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In this example, you ll add a custom dialog box to the Set Up Finder and TextEdit script you created in 3. The dialog box tells the user what the script will do and lets the user choose between running the script and stopping it in its tracks. Follow these steps:
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Table 12-12. Streamlined process for solving the equation 18x + 7 = 2.
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siently to 15,000/mm3, a higher gure than in thrombosis. The sedimentation rate is mildly elevated in some patients. Course and Prognosis The immediate prognosis for large and medium-sized cerebral clots is grave; some 30 to 35 percent of patients die in 1 to 30 days. Either the hemorrhage extends into the ventricular system or intracranial pressure is elevated to levels that preclude normal perfusion of the brain. Sometimes the hemorrhage itself seeps into vital centers such as the hypothalamus or midbrain. A formula that predicts outcome of hemorrhage based on clot size has been devised by Broderick and coworkers; it is mainly applicable to putaminal and thalamic hemorrhages. They found a close correlation with outcome. A volume of 30 mL or less, calculated from the CT scan, predicted a generally favorable outcome; only 1 of their 71 patients with clots larger than 30 mL had regained independent function by 1 month. By contrast, in patients with clots of 60 mL or larger and an initial Glasgow Coma Scale score of 8 or less, the mortality was 90 percent (this scale is detailed on page 754). As remarked earlier, it is the location of the hematoma, not simply its size, that determines the clinical effects. A clot 60 mL in volume is almost uniformly fatal if situated in the basal ganglia but may be more benign if located in the frontal or occipital lobe. From the studies of Diringer and colleagues, it appears that hydrocephalus is also an important predictor of poor outcome, and this accords with our experience. In patients who survive i.e., in those with smaller hemorrhages there can be a surprising degree of restoration of function, since, in contrast to infarction, the hemorrhage has to some extent pushed brain tissue aside rather than destroyed it. Function may return very slowly, however, because extravasated blood takes time to be removed from the tissues. Also, since rebleeding from the same site is unlikely, the patient may live for many years. In some instances of medium-sized cerebral and cerebellar hemorrhages, papilledema appears after several days of increased intracranial pressure. This does not mean that the hemorrhage is increasing in size or swelling only that papilledema is slow to develop. Healed scars impinging on the cortex are liable to be epileptogenic; the frequency of seizures after each type of hemorrhage has not been established, but it is lower than for ischemic strokes. There is probably no need to administer anticonvulsive medication unless a seizure has occurred. The poor prognosis of all but the smallest pontine hemorrhages has already been mentioned. Cerebellar hemorrhages present special problems that are discussed below. Treatment The management of patients with large intracerebral hemorrhages and coma includes the maintenance of adequate ventilation, use of controlled hyperventilation to a PCO2 of 25 to 30 mmHg, monitoring of intracranial pressure in some cases and its control by the use of tissue-dehydrating agents such as mannitol (osmolality kept at 295 to 305 mosmol/L and Na at 145 to 150 meq), and limiting intravenous infusions to normal saline. Qureshi s group has offered data suggesting that aggressive measures to reduce intracranial pressure may be lifesaving and result in good outcome even in patients who have signs of transtentorial herniation. In our experience, this type of recovery is exceptional, but treatment may be justi ed in some patients whose medical condition allows it. As mentioned, virtually all patients with intracerebral hemorrhage are hypertensive immediately after the stroke because of a generalized sympathoadrenal response. The natural trend is for the
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Table 4-3.
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gests a maturational failure of certain modulating nervous in uences. An enuretic episode is most likely to occur 3 to 4 h after sleep onset and usually but not necessarily in stages 3 and 4 sleep. It is preceded by a burst of rhythmic delta waves associated with a general body movement. If the patient is awakened at this point, he does not report any dreams. Imipramine (10 to 75 mg at bedtime) has proved to be an effective agent in reducing the frequency of enuresis. A series of training exercises designed to increase the functional bladder capacity and sphincter tone may also be helpful. Sometimes all that is required is to proscribe uid intake for several hours prior to sleep and to awaken the patient and have him empty his bladder about 3 h after going to sleep. One interesting patient, an elderly physician with lifelong enuresis, reported that he had nally obtained relief (after all other measures had failed) by using a nasal spray of an analogue of antidiuretic hormone (desmopressin) at bedtime. This has now been adopted for the treatment of intractable cases. Diseases of the urinary tract, diabetes mellitus or diabetes insipidus, epilepsy, sleep apnea syndrome, sickle cell anemia, and spinal cord or cauda equina disease must be excluded as causes of symptomatic enuresis.
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