Chapter 3

Fig.5.—Left Hemisphere of Dog's Brain, after Ferrier.A, the fissure of Sylvius.B, the crucial sulcus.O, the olfactory bulb.I, II, III, IV,indicate the first, second, third, and fourth external convolutions respectively. (1), (4), and (5) are on thesigmoidgyrus.

Fig.5.—Left Hemisphere of Dog's Brain, after Ferrier.A, the fissure of Sylvius.B, the crucial sulcus.O, the olfactory bulb.I, II, III, IV,indicate the first, second, third, and fourth external convolutions respectively. (1), (4), and (5) are on thesigmoidgyrus.

Fig.6.—Left Hemisphere of Monkey's Brain. Outer Surface.

Fig.6.—Left Hemisphere of Monkey's Brain. Outer Surface.

Even when the entire motor zone of a dog is removed, there is no permanent paralysis of any part, but only this curious sort of relative inertia when the two sides of the body are compared; and this itself becomes hardly noticeable after a number of weeks have elapsed. Prof. Goltz has described a dog whose entire left hemisphere was destroyed, and who retained only a slight motor inertia on the right half of the body. In particular he could use his right paw for holding a bone whilst gnawing it, or for reaching after a piece of meat. Had he been taught to give his paw Before the operations, it would have been curious to see whether that faculty also came back. His tactile sensibility was permanently diminished on the right side.[12]Inmonkeysa genuine paralysis follows upon ablations of the cortex in the motor region. This paralysis affects parts of the body which vary with the brain-parts removed. The monkey's opposite arm or leg hangs flaccid, or at most takes a small part in associated movements. When the entire region is removed there is a genuine and permanent hemiplegia in which the arm is more affected than the leg; and this isfollowed months later by contracture of the muscles, as in man after inveterate hemiplegia.[13]According to Schaefer and Horsley, the trunk-muscles also become paralyzed after destruction of themarginalconvolution onbothsides (see Fig. 7). These differences between dogs and monkeys show the danger of drawing general conclusions from experiments done on any one sort of animal. I subjoin the figures given by the last-named authors of the motor regions in the monkey's brain.[14]

Fig.7.—Left Hemisphere of Monkey's Brain. Mesial Surface.

Fig.7.—Left Hemisphere of Monkey's Brain. Mesial Surface.

In manwe are necessarily reduced to the observationpost-mortemof cortical ablations produced by accident or disease (tumor, hemorrhage, softening, etc.). What results during life from such conditions is either localized spasm, or palsy of certain muscles of the opposite side. The cortical regions which invariably produce these results are homologous with those which we have just been studying in the dog, cat, ape, etc. Figs. 8 and 9 show the result of169 cases carefully studied by Exner. The parts shaded are regions where lesions producednomotor disturbance. Those left white were, on the contrary, never injured without motor disturbances of some sort. Where the injury to the cortical substance is profound in man, the paralysis is permanent and is succeeded by muscular rigidity in the paralyzed parts, just as it may be in the monkey.

Fig.8.—Right Hemisphere of Human Brain. Lateral Surface.

Fig.8.—Right Hemisphere of Human Brain. Lateral Surface.

Fig.9.—Right Hemisphere of Human Brain. Mesial Surface.

Fig.9.—Right Hemisphere of Human Brain. Mesial Surface.

(3)Descending degenerationsshow the intimate connection of the rolandic regions of the cortex with the motor tracts of the cord. When, either in man or in the lower animals, these regions are destroyed, a peculiar degenerative change known as secondary sclerosis is found to extend downwards through the white fibrous substance of the brain in a perfectly definite manner, affecting certain distinct strands which pass through the inner capsule, crura, and pons, into the anterior pyramids of the medulla oblongata, and from thence (partly crossing to the other side) downwards into the anterior (direct) and lateral (crossed) columns of the spinal cord.

(4)Anatomical proofof the continuity of the rolandic regions with these motor columns of the cord is also clearly given. Flechsig's 'Pyramidenbahn' forms an uninterrupted strand (distinctly traceable in human embryos, before its fibres have acquired their white 'medullary sheath') passing upwards from the pyramids of the medulla, and traversing the internal capsule and corona radiata to the convolutions in question (Fig. 10). None of the inferior gray matter of the brain seems to have any connection with this important fibrous strand. It passes directly from the cortex to the motor arrangements in the cord, depending for its proper nutrition (as the facts of degeneration show) on the influence of the cortical cells, just as motor nerves depend for their nutrition on that of the cells of the spinal cord. Electrical stimulation of this motor strand in any accessible part of its course has been shown in dogs to produce movements analogous to those which excitement of the cortical surface calls forth.

Fig.10.—Schematic Transverse Section of Brain showing Motor Strand.—After Edinger.

Fig.10.—Schematic Transverse Section of Brain showing Motor Strand.—After Edinger.

One of the most instructive proofs of motor localization in the cortex is that furnished by the disease now called aphemia, ormotor Aphasia. Motor aphasia is neither loss of voice nor paralysis of the tongue or lips. The patient's voice is as strong as ever, and all the innervations of his hypoglossal and facial nerves, except those necessary for speaking, may go on perfectly well. He can laugh and cry, and even sing; but he either is unable to utter any words at all; or a few meaningless stock phrases form his only speech; or else he speaks incoherently and confusedly, mispronouncing,misplacing, and misusing his words in various degrees. Sometimes his speech is a mere broth of unintelligible syllables. In cases of pure motor aphasia the patient recognizes his mistakes and suffers acutely from them. Now whenever a patient dies in such a condition as this, and an examination of his brain is permitted, it is found thatthe lowest frontal gyrus (see Fig. 11) is the seat of injury. Broca first noticed this fact in 1861, and since then the gyrus has gone by the name of Broca's convolution. The injury in right-handed people is found on the left hemisphere, and in left-handed people on the right hemisphere. Most people, in fact, are left-brained, that is, all their delicate and specialized movements are handed over to the charge of the left hemisphere. The ordinary right-handedness for such movements is only a consequence of that fact, a consequence which shows outwardly on account of that extensive decussation of the fibres whereby most of those from the left hemisphere pass to the right half of the body only. But the left-brainedness might exist in equal measure and not show outwardly. This would happen wherever organs onbothsides of the body could be governed by the left hemisphere; and just such a case seems offered by the vocal organs, in that highly delicate and special motor service which we call speech. Either hemispherecaninnervate them bilaterally, just as either seems able to innervate bilaterally the muscles of the trunk, ribs, and diaphragm. Of the special movements of speech, however,it would appear (from the facts of aphasia) that the left hemisphere in most persons habitually takes exclusive charge. With that hemisphere thrown out of gear, speech is undone; even though the opposite hemisphere still be there for the performance of less specialized acts, such as the various movements required in eating.

Fig.11.—Schematic Profile of Left Hemisphere, with the parts shaded whose destruction causes motor ('Broca') and sensory ('Wernicke') Aphasia.

Fig.11.—Schematic Profile of Left Hemisphere, with the parts shaded whose destruction causes motor ('Broca') and sensory ('Wernicke') Aphasia.

It will be noticed that Broca's region is homologous with the parts ascertained to produce movements of the lips, tongue, and larynx when excited by electric currents in apes (cf. Fig. 6). The evidence is therefore as complete as it well can be that the motor incitations to these organs leave the brain by the lower frontal region.

Victims of motor aphasia generally have other disorders. One which interests us in this connection has been calledagraphia: they have lost the power towrite. They can read writing and understand it; but either cannot use the pen at all or make egregious mistakes with it. The seat of the lesion here is less well determined, owing to an insufficient number of good cases to conclude from.[15]There is no doubt, however, that it is (in right-handed people) on the left side, and little doubt that it consists of elements of the hand-and-arm region specialized for that service, The symptom may exist when there is little or no disability in the hand for other uses. If it does not get well, the patient usually educates his right hemisphere, i.e. learns to write with his left hand. In other cases of which we shall say more a few pages later on, the patient can write both spontaneously and at dictation, but cannotreadeven what he has himself written! All these phenomena are now quite clearly explained by separate brain-centres for the various feelings and movements and tracts for associating these together. But their minute discussion belongs to medicine rather than to general psychology, and I can only use them here to illustrate the principles of motor localization.[16]Under the heads of sight and hearing I shall have a little more to say.

The different lines of proof which I have taken up establish conclusively the proposition thatall the motor impulses which leave the cortex pass out, in healthy animals,from the convolutions about the fissure of Rolando.

When, however, it comes to defining precisely what is involved in a motor impulse leaving the cortex, things grow more obscure. Does the impulse start independently from the convolutions in question, or does it start elsewhere and merely flow through? And to what particular phase of psychic activity does the activity of these centres correspond? Opinions and authorities here divide; but it will be better, before entering into these deeper aspects of the problem, to cast a glance at the facts which have been made out concerning the relations of the cortex to sight, hearing, and smell.

Ferrier was the first in the field here. He found, when theangularconvolution (that lying between the 'intra parietal' and 'external occipital' fissures, and bending round the top of the fissure of Sylvius, in Fig. 6) was excited in the monkey, that movements of the eyes and head as if for vision occurred; and that when it was extirpated, what he supposed to be total and permanent blindness of the opposite eye followed. Munk almost immediately declared total and permanent blindness to follow from destruction of theoccipital lobein monkeys as well as dogs, and said that the angular gyrus had nothing to do with sight, but was only the centre for tactile sensibility of the eyeball. Hunk's absolute tone about his observations and his theoretic arrogance have led to his ruin as an authority. But he did two things of permanent value. He was the first to distinguish in these vivisections between sensorial andpsychicblindness, and to describe the phenomenon ofrestitutionof the visual function after its first impairment by an operation; and the first to notice thehemiopiccharacter of the visual disturbances which result when only one hemisphere is injured. Sensorial blindness is absolute insensibility to light; psychic blindness is inability to recognize themeaningof the optical impressions, as when wesee a page of Chinese print but it suggests nothing to us. A hemiopic disturbance of vision is one in which neither retina is affected in its totality, but in which, for example, the left portion ofeachretina is blind, so that the animal sees nothing situated in space towards its right. Later observations have corroborated this hemiopic character of all the disturbances of sight from injury to a single hemisphere in the higher animals; and the question whether an animal's apparent blindness is sensorial or only psychic has, since Munk's first publications, been the most urgent one to answer, in all observations relative to the function of sight.

Goltz almost simultaneously with Ferrier and Munk reported experiments which led him to deny that the visual function was essentially bound up with any one localized portion of the hemispheres. Other divergent results soon came in from many quarters, so that, without going into the history of the matter any more, I may report the existing state of the case as follows:[17]

Infishes, frogs, andlizardsvision persists when the hemispheres are entirely removed. This is admitted for frogs and fishes even by Munk, who denies it for birds.

All of Munk'sbirdsseemed totally blind (blind sensorially) after removal of the hemispheres by his operation. The following of a candle by the head and winking at a threatened blow, which are ordinarily held to prove the retention of crude optical sensations by the lower centres in supposed hemisphereless pigeons, are by Munk ascribed to vestiges of the visual sphere of the cortex left behind by the imperfection of the operation. But Schrader, who operated after Munk and with every apparent guarantee of completeness, found that all his pigeons saw after two or three weeks had elapsed, and the inhibitions resulting from the wound had passed away. They invariably avoided even the slightest obstacles, flew very regularly towards certain perches, etc., differingtoto cœloin these respects with certain simplyblindedpigeons who were kept withthem for comparison. They did not pick up food strewn on the ground, however. Schrader found that they would do this if even a small part of the frontal region of the hemispheres was left, and ascribes their non-self-feeding when deprived of their occipital cerebrum not to a visual, but to a motor, defect, a sort of alimentary aphasia.[18]

In presence of such discord as that between Munk and his opponents one must carefully note how differently significant isloss, frompreservation, of a function after an operation on the brain. Thelossof the function does not necessarily show that itisdependent on the part cut out; but itspreservationdoes show that it isnotdependent: and this is true though the loss should be observed ninety-nine times and the preservation only once in a hundred similar excisions. That birds and mammalscanbe blinded by cortical ablation is undoubted; the only question is,mustthey be so? Only then can the cortex be certainly called the 'seat of sight.' The blindness may always be due to one of those remote effects of the wound on distant parts, inhibitions, extensions of inflammation,—interferences, in a word,—upon which Brown-Séquard and Goltz have rightly insisted, and the importance of which becomes more manifest every day. Such effects are transient; whereas thesymptoms of deprivation(Ausfallserscheinungen, as Goltz calls them) which come from the actual loss of the cut-out region must from the nature of the case be permanent. Blindness in the pigeons,so far as it passes away, cannot possibly be charged to their seat of vision being lost, but only to some influence which temporarily depresses the activity of that seat. The same is truemutatis mutandisof all the other effects of operations, and as we pass to mammals we shall see still more the importance of the remark.

In rabbitsloss of the entire cortex seems compatible with the preservation of enough sight to guide the poor animals' movements, and enable them to avoid obstacles. Christiani's observations and discussions seem conclusivelyto have established this, although Munk found that allhisanimals were made totally blind.[19]

In dogsalso Munk found absolute stone-blindness after ablation of the occipital lobes. He went farther and mapped out determinate portions of the cortex thereupon, which he considered correlated with definite segments of the two retinæ, so that destruction of given portions of the cortex produces blindness of the retinal centre, top, bottom, or right or left side, of the same or opposite eye. There seems little doubt that this definite correlation is mythological. Other observers, Hitzig, Goltz, Luciani, Loeb, Exner, etc., find, whatever part of the cortex may be ablated on one side, that there usually results ahemiopicdisturbance ofbotheyes, slight and transient when the anterior lobes are the parts attacked, grave when an occipital lobe is the seat of injury, and lasting in proportion to the latter's extent. According to Loeb, the defect is a dimness of vision ('hemiamblyopia') in which (however severe) the centres remain the best seeing portions of the retina, just as they are in normal dogs. The lateral or temporal part of each retina seems to be in exclusive connection with the cortex of its own side. The centre and nasal part of each seems, on the contrary, to be connected with the cortex of the opposite hemispheres. Loeb, who takes broader views than any one, conceives the hemiamblyopia as he conceives the motor disturbances, namely, as the expression of an increased inertia in the whole optical machinery, of which the result is to make the animal respond with greater effort to impressions coming from the half of space opposed to the side of the lesion. If a dog has right hemiamblyopia, say, and two pieces of meat are hung before him at once, he invariably turns first to the one on his left. But if the lesion be a slight one,shakingslightly the piece of meat on his right (this makes of it a stronger stimulus) makes him seize upon it first. If only one piece of meat be offered, he takes it, on whichever side it be.

EngravingsFigs.12 and 13. The Dog's visual centre according to Munk, the entire striated region,A, A, being the exclusive seat of vision, and the dark central circle,A1, being correlated with the retinal centre of the opposite eye.

Figs.12 and 13. The Dog's visual centre according to Munk, the entire striated region,A, A, being the exclusive seat of vision, and the dark central circle,A1, being correlated with the retinal centre of the opposite eye.

When both occipital lobes are extensively destroyed total blindness may result. Munk maps out his 'Sehsphäre'definitely, and says that blindnessmustresult when the entire shaded part, markedA, A,in Figs. 12 and 13, is involved in the lesion. Discrepant reports of other observations he explains as due to incomplete ablation. Luciani, Goltz, and Lannegrace, however, contend that they have made complete bilateral extirpations of Munk's Sehsphäre more than once, and found a sort of crude indiscriminating sight of objects to return in a few weeks.[20]The question whether a dog is blind or not is harder to solve than would at first appear; for simply blinded dogs, in places to which they are accustomed, show little of their loss and avoid all obstacles; whilst dogs whose occipital lobes are gone may run against things frequently and yet see notwithstanding. The best proof that they may see is that which Goltz's dogs furnished: they carefully avoided, as it seemed, strips of sunshine or paper on the floor, as if they were solid obstacles. This no really blind dog would do. Luciani tested his dogs when hungry (a condition which sharpens their attention) by strewingpieces of meat and pieces of cork before them. If they went straight at them, theysaw; and if they chose the meat and left the cork, theysaw discriminatingly. The quarrel is very acrimonious; indeed the subject of localization of functions in the brain seems to have a peculiar effect on the temper of those who cultivate it experimentally. The amount of preserved vision which Goltz and Luciani report seems hardly to be worth considering, on the one hand; and on the other, Munk admits in his penultimate paper that out of 85 dogs he only 'succeeded' 4 times in his operation of producing complete blindness by complete extirpation of his 'Sehsphäre.'[21]The safe conclusion forusis that Luciani's diagram, Fig. 14, represents something like the truth. The occipital lobes are far more important for vision than any other part of the cortex, so that their complete destruction makes the animal almost blind. As for the crude sensibility to light whichmaythen remain, nothing exact is known either about its nature or its seat.

Fig.14.—Distribution of the Visual Function in the Cortex, according to Luciani.

Fig.14.—Distribution of the Visual Function in the Cortex, according to Luciani.

In the monkey, doctors also disagree. The truth seems, however, to be that theoccipital lobesin this animal also are the part connected most intimately with the visual function. The function would seem to go on when very small portions of them are left, for Ferrier found no 'appreciable impairment' of it after almost complete destruction of them on both sides. On the other hand, he found complete and permanent blindness to ensue when they and theangular gyriin addition were destroyed on both sides. Munk, as well asBrown and Schaefer, found no disturbance of sight from destroying theangular gyrialone, although Ferrier found blindness to ensue. This blindness was probably due to inhibitions exertedin distans, or to cutting of the white optical fibres passing under the angular gyri on their way to the occipital lobes. Brown and Schaefer got complete and permanent blindness in one monkey from total destruction of both occipital lobes. Luciani and Seppili, performing this operation on two monkeys, found that the animals were only mentally, not sensorially, blind. After some weeks they saw their food, but could not distinguish by sight between figs and pieces of cork. Luciani and Seppili seem, however, not to have extirpated the entire lobes. When one lobe only is injured the affection of sight is hemiopic in monkeys: in this all observers agree. On the whole, then, Munk's original location of vision in the occipital lobes is confirmed by the later evidence.[22]

In manwe have more exact results, since we are not driven to interpret the vision from the outward conduct. On the other hand, however, we cannot vivisect, but must wait for pathological lesions to turn up. The pathologists who have discussed these (the literature is tediousad libitum) conclude that the occipital lobes are the indispensable part for vision in man. Hemiopic disturbance in both eyes comes from lesion of either one of them, and total blindness, sensorial as well as psychic, from destruction of both.

Hemiopia may also result from lesion in other parts, especially the neighboring angular and supra-marginal gyri, and it may accompany extensive injury in the motor region of the cortex. In these cases it seems probable that it is due to anactio in distans, probably to the interruption offibres proceeding from the occipital lobe. There seem to be a few cases on record where there was injury to the occipital lobes without visual defect. Ferrier has collected as many as possible to prove his localization in the angular gyrus.[23]A strict application of logical principles would make one of these cases outweigh one hundred contrary ones. And yet, remembering how imperfect observations may be, and how individual brains may vary, it would certainly be rash for their sake to throw away the enormous amount of positive evidence for the occipital lobes. Individual variability is always apossibleexplanation of an anomalous case. There is no more prominent anatomical fact than that of the 'decussation of the pyramids,' nor any more usual pathological fact than its consequence, that left-handed hemorrhages into the motor region produce right-handed paralyses. And yet the decussation is variable in amount, and seems sometimes to be absent altogether.[24]If, in such a case as this last, the left brain were to become the seat of apoplexy, the left and not the right half of the body would be the one to suffer paralysis.

Theschemabelow [Fig. 15], copied from Dr. Seguin, expresses, on the whole, the probable truth about the regions concerned in vision. Not the entire occipital lobes, but the so-called cunei, and the first convolutions, are the cortical parts most intimately concerned. Nothnagel agrees with Seguin in this limitation of the essential tracts.[25]

Fig.15.—Scheme of the mechanism of vision, after Seguin. Thecuneusconvolution (Cu) of the right occipital lobe is supposed to be injured, and all the parts which lead to it are darkly shaded to show that they fail to exert their function.F. O.are the intra-hemispheric optical fibres.P. O. C.is the region of the lower optic centres (corpora geniculata and quadrigemina).T. O. D.is the right optic tract;C, the chiasma;F. L. D.are the fibres going to the lateral or temporal halfTof the right retina; andF. C. S.are those going to the central or nasal half of the left retina.O. D.is the right, andO. S.the left eyeball. The rightward half of each is therefore blind: in other words, the right nasal field,R. N. F., and the left temporal fieldL. T. F., have become invisible to the subject with the lesion atCu.

Fig.15.—Scheme of the mechanism of vision, after Seguin. Thecuneusconvolution (Cu) of the right occipital lobe is supposed to be injured, and all the parts which lead to it are darkly shaded to show that they fail to exert their function.F. O.are the intra-hemispheric optical fibres.P. O. C.is the region of the lower optic centres (corpora geniculata and quadrigemina).T. O. D.is the right optic tract;C, the chiasma;F. L. D.are the fibres going to the lateral or temporal halfTof the right retina; andF. C. S.are those going to the central or nasal half of the left retina.O. D.is the right, andO. S.the left eyeball. The rightward half of each is therefore blind: in other words, the right nasal field,R. N. F., and the left temporal fieldL. T. F., have become invisible to the subject with the lesion atCu.

A most interesting effect of cortical disorder ismental blindness. This consists not so much in insensibility to optical impressions, as ininability to understand them. Psychologically it is interpretable asloss of associationsbetween optical sensations and what they signify; and any interruption of the paths between the optic centres and the centres for other ideas ought to bring it about. Thus,printed letters of the alphabet, or words, signify certain sounds and certain articulatory movements. If the connection between the articulating or auditory centres, on the one hand, and the visual centres on the other, be ruptured we oughta priorito expect that the sight of words would fail to awaken the idea of their sound, or the movement for pronouncing them. We ought, in short, to havealexia, or inability to read: and this is just what we do have in manycases of extensive injury about the fronto-temporal regions, as a complication ofaphasicdisease. Nothnagel suggests that whilst thecuneusis the seat of opticalsensations, the other parts of the occipital lobe may be the field of opticalmemories and ideas, from the loss of which mental blindness should ensue. In fact, all the medical authors speak of mental blindness as if it must consist in the loss of visual images from the memory. It seems to me, however, that this is a psychological misapprehension. A man whose power of visual imagination has decayed (no unusual phenomenon in its lighter grades) is not mentally blind in the least, for he recognizes perfectly all that he sees. On the other hand, hemaybe mentally blind, with his optical imagination well preserved; as in the interesting case published by Wilbrand in 1887.[26]In the still more interesting case of mental blindness recently published by Lissauer,[27]though the patient made the most ludicrous mistakes, calling for instance a clothes-brush a pair of spectacles, an umbrella a plant with flowers, an apple a portrait of a lady, etc. etc., he seemed, according to the reporter, to have his mental images fairly well preserved. It is in fact the momentary loss of ournon-optical images which makes us mentally blind, just as it is that of ournon-auditory images which makes us mentally deaf. I am mentally deaf if,hearinga bell, I can't recall how itlooks; and mentally blind if,seeingit, I can't recall itssound or its name. As a matter of fact, I should have to be not merely mentally blind, but stone-blind, if all my visual images were lost. For although I am blind to the right half of the field of view if my left occipital region is injured, and to the left half if my right region is injured, such hemianopsia does not deprive me of visualimages, experience seeming to show that the unaffected hemisphere is always sufficient for production of these. To abolish them entirely I should have to be deprived of both occipital lobes, and that would deprive me not only of my inward images of sight, but of mysight altogether.[28]Recent pathological annals seem to offer a few such cases.[29]Meanwhile there are a number of cases of mental blindness, especially for written language, coupled with hemianopsia, usually of the rightward field of view. These are all explicable by the breaking down, through disease, of theconnecting tractsbetween the occipital lobes and other parts of the brain, especially those which go to the centres for speech in the frontal and temporal regions of the left hemisphere. They are to be classed among disturbances ofconductionor ofassociation; and nowhere can I find any fact which should force us to believe that optical images need[30]be lost in mental blindness, or that the cerebral centres for such images are locally distinct from those for direct sensations from the eyes.[31]

Where an object fails to be recognized by sight, it often happens that the patient will recognize and name it as soon as he touches it with his hand. This shows in an interestingway how numerous the associative paths are which all end by running out of the brain through the channel of speech. The hand-path is open, though the eye-path be closed. When mental blindness is most complete, neither sight, touch, nor sound avails to steer the patient, and a sort of dementia which has been calledasymboliaorapraxiais the result. The commonest articles are not understood. The patient will put his breeches on one shoulder and his hat upon the other, will bite into the soap and lay his shoes on the table, or take his food into his hand and throw it down again, not knowing what to do with it, etc. Such disorder can only come from extensive brain-injury.[32]

Themethod of degenerationcorroborates the other evidence localizing the tracts of vision. In young animals one gets secondary degeneration of the occipital regions from destroying an eyeball, and,vice versâ, degeneration of the optic nerves from destroying the occipital regions. The corpora geniculata, thalami, and subcortical fibres leading to the occipital lobes are also found atrophied in these cases. The phenomena are not uniform, but are indisputable;[33]so that, taking all lines of evidence together, the special connection of vision with the occipital lobes is perfectly made out. It should be added, that the occipital lobes have frequently been found shrunken in cases of inveterate blindness in man.

Hearing is hardly as definitely localized as sight.In the dog, Luciani's diagram will show the regions which directly or indirectly affect it for the worse when injured. As with sight, one-sided lesions produce symptoms on both sides. The mixture of black dots and gray dots in the diagram is meant to represent this mixture of 'crossed' and 'uncrossed' connections, though of course no topographical exactitude is aimed at. Of all the region, the temporal lobe is the most important part; yet permanent absolute deafness did notresult in a dog of Luciani's, even from bilateral destruction of both temporal lobes in their entirety.[34]

Fig.16.—Luciani's Hearing Region.

Fig.16.—Luciani's Hearing Region.

In the monkey, Ferrier and Yeo once found permanent deafness to follow destruction of the upper temporal convolution (the one just below the fissure of Sylvius in Fig. 6) on both sides. Brown and Schaefer found, on the contrary, that in several monkeys this operation failed to noticeably affect the hearing. In one animal, indeed, both entire temporal lobes were destroyed. After a week or two of depression of the mental faculties this beast recovered and became one of the brightest monkeys possible, domineering over all his mates, and admitted by all who saw him to have all his senses, including hearing, 'perfectly acute.'[35]Terrible recriminations have, as usual, ensued between the investigators, Ferrier denying that Brown and Schaefer's ablations were complete,[36]Schaefer that Ferrier's monkey was really deaf.[37]In this unsatisfactory condition the subject must be left, although there seems no reason to doubt that Brown and Schaefer's observation is the more important of the two.

In manthe temporal lobe is unquestionably the seat of the hearing function, and the superior convolution adjacent to the sylvian fissure is its most important part. The phenomena of aphasia show this. We studied motor aphasia a few pages back; we must now considersensory aphasia.Our knowledge of this disease has had three stages: we may talk of the period of Broca, the period of Wernicke, and the period of Charcot. What Broca's discovery was we have seen. Wernicke was the first to discriminate those cases in which the patient cannot even understandspeech from those in which he can understand, only not talk; and to ascribe the former condition to lesion of the temporal lobe.[38]The condition in question isword-deafness, and the disease isauditory aphasia. The latest statistical survey of the subject is that by Dr. Allen Starr.[39]In the seven cases ofpureword-deafness which he has collected, cases in which the patient could read, talk, and write, but not understand what was said to him, the lesion was limited to the first and second temporal convolutions in their posterior two thirds. The lesion (in right-handed, i.e. left-brained, persons) is always on the left side, like the lesion in motor aphasia. Crude hearing would not be abolished, even were the left centre for it utterly destroyed; the right centre would still provide for that. But thelinguistic useof hearing appears bound up with the integrity of the left centre more or less exclusively. Here it must be that words heard enter into association with the things which they represent, on the one hand, and with the movements necessary for pronouncing them, on the other. In a large majority of Dr. Starr's fifty cases, the power either to name objects or to talk coherently was impaired. This shows that in most of us (as Wernicke said) speech must go on from auditory cues; that is, it must be that our ideas do not innervate our motor centres directly, but only after first arousing the mental sound of the words. This is the immediate stimulus to articulation; and where the possibility of this is abolished by the destruction of its usual channel in the left temporal lobe, the articulation must suffer. In the few cases in which the channel is abolished with no bad effect on speech we must suppose an idiosyncrasy. The patient must innervate his speech-organs either from the corresponding portion of the other hemisphere or directly from the centres of ideation,those, namely, of vision, touch, etc., without leaning on the auditory region. It is the minuter analysis of the facts in the light of such individual differences as these which constitutes Charcot's contribution towards clearing up the subject.

Every nameable thing, act, or relation has numerous properties, qualities, or aspects. In our minds the properties of each thing, together with its name, form an associated group. If different parts of the brain are severally concerned with the several properties, and a farther part with the hearing, and still another with the uttering, of the name, there must inevitably be brought about (through the law of association which we shall later study) such a dynamic connection amongst all these brain-parts that the activity of any one of them will be likely to awaken the activity of all the rest. When we are talking as we think, theultimateprocess is that of utterance. If the brain-part forthatbe injured, speech is impossible or disorderly, even though all the other brain-parts be intact: and this is just the condition of things which, onpage 37, we found to be brought about by limited lesion of the left inferior frontal convolution. But back of that last act various orders of succession are possible in the associations of a talking man's ideas. The more usual order seems to be from the tactile, visual, or other properties of the things thought-about to the sound of their names, and then to the latter's utterance. But if in a certain individual the thought of thelookof an object or of thelookof its printed name be the process which habitually precedes articulation, then the loss of thehearingcentre willpro tantonot affect that individual's speech. He will be mentally deaf, i.e. hisunderstandingof speech will suffer, but he will not be aphasic. In this way it is possible to explain the seven cases ofpureword-deafness which figure in Dr. Starr's table.

If this order of association be ingrained and habitual in that individual, injury to hisvisualcentres will make him not only word-blind, but aphasic as well. His speech will become confused in consequence of an occipital lesion. Naunyn, consequently, plotting out on a diagram of the hemisphere the 71 irreproachably reported cases ofaphasia which he was able to collect, finds that the lesions concentrate themselves in three places: first, on Broca's centre; second, on Wernicke's; third, on the supra-marginal and angular gyri under which those fibres pass which connect the visual centres with the rest of the brain[40](see Fig. 17). With this result Dr. Starr's analysis of purely sensory cases agrees.

Fig.17.

Fig.17.

In a later chapter we shall again return to these differences in the effectiveness of the sensory spheres in different individuals. Meanwhile few things show more beautifully than the history of our knowledge of aphasia how the sagacity and patience of many banded workers are in time certain to analyze the darkest confusion into an orderly display.[41]There is no 'centre of Speech' in the brain any more than there is a faculty of Speech in the mind. The entire brain, more or less, is at work in a man who uses language. The subjoined diagram, from Boss, shows the four parts most critically concerned, and, in the light of our text, needs no farther explanation (see Fig. 18).

Fig.18.

Fig.18.

Everything conspires to point to the median descending part of the temporal lobes as being the organs of smell. Even Ferrier and Munk agree on the hippocampal gyrus, though Ferrier restricts olfaction, as Munk does not, to the lobule or uncinate process of the convolution, reserving the rest of it for touch. Anatomy and pathology also point to the hippocampal gyrus; but as the matter is less interesting from the point of view of human psychology than were sight and hearing, I will say no more, but simply add Luciani and Seppili's diagram of the dog's smell-centre.[42]Of

we know little that is definite. What little there is points to the lower temporal regions again. Consult Ferrier as below.

Fig.19.—Luciani's Olfactory Region in the Dog.

Fig.19.—Luciani's Olfactory Region in the Dog.

Interesting problems arise with regard to the seat of tactile and muscular sensibility. Hitzig, whose experiments ondogs' brainsfifteen years ago opened the entire subject which we are discussing, ascribed the disorders of motility observed after ablations of the motor region to a loss of what he called muscular consciousness. The animals do not notice eccentric positions of their limbs, will stand with their legs crossed, with the affected paw resting on its back or hanging over a table's edge, etc.; and do not resist our bending and stretching of it as they resist with the unaffected paw. Goltz, Munk, Schiff, Herzen, and others promptly ascertained an equal defect of cutaneous sensibility to pain, touch, and cold. The paw is not withdrawn when pinched, remains standing in cold water, etc. Ferrier meanwhile denied that there was any true anæsthesia produced by ablations in the motor zone, and explains the appearance of it as an effect of the sluggish motor responses of the affected side.[43]Munk[44]and Schiff[45], on thecontrary, conceive of the 'motor zone' as essentially sensory, and in different ways explain the motor disorders as secondary results of the anæsthesia which is always there, Munk calls the motor zone the Fühlsphäre of the animal's limbs, etc., and makes it coördinate with the Sehsphäre, the Hörsphäre, etc., the entire cortex being, according to him, nothing but a projection-surface for sensations, with no exclusively or essentially motor part. Such a view would be important if true, through its bearings on the psychology of volition. What is the truth? As regards the fact of cutaneous anæsthesia from motor-zone ablations, all other observers are against Ferrier, so that he is probably wrong in denying it. On the other hand, Munk and Schiff are wrong in making the motor symptomsdependon the anæsthesia, for in certain rare cases they have been observed to exist not only without insensibility, but with actual hyperæsthesia of the parts.[46]The motor and sensory symptoms seem, therefore, to be independent variables.

In monkeysthe latest experiments are those of Horsley and Schaefer,[47]whose results Ferrier accepts. They find that excision of the hippocampal convolution produces transient insensibility of the opposite side of the body, and that permanent insensibility is produced by destruction of its continuation upwards above the corpus callosum, the so-calledgyrus fornicatus(the part just below the 'calloso-marginal fissure' in Fig. 7). The insensibility is at its maximum when the entire tract comprising both convolutions is destroyed. Ferrier says that the sensibility of monkeys is 'entirely unaffected' by ablations of the motor zone,[48]and Horsley and Schaefer consider it by no means necessarilyabolished.[49]Luciani found it diminished in his three experiments on apes.[50]


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