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MRI in the early stages, often with edema extending many segments above and below the area of primary disease, and later became atrophic Up to 50 cells are typical in the CSF and the protein is elevated, but the spinal uid may be normal during periods of clinical stability Several of these cases have had positive IgG antibodies as tested in Weinshaker s laboratory (see above), further supporting the notion that these cases are allied with Devic disease but leaving ambiguous the relationship of both entities to MS Treatment The treatment of neuromyelitis optica and of subacute necrotic myelopathy has been largely unsuccessful, most cases progressing despite aggressive therapy, including high-dose corticosteroids, plasma exchange, intravenous immunoglobulin, azathioprine, and cyclophosphamide A study of several patients by Mandler and colleagues (1998) suggested that perhaps a combination of high-dose methylprednisolone and azathioprine led to clinical improvement; we cannot af rm this approach, but most other treatments have given poor results in our experience Because some individuals respond (albeit infrequently) to them, it is appropriate to try one or more of these therapies in these cases Diffuse Cerebral Sclerosis of Schilder (Schilder Disease, Encephalitis Periaxialis Diffusa) Exceptionally the cerebrum is the site of massive demyelination, occurring in multiple foci or as a single large focus Such cases are more frequent in childhood and adolescence than in adult life Despite the undoubted occurrence of such cases, to call them Schilder disease is to refer to a clinical entity of ambiguous standing The term diffuse sclerosis was probably rst used by Strumpell (1879) to describe the hard texture of the freshly removed brain of an alcoholic; later the term was applied to widespread cerebral gliosis of whatever cause In 1912, Schilder described an instance of what he considered to be diffuse sclerosis The case was that of a 14-year-old girl with progressive mental deterioration and signs of increased intracranial pressure, terminating fatally after 19 weeks Postmortem examination disclosed large, well-demarcated areas of demyelination in the white matter of both cerebral hemispheres as well as a number of smaller demyelinative foci, resembling the common lesions of MS Because of the similarities of the pathologic changes to those of MS (prominence of the in ammatory reaction and relative sparing of axons), Schilder called this disease encephalitis periaxialis diffusa, bringing it in line with encephalitis periaxialis scleroticans, a term that Marburg had used to describe a case of acute MS Unfortunately, in subsequent publications, Schilder applied the same term to two other conditions of different type One appears to have been a familial leukodystrophy (probably adrenoleukodystrophy) in a boy, and the other, quite unlike either of the rst two cases, was suggestive of an in ltrative lymphoma The last two reports seriously confused the subject, and for many years the terms Schilder disease and diffuse sclerosis were therefore indiscriminately attached to quite different conditions One group of diseases of the cerebral white matter, which can be readily culled from the overall category of diffuse sclerosis, is the leukodystrophies, including adrenoleukodystrophy of boys and young men, globoid-cell leukodystrophy of Krabbe, sudanophilic leukodystrophy, and metachromatic leukodystrophy all of which may involve peripheral nerves as well as the CNS tissue The leukodystrophies (discussed in detail in Chap 37) are characterized clinically by progressive visual failure, mental deterioration, and spastic paralysis and pathologically by massive and more or less symmetrical destruction of the white matter of the cerebral hemi-.

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spheres In each of them there is a speci c inherited biochemical defect in the metabolism of myelin proteolipids If one sets aside the hereditary metabolic leukodystrophies and other childhood disorders of cerebral white matter that were incorrectly included under the rubric of Schilder disease or diffuse sclerosis, there remains a characteristic group of cases that does indeed correspond to Schilder s original case description They are nonfamilial and are most frequently encountered in children or young adults As with the case reported by Ellison and Barron, the disease may follow the course of MS, either steady and unremitting or punctuated by a series of episodes of rapid worsening In rare instances the disease may become arrested for many years, or the patient may even improve for a time Dementia, homonymous hemianopia, cerebral blindness and deafness, varying degrees of hemiplegia and quadriplegia, and pseudobulbar palsy are the usual clinical ndings Optic neuritis may occur before or after the cerebral symptoms The CSF may show changes similar to those in chronic relapsing MS, but often there are no oligoclonal bands; instead, myelin basic protein is found in large quantity in the CSF Death occurs in most patients within a few months or years, but some survive for a decade or longer In the differential diagnosis, a diffuse cerebral neoplasm (gliomatosis or lymphoma), adrenoleukodystrophy, and progressive multifocal leukoencephalopathy (Chap 33) are the main considerations The characteristic lesion in these cases is a large, sharply outlined, asymmetrical focus of myelin destruction often involving an entire lobe or cerebral hemisphere, typically with extension across the corpus callosum and involvement of the opposite hemisphere (Fig 36-2) In some cases both hemispheres may be symmetrically involved A careful examination of the optic nerves, brainstem, and spinal cord often discloses the typical discrete lesions of MS Histologically, the large single focus as well as the smaller disseminated ones show the characteristic features of MS.

Figure 36-2 Diffuse cerebral sclerosis (Schilder disease) MRI showing large asymmetrical foci of involvement of white matter in a 12-year-old boy 2 1/2 months after onset of symptoms The clinical picture was one of rapidly worsening episodes of bilateral hemiplegia and hemianopia (Reproduced by permission from Bisese JH, Cranial MRI, New York, McGraw-Hill, 1991)

overwrite individual Web items or data providers When you integrate a Web item into your Web template from the Web item groupings in the Web Items screen area and define your settings, you might want to use this Web item again in this form in other Web templates, without having to define the settings over again The WAD enables you to use your own version of a Web item as the Web template for other items You store this Web item as a template You can then access your Web items from the Reusable Web Items tab Any changes that you make to the settings of the reusable Web item (as previously described) have a global effect, meaning the changes are effective in all saved Web templates in which you use that specific Web item This does not apply to Web templates in which you changed the parameters of a reusable Web item locally In this case, the settings that you make locally are effective If you want to change the settings in a reusable Web item locally (that is, in a specific Web template in which you are using this Web item), proceed as follows: 1 Open the Web template 2 Select the reusable Web item in the Web template 3 Change the parameters of this Web item on the Web Item Parameters tab in the Properties screen area 4 Save the Web template The changes that you made to the reusable Web item apply only in this second Web template The parameter settings of the reusable Web item are not affected by the changes

long strangles, 175 180 ratio, 147 155 for risk management, 276 risk reversals, 134 146 sell-buy-sell, 143 146 short straddles, 180 183, 185 189 short strangles, 183 189 strangles and straddles, 166 189 synthetic long or short, 134, 142 143 uses of, 114 vertical, 114 (See also Wingspreads) Stock settled index options, 223 Stops, 80 85 hard, 80, 85 implied volatility, 83 84 monetary, 80 81 price, 81 82 soft, 80 time, 82 trailing, 84 85 Straddles, 166 167 de ned, 167 key to success in, 172 long, 167 175, 177 180 short, 180 183, 185 189 Strangles, 166 167 de ned, 167