from these points on ill-defined lines or angles. A simpler and probably more accurate plan is advocated by Drs. Anderson and Makins, of London, based upon a series of forty observations upon adult male and female heads and the heads of children. The system depends upon averages and proportions, making it of wider application than the others. It has served the writer well in many cases.

First a line, the sagittal line, is drawn in the median plane from the glabellar point to the external occipital protuberance. The glabellar point is determined by drawing a horizontal line at the level of the upper border of the orbital openings, and marking its intersection with the median plane. It corresponds very nearly to the union between the nasal and frontal bones. At exactly one-half the length of this line

commencement

Fig. 68. Craniocerebral guiding lines traced upon a cast of Professor Cunningham's (from a photograph). GP, Glabellar point, glabella opposite superior border of orbit; IP, inial point, at external occipital protuberance; MSP, mid-sagittal point, midway between GP and IP; Ang.P, angular point, external angular process opposite upper border of orbit; Sq.P, squamosal point, intersection of oblique and frontal lines at junction of middle and lower thirds of latter; PP, parietal point, termination of oblique line, equidistant with FS2 from squamosal point; Aur.P, pre-auricular point, depression in front of tragus, at the level of upper border of external auditory meatus; FS1 of fissure of Sylvius, five-twelfths of distance from Ang. P to Sq.P; FS2, bifurcation of fissure of Sylvius, seven-twelfths of distance from Ang.P to Sq.P; FS3, termination of fissure of Sylvius, 1⁄2 of an inch above PP, in a direction parallel to frontal line; FR1, upper extremity of fissure of Rolando carried to sagittal line in direction of fissure, 3% of an inch behind mid-sagittal point; FR2, lower extremity of fissure of Rolando carried to oblique line in direction of fissure, 3 of an inch in front of squamosal point; PO. external parieto-occipital fissure carried to sagittal line in direction of fissure, seven-twelfths of distance from MSP to IP.

From

is marked a vertical point. Seven-twelfths of the distance from the vertical point to the external occipital protuberance, which can always be readily located, is a point corresponding to the parieto-occipital fissure, marking the limits of the parietal and occipital lobes. the depressions immediately in front of the tragus of each ear, at the level of the upper margin of the external auditory meatus, lines called frontal lines are drawn to the vertical point already mentioned. At the junction of the middle and lower thirds of the frontal line lies the fissure of Sylvius, and this point, corresponding fairly well to the squamous suture of the temporal bone, is called the squamosal point. From the squamosal point a line, the oblique line, is drawn downward and forward to the external angular process of the frontal bone, at the upper orbital

border level, as in fixing the glabellar point. Divide this line into twelfths. Five-twelfths of the distance from the angular point to the squamosal point begins the fissure of Sylvius; at seven-twelfths it bifurcates and extends by its horizontal line backward under the oblique line, and in its continuation to a distance posterior to the squamosal point equal to the distance of the point of bifurcation anterior to this intersection of oblique and frontal lines. At the termination of the oblique line the Sylvian fissure turns upward about of an inch parallel to the frontal line, to terminate approximately under the parietal boss. To mark the fissure of Rolando, draw a line from the sagittal line of an inch posterior to the vertical point downward and forward, at an angle of about sixty-seven degrees, to terminate of an inch anterior to the squamosal point on the oblique line. The fissure of Rolando lies under this line, but terminates, as a rule, of an inch above the Sylvian, though very rarely opening into it.

Having thus fixed these two important and tolerably uniform fissures, the marking off of the principal convolutions is simple. Owing to the fact that there is no absolute relation between the cranium and the convolutions, it is necessary, when they are exposed, to verify them, if they are motor in character, by the application of the faradic current. This is done by means of an electrode bearing two probepointed terminals and may be accomplished through the unopened dura.

CHAPTER II.

SPEECH AND THE CORTEX-APHASIA.

General Conditions.-A word has four principal cortical qualities: it can be heard and seen, and it can be spoken and written. The first two are afferent qualities of perception. The second two are efferent qualities of expression. We, therefore, have four groups of word memories: (1) Those of sound, or auditory word memories; (2) those of sight, or visual word memories; (3) those of the motions necessary to express words in speech, vocal motor word memories, and (4) probably those of the motions required to express them by written symbols, graphic motor word memories. For these four memory groups we have four cortical memory depots, as indicated in Fig. 69. These memory word-centers are brought into mutual relations by systems of connecting fibers and into relation with their corresponding receptive and emissive peripheral organs by afferent and efferent tracts. We may indicate these connections by a diagram (Fig. 70). Thus, take the word apple; when it is spoken we hear it in the temporal lobe, and when written we see it in the angular gyre of the parietal lobe. We call up the memory of muscular move

ments in the third left frontal gyre when we would utter it vocally, and those probably in the neighborhood of the hand-center when we would express it by writing.

As one or another of these speech-centers is diseased we have corresponding varieties of cortical speech defect, or aphasia. They are: (1) Auditory aphasia, or word-deafness; (2) visual aphasia, or word-blind

Fig. 69.-Speech areas in the cortex. A, Auditory word memories; B, memories for motor vocal speech; C, visual speech memories, including written characters and lip positions; D, graphic motor word memories (after Wyllie).

ness; (3) motor aphasia, or aphemia; and (4) graphic motor aphasia, or agraphia. Disturbance of the connecting fibers also disturbs speech, giving rise to a number of secondary or connecting aphasias. Again, more than one center may be simultaneously affected, causing combined aphasias. The four primary word-centers are, to a varying degree, mutually dependent. Word-blindness is often attended by agraphia, as the mind is unable to recall the visual image of the word, which is to

Fig. 70.-Diagram showing receptive and emissive speech-route, and the primary interrelations of the memory depots for speech. A, B, C, D correspond to the memory depots similarly indicated in the preceding figure (after Wyllie).

be copied, as it were, through the action of the graphic center. Again, if there is word-deafness, the patient can not write to dictation, though he may copy perfectly.

Individuals vary greatly in the local storage of their word memories. As first emphasized by Charcot, one may have his words principally stored in the auditory area (auditif), another in the motor area (moteur), and

a third in the visual area. If we learn a new language by ear its memories are mainly auditory, and if by the book, they are visual. It is only when we have acquired oral proficiency that our motor memories are fully established and may finally, perhaps, predominate. Probably only those who constantly express themselves in writing for many years so fully establish the graphic motor memories that they become relatively independent of the other word-centers. It follows that children always have auditory word memories first developed, the motor or verbal expression following. The visual and graphic memories then in turn are acquired. From these considerations we can understand how it is that apparently identical lesions may produce results differing in degree in different cases.

The stability of word memories depends upon the intensity with which they are imprinted upon the convolutions, either by some special emphasis or by frequent use and repetition. Thus, words as well as incidents that come with the shock, for instance, of fright, are always readily recalled. Every one knows the value of repetition in fixing a point in the student's mind. Nouns, being least frequently used, are the most easily displaced, and proper nouns suffer the earliest of all. Verbs, adjectives, adverbs, and prepositions follow in a methodical order, governed by the rule of depth of imprint due to repetition in daily use. This necessarily varies with the individual. An oft-repeated oath, yes, and no are the most persistent of all.

It sometimes happens that the word or phrase on the patient's lips, at the moment of the stroke producing the aphasia, remains his only vocal expression. This he repeats at every attempt to speak, being, as it were, saturated or intoxicated with it. It has been suggested that its imprint under the circumstances of the stroke has made it indelible. In writing, the same thing is often indicated by the repetition of letters or words. The name is usually signed promptly, if the patient has been accustomed to the act, which has in time become automatic. Sometimes only the first few letters of a word are accomplished, and then repeated again and again, or words are repeated. The tendency to echolalia is also very noticeable, the patient repeating some word or expression he has himself uttered or just heard others employ.

In many cases of aphasia the patient miscalls objects or uses wrong words, especially names and personal pronouns. This is denominated paraphasia, and is most marked in lesions of the auditory word memory depot. In this case the patient does not make persistent attempts to correct himself, as he is unable to recognize his own mistakes. When the auditory centers are not primarily involved paraphasia is recognized by the patient, who constantly manifests his annoyance at being unable to utter the proper word.

The mental capacity of aphasics varies greatly, and must be carefully estimated in a given case. As a rule, it is somewhat modified, as is clearly indicated by the changed temperament and disposition practically always present, even in the slightest cases. The organic mischief producing the cortical lesion may induce complete dementia, and in any event the mind works somewhat clumsily. According to Bastian and

others the sensory forms of aphasia, those due to auditory and visual disturbance, are more likely to present mental deterioration and to develop insanity than the motor varieties. In such cases hallucinations of sight and hearing, due to irritation of the cortex, are not infrequent. Besides the loss of visual word memories, the patient is unlikely to recall figures, algebraic or other conventional signs, and musical notation. Mind-blindness, in which all objects are unrecognized, their visual memories being destroyed, is due, it will be recalled, to a bilateral lesion. In some cases of auditory aphasia the patient has shown a loss of musical appreciation, a condition termed amusia, and, as far as music is an acquired educated faculty, it is presumably associated with the left temporal lobe. Most motor aphasics whistle or hum tunes with more or less precision, and cases are of record where motor speech was lost, but the patient could sing the words of a song correctly. One case recently seen replied "God damn" to every question, but got out most of the words of "Annie Rooney" with distinctness when he attempted to sing.

Secondary means of expression, such as pantomime, facial expression, and gestures, are usually retained, but in rare cases the patient neither correctly produces nor understands them. This may go to the extent of nodding the head when negation is intended. The loss of gesture and mimicry is called amimia; the misuse of these is paramimia. Emotional facial expression is generally retained, so that when the mind is not too much impaired the feelings of the patient are vividly portrayed in his countenance. There is some reason to locate these expressional centers in the basal ganglia, especially in the optic thalamus.

The motor cortex subserving speech is all within the domain of the middle cerebral artery, and aphasia is most frequently due to diseases of the branches or the trunk of this vessel. Trauma, meningitic disease, and new growths may also cause it. The most common simple variety of aphasia is the motor form, next the auditory, and then the visual. Distinct cases of graphic motor aphasia are extremely rare, but a convincing instance has been recorded. A combination of motor aphasia with the auditory and visual varieties is that ordinarily encountered. In this connection the various memory areas may be affected in different degree. No two cases in any one man's experience are exactly alike. Variations due to improvement or failure. in the various speech qualities in any given case furnish constant study. It is important to know the initial conditions, when usually the picture is complete, in order to estimate the extent of the lesion. After a few weeks or months, through education of the opposite cortex and partial local recovery, the clinical picture may be entirely altered and quite deceptive.

Before taking up the various forms of aphasia the reader is referred to the methods of examination in such cases described in Part I, page 23. It may be well to call attention to the fact that the blind read type with their fingers, and that the deaf, by lip reading, cultivate special verbal memories, which must be specially localized in the cortex. We must also bear in mind that the word and the object are not the same, but that one is the symbol, sign, or name of the other. The word