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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 81-year-old woman with right lower limb ischemia was scheduled for revascularization of a femoropopliteal bypass grafted 10 years earlier. A popliteal blockade, attempted as part of regional anesthesia with the aid of a nerve stimulator, was not achieved because the posterior tibial nerve could not be located. After surgery, the patient mentioned symptoms in the region of the right knee consistent with complex regional pain syndrome (Ducke's stage 3); the symptoms appeared after the first operation and would explain the absence of response to the nerve stimulator. Using a nerve stimulator to facilitate location of the various nerve trunks for anesthesia involves obtaining a motor response to electrical stimulation. The procedure is becoming more and more frequent because of its many advantages over other more traditional methods. However, it may be impossible to locate a nerve for a variety of reasons.
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PMID:[Constraints on the use of a nerve stimulator in peripheral conduction blocks when there is disturbance in the neuromuscular junction]. 1073 90

A neuropathic-like pain syndrome was produced in rats following prolonged hindpaw ischemia and reperfusion, creating an animal model of complex regional pain syndrome-Type I (CRPS-I; reflex sympathetic dystrophy) that we call chronic post-ischemia pain (CPIP). The method involves placing a tourniquet (a tight fitting O-ring) on one hindlimb of an anesthetized rat just proximal to the ankle joint for 3 h, and removing it to allow reperfusion prior to termination of the anesthesia. Rats exhibit hyperemia and edema/plasma extravasation of the ischemic hindpaw for a period of 2-4 h after reperfusion. Hyperalgesia to noxious mechanical stimulation (pin prick) and cold (acetone exposure), as well as mechanical allodynia to innocuous mechanical stimulation (von Frey hairs), are evident in the affected hindpaw as early as 8 h after reperfusion, and extend for at least 4 weeks in approximately 70% of the rats. The rats also exhibit spontaneous pain behaviors (hindpaw shaking, licking and favoring), and spread of hyperalgesia/allodynia to the uninjured contralateral hindpaw. Light-microscopic examination of the tibial nerve taken from the region just proximal to the tourniquet reveals no signs of nerve damage. Consistent with the hypothesis that the generation of free radicals may be partly responsible for CRPS-I and CPIP, two free radical scavengers, N-acetyl-L-cysteine (NAC) and 4-hydroxy-2,2,6,6-tetramethylpiperydine-1-oxyl (Tempol), were able to reduce signs of mechanical allodynia in this model.
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PMID:Chronic post-ischemia pain (CPIP): a novel animal model of complex regional pain syndrome-type I (CRPS-I; reflex sympathetic dystrophy) produced by prolonged hindpaw ischemia and reperfusion in the rat. 1549 78

The transradial approach for coronary catheterization is now a routine technique without serious complications at the puncture site. We report a case of complex regional pain syndrome type II (CRPS type II) in the hand after the transradial coronary intervention, which may alert medical personnel that the technique may cause serious regional pain with disability. A 61-year-old woman underwent coronary intervention via the right radial artery for the treatment of unstable angina. After the operation she complained of severe pain in the right hand, consistently felt along the median nerve distribution. The nerve conduction study suggested carpal tunnel syndrome. We made a diagnosis of CRPS type II, and the patient received stellate ganglion blockade, cervical epidural blockade, and administration of amitriptyline and loxoprofen. The symptoms gradually improved and her activities of daily living markedly improved. The median nerve appeared to be damaged by local compression and potential ischemia. Careful attention should be paid to avoid CRPS type II, associated with excess compression.
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PMID:A case of complex regional pain syndrome type II after transradial coronary intervention. 1554 77

Spinal cord stimulation is the most common mode of neuromodulation used in managing chronic low back pain. It is minimally invasive and reversible as opposed to nerve ablation. The basic scientific background of the initial spinal cord stimulation trials was based on the gate control theory of Melzack and Wall. It has been demonstrated in multiple studies that dorsal horn neuronal activity caused by peripheral noxious stimuli could be inhibited by concomitant stimulation of the dorsal columns. Various other mechanisms, which may play a significant role in the mechanism of action of spinal cord stimulation, include the suppressive effect of spinal cord stimulation on tactile allodynia, increased dorsal horn inhibitory action of gamma-aminobutyric acid (GABA), prevention or abolition of peripheral ischemia, and effects on human brain activity. Spinal cord stimulation is indicated in low back pain with radiculopathy, failed back surgery syndrome, complex regional pain syndrome, peripheral vascular disease, and ischemic heart disease. There is substantial scientific evidence on the efficacy of spinal cord stimulation for treatment of low back and lower extremity pain of neuropathic nature. Clinical studies revealed a success rate of from 50% to 70% with spinal cord stimulation, with decreased pain intensity scores, functional improvement and decreased medication usage. This review discusses multiple aspects of spinal cord stimulation, including pathophysiology and mechanism of action, rationale, indications, technique, clinical effectiveness, and controversial aspects.
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PMID:Spinal cord stimulation. 1690 66

Electrical spinal neuromodulation in the form of spinal cord stimulation is currently used for treating chronic painful conditions such as complex regional pain syndrome, diabetic neuropathy, postherpetic neuralgia, peripheral ischemia, low back pain, and other conditions refractory to more conservative treatments. To date, there are very few published reports documenting the use of spinal cord stimulation in the treatment of head/neck and upper limb pain. This paper reports a case series of 5 consecutive patients outlining the use of spinal cord stimulation to treat upper extremity pain. All subjects had previously undergone cervical fusion surgery to treat chronic neck and upper limb pain. Patients were referred following failure of the surgery to manage their painful conditions. Spinal cord stimulators were placed in the cervical epidural space through a thoracic needle placement. Stimulation parameters were adjusted to capture as much of the painful area(s) as possible. In total, 4 out of 5 patients moved to implantation. In all cases, patients reported significant (70-90%) reductions in pain, including axial neck pain and upper extremity pain. Interestingly, 2 patients with associated headache and lower extremity pain obtained relief after paresthesia-steering reportedly covered those areas. Moreover, 2 patients reported that cervical spinal cord stimulation significantly improved axial low back pain. Patients continue to report excellent pain relief up to 9 months following implantation. This case series documents the successful treatment of neck and upper extremity pain following unsuccessful cervical spine fusion surgery. Given this initial success, prospective, controlled studies are warranted to more adequately assess the long term utility and cost effectiveness of electrical neuromodulation treatment of chronic neck and upper extremity pain.
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PMID:Neuromodulation of the cervical spinal cord in the treatment of chronic intractable neck and upper extremity pain: a case series and review of the literature. 1752 88

Spinal cord stimulation (SCS) is used in the treatment of chronic pain, ischemia because of obstructive arterial disease, and anginal pain. Recently, a number of studies have described the effects of the high cervical SCS, including increased cerebral blood flow, although the underlying mechanisms are unknown. This case report describes a patient with a severe complex ischemic condition affecting both cerebral and upper limb blood flow with an associated complex regional pain syndrome in upper limb. While all previous clinical treatments proved ineffective, cervical SCS afforded satisfactory results. Possible mechanisms underlying the cervical SCS effect are discussed.
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PMID:The beneficial effect of spinal cord stimulation in a patient with severe cerebral ischemia and upper extremity ischemic pain. 1755 83

Electric energy have been in use for the treatment of various ailments, including pain, since the time of Pharaohs. The theoretical basis of electrotherapy of pain was provided by the Gate Control Theory of Melzak and Wall. In 1965, Shealey et al. first introduced electrical stimulation of spinal cord for treating pain. At present spinal cord stimulation (SCS) is a well established form of treatment for failed back surgery syndrome, complex regional pain syndrome and refractory pain due to ischemia. The indications for SCS is growing and the technology involved in this is rapidly advancing, however, high level of scientific evidence is still lacking to support this form of therapy due to difficulties in blinding and comparing with control groups. Future developments in SCS could include, combined SCS-drug delivery system, bio feedback and closed loop systems.
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PMID:Spinal cord stimulation: principles of past, present and future practice: a review. 1972 20

Ischemic-reperfusion (I/R) is common in various pathological conditions like diabetic complication, complex regional pain syndrome type II (CRPS II), necrotizing vascular occlusive disease and trauma. We have developed an animal model of ischemic-reperfusion injury induced nociceptive sensory neuropathy in rats. The model was validated after 2, 4 and 6h of ischemia followed by prolonged reperfusion. The sensory behavioral assessment revealed thermal and mechanical hyperalgesia in paw and in tail which expressed the peripheral and central neuropathic pain respectively. We observed a decrease in the serum IL-10 and nerve conduction velocity and increase in the serum nitrate, malondialdehyde (MDA) and TNF-alpha levels in the 4 and 6h I/R groups in biochemical and electrophysiological evaluations. Histopathological study had revealed the decrease in nerve fiber density in the moderate and severe I/R groups. We selected the moderate (4h) ischemic-reperfusion injury as beneficial model because of the good correlation with clinical status for the development of neuropathy in human associated with severe pain disorders. This model can be used to explore pathophysiological mechanisms implied in the genesis of neuropathic pain and also to evaluate the new analgesic agents, peripheral neuro-vasoactive substances and neuroprotective drugs.
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PMID:Development of animal model for vasculatic neuropathy: Induction by ischemic-reperfusion in the rat femoral artery. 2002 13

Transradial access for cardiac catheterization is now widely accepted among the invasive cardiology community as a safe and viable approach with a markedly reduced incidence of major access-related complications compared with the transfemoral approach. As this access technique is now being used more commonly for cardiac catheterization, it is of paramount importance to be aware of its complications and to understand their prevention and management. Some of the common complications of transradial access include asymptomatic radial artery occlusion, nonocclusive radial artery injury and radial artery spasm. Among these complications, radial artery spasm is still a significant challenge. Symptomatic radial arterial occlusion, pseudoaneurysm and radial artery perforation are rarely reported complications of the transradial approach. Early identification of these rare complications and their immediate management is of vital importance. Arteriovenous fistula, minor nerve damage and complex regional pain syndrome are very rare but have been reported. Recently, granulomas have been reported to be associated with the use of a particular brand of hydrophilic sheaths during the procedure. Generally, access-site complications can be minimized by avoiding multiple punctures, selection of smaller sheaths, gentle catheter manipulation, adequate anticoagulation, use of appropriate compression devices and avoiding prolonged high-pressure compression. In addition, careful observation for any ominous signs such as pain, numbness and hematoma formation during and in the immediate postprocedure period is essential in the prevention of catastrophic hand ischemia.
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PMID:Access-site complications and their management during transradial cardiac catheterization. 2265 38

This study investigated the involvement of the adenosinergic system in antiallodynia induced by exercise in an animal model of complex regional pain syndrome type I (CRPS-I). Furthermore, we analyzed the role of the opioid receptors on exercise-induced analgesia. Ischemia/reperfusion (IR) mice, nonexercised and exercised, received intraperitoneal injections of caffeine (10mg/kg, a non selective adenosine receptor antagonist), 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (0.1mg/kg, a selective adenosine A receptor antagonist), ZM241385 (3mg/kg, a selective adenosine A receptor antagonist), adenosine deaminase inhibitor erythro-9-(2-hydroxy-3nonyl) adenine [(EHNA), 5mg/kg, an adenosine deaminase inhibitor] or naloxone (1mg/kg, a nonselective opioid receptor antagonist). The results showed that high-intensity swimming exercise reduced mechanical allodynia in an animal model of CRPS-I in mice. The antiallodynic effect caused by exercise was reversed by pretreatment with caffeine, naloxone, DPCPX but it was not modified by ZM241385 treatment. In addition, treatment with EHNA, which suppresses the breakdown of adenosine to inosine, enhanced the pain-relieving effects of the high-intensity swimming exercise. This is the first report demonstrating that repeated sessions of high-intensity swimming exercise attenuate mechanical allodynia in an animal model of CRPS-I and that the mechanism involves endogenous adenosine and adenosine A receptors. This study supports the use of high-intensity exercise as an adjunct therapy for CRPS-I treatment.
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PMID:High-intensity swimming exercise reduces neuropathic pain in an animal model of complex regional pain syndrome type I: evidence for a role of the adenosinergic system. 2329 54


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