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In both myotonia congenita and hyperkalemic paralysis, the absence of major morphologic changes and the prominence of the myotonic phenomenon in individual muscle bers point to the existence of a physiologic aberration in the sarcolemma or some other part of the electrical conducting apparatus of the muscle bers This is consistent with the observation that myotonia persists after the administration of curare, thereby exonerating neural input as the source of myo ber hyperexcitability The electromyographic pattern of a myotonic muscle reveals highly characteristic discharges that persist following the cessation of voluntary contraction The tension of the myotonic muscle bers is slow to diminish as a result of these greatly prolonged trains of muscle action potentials (see Fig 45-8) Some of these afterdischarge potentials are the size of brillations but others are as large as normal motor units Thus myotonia can be distinguished electrophysiologically from contracture (eg, that encountered in McArdle disease, in which the muscle is electrically silent) In classic experiments conducted in the 1940s, Denny-Brown and Foley, stimulating single muscle bers directly, found that myotonic discharges could be elicited only by a volley of stimuli and not by a single stimulus They also noted that the series of myotonic potentials progressively diminished in size Percussion elicits myotonia by imparting a brief but relatively intense repetitive excitation of the muscle membrane The biophysical basis of myotonia is now well understood in terms of the functioning of chloride and sodium channels The correspondence between mathematical models of the electrical properties of the muscle membrane and the clinical features of the myotonic and periodic paralyses is quite remarkable During the normal action potential in all neural and muscular tissue, membrane depolarization is terminated by two events: the depolarizationinduced inactivation of the sodium channel (which ends the inward sodium current) and the subsequent action of the outward potassium current In muscle, the termination of an action potential requires an additional factor Because of its large size, excitation of the muscle ber involves depolarization that propagates not only along the cell surface but also radially into the center of the muscle cell through the transverse tubules (T tubules) The tubules are very narrow structures whose internal spaces are in continuity with the extracellular space When the repolarizing outward potassium current is activated, potassium ions ood into the tubules from the muscle cytoplasm By itself, this tubular K accumulation would depolarize the muscle membrane and prolong excitation Normally, this does not occur because there is a large opposing chloride conductance in the tubules that counteracts the in uence of potassium accumulation The rst clues to the importance of the chloride channel in this electrical stabilizing process were obtained by Bryant who performed in vitro studies of myotonic goat muscle and found a reduced chloride conductance in the transverse tubular system Subsequent studies of muscle from patients with myotonia congenita by Lipicky and Bryant demonstrated a similarly low chloride conductance That a mutation in a muscle chloride channel could pro-.

duce myotonia was con rmed in a mouse model by Jentsch and Steinmeyer and colleagues (see Koch et al), who subsequently also described the rst human chloride channel (CLCN1) mutations As indicated, an essential event for normal repolarization of an excitable membrane is the rapid inactivation of the inward sodium current This process of rapid, complete sodium channel inactivation is impaired by the sodium channel mutations implicated in hyperkalemic periodic paralysis The sodium channel mutations cause imperfect inactivation of the channel and lead to aberrant and early reopenings Repolarization is then incomplete, rendering the muscle cell more readily re-excited; it is this hyperexcitability that causes the myotonia of hyperkalemic periodic paralysis The physiologic problem becomes self-reinforcing because, as the membrane fails to repolarize fully, its electrolytic inactivation becomes increasingly less effective If this process is not aborted, the result is such excessive depolarization to a degree that the muscle cell ultimately becomes unexcitable a state that corresponds to the paralytic phase of hyperkalemic periodic paralysis These features are evident in hyperkalemic muscle in vitro (Cannon) and can be recapitulated in computer simulations Presumably, over several hours, a variety of compensatory mechanisms [eg, activation of Na-K adenosine triphosphatase (ATPase) pumps] restores the baseline excitability of the muscle membrane

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reports based on the data from the Management Repository, and does not get real-time data from the Exadata Storage Servers Some of the built-in reports available in Enterprise Manager are performance reports of Exadata Storage Server components such as cell disks, grid disks, and I/O Resource Manager, as well as configuration reports of the Exadata Storage Server and the cell disks Figure 5-11 shows a sample report

When a computer is started, the BIOS performs a POST (power-on self-test) to check for the presence and status of existing components Errors found during the POST are typically indicated by a visual error message on the screen or by a series of beeps These visual and audio error codes can differ from BIOS to BIOS, so it s best to consult the manufacturer s documentation for the meaning of each code However, some BIOS error codes are considered common because they are used in most machines For example, most error codes in the 1** series, such as 120 or 162, indicate a problem with the system board or processor It is rare to see a 1** error code, since most system board and processor errors are serious enough to prevent the computer from issuing the error code at all Memory errors detected by the POST are typically indicated by a 2** error, and keyboard errors are indicated by a 3** error Fortunately, most visual error codes are also accompanied by a brief description of the problem Again, consult the documentation for your specific BIOS, because these messages can often be cryptic (for example, 213: DMA arbitration time-out ) Some BIOSes use a series of beeps rather than a visual message when there is a POST error Typically, one beep indicates that all components passed the POST This doesn t mean that there are no problems in the computer; it simply means that none of the components has a problem that was detected by the BIOS When the BIOS issues an audio error code, carefully count the beeps and note whether they are long or short Again, consult the BIOS documentation for the proper meaning of each code, because these differ from system to system For example, one BIOS might indicate a video problem by issuing eight short beeps, while another might use one short and two long beeps The manufacturer s website is a terrific place to get specific information on the diagnostics and BIOS messages that a motherboard uses While there is a high level of standardization in codes, it is not unusual for manufacturers to implement codes of their own.

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