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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. upc czech internet Zkušenosti z UPC internet | DSL.cz
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Internet pre častých surferov. Sťahujte, odosielajte, streamujte hudbu & videá v mihnutí oka a extrémnou rýchlosťou. Vybere si rýchlosť vhodnú pre svoje potreby ... . potension induces cerebral vasodilation in order to maintain normal blood ow Upon recovery of the blood pressure, the response in cerebrovascular tone is delayed, thereby allowing intracranial blood volume to accumulate in the dilated vascular bed and raising ICP In support of this explanation is the observation that a brief period of induced elevation of blood pressure paradoxically restores the normal cerebrovascular tone and leads to an abrupt cessation of a plateau wave It has been demonstrated that the high mortality and morbidity of acute cerebral mass lesions is in large part related to uncontrolled elevation in ICP In a normal adult reclining with the head and trunk elevated to 45 degrees, the ICP is in the range of 2 to 5 mmHg Levels up to 15 mmHg are not in themselves hazardous; in fact, adequate cerebral perfusion can be maintained at an ICP of 40 mmHg provided blood pressure (BP) remains normal A higher ICP or a lower BP may combine to reduce cerebral perfusion pressure and cause diffuse ischemic damage, as discussed further on Causes of Raised ICP In clinical practice, one of several general mechanisms causing elevated ICP can be identi ed: 1 A cerebral or extracerebral mass such as brain tumor; massive infarction with edema; extensive traumatic contusion; parenchymal, subdural, or extradural hematoma; or abscess, all of which tend to be localized and deform the adjacent brain The brain deformation is greatest locally, being compartmentalized to a varying degree by dural partitions as already noted Generalized brain swelling, as occurs in ischemic-anoxic states, acute hepatic failure, hypertensive encephalopathy, hypercarbia, and the Reye hepatocerebral syndrome Here the increase in pressure reduces the cerebral perfusion pressure, but tissue shifts are minimal because the mass effect is widely distributed throughout the cranial contents An increase in venous pressure due to cerebral venous sinus thrombosis, heart failure, or obstruction of the superior mediastinal or jugular veins Obstruction to the ow and absorption of CSF If the obstruction is within the ventricles or in the subarachnoid space at the base of the brain, hydrocephalus results Extensive meningeal disease from any number of causes (infectious, carcinomatous, granulomatous, hemorrhagic) is another mechanism If the block is con ned to the absorptive sites adjacent to the cerebral convexities and superior sagittal sinus, the ventricles remain normal in size or enlarge only slightly, because the pressure over the convexities approximates the pressure within the lateral ventricles (see further on) Any process that expands the volume of CSF (meningitis, subarachnoid hemorrhage) or, less commonly, increases CSF production (choroid plexus tumor). FIGURE 8-2 . upc internet praha Compare Internet - UPC
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