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tality rate (due mainly to heart disease) had risen to 21 percent and the incidence of stroke to 13 percent (compared to expected gures of 15 and 3 percent, respectively, in an age-matched population) Of the patients who were alive at the end of the observation period, 43 percent had had no further attacks of amaurosis fugax following the initial episode Noteworthy also was the nding that among patients with normal carotid arteriograms, only 1 of 35 had had a stroke during the follow-up period, whereas stroke had occurred in 8 of 21 patients in whom the internal carotid artery was occluded or stenotic These gures are in keeping with those of Ackerman; in his series of 139 patients with amaurosis fugax and normal lumens of the common and internal carotid arteries, only 3 had a subsequent hemispheric stroke (personal communication) As pointed out by Benavente and colleagues, the risk of stroke over the 3 years following an attack is as low as 2 percent if there are no other issues such as diabetes, but it may be as high as 24 percent in older patients with risk factors for atherosclerosis The age of the patient with amaurosis fugax is of particular signi cance In the series of Poole and Ross Russell, the youngest patient to have a stroke after amaurosis fugax was 57 years old Tippin and coworkers reviewed the records of 83 patients with onset of amaurosis fugax before the age of 45 years and found evidence of stroke in none; moreover, 42 of these patients were examined after a mean period of 58 years during which no stroke had occurred It is evident that in this early-onset, good-prognosis group, a mechanism other than atherosclerosis was operative, such as migraine or an antiphospholipid antibody (discussed further on) Brainstem Transient Ischemic Attacks (Vertebrobasilar Circulation) Recurrent TIAs referable to vertebrobasilar disease tend to be less stereotyped and more prolonged than those related to the carotid circulation They are also more likely to culminate in a stroke The clinical picture of TIAs in the vertebrobasilar territory is diverse, since this circulation sustains such a varied sensorimotor traf c Vertigo, diplopia (vertical or horizontal), dysarthria, bifacial numbness, ataxia, and weakness or numbness of part or all of one or both sides of the body (ie, a disturbance of the long motor or sensory tracts bilaterally) are the hallmarks of vertebrobasilar involvement Transient vertigo, diplopia, or headache occurring as solitary symptoms should not be interpreted as a TIA Also, in some patients, the complaint of dizziness will prove, however infrequently, to be part of a carotid TIA; hence this symptom, in our experience and that of Ueda et al, is not a totally reliable indicator of the vascular territory involved Other manifestations of vertebrobasilar TIAs, in their approximate order of frequency, include staggering, veering to one side, a feeling of cross-eyedness, dark vision, blurred vision, tunnel vision, partial or complete blindness, pupillary change, ptosis, paralysis of gaze, dysarthria, and dysphagia Less common symptoms include hemiplegia, noise or pounding in the ear or in the head, pain in the head or face or other peculiar head sensations, vomiting, hiccups, sense of tilting, lapse of memory, confused behavior, drowsiness, transient unconsciousness (rare), impaired hearing, deafness, hemiballismus, hallucinosis, and forced deviation of the eyes So-called drop attacks (page 329), according to Ross Russell, have been recorded in 10 to 15 percent of patients with vertebrobasilar insuf ciency, but we have never observed such attacks as a recurrent ischemic phenomenon or a manifestation of other forms of cerebrovascular disease Vertebrobasilar TIAs may be identical from one episode to another, or they may vary in detail while maintaining the same basic pattern, the latter occurrence being more typical For exam-.

Figure 44-5 MRI of necrotic myelopathy in a patient without optic neuritis Atrophy of the cord was evident several months later

not clear The electromyogram (EMG) after several weeks reveals denervation of several contiguous myotomes, re ecting damage to the gray matter of those segments The nding by Lennon and colleagues of a speci c serum IgG antibody in half of cases of Devic disease is notable The antibody is directed against capillaries of the brainstem and cerebellum, but its role in the pathogenesis of the disease has not been established As mentioned, the characteristic feature in most of our cases of necrotic myelopathy that are not af liated with optic neuritis, has been a subacute and relapsing course, usually with stepwise worsening and occasionally punctuated by brief and limited remissions The neurologic de cits of necrotic myelopathy unlike those of the demyelinative and postinfectious myelitides described earlier tend to be profound and lasting; in a few cases, they have reached a stage of accid tetraplegia within several weeks or months In several cases coming to postmortem examination at variable times after the onset of symptoms, the lesion has proved to be a necrotizing myelitis with widespread loss of spinal cord tissue The pattern of tissue destruction appears at least in part infarctive, ie, not respecting the borders of gray and white matter However,

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We are interested in the BI Patterns with Pattern Wizard option, commonly known as the Information Consumer Pattern Using this wizard is the approach within the WAD that will help speed up your implementation of the WAD component and offer a business user the option to work within the WAD without requiring them to have a significant amount of training; to configure something, they would only have to get comfortable using the BI Pattern Wizard This wizard is very similar to any wizard that you come across in SAP environments It s a step-by-step process that you can use to build some basic customization into the Web templates without having to work through all the settings In this section we will look at some examples of using this wizard to demonstrate in what situations we can use this tool to our advantage