In any large group of cases of general paralysis, there are such differences in the mental symptoms, the paretic signs, the mode of onset, the course, intercurrent affections, duration, variability and mobility of symptoms, and pathological anatomy of the several cases, that one must feel that there are varieties of the disease. This has led to subdivisions of the affection, or grouping of its cases, scarcely any of which have had a pathological basis. True it is that Bayle, who was the first to differentiate general paralysis, and who attributed its striking phenomena each to a special morbid change, was led to place his cases in five series, in the first of which were simply the lesions of chronic meningitis, and in the second abundant serous effusion was added to these; in the third consecutive inflammation of the grey cortex; in the fourth arachnoid false membranes (cysts); and in the fifth various cerebral affections, complicated the chronic inflammation of the soft membranes. Yet many of his explanations are obviously incorrect, although his work marks a marvellous advance in science. Again, Baillarger, Requin, Prus, Duhamel, Duchenne, Sandras and others, held that general paralysis occurred either with or without insanity, and the first-named of these denied that the insanity is anything more than secondary and accessory in general paralysis of the insane.∗ Further, he speaks, and in this is followed by Lunier, of the symptoms of general paralysis as being produced by (1) chronic meningo-encephalitis, and by (2) chronic hydrocephalus (Dance, Moulin), or serous effusion following apoplexy (Rochoux, Moulin), or symptomatic of organic lesions. But they do not in any way distinguish between the cases arising from the two kinds of lesion, further than that Lunier asserts an absence of trembling of the limbs in those from lesions of the second kind.
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