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1 Open a new Web Site with the name TableRepeater 2 Open the ASPNET portion of the application, and open the Data menu in the Toolbox 3 Drag a Repeater web control to the editor in the <div> container 4 Begin to type <H and IntelliSense provides you with the <HeaderTemplate>

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Bhatia and Marsden, relying on published imaging studies, some quite crude, reviewed some 240 cases in which there were lesions in the caudate, putamen, and globus pallidus associated with movement and behavioral abnormalities Dystonia had occurred in 36 percent, chorea in 8 percent, parkinsonism in only 6 percent, and dystonia-parkinsonism in 3 percent Bilateral lesions of the lenticular nuclei resulted in parkinsonism in 19 percent and dystonia-parkinsonism in 6 percent It is also notable that a common persisting behavioral abnormality was abulia (apathy and loss of initiative, spontaneous thought, and emotional responsivity), occurring in 28 percent of those with caudate lesions The de ciencies of this type of case analysis, conceded by the authors to be imprecise (eg, computed tomography studies) and obtained without regard to the temporal aspects of the functional disorder time of onset, duration, and changes during the course of the illness, are obvious We nd it surprising that choreoathetosis was not more frequent Needed, of course, are detailed anatomic (postmortem) studies of cases in which the disturbances of function were stable for many months or years Such an example is the case of generalized dystonia with pallidoluysian atrophy reported by Wooten and coworkers Table 4-3 summarizes the clinicopathologic correlations of extrapyramidal movement disorders that are accepted by most neurologists; it must be emphasized, however, that there is still some uncertainty as to the ner details

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option to complete the tag as shown in Figure 13-4

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gress, or even remit to some extent on its own or with therapy, most of the patients succumb to the underlying tumor within a year Treatment If the tumor can be treated effectively, the neuropathy may improve, the exception being the pure sensory neuronopathy Treatment with plasma exchange, gamma globulin, or immunosuppression has had only a minimal effect, but there are anecdotal reports of success with very early immune treatment In the report by Uchuya and colleagues, only 1 of 18 patients with a subacute sensory neuropathy improved and another became dependent for sustained improvement on immune globulin; most of the others stabilized or worsened, and the authors concluded that treatment was of doubtful value Corticosteroids have not been tested in a systematic way but there is little clinical evidence to support their use

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Arsenical Polyneuropathy Of the neuropathies caused by metallic poisoning, that due to arsenic is particularly well known In cases of chronic poisoning, the neuropathic symptoms develop rather slowly, over a period of several weeks or months, and have the same sensory and motor distribution as the nutritional polyneuropathies Gastrointestinal symptoms, the result of ingestion of arsenic compounds, may precede the polyneuropathy, which is nearly always associated with anemia, jaundice, brownish cutaneous pigmentation, hyperkeratosis of palms and soles, and later with white transverse banding of the nails (Mees lines) The disease is accompanied by an excess of arsenic in the urine and hair Pathologically, this form of arsenical neuropathy is generally categorized as of the dying-back (axonal degeneration) type In patients who survive the ingestion of a single massive dose of arsenic, a more rapidly evolving polyneuropathy may appear after a period of 8 to 21 days as discussed earlier The neuropathy may be preceded by severe gastrointestinal symptoms, renal and hepatic failure, and mental disturbances, convulsions, confusion, and coma ie, arsenical encephalopathy the pathologic basis of which is a brain purpura, or pericapillary hemorrhages Initially, the neuropathy that develops in this setting may resemble GBS, both clinically and electromyographically (partial conduction block, prolonged F responses) Diagnosis and treatment of arsenical poisoning are discussed further in Chap 43 Lead Neuropathy (Plumbism) Lead neuropathy is an uncommon disorder In adults, as a rule, it occurs following chronic exposure to lead paint or fumes (from smelting industries or burning batteries) or from ingestion of liquor distilled in lead pipes Its most characteristic presentation is a predominantly motor mononeuropathy in the distribution of the radial nerves (wrist and nger drop) In a few personally observed patients, this was the main abnormality but there was also a slight sensory loss in the radial territory of the hand Less commonly there is foot drop occurring alone or in combination with weakness of the proximal arm and shoulder girdle muscles As pointed out in Chap 43, lead neuropathy seldom occurs in children, in whom lead poisoning usually results in a devastating encephalopathy Although the neuropathy has been known since ancient times, details of the pathology are still obscure Axonal degeneration with secondary myelin change and swelling and chromatolysis of anterior horn cells has been described Lead accumulates in the nerve and may be toxic to Schwann cells or to endothelial capillary cells, causing edema.

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