Volume 1

A clinical treatise on the diseases of the nervous system / by M. Rosenthal ; with a preface by Professor Charcot ; translated from the author's revised and enlarged edition by L. Putzel.

  • Rosenthal, Moriz, 1833-1889.
Date:
1881
Catalogue details

Licence: Public Domain Mark

Credit: A clinical treatise on the diseases of the nervous system / by M. Rosenthal ; with a preface by Professor Charcot ; translated from the author's revised and enlarged edition by L. Putzel. Source: Wellcome Collection.

Provider: This material has been provided by University of Bristol Library. The original may be consulted at University of Bristol Library.

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    transmission of sensory impressions to the centres of co-ordination in the cerebellum and mesocephalon. Serious lesions of these conductors destroy the intermediate paths and, consequently, the essential unity of the ap- paratus of co-ordination. From the statements hitherto made, we must therefore conclude that progressive locomotor ataxia is a paralysis of co- ordination, a synergic paralysis of spinal origin. Diagnosis. The appearance of lancinating pains in the lower or upper limbs, ap- pearing periodically and increasing after exertion or excitement should lead us to suspect the beginning of locomotor ataxia. Pains in the spinal column, and especially sciatic pains (with or without partial cutaneous hyperaesthesia), persistent upon one side and intermittent upon the other, are very significant. Intercurrent diplopia, marked inequality of the pupils, changes in the optic nerves recognizable with the ophthalmoscope, disturbances of vision and color-blindness, and the less frequent irritative phenomena on the part of the digestive and genito-urinary organs, are also very characteristic symptoms. Rapidly developing fatigue, especially in the vertical position; tremor and oscillations occurring when the patient attempts to stand upon one foot, with the eyes closed; phenomena of irritation on the part of the genital organs (increased sexual desire, fre- quent pollutions, incomplete erections, etc.); extreme sensibility to atmos- pheric changes; finally, the abnormal electrical excitability of the nerves, —all these symptoms, together with their manner of appearance and their characteristic relations, will usually enable us to detect the latent course of ataxia at an early period. In its more advanced stages, ataxia will hardly be overlooked by even the most careless observer. With regard to differential diagnosis, we must especially take into consideration certain central affections whose symptoms are similar to those of ataxia. Chronic myelitis is distinguished from ataxia by an evident diminu- tion of motor power (varying from abolition of certain isolated movements to general paralysis); in walking, the patient drags the limbs slowly and with difficulty. There are no disorders of co-ordination or intermittent ocular paralyses. The different varieties of sensibility disappear rapidly, and galvanic excitability is more frequently diminished than in ataxia. Chronic spinal ymningitis also presents the signs of a chronic myelitis, with the trophic disorders and electrical reactions resulting from local com- pression of the cord (vide p. 189). In general paralysis we sometimes observe movements of projection of the limbs at an advanced stage of the disease. But general paralysis commences with tremor of the limbs, tongue, and lips, followed by em- barrassment of speech, dullness of the senses, disorders of memory and judgment. Not infrequently certain filaments of the facial nerve are more or less paretic at the onset. On the other hand, ocular paralysis and amaurosis do not occur. If ataxia is complicated with insanity (a very rare occurrence), this will only develop after secondary affection of the cerebral cortex, and we must then rely, for diagnosis, upon the previous history of the patient. The differential diagnosis between ataxia and cerebellar affections has been discussed upon p. 134. Unilateral ataxia is rare, and is readily dis- tinguished, with a little care, from cerebral hemiplegia. We can recog-