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Other closely related phenomena are spasms or involuntary movements of the toes and feet The latter, referred to by Spillane and colleagues as the syndrome of painful legs and moving toes, is attributed by Nathan to ectopic discharges in sensory roots, ganglia, or nerves, evoking both pain and organized movements This is one cause of a nocturnal restless leg syndrome, the more common type being idiopathic and not associated with features of peripheral nerve disease Other possible mechanisms for cramps and spasms are ephaptic cross-transmission, segmental hyperactivity from deafferentation, and neuronal sprouting during reinnervation In yet other instances, the muscle activity induces odd postures or slow writhing movements that Jankovic and van der Linden have likened to dystonia The precise pathophysiology of these spontaneous and asynchronous activities of motor neurons is not known.

Stimulation of a motor nerve, instead of causing a brief burst of action potentials in the muscle, results in a prolonged or dispersed series of potentials lasting several hundred milliseconds Evidently, branched axons involved in.

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By the triangle inequality, these bypasses can only make the overall tour shorter. General TSP But what if we are interested in instances of TSP that do not satisfy the triangle inequality It turns out that this is a much harder problem to approximate. Here is why: Recall that on page 255 we gave a polynomial-time reduction which given any graph G and integer any C > 0 produces an instance I(G, C) of the TSP such that: (i) If G has a Rudrata path, then

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98. A URL such as http://localhost/localstart.asp would be the virtual path to the web page, whereas a file path such as C:\Inetpub\Wwwroot\localstart .asp would be the physical path to the web page. 99. MapPath is the method of the HttpServerUtility class that returns the physical file path that corresponds to (is mapped to) the specified virtual path on a web server. 100. Page is the name of the class that is the web application equivalent of the Form class in a Windows application.

suf cient quantities to destroy the cells, probably by interfering with mitochondrial function In monkeys made parkinsonian by the administration of MPTP, electrophysiologic studies have shown increased activity in the medial globus pallidus and decreased activity in the lateral globus pallidus, as predicted from the previously described models This comes about because of the differential loss of activity of dopaminergic striatal neurons that project to each of these parts of the pallidum The end result is increased inhibition of thalamocortical neurons It is, however, dif cult to explain why medial pallidal lesions do not regularly cause parkinsonism, as pointed out by Bhatia and Marsden Perhaps it is because the subtle imbalance between the medial and lateral pallidal circuits that exists in Parkinson disease is not reproduced.

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This subtlety may also explain why crude lesions such as infarcts, hemorrhages, and tumors rarely produce the complete parkinsonian syndrome of tremor, bradykinesia, and rigidity without paralysis or re ex changes Indeed, striking improvements in parkinsonian symptoms are obtained by placing lesions in the medial pallidum (pallidotomy), as discussed on page 924 However, there are de ciencies in all current models, particularly as they relate to Parkinson disease and its treatment For example, the abatement of drug-induced dyskinesias by a lesion in the subthalamic nucleus is an anomaly, and the effects of thalamic lesions are not easily explained (see Chap 39) It is likely that the static model of inhibitory and excitatory pathways and the parsing of a direct and an indirect pathway, as useful as it is as a mnemonic, does not account for the dynamic activities of the basal ganglia.

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