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In the past, this syndrome was almost invariably the result of infection by one of the three types of poliovirus However, illnesses that clinically resemble poliovirus infections can be caused by other enteroviruses, such as Coxsackie viruses groups A and B and Japanese encephalitis virus as well as by West Nile virus Epidemics of hemorrhagic conjunctivitis (due to enterovirus 70 and formerly common in Asia and Africa) are also, in a small percentage of cases, associated with a lower motor neuron paralysis resembling poliomyelitis (Wadia et al) In countries with successful poliomyelitis vaccination programs, these other viruses are now the most common causes of the anterior poliomyelitis syndrome, as discussed further on In some cases, the illnesses induced by these viruses are generally benign and the associated paralysis is in signi cant West Nile virus may be an exception in that several instances of encephalitis have been associated with a severe asymmetrical accid poliomyelitis Of course, the important (paralytic) disease in this category is poliomyelitis Although no longer a scourge in areas where vaccination is practiced, its lethal and crippling effects are still fresh in the memory of physicians who practiced in the 1950s In the summer of 1955, when New England experienced its last epidemic, 3950 cases of acute poliomyelitis were reported in Massachusetts alone, and 2771 of these were paralytic The details of this epidemic, described by Pope and colleagues, are worth reviewing by any student of the disease Now, only about 15 cases of paralytic poliomyelitis are reported annually in the United States about equally divided between unvaccinated children and unvaccinated adults, the latter exposed to a recently vaccinated infant Furthermore, the paralytic residua of previous epidemics can still be seen everywhere In these cases, a delayed progression of muscle weakness may sometimes seem to appear many years after the acute paralytic illness a condition termed postpolio syndrome (page.

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01-25-2005

Option models are a necessary evil and rather than heading for that bottle of aspirin over a bunch of calculus, let s look at the pros and cons of a couple of the popular systems At the least it s important to understand the history and rationale of these formulas as well as their bene ts and shortcomings Let s look at the most popular formulas used to calculate theoretical option value and implied volatility and then we ll look at what is relevant and what is not relevant about these models The most prevalent formula for option pricing is the BlackScholes option pricing model The Black-Scholes formula was created in 1973 by Fisher Black and Myron Scholes The model essentially changed nancial markets by providing a means to estimate the future value of derivative positions given a certain set of variables The Black-Scholes model makes certain assumptions that are important to understand because they represent some of the limitations of the model:

mal for 48 h The distribution of spinal paralysis is quite variable; rarely there may be an acute symmetrical paralysis of the muscles of the trunk and limbs as occurs in the Guillain-Barre syndrome Excessive physical activity and local injections during the period of asymptomatic infection were thought to favor the development of paralysis of the exercised muscles or injected limbs Coarse fasciculations are seen frequently as the muscles weaken; they are transient as a rule, but occasionally they persist Tendon re exes are diminished and lost as the weakness evolves and paralyzed muscles become accid Patients frequently complain of paresthesias in the affected limbs, but objective sensory loss is seldom demonstrable Retention of urine is a common occurrence during the early phase in adult patients, but it does not persist Atrophy of muscle can be detected within 3 weeks of onset of paralysis, is maximal at 12 to 15 weeks, and is permanent Bulbar paralysis is more common in young adults, but usually such patients have spinal involvement as well The most frequently involved cranial muscles are those of deglutition, re ecting involvement of the nucleus ambiguus The other great hazards of bulbar disease are disturbances of respiration and vasomotor control hiccough, shallowness and progressive slowing of respiration, cyanosis, restlessness and anxiety (air hunger), hypertension, and ultimately hypotension and circulatory collapse When these disturbances are added to paralysis of diaphragmatic and intercostal musculature, the patient s survival is threatened and the institution of respiratory assistance and intensive care becomes urgent Pathologic Changes and Clinicopathologic Correlations In fatal infections, lesions are found in the precentral (motor) gyrus of the brain (usually of insuf cient severity to cause symptoms), brainstem, and spinal cord The brunt of the disease is borne by the hypothalamus, thalamus, motor nuclei of the brainstem and surrounding reticular formation, vestibular nuclei and roof nuclei of the cerebellum, and mainly, giving the illness its name, the neurons of the anterior and intermediate gray matter of the spinal cord In these areas, nerve cells are destroyed and phagocytosed by microgliacytes (neuronophagia) A leukocytic reaction is present for only a few days, but mononuclear cells persist as perivascular accumulations for many months Nuclear or cytoplasmic inclusion bodies are not seen The earliest histopathologic changes are central chromatolysis of the nerve cells, along with an in ammatory reaction These changes correlate with a multiplication of virus in the CNS and, in the infected monkey, precede the onset of paralysis by one or several days In Bodian s experimental material, the infected motor neurons continued to function until a stage of severe chromatolysis was reached Moreover, if damage to the cell had attained only the stage of central chromatolysis, complete morphologic recovery could be expected a process that took a month or longer After this time, the degrees of paralysis and atrophy were closely correlated with the number of motor nerve cells that had been destroyed; where limbs remain atrophic and paralyzed, less than 10 percent of neurons survived in corresponding cord segments Lesions in the motor nuclei of the brainstem are associated with paralysis in corresponding muscles, but only if severe in degree The disturbances of swallowing, respiration, and vasomotor control are related to neuronal lesions in the medullary reticular formation, centered in the region of the nucleus ambiguus Atrophic, are exic paralysis of muscles of the trunk and limbs relates, of course, to destruction of neurons in the anterior and intermediate horns of the corresponding segments of the spinal cord.

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