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the illness is not much longer than 3 weeks in duration Performing plasma exchanges after the use of IVIG does not make sense to us (but this notion has not been tested); therefore, we either follow exchanges with IVIG or, more often, repeat a course of IVIG as suggested by Farcas and colleagues The value of corticosteroids alone in the treatment of GBS has been disputed for decades Many clinicians were persuaded of their bene t However, two randomized controlled studies, one with conventional-dose prednisolone and the other with high-dose methylprednisolone, have failed to demonstrate any bene cial effect (Hughes et al) Although corticosteroids can no longer be recommended as routine treatment for acute GBS, we have observed a few instances in which the administration of intravenous high-dose corticosteroids seemingly halted the progress of the acute disease Prognosis As already indicated, approximately 3 to 5 percent of patients do not survive the illness, even in the best-equipped hospitals In the early stages, death is most often due to cardiac arrest, perhaps related to dysautonomia, adult respiratory distress syndrome, pneumo- or hemothorax, or some type of accidental machine failure Later in the illness, pulmonary embolism and other medical complications (usually bacterial) of prolonged immobilization and respiratory failure are the main causes The majority of patients recover nearly completely (with mild motor de cits or sensory complaints in the feet or legs) In about 10 percent, however, the residual disability is pronounced; this occurs in those with the most severe and rapidly evolving form of the disease, when there has been evidence of widespread axonal damage (see later), and in those requiring early and prolonged mechanical ventilatory assistance A consistent predictor of residual weakness is the EMG nding of severely reduced amplitudes of muscle action potentials and widespread denervation, both indicative of axonal damage In patients with respiratory failure, the average period of machine-assisted respiration has been 22 days and the period of hospitalization approximately 50 days (these were twice as long prior to the introduction of PE and IVIG) As a rule, older adults recover more slowly than younger ones and children and have more residual weakness The most common residual dif culties are weakness of the lower leg muscles, numbness of the feet and toes, and mild bifacial weakness A few patients are left with a sensory ataxia; when this occurs, it tends to be severe and quite disabling Distal neuropathic pain and persistent autonomic problems occur but are infrequent All manner of other late symptoms are attributed with little evidence to the illness and should be addressed on their own merits fatigue and asthenia, muscle cramps, dizziness, pain, and breathlessness Depression has not been frequent The speed of recovery varies but its pace is steady Often it occurs within a few weeks or months; however, if axons have degenerated, their regeneration may require 6 to 18 months or longer In our experience, little improvement can be expected in disabilities that have lasted 3 or more years Some 5 to 10 percent of patients suffer one or more recurrences of the acute polyneuropathy as mentioned An illness that in the beginning appeared to be an acute in ammatory polyradiculoneuropathy may fail to stabilize and continue to progress steadily, or there may be an incomplete remission followed by a chronic, uctuating, slowly progressive neuropathy These chronic forms of in ammatory neuropathy are described in a later section of this chapter.

.

( r5 2 1 )

AdRotator tag and the C# event handler Change the name of the event handler to Sandlight_AdCreated in both the ASPNET and C# portions of the application While you re at it, remove the Page_Load function from the C# portion of the application The following listings provide the code for both the ASPNET and C# portions of the application:

In the recumbent position, ICP and consequently CSF pressure measured by lumbar puncture is normally about 8 mmHg or 110 mmH2O (1 mmHg equals 137 mmH2O) As the head and trunk are progressively elevated, the weight of the column of CSF is added incrementally to the pressure in the lumbar subarachnoid space, and the ICP drops correspondingly, so that it is close to zero in the standing position As described above, the CSF pressure is in equilibrium with the capillary or prevenous vascular pressure, which is in uenced mainly by circulatory changes that alter arteriolar tone Rises in systemic arterial pressure cause little or no increase of pressure at the capillary level (because of autoregulation) and hence little increase in CSF pressure The inhalation or retention of CO2 raises the blood PCO2 and correspondingly decreases the pH of the CSF By a mechanism that is not fully understood, this acidi cation of the CSF acts as a potent cerebral vasodilator, causing an increase in cerebral blood ow and leading to intracranial hypertension Hyperventilation, which reduces PCO2, has the opposite effect ie, it increases the pH and the cerebral vascular resistance and thereby decreases CSF pressure; this maneuver of lowering the arterial CO2 content by hyperventilation is utilized in the treatment of acutely raised ICP In contrast to the limited effect caused by changes in arterial blood pressure, increased venous pressure exerts an almost immediate effect on CSF pressure by increasing the volume of blood in the cerebral veins, venules, and dural sinuses If jugular veins are compressed, there is a rise of intracranial pressure that is transmitted to the lumbar subarachnoid space (unless there is a spinal subarachnoid block) This is the basis of the Queckenstedt test, mentioned in Chap 2 In the case of a spinal block, pressure on the abdominal wall, which affects the spinal veins below the point of subarachnoid block, will still increase the lumbar CSF pressure The Valsalva maneuver as well as coughing, sneezing, and straining also causes an increased intrathoracic pressure, which is transmitted to the jugular and then to the cerebral and spinal veins The ICP rises in heart failure, when central and jugular venous pressures become elevated Mediastinal tumors, by obstructing the superior vena cava, have the same effect These increases are manifest despite the presence of valves in the jugular veins When the heart stops, the CSF pressure falls to zero.

<%@ Page Language="C#" AutoEventWireup="true" CodeFile="AdRotateaspxcs" Inherits="RollAd" %> <!DOCTYPE html PUBLIC "-//W3C//DTD XHTML 10 Transitional//EN" "http://wwww3org/TR/xhtml1/DTD/xhtml1-transitionaldtd"> <html xmlns="http://wwww3org/1999/xhtml"> <head runat="server"> <title>ADRotator At Work</title> </head>

N o t i c e l r o w t h e f l r s t t e r n r i s e q u a l t o / ( r 1 ) aa n d i s e q u a l t o z e r o a t r 2 a n d r - l T h e o t h e r t11 terms work in a similar fashion Both the first- and second-order versionsas well as higher-order Lagrangepolynomials can be represented conciselyas

.

(continued )

(1s22)