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disturbances were caused by disease of the two anterior lobes of the brain and by them alone. The second was Marc Dax, who in 1836, from the study of one hundred and forty cases of aphasia attended with right hemiplegia, came to the conclusion that not both anterior lobes of the brain, but the left only, was the seat of disease in speech disorders. M. Broca was the third. Two autopsies made in 1861, and revealing in both cases destruction of the third frontal and neighboring convolutions, which had coincided with total aphasia without hemiplegia, enabled him in the light of previous investigations to designate the convolution which bears his name, as the seat of the faculty of articulate speech.

During the next ten years, important differentiations in the nature of the speech processes were made by a number of British writers. In particular, Jackson in 1864, showed the difference between emotional speech in oaths, interjections, etc., and propositional speech, expressing an idea. Marse, 1865, was the first to conclude that the centers of spoken and written language were separate. Bastian, 1869, called attention to the sensory nature of alexia and word blindness.

The Germans date their contributions to the elucidation of these problems from 1870. Moeli remarks: “the great discovery of Broca took on a quite new significance after the doctrine of cerebral localization had been established by the investigation of Fritsch and Hitzig." Though late, the value of their work can hardly be overestimated. Wernicke, in 1874, was enabled to locate the center for the understanding of spoken language, in the first temporal convolution, and gave us the new designations of motor sensory and conduction aphasia. Kussmaul's name is connected with word deafness. Munk's with psychical blindness. Grashey brought out still a new cause of aphasia which has been generally accepted.

In our own country, Flint, Seguin, Fisher, Bartholow, and Starr, have all made valuable contributions to the literature of the subject, early and recent. These names are but few of a host, but certainly they illustrate the solidarity of the race in the fields of science.

For convenience of diagnosis, three general forms of aphasia may be recognized: functional, toxic, and organic.

Functional aphasia may be due to powerful emotions, for example; fear, or to reflex causes, such as operations, the presence of worms or other irritating ingesta, or to exhaustion and inanition. It has been known to accompany migraine. This. form of aphasia is transitory.

Toxic aphasia occurs in the course of typhoid, puerperal, and other infections, in uræmia, and cancer.

Organic aphasia, due to lesions of language centers or their connecting fibre bundles, is the common form inet by the general practitioner, and is the subject for discussion in this paper.

It is important to bear in mind that the term aphasia does not include those disorders of speech caused by any peripheral lesion, not even those in the medulla, to which the terın anarthria has been fittingly applied. The lesions of aphasia are cortical or immediately subcortical. Even disease foci in the internal capsule or basal ganglia do not cause permanent aphasia, unless they exert pressure on the cortical language areas. This statement made by the highest authorities, explains the many cases of complete right hemiplegia, including face and tongue muscles, but without disturbances of speech except such as are plainly due to the peripheral conditions. This statement explains also those cases of complete right hemiplegia with an aphasia of a few hours' or days' duration. The reason appears to be that the corpus callosum and right hemisphere furnish another way of exit for the outgoing currents from cortical language centers. To repeat, the lesions of aphasia do not cause paralysis of coarse muscular movements and are situated in the cortex or in those subcortical fibre bundles specialized for the transmission of the sensory and motor impulses connected with language processes. Thus cortical hæmorrhages, and far oftener softenings, which are usually cortical, are the most frequent causes of aphasia. Embolism indeed is the most frequent cause, as Hughlings Jackson long ago pointed out, since it involves most frequently the artery of the Sylvian fissure which supplies by one branch or another nearly all the cortical language areas. Thrombosis is another frequent cause, being likewise predominantly cortical in situation. Of course abscesses, tumors, tubercle, wounds, etc., may be causes.

It is rare to find a case of aphasia in which an isolated form of speech disorder occurs. On the contrary, several forms of disorder are usually present together, and to arrive at just conclusion as to the seat of the lesion is no easy task. I have found that the clearest understanding of the matter was to be obtained by keeping before me the order of training of language areas, and their true relations to each other. The average child at two years can understand a large amount of spoken language, though his own vocabulary contains but a score of words. That is to say, the auditory areas have eighteen months or two years the start in training, and store up doubtless many times more word

sounds than are ever transferred to the areas of articulation. The child then strives to repeat or imitate the word sounds with an ever increasing degree of accuracy. Thus the ear is the guide to the tongue, or rather the temporal convolutions to the frontal. Bastian ascribes to the temporal area the initiation of all the forms of language processes. It is easy then to see that, while a lesion of Broca's center need not disturb the functions of the temporal convolutions, on the other hand a lesion of the temporal convolutions would be likely to have a decided effect on the functions of Broca's center This is perceived in such symptoms as amnesic aphasia, paraphasia and even pure jargon. So with the writing center, as Grashey pointed out some years ago. The sound image of a word always comes up in consciousness before it is transferred to the pen. Agraphia is therefore usually a con-comitant of lesion of the temporal gyri, and the same is true of alexia, especially in uneducated people. Thus, to sum up, in lesion of the temporal gyri we are likely to find, in varying degrees, word deafness, amnesic aphasia, paraphasia, agraphia, alexia, and even motor aphasia.

Lesion of Broca's center is indicated first and foremost by lost or impaired power of speaking. The patient may be either reduced to the articulation of a single word or a few monosyllables, or the impairment may be so slight as only to be indicated by the omission or misplacement of some letters, which the Germans call syllable stumbling. It has to do primarily with the formation of words, while the understanding of the meaning of the word is perfectly clear. It, of course, comes out in spontaneous speech, in reading aloud, or in repeating after another. asmuch as many people, in both reading and writing, pronounce their letters first, agraphia and alexia may be found with motor aphasia. Dejerine and Mirallie examined eighteen patients recently, suffering with motor aphasia and found coexisting not only agraphia, which has long been known as a frequent concomitant, but also a certain degree of alexia. In those cases which recovered, the alexia often improved before the aphasia. The explanation they give is that the alexia is really functional, and conditioned by the unity of the entire cerebral speech mechanism. A lesion at any point of the speech circuit causes a functional disturbance of a certain degree of all speech processes. The predominance and persistence of disturbance in any individual speech process indicates the location of the lesion.

As I have already said, the initiation of spontaneous speech is generally believed to be the function of the temporal convolu

tions, so far as the speech circuit is concerned, that is to say, leaving out of account any higher center, which may or may not exist. While this is probably true of the average man, evidence is not wanting that other centers usually subordinate, may become independent and controlling. In the Berlin Medical Weekly, No. 14, 1895, Bianchi reports the case of a printer with right hemiplegia. He comprehended spoken language and had perfect articulation and could write to dictation, thus showing no lesion of the first temporal or third frontal or the writing area. On the other hand spontaneous speech and spontaneous writing were defective and he could not read or write to copy. Autopsy showed, besides lesions, softening in the right hemisphere; in the left hemisphere a spot of softening in the angular gyrus, and the inference was made, as it seems to me correctly, that in the case of this printer, the memory images of internal speech came not from the auditory but from the visual areas. Unquestionably in certain educated people, in the progress of life, a greater training may be bestowed upon the visual or articulative areas than upon the auditory, which must be taken into account in the making up of the diagnosis.

Alexia, when it is the only or the most prominent symptom, points to lesion of the posterior part of the brain, especially of the angular syrus. The distinction has been made by a number of investigators between cortical and subcortical alexia. The first is caused by lesion of the angular gyrus, and is indicated by word blindness and total agraphia. The second is due to a lesion cutting the connection between the angular gyrus and centers of common vision in the accipital lobe, and is distinguished by the fact that the agraphia is not total, spontaneous and dictation writing being preserved, while reading and copying are lost.

As I have already shown, alexia may be a functional symptom occurring in connection with lesion of either Broca's convolution or the first-temporal. The reading centers are trained after the age of five or six and under the control and guidance of the first two. Uncultivated people are obliged to read aloud in order to take in the meaning of any passage.

The writing-center is latest developed, usually by several years and under the guidance of the other three. Its situation is uncertain, the base of the second frontal being selected by most authorities. An isolated agraphia with post-mortem is unknown. As a symptom, agraphia is most frequently joined to sensory aphasia or lesion of the temporal convolutions, since in most men the sound image of a word comes up in consciousness before they write it or can write it. Agraphia is also a frequent concomitant

of motor aphasia and also of alexia as an isolated symptom. Wiessenburg in 1893 reported a case where the early symptoms were alexia and agraphia. Later on word-deafness and aninesic aphasia appeared. The lesion proved to be a tumor in the occipital lobe. The subordinate relation of the agraphia to the alexia is clearly seen here. Paraphasia is usually due to lesion of the temporal gyri or the fibre bundles connecting them with Broca's center, and passing beneath the Island of Reil. Amnesic aphasia, or the loss of power to speak spontaneously, due to forgetfulness of words, is probably most frequently connected with lesion of the temporal gyri or the subjacent fibres. Yet from the foregoing considerations, one might expect to find it in some degree present with lesion of any language center.

The two following cases seen recently, illustrate the two main divisions of aphasia, motor and sensory.

Case I. M-, aged fifty-six, burnisher, history of cardiac hypertrophy and valvular defect. March 7th, while at work felt a sudden numbness in right side, and found he couldn't use right arm or leg. No loss of consciousness. Present state on examination, four weeks later, April 8th, moderate right hemiplegia, including face muscles, grip R. 25, L. 50. Examination for aphasia shows -ist, perfect understanding of what is said to him; 2d, articulation defective, defect consisting in stammering and repeating words, the rhythm being jerky and the words sometimes so run together as to be distinguished with difficulty; letters sometimes misplaced; says he knows what he wants to say but can't say it; 3d, ability to read aloud as good as ever excepting the foregoing articulative defect; 4th, can write spontaneously, to copy, and to dictation, but writing very poor, partly on account of perepheral paralysis, and probably never very good. The idea of writing evidently unimpaired; 5th, no degree of paraphasia or amnesic aphasia.

Diagnosis was embolism of the left middle cerebral, affecting the integrity of those parts supplied by the initial branches, namely, the internal capsule and third frontal convolution. Six months subsequently the condition was about the same.

Case II., L. 62. History of heart trouble which had not been definitely made out. On June 19th, while in a hall on a hot day, something came over him like a bright light. came out, tried to say something, and couldn't say what he wanted to. Instead said something else; could walk and see perfectly, but couldn't talk straight and went home.

Present state--1, Understands spoken language; 2, articulation good, though occasionally a letter misplaced; 3, if speaks

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