an almost complete loss of smell-a fact which seems to indicate to us that this portion of the brain is the central point of the olfactory sphere. Some of my experiments show, in addition, that the more or less extensive destruction of the gyrus hippocampi, as well as the partial ablation of the cornu ammonis, produces evident troubles, and chiefly an almost absolute loss of olfaction, a fact which seems to show us that we have here the true centre, or fundamental nucleus, of the olfactory sphere.

cutaneous and muscular anesthesia. When the lesion is not very extensive, one may, within a few days, obtain an almost perfect compensation of the paralysis of motion and sense; but when it involves the whole motor zone, or even if it is deep enough to reach the opto-striate tract, the phenomena are persistent, and one may have clear evidence of them (though less marked than at first) several months after the operation. After decortication of any one region which responds to electrical excitation with reactions circumscribed to a single part of the body, the sensori-motor paralytical effects are not limited to that part, but are diffused more or less to other parts of the body on the same side. Thus after extirpation of the motor zone of the posterior limb, there is a diffusion of the paralytic effects into the anterior limb, and vice verså; after extir

limb and face, or of the face only, or of the neck and trunk, there is diffusion throughout the same half of the body. We have already asserted, that these effects are more intense in that portion of the body of which the cortical area has been chiefly or solely removed. Thus, to quote but one instance, after decortication of the excitable area of the anterior limb only, the paralytical phenomena, though they extend into the posterior limb, are mainly localised in the anterior.

These experiments, besides proving the great importance of the cornu ammonis in this respect, seem to point to a partial inter-hemispheric decussation of the olfactory fibres, analogous to what we said of the acoustic nerve -with this difference, however, that an opposite condition would prevail here, the direct appearing to be larger than the crossed fasciculus. Fig. C gives a schematic representa-pation of the excitable zone of the anterior tion of the olfactory sphere, according to these views; but it shows only the part of it which emerges from the base of the hemisphere (hippocampal region) towards its external aspect. The region extends from below the Sylvian fissure upwards and forwards, and spreads out as far as the parietal lobe of the hemisphere, and to a less degree towards the frontal lobe. The dark dots, which are more numerous, indicate the relations of the direct fibres with the cortex; the light dots, present in smaller number, those of the crossed fibres. We cannot state much concerning the localisation of the question for the sense of taste. The insufficiency of the means of testing it in animals, and possibly the hidden position they occupy in the cortex, may explain this want of success. Among our numerous researches we only once succeeded in proving a disordered condition of taste. After a unilateral extirpation of the fourth external convolution, and of a portion of the gyrus hippocampi, we discovered a diminished sensibility to the taste of bitters (powder of digitaline) on the half of the tongue corresponding to the lesion, as compared with the opposite half. From this fact we can only draw the presumption, that the gustatory is to be found in close relationship with the olfactory centre. And in fact, in the same dog, we were able to note the deepest alteration of the sense of smell.

My studies concerning the localisation of the tactile sense, or in other words concerning the general sensorial sphere, though still unpublished, were made in greater part in conjunction with Dr. G. Seppili, now physician-in-chief of the Asylum at Imola. Our results may easily be resumed as follows: consequently to the total or partial extirpation of the motor zone in the dog and the monkey, one constantly observes effects not only of motor paralysis, but also of

From these results we must necessarily conclude, that a localisation or precise delimitation of single centres in the sensory-motor zone, based upon not their reactions to electrical excitation of various points of the area, as Hitzig and Ferrier were the first to do, but upon the effects of partial extirpations, as Munk pretends,-that such a localisation is not practicable. We are led to believe that this is due to the fact, that the single centres in the sensory-motor zone are so completely bound up with, and, so to speak, let into, one another, that it is not possible to divide them with a clear and definite line, such as is the case when the cortex is incised and removed; so that in destroying a centre one necessarily eliminates a portion of the neighbouring centres.

The almost perfect compensation of paralytical effects consecutive to the extirpation of a single excitable area, and which takes place after a few days, even in the part of the body corresponding to it, is a fact which argues in favour of the partial overlapping of the special centres contained in the general sensorial sphere. We must not forget the fact, demonstrated by myself in previous papers, that the centres of the limbs in the dog are not limited to the external cortex of the sigmoid gyrus, but extend over the whole still wider surface of the sulcus cruciatus, and it renders very difficult

the complete extirpation of a single one of these centres. Considering the general sensory sphere as a whole, there remains the question whether it is limited to the frontal lobe, or whether it spreads out more or less into the other cerebral lobes. My recent researches exclude the occipital and temporosphenoidal lobes, but show that it does extend into the parietal lobe, extirpations of which constantly give rise to more or less extensive and durable tactile paralyses or pareses.

lobes, Goltz-this diligent and able observer, but who starts from a point of view totally opposed to ours-has noted a notable alteration in the character of the animal; goodtempered and affectionate before the operation, they become peevish, quarrelsome, and refractory. He gives no explanation for this fact (which I have confirmed in a dog), and could not possibly give it on the grounds of his wellknown theory. To me, on the other hand, this deep alteration in the psychical characteristics, appears to be referable to the loss of this important cortical area, in which the several sensory spheres meet and coalesce, and the removal of which necessarily produces the loss of the normal association of the psychical perceptions and images. -Brain, July.

Let us remark finally, that in all experiments upon the tactile sphere there was a manifest and constant crossing of the relations between the peripheral sensory fibres and their respective cortical centres. Fig. D represents schematically the probable extension of the general sensorial sphere on the external aspect of the brain of the dog, comprising the several ON ALCOHOLIC PARALYSIS. sensory-motor centres for the various parts of BY J. DRESCHFELD, M.D., F.R.C.P. the body. One sees that what one calls "motor THE effects of alcohol on the nervous system zone" is the central focus of the large portion manifest themselves in various ways, chiefly of the sensorial sphere visible on the external according to the particular part of the nervous aspect of the hemisphere-focus from which sphere attacked. Whilst in many forms of the latter is irradiated forwards towards the tip chronic alcoholism the brain seems to be the of the frontal lobe, backwards towards the chief organ to suffer, there is one affection, parietal lobe, entering thus into intimate con-alcoholic paralysis or alcoholic paraplegia, in nection by "engrenage" with the visual, auditory, and olfactory spheres.

which cerebral symptoms are either altogether absent, or play a mere subordinate part, while If we compare together the four figures most of the symptoms are referable to the which indicate the localisation of these centres spinal cord or to the peripheral nerves. The in the cerebral cortex, and ideally superpose symptomatology of this affection has been well them upon one another, we discover a remark- described in this country by Wilks (' Diseases able fact, which I consider as one of the newest of the Nervous System'), Lockhart Clarke and most important results of my new inquiry.('Lancet,' 1872), Reginald Thompson, (Med. The four sensorial spheres, besides possessing each a territory of their own in the cortical substance, have, in addition, a common territory which is represented by the area of the parietal lobe, or more precisely by the zone F of Munk, which the latter calls the region of the eyes, attributing to it the humble functions | 1881), Moëli (Berl. Klin. Wochenschr. No. 14, of providing for the tactile sensibility of the eyeballs and conjunctiva.

In this region the mutual overlapping, or "'engrenage," and consequently the partial fusion takes place of the single sensorial centres (excepting the gustatory centre, of which we know but little). Every one will thus see how this region is the most important in the hemisphere of the dog, where it represents, so to speak, the centre of centres. And indeed extirpation of this region, whilst it affects more particularly the visual perceptions, injures at the same time the auditory, olfactory, and tactile perceptions. There is no other portion of the brain of the dog lesions of which are capable of giving rise to effects so complicated, and so liable to set up profound psychical disturbances in the animal.

Chir. Trans.' 1868), and more recently by Glynn, ('Liverpool Medico-Chir. Journal'), and Broadbent ('Lancet,' Feb. 16, 1884). On the Continent, the principal workers at this subject have been Leudet ('Arch. Gén, de Méd.' 1867), Lancereaux (Gaz. Hebd,' 1865 and

1884), and Charcot (see article by Féré in 'Prog. Méd.' June 14, 1884).

Our knowledge of the pathological anatomy of this affection is, however, still meagre, although the observations of Lancereux, Moëli, and Broadbent, tend to show that the lesions concern chiefly, if not entirely, the peripheral nerves.

Considering the more prominent characteristics, we may divide alcoholic paralysis into certain types. The first may be fitly designated Alcoholic Ataxia. Wilks mentions the case of a young woman whose symptoms very much resembled those of locomotor ataxy, both in the character of the pains, which were like electric shocks, and also in the mode of progression." Leudet alludes to the difficulty of distinguishing such cases from true ataxia, and And in fact, after extirpation of the parietal Lancereaux and Charcot also mention the

ataxic symptoms. The cases of this description which I have seen were men, from 30 to 40 years old; the symptoms had come on more or less gradually, and consisted chiefly of marked inco-ordination in the lower extremities, absence of tendon-reflex, and lancinating pains. There was neither atrophy nor paralysis. A patient I saw recently who had been greatly addicted to alcohol for years, had already had one attack of paralysis, from which he completely recovered, after giving up alcohol. Having again fallen into bad habits, the old symptoms recurred (inco-ordination, lancinating pain, absence of tendon-reflex and slight loss of control over the bladder at night). Dr. Roe informs me that the patient's habits are still very intemperate, that his ataxic symptoms have remained unaltered, but that the patient is now suffering from rapidly advancing phthisis.

A very similar case I saw with my colleague, Mr. Jones here also the symptoms came on after a series of alcoholic excesses, and have now quite subsided. Patient's family history was free from any neurotic taint, and he had not had syphilis at the time I saw him, though he has contracted it since.

the alcoholic ataxia. The symptoms observed harmonise well with the pathological anatomy which underlies the alcoholic paraplegia,—for as the changes observed chiefly concern peripheral nerves, we can understand the symptoms if we suppose that in the ataxic type we have an affection, a multiple neuritis, especially of the sensory nerves.

The second type of alcoholic paralysis, which deserves better the name of paralysis, is far more common, and is that which most observers have described. This affection chiefly attacks females, who, though they deny the abuse of alcohol, have suffered from symptoms of chronic alcoholism (morning vomiting, chronic gastric catarrh, hæmatemesis, &c.), previous to the appearance of the nervous troubles. These commence more or less acutely, and consist of sensory, motor, vasomotor, and trophic disturbances.

The sensory disturbances are, as a rule, well marked and very characteristic, and consist of extreme hyperesthesia of the feet and other parts of the lower extremities, with or without hyperalgesia; perversion of the sense for temperature (all objects when brought in contact with the skin feel cold); there are often present, in addition, lancinating pains in the lower extremities, and pain when pressure is applied along the vertebral column. The hyperæsthesia is often followed by anææsthesia or retarded sensibility, the hyperalgesia by analgesia.

The motor troubles consist of more or less marked paralysis, attacking the lower, and sometimes the upper extremities; in many cases the extensor muscles are chiefly affected, while in not a few cases the paralysis is more general. The superficial and mechanical reflexes are often diminished, the tendon-reflexes are nearly always absent; contractures have only been noticed by a few observers (Wilks, Buzzard). The vaso-motor affections consist chiefly of redness of the feet or hands, occasionally also of other parts of the body, and oedema, especially seen at the ankle, the dorsum or the foot, and the back of the hand. The nerves and muscles show marked degenerative reaction, though we have but few detailed statements on this subject.

A man, æt. 35, an excessive drinker, suffered from the symptoms described above, which came on in the course of three weeks, but subsided completely in three months. The recovery in this case was complete, the tendonreflex being again established some months after all the other symptoms had disappeared. These cases differ from those of the second type to be described below, in the absence of hyperæsthesia, hyperalgesia, vaso-motor disturbances, paralysis, atrophies and mental disturbances. The individuals attacked are chiefly men, and the symptoms disappear with the discontinuance of alcohol. In the diagnosis of such cases of pure alcoholic ataxia, one has of course to bear in mind how far alcohol may simply play the part of an etiological factor, and how far alcoholism and ataxia may be mere coincidences; moreover in the ordinary cases of ataxia, the symptoms, especially if they come on somewhat acutely, often show for a time a marked improvement. In the above cases, however, the ataxia followed so Cerebral symptoms, such as insomnia, restsoon after the excesses, and so completely dis-lessness, more or less delirium and hebetude, appeared, that I have no hesitation in pronouncing them alcoholic. This view is still further supported by the fact, that symptoms of ataxia are again seen in the second type to be described (especially the absence of tendonreflex and the lancinating pains); moreover, some of the symptoms of ordinary locomotor ataxy, such as the arthropathies, the oculomotor pareses, spinal myosis, &c., symptoms which we may consider spinal, are absent in

though absent at first, often make their appearance during the course of the disease, and are frequently the cause of death, unless other complications should occur, such as phthisis, fatty degeneration of liver, &c.

Disorders of the circulatory, digestive and respiratory organs, are often seen during the progress of the disease, but are rather complications, or the primary effects of alcohol on these organs, than secondary manifestations

of the nervous affection under consideration. whole of the vertebral column; there are no The prognosis varies very much. Many spots of either anæsthesia or analgesia; all the cases recover when they come early under muscles seem equally atrophied and flabby; care, and when uncomplicated; some recover for a time, and afterwards relapse; whilst in others the disease pursues a steady downward course, death ensuing from the cerebral symptoms, from exhaustion, or from some intercurrent affection, as is so often seen in other forms of chronic alcoholism.

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tuberculosis of the kidney and bladder of more recent date. The diagnosis of alcoholic paralysis was thus confirmed by the post-mortem appearances, which were exactly those described by Lancereaux and Moëli.

There remained, therefore, scarcely any neuritis, chronic tuberculosis of the lungs, and other disease but multiple peripheral neuritis, and with the history before us, and the absence of any evidence showing that any other toxic agent, such as lead, arsenic, &c., was the cause of the symptoms (though such poisons would scarcely produce the sensory disturbances observed), we had no difficulty in arriving at the diagnosis stated.

April 7. Patient much worse; delirious at night; speech slow and muttering; lies with legs flexed, and can only extend them with great difficulty. April 9. Patient much worse; delirium constant; temp. 95; extremities cold and cyanotic; pulse, very feeble, 80; the paralysis more extensive. April 10. Became comatose, and died early this morning.

Autopsy, by Dr. Maguire. Some fluid in pleural cavity, a little fluid in pericardium; aortic valves showed some chronic thickening; the lungs, slightly emphysematous, contained a few caseous nodules in both apices. Liver enlarged, pale and soft. Kidneys showed several patches of caseation in the cortex ; pelvis full of pus; capsule thickened, but peeled off easily, and showed surface of the kidney affected by tubercular deposit. Bladder greatly inflamed, its inner surface covered with muco-pus, its walls thickened and infiltrated with tubercular deposit.

Brain found normal, the pia slightly thickened; the dura mater showed numerous Pacchionian bodies. The spinal cord and its membranes, when examined in the fresh condition, appeared perfectly normal. Some peripheral nerves, which were reserved for microscopic examination, also appeared normal. The muscles were pale, but otherwise normal.

After hardening the cord, I examined portions of it microscopically, without finding any changes examined by Weigert's method, numerous small nerve fibres were found in Clarke's columns. The ganglion cells in all parts of the spinal cord were perfectly healthy. Several posterior roots of the lumbar region were examined and found perfectly healthy.

Though hyperesthesia and hyperalgesia are prominent symptoms in this form of alcoholic paralysis, yet I think that both these symptoms may be occasionally absent, and the motor nerves may be principally affected. Thus, not long since, I observed the case of a man, æt. 38, who suffered from far-advanced alcoholic cirrhosis of the liver, and who in the course of a few days lost the use of his arms and legs. When admitted, about three weeks after the onset of the paralysis, there was noticed, besides the ascites and enlarged spleen, marked atrophy and paralysis of the upper extremity, affecting chiefly the muscles supplied by the radial, the posterior interosseous and median nerves, and more pronounced on left than on right side. The back of the hand was cedematous. There was also observed some paralysis of the lower extremities, affecting chiefly the extensors of the toes and ankle. In the sensory system there was found a perversion of the sense for temperature, namely, the patient felt, as intensely cold, anything that touched his arms or his legs. (I find this symptom stated in several of the recorded cases of alcoholic paralysis.) There was absence of tendon and superficial reflexes.

The electric reactions of the muscles showed marked degenerative reaction. The special sense-organs were normal. The cerebral symptoms consisted chiefly of sleeplessness. Patient was in hospital some time, without showing any improvement. He left, and died at home.

The nervous symptoms in this case resembled more those seen in chronic poliomyelitis; yet the history, the onset, the perversion of the sense for temperature, the marked degenerative electric reaction and the associated cerebral symptoms (though these might have been due to the cirrhosis), induced me to look upon this case as one of peripheral multiple neuritis, affecting chiefly the motor nerves and caused by alcohol. The combination of cirrhosis with alcoholic paralysis has already been noticed by Lancereaux.

Of the peripheral nerves, there were examined the two sciatics, the musculo-spiral and the anterior crural. These nerves showed the characteristic changes described by Lancereaux in a very marked fashion. In the sciatic, longitudinal and transverse sections showed The Anatomical lesions then which underlie most markedly the breaking up of the myeline, alcoholic paralysis, to judge from the postand in many places the breaking up of the axis mortem results of Lancereaux and Moëli, and cylinder also. Longitudinal sections showed those given in the case above, consist of a the segmental changes described by Gombault, peripheral multiple progressive neuritis. and seen by me in a case of lead paralysis. Broadbent, in his case, found the cord norThe muscles showed no peculiar changes when mal, but was not allowed to examine any other microscopically examined. The post-mortem part of the body. In one of Lancereaux's changes showed then a multiple peripheral | older observations the antero-lateral columns