I JEW PHYSIOL' G IN SURGICAL AND HKNKRAL PJ 6 6O S> ^ C C o» 5. J IH I-. cn «J rt •»H P C^ hJ C M t5 H • • ' ^B ' ' ' W S O w z w o u • < a o fc C a g S3 2 ^ s G ° i3 § 1 •§ js^* § ts o « g go^ « „ ^VM "35^ OO 1— I 8 nS M 4_J «._, O ,. . I™" Cj JH -1 £ <; t> z M Crt ^) ^ CD TO 3 rt .tj ^ " "3 "^ -"^ 5ZJ fc 0 § G PH K ,5 Q o : : : : : : : Q- Z . . £> i 1— I o * u 1— 1 u 1— 1 hH 4 J •— " ' Q i-T I-H ^ > > > > a" a OF THE SPINAL CORD 145 rt bb p c CD ^ g CD N t/j 73 Cfl G •+J CJ bo ^rt ro 0 •> C 3 3 (/} 3 ~H £* +J cn~ rt 0) rM 0 a Lg I m •rt 'S S 0 B C M cn 1 rt CX 5) M 6 S 73 . 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It is hoped that the bare elements set down below may be found easier to remember, and adequate for most purposes. No two accounts agree exactly. The main points may be emphasized first. With regard to the sensory distribution, there is a good deal of overlap, especially in the hand, where the seventh cervical supplies the radial half, the eighth cervical the inner half, and the first dorsal the one and a half fingers to which the ulnar nerve may be traced. The twelve dorsal nerves supply the chest and abdomen in bands like successive strips of plaster stretched round the body ; the nipple lies between the fourth and fifth dorsal, and the umbilicus between the ninth and tenth. If we place the open hand on the thigh just below and parallel to Poupart's ligament, we cover the first lumbar area ; the next handbreadth below is the second lumbar, and the next, including the region of the patella, is the third lumbar. The small sciatic nerve area corresponds to the second sacral. With regard to motor distribution, the fifth cervical supplies the deltoid + biceps + supinator longus group, as well as the dorsal scapular muscles and rhomboids. In infantile palsy and other anterior horn or nerve- root affections, these muscles may be found paralysed and atrophied in company. On the other hand, a fracture of the spine irritating this area brings about a characteristic position of the arms ^ . The first dorsal gives off sympathetic branches dilating the pupil. The hand and foot are each supplied by OF THE SPINAL CORD 147 the two lowest nerves entering the brachial and sacral plexuses respectively. The anatomy of the lumbo-sacral plexus makes it easy to remember that the quadriceps and adductors must be supplied from the lumbar nerves, whereas the hamstrings and crural muscles are innervated from the sciatic nerve. There is a general tendency for flexors to derive their nerve supply from a level slightly below that for the extensors. It is easy to see why this should be the case if we glance at a quadruped, where the flexors are posterior to the extensors. THE EXACT DIAGNOSIS OF INJURIES OF THE SPINAL CORD. The following lesions of the cord may be responsible for symptoms of paralysis or anaesthesia after an injury to the back. 1. Simple concussion, the injuries being micro- scopical or functional only, and the paralysis transient. 2. Complete division of ah1 the nervous elements. 3. Pressure on the cord due to bone, callus, or a foreign body, not causing a total transection. 4. Haemorrhage into the spinal membranes. 5. Haemorrhage into the cord itself. 6. Later complications such as myelitis, traumatic neurasthenia, etc. This is not the place to consider all these in their surgical bearing. We want to look at them in relation to the physiology of the spinal cord. A total transection of the cord in man, not in animals, affects profoundly the functions of the 148 THE SURGICAL PHYSIOLOGY segments below the injury, and either from the first or after the lapse of a little time they lose their reflex functions, the bladder and rectum and their sphincters become paralysed, and the effect is much the same as it would have been if the isolated portion of the cord had been removed in toto. In animals, the reflex functions persist. Considerable difficulty may be experienced for a day or two in deciding whether a patient is suffering from a complete division of the cord due to the nip at the moment of fracturing the spine, or whether the symptoms are due merely to concussion. In the latter case a few days' rest will effect a cure. Sometimes one can get a hint earlier. If the distri- bution of the paralysis does not correspond with the distribution of the anaesthesia, and if the sym- ptoms are asymmetrical, it is probable that they are due partly at least to concussion. In either case it is very seldom that any useful purpose will be served by operating, unless the injury involves the cervical region or the cauda equina. When the cord is involved, but has not suffered a functional transection, the paralysis will probably be spastic in nature, and operation is more hopeful because there may be something exercising injurious pressure which can be removed. Haemorrhage into the spinal membranes produces pain and spasm by involving the issuing nerve roots. In addition, there will probably be some evidence of pressure on the cord, producing spastic paralysis and some anaesthesia below the lesion. Haemorrhage into the centre -of the cord sometimes OF THE SPINAL CORD 149 abolishes the pain and temperature senses while tactile sense escapes. There will probably be spastic paraplegia as well. It will not be necessary to refer here to the diagnosis of the later complications, such as myelitis and the various neuroses. Unfortunately the central nervous system is so highly specialized that it has lost the power of regeneration after injury, not only in man (unless we accept the evidence of the famous Stewart-Harte case !) but also in nearly all animals. The newt, it is true, can form a new cord if its tail is lopped off, but the newt has marvellous powers of regeneration, and can even grow a new lens if the front of its eye is removed ! REFERENCES. FORSTER. — Zeitschrift f. orthopad Chirurgie, 1908, Bd. xxii., p. 203. HEAD AND THOMPSON. — " The Grouping of Afferent Impulses in the Spinal Cord," Brain, 1906, p. 537. 150 CHAPTER XL CEREBRAL LOCALIZATION. The causation and significance of optic neuritis. — Localization in the cerebellum. — Tumours in the cerebello-pontine angle. Localization of sensation in the cerebral cortex. — Functions of the frontal cortex. — Spasticity. — Apraxia. — Aphasia. — Misleading localizing signs of cerebral tumour. — The cerebrospinal fluid. IT will be necessary here to assume that the reader has an ordinary acquaintance with the structure and functions of the brain. We shall confine our- selves to a brief reference to the most important advances of the past decade in providing evidence for the localization of tumours, abscesses, and traumatic lesions, and therefore for their successful treatment by operation. OPTIC NEURITIS. It has long been in doubt why optic neuritis should develop in cases of cerebral tumour. It has been attributed to the effects of chronic meningitis, and to over-filling of the third ventricle, with consequent pressure on the underlying optic chiasma. It is now definitely established by the experiments of Gushing and Bordley, and confirmed by clinical experience, that it is a pressure effect. The growth of the neoplasm causes a great and continued rise of intracranial pressure ; this tends to dam back the lymph flow returning in the sheath of the optic nerve. The usual consequence of lymphatic obstruc- CEREBRAL LOCALIZATION 151 tion is produced, namely, cedematous swelling of the area drained. So the optic cup fills up, the disc is obscured by transudate, and the vessels are buried from view in the oedema fluid. All this may be exactly reproduced by intracranial pressure in dogs, and when the pressure is removed, restitution to normal takes place. Several methods of raising the intracranial pressure were employed, the best results being obtained by the insertion of sponge-tent material inside the skull. Swelling and oedema of the disc, tortuosity of the veins, and over-distention of the lymph- sheath around the optic nerve, were all marked. Relief of the pressure rapidly cured them. Although we use the conventional term " neuritis," the histological changes are not those of inflammation. For instance, there is no arterial hyperaemia, and the principal infiltration is with cells of connective tissue origin, not leucocytes. Further, it has been stated by many observers, and recently defended, with all his great authority and experience, by Sir Victor Horsley, that the degree of the neuritis in the two eyes is a most reliable guide as to the side of the tumour. It is not so much the amount of swelling that is to be taken into account as the age and extent of the changes. These nearly always commence at the upper nasal quadrant of the disc. Thus, optic neuritis best marked in the right eye is of great value in pointing to a right-sided tumour. The further forwards the tumour, the more constant does this rule become. It is well known that even if a cerebral tumour 152 cannot be localized, palliative trephining should be performed to relieve headache and save the sight. If this is undertaken early, the optic neuritis passes off. As the tentorium transmits pressure badly, the trephining should be in the temporal region for supratentorial tumours, and in the occipital region for cerebellar tumours. Another valuable observation which we owe to Gushing is that raised intracranial pressure, par- ticularly by cerebral tumour, induces a considerable limitation of the field of vision for blue ; indeed, there may be actual blue-blindness. THE CEREBELLUM. We have been in urgent need of some improvement in our means of localizing tumours and abscesses in the cerebellum. It remains to be seen how far the fresh light recently thrown on the subject and herein set forth will help us to obtain materially better results. During the past ten years, at the Bristol Royal Infirmary there have been eight cases of temporo-sphenoidal abscess, all of which have been successfully diagnosed, and ten cases of cere- bellar abscess, of which only three were correctly located ; in three of these ten cases the cerebrum was explored in vain, and in two the lateral sinus was thought to be the cause of the symptoms. Sir Victor Horsley and R. H. Clarke have recently revised our knowledge of the functions and relation- ships of the cerebellum by an ingenious method. Reconstructions of a monkey's head have been made by cutting frozen sections and then piecing them CEREBRAL LOCALIZATION 153 together again ; by this means it was possible to build a frame of metal to fit about the head of a living monkey, carrying an insulated needle which could be thrust, through a small trephine hole, into any desired portion of the cerebellum, its cortex, or its deep nuclei (roof nuclei) , the exact position of the point of the needle having been determined by a study of the head reconstructed from the frozen sections. By this means various parts could be stimulated electrically without doing any but the slightest damage to the overlying structures ; more- over, by passing in a strong current and using a double needle shielded nearly to the points, small electrolytic lesions either of the cortex or of the roof nucleus could be made, and the resulting degenerations studied by suitable staining some weeks afterwards. The general result was to prove that the cortex cerebelli is a receiving platform, and that its axons merely pass to the roof nuclei, from which the efferent tracts start. Stimulation of the cerebellar cortex by ordinary currents produces no obvious response ; stimulation of the roof nuclei causes movements of the eyes and sometimes of the limbs. We see here the reason why laterally situated tumours or abscesses lie so quiet. The classic signs of a lesion of the cerebellum, determined both by physiologists and by clinicians, are the following : — (i) Ataxia;' (2) Atonia; (3) Asthenia; (4) Tremor; these all affect the same side as the lesion. (5) Nystagmus ; (6) Vertigo. 154 CEREBRAL LOCALIZATION 1. Ataxia. — This, one of the most constant signs, is easily detected if the patient is able to walk. When he is in bed, it may be brought out by making him try to pronate and supinate rapidly for a minute or two ; or to make and unmake a fist quickly, over and over again. This sign is the more convincing if it is unilateral. 2. Atonia is very variable ; the knee-jerks may be absent, normal, or excessive, and may change day by day. Thiele and others have proved that the great increase of tone noticed in man or animals after lesions involving the pyramidal and other long descending tracts depends on the integrity of Deiter's nucleus. This lies just at the junction of the pons and medulla, beneath the outer part of the floor of the fourth ventricle, and therefore in close relation to the cerebellum. If it is destroyed, or if it is cut off from influencing the spinal cord by a complete transverse division below Deiter's nucleus, the spasticity and increased reflexes which ordinarily foUow lesions of the motor paths will fail to develop. Some cerebellar abscesses and tumours press on the pyramids (above their decussation) but not on Deiter's nucleus. These cause increase of tone on the opposite side. Others destroy Deiter's nucleus, and cause loss of tone on the same side. Others do not involve either, and tone may be normal, or a little increased on the same side as the lesion. 3. Asthenia may be evidenced by weakening of the grip, tendency to fall, or drooping of the head on the affected side. It is not very constant. CEREBRAL LOCALIZATION 155 4. Tremor is only occasionally in evidence. 5. Nystagmus. — These curious jerkings of the eyes are of considerable importance in the diagnosis of cerebellar affections, because, although seen in such conditions as disseminated sclerosis, they are very unusual with localized intracranial tumours. Un- fortunately they are not constantly present even when the lesion is in the cerebellum, and, on the other hand, are usually to be observed in patients with disease of the labyrinth (vestibule and semi- circular canals). Seeing that most cases of cerebellar abscess follow otitis media, it has been very difficult to be certain, in the past, whether any nystagmus in a patient with a suppurating ear was due to the labyrinth, or the cerebellum, or both. Barany, of Vienna, has shown that it is possible to induce nystagmus in a normal person by stimulat- ing the labyrinth. This may be done either by rotating the patient, or by allowing hot or cold (not tepid) water to trickle in as far as the membrana tympani. Hot water in the right ear causes a nystagmus in which the eyes slowly turn to the left and are corrected by rapid jerkings to the right ; with cold water the rapid jerkings would be to the left. If a patient with a suppurating ear has nystagmus, and it is desired to know whether this is due to affection of the labyrinth or of the cerebellum, hot or cold water should be injected to see if the nystagmus can be reversed in direction. If it can, the labyrinth cannot be at fault ; it must be the cerebellum. Again, a patient with severe vertigo following on 156 CEREBRAL LOCALIZATION otitis media may be suffering from labyrinthitis or from cerebellar abscess. If injection causes no nystagmus, the labyrinth is destroyed. TUMOURS IN THE CEREBELLO-PONTINE ANGLE. This is a very common location for cerebellar tumours, and a comparatively favourable one for surgery, seeing that in many instances the growth is simple, and can be enucleated without recurrence. Allen Starr finds in the literature sixty-nine cases cured by removal. In many of these there was restoration to good, in some to perfect, health. Diagnosis, therefore, becomes peculiarly important. In addition to the signs mentioned above, certain nerve-root symptoms may develop, and the pons may be pressed on. Mental trouble is quite unusual. We may classify the evidence as follows : — 1. General : headache, vomiting, optic neuritis, slow pulse, blue-blindness, perhaps convulsions. 2. Cerebellar signs : staggering, vertigo, ataxia, weakness, tremor, and perhaps absent knee-jerk ; these may be unilateral, on the same side as the growth. Nystagmus. 3. Nerve-root symptoms affecting the same side : pressure on the fifth, with corneal anaesthesia and loss of reflex, and weakness of jaw muscles ; pressure on the sixth, with internal strabismus; pressure on the seventh, with facial weakness ; pressure on the eighth, with tinnitus, loss of perception for upper notes (tested by Galton's whistle), or absolute deaf- ness ; pressure on the ninth, tenth, and eleventh, CEREBRAL LOCALIZATION 157 with dysphagia, laryngeal palsy, cardiac attacks, etc. ; pressure on the twelfth, with deviation of the protruded tongue. Of these, the facial and auditory nerves are most often affected, there being complete unilateral deafness in most of the cases. In cerebellar tumours these two nerves may be interfered with, but not to any considerable degree. 4. Pressure on the pons, causing crossed hemiplegic weakness, with exaggerated reflexes and extensor response. The cases may live for years, but there is a liability to sudden death by crowding of the cerebellum down through the foramen magnum. LOCALIZATION OF SENSATION IN THE CEREBRAL CORTEX. HEARING. — Although it is certain that monkeys which have suffered bilateral removal of the temporal cortex give every evidence that they can hear, it is very difficult to be certain that sounds are still appreciated in consciousness by them, and recognized for what they signify. It is no more evidence of conscious hearing that a monkey looks round when a bell sounds, than it is of conscious pain that a man with a fractured spine withdraws a foot pricked by a pin. At any rate, there is a fair amount of evidence, both anatomical and clinical, to locate this function in the temporal region, and none to locate it else- where. The most convincing observation on record was made by Gushing, who stimulated the exposed temporal cortex in a conscious man, and the patient said that he noticed a buzzing noise. 158 CEREBRAL LOCALIZATION VISION. — There is abundant evidence that visual sensations are received on the mesial surfaces of the occipital lobes, just above and just below the calcarine fissure. Histologically, the area is mapped out by the white line of Gennari ; it barely encroaches posteriorly on the convexity of the hemisphere. The left half of each retina is represented in the left cerebral cortex, and the right half of each retina in the right cortex. The fovea centralis of each eye has a bilateral representation. The upper half of each retina is projected above the calcarine fissure ; the lower half of each retina below the fissure. Therefore a tumour of the left cortex above the calcarine fissure would render the upper left quadrant of each eye psychically blind, and the patient would be unable to see objects downwards and to his right. A smaller lesion, however, does not produce a smaller patch of blindness ; it merely reduces the visual acuity over the whole of the corresponding quadrant. CUTANEOUS SENSATION. — There is some evidence that the cortical representation of heat, cold, pain, and tactile sense is identical. Possibly muscular sense has a somewhat different location. It is universally agreed that the main receiving platform for cutaneous sensation is situated in the postcentral (ascending parietal) gyms, just behind the fissure of Rolando, and that the general arrangement is the same as that of the motor centres ; thus, the sensory centre for the leg is nearest the vertex, opposite the origin of the pyramidal fibres for the leg ; next come the arm centres, and lowest of all those for the face and head. CEREBRAL LOCALIZATION 159 The localization in the limbic lobe once advocated by Schafer and others following him, has now been given up, even by its author. Doubt still remains, however, whether the precentral or motor cortex takes any share in appreciating cutaneous sensation. If so, it is quite secondary to the part played by the postcentral convolution. It is very difficult to be sure to what extent animals feel after the removal of small parts of either the postcentral or precentral convolutions, and very diverse views have been expressed ; it is quite certain that a small lesion does not induce com- plete anaesthesia. It is probably wiser to put faith principally in the human evidence on such a subject. It is abundantly proved that lesions involving the ascending parietal convolution almost always cause a certain degree of interference with sensation, never amounting to a complete hemianaesthesia, which, indeed, occurs only in hysteria, or very transitorily after an apoplectic stroke. Bergmark quotes thirty- three cases of lesions of this gyrus with sensory symptoms but no paralysis. Gushing excited the postcentral convolution in two conscious patients who had previously been trephined, by unipolar faradic stimulation. He found that the brain itself was devoid of any sort of feeling, but that sensations of stroking, tingling, or warmth were produced, referred to the hand of the opposite side. The sensation was quite well denned and localized ; one area corresponded to the index finger, and another to the back of the hand. When the electrode was applied in front of the fissure 160 CEREBRAL LOCALIZATION of Rolando instead of behind, the fingers or hand moved, but there was no sensation. An incision in the postcentral convolution was quite painless, and caused some numbness of all forms of sensation in the hand. It is more difficult to be certain whether the ascending frontal or motor convolution has also any sensory function ; if so, it is less obvious than in the case of the postcentral convolution. Naturally occurring lesions limited to the front of the fissure of Rolando, and carefully studied before and after death, are rare, and the evidence is conflicting ; some showed paralysis but no sensory loss, whereas others had both motor and sensory impairment. Many years ago, before it was realized that the convolutions in front of and behind the fissure of Rolando differed in function, Ransom and also Laycock observed that a tingling sensation was elicited when they stimulated the exposed cortex in a conscious man, and apparently they both applied the electrodes .in front of the fissure ; Gushing and others have failed to confirm this. Recently Sir Victor Horsley has published an account of the only case in which he has removed a cortical centre (part of the hand area) without encroaching upon the ascending parietal gyms (for athetosis). Immediately after the operation there was complete flaccid paralysis of the arm, and some interference with sensation. The hand could detect cold, but not warmth, stroking with a wool pencil was not felt on the ungual phalanges, there were inaccuracy of location of pain and touch, loss of the sense of position, and objects placed in the hand were not CEREBRAL LOCALIZATION 161 recognized by touch (astereognosis). A year later, movement was recovered, except for some spastic paralysis in the two ulnar fingers ; there were still astereognosis, inaccuracy of location, and slight dulling of sensation over the ulnar border of the hand. If the lesion had involved the postcentral convolution, the sensory symptoms, in his experience, would have been much more marked. The athetosis was cured. Interference with sensation is of course no proof that a cerebral tumour is in the cortex ; it may be found with a lesion of the optic thalamus, internal capsule, isthmus, pons, or medulla. In twenty-six cases of hemiplegia due to some trouble in the internal capsule, Bergmark found evidence of sensory im- pairment in all who were intelligent enough to be tested with accuracy by modern methods, although there was never complete hemiansesthesia to all forms of stimuli. FUNCTIONS OF THE FRONTAL CORTEX: It is well known, of course, that the great motor centres are limited to the ascending frontal or pre- central convolution. This has been abundantly proved by many methods : by the study of paralysis following localized lesions in man or removals in man or apes ; by electrical stimulation in man and apes ; and histologically, by the limitation to this region of the giant pyramidal or Betz cells, which are the only cells to undergo chromatolysis when the pyramidal tracts are destroyed in the spinal cord. It often becomes of great importance to the surgeon II 162 CEREBRAL LOCALIZATION to know whether a tumour causing hemiplegia is accessible, either in the cortex or close beneath it, or inaccessible, in the internal capsule or isthmus. The principal evidences of the former are the occur- rence of monoplegias, the face, arm, or leg being affected alone without the others, whereas lesions of the internal capsule would paralyse all three ;* secondly, persistent aphasia may be present ; and thirdly, there may be recurring convulsions. The degree of sensory impairment is not of much assistance. There is a good deal of evidence that if the paralysis is of a flaccid type, the lesion is most probably cortical, though the converse is not necessarily true. Thiele has demonstrated in animals that tone is increased by impulses from Deiter's nucleus in the medulla, and inhibited by impulses generated in the optic thalamus and conducted by the rubrospinal tract (Monakow's bundle). It is this tract wrhich subserves the stock movements such as standing and walking, which can often be carried out after complete destruction of the pyramidal tract. In man, a cortical lesion is often (not always) accompanied by a flaccid paralysis with no Babinski sign and with normal or diminished reflexes (see cases quoted by Bergmark) , but when the optic thalamus and internal capsule are involved, there is always marked rigidity. Pressure on the isthmus, pons, medulla, or spinal cord will probably damage the rubrospinal tract as * In monkeys the fibres to the head, arm, and leg are grouped in bundles in the internal capsule, but apparently this is not the case in man, and consequently small lesions cause mild hemiplegia, not monoplegia. CEREBRAL LOCALIZATION 163 well as the adjacent pyramidal tracts, and so set up spasticity, unless the whole cord is functionally divided, in which case impulses descending from Deiter's nucleus (possibly in the vestibulospinal tract), are also cut off, and a flaccid paralysis results. It is, however, true that irritation of the cortex, such as may be present just after a traumatic lesion, or during the growth of a tumour, may cause early contracture, so we should regard the presence of rigidity as an equivocal sign, but absence of rigidity as evidence of a cortical lesion. The frontal cortex lying in front of the motor region is described as a " silent area," and extensive tumours, degenerations, or injury may produce few or no symptoms. In a case under the writer's care a wound one inch deep into the brain caused by a chopper, from the vertex to the nose, made absolutely no difference to the woman's character, capacity, or intelligence, and indeed produced no symptoms at all beyond concussion, although she was under observation for many months. In the famous American crowbar case, where a large part of the frontal cortex on both sides was destroyed, there was no paralysis, but on returning to work the man, previously a capable foreman, had become weak, vacillating, inattentive, and profane. There are quite commonly signs of mental dullness in patients with frontal lesions. In cats there are, after excisions of the frontal cortex, changes in the disposition, and recently acquired tricks may be lost. 164 CEREBRAL LOCALIZATION APRAXIA. More definite evidence, however, is now available. There are a number of carefully studied cases on record in which, with no actual paralysis, there has been a remarkable clumsiness in the performance of movements requiring any skill, and in which the patient has been quite unable to make some movement voluntarily or in response to command, although he may unconsciously do that very thing under the influence of emotion or by accident. This condition is called apraxia. It is most convincing when it is unilateral. Thus, a musician may lose the power of playing his instrument, or the clerk his power of writing. In Liepmann's classic case, one of the first to be described, there was apraxia of the right arm and leg. " Asked to put his right forefinger on his nose, he said, ' Yes,' and with his stretched forefinger executed wide circling movements in the air. He made the correct movement at once with his left hand. Asked to close his right hand into a fist, he performed various absurd movements of his arm and body, but attained the required goal at once with his left hand. When asked to give the examiner a certain object with his right hand, he frequently picked up the wrong thing, and still holding it in his hand, used the left to take up the required object and present it to the physician." A patient of de Buck's, asked to lift her right arm, crossed it over her body, put it in her left axilla, and after making various other vigorous but futile efforts, said plain- tively, " Je comprends bien ce que vous voulez, CEREBRAL LOCALIZATION 165 mais je ne parviens pas a le faire " : this' just expresses the condition. In some of the cases, there is imperfect recognition of objects or of their uses (agnosia), but these are complicated and cannot be described here. It is an important fact that apraxia of the left arm is common in right hemiplegics, whereas apraxia of the right arm rarely occurs in left hemiplegics ; moreover, in the cases where there are apraxia of the left side and hemiplegia of the right, there is evidence that the lesion is cortical, not in the internal capsule. Thus Liepmann examined eighty-three hemiplegic patients, with these results : — Forty-two had left hemiplegia ; they could nearly all obey directions with the right arm. Forty-one had right hemiplegia ; of these 20 had apraxia of the left arm, and 14 in this group also had aphasia ; 21 had no apraxia, and of these only 4 had aphasia (in most of the other 17 cases, the lesion was probably in the internal capsule). Of course, as left-handed persons form one-twentieth of the community, it is possible to find a few cases of left hemiplegia with right apraxia. There is good ground, then, for believing that the centres which consciously initiate voluntary move- ments for both sides of the body are limited to the left cortex in right-handed people, and that the pre- central convolutions are merely the departure platforms for messages from the brain to the cord. Instructions are sent to the right precentral convolu- tion by way of the corpus callosum. It is still in doubt whether the above-mentioned initiating centre 166 CEREBRAL LOCALIZATION is in the left precentral gyms, or whether it lies in front of this, in the first and second frontal convolu- tions, as most neurologists maintain. It is quite certain that a lesion of the front part of the corpus callosum is characterized by apraxia of the left arm ; this important discovery may well lead to successful surgical removal of tumours there situated. A lesion in the left frontal cortex may cause apraxia of both arms ; there will probably be right hemiplegia as well, which would mask the condition in the right arm. To sum up, a lesion is cortical if there are present : — 1. A monoplegia. 2. Hemiplegia with either (i) Aphasia which persists ; (ii) Recurring convulsions ; (iii) Flac- cidity ; (iv) Apraxia of the opposite side. Left-sided apraxia without hemiplegia indicates a lesion of the corpus callosum. APHASIA. The various types of aphasia have always presented problems of great complexity but of great interest. Recent studies of the subject have been very revolu- tionary in their tendency. We used to learn that there were three great centres for the appreciation and utterance of language, namely : — 1. The motor centre, controlling utterance, in Broca's convolution (the third left frontal). 2. The auditory word centre, appreciating spoken language, in the posterior part of the second left temporal convolution. This was also regarded as dominating and being necessary for the activity of the other two centres. CEREBRAL LOCALIZATION 167 3. The visual word centre, appreciating written language, in the left angular gyms, behind and above the auditory word centre. Now, however, the searching analyses of Marie and his pupils have raised very grave doubts about the first and third of the above, and many neurologists have agreed that Broca's convolution has no speech function at all ; very few now defend the existence of a separate visual word centre. Briefly, the contention of Marie and Moutier may be put thus. Between 1861 and 1906, there have been published 304 cases of aphasia with autopsy. Of these 201 were useless and 103 were relevant. Useless f Lesion too extensive - ( Badly described 175 26 201 Favourable to I Corti'al -lesions ™th Rrnra'« Wai aphasia Broca s local- , Subcortical lesions lzatlon I with aphasia - Relevant < Unfavourable to Broca's localization Aphasia, but Broca's convolution normal 57 No aphasia, but Broca's convolu- tion destroyed (in two caseSjbilateral destruction) - 27 304 The majority even of the nineteen cases allowed by these writers they consider to be inconclusive for various reasons. Two cases of Burckhart's are of sufficient surgical interest to be worth quoting. In the first, he removed 5 grams of grey matter from the foot of the first and 168 CEREBRAL LOCALIZATION second left temporal gyri, but no word-deafness resulted. Eight months later he resected the cap and foot of the left third frontal gyms (Broca's convolution) , but no aphasia followed. In the second case he resected, in several operations, the left supramarginal, temporal, and third frontal gyri, but he failed to induce any speech defect. The patients were demented, with verbal delusions and logorrhoea. Marie maintains further that all patients with aphasia are mentally deficient ; thus, the cook can no longer compound an omelette, and the pianist can no longer play the piano. He locates all the speech functions diffusely in the left temporo- parietal region, maintaining that this is merely a region of intelligence specialized for language, and not a storehouse of sensory images ; a mild lesion destroys the function last acquired, viz., reading, andja severer lesion produces loss of voluntary speech and of recognition of spoken language as well. What Marie calls " anarthria " — a word previously used in another sense — meaning loss of the power to utter speech, although the individual can say the words over to himself, is due to a lesion in " the quadrilateral," bounded in front and behind by the anterior and posterior limiting sulci of the island of Reil, internally by the wall of the lateral ventricle, and externally by the surface of the island of Reil. In most cases of so-called Broca's aphasia, both the temporal cortex and the " quadrilateral " are injured. Defenders of the classical view, Dejerine in par- ticular, have replied by advancing fresh cases with CEREBRAL LOCALIZATION 169 a lesion in Broca's gyrus with aphasia resulting ; they contend that Marie's " quadrilateral " contains the projection fibres of the third frontal convolution, which in their view explains the anarthria ; and they maintain that most of the fifty-seven cases of aphasia in which Broca's convolution was intact were associated with much defect in understanding language spoken or written, and that the lesion was one of the dominant auditory word centre in the temporal lobe, without which Broca's convolution cannot work. If it were proved that in cases of apraxia, previously referred to, the lesion was in the first frontal con- volution for the legs, and in the second frontal for the arms, the location of speech just in front of the motor centres for the face and mouth would receive strong support by analogy, but all this is still very uncertain. To sum up, we may express current opinion by accepting the existence of a large diffuse centre in the left temporo-parietal region in which recognition of spoken and written language and " internal speech " take place ; when it is seriously damaged these are all lost and the intelligence is impaired. Whether there is a special departure platform in Broca's convolution for uttering speech is uncertain, but probably there is. Lesions of the projection fibres from the cortex ( (?) of Broca's convolution) will cause " anarthria," that is, loss of external but not of internal speech. Practical deductions are not to trust aphasia as conclusive localizing evidence of a lesion in the left 170 CEREBRAL LOCALIZATION third frontal gyms, but rather to look to the temporal region, especially if there is any defective appreciation of what is said or written. Moreover, we receive encouragement that there is no need to fear that small cortical injuries inflicted by the surgeon will cause aphasia ; subcortical injuries are much more likely to do so, by cutting off projection fibres. MISLEADING LOCALIZING SIGNS OF INTRA- CRANIAL TUMOUR. It is very disappointing when definite signs usually regarded as of importance in localization give colour to a diagnosis as to the position of a cerebral tumour, but on the operation table nothing is found in that region. It is more than disappointing, because un- successful attempts to find the tumour are more fatal than actual removals. Some study therefore of the physiology of the production of misleading signs may be useful. The principal traps are furnished by the following : i. CRANIAL NERVE PALSIES. — Paralysis of one or both sixth cranial nerves is quite common, and by no means proves that the nerve itself or its nucleus is involved in the lesion. It has been accounted for by stretching, due to a supposed backward dis- placement of the whole brain late in the development of a growth ; the abducent nerves run straight forwards and are slender, so the first sign of the displacement is a convergent squint. Other cranial nerves, including the third, fifth, seventh, and eighth, are occasionally affected by dis- placements of the brain or by pressure. CEREBRAL LOCALIZATION 171 2. LOCALIZED OR GENERAL CONVULSIONS. — Mis- takes are particularly apt to arise if the fit starts in some definite area, follows a slow and orderly march to other areas, and perhaps affects only one side, consciousness being lost late if at all (Jacksonian epilepsy). It must, however, be remembered that all this may occur without any obvious cortical lesion ; indeed, the commonest cause of a localized convulsion is ordinary idiopathic epilepsy. Again, localized or general convulsions may give a wrong impression when arising late in the course of an intracranial tumour or abscess, especially if it presses on the ventricular system of the brain and dams back the cerebrospinal fluid, causing hydro- cephalus. The accumulation of fluid in one or both lateral ventricles stretches the overlying cortex, and may give rise to fits, sometimes of a Jacksonian type. 3. BILATERAL SPASTIC PARESIS. — In many cases a hint is given of the true nature of these seizures, by the presence of a slight degree of bilateral spastic paresis, with clumsiness of movement, exaggerated reflexes, extensor plantar response, and a little rigidity. Of course, if this should chance to be associated with paralysis of a cranial nerve, such as the sixth, the temptation to diagnose a lesion of the pons would be very great. Fortunately, this would not be of much surgical importance, as the pons is not an accessible structure. Pontine tumours are often unilateral, and optic neuritis is usually absent ; whereas in the class of cases we are now considering, optic neuritis is marked and old-standing, and there 172 CEREBRAL LOCALIZATION is a long history of headache, vomiting, or other signs, previous to the development of spasticity or cranial nerve palsy. In other cases, misleading localizing signs may arise from patches of secondary thrombosis, spreading oedema, or meningitis ; but none of these are common. The suspicious feature about all the signs here mentioned is their late development. Localizing symptoms appearing when headache, vomiting, optic neuritis or other evidences have been present for months or years are little to be trusted. Early localizing signs, on the other hand, are trustworthy in the main. A few words may be said about the significance of ataxia. This is of course evidence of a lesion of the cerebellum, but it may be seen in other conditions also. Putting aside ataxia due to affections of the labyrinth, Friedreich's ataxia, and other general nervous diseases, it may also be caused by a tumour in the neighbourhood of the red nucleus in the isthmus, or in the pons. THE CEREBROSPINAL FLUID. This fluid is clear, watery, and of low specific gravity ; it contains almost no albumin, but some sugar. Until recently this reducing substance was thought to be a pyrocatechin body. It contains no cells in health, nor does it contain the antitoxins, opsonins, or alexins which are present in plasma, lymph, and most serous fluids. This explains the great liability to septic meningitis after injuries to or operations on the central nervous system. As CEREBRAL LOCALIZATION 173 urotropin is excreted into the cerebrospinal fluid when given by mouth, it may usefully be administered to prevent septic complications such as the above, or following on suppurative otitis media. Some success is already claimed for this procedure. The fluid is secreted by the choroid plexus into the lateral and third ventricles ; it passes by the Sylvian aqueduct into the fourth ventricle, escapes by the foramina in the roof into the subarachnoid space, and is absorbed, partly by the aid of the Pacchionian bodies, into the superior longitudinal sinus and other veins. Hydrocephalus is produced by blocking of the foramina in the roof of the fourth ventricle. If an exit is provided, large quantities of cerebrospinal fluid may be lost daily. Lumbar puncture is a very valuable aid to diag- nosis in various forms of meningitis, parasyphilitic affections etc., and the fluid may be blood-stained after cerebral haemorrhage or injury. It is also valuable in treatment as a means of reducing intra- spinal and intracranial pressure, particularly if the trouble lies below the tentorium. REFERENCES. GUSHING AND BORDLEY. — " Observations on experimentally induced choked disc." Bulletin Johns Hopkins Hospital, 1909, xx., p. 95. HORSLEY. — " Optic Neuritis." British Medical Journal, 1910, i., p. 553. HORSLEY AND CLARKE. — " The structure and functions of the cerebellum." Brain, 1908, xxxi., p. 45. THIELE. — •" The optic thalamus and Deiter's nucleus." Journ. of Physiology, 1905, xxxii., p. 358. ALLEN STARR. — " Tumours of the acoustic nerve." Amer. Journ. of Medical Sciences, 1910, cxxxix., p. 551. 174 CEREBRAL LOCALIZATION BERGMARK. — " Cerebral monoplegia." Brain, 1909, xxxii., P- 342. GUSHING. — " A note on faradic stimulation of the post- central gyms in conscious patients." Brain, 1909, xxxii., p. 44. WILSON. — " A contribution to the study of apraxia." Brain, 1908, xxxi., p. 164. COLLIER. — " Recent work on aphasia." Brain, 1908, xxxi., P- 523- COLLIER. — " The false localizing signs of intracranial tumour." Brain, 1904, xxvii., p. 490. 175 CHAPTER XII. THE ACTION OF CUTANEOUS ANESTHETICS. Local anaesthetics given hypodermically ; cocaine, novocain, eucain, stovain. — Drugs applied to the unbroken skin ; opium, belladonna. — Counter-irritants ; the theory of their action. THE drugs which may be used as local anaesthetics and analgesics fall into three groups. Some of them are commonly given by hypodermic injection beneath the skin, although they may be painted or sprayed on mucous membranes with satisfactory results. Here we put cocaine and its derivatives, eucain (more precisely, /3-eucain lactate), novocain, stovain, and tropocaine. In another group we place the drugs which are applied to the unbroken skin in the form of ointments, liniments, and plasters, including pre- parations of belladonna, opium, aconite, cocaine, and menthol. In the third group we place the drugs which are not credited with any local anaesthetic action, but which are classed as counter-irritants. This is an immense collection ; it comprises all the volatile oils, especially mustard, camphor, and tur- pentine, also such substances as alcohol, iodine, cantharides, and ammonia. The thermo-cautery is not a drug, but its action calls for similar inter- pretation. 176 THE ACTION OF LOCAL ANESTHETICS GIVEN HYPODERMICALLY. We have to compare in this group the value of cocaine, novocain, eucain, and stovain. A luminous report was published on these by a Committee of the British Medical Association in 1909. The ideal local anaesthetic should have the maximum power to relieve pain, it should not be toxic, it should not irritate the tissues, and it should be capable of sterili- zation by boiling. The table below gives the comparison of these four drugs at a glance. DRUG AN/ESTHETIC POWER TOXICITV EFFECT ON TISSUES EFFECT OF BOILING Cocaine Powerful Most toxic Rather Spoiled irritant Eucain Powerful Least toxic Very No effect irritant Stovain Most power- Rather toxic Very No effect ful irritant Novocain Powerful Least toxic Not No effect irritant It will be seen that novocain is the most satis- factory, and cocaine the least so. It is common knowledge that cocaine, like chloral, is very variable in its effects on different people, and a safe dose for one is fatal for another. With some patients the margin of safety between a dose that produces no effect at all and a dose that causes alarming symptoms is exceedingly narrow. The symptoms, again, vary widely.^ Some get headache, others CUTANEOUS ANAESTHETICS 177 vomiting, and yet others fainting and collapse. Fatal cases have often occurred even after moderate doses, and it is never safe to give more than a quarter of a grain of cocaine unless the patient has had it before. Most surgeons will doubt if eucain is really as powerful an anaesthetic as cocaine, but in its main details the correctness of the above table has been abundantly demonstrated by many independent observers. Mr. Barker, and others following his example, have claimed great advantage from combining adrenalin with the cocaine or its derivative. The suggestion is that the vasoconstriction induced keeps the cocaine from being carried rapidly away by the circulation. Thus we increase the local effect, which is desired, and diminish the general or systemic effect, which is not desired. There is no doubt that the method is often most efficacious, but adrenalin is a powerful agent, and occasionally it seems to be responsible for alarming collapse. Whatever drug or combination of drugs is used for hypodermic injection as an anaesthetic for opera- tive purposes, it is of cardinal importance that it should be correctly given, and an extraordinary number of surgeons do not appear to know how to secure a good result. Again and again one sees cocaine injected, and one can foretell with certainty that the patient will scream with pain when the incision is made. In another case half the dose gives a perfect anaesthesia. The whole point is that the sensitive nerve-endings are not in the subcutaneous 12 178 THE ACTION OF fat, but in the cells of the Malpighian layer of the skin, and the injection must be made into the skin, not into the fat. When the anaesthetic has been properly given, the skin will be white, and will present a flat-topped infiltration with a sharp edge, like that which is so characteristic of erysipelas. To make a satisfactory intradermic injection a small hypo- dermic syringe is seldom good enough. One needs a powerful syringe with a fine needle. An anti- toxin syringe does excellently. DRUGS APPLIED TO THE UNBROKEN SKIN. It has been customary to relieve abdominal pain by the application of hot fomentations containing opium, to treat sprains and bruises with lead and opium, and to smear on glycerin of belladonna for the discomfort of white leg. What dyspeptic old lady has not worn a belladonna plaster over her heart, and what practitioner has not prescribed a belladonna liniment for vague aches and pains ? The rationale of the treatment has been that bella- donna, opium, and menthol are alleged local anaesthetics, and it is further supposed that they are absorbed by the unbroken skin. The truth is that they are not local anaesthetics, and that they are scarcely if at all absorbed through the unbroken skin. Neither aconite, cocaine, carbolic acid, bella- donna, nor opium has any power to relieve pain when applied to the unbroken skin. It has been well said that " You have not proved a lie to be a lie, until you have shown how it came to be believed." This is very true in science, and CUTANEOUS ANAESTHETICS 17fc especially in medical science. The use of belladonna and opium to relieve local pain was an obvious deduction from their great power, when given by the mouth, to relieve general pain by inducing sleep or allaying colicky contractions. In the case of bella- donna and its alkaloid atropine, the fallacy was the more natural in that they have a very genuine effect in paralysing nerve-endings, but, unfortunately, it is only the nerve-endings in glands and unstriped muscle that are paralysed, not the sensory twigs in the skin. The fallacy has been maintained by the practice of combining these drugs with other and more potent treatment ; thus, belladonna is given with counter- irritants such as camphor or alcohol ; warmth may be applied with the opium ; friction helps the bella- donna liniment to make a reputation, and even the support of the strapping, with counter-irritants in it, assists the patient to believe in the value of a belladonna plaster. We may go one step further, and say that the application of opium and belladonna to mucous membranes is equally futile. There is no evidence that opium suppositories after the operation for piles, or laudanum dropped into aching ears, have any direct local effect. Of course, morphia may be absorbed from the suppository, but in that case it presents no advantage over a dose given by mouth or hypodermically, and is less certain in its action. To sum up, there is no drug in common use capable of acting as an anaesthetic on the unbroken skin, except ether and ethyl chloride, which freeze it, and 180 THE ACTION OF the only drugs which relieve deep-seated pain when painted on or rubbed into the skin are the counter- irritants. Full details of the experimental data for these conclusions, which are accepted by the leading pharmacologists, will be found elsewhere. Briefly, the methods adopted were as follows. Strong, even dangerously strong solutions and ointments containing opium, atropine or belladonna, aconite, cocaine, carbolic acid, and menthol were tested on the skin of the finger, and on the tongue, and these were then examined to see if their sensi- bility was in any way altered. The methods of examining the skin of the finger were as follows. Each test was applied on more than one observer and after varying intervals of time. 1. The Intolerable Temperature Test. — For each observer there was a certain constant temperature which was just not intolerably hot, when the finger was dipped into warm water for half a minute. This was determined before and after applying the drug under consideration. 2. The Faradic Pain Test. — The strength of current was determined, before and after the application of each drug, at which the damp finger first found electrical stimulation by means of electrodes led off from a faradic coil actually painful, the current used being small at first and gradually augmented. 3. Thermal Discrimination Test. — We found that we were able, by immersing the finger first in one beaker of warm water and then in another, to detect a difference in temperature of not less than one degree. CUTANEOUS ANAESTHETICS 181 This was tested before and after the application of each drug. 4. General Testing by means of a pin point, the sesthesiometer, a wool pencil, etc., was also used. In testing the sensibility of the tongue, we used the faradic pain test as described above ; we examined thermal discrimination by applying warm metal points at various temperatures ; we used the aesthesio- meter, and studied the effect of the drugs on taste. Judged by these standards, the various drugs fared as follows : — Opium. — A 5 per cent solution of morphine tartrate in water had no effect on skin or tongue. Belladonna. — Very strong liniments had no anaes- thetic effect. Indeed, if they had, the drug could be used instead of cocaine for eye surgery. The only sign we could obtain was diminution of sweating over the skin area treated. There was no flushing or blanching of the skin or mucous membrane. Aconite. — Neither the B.P. liniment nor ointment had any effect on the skin. Solutions produced tingling of the tongue, but we were not quite confident whether there was or was not a little reduction in sensibility. Cocaine. — Strong ointments and alcoholic solutions had no effect on the unbroken skin. Of course, if the skin is broken, the effect is marked. A 10 per cent solution applied to the tongue produced con- siderable reduction of sensibility, by all our tests. Menthol produces a curious stimulation of the nerve-endings which detect cold, as is well known. A discussion of its other actions would lead us too 182 THE ACTION OF far, but any anaesthetic effect is purely that of a counter-irrita nt . Carbolic Acid rather increases the sensitiveness of the finger to painful stimuli. Its undoubted value in relieving toothache is due to its Caustic action in destroying irritated nerve-endings. The numb feel- ing we get after prolonged soaking in I in 20 carbolic is due to the formation of a thin coating of killed epidermis over the hands. The fact that even cocaine, which is thoroughly proved to paralyse sensory nerves, fails to produce the slightest effect when a 10 per cent solution in alcohol, or a 10 per cent ointment made with lanolin is rubbed into the skin, is strong evidence that little if any of these alkaloids reaches the nerve-endings at all. Atropine finds its way into the sweat ducts sufficiently to reduce but not to abolish sweating by its action on the sweat glands. It may be objected that there is sufficient clinical evidence of benefit from these drugs to defy negative results by experimental methods, but any who claim this must not confuse the issue by combining the belladonna or opium with camphor, heat, rest, or strapping. Again, it may be suggested that atropine, at least, has some vasomotor effect, but we failed to observe any, and indeed we doubt if it ever reaches the blood-vessels when rubbed into the unbroken skin. It is a thankless task to pull down strongholds of belief, but it is necessary if only to direct more attention to the true means of giving relief to pain, including general drug treatment, rest, massage, counter-irritation, heat, and passive hyperaemia. CUTANEOUS ANAESTHETICS 183 Moreover, a recognition of the failure of drugs saves useless expense, and may banish from patients' houses some of the commonest of powerful poisons. Belladonna liniment, for instance, has been respon- sible for an immense number of alarms, illnesses, and even fatalities. COUNTER-IRRITANTS. In order to have a clear conception of the subject before us, let us take three illustrations of the use of counter-irritants : (i) The application of diluted tincture of capsicum to the loin for lumbago ; (2) Rubbing in soap liniment for a painful sprained ankle ; and (3) Putting a blister behind the ear for earache. These are old and tried remedies ; have we any evidence of their value ; and if so, how do they act ? Why should an irritation of the cutaneous nerve- endings make any difference to the sensations received from deep fasciae, synovial membranes, or the middle ear ? No one can deny the great relief given by the above measures. The effect of the first is often marvellous, to which some of us can bear personal testimony. The liniments and other applications mentioned in the group we have just considered have traded for their reputation on the counter-irritation they produced. We have the analogous means of relieving pain, the use of hot fomentations and of the thermo-cautery, waiting for an explanation on similar lines. Before considering why counter-irritants relieve 184 THE ACTION OF pain, we should first inquire why inflammation is painful ; in what way do the vascular and other changes that take place in inflamed areas irritate nerve-endings ? It cannot be merely by the flushing with blood, because Bier's bandage greatly increases this, and yet relieves pain. It may be by the chemical irritation produced by the toxins, or more probably by stretching of nerve-endings owing to the swelling up of the tissues with inflammatory exudate. That stretching will cause acute pain is shown by its occurrence in colic. Dropsy is not painful, because in that condition the fluid passes out passively where the resistance is least, as in the subcutaneous tissues ; whereas inflammatory exudation is an active process affecting all the tissues involved in the inflammation, even when they are tense and full of nerves. It seems strange to claim that vascular dilatation should relieve such a condition. Would it not rather add to the painful tension ? In unyielding structures this may be true ; the general vasodilatation and falling blood-pressure just as we go to sleep will exaggerate the aching of chronic bone inflammation. But we must consider how the painful exudation of plasma into all the interstices of the tissues is to be removed ; it can only be by increasing the lymph flow, by increasing the absorption of fluid by the venules, and by washing away the toxins which set up the exudation. To increase the lymph flow, the part must be elevated and a better " head " of water provided by vasodilatation. To increase absorption by the blood-stream, there must be vasodilatation. CUTANEOUS ANESTHETICS 185 To carry off and dilute toxins, again, there must be vasodilatation. It is true that in the early stages, before any quantity of exudate has been poured out, and where the cause of the trouble is mechanical injury, not bacterial toxins, the vasoconstriction obtained by cold may prevent the increase of the fluid in the tissues. But when the outpouring has already taken place, we need some means of inducing vasodilatation. We need not explain how heat and Bier's bandage will produce this effect, but at once turn to ask why putting irritants on the skin can cause vasodilatation in the deeper parts. Each segment of the spinal cord, medulla, pons, and isthmus receives sensory impulses from the skin, and also from a viscus. Messages from the former we can localize accurately. Messages from the latter the segment cannot localize at all, but we know vaguely that the discomfort is in the visceral area which is innervated from that segment. Mis- interpretations are common, and consequently there may be incorrect localizing of a pain, and tenderness of the corresponding skin area when really the viscus is at fault. To quote a few instances, earache without deafness is usually due to a carious lower back molar ; skin tenderness of the right eleventh dorsal area is associated with commencing appendi- citis ; and painful affections of the ovary or testis may cause girdle pain in the tenth dorsal area. The liver, heart, and stomach all have their areas of referred pain. Dr. Head has published much research on these topics. 186 CUTANEOUS ANAESTHETICS Irritation of the cutaneous nerves by iodine, camphor, cantharides, menthol, or heat will be inter- preted by the spinal segment as a call for local vaso- dilatation, and in responding to the appeal more blood is supplied not only to the skin area but also to the corresponding viscus. As we have seen, the better blood-supply will give some relief, if such relief is possible, to the pain. This is the theory of counter-irritation. The practical corollary is that our counter-irritants should be those having a powerful and prolonged effect on the cutaneous nerves. REFERENCES. REPORT OF B.M.A. COMMITTEE. British Medical Journal, (i.), 1909, p. 783. A. RENDLE SHORT AND WALTER SALISBURY, British Medical Journal, 1910, (i.), p. 560. 187 APPENDIX. URINE ANALYSIS IN CASES FED BY NUTRIENT ENEMATA. I AM given kind permission to set forth the following unpublished observations by Dr. R. E. Thomas on patients under Dr. Nixon in the Bristol Royal Infirmary. CASE I. — L. W., a girl aged 22, was admitted for haematemesis on Nov. 9, 1909, and was treated with nutrient enemata consisting of 4 oz. of milk with one egg peptonized for twenty minutes, given every four hours. One to two pints of saline were also given daily by the rectum, and the bowel was washed out every morning. Nothing was given by mouth, except a little ice, until Nov. 22. The urea was estimated by the hypobromite method, the ammonia nitrogen by the formalin method, and diacetic acid and acetone by the tests described in Chapter VII. (See Table, pp. 188, 189). CASE II. — M. H., a girl aged 20, was admitted for haematemesis on June i, 1909. The treatment was exactly as in Case I., but no analyses of the urine were made until June 19, on which day mouth feeding began as well as the nutrients, which latter went on till July 7. (See Table, p. 190). 188 APPENDIX "^J CO CO V0 0s* t^» ^h HI M M M •*• O HI M i ii s « 2 \O ^" ^O *O O O rf- ro O O OO V> •f ro •«t- CO < DM O M W M M M HI HI rx - c V o ^00 O-ONOO'S'3^ HI t^ a t, \O HI CO d d M n» tO W) fO < & ON ON 00 00 OO rt OO oo oo 5 .is 11 ^3 en en <0 0 CU c».oo ^j^j'r rnt^OO OOO OQ^ •S o* Vf b «o 60 ^ ^ do 00 O M OO 60 ib x c •4-* M M M en B u o z o g u < ^7" O O "^ ^ ^ ^"^ "3 u o o J? <-> rt B 333 53 i3 s a a a > a o o 3 3 8 8 DIACETIC ACID 53 1) 4) ifl J3 ^3 § i isi § u O O fl fl fl -*j en •HP R 1 1 8 8 Z v en ~~ U , O , , z z O O ^ O t^ w M N XT CO ~O Mg N HI •"' o 1 i m. 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C ,1^3 +3^^2 ; :—,Hy •^ JH C QC ^ t>2 JJ QO U 4; 5 * h "~" -rt O rt <1 X O P -n VM 71 g-g - 5 ^ C 0 O ** CO - ~ - cu * •• - : 5 ™ S""^S "rt ^MC^ S ^ e S ^ ** ^ *5 -TH •Si, "i 5! 11 s s2iii 360SO ^=?o^3 § ?| = * • " 52! ^ VI 00 10 o _ rxj LM *>• en 5> ^ DA* f C F FAST 1 2 3 4 5 6 7 8 9 10 ii 12 13 14- 15 16 17 18 19 20 21 1 A / \ / \ 5 «., «•• •»• -* \ \ f -*, \\ T ? X w 1 Mf V V A \1 •u- «. ^ V •0* -* ]l > A • f" ••H m »• -•x • ' \ / •: •» Case I. — - — - — Case II. - - Average of Fasting Cases. INDEX A BSORPTION in the colon /\ — of proteins Acetonaemia after chloroform — conditions in which seen — treatment of Acetone in urine normally test for . . — origin of, from fat Acid dyspepsia of infants Acids in dyspepsia Acidosis after chloroform — conditions in which seen — in diabetes . , — pathology of — treatment of Aconite as local analgesic Acromegaly — treatment of Addis on haemophilia . . Addison's diseas sure in . Adenin . . Adiposity from removal pituitary gland — treatment of Adrenalin, influence o pressure — toxic symptoms from — transfusion for shock — useless in haemoptysis — uses of Albuminuria, tra salts for Alcohol, effect on digestion — in shock Alkalies, effect on digestion Amino-acids Ammonia nitroj in Amputations, in with cocaine before Amyl nitrite for haemoptysis Anaesthesia, testing for Anaesthetics, local, how Anderson and Langley generation of nerve Anterior horn cell cl division of nerve-roots Antipepsin Antithrombin . . Aphasia . . PJ IGE p AGE ic colon 52 Appendicitis, hyperchlorhydria 46 with 36 oroform 1 20 Appendicostomy 5i i seen . . 97 Appetite juice 28 108 Apraxia 164 lally 98 Ataxia, cerebellar 154 109 — not always cerebellar 172 98 — from division of posterior ints 38 nerve-roots 138 3i Atheroma in cretin animals . . 5 arm I2O — and myxoedema 13 li seen . . 97 Atropine for chloroform poison- 108 ing 118 101 Auditory nerve, tumours of . . 156 108 — word centre 166 ;esic 178, 181 21 25 Baldwin, Helen, on oxaluria . . 92 73 Ballance and Stewart on re- ood-pres- generation of nerve 129 61 Ballance on nerve anastomosis 136 84 Bar any on nystagmus 155 loval of Barker on local anaesthesia . . 177 1 20 , 22 Barnard and Hill's sphygmo- 25 meter 57 sn blood- Baumann on thyroid 6 60 Bayliss and Starling on secretiu 42 •om 61 Belladonna as local analgesic ick 63 178, 181 ysis 67 Bergmark on cerebral cortex 61 159, 161 t, calcium Bethe on regeneration of nerve 131 Ro Bile 45 jestion 30 , 32 Billroth on tetany from thy- 63 roidectomy 3 ;estion . . 3° Bismuth feeding to map out 47 stomach 32 variations Bitemporal haemianopsia 22 103, 187 Bitters, effect on digestion . . 30 ig nerves Blood-clotting 69 :fore 62 Blood-pressure, arterial 57 optysis 67 — capillary, how measured . . 58 sr 125 — normal 58 >w to use 177 — venous, how measured 58 •y on re- — instruments for measuring 57 lerve 131 — falls during sleep . . 65 tiges after — in surgical shock . . 62 posterior — influence of respiratory 139 movements on . . 59 37 — lowered by chloroform 119 70 — raised by intracranial pres- 166 sure 65 I3A 196 INDEX PAGE Blue blindness in cerebral tumour . . . . . . 152 Bode on operations on the pituitary gland . . 22 Bordhy and Gushing on choked disc . . . . . . 150 /3-oxybutyric acid, origin of, from fat . . . . 98 in urine, test for . . 109 Brain, circulation in . . . . 64 — localization of sensation in 157 Broca's convolution .. .. 166 Broths and gastric juice . . 29 Brown, Langdon, on nutrient enemata . . 54, 193 Brown on parathyroid grafting 16 Brown-Sequard phenomenon 143 Bullock on haemophilia . . 72 Burckhardt on removal of speech centres . . 167 Burdach's tract . . . . 141 CAFFEINE, effects of . . . . 87 Calcium oxalate in urine . . 90 — salts for haemophilia . . 77 in tetany .. 15, 80 treatment by . . . . 80 Calculi, laws governing forma- tion of . . . . . . 94 Calculus, prevention of 89, 92 Cameron on gastrojejuno- stomy . . . . . . 41 Cancer, gastric, HC1 deficient in 40 Cannon on skiagraphy of stomach . . 32, 40 Cannon and Murphy on peri- stalsis . . . . . . 51 Capillary blood-pressure, how measured . . . . 58 Carbolic acid as local anaesthetic 178, 182 Cerebellar tracts . . . . 141 Cerebello-pontine angle, tu- mours of . . . . 156 Cerebellum, lesions of . . 152 Cerebral localization . . 150 et seq. — ^ tumour, blue blindness in 152 late signs misleading . . 172 misleading localizing signs of . . . . 170 optic neuritis in .. 151 Cerebrospinal fluid . . . . 172 Chilblains, treatment of . . 80 Chloroform causing sudden death .. .. .. 116 — effects of overdose of . . 119 — poisoning, delayed . . 120 treatment of . . . . 118 — possible dangers of .. 116 PAGE Choked disc, cause of . . 150 Chromatolysis of anterior horn cells . . . . . . 139 Clarke and Horsley on func- tions of cerebellum . . 152 Coagulation of blood, physi- ology of . . • . . 69 Coagulimeter . . . . . . 70 Cocaine as local anaesthetic 175, 176, 181 — injected into nerves to pre- vent shock . . . . 62 Cohnheim on pancreatic dia- betes . . . . . . 107 Collier on misleading signs of cerebral tumour . . 170 Colon, functions of . . 49 Coma, prolonged after chloro- form . . . . . . 120 Concretionary action . . . . 94 Concussion, blood-pressure after 66 — of the spinal cord . . . . 147 — treatment of . * . . 66 Congenital goitre . . 3, 9, 10 Convulsions in cerebral tumour 170 — localized .. .. .. 171 Corpus callosum, tumours of. . 165 — luteum, secretion of . . 43 n. Cortex, localization of sensation in 157 Cortical tumours, localization of 161, 166 21 of Cotter, Patrick, the giant Counter-irritants, mode action of . . . . 183 Cretin lambs . . . . . . 8 Cretinism, experimental, in animals . . . . 5 — treatment of . . . . 15 Crile on surgical shock . . 61 Gushing and Bordley on choked disc 150 Gushing on blue blindness . . 152 — on localization of sensation in cortex . . 157, 159 — on removal of pituitary 18, 19, 20 Cyclical vomiting . . 98, 100 Cystin, origin of . . . . 93 Cystinuria .. .. .. 93 Davis, O. C. M., on oxaluria . . 90 Better's nucleus, influence on tone . . . . . . 154 Dejerine on aphasia . . . . 168 Dextrose, absorption of by colon 55 Diabetes, causation of . . 103 Diabetic coma, prevention of nr treatment of .. .. 114 INDEX 197 PAGE Diabetics, operations on . . 1 1 1 Diacetic acid, origin of, from fat 98 — — in urine, test for . . no Diagnosis of starvation . . 103 Diphtheria antitoxin for haemo- philia . . . . . . 78 Diuretic, pituitary extract as a 24 Dixon on chloroform poisoning 119 Dunlop on estimation of oxa- lates in urine . . . . 90 Dyspepsia, treatment by drugs 30 Edkins on gastric secretion . . 29 Edmunds on goitre . . . . 8 — — myxoedema . . . . 3, 4 parathyroids . . . . 4 tetany . . . . . . 15 Eiselsberg on experimental cretinism . . . . 5, 13 Enemata, nutrient 49, 53, 187, 193 Enophthalmos from thyroid- ectomy . . . . . . 3 Epicritic sense .. .. 123, 124 Erepsin . . . . . . 47 Ergot useless in haemoptysis . . 67 Eucaiii as local anaesthetic 175, 176 Exophthalmos from thyroid feeding . . . . . . 6 Exophthalmic goitre . . . . 14 due to iodoform . . 12 Extractives and gastric juice 29 Fabre and Thevenot on con- genital goitre . . . . 10 Facial palsy, treatment of . . 136 . Fats .cause pancreatic secretion 44 — inhibit gastric juice . . 32 Fawcett on skeleton of a giant 21 Fenwick, Soltau, on hyper- chlorhydria . . . . 39 Fibrinogen . . . . . . 69 Fischer on the protein molecule 47 uric acid . . . . . . 83 Forssman on regeneration of nerve . . . . . . 133 Forster on division of pos- terior nerve-roots . . 139 Frohlich's symptom complex 22 Frontal cortex, functions of . . 161 GASTRIC juice, factors control- ling flow of . . 28, 29 inhibited by fat . . 32 — secretin . . . . . . 29 — ulcer, cause of . . . . 37 — hyperchlorhydria in . . 36 Gastrojejunostomy, course of food after . . . . 40 — for hyperchlorhydria or ulcer . . . . . . 39 Gastrojejunostomy, nutrition after . . " . . . . 41 Gastrostomy, feeding after . . 41 Gee on uric acid shower . . 90 Generali on parathyroids . . 4 Gigantism . . . . . . 21 Gley investigated parathyroids 4 Glucose, relation to acidosis . . 100 Glycosuria . . . . . . 103 Goitre, causation of . . . . 9 — iodothyrin in . . • • 7, 9 — relation to drinking water 7 — treatment of . . . . 15 Coil's tract . . . . . . 141 Goodman on transfusion for hiemophilia . . . . 78 Gout, pathology of . . . . 88 — treatment of . . . . 90 Grafting for myxoedema, cre- tinism, or tetany . . 16 Graves' disease . . . . 14 caused by iodoform . . 12 treatment of . . .. 16 Gravity, effect of on blood- pressure.. .. .. 59 Gray on skiagraphy of stomach 32, 40 Groves, Hey, on the colon . . 53 Guanin . . . . . . . . 84 Gull on myxoedema . . . . 2 H.EMATEMESIS, treatment by nutrient enemata . . 187 Haemophilia, pathology of ..71,72 — treatment of . . . . 76 Haemoptysis, treatment of . . 67 Haemorrhage into spinal cord 148 — membranes. . . . 148 Haemorrhages, profuse . . 68 Haemorrhagic diathesis, cause of 68 Hall, Walker, on the colon . . 53 on gout . . . . 89 the purinometer . . 90 Halliburton and Mott on re- generation of nerve . . 132 Hahtead on partial thyroid- ectomy . . . . . . 3 Harrison, Ross, on developing nerve fibres . . . . 132 Head on cutaneous sensation 124 referred pain . . . . 185 spinal segmental areas 138 Head and Thompson on spinal tracts . . 141, 142, 143 Headache, lymphatic, calcium salts for . . . . 80 Hearing, cortical localization of 157 Heart, massage of for chloro- form poisoning . . 118 Hele on cystinuria . . . . 93 198 INDEX PAGE Hemianaesthesia, not cortical 159 Hertz on gastric sensation . . 34 skiagraphy of stomach .. 33 Hill, L., on influence of gravity on blood-pressure . . 59 — on intracranial circulation 64 capillary pressure . . 58 Hill and Barnard's sphygmo- meter . . . . . . 57 Hormones . . . . . . 43 n. Horsley and Clarke on func- tions of cerebellum . . 152 Horsley, Sir V ., on cerebral cortex . . . . . . 160 on optic neuritis .. 151 • myxoedema . . . . 3 Hour-glass stomach, diagnosis of 34 Hunger, explanation of . . 33 Hunger-pain . . . . . . 36 Hunt and Seidel on iodothyrin 8 Hydrocephalus, pathology of 173 Hydrochloric acid, deficient in gastric juice . . . . 40 Hydrochloric acid, variations in stomach . . . . 35 Hyperchlorhydria . . . . 36 Hypoxanthin . . . . . . 83 Hypnotics, mode of action of 115 ILEOSIGMOIDOSTOMY, a draw- back of. . . . .. 51 Infantile palsy, nerve anasto- mosis for . . . . 136 Infantilism from removal of pituitary gland 20, 22 — treatment of . . . . 25 Intestinal paralysis, treatment of 52 — peristalsis, arrest of . . 52 Intestine, functions of large . . 49 Intracranial circulation . . 64 — pressure, effect on blood- pressure . . . . . . 65 Iodides, action on gummata and atheroma . . . . 13 — for goitre . . . . . . 8 Iodine in foodstuffs . . . . 10 — thyroid . . . . . . 6 lodof orm poisoning . . . . 1 1 — and the thyroid . . . . i r Iodothyrin . . . . . . 6 JACKSONIAN epilepsy . . 171 Jackson-Taylor's test for ace- tone . . . . . . 109 Jaundice, hsemorrhagic ten- dency in . . . . 76 Kilvington and Osborne on nerve anastomosis . . 136 PAGE Knee-jerk absent with posterior nerve-roots divided . . 138 Kocher on tetany . . . . 15 -- the thyroid . . . . 1,3 K ohn on parathyroids . . 4 Kossel on the protein molecule 47 Kropfbrunnen . . . . . . 7 LABYRINTH and nystagmus . . 155 Lactation, cause of . . . . 43 n. Laidlaw and Ryffel on nutrient enemata . . . . 54 Langley and Anderson on re- generation of nerve . . 131 -- nerve anastomosis .. 135 Leukaemia, uric acid in . . 87 Liepmann on apraxia.. .. 164 Liver, action on uric acid . . 86 Local anaesthetics, how to use 177 Localization, cerebral., isoetseq. Lossen and Morawitz on haemo- philia 73 Lumbar puncture in diagnosis 173 -- for intracranial pressure 66 Lungs, circulation in . . . . 66 Macallum on tetany . . . . 15 Magnesium salts, treatment by 81 Magnus-Levy on acidosis . . 99 — thyroid feeding . . . . 6 Marie on aphasia . . . . 167 Marine on cretin lambs . . 8 Mayo on Graves' disease . . 16 — — hyperchlorhydria . . 39 Mellanby on blood-clotting 69, 75 Meningitis, prevention of . . 172 Menopause, treatment of . . ' 80 Menthol as local analgesic 178, 181 Meyer, Hans, on action of hypnotics . . . . 115 Milk, cause of secretion of . . 43n. Miller, Reg., on infantile dyspepsia . . . . 38 Misleading localizing signs of cerebral tumour . . i/o Monakow's bundle . . . . 140 Monoplegia from cortical tumours .. .. 162 Moore, B., on calculi . . . . 92 Morawitz and Lossen on haemo- philia . . . . . . 73 Mott and Halliburton on re- generation of nerve . . 132 Moussu on parathyroids . . 4, 5 Movements of stomach . . 32 Murray on myxosdema and cretinism . . . . 2 Murray and Warrington on nerve anastomosis for infantile palsy . . . . 137 Mummery on surgical shock.. 62 INDEX 199 Murphy on operations on jejunum . . . . 33 Murphy and Cannon on peri- stalsis . . . . . . 51 Myxoedema and atheroma . . 13 — experimental , . . . 2, 5 — treatment of . . . . 15 NERVE Anastomosis . . . . 135 — grafting .. . . . . 135 — injuries, effects of . . 123 regeneration . . . . 128 — -roots, development of . . 132 — distribution, table of 144, 145 effects of division of . . 138 — surgical indications for dividing posterior . . 139 — section, effects of incomplete 128 — suture, on bridging gaps . . 135 recovery after . . . . 134 — transplantation . . . . 135 Newt, regeneration in the . . 149 Nissl's degeneration in anterior horn cells after division of posterior nerve-roots 139 Nitrites for haemoptysis . . 67 Nitrogen output on nutrient enemata . . 187, 194 Novocain injected into nerves to prevent shock . . 62 — as local anaesthetic .. 175, 176 Nucleoprotein and purin bodies 83 Nutrient enemata 49, 53, 187, 193 Nystagmus, cerebellar .. 155 — labyrinthine . . . . 155 O'BYRNE, Patrick, the giant. . 21 Occipital lobe, function of . . 158 Olive oil, action on bile flow . . 46 Operations on diabetics . . 1 1 1 Opium as local analgesic 178, 181 Optic neuritis, cause of . . 150 Ord on myxcedema . . . . 2 Osborne and Kilvington on nerve-anastomosis . . 136 Osier, cases of haemophilia 72 n. Oxaluria . . . . . . 90 — prevention of . . . . 92 PAIN sense, conduction in spinal cord . . . . . . 141 Pancreatic diabetes . . . . 105 — fistulas . . . . . . 44 — juice, secretion of . . . . 42 Parathyroids, effects of removal of 5 Paterson on gastro-jejunostomy 41 — — hyperchlorhydria . . 39 Paulesco on removal of pitui- tary . . . . 18, 19 Pawlow on gastric juice . . 27 pancreatic secretion . . 43 Pawlow on peristalsis Pepsin, relation to diet Peristalsis in colon — gastric Perroncito on regeneration of nerve Phloridzin and glycosuria Pituitary extracts, feeding or injecting with for shock — gland, effects of removal of functions of structure of operations for removal of Pons, tumours of Post-central convolution, func- tion of . . Posterior columns of Goll and Burdach Posterior nerve-roots, effects of division of Posterior nerve-roots, surgical indications for dividing PAGE 15 30 49 33 132 104 63 19 156 159 138 139 Precentral convolution, function of . . . . . . 160 Prevention of shock . . . . 62 Proteins, absorption of . . 46 Prothrombin . . . . . . 69 — • at fault in haemophilia . . 74 Protopathic sense . . 123, 124 Pulmonary circulation . . 66 Parathyroids, anatomy of 4 Purin bodies, effects of . . 87 estimation of in urine . . 90 in food . . . . . . 83 Purinometer . . . . . . 90 Pyloric spasm . . . . . . 37 Pylorus, movements of . . 33 — stenosis of . . . . . . 38 Pyramidal tract . . . . 140 Pyrosis . . . . . . 37 QUADRILATERAL, Marie's . . 168 REACTION of degeneration after nerve section . . . . 123 partial nerve section 128 Recurrent sensibility .. .. 129 Reflexes lost from division of posterior nerve-roots . . 138 Regeneration of nerve . . 128 — not in the spinal cord . . 149 Respiratory movements, in- fluence on blood-pressure 59 Rhubarb, oxaluria from . . 91 Richardson on thyroid and parathyroid glands . . t Riva-Rocci sphygmometer . . 57 Roos on iodothyrin . . . . 8 thyroid feeding . . 6 200 INDEX PAGE Rubrospinal tract . . . . 140 Ryffel and Laidlaw on nu- trient enemata . . 54 SaJili on haemophilia . . . . 74 Salicylates poisoning . . 98, 101 Salisbury and Rendle Short on cutaneous anaesthetics 178, 180 Saliva, factors controlling flow of 26 Sandstrom discovered para- thyroids . . . . 4 Satta on atidosis . . . . 100 Schafer on pituitary . . 18, 20 Schiff on removal of thyroid i, 2 Secretin. . . . . . 42, 46 Seidcl and Hunt on iodoth5Trin 8 Segmental areas, table of 144, 145 Semicircular canals and nys- tagmus . . . . 155 Sensation, conduction in spinal cord . . . . . . 141 — localization of in cortex . . 157 — in stomach . . . . . . 34 Sensibility, recurrent . . . . 129 Serum of horse, for haemor- rhagic tendency . . 78 Sharkey on nutrient enemata 54 Sherren on cutaneous sensation 124 nerve suture . . . . 134 Sherrington on concentration of blood in shock . . 62 spinal segmental areas. . 138 Shock absent when posterior nerve-roots are divided 138 — contributed to by chloro- form . . . . . . 119 — imitated in animals . . 60 — pituitary extract in 24 — surgical, causes of . . . . 61 how to prevent . . 62 Short, Rendle, on division of posterior nerve-roots 139 iodoform and thy- roidism .-. . . 12 oxaluria . . . . 90 Short, Rendle, and Salisbury on cutaneous anaes- thetics . . 178, 180 Sight, cortical localization of .. 158 Soups and gastric juice . . 29 Spastitity, division of posterior nerve-roots for. . .. 139 Spastic paresis in cerebral tumour . . . . . . 171 Speech centres .. .. .. 166 Sphygmometers . . . . 57 Spinal cord, ascending tracts of 141 — • — descending tracts of . . 140 — — does not regenerate . . 149 PAGE Spinal cord, injuries of . . 147 tumours of . . 140, 142 — nerve-roots, effects of divi- sion of . . . . . . 138 — segmental areas, table of 144, 145 Spleen forming uric acid . . 85 Squint, divergent, in cerebral tumour . . . . . . 1 70 Squire, case of haemophilia 72 n. Standardization of thyroid extract . . . . 17 Starling and Bayliss on secre- tin . . . . . . 42 Starr, Allen, on tumours of auditory nerve .. .. 156 Starvation, diagnosis of . . 103 — survival in . . . . . . 56 Stereognosis . . . . . . 141 Stewart and Ballance on re- generation of nerve . . 129 Stewart-Harte case . . . . 149 Stomach, movements of . . 32 Stovain as local anaesthetic 175, 176 Strychnine for shock . . . . 63 Stuart-Hart's test for /3-oxy- butyric acid . . . . 109 Sudden death from chloroform 16 Suprarenal glands, influence in maintaining blood- pressure . . . . . . 60 TACTILE sense, conduction in spinal cord . . . . 142 Temperature sense, conduction in spinal cord . . . . 141 Temporal lobe, functions of . . 157 Tetany, experimental. . . . 2, 4 — treatment of . . 5, 15, 80 Thnenot and Fabre on con- genital goitre . . . . 10 Thiele on muscular tone . . 154 Thomas, R. E., on nutrient enemata . . 54, 187 Thompson and Head on spinal tracts . . 141, 142, 143 Thrombogen . . . . . . 69 Thrombokinase . „ . . 69 Thyroid colloid, chemistry of 6 — effects of removal of . . 2, 5 — extract, standardization of 17 — feeding . . . . . . 5 — intoxication . . . . 14 from iodoform . . . . 1 1 Transfusion for haemophilia . . 78 Transplantation of nerve . . 135 Trephining, palliative, for tumour . . . . . . 151 Trophic changes from division of posterior nerve- roots 138 INDEX 201 PAGE Trophic lesions, cause of 124, 126 Trotter on nerve suture . . 134 Tone, Deiter's nucleus and . . 154 — in diagnosis of cortical tumours . . . . 162 — influence of tracts on 140, 141 — loss of from division of posterior nerve-roots . . 138 — lost in cerebellar lesions 154 Treatment of acetonaemia . . 108 — acidosis . . . . . . 108 — acromegaly. . .. .. 25 — adiposity . . . . . . 25 — to prevent calculus ..89,92 — of chilblains . . . . 80 — chloroform poisoning .. 118 — late chloroform poisoning 121 to prevent . . . . 121 — of coma from starvation., no — concussion . . . . . . 66 — cyclical vomiting .. .. no — diabetic coma . . . . 114 — to prevent diabetic coma . . in — of dyspepsia by drugs . . 30 — epigastric pain . . . . 39 — facial palsy . . . . 136 — gastric carcinoma . . . . 43 — gastric crises . . . . 140 — gastric ulcer . . . . 39 — after gastrostomy . . . . 41 — of gigantism . . . . 25 — goitre . . . . . . 15 — gout.. 90 — Graves' disease . . . . 16 — haemophilia . . . , 76 — haemoptysis . . . . 67 — haemorrhagic tendency in jaundice . . . . 76 — hyperchlorhydria . . . . 38 — infantilism . . . . . . 25 — infantile palsy by nerve anastomosis . . . . 136 — injuries of spinal cord . . 148 — intestinal paralysis . . 52 — intracranial pressure . . 173 — lymphatic headache . . 80 — to prevent meningitis . . 172 — of menopause . . . . 80 — myxoedema . . . . 15 — nerve injuries . . . . 134 — by nutrient enemata 49, 53, 187, 193 — of oxaluria — painful inoperable cancer — pancreatic fistulae . . — post-anaesthetic vomiting — to prevent salicylate poison- ing in — of shock . . . . 62, 63 — spasticity 139 92 140 44 121 Treatment of transient albu- minuria . . . . . . 80 — tetany I5( 80 — uric acid deposit . . . . 89 — urticaria . . . . . . 80 Tumour of brain, misleading localizing signs of . . 170 Tumours in cerebello-pontine angle 156 — of cortex, localization of . . 161 — spinal cord.. .. 140, 142 UI.NAR palsy, symptoms of.. 124 Urates, origin of, in the body . . 82 Urea output on nutrient ene- mata . . . . 187, 194 Uric acid, origin of in body . . 82 deposit, treatment of . . 89 Urticaria, treatment of . . 80 VAGUS, action of chloroform on 116 — influence on gastric juice. . 28 Vasomptor reflexes . . 127 V as soli on parathyroids . . 4 Venous blood-pressure, how measured . . . . 58 Vestibulospinal tract . . . . 140 Vision, cortical localization of 158 Visual word centre . . . . 166 Vomiting, prolonged, after chloroform . . . . 120 Von Noorden on diabetic coma 112 pancreatic diabetes 107 WALLERIAN degeneration in nerve fibres . . 124, 133 spinal tracts . . 139 Walton on shock . . . . 61 intestinal shock . . 52 Warrington on division of posterior nerve-roots . . 139 Warrington and Murray on nerve anastomosis for infantile palsy . . . . 137 Water, absorption of by bowel 53 — supply and'goitre . . . . 7 Watson, Chalmers, on goitre . . 8 Weil on horse serum for haemophilia . . . . 78 Wells on Hodothyrin . . . . 6 Wells and goitre .. ..7,11 Wilms on goitre . . . . 1 1 Willcox on gastric HC1 . . 35 infantile dyspepsia . . 38 Wright, Sir Almroth, on haemo- philia . . . . . . 72 XANTHIN . . . . . . 83 X-rays in mapping out stomach 32 MEDICAL WORKS JOHN WRIGHT & SONS LTD., PUBLISHERS, BRISTOL. 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