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[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 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.[32] 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;[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._ 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.[34] _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 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.[38] 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.[39] 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, on page 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 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[40] (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.[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).
_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.[42] 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.[43] Munk[44] and Schiff[45], 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.[46] The motor and sensory symptoms seem, therefore, to be independent variables.
_In monkeys_ the 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 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,[48] and Horsley and Schaefer consider it by no means necessarily abolished.[49] Luciani found it diminished in his three experiments on apes.[50] _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;[51] and Dr. Mills, carefully reviewing the evidence, adds the gyri fornicatus and hippocampi to the cutaneo-muscular region in man.[52] 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.[53] The lower we go in the animal scale the less differentiated the functions of the several brain-parts seem to be.[54] 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."[55] He fails, however, to convince more competent critics than the present writer,[56] 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.
* * * * * I must add a word about the connection of aphasia with the tactile sense. On p. 40 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.[57] 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.
* * * * * 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.[58] 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."[59] The accompanying figure from Paneth shows just how the matter stands in the dog.[60] 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;[61] 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.).[62] 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 on p. 30 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._[63] 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,[64] and Exner and Paneth[65] 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;[66] 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.
MAN'S CONSCIOUSNESS LIMITED TO THE HEMISPHERES.
_But is the consciousness which accompanies the activity of the cortex the only consciousness that man has?_ or _are his lower centres conscious as well?_ This is a difficult question to decide, how difficult one only learns when one discovers that the cortex-consciousness itself of certain objects can be seemingly annihilated in any good hypnotic subject by a bare wave of his operator's hand, and yet be proved by circumstantial evidence to exist all the while in a split-off condition, quite as 'ejective'[67] to the rest of the subject's mind as that mind is to the mind of the bystanders.[68] The lower centres themselves may conceivably all the while have a split-off consciousness of their own, similarly ejective to the cortex-consciousness; but whether they have it or not can never be known from merely introspective evidence. Meanwhile the fact that occipital destruction in man may cause a blindness which is apparently absolute (no feeling remaining either of light or dark over one half of the field of view), would lead us to suppose that if our lower optical centres, the corpora quadrigemina, and thalami, do have any consciousness, it is at all events a consciousness which does not mix with that which accompanies the cortical activities, and which has nothing to do with our personal Self. In lower animals this may not be so much the case. The traces of sight found (supra, p. 46) in dogs and monkeys whose occipital lobes were entirely destroyed, may possibly have been due to the fact that the lower centres of these animals saw, and that what they saw was not ejective but objective to the remaining cortex, i.e. it formed part of one and the same inner world with the things which that cortex perceived. It may be, however, that the phenomena were due to the fact that in these animals the cortical 'centres' for vision reach outside of the occipital zone, and that destruction of the latter fails to remove them as completely as in man. This, as we know, is the opinion of the experimenters themselves. For practical purposes, nevertheless, and limiting the meaning of the word consciousness to the personal self of the individual, we can pretty confidently answer the question prefixed to this paragraph by saying that _the cortex is the sole organ of consciousness in man_.[69] If there be any consciousness pertaining to the lower centres, it is a consciousness of which the self knows nothing.
THE RESTITUTION OF FUNCTION.
Another problem, not so metaphysical, remains. The most general and striking fact connected with cortical injury is that of the _restoration of function_. Functions lost at first are after a few days or weeks restored. _How are we to understand this restitution?_ Two theories are in the field: 1) Restitution is due to the vicarious action either of the rest of the cortex or of centres lower down, acquiring functions which until then they had not performed; 2) It is due to the remaining centres (whether cortical or 'lower') resuming functions which they had always had, but of which the wound had temporarily inhibited the exercise. This is the view of which Goltz and Brown-Séquard are the most distinguished defenders.
Inhibition is a _vera causa_, of that there can be no doubt. The pneumogastric nerve inhibits the heart, the splanchnic inhibits the intestinal movements, and the superior laryngeal those of inspiration.
The nerve-irritations which may inhibit the contraction of arterioles are innumerable, and reflex actions are often repressed by the simultaneous excitement of other sensory nerves. For all such facts the reader must consult the treatises on physiology. What concerns us here is the inhibition exerted by different parts of the nerve-centres, when irritated, on the activity of distant parts. The flaccidity of a frog from 'shock,' for a minute or so after his medulla oblongata is cut, is an inhibition from the seat of injury which quickly passes away.
What is known as 'surgical shock '(unconsciousness, pallor, dilatation of splanchnic blood-vessels, and general syncope and collapse) in the human subject is an inhibition which lasts a longer time. Goltz, Freusberg, and others, cutting the spinal cord in dogs, proved that there were functions inhibited still longer by the wound, but which re-established themselves ultimately if the animal was kept alive.
The lumbar region of the cord was thus found to contain independent vaso-motor centres, centres for erection, for control of the sphincters, etc., which could be excited to activity by tactile stimuli and as readily reinhibited by others simultaneously applied.[70] We may therefore plausibly suppose that the rapid reappearance of motility, vision, etc., after their first disappearance in consequence of a cortical mutilation, is due to the passing off of inhibitions exerted by the irritated surface of the wound. The only question is whether _all_ restorations of function must be explained in this one simple way, or whether some part of them may not be owing to the formation of entirely new paths in the remaining centres, by which they become 'educated' to duties which they did not originally possess. In favor of an indefinite extension of the inhibition theory facts may be cited such as the following: In dogs whose disturbances due to cortical lesion have disappeared, they may in consequence of some inner or outer accident reappear in all their intensity for 24 hours or so and then disappear again.[71] In a dog made half blind by an operation, and then shut up in the dark, vision comes back just as quickly as in other similar dogs whose sight is exercised systematically every day.[72] A dog which has learned to beg before the operation recommences this practice quite _spontaneously_ a week after a double-sided ablation of the motor zone.[73] Occasionally, in a pigeon (or even, it is said, in a dog) we see the disturbances less marked immediately after the operation than they are half an hour later.[74] This would be impossible were they due to the subtraction of the organs which normally carried them on. Moreover the entire drift of recent physiological and pathological speculation is towards enthroning inhibition as an ever-present and indispensable condition of orderly activity. We shall see how great is its importance, in the chapter on the Will. Mr. Charles Mercier considers that no muscular contraction, once begun, would ever stop without it, short of exhaustion of the system;[75] and Brown-Séquard has for years been accumulating examples to show how far its influence extends.[76] Under these circumstances it seems as if error might more probably lie in curtailing its sphere too much than in stretching it too far as an explanation of the phenomena following cortical lesion.[77] On the other hand, if we admit _no_ re-education of centres, we not only fly in the face of an _a priori_ probability, but we find ourselves compelled by facts to suppose an almost incredible number of functions natively lodged in the centres below the _thalami_ or even in those below the _corpora quadrigemina_. I will consider the _a priori_ objection after first taking a look at the facts which I have in mind.
They confront us the moment we ask ourselves just _which are the parts which perform the functions abolished by an operation after sufficient time has elapsed for restoration to occur?_ The first observers thought that they must be the _corresponding parts of the opposite or intact hemisphere_. But as long ago as 1875 Carville and Duret tested this by cutting out the fore-leg-centre on one side, in a dog, and then, after waiting till restitution had occurred, cutting it out on the opposite side as well. Goltz and others have done the same thing.[78] If the opposite side were really the seat of the restored function, the original palsy should have appeared again and been permanent. But it did not appear at all; there appeared only a palsy of the hitherto unaffected side. The next supposition is that _the parts surrounding the cut-out region_ learn vicariously to perform its duties. But here, again, experiment seems to upset the hypothesis, so far as the motor zone goes at least; for we may wait till motility has returned in the affected limb, and then both irritate the cortex surrounding the wound without exciting the limb to movement, and ablate it, without bringing back the vanished palsy.[79] It would accordingly seem that _the cerebral centres below the cortex_ must be the seat of the regained activities. But Goltz destroyed a dog's entire left hemisphere, together with the _corpus striatum_ and the _thalamus_ on that side, and kept him alive until a surprisingly small amount of motor and tactile disturbance remained.[80] These centres cannot here have accounted for the restitution. He has even, as it would appear,[81] ablated both the hemispheres of a dog, and kept him alive 51 days, able to walk and stand. The corpora striata and thalami in this dog were also practically gone. In view of such results we seem driven, with M. François-Franck,[82] to fall back on the _ganglia lower still_, or even on the _spinal cord_ as the 'vicarious' organ of which we are in quest. If the abeyance of function between the operation and the restoration was due _exclusively_ to inhibition, then we must suppose these lowest centres to be in reality extremely accomplished organs. They must always have done what we now find them doing after function is restored, even when the hemispheres were intact. Of course this is conceivably the case; yet it does not seem very plausible. And the _a priori_ considerations which a moment since I said I should urge, make it less plausible still.
For, in the first place, the brain is essentially a place of currents, which run in organized paths. Loss of function can only mean one of two things, either that a current can no longer run in, or that if it runs in, it can no longer run out, by its old path. Either of these inabilities may come from a local ablation; and 'restitution' can then only mean that, in spite of a temporary block, an inrunning current has at last become enabled to flow out by its old path again--e.g., the sound of 'give your paw' discharges after some weeks into the same canine muscles into which it used to discharge before the operation. As far as the cortex itself goes, since one of the purposes for which it actually exists is the production of new paths,[83] the only question before us is: Is the formation of _these particular 'vicarious' paths_ too much to expect of its plastic powers? It would certainly be too much to expect that a hemisphere should receive currents from optic fibres whose _arriving-place_ within it is destroyed, or that it should discharge into fibres of the pyramidal strand if their _place of exit_ is broken down. Such lesions as these must be irreparable _within that hemisphere_. Yet even then, through the other hemisphere, the _corpus callosum_, and the bilateral connections in the spinal cord, one can imagine some road by which the old muscles might eventually be innervated by the same incoming currents which innervated them before the block. And for all minor interruptions, not involving the arriving-place of the 'cortico-petal' or the place of exit of the 'cortico-fugal' fibres, roundabout paths of some sort through the affected hemisphere itself must exist, for every point of it is, remotely at least, in potential communication with every other point. The normal paths are only paths of least resistance. If they get blocked or cut, paths formerly more resistant become the least resistant paths under the changed conditions. It must never be forgotten that a current that runs in has got to run out _somewhere_; and if it only once succeeds by accident in striking into its old place