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The extrapyramidal motor syndrome as we know it today was rst delineated on clinical grounds and so named by S. A. K. Wilson in 1912. In the disease that now bears his name and that he called hepatolenticular degeneration, the most striking abnormality in the nervous system was a bilaterally symmetrical degeneration of the putamens, sometimes to the point of cavitation. To these lesions Wilson correctly attributed the characteristic symptoms of rigidity and tremor. Shortly thereafter, van Woerkom described a similar clinical syndrome in a patient with acquired liver disease (Wilson s cases were familial); in the acquired form also, the most prominent lesions consisted of foci of neuronal degeneration in the striatum. Clinicopathologic studies of Huntington chorea beginning with those of Meynert (1871) and followed by those of Jelgersma (1908) and Alzheimer (1911) related the movement disorder as well as the rigidity to a loss of nerve cells in the striatum. In 1920, Oskar and Cecile Vogt gave a detailed account of the neuropathologic changes in several patients who had been af icted with choreoathetosis since early infancy; the changes, which they described as a status brosus or status dysmyelinatus, were con ned to the caudate and lenticular nuclei. Surprisingly, it was not until 1919 that Tretiakoff demonstrated the underlying cell loss of the substantia nigra in cases of what was then called paralysis agitans and is now known as Parkinson disease. A series of observations, culminating with those of J. Purdon Martin and later of Mitchell and colleagues, related hemiballismus to lesions in the subthalamic nucleus of Luys and its immediate connections.
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sensory nerve since the dorsal root ganglion cells maintain the integrity of the distal axon. In other words, destruction of axons results within several days in a wallerian degeneration of all the myelin distal to the point of injury. The myelin breaks down into blocks or ovoids in which lie fragments of axons (digestion chambers of Cajal). The myelin fragments are then converted, through the action of macrophages, into neutral fats and cholesterol esters and carried by these cells to the bloodstream. Certain diseases affect the neuron primarily rather than the axon and cause either a motor or sensory neuronopathy. In the former case the anterior horn cell is affected by a disease process (motor neuron disease, or motor neuronopathy), and in the latter, the sensory ganglion cell (ganglionopathy) is destroyed. Degeneration of the respective nerve bers follows. These pathologic reactions are more easily understood if one considers certain features of cytoskeletal structure and function of nerve cells and their axons. The axon contains longitudinally oriented neuro laments and microtubules, which are separated but interconnected by cross-bridges. Their main function involves the transport of substances from nerve cell body to axon terminal (anterograde transport) and from the distal axon back to the cell body (retrograde transport). Thus, when the axon is severed, organelles cannot be transmitted to the distal axon for the purpose of renewing membrane and neurotransmitter systems. By means of retrograde axonal transport, the cell bodies receive signals to increase their metabolic activity and to produce growth factors and other materials needed for axonal regeneration. In some incompletely de ned way the axon creates a local environment that allows the Schwann cell to maintain the integrity of the adjacent myelin sheath. Loss
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Our objective is to nd b(t2 ) when b(t1 ) is known and Q(t) is constant for t (t1 , t2 ] where T = t2 t1 . Given these assumptions, for t (t1 , t2 ] we have that 0 1 1 Q(t) = Q = 2 2 3 and we de ne the integrating factor (t) = e
After modifying build.xml, you can then try to run ant again.
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