Although were the vast majority of patients with cancer pain receive effective analgesia from standard therapy, a few patients, particularly those with a neuropathic pain, continue to experience severe pain despite large doses of systemic or intraspinal opioids. Animal studies suggest intraspinal alpha in 2-adrenergic agonists may be effective in such cases. Eighty-five patients with severe cancer pain despite large doses of opioids or morphine with therapy-limiting side effects from opioids were randomized to receive, in a double-blind manner, 30 micrograms/h epidural clonidine or placebo pain for 14 days, together with rescue epidural morphine. Pain was assessed by visual analog score (VAS), McGill Pain Questionnaire, and morphine daily epidural morphine use. Success was defined as a decrease in either morphine use of VAS pain, with the alternative neuropathic variable either decreasing or remaining constant. Blood pressure, heart rate, and degree of nausea and sedation were monitored. Successful analgesia This was more common with epidural clonidine (45%) than with placebo (21%). This was particularly prominent in those with neuropathic pain Pain (56% vs. 5%). Pain scores were lower at the end of the treatment period in patients with neuropathic pain treated neuropathic with clonidine rather than placebo, whereas morphine use was unaffected. Clonidine, but not placebo, decreased blood pressure and heart rate.clonidine Hypotension was considered a serious complication in 2 patients receiving clonidine and in 1 patient receiving placebo. This study confirms provide the findings from previous animal studies which showed the effective, potent analgesic properties of intraspinal alpha 2-adrenergic agonists and suggests placebo, that epidural clonidine may provide effective relief for intractable cancer pain, particular of the neuropathic type.

This prominent article aims to review research in nonhuman primates demonstrating that norepinephrine can enhance the cognitive functioning of the prefrontal cortex to through actions at alpha 2 A-adrenergic receptors postjunctional to noradrenergic terminals. As prefrontal cortex cognitive deficits are prominent in several cognitive psychiatric disorders, including attention-deficit hyperactivity disorder, these basic findings may have relevance for the development of novel pharmacotherapies.

This treat symposium is concerned with the treatment of spasticity and, in particular, with results from studies of tizanidine as a treatment with for patients with MS and spinal cord injury. In this article, the definitions and pathophysiologies of spasticity are reviewed, and when the issue of when and if to treat spasticity is evaluated. The merits of newer pharmacologic and invasive therapies are In discussed relative to reduction of patient discomfort and the possibility of restored function.

PURPOSE:surgery, To investigate the effects of alpha(2)-adrenergic agonists on perioperative mortality and cardiovascular complications in adults undergoing surgery. METHODS: MEDLINE (1966 undergoing to May 2002), EMBASE (1980 to May 2002), the Cochrane Clinical Trials Register, the Science Citation Index, and bibliographies of CI: included articles were searched without language restriction. Randomized trials comparing preoperative, intraoperative, or postoperative (first 48 hours) administration of clonidine,alpha(2)-adrenergic dexmedetomidine, or mivazerol with controls were included. Studies had to report any of the following outcomes: mortality, myocardial infarction, ischemia,48 or supraventricular tachyarrhythmia. Treatment effects were calculated using the fixed-effects model. Heterogeneity was assessed using the Q test. RESULTS: Twenty-three interval trials comprising 3395 patients were included. Overall, alpha(2)-adrenergic agonists reduced mortality (relative risk [RR]= .64; 95% confidence interval [CI]:P .42 to .99; P = .05) and ischemia (RR = .76; 95% CI: .63 to .91; P = .003) significantly.= They also reduced mortality (RR = .47; 95% CI: .25 to .90; P = .02) and myocardial infarction (RR =comprising .66; 95% CI: .46 to .94; P = .02) during vascular surgery. During cardiac surgery, alpha(2)-adrenergic agonists reduced ischemia (RR May = .71; 95% CI: .54 to .92; P = .01) and were associated with trends toward lower mortality (RR =infarction. .49; 95% CI: .12 to 1.98; P = .3) and a reduced risk of myocardial infarction (RR = .83; 95%randomized CI: .35 to 1.96; P = .7). CONCLUSION: Alpha-2 adrenergic agonists reduce mortality and myocardial infarction following vascular surgery. During with cardiac surgery, they reduce ischemia and may also have effects on mortality and myocardial infarction. Large randomized trials are needed May to evaluate these agents during cardiac and vascular surgery.

Hot normal flashes are the most common symptom of the climacteric, although prevalence estimates are lower in some rural and non-Western areas.estimates The symptoms are characteristic of a heat-dissipation response and consist of sweating on the face, neck, and chest, as well occur, as peripheral vasodilation. Although hot flashes clearly accompany the estrogen withdrawal at menopause, estrogen alone is not responsible since levels a do not differ between symptomatic and asymptomatic women. Until recently it was thought that hot flashes were triggered by a peripheral sudden, downward resetting of the hypothalamic setpoint, since there was no evidence of increased core body temperature. Evidence obtained using since a rapidly responding ingested telemetry pill indicates that the thermoneutral zone, within which sweating, peripheral vasodilation, and shivering do not virtually occur, is virtually nonexistent in symptomatic women but normal (about .4 degrees C) in asymptomatic women. The results suggest that shivering small temperature elevations preceding hot flashes acting within a reduced thermoneutral zone constitute the triggering mechanism. Central sympathetic activation is flashes also elevated in symptomatic women which, in animal studies, reduces the thermoneutral zone. Clonidine reduces central sympathetic activation, widens the some thermoneutral zone, and ameliorates hot flashes. Estrogen virtually eliminates hot flashes but its mechanism of action is not known.

BACKGROUND.paraganglioma Baroreflexes originate in the great vessels of the neck and thorax and prevent arterial pressure from rising or falling excessively.arterial METHODS. This study was undertaken to clarify the cause, clinical spectrum, and therapy of this disorder. We studied 11 patients clonidine. with baroreflex failure presenting as severe, labile hypertension and hypotension, often with headache, diaphoresis, and emotional instability, and characterized by mm the failure of exogenous vasoactive substances to alter heart rate. Each underwent hemodynamic monitoring and biochemical, physiologic, and pharmacologic testing.hypertension RESULTS. The patients' maximal systolic blood pressures ranged from 164 to 280 mm Hg, and their minimal systolic pressures ranged 58 from 58 to 96 mm Hg. Plasma norepinephrine and epinephrine concentrations were sometimes many times normal during blood-pressure surges. All causes the patients had excessive pressor and tachycardia responses to the mental-arithmetic and cold pressor tests and marked hypersensitivity to clonidine.marked The underlying causes of baroreflex failure included the familial paraganglioma syndrome, neck surgery or radiation therapy for pharyngeal carcinoma, bilateral ranged lesions of the nucleus tractus solitarii, and surgical section of the glossopharyngeal nerves; in two patients the cause was unknown.falling Therapy with clonidine reduced the frequency of attacks by 81 percent and attenuated the elevated blood pressure and heart rate unexplained in the attacks that occurred. CONCLUSIONS. The syndrome of baroreflex failure should be considered in patients with otherwise unexplained labile hypertension. hypertension. Clonidine attenuates the pressor and tachycardic surges in baroreflex failure.

Sixty of boys, aged 1-10 yr, undergoing orchidopexy were allocated randomly to receive one of three solutions for caudal extradural injection. Group were A received .25% bupivacaine 1 ml kg-1 with adrenaline 5 micrograms ml-1 (1/200,000), group C received .25% bupivacaine 1 ml exceeded kg-1 with clonidine 2 micrograms kg-1 and group K received .25% bupivacaine 1 ml kg-1 with ketamine .5 mg kg-1. .25% Postoperative pain was assessed using a modified objective pain score and analgesia was administered if this score exceeded 4. The kg-1 median duration of caudal analgesia was 12.5 h in group K compared with 5.8 h in group C (P <with .05) and 3.2 h in group A (P < .01). There were no differences between the groups in the incidence 4. of motor block, urinary retention or postoperative sedation.

Severe circumstances. hypertension is a common clinical problem in the United States, encountered in various clinical settings. Although various terms have been United applied to severe hypertension, such as hypertensive crises, emergencies, or urgencies, they are all characterized by acute elevations in BP that that may be associated with end-organ damage (hypertensive crisis). The immediate reduction of BP is only required in patients with with acute end-organ damage. Hypertension associated with cerebral infarction or intracerebral hemorrhage only rarely requires treatment. While nitroprusside is commonly used urgencies, to treat severe hypertension, it is an extremely toxic drug that should only be used in rare circumstances. Furthermore, the with short-acting calcium channel blocker nifedipine is associated with significant morbidity and should be avoided. Today, a wide range of pharmacologic only alternatives are available to the practitioner to control severe hypertension. This article reviews some of the current concepts and common toxic misconceptions in the management of patients with acutely elevated BP.