Careers in Governance and Control of Education in Software

Integrating UPC-A Supplement 2 in Software Careers in Governance and Control of Education

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causing the patient to freeze in place. Getting in and out of a car or elevator or walking into a room or in a hall are then particularly dif cult. Dif culty in turning over in bed is a characteristic feature as the illness advances, but the patient rarely volunteers this information; several of our patients have fallen out of bed at a frequency that suggests a connection to their reduced mobility. Shaving or applying lipstick becomes dif cult, as the facial muscles become more immobile and rigid. Persistent extension or clawing of the toes, jaw clenching, and other fragments of dystonia, often painful, may enter the picture but are not usually early ndings. (These are particularly resistant to treatment.) As noted above, these various motor impediments and tremors characteristically begin in one limb (more often the left) and spread to one side and later to both sides, until the patient is quite helpless. Yet in the excitement of some unusual circumstance (as escaping from a re, for example), the patient with all but the most advanced disease is capable of brief but remarkably effective movement (kinesis paradoxica). Regarding other elicitable neurologic signs, there is an inability to inhibit blinking in response to a tap over the bridge of the nose or glabella (Myerson sign), but grasp and suck re exes are not present and buccal and jaw jerks are rarely enhanced. Commonly there is an impairment of upward gaze and convergence; if prominent or noted early in the disease, this sign suggests more the possibility of progressive supranuclear palsy. The bradykinesia may extend to eye movements, in that there is a delay in the initiation of gaze to one side, slowing of conjugate movements (decreased maximal saccadic velocity), hypometric saccades, and breakdown of pursuit movements into small saccades. There are no sensory changes, but a variety of paresthetic complaints are common. Drooling is troublesome; an excess ow of saliva has been assumed, but actually the problem is one of failure to swallow with normal frequency. Seborrhea and excessive sweating are probably secondary as well, the former due to failure to cleanse the face suf ciently, the latter to the effects of the constant motor activity. Postural instability can be elicited by tugging at the patient s shoulders from behind and noting the lack of a small step backward to maintain balance. The tendon re exes vary, as they do in normal individuals, from being barely elicitable to brisk. Even when parkinsonian symptoms are con ned to one side of the body, the re exes are usually equal on the two sides, and the plantar responses are exor. Exceptionally, the re exes on the affected side are slightly brisker, which raises the question of corticospinal involvement; but the plantar re ex remains exor. In these respects, the clinical picture differs from that of corticobasal ganglionic degeneration, in which rigidity, hyperactive tendon re exes, and Babinski signs are combined with apraxia (see further on). There is a tendency to orthostatic hypotension and sometimes syncope; this has been attributed by Rajput and Rozdilsky to cell loss in the sympathetic ganglia. However, syncope is never as prominent as in the Shy-Drager type of striatonigral degeneration (page 925). It is worth mentioning that two of our younger Parkinson patients with recurrent syncope proved to have cardiac arrhythmias, which were cured by the insertion of a pacemaker, hence other causes of fainting are still to be considered. At times, Parkinson disease is complicated by a dementia, a feature that had been commented upon by Charcot. The reported frequency of this combination varies considerably, based on the selection of patients and type of testing. An estimate of 10 to 15 percent (Mayeux et al) is the generally accepted gure and matches
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neurologic syndrome; it appears to be identical to the one described by Strachan. The core disorder is an affection of the peripheral and optic nerves. The former consists mainly of sensory symptoms and signs, and the latter is characterized by the subacute evolution of failing vision, which, if untreated, may progress to complete blindness and pallor of the optic discs. Deafness and vertigo are generally uncommon, but in some outbreaks among prisoners of war these symptoms were frequent enough to earn the epithet camp dizziness. In all these respects the syndrome differs from beriberi. Along with the neurologic signs there may be varying degrees of stomatoglossitis, corneal degeneration, and genital dermatitis (the orogenital syndrome). These mucocutaneous lesions are unlike those of pellagra and ribo avin de ciency. There have been only a few neuropathologic studies of this syndrome. Aside from the changes in the papillomacular bundle of the optic nerve, which are similar to the de ciency amblyopia discussed above, the most consistent abnormality has been a loss of myelinated bers in each column of Goll adjacent to the midline. Fisher has interpreted this change to indicate a degeneration of the central processes of the bipolar sensory neurons of the dorsal root ganglia. The fact that the primary sensory neuron is the main site of the neuropathic disorder is consistent with the predominantly sensory symptomatology. The present authors nd it dif cult to draw a sharp dividing line between the nutritional peripheral (and optic) neuropathy described above and the Strachan syndrome.
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i f hh>h, h]-i = h; end while(1) i f ct+hh>tend, hh = tend-tt,'end : })' ; :),vararqin{ kl = dydt (tt.y1i, ymid = y(1,:) + kL.*hrh,./2; : ] )' ; k2 = dydt |.tt+hY\/2,ymid,varargini ymid = y(i,:) + k2*hrh/2; k3 - dydt (tt+hh,/2,ymid,vararqrin{ : } )' ; +k3*hh; Vei-rd=y(i,:) ; } )' ; k4 = dydL(tL+hh,yend,varargin{ phi = (k1+2*(k2+k3) +k4) /6; = y(i,:) y(i+l,:) + phi*hh;
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