gested to Broca and Trousseau that the motor speech-center must control this form of emissive expression as well as that by the oral apparatus. There is a general inclination to return to this view.

Conduction Aphasias.-The aphasias thus far considered are due to lesions of single memory depots. There are others due to lesions of the conducting tracts that bring these depots into mutual and coördinate relations. The most important is the one produced by breaking the path between the auditory and motor word-centers. This is usually due to a lesion of or in the neighborhood of the island of Reil. It was first described by Wernicke and is sometimes called Wernicke's conduction aphasia. These patients present no particular auditory or articulative difficulty, but, owing to the loss of correlation between auditory and motor memories, they lose selective ability when they try to express themselves, and a most marked paraphasia and paragraphia result. They are obedient to direction, but can not repeat dictation orally or in writing, though they copy with perfect precision. Neither can they read or pronounce aloud, though they seem to read understandingly. There is very little attempt to correct errors of spoken or written speech. The writer has seen such a case, due to traumatic hemorrhage, which was relieved by operation, the clot being found under the operculum on the surface of the insular convolutions, where it had been located from the symptoms. The recovered patient now states that there was considerable mental confusion during the aphasia, to which the verbal disturbance no doubt would conduce.

Wernicke, Lichtheim, Wyllie, and others describe four other varieties of conduction aphasia depending upon the location of the lesion in relation to the conducting tracts to and from the auditory and motor word memories. Some quoted cases also are given in their support. Anatomical findings as yet are scarcely adequate to firmly establish these varieties, which, however, serve to complete the pathological study of the subject. By their aid some rare instances can be deciphered.

Combined Aphasias.-It has been pointed out that all the wordmemory depots are in the arterial territory of the middle cerebral. Consequently from this source, as well as by trauma, meningitis, or cerebritis, they may all be thrown out at once. Simultaneous injury to the auditory and visual word memories is comparatively frequent, and it has been seen that graphic-motor memories usually disappear with vocal motor memories-a combination due not only to association in function, but to proximity of centers, if a special one for writing is admitted. The loss of auditory and motor memories practically entails a loss of all speech attributes, as the visual and graphic-motor centers are so thoroughly dependent upon them. Again, the centers may be unequally affected, so that sensory disturbance preponderates over motor, or the contrary. The type cases indicated in the foregoing pages are indeed rare, but only by their full comprehension can we unravel the combined forms.

The mental disturbance is usually proportionate to the speech defect, and in total aphasia is very marked.

Reeducation of Aphasics.-One of the most important questions in

a given case of aphasia regards recovery from the speech defect. Pure motor aphasia is perhaps the most hopeful variety in this respect, as verbal motor memories are the most easily built up. Reading usually follows much more slowly and writing is even more tardy. The forms of aphasia connected with the loss of sensory word memories are the most persistent. As often mentioned, a majority of persons are auditif, and all are necessarily so in childhood, though the child intently watches the lips of those teaching it to speak and probably acquires visual memories in association with the auditory impressions. In the sensory aphasias the mental disturbance is usually greatest. The loss of these earliest and usually most deeply graven memories, which become dominant in the speech mechanism, is the most difficult to overcome.

The first step is to determine by which route the intelligence may best be reached. Even when both auditory and visual memories are gone some patients can use the sense of touch to good advantage, and it will often be found an aid to put familiar objects into their hands when encouraging them to name them. If they are capable of giving attention, much may be expected. Simple sounds, such as a child first utters, like ba, pa, ma, may be indicated to them and repeated by the voice and in writing, by the position of the lips, mouth, and tongue of the instructor, or by taking the patient's hand and tracing the letters either in air or on a blackboard. If some object can be used,—say, a knife or pen,-it should be kept before the patient and placed in his hand when he attempts to name it. When simple sounds are mastered they can then be grouped into words, and the words associated with objects or actions, and so a vocabulary built up, which must be frequently and repeatedly and patiently rehearsed. By unremitting, intelligent effort, some emissive speech may be taught even the most hopeless cases. adds greatly to their comfort and makes their care less burdensome.

It

CHAPTER III.

THE CEREBRAL WHITE MATTER, BASAL GANGLIA, AND CEREBELLUM.

DESCENDING from the cortex in converging lines we have the corona radiata, the fibers of which bring the brain-mantle into relation with the lower brain parts and the spinal cord. Through the corpus callosum the homologous cortical elements on the two sides of the brain are brought into harmonious relation. The descending tracts reaching the basal ganglia are condensed into the internal capsule, in which the cortical motor fields are represented from head to foot, in an order from before backward, as indicated in figure 73.

Fig. 73.-Arrangement of motor paths in the internal capsule (after Ferrier).

The internal capsule lies between the lenticular part of the striate body externally and the caudate nucleus and the optic thalamus on its median aspect, but is not dependent upon them. Its anterior portion, or limb, is supposed to contain psychic paths to the frontal lobes. Lesions of this part of the internal capsule produce no distinctive symptoms. The motor routes lower down are continued in the under portion of the crura and so on through the pons into the medulla and cord. The motor paths and their relations are indicated in figure 74,

which shows that the face mechanism is inferiorly situated in the cortex, anteriorly in the capsule, and internally in the crus.

The sensory paths, situated in the posterior columns of the cord, pass upward into the posterior third of the hinder limb of the internal capsule. They reach the cortex of both hemispheres, according to Brissaud and others, directly on the same side and indirectly on the opposite side, by sending off a branching path through the corpus callosum, as shown in figure 75. Bilateral sensory representation is thus provided for. Doubtless motion is originally equally symmetrical in its cortical representation, the apparent functional difference arising from the specializing of unilateral motility in the opposite or most intimately related cortex, by practice, habit, and education.

From these diagrams we can understand that lesions in the cerebral

Fig. 74.-Diagram to show the relative position of the several motor tracts in their course from the cortex to the crus. The section through the convolutions is vertical; that through the internal capsule, 1, C, horizontal; that through the crus is again vertical; CN, caudate nucleus; O, TH, optic thalamus; L2 and L3, the middle and outer parts of the lenticular nucleus; f, a, l, face, arm, and leg fibers. The words in italics indicate the corresponding cortical centers (after Gowers).

white matter must be close to the cortex or in the internal capsule to produce permanent and definite sensory symptoms, as otherwise placed they do not intercept the pathways to both hemispheres. The symptoms in subcortical lesions correspond to the function of the related cortex, and in capsular lesions to the function of the particular tracts involved. The radiations to and from the cortex in the area of latent lesions may be, and often are, involved without giving rise to any symptoms.

The corpus callosum may be diseased to almost any extent without presenting any peculiar symptoms. Bristowe, Sharkey, and Schuffer1 contend that tumors of the corpus callosum are likely to produce hebetude, apathy, and prolonged placid coma. If its function is but

1 "Rev. Speriment.," vol. xxviii, p. 2.

to furnish correlating tracts between the two sides of the brain, their destruction would not materially interfere, perhaps, with the independent action of the half-brain.

Lesions involving the optic radiations in the occipital lobes produce hemianopsia, and when, on the left side, they cut the radiations from the occipital apex to the angular gyre, word-blindness ensues, as described on page 171. Lesions beneath the auditory word-centers likewise pro

duce word-deafness.

The corpora striata can be completely destroyed on both sides without giving rise to motor or sensory disturbance if the internal capsule escapes. Their function is still a matter of speculation. Lesions affecting them, however, almost invariably implicate the capsular tracts.

In this

Fig. 75.-Schematic vertical transverse section of the hemispheres passing through the internal capsule and representing the sensory pathways. G, Left hemisphere; D, right hemisphere; cc, corpus callosum; ei, internal capsule; SG, sensory pathway from left side of cord; SD, sensory pathway from right side of cord. Both sides are brought into intimate relation through the corpus callosum, and the sensory representation is uniformly bilateral (after Brissaud).

locality we encounter the hemorrhagic lesion that is preeminently causative of apoplectic hemiplegia. Whether or not posthemiplegic choreic movements and athetosis are due to disease of the basal ganglia can not be definitely stated.

The optic thalami, when diseased, give rise to no definite symptoms if the lesions are confined to their anterior portions and do not invade the capsule. When the hinder portion of the optic thalamus is involved. we are likely to have either a crossed blindness or a double hemianopsia, probably from simultaneous injury to the optic tract. Bechterew claims, with much probability, that facial emotional expressions are controlled by the thalamus in some manner. Brissaud, in cases of postparalytic spasmodic crying and laughing, locates the lesion near the knee of the internal capsule. The loss of facial emotional expression at least