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Encephalitis Lethargica (Von Economo Disease, Sleeping Sickness) Although examples of a somnolent-ophthalmoplegic encephalitis dot the early medical literature (eg, nona, febre leth argica, Schlafkrankheit), it was in the wake of the in uenza pandemic of World War I that this disease appeared prominently and continued to reappear for about 10 years The viral agent was never identi ed, but the clinical and pathologic features were typical of viral infection The importance of encephalitis lethargica relates to its unique clinical syndromes and sequelae and to its place as the rst recognized slow virus infection of the nervous system in human beings The unique symptoms were ophthalmoplegia and pronounced somnolence, from which the disease took its name Some patients were overly active, and a third group manifested a disorder of movement in the form of bradykinesia, catalepsy, mutism, chorea, or myoclonus Lymphocytic pleocytosis was found in the spinal uid of half the patients, together with variable elevation of the CSF protein content More than 20 percent of the victims died within a few weeks, and many survivors were left with varying degrees of impairment of mental function However, the most extraordinary feature was the appearance of a Parkinsonian syndrome, after an interval of weeks or months (occasionally years), in a high proportion of survivors This is the only form of encephalitis known to cause a delayed extrapyramidal syndrome of this type (a similar though not identical syndrome with a much shorter latency may follow Japanese B encephalitis and occasionally other arboviral encephalitis, as occurred in one of our cases after Eastern equine encephalitis) Myoclonus, dystonia, oculogyric crises (page 227) and other muscle spasms, bulimia, obesity, reversal of the sleep pattern, and, in children, a change in personality with compulsive behavior were other distressing sequelae The pathology was typical of a viral infection, localized principally to the midbrain, subthalamus, and hypothalamus In the patients who died years later with a Parkinson syndrome, the main ndings were depigmentation of the substantia nigra and locus ceruleus due to nerve cell destruction Neuro brillary changes in the surviving nerve cells of the substantia nigra and the oculomotor and adjacent nuclei were also described, indistinguishable from those of progressive supranuclear palsy Lewy bodies were not seen, in contrast to idiopathic Parkinson disease (paralysis agitans), where they are consistently present Only a few new questionable cases of postencephalitic type have been seen in the United States and western Europe since 1930 Sporadic cases, such as the four reported by Howard and Lees, may be examples of this disease, but there is no way of proving their identity Other Forms of Subacute Encephalitis A number of uncommon conditions not covered above are characterized by regional in ammation in the cerebrum Among these, Rasmussen encephalitis, which causes intractable focal seizures and progressive hemiparesis, has been connected to infections by CMV and HSV-I in various studies that used PCR techniques However, a speci c immune reaction consisting of antibodies to glutamate receptors has been implicated more consistently and immunosupressive treatments may be effective It is not clear whether this process can be classed with the infectious encephalitides; it is discussed in detail with other epileptic diseases on page 289 Similarly, the restricted in ammatory conditions called limbic encephalitis and brainstem encephalitis most often a distant effect of lung cancer have some characteristics of a subacute viral encephalitis, but no agent has been consistently isolated and they are also best considered.

THE TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES (PRION DISEASES)

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This category includes a quartet of human diseases so-called Creutzfeldt-Jakob disease (and a variant that infects cows and may be rarely transmitted to humans), the Gerstmann-Straussler Scheinker syndrome, kuru, and probably, fatal familial insomnia Although this group of diseases has been included for discussion in the chapter on viral diseases of the nervous system, it has been evident for some time that the cause of these slow infections is neither a virus nor a viroid (nucleic acid alone, without a capsid structure) During the past 20 years, Prusiner is credited with doggedly pursuing this problem, for which he was awarded the Nobel prize He and his colleagues have presented compelling evidence that the transmissible pathogen is a proteinaceous infectious particle that is devoid of nucleic acid, resists the action of enzymes that destroy RNA and DNA, fails to produce an immune response, and electron microscopically does not have the structure of a virus To distinguish this pathogen from viruses and viroids, Prusiner introduced the term prion The prion protein (PrP) is encoded by a gene on the short arm of chromosome 20 The discovery of mutations in the PrP genes of patients with familial Creutzfeldt-Jakob disease and Gerstmann-Straussler-Scheinker syndrome (described below) attests to the fact that prion diseases are both genetic and infectious In this respect, prions are unique among all infectious pathogens It is now possible to detect inherited types of prion disease during life, using DNA extracted from leukocytes How prions arise in sporadic forms of spongiform encephalopathy is not fully understood; probably the conversion of the normal cellular protein to the infectious form involves a conformational change in the protein structure as described in Prusiner s review in 2001 What is remarkable is the current theory that abnormally folded prion protein can act as a template for the conversion of normal PrP to PrPsc (the latter denoting the scrapie prion; see further on) A description of the human prion diseases follows, the most important by far being Creutzfeldt-Jakob disease.

03-15-2005

With these assumptions in mind, the Black-Sholes model is the standard option model for most online and software applications Most option analysis software has two or three choices for pricing formulas built in for the various needs of the user, but in general you will nd that the default for the application is Black-Sholes Some of the disadvantages of the Black-Sholes model are corrected in the binomial pricing model or the Cox, Ross, Rubenstein model Cox, Ross, and Rubinstein introduced the binomial model for pricing US stock options in 1979 This model is a tree model with nodes or branches and, when viewed graphically, the stock price and option price steps through each interval period from origin to expiration At each step, the stock price will either move up or down, with a probability de ned by the volatility of the stock Each step or node in the tree represents a period in which the stock price can branch up or down From each of these two points the stock price can either branch up or down at another point, creating another probability The branches continue, making a larger structure through expiration Like the Black-Scholes model, the binomial model assumes a risk-free interest rate, but in contrast to Black-Scholes, this model can account for dividend yield Because of the tree structure of the binomial model, options can be evaluated as exercised prior to expiration The model assumes that once time value has completely disappeared, the option would be exercised or expired The Cox, Ross, Rubenstein model corrects two issues with the Black-Scholes model, American option expiration and the model is able to account for dividend yield in the formula The binomial model is said to be more accurate, but also takes signi cantly longer to calculate by hand

Subacute Spongiform Encephalopathy (Creutzfeldt-Jakob Disease)