat pain threshold distally on the affected limb. In patients with sensory deficits limited to the affected limb, the touch threshold was significantly higher only in the distal part of the affected limb when compared with the contralateral limb. In these patients, thermal testing revealed almost no differences in cool, warm and heat pain thresholds when comparing both sides. Repeated thermal testing conducted in five patients with generalized sensory impairment reproduced the significant differences between both sides for cool, warm and heat pain thresholds. However, the correlation between the results obtained in the first and second examinations was poor. Neurophysiological recordings revealed pathological results in 46% for nerve conduction studies, 24% for somatosensory evoked potentials and 39% for sympathetic skin response. For all methods applied, there was no statistically significant difference in the incidence of pathological results between patients with generalized and patients with spatially restricted sensory abnormalities. Psychological examination using the structured clinical interview on DSM-IV (SKID) demonstrated a high frequency of affective and anxiety disorders, however, without significant differences between both groups.We conclude that hemisensory impairment in patients with CRPS Type I is probably related to functional disturbances in processing of noxious events in the thalamus and may be a clinical correlate of subcortical brain plasticity in chronic pain.
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PMID:Quantitative sensory testing, neurophysiological and psychological examination in patients with complex regional pain syndrome and hemisensory deficits. 1151 87

As suggested by this article, considerable advances in clinical management and research have taken place during the past 20 years. Although mechanisms underlying the pain syndrome CRPS I and CRPS II remain far from one's understanding, glimpses of the pathophysiology are beginning to take shape. There is now strong evidence that these syndromes exemplify a complex neurologic disease involving the brain at several integrated levels. The changes that occur in CRPS I patients involve somatosensory, sympathetic, and somatomotor systems. The diagnostic criteria have helped to focus on aspects of these foregoing systems and whereas there is no specific laboratory test for CRPS, enough is now known about the pathophysiology to use the following tests: quantitative sensory testing (QST), autonomic testing that include quantitative sudomotor axon reflex test (QSART) for sweating abnormalities, the cold pressor test in conjunction with thermographic imaging to observe the vasoconstrictor response, and laser Doppler flowmetry to monitor background vasomotor control. Recognition of a motor disorder requires accurate documentation and may be a component of the diagnostic criteria in the future. Until a better understanding of mechanistic overtones that would help to put in place mechanism-based therapeutic strategies, current management is built around a rehabilitation model. For this to be successful, as described in the foregoing pages, different non-interventional and interventional modalities are applied in a time-restricted manner to facilitate those modalities that favor progress in the treatment algorithm. As has been described, it is important when using physiotherapeutic maneuvers to minimize joint movement in the affected region to reduce the mechanorecpetor barrage and its increase in perceived pain to encourage and maintain a patient's compliance with their rehabilitation. Finally, of greater significance is the understanding that sympatholysis per se is not a "diagnostic" test for CRPS, but rather a useful procedure that may facilitate treatment for pain that is sympathetically maintained.
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PMID:Complex regional pain syndrome. 1471 16

As CRPS I frequently develops after tissue trauma, we proposed that an exaggerated inflammatory response to tissue trauma may underlie CRPS I. Therefore, we studied the vascular inflammatory, nociceptive and apoptotic sequelae of (i) soft tissue trauma and (ii) exaggerated soft tissue trauma in comparison to those of (iii) sciatic nerve chronic constriction injury, modeling CRPS II. Standardized soft tissue trauma (TR) was induced by means of a controlled impact injury technique in the hind limb of pentobarbital-anesthetized rats. Additional animals received soft tissue trauma and femoral arterial infusion of mediator-enriched supernatant achieved by homogenization and centrifugation of traumatized muscle tissue in order to provoke an exaggerated trauma response (ETR). Infusion of supernatant of non-traumatized muscle served as control intervention (STR, sham trauma response). Neuropathy was induced by chronic constriction injury of the sciatic nerve (CCI). Untreated animals served as controls (CO). Detailed nociceptive testing showed temporarily decreased mechanical pain thresholds in ETR animals that resolved within 14 days, while TR and STR animals, i.e. those with singular limb trauma, and controls remained free of pain. Neither cold- nor heat-evoked allodynia developed in post-traumatic animals, whereas CCI animals presented the well-known pattern of ongoing neuropathic pain. Using high-resolution in vivo multifluorescence microscopy, muscle tissue of traumatized animals revealed an enhanced inflammatory response that was found most pronounced in ETR animals. CCI of the sciatic nerve was not accompanied by tissue inflammation; however, induced myocyte apoptosis. Collectively, these data indicate that exaggeration of trauma response induces signs and symptoms of acute CRPS I. Pain perception displays differences to that in CRPS II. Apoptosis turns out to be a distinctive marker for CRPS, warranting further evaluation in clinical studies.
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PMID:Exaggeration of tissue trauma induces signs and symptoms of acute CRPS I, however displays distinct differences to experimental CRPS II. 1667 12

We present the case of a 33-year-old woman with benign sporadic monomelic amyotrophy of the distal part of the arm, called Hirayama disease. Clinical features included forearm amyotrophy sparing the brachioradialis muscle, cold paresis and causalgia. Neck magnetic resonance imaging was normal in neutral and flexion position. Electromyography showed denervated patterns in the extensor digitorum communis, and conduction studies ruled out multifocal motor neuropathy. Motor evoked potentials were normal. Serum IgG anti-GM1 antibodies were moderately raised but were negative 8 months later. Outcome was favourable within 15 months, with partial motor recovery. Pathogenesis remains controversial: neck flexion induced myelopathy via chronic anterior horn ischaemia due to forward displacement of the posterior wall of the dura mater, or benign variant of lower motor neuron disease? Whatever the pathomechanism is, the clinical features and outcome are the same.
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PMID:A woman with forearm amyotrophy. 2217 Dec 30