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surable decrease in the uptake of amino acids and protein synthesis by muscle cells Acute Steroid Myopathy (Critical Illness Myopathy; Acute Quadriplegic Myopathy) In addition to the well-known proximal myopathy induced by the long-term use of steroids, an acute and severe myopathy has been recognized in critically ill patients It was described initially in patients with severe asthma who were exposed to high doses of steroids Subsequently this acute myopathy has been recognized with numerous critical systemic diseases and organ failures, again, in the context of treatment with high doses of corticosteroids and, in a few cases, with sepsis and shock alone The use of neuromuscular blocking agents appears to play an important complementary role in the genesis of the myopathy, being a factor in over 80 percent of reported cases, but it is uncertain whether these agents alone can produce a similar process (see reviews by Gorson and Ropper, Lacomis et al, and Barohn et al) Patients who acquire this problem have generally been exposed to high doses of corticosteroids, sometimes for only brief periods Exceptional instances have been reported in which the myopathy was induced by doses as low as 60 mg prednisone administered for 5 days, but we have not encountered such a case The degree and type of simultaneous exposure to neuromuscular blocking agents has varied, but the doses have generally been quite high, falling in the range of a total dose of 500 to 4000 mg of pancuronium or its equivalent over several days The severe muscle weakness usually becomes evident when the systemic illness subsides, as attempts are made to wean the patient from the ventilator The tendon re exes are normal or diminished and there may be confounding features of a polyneuropathy, which is also known to be induced by critical illness and sepsis (page 1128) Most of our patients with acute myopathy have recovered over a period of many weeks after the corticosteroid agent has been withdrawn, but a few have remained weak for as long as a year Serum CK is elevated, at least early in the process The EMG discloses the characteristic features of a myopathy; often there are brillations as well, theorized to be due to separation of the motor end-plate region from intact segments of muscle bers Polyneuropathy and residual effects of neuromuscular blockade can be excluded by appropriate electrophysiologic studies Muscle biopsy shows varying degrees of necrosis and vacuolation affecting mainly type 2 bers The most characteristic feature is a striking loss of thick (myosin) laments Severe degrees of muscle necrosis have been accompanied by massively elevated CK levels and by myoglobinuria and renal failure Several experimental observations may explain the apparent additive effect on muscle of corticosteroids and neuromuscular blocking agents Animals exposed to high doses of steroids soon after muscle denervation display a selective loss of myosin, the characteristic nding of acute steroid myopathy This depletion of myosin is reversed by reinnervation but not by withdrawal of the corticosteroids Furthermore, denervation of muscle has been found to induce an increase in glucocorticoid receptors on the surface of the muscle Dubois and Almon have postulated that exposure to neuromuscular blocking agents creates a functional denervation, rendering the muscle ber vulnerable to the damaging effects of steroids It is curious that this myopathy has not been seen after high-dose corticosteroid administration for neurologic diseases such as multiple sclerosis, but the observation of Panegyres and colleagues of a patient with myasthenia who developed a severe,.

688 Final exam D Runs parallel to lines of latitude E Is circular in shape 51 One of the main shortcomings of MOSFETs is that they: A Are easily damaged by static electricity B Require high voltages C Consume large amounts of current D Have very low gain E Do not have good sensitivity 52 Resistivity of wire can be specified in: A Volts per ohm B Ohms per volt C Ohms per meter D Amperes per ohm E Ohms per ampere 53 A complementary-metal-oxide-semiconductor (CMOS) IC: A Employs diodes and NPN transistors on a single chip B Employs N-channel and P-channel FETs on a single chip C Uses two chips connected together in a special way D Uses resistors and PNP transistors on a single chip E Consists of metal oxide sandwiched between two layers of P-type material 54 A piano sounds different than a saxophone, even if the notes are at the same frequency, because of a difference in: A Bias B Waveform C Voltage D Current E The way you imagine it 55 Inductances in parallel, assuming there is no mutual inductance, add up like: A Resistances in series B Resistances in parallel C Capacitances in parallel D Batteries in parallel E No other type of electrical component 56 A reactance modulator produces: A CW B AM

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SCHWARTZMAN RJ, MCLELLAN TL: Re ex sympathetic dystrophy: A review Arch Neurol 44:555, 1987 SILVERMAN DH, MUNAKATA JA, ENNES H, et al: Regional cerebral activity in normal and pathological perception of visceral pain Gastroenterology 112:64, 1997 SINCLAIR D: Mechanisms of Cutaneous Sensation Oxford, England, Oxford University Press, 1981 SNYDER SH: Opiate receptors in the brain N Engl J Med 296:266, 1977 TAUB A, CAMPBELL JN: Percutaneous local electrical analgesia: Peripheral mechanisms, in Advances in Neurology Vol 4: Pain New York, Raven Press, 1974, pp 727 732 TROTTER W, DAVIES HM: Experimental studies in the innervation of the skin J Physiol 38:134, 1909 US DEPARTMENT OF HEALTH AND HUMAN SERVICES: Management of Cancer Pain: Clinical Practice Guideline Number 9 AHCPR Publications No 94-0592 and 94-0593 March 1994 VON FREY M: Untersuchungen uber die Sinnesfunctionen der men schlichen Haut: I Druckemp ndung und Schmerz Konigl Sachs Ges Wiss Math Phys Kl 23:175, 1896

WALL PD, MELZACK R (eds): Textbook of Pain, 4th ed New York, Churchill Livingstone, 1999 WALSHE FMR: The anatomy and physiology of cutaneous sensibility A critical review Brain 65:48, 1942 WEDDELL G: The anatomy of cutaneous sensibility Br Med Bull 3:167, 1945 WELLS KB, STEWART A, HAYS RD, et al: The functioning and well-being of depressed patients JAMA 262:914, 1989 WHITE D, HELME RD: Release of substance P from peripheral nerve terminals following electrical stimulation of sciatic nerve Brain Res 336: 27, 1985 WOOLF CJ: Pain: Moving from symptom control toward mechanism-speci c pharmacologic management Ann Intern Med 140:441, 2004 WOOLF CJ, MANNION RJ: Neuropathic pain: Aetiology, symptoms, mechanisms, and management Lancet 353:1959, 1999 YAKSH TL, HAMMOND DL: Peripheral and central substrates involved in the rostrad transmission of nociceptive information Pain 13:1, 1982

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