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measured by intracellular recordings are initially normal despite the failure of impulse propagation by the sarcolemma One would expect the muscle ber to be hyperpolarized as K moves into it, but it actually becomes depolarized Rudel and associates attribute the latter change to an increased Na conductance The ECG changes also begin at levels of K that are slightly below normal (about 3 meq/L); they consist of prolonged PR, QRS, and QT intervals and attening of T waves Diagnosis at a time when the patient is normal may be facilitated by provocative tests With the patient carefully monitored, including the use of an ECG, the oral administration of 50 to 100 g of glucose or loading with 2 g of NaCl every hour for seven doses, followed by vigorous exercise, brings on an attack, which then can be terminated by 2 to 4 g of oral KCl (the opposite of what pertains in hyperkalemic periodic paralysis) Pathologic Changes The nervous system is entirely normal The muscle bers are uniformly somewhat large, but the most striking change, particularly in the late degenerative phases of the disease, is vacuolization of the sarcoplasm The myo brils are separated by round or oval vacuoles containing clear uid, presumably water, and a few PAS-positive granules There are pathologic changes in myo brils and mitochondria as well and focal increases in muscle glycogen Isolated muscle bers may undergo segmental degeneration Electron microscopic studies have shown that the vacuoles arise as a result of proliferation and degeneration of membranous organelles within the sarcoplasmic reticulum and transverse tubules (A G Engel) Treatment A low-sodium diet (160 meq/day), avoidance of large meals and exposure to cold, and acetazolamide 250 mg three times daily may be helpful in preventing attacks That acetazolamide reduces attacks is somewhat surprising since it is kaluretic, but it may work through the production of acidosis; a few patients have worsened with the drug Patients who are unresponsive to acetazolamide may be treated with the more potent carbonic anhydrase inhibitor, dichlorphenamide, 50 to 150 mg per day or with the potassium-sparing diuretics spironolactone or triamterine (both in doses of 25 to 100 mg/day) but caution must then be exercised with the simultaneous administration of oral potassium supplements The daily administration of 5 to 10 g of KCl orally in an unsweetened aqueous solution prevents attacks in many patients, and apparently this program can be maintained inde nitely If this approach fails, a low-carbohydrate, low-salt, high-K diet combined with a slow-release K preparation may be effective For an acute attack, 025 meq KCl/kg should be given orally or, if this is not tolerated, some other K salt may be tried This dose may be insuf cient, and if there is no improvement in 1 or 2 h, KCl may have to be given intravenously 005 to 01 meq/kg intravenously initially in a bolus at a safe rate, followed by 20 to 40 meq KCl in 5% mannitol, avoiding glucose or NaCl as the carrier solution For the late progressive polymyopathy that follows many severe attacks of periodic paralysis, Dalakas and Engel report successful restoration of strength by the long-term administration of the carbonic anhydrase inhibitor dichlorphenamide Regular exercise (not too strenuous) to keep the patient t is desirable.

Sensory Nerves Fibers that mediate super cial sensation are located in cutaneous sensory or mixed sensorimotor nerves In cutaneous nerves, unmyelinated pain and autonomic bers exceed myelinated bers by a ratio of 3 or 4 : l In contrast, proprioceptive bers are located in deeper, predominantly motor nerves The myelinated bers are of two types, small, lightly myelinated, A- bers for pain and cold, as discussed in Chap 8, and larger, fasterconducting A- bers for touch and pressure The nonmyelinated autonomic bers are efferent (postganglionic) and innervate piloerector muscles, sweat glands, and blood vessels In addition, these nerves contain afferent and efferent spindle and Golgi tendon organ bers and thinner pain afferents The differing conduction velocities of these bers are discussed in Chap 45 A single cutaneous (touch, pain, and temperature) axon con-

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In most cases, processor and memory problems are fatal, meaning that when there is such a problem, the computer will not boot at all However, you should be aware of some nonfatal error indicators As described, 1** error codes are typical of processor problems, and 2** error codes are typical of memory problems If you turn on the computer and it does not even complete the POST or it does nothing at all, and you have eliminated power problems, there might be a problem with the processor or memory The solution to a processor or memory problem is to remove the offending component and replace it with a new one If the error persists, there might be a problem with the slot or socket that the memory or processor uses to connect to the motherboard In this case, the motherboard needs to be replaced On a final note: Some RAM errors are not reported by the computer at all That is, if an entire memory module does not work, the computer might just ignore it and continue to function normally without it Watch as the RAM is counted on the screen at startup to ensure that the total amount matches the capacity installed in the machine If this amount comes up significantly short, you probably have to replace the memory module Memory failures may not cause a system to appear to malfunction at all Most modern systems will simply ignore a memory card that has malfunctioned and normal operations will continue The user may note performance loss, which is a key symptom of a memory card failure

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