Principles Of Psychology Vol1
The Localization of Functions in the Hemispheres
Up to 1870, the opinion which prevailed was that which the experiments of Flourens on pigeons’ brains had made plausible, namely, that the different functions of the hemispheres were not locally separated, but carried on each by the aid of the whole organ. Hitzig in 1870 showed, however, that in a dog’s brain highly specialized movements could be produced by electric irritation of determinate regions of the cortex; and Ferrier and Munk, half a dozen years later, seemed to prove, either by irritations or excisions or both, that there were equally determinate regions connected with the senses of sight, touch, hearing, and smell. Munk’s special sensorial localizations, however, disagreed with Ferrier’s; and Goltz, from his extirpation-experiments, came to a conclusion adverse to strict localization of any kind. The controversy is not yet over. I will not pretend to say anything more of it historically, but give a brief account of the condition in which matters at present stand.
The one thing which is perfectly well established is this, that the ‘central’ convolutions, on either side of the fissure of Rolando, and (at least in the monkey) the calloso-marginal convolution (which is continuous with them on the mesial surface where one hemisphere is applied against the other), form the region by which all the motor incitations which leave the cortex pass out, on their way to those executive centres in the region of the pons, medulla, and spinal cord from which the muscular contractions are discharged in the last resort. The existence of this so-called ‘motor zone’ is established by the lines of evidence successively given below:
(1) Cortical Irritations. Electrical currents of small intensity applied to the surface of the said convolutions in dogs, monkeys, and other animals, produce well-defined movements in face, fore-limb, hind-limb, tail, or trunk, according as one point or another of the surface is irritated. These movements affect almost invariably the side opposite to the brain irritations: If the left hemisphere be excited, the movement is of the right leg, side of face, etc. All the objections at first raised against the validity of these experiments have been overcome. The movements are certainly not due to irritations of the base of the brain by the downward spread of the current, for: a) mechanical irritations will produce them, though less easily than electrical; b) shifting the electrodes to a point close by on the surface changes the movement in ways quite inexplicable by changed physical conduction of the current; c) if the cortical ‘centre’ for a certain movement be cut under with a sharp knife but left in situ, although the electric conductivity is physically unaltered by the operation, the physiological conductivity is gone and currents of the same strength no longer produce the movements which they did; d) the time-interval between the application of the electric stimulus to the cortex and the resultant movement is what it would be if the cortex acted physiologically and not merely physically in transmitting the irritation. It is namely a well-known fact that when a nerve-current has to pass through the spinal cord to excite a muscle by reflex action, the time is longer than if it passes directly down the motor nerve: the cells of the cord take a certain time to discharge. Similarly, when a stimulus is applied directly to the cortex the muscle contracts two or three hundredths of a second later than it does when the place on the cortex is cut away and the electrodes are applied to the white fibres below.
(2) Cortical Ablations. When the cortical spot which is found to produce a movement of the fore-leg, in a dog, is excised (see spot 5 in Fig. 5), the leg in question becomes peculiarly affected. At first it seems paralyzed. Soon, however, it is used with the other legs, but badly. The animal does not bear his weight on it, allows it to rest on its dorsal surface, stands with it crossing the other leg, does not remove it if it hangs over the edge of a table, can no longer ‘give the paw’ at word of command if able to do so before the operation, does not use it for scratching the ground, or holding a bone as formerly, lets it slip out when running on a smooth surface or when shaking himself, etc., etc. Sensibility of all kinds seems diminished as well as motility, but of this I shall speak later on. Moreover the dog tends in voluntary movements to swerve towards the side of the brain-lesion instead of going straight forward. All these symptoms gradually decrease, so that even with a very severe brain-lesion the dog may be outwardly indistinguishable from a well dog after eight or ten weeks. Still, a slight chloroformization will reproduce the disturbances, even then. There is a certain appearance of ataxic in-coordination in the movements—the dog lifts his fore-feet high and brings them down with more strength than usual, and yet the trouble is not ordinary lack of co-ordination. Neither is there paralysis. The strength of whatever movements are made is as great as ever—dogs with extensive destruction of the motor zone can jump as high and bite as hard as ever they did, but they seem less easily moved to do anything with the affected parts. Dr. Loeb, who has studied the motor disturbances of dogs more carefully than any one, conceives of them en masse as effects of an increased inertia in all the processes of innervation towards the side opposed to the lesion. All such movements require an unwonted effort for their execution; and when only the normally usual effort is made they fall behind in effectiveness.
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. In monkeys a 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 is followed months later by contracture of the muscles, as in man after inveterate hemiplegia. According to Schaefer and Horsley, the trunk-muscles also become paralyzed after destruction of the marginal convolution on both sides (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.
In man we are necessarily reduced to the observation post-mortem of 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 of 169 cases carefully studied by Exner. The parts shaded are regions where lesions produced no motor 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.
(3) Descending degenerations show 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 proof of 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.
One of the most instructive proofs of motor localization in the cortex is that furnished by the disease now called aphemia, or motor 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 that the 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 on both sides 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 hemisphere can innervate 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.
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 called agraphia: they have lost the power to write. 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. 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 cannot read even 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. 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 that all 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.
Sight.
Ferrier was the first in the field here. He found, when the angular convolution (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 the occipital lobe in 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. Munk’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 and psychic blindness, and to describe the phenomenon of restitution of the visual function after its first impairment by an operation; and the first to notice the hemiopic character 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 the meaning of the optical impressions, as when we see 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 of each retina 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:
In fishes, frogs, and lizards vision 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’s birds seemed 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., differing toto cœlo in these respects with certain simply blinded pigeons who were kept with them 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.
In presence of such discord as that between Munk and his opponents one must carefully note how differently significant is loss, from preservation, of a function after an operation on the brain. The loss of the function does not necessarily show that it is dependent on the part cut out; but its preservation does show that it is not dependent: 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 mammals can be blinded by cortical ablation is undoubted; the only question is, must they 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 the symptoms 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 true mutatis mutandis of all the other effects of operations, and as we pass to mammals we shall see still more the importance of the remark.
In rabbits loss 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 conclusively to have established this, although Munk found that all his animals were made totally blind.
In dogs also 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 a hemiopic disturbance of both eyes, 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, shaking slightly 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.
When both occipital lobes are extensively destroyed total blindness may result. Munk maps out his ‘Sehsphäre’ definitely, and says that blindness must result when the entire shaded part, marked A, 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. 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 strewing pieces of meat and pieces of cork before them. If they went straight at them, they saw; and if they chose the meat and left the cork, they saw 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.’ The safe conclusion for us is 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 which may then remain, nothing exact is known either about its nature or its seat.
In the monkey, doctors also disagree. The truth seems, however, to be that the occipital lobes in 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 the angular gyri in addition were destroyed on both sides. Munk, as well as Brown and Schaefer, found no disturbance of sight from destroying the angular gyri alone, although Ferrier found blindness to ensue. This blindness was probably due to inhibitions exerted in 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.
In man we 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 tedious ad 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 an actio in distans, probably to the interruption of fibres 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. 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 a possible explanation 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. 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.
The schema below [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.
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A most interesting effect of cortical disorder is mental blindness. This consists not so much in insensibility to optical impressions, as in inability to understand them. Psychologically it is interpretable as loss of associations between 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 ought a priori to 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 have alexia, or inability to read: and this is just what we do have in many cases of extensive injury about the fronto-temporal regions, as a complication of aphasic disease. Nothnagel suggests that whilst the cuneus is the seat of optical sensations, the other parts of the occipital lobe may be the field of optical memories 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, he may be mentally blind, with his optical imagination well preserved; as in the interesting case published by Wilbrand in 1887. In the still more interesting case of mental blindness recently published by Lissauer, 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 our non-optical images which makes us mentally blind, just as it is that of our non-auditory images which makes us mentally deaf. I am mentally deaf if, hearing a bell, I can’t recall how it looks; and mentally blind if, seeing it, I can’t recall its sound 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 visual images, 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 my sight altogether. Recent pathological annals seem to offer a few such cases. 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 the connecting tracts between 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 of conduction or of association; and nowhere can I find any fact which should force us to believe that optical images need be lost in mental blindness, or that the cerebral centres for such images are locally distinct from those for direct sensations from the eyes.
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 interesting way 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 called asymbolia or apraxia is 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.
The method of degeneration corroborates 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; 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.
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 not result in a dog of Luciani’s, even from bilateral destruction of both temporal lobes in their entirety.
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.’ Terrible recriminations have, as usual, ensued between the investigators, Ferrier denying that Brown and Schaefer’s ablations were complete, Schaefer that Ferrier’s monkey was really deaf. 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 man the 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 consider sensory 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 can not even understand speech from those in which he can understand, only not talk; and to ascribe the former condition to lesion of the temporal lobe. The condition in question is word-deafness, and the disease is auditory aphasia. The latest statistical survey of the subject is that by Dr. Allen Starr. In the seven cases of pure word-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 the linguistic use of 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, the ultimate process is that of utterance. If the brain-part for that be injured, speech is impossible or disorderly, even though all the other brain-parts be intact: and this is just the condition of things which, 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 the look of an object or of the look of its printed name be the process which habitually precedes articulation, then the loss of the hearing centre will pro tanto not affect that individual’s speech. He will be mentally deaf, i.e. his understanding of speech will suffer, but he will not be aphasic. In this way it is possible to explain the seven cases of pure word-deafness which figure in Dr. Starr’s table.
If this order of association be ingrained and habitual in that individual, injury to his visual centres 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 of aphasia 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 (see Fig. 17). With this result Dr. Starr’s analysis of purely sensory cases agrees.
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. 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 Ross, shows the four parts most critically concerned, and, in the light of our text, needs no farther explanation (see Fig. 18).
Smell.
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.
_Taste._
Of taste we know little that is definite. What little there is points to the lower temporal regions again. Consult Ferrier as below.
Touch.
Interesting problems arise with regard to the seat of tactile and muscular sensibility. Hitzig, whose experiments on dogs’ brains fifteen 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. Munk and Schiff, on the contrary, 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 symptoms depend on the anæsthesia, for in certain rare cases they have been observed to exist not only without insensibility, but with actual hyperæsthesia of the parts. The motor and sensory symptoms seem, therefore, to be independent variables.
In monkeys the latest experiments are those of Horsley and Schaefer, 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-called gyrus 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, and Horsley and Schaefer consider it by no means necessarily abolished. Luciani found it diminished in his three experiments on apes.
In man we have the fact that one-sided paralysis from disease of the opposite motor zone may or may not be accompanied with anæsthesia of the parts. Luciani, who believes that the motor zone is also sensory, tries to minimize the value of this evidence by pointing to the insufficiency with which patients are examined. He himself believes that in dogs the tactile sphere extends backwards and forwards of the directly excitable region, into the frontal and parietal lobes (see Fig. 20). Nothnagel considers that pathological evidence points in the same direction; and Dr. Mills, carefully reviewing the evidence, adds the gyri fornicatus and hippocampi to the cutaneo-muscular region in man. If one compare Luciani’s diagrams together (Figs. 14, 16, 19, 20) one will see that the entire parietal region of the dog’s skull is common to the four senses of sight, hearing, smell, and touch, including muscular feeling. The corresponding region in the human brain (upper parietal and supra-marginal gyri—see Fig. 17) seems to be a somewhat similar place of conflux. Optical aphasias and motor and tactile disturbances all result from its injury, especially when that is on the left side. The lower we go in the animal scale the less differentiated the functions of the several brain-parts seem to be. It may be that the region in question still represents in ourselves something like this primitive condition, and that the surrounding parts, in adapting themselves more and more to specialized and narrow functions, have left it as a sort of carrefour through which they send currents and converse. That it should be connected with musculo-cutaneous feeling is, however, no reason why the motor zone proper should not be so connected too. And the cases of paralysis from the motor zone with no accompanying anæsthesia may be explicable without denying all sensory function to that region. For, as my colleague Dr. James Putnam informs me, sensibility is always harder to kill than motility, even where we know for a certainty that the lesion affects tracts that are both sensory and motor. Persons whose hand is paralyzed in its movements from compression of arm-nerves during sleep, still feel with their fingers; and they may still feel in their feet when their legs are paralyzed by bruising of the spinal cord. In a similar way, the motor cortex might be sensitive as well as motor, and yet by this greater subtlety (or whatever the peculiarity may be) in the sensory currents, the sensibility might survive an amount of injury there by which the motility was destroyed. Nothnagel considers that there are grounds for supposing the muscular sense to be exclusively connected with the parietal lobe and not with the motor zone.
“Disease of this lobe gives pure ataxy without palsy, and of the motor zone pure palsy without loss of muscular sense.” He fails, however, to convince more competent critics than the present writer, so I conclude with them that as yet we have no decisive grounds for locating muscular and cutaneous feeling apart. Much still remains to be learned about the relations between musculo-cutaneous sensibility and the cortex, but one thing is certain: that neither the occipital, the forward frontal, nor the temporal lobes seem to have anything essential to do with it in man. It is knit up with the performances of the motor zone and of the convolutions backwards and midwards of them. The reader must remember this conclusion when we come to the chapter on the Will.
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I must add a word about the connection of aphasia with the tactile sense. Earlier I spoke of those cases in which the patient can write but not read his own writing. He cannot read by his eyes; but he can read by the feeling in his fingers, if he retrace the letters in the air. It is convenient for such a patient to have a pen in hand whilst reading in this way, in order to make the usual feeling of writing more complete. In such a case we must suppose that the path between the optical and the graphic centres remains open, whilst that between the optical and the auditory and articulatory centres is closed. Only thus can we understand how the look of the writing should fail to suggest the sound of the words to the patient’s mind, whilst it still suggests the proper movements of graphic imitation. These movements in their turn must of course be felt, and the feeling of them must be associated with the centres for hearing and pronouncing the words. The injury in cases like this where very special combinations fail, whilst others go on as usual, must always be supposed to be of the nature of increased resistance to the passage of certain currents of association. If any of the elements of mental function were destroyed the incapacity would necessarily be much more formidable. A patient who can both read and write with his fingers most likely uses an identical ‘graphic’ centre, at once sensory and motor, for both operations.
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I have now given, as far as the nature of this book will allow, a complete account of the present state of the localization-question. In its main outlines it stands firm, though much has still to be discovered. The anterior frontal lobes, for example, so far as is yet known, have no definite functions. Goltz finds that dogs bereft of them both are incessantly in motion, and excitable by every small stimulus. They are irascible and amative in an extraordinary degree, and their sides grow bare with perpetual reflex scratching; but they show no local troubles of either motion or sensibility. In monkeys not even this lack of inhibitory ability is shown, and neither stimulation nor excision of the prefrontal lobes produces any symptoms whatever. One monkey of Horsley and Schaefer’s was as tame, and did certain tricks as well, after as before the operation. It is probable that we have about reached the limits of what can be learned about brain-functions from vivisecting inferior animals, and that we must hereafter look more exclusively to human pathology for light. The existence of separate speech and writing centres in the left hemisphere in man; the fact that palsy from cortical injury is so much more complete and enduring in man and the monkey than in dogs; and the farther fact that it seems more difficult to get complete sensorial blindness from cortical ablations in the lower animals than in man, all show that functions get more specially localized as evolution goes on. In birds localization seems hardly to exist, and in rodents it is much less conspicuous than in carnivora. Even for man, however, Munk’s way of mapping out the cortex into absolute areas within which only one movement or sensation is represented is surely false. The truth seems to be rather that, although there is a correspondence of certain regions of the brain to certain regions of the body, yet the several parts within each bodily region are represented throughout the whole of the corresponding brain-region like pepper and salt sprinkled from the same caster. This, however, does not prevent each ‘part’ from having its focus at one spot within the brain-region. The various brain-regions merge into each other in the same mixed way. As Mr. Horsley says: “There are border centres, and the area of representation of the face merges into that for the representation of the upper limb. If there was a focal lesion at that point, you would have the movements of these two parts starting together.” The accompanying figure from Paneth shows just how the matter stands in the dog.
I am speaking now of localizations breadthwise over the brain-surface. It is conceivable that there might be also localizations depthwise through the cortex. The more superficial cells are smaller, the deepest layer of them is large; and it has been suggested that the superficial cells are sensorial, the deeper ones motor; or that the superficial ones in the motor region are correlated with the extremities of the organs to be moved (fingers, etc.), the deeper ones with the more central segments (wrist, elbow, etc.). It need hardly be said that all such theories are as yet but guesses.
We thus see that the postulate of Meynert and Jackson which we started with is on the whole most satisfactorily corroborated by subsequent objective research. _The highest centres do probably contain nothing but arrangements for representing impressions and movements, and other arrangements for coupling the activity Of these arrangements together._ Currents pouring in from the sense-organs first excite some arrangements, which in turn excite others, until at last a motor discharge downwards of some sort occurs. When this is once clearly grasped there remains little ground for keeping up that old controversy about the motor zone, as to whether it is in reality motor or sensitive. The whole cortex, inasmuch as currents run through it, is both. All the currents probably have feelings going with them, and sooner or later bring movements about. In one aspect, then, every centre is afferent, in another efferent, even the motor cells of the spinal cord having these two aspects inseparably conjoined. Marique, and Exner and Paneth have shown that by cutting round a ‘motor’ centre and so separating it from the influence of the rest of the cortex, the same disorders are produced as by cutting it out, so that really it is only the mouth of the funnel, as it were, through which the stream of innervation, starting from elsewhere, pours; consciousness accompanying the stream, and being mainly of things seen if the stream is strongest occipitally, of things heard if it is strongest temporally, of things felt, etc., if the stream occupies most intensely the ‘motor zone.’ It seems to me that some broad and vague formulation like this is as much as we can safely venture on in the present state of science; and in subsequent chapters I expect to give confirmatory reasons for my view.