By P. Sanford. University of Massachusetts at Dartmouth. 2018.
While this This botulinum toxin treatment has now become an surgical procedure results in a permanent loss of power indispensable part of the modern management of cere- when performed on normal muscle discount 100 mg kamagra gold amex erectile dysfunction young age treatment, the power declines bral palsy proven kamagra gold 100mg strongest erectile dysfunction pills. It has also been suggested that, if employed at only temporarily after the aponeurotic technique and a very early age (2 or 3 years), pathological compensa- subsequently recovers completely. On the other hand, the lengthening of a The correct location of the needle in the desired contracted muscle can restore the optimal muscle length muscle must be checked before the drug is injected, either at which the muscle produces its maximum force, so that by a functional movement test (accompanying movement it again acts within the correct range of motion of the of the needle), or by checking the position by EMG or joint. No more than 50 U of Botox per injection explains the contradictory results reported after tendon site should be administered. To achieve muscle differs depending on the respective muscle, the a reduction in power the tendon must be lengthened age of the patient and the preparation. A prior test injection with botulinum toxin will signs of weakness can even occur at this level, we avoid help avoid any incorrect indications. The injection can be administered fering periods (from a few hours to months) by means of under local anesthesia, sedation or, if extensive, under a nerve blocks involving the instillation of local anesthetics, general anesthetic. If only the motor sec- We administer a general anesthetic for the injection tions of the nerves are infiltrated, this method is a good of very deep muscles (e. Only a joint and coordinated approach will treatment for spasticity resulting from traumatic lesions be able to give the patient the ideal rehabilitation. Braces The various braces available cover a wide range, from the Uncontrolled muscle activity simple shoe insert to the complex, individually adapted Patients with uncontrolled muscle activity lack a suffi- electric wheelchair. Most braces are discussed in connec- 4 ciently stable basis for standing and walking. Orthopaedic tion with other therapeutic methods in relation to indi- braces that guide the joints of the lower extremity while al- vidual body regions. The basic principles are outlined in lowing free movement in the sagittal plane can help such Chapter 4. Orthoses replace deficient muscle ac- The therapeutic options include the various »therapies« tivity, stabilize joints and preserve the balance in relation (physical therapy, occupational therapy, speech therapy to muscle lengths, which is more important than actual etc. Unfortunately, this form of muscle length- depending on their purpose: one for diagnosis and the ening is invariably associated with atrophy, and relapses as other for treatment. All patients must be investigated in- soon as the muscle power is restored are not infrequent. Nevertheless, such cast treatments are very helpful and This includes extensive testing of daily activities, record- useful and can be repeated. As with orthoses, it is im- ing the neurological development, sensory function and portant that the plastered section of the skeleton should coordination skills. As well as all the problems associated be corrected and held in the optimal position in order with the actual musculoskeletal system, any deficits in to achieve efficient stretching. Since structural changes neuromotor control must be diagnosed and treated. The can arise in the muscles after a cast treatment lasting various therapies (occupational therapy, physical therapy, 4–6 weeks, the cast should not be applied for more than speech therapy etc. Training is required both for global cast treatment after several months. The cast treatment is functions such as balance or coordination and cogni- more efficient if administered two weeks after an injection tive deficits, and for the functions of individual muscles, of botulinum toxin. The botulinum toxin also appears to sensory problems or joint contractures. Skeletal deformities can merely be checked or training, particularly in neurophysiology. Hippotherapy for the training of balance and body control is also included in this group. For the purposes of general practice, however, the specific neurophysiological Orthopaedic surgical measures basis is probably less important than an understanding of Before any operation, troublesome functional changes the problems of the patients in relation to their everyday must be differentiated from useful ones. This requires a flexible approach to their evaluation who are capable of walking, a gait analysis, ideally in and type of treatment. The basic aim of surgical The ideal treatment can probably be formulated as fol- treatment is to restore muscle lengths and, if possible, lows: Out of all the available therapeutic methods, those muscle strength, and lever arms. A muscle becomes steps that are required for the patient must be picked out, contracted when it cannot be stretched properly be- like raisins from a cake, and applied in a coordinated cause of spastic activity. Which therapist tackles which joint or problem muscles require regular stretching in order for them to 719 4 4. In recurrence occurs, the muscle belly will shorten even spastic muscles, however, stretching occurs to a much more.
Inhibition of traumatic immunosuppression buy 100 mg kamagra gold free shipping erectile dysfunction protocol video, nitrogen balance purchase kamagra gold 100mg fast delivery xyzal impotence, and cyclooxygenase attenuates the metabolic response to endo- acute-phase reactant proteins. Inhibition of neous activity in dorsal root ganglion cells) to spe- prostaglandin synthesis improves postoperative nitrogen bal- cific features of pain phenomenology could improve ance Clin Nutr. Topical flurbiprofen decreases burn wound induced hypermetabolism and sys- temic lipid peroxidation. Immunoprotective PHARMACOLOGIC MECHANISMS OF effects of cyclooxygenase inhibition in patients with major ANTINOCICEPTION surgical trauma. Effect of DESCENDING INHIBITION ibuprofen in patents with severe sepsis: A randomized dou- ble blind multicenter study. Indomethacin and the pressants is mediated primarily by the blockade of stress response to hysterectomy. Prophylactic diclofenac infu- enhances the activation of descending inhibitory neu- sions in major orthopedic surgery: Effects of analgesia and acute phase proteins. The effects of periop- Antidepressants, however, may produce antinocicep- erative ketorolac infusion on postoperative pain an endocrine tive effects through a variety of pharmacologic mech- metabolic response. Clark, MD, MPH MONOAMINE MODULATION INTRODUCTION Investigations have demonstrated differential effects of ANTIDEPRESSANTS AND PAIN monoamine receptor subtypes in antidepressant- induced antinociception in the rat formalin test. The Since the first report of imipramine use for trigeminal effects of antidepressants with varying degrees of nor- neuralgia was published in 1960, antidepressants, par- epinephrine and serotonin reuptake inhibition as well as ticularly tricyclic antidepressants (TCAs), have been those of their antagonists indicate that α1 adrenoceptors commonly prescribed for the treatment of many and several serotonin receptor subtypes (5-HT2, 5-HT3, chronic pain syndromes, especially those involving and 5-HT4) contribute to antinociception. OPIOID INTERACTIONS MONOAMINE RECEPTORS CLASSIFICATION SYSTEMS Because they interact with opioids or their antago- nists, antidepressants may interact with opioid recep- Neuropathic pain has been classified according to tors or stimulate endogenous opioid peptide release. In contrast, systemic kappa-3, and delta opioid receptor subtypes as well as and spinal administration of antidepressants produce by the α2 adrenergic receptor. CLINICAL APPLICATIONS SYNERGISTIC EFFECTS SEROTONIN AND NOREPINEPHRINE In the rat tail-flick model, the antinociception produced by individual intrathecal administration of serotonin, Antidepressants are typically characterized according desipramine, and morphine can be achieved with sub- to the specificity of their neurotransmitter reuptake threshold doses of combinations of these agents. For example, TCAs Fluoxetine (Prozac) 10–80 mg 5-HT NE reuptake may reduce hyperalgesia but not tactile allodynia inhibition because different neuronal mechanisms underlie dif- Sertraline (Zoloft) 50–200 mg ferent manifestations of neuropathic pain. Paroxetine (Paxil) 10–40 mg The blocking by caffeine of this effect induced with Fluvoxamine (Luvox) 100–300 mg Citalopram (Celexa) 20–40 mg amitriptyline indicates a role for endogenous adeno- sine systems. ATYPICAL ANTIDEPRESSANTS Venlafaxine (Effexor) 75–450 mg 5-HT NE DA reup- ION CHANNELS take inhibition 2+ + (dose dependent) The opening of voltage-gated and Ca -gated K Nefazodone (Serzone) 100–600 mg 5-HT NE reuptake channels has been implicated in the central antinoci- Trazodone (Desyrel) 100–600 mg inhibition with ception induced by amitriptyline and clomipramine in 5-HT2 receptor the mouse hot plate test. Intravenous amitriptyline blockade + Bupropion (Wellbutrin) 100–450 mg DA and NE reuptake impairs the function of tetrodotoxin-resistant Na inhibition channels in rat dorsal root ganglia, particularly in con- Mirtazapine (Remeron) 15–90 mg α2-NE and 5-HT2 ditions of repetitive firing and depolarizing mem- presynaptic agonist with 5-HT2/3 receptor brane potential, which may reduce firing frequency in blockade ectopic sites of damaged nociceptive fibers. The fact that 73% of treated patients were prescribed the equivalent of 50 mg or less of SELECTIVE SEROTONIN amitriptyline, however, suggests there is a potential REUPTAKE INHIBITORS for additional pain relief with higher doses. This antinociception is blocked by sero- guidelines have been established. TERTIARY VERSUS SECONDARY In human clinical trials, the efficacy of SSRIs in Generally, the tertiary TCAs with balanced effects on chronic pain syndromes has been variable and incon- 5-HT and NE reuptake (imipramine, amitriptyline, sistent:14 doxepin) are considered more effective analgesic Desipramine was superior to fluoxetine in the treat- agents than the secondary TCAs with more selective ment of painful diabetic peripheral neuropathy. NE reuptake inhibition (desipramine, nortriptyline, Paroxetine and citalopram were beneficial in maprotiline). A 12-week course of fluoxetine also decreased gastrointestinal motility and urinary reten- improved a variety of self-reported outcome meas- tion. The fact that desipramine and nortriptyline had ures in women with fibromyalgia. Nor- In a study of chronic tension-type headache, triptyline, the major metabolite of amitriptyline, amitriptyline significantly reduced the duration of causes less sedation, orthostatic hypotension, and headache, headache frequency, and the intake of falls than does imipramine and is as effective as analgesics, but citalopram, an SSRI, did not. Studies of mianserin, an older analog of mir- serotonin and norepinephrine and, to a lesser extent, tazapine, produced mixed results. Additional analyses suggested that response improved with higher doses of venlafaxine. FUTURE ANTIDEPRESSANTS Reboxetine is a selective noradrenaline reuptake NEWER ANTIDEPRESSANTS inhibitor not yet available in the United States. In a placebo-controlled study of laser-evoked somato- Norepinephrine and dopamine reuptake inhibitors, sensory potentials in healthy humans, reboxetine such as bupropion, produced antinociception in stud- reduced N1 and P2 amplitudes along with subjec- ies of thermal nociception. In a randomized, double- tive pain feelings and measurements, suggesting blind, placebo-controlled, crossover study of patients central and peripheral mechanisms of antinoci- with neuropathic pain but without depression, bupro- ception. In an open-label trial of diabetic neuropathy in as well as neuropathic pain are underway. No controlled trials have been per- and other pharmacologic agents used in the treatment formed on the efficacy of mirtazapine in the treatment of pain is difficult. TABLE 11–2 Numbers Needed to Treat for Antidepressants and Chronic Pain Conditions* DIABETIC POSTHERPETIC PERIPHERAL ALL ANTIDEPRESSANT NEUROPATHY NEURALGIA NERVE INJURY CENTRAL PAIN CONDITIONS All types 3.
The fifth edition of the American Medical Association Guides to the Evaluation of Permanent Impairment (AMA buy 100mg kamagra gold with amex erectile dysfunction pump infomercial, 2000) provides similar illustrations 100 mg kamagra gold visa impotence symptoms, pointing out that pain without an apparent underlying biological basis is common- place, as is asymptomatic pathophysiology. It noted that “For example, in up to 85% of individuals who report back pain, no pain-producing pathology can be identified; conversely, some 30% of asymptomatic people have sig- nificant pathology on magnetic resonance imaging (MRI) and computed tomographic (CT) scans that might be expected to cause pain” (p. The AMA Guides (AMA, 2000) provided an illustrative list of other well-established pain syndromes without significant, identifiable organ dysfunction capable of explaining the pain, including postherpetic neuralgia, tic douloureux, erythromelalgia, complex regional pain syndrome, type 1 (reflex sympathetic dystrophy), and any injury to the nervous system. It seems clear that practitioners whose focus is on identify- ing organic etiology and providing biologically oriented treatments will of- ten fail to have satisfactory assessment methods or interventions available for the vast majority of their patients. The risk of iatrogenic factors com- pounding initial problems was observed by Kouyanou, Pither, and Wessely (1997), who reported overinvestigation, and inappropriate information and advice given to patients. The same researchers also observed misdiagnosis, overtreatment, and inappropriate prescription of medication in a group of 125 chronic pain patients. Given the inadequacies of medical investigations focusing exclusively on the organic basis of pain, psychological methods 310 CRAIG AND HADJISTAVROPOULOS are increasingly employed in the assessment of the genuineness of pain complaints, although there are limitations (Rogers, 1997). Neuroscience Questions The neurosciences are working effectively and rapidly toward an under- standing of biological substrates of pain that would account for the dy- namic process whereby the individual’s life history of past experiences with pain combined with current thoughts and feelings continuously inter- act with sensory input to determine the complex experience of pain. Under- standing peripheral pathophysiological events is no longer sufficient be- cause past experiences and current brain activity are capable of modifying neural input. Pain experiences early in life have a potential for powerful structural and functional impact (Porter, Grunau, & Anand, 1999). Anand and Scalzo (2000) demonstrated that multiple exposures to unintended or culturally sanc- tioned pain may alter the biological systems that control pain. For example, these experiences could potentially dampen reactivity or produce hyper- sensitivity, among other possibilities. Grunau (2001) observed that re- peated pain early in life affects how children interact with others. For exam- ple, children who are born early with low birth weights, and who are exposed frequently to pain in neonatal intensive care nurseries, become predisposed to increased somatization in interactions with their mothers (Grunau, Whitfield, Petrie, & Fryer, 1994). In adults, an appreciation of the substantial central modulation and plasticity of the nervous system has al- lowed us to begin to understand the basic mechanisms whereby acute pain evolves into chronic pain (Coderre, Katz, Vaccarino, & Melzack, 1993). Through numerous mechanisms, the brain is capable of attenuating, magni- fying, and prolonging perception of noxious events. Phenomena of periph- eral and central sensitization, increased adrenergic sensitivity in injured nociceptive fibers, accumulation of ion channels at sites of nerve injury, and other factors appear capable of producing severe pain in response to trivial stimulation (allodynia) (Covington, 2000). Melzack and Katz’s chapter in this volume provides extensive discussion of related mechanisms. PSYCHOLOGICAL PERSPECTIVES: CONTROVERSIES 311 that challenge explanations of pain that require strong correlations be- tween peripheral pathology and subjective experiences of pain. Complementing an appreciation of the complexity are the current ad- vances in imaging brain activity during painful events (Casey & Bushnell, 2000; Price, 2000). The diverse qualities of painful experience are reflected in the distributed processing of pain in the brain, leading to rejection of the proposition that there should be a “pain center” and further appreciation of the heterogeneity of painful experiences, despite common features. Varia- tion in brain activation is reflected in studies demonstrating that psycholog- ical interventions, such as hypnoanalgesia, have a powerful impact on brain activity (Rainville, Carrier, Hofbauer, Duncan, & Bushnell, 1999). The re- search on central neuroplasticity and functional brain imaging is relatively uncontroversial, given the impeccable scientific controls that are intro- duced, and has created major changes in the thinking of theoreticians and practitioners. Although our understanding of the role of the central nervous system during pain is rapidly developing, major questions remain concerning how neural activity relates to the experience of pain. This is “the big question” in philosophy and consciousness research: How do conscious experiences arise from biological activity? The role of consciousness has been particularly contentious in the study of pain in infants, as it has been proposed that newborns and infants roughly throughout the first year of life could not ex- perience pain because they do not have a capacity to understand the na- ture of the experience (Derbyshire, 1996, 1999; Leventhal & Sherer, 1987). Anand and Craig’s (1996) appeal for improved sensitivity and management of infant pain was met by a characterization of this position as “dangerous,” because it promoted the use of potent analgesics early in life (Derbyshire, 1996). Similar unfortunate beliefs and positions seem pervasive among health care practitioners and the public. An example of these attitudes is found in a recently published and widely available book written by a neuro- surgeon (Vertosick, 2000), Why We Hurt: The Natural History of Pain.
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