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DEGENERATIVE DISEASES OF THE NERVOUS SYSTEM
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ever, exceptions Inability to produce vertical saccades and, later, paralysis of upward and downward gaze and eventually of lateral gaze with retention of re ex eye movements establish the diagnosis in most cases Strict adherence to the diagnostic criteria for Parkinson disease also permits its differentiation from corticostriatospinal, striatonigral, and corticobasal ganglionic degeneration as well as Machado-Joseph disease all of which are discussed in other parts of this chapter The rapid onset of parkinsonism should suggest exposure to neuroleptic medications or a variant of Creutzfeldt-Jakob disease Paucity of movement, unchanging attitudes and postural sets, and a slightly stiff and unbalanced gait may be observed in patients with an anergic or hypokinetic ( retarded ) type of depression Since as many as 25 to 30 percent of parkinsonian patients are depressed, the separation of these two conditions is at times dif cult The authors have seen patients who were called parkinsonian by competent neurologists but whose movements became normal when antidepressant medication or electroconvulsive therapy was given Several such patients have nonetheless insisted that levodopa helps them in some nondescript way The rapid onset of the Parkinson syndrome, especially in conjunction with other medical diseases, should always raise the suspicion of drug effects; phenothiazines, haloperidol, and the neuroleptics pimozide and metoclopramide, used at times as antiemetics, all cause a slight masking of the face, stiffness of the trunk and limbs, lack of arm swing, ne tremor of the hands, and mumbling speech They may also evoke an inner restlessness, a muscular impatience, an inability to sit still, and a compulsion to move about much like that which occurs at times in the parkinsonian patient (akathisia; page 97) Spasms of the neck, face, and jaw muscles (open mouth, protruded tongue, retrocollis or torticollis, grimacing) may also be provoked by such drugs Even the newer antipsychotic medications, favored speci cally because of a putative lack of extrapyramidal effects, may be at fault A mild, localized rigidity of an arm due to local tetanus was studied by R D Adams in a patient who had been referred as a case of acute parkinsonism All in all, if one adheres to the strict de nition of Parkinson disease bradykinesia, resting tremor, postural changes and instability, cogwheel rigidity, and response to L-dopa errors in diagnosis are few Yet in a series of 100 cases, studied clinically and pathologically by Hughes and associates, the diagnosis was inaccurate in 25 percent The reasons are that about this number of Parkinson patients fail to display the characteristic tremor and about 10 percent are said to not respond to L-dopa These authors noted that early dementia and autonomic disorder and the presence of ataxia and corticospinal signs were reliable guides to an alternate diagnosis Pathology and Pathogenesis The most constant and pertinent nding in both idiopathic and postencephalitic Parkinson disease is a loss of pigmented cells in the substantia nigra and other pigmented nuclei (locus ceruleus, dorsal motor nucleus of the vagus) The substantia nigra is visibly pale to the naked eye; microscopically, the pigmented nuclei show a marked depletion of cells and replacement gliosis, and some of the remaining cells have reduced quantities of melanin, ndings that enable one to state with con dence that the patient must have suffered from Parkinson disease Also, many of the remaining cells of the pigmented nuclei contain eosinophilic cytoplasmic inclusions, surrounded by a faint halo, called Lewy bodies (Fig 39-5) These are seen in practically all
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Figure 39-5 Photomicrograph of a round Lewy body inclusion in the cytoplasm of a nigral neuron (Taken from H and E) (Courtesy of M Frosch, MD, PhD)
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cases of idiopathic Parkinson disease They were generally absent in postencephalitic cases, but neuro brillary tangles were the usual nigral cell abnormalities Both of these cellular abnormalities appear occasionally in the substantia nigra of aged, nonparkinsonian individuals Possibly the individuals with Lewy bodies would have developed Parkinson disease if had they lived a few more years Noteworthy is the nding by McGeer et al that nigral cells normally diminish with age, from a maximal complement of about 425,000 to 200,000 at age 80 Tyrosine-hydroxylase, the rate-limiting enzyme for the synthesis of dopamine, diminishes correspondingly However, these authors and others have found that in patients with Parkinson disease, the number of pigmented neurons was reduced to 30 percent or less of that in age-matched controls Using more re ned counting techniques, Pakkenberg and coworkers estimated the average total number of pigmented neurons to be 550,000 and to be reduced in absolute numbers by 66 percent in Parkinson patients (The number of nonpigmented neurons was reduced in Parkinson cases by only 24 percent) Thus, aging contributes importantly to nigral cell loss, but the cell depletion is so much more marked in Parkinson disease that some factor other than aging must also be operative Other depletions of cells are widespread as mentioned, but they have not been quantitatively evaluated and their signi cance is less clear There is neuronal loss in the mesencephalic reticular formation, near the substantia nigra These cells project to the thalamus and limbic lobes In the sympathetic ganglia, there is slight neuronal loss and Lewy bodies are seen This is also true of the pigmented nuclei of the lower brainstem as well as of neuronal populations in the putamen, caudatum, pallidum, and substantia innominata On the other hand, dopaminergic neurons that project to cortical and limbic structures, to caudate nucleus and nucleus accumbens, and to periaqueductal gray matter and spinal cord are affected little or not at all The lack of a consistent lesion in either the striatum or the pallidum is noteworthy in view of the reciprocal connections between the striatum and the substantia nigra and the depletion of striatal dopamine, based on the loss of nigral projections, that characterizes the disease
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