THERAPY—NERVE BLOCKS: SOMATIC AND LESION TECHNIQUES
Kate M. Grady, Andrew M. Severn, Paul R. Eldridge in Key Topics in Chronic Pain, 2002
Sensory nerve blocks are widely used in chronic pain management for diagnostic and therapeutic purposes. Local anaesthetic agents and neurolytic substances such as phenol, alcohol, or glycerol can be used, depending on the indication. Radiofrequency (heating) or cryotherapy (freezing) probes can be used to cause a lesion in a nerve after precise localization with X-ray and nerve stimulation. Drugs with differing mechanisms of action, such as depot steroids, clonidine and opioids can be added to local anaesthetic. Historically, nerve block procedures were the cornerstone of pain clinic practice: their role has changed as more techniques for medical management are available and as pain relief is seen as part of a strategy of rehabilitation.
Medicating Children
Shawna S. Brent in A Guide to Psychiatric Services in Schools, 2012
Children, particularly those under the age of 15 years, tend to require higher dosages of medication per body weight than an adult. The other way in which psychiatric care is appropriately ended is when there has been an ongoing period of symptom stability without medication changes. Stimulant and nonstimulant medications show a more rapid treatment response than other psychotropic medications. Throughout treatment and follow-up visits, compliance with medication has been assessed. The psychiatrist should ensure that the person has continued to take the medications as prescribed. Some examples of medications where an EKG should be considered include stimulants, clonidine, and tricyclic antidepressants. As with the traditional mood stabilizers, these medications frequently cause a dramatic increase in appetite, which can lead to weight gain and other metabolic problems. A final common reason that polypharmacy occurs is that a second medication may be needed to treat emergent side effects from an effective medication.
Other Regional and Local Analgesia
Pamela E. Macintyre, Stephan A. Schug in Acute Pain Management, 2021
The use of regional and local anesthetic techniques other than neuraxial blockade to provide postoperative and postinjury analgesia continues to gain in popularity. The technique provides extended regional analgesia with minimal systemic adverse effects, facilitating recovery and ongoing physiotherapy and rehabilitation. However, there are no clinical benefits from adding either clonidine or epinephrine to solutions used for CPNB; epinephrine may even carry an increased risk of reduced blood flow to nerves due to prolonged vasoconstriction. Newer pumps have the capability to deliver bolus doses on patient request or automatically at set dosing intervals. Standard orders for CPNB should cover monitoring and documentation, medication orders and responses required for inadequate analgesia or management of adverse effects. However, patient-controlled CPNB, using patient-controlled bolus doses with a continuous background infusion, consistently reduce total consumption of local anesthetic and often supplemental systemic analgesic requirements compared to continuous infusions.
An evidence for presynaptic excitatory alpha
Published in Archives Internationales de Physiologie et de Biochimie, 1988
Y. Sarioglu, M. Ilhan, S. O. Kayaalp
This study was undertaken to determine the effects of clonidine on sympathetic neurotransmission in frog myocardium. In the electrically driven ventricular strips of frog heart, clonidine was found to be ineffective on contractility. However, clonidine increased the positive inotropic responses to transient additional stimulations. This effect of clonidine was antagonized by yohimbine, an α2-adrenergic receptor antagonist. Clonidine did not change the positive inotropic effects of exogenously applied noradrenaline. These results suggest that clonidine facilitates sympathetic neurotransmission in frog myocardium via an action on α2-adrenergic receptors located on sympathetic nerve terminals.
Transdermal and Oral Clonidine
Published in Annals of Medicine, 1991
Mauno Lilja, Heikki Juustila, Seppo Sarna, Antti J. Jounela
The antihypertensive efficacy and side effects of transdermal clonidine (Catapres-TTS) and oral clonidine in equivalent doses on a weight basis were compared under double blind (double dummy) and cross over conditions in 16 outpatients with mild to moderate hypertension. After four weeks of placebo TTS and placebo tablet treatment, the patients were randomly placed into groups for six weeks of active treatment and, after an intervening week of placebo treatment, a second six week treatment period. Transdermal clonidine reduced supine and standing blood pressures (P < 0.01) and heart rates (P < 0.05) compared with the values at the end of the placebo periods, while oral clonidine did so to the extent of supine systolic blood pressure (P < 0.01) and standing heart rate (P < 0.05), respectively. There were, however, no differences in the values between transdermal and oral clonidine at the end of these six week periods. The plasma clonidine concentration was lower 12 hours after a dose of oral clonidine than after transdermal clonidine (P < 0.05). The side effects did not differ. Seven patients said afterwards that they preferred the transdermal treatment, two preferred the oral treatment and four could not state any preference. It is concluded that transdermal clonidine is similar in its effect to oral clonidine in mild to moderate hypertension. Transdermal clonidine once a week may increase patients' compliance with antihypertensive treatment.
Tachycardic and Hypertensive Effects of Centrally Administered Clonidine in Conscious Rats
Published in Clinical and Experimental Hypertension. Part A: Theory and Practice, 1986
Yutaka Imai, Peter L. Nolan, Colin I. Johnston
The centrally mediated cardiovascular changes induced by clonidine were studied in conscious rats. Clonidine administered intracerebroventricularly (i.c.v.), and intravenously (i.v.) caused hypotension following an initial pressor response. I.v. clonidine caused significant greater hypotension than i.c.v. clonidine (30 μg/kg; p < 0.05). With the 30 μg/kg i.c.v. dose, a tachycardia was observed in all rats following initial transient bradycardia. No tachycardia was observed when clonidine was administered i.v. Propranolol (3 mg/kg i.v.) did not modify the cardiovascular actions of i.c.v. clonidine except initial pressure response. While combined treatment with propranolol (3 mg/kg i.v.) and atropine (1 mg/kg i.v.) abolished both the bradycardic and tachycardic actions of i.c.v. clonidine (30 μg/kg), but did not modulate the hypotensive action. Yohimbine (30 μg/kg i.c.v.) converted the hypotension induced by i.c.v. clonidine (30 μg/kg) to hypertension, attenuated the bradycardia but did not modulate the tachycardia. The same dose of i.c.v. yohimbine attenuated the hypotensive effect of i.v. clonidine (30 μg/kg) but did not affect the initial pressor response. Prazosin (30 μg/kg i.c.v.) did not modulate either phase of the heart rate response to i.c.v. clonidine. These results provide evidence of centrally mediated pressor and tachycardic actions of clonidine in conscious rats. The tachycardia appears to be mediated through the inhibition of parasympathetic tone and is not dependent on α -adrenoceptor mechanism. In conscious rats the opposing influence of centrally mediated pressor and depressor actions may result in the apparently low hypotensive potency of i.c.v. clonidine.
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