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capillary blood-supply, that the two functions go on without in any way disturbing one another; and if from any extraneous cause the blood-stream be temporarily either considerably quickened or retarded, we do not find that any immediate increase or decrease of the tissues results. On the other hand, when a part is undergoing great exertion or employment, therefore great nutritive activity, the blood-stream is immediately and instantaneously increased. This amounts to saying, that the supply of blood does not regulate the nutritive activity of a part, but that the nutritive activity regulates the supply of blood. If, then, inflammation be a disturbance in the nutritive activity, it begins where that function is situated in the tissue itself, not in the vessels, the changes in which are only secondary.
It seems, then, that inflammation begins in the substance of tissue which is extra-vascular, and no one can affirm that this non-vascular islet must be of a certain definite minuteness, in order to permit of inflammation, since we do not find that the tendency to that action is in any direct ratio with the minuteness of the intra-plexural parts. It seems rather probable that every organ which is capable of nutrition must also be capable of inflammation, and it therefore is impossible to affirm that cartilage, because there are no vessels in its substance, cannot assume that disorder of its usual nutritive action which constitutes inflammation.
But again, the sceptic may still say, "How can inflammation be present when its symptoms, heat, pain, redness, swelling, are absent?" The signs of a thing are not the thing itself, and are very often not even essentials, although, as far as our knowledge at present goes, they may be constant accompaniments. Thus, a potentate of India had always been accustomed to consider fluidity so essentially characteristic of water, that he either bastinadoed or bowstringed a gentleman who mentioned that he had seen that substance solid. The phenomena, which we have been accustomed to consider as signs of inflammation are not signs of the disturbed nutritive action, which we find to be situated on the tissue, but of the vascular disorder produced thereby; and if it be admitted that inflammation may begin in the tissue, and that vascular disturbance is only a secondary action, it must also be admitted that inflammation can proceed to a certain distance without producing such symptoms of disorder. We have other signs of inflammation which are likely to be more infallible than mere hyperæmia, which is often present in non-inflamed parts under the name congestion. When we find evidences of superabundant action in the tissue, with effusion of lymph, hardening, softening, &c., we know that inflammation has been present, even if we do not find any vascular engorgement in its immediate neighbourhood. Now, this increased action and subsequent alteration of texture is found to take place in cartilage, the simplicity of whose structure and purity of whose action render such changes easier to follow, though its symptoms be not striking, because free from secondary actions, which being prominent, have been seized upon as invariable characteristics of inflammation. Therefore it appears to me that this increased action occurring in cartilage should serve as
the type of the inflammatory process in the simplest form, unmasked by any secondary action.
In the experiments which Dr. Redfern made upon the costal cartilages of dogs, he performed certain operations, which, in ordinary textures, would have produced inflammation; and the results were increased action of the cartilage cells, and hyperemia of the neighbouring parts which supply that structure with nutriment. When a synovitis has lasted some time, the cartilages will in places be found ulcerated and fibrous; in some parts the free surface only will be affected, in others the deep only will be altered and detached from the bone, sometimes the two lesions occur together. The detachment of the cartilage from the bone takes place not by ulceration of the deep surface, but by separation of the articular lamella from the rest of the bone, and the ulceration on that deep surface takes place subsequently. Now in all these instances the microscope will present the same, or very nearly the same, appearances-the differences being only in degree. There will be great increase in the activity, in the number and in the nuclear contents of the cells, producing absorption of the hyaline substance, either slowly after its conversion into fibres, or more rapidly without such change; subsequently, before the bone be laid bare, before fibrification of the cartilage shall have reached its osseous surface, the articular lamella will have become detached-a process which can only take place by the disease having passed through the cartilage to the bone. If we saw through the bone of any joint, in which pretty active ulceration of cartilage is going on, we shall find close to its articular surface a deep red blush. This is the true hyperemia of inflamed cartilage, which we miss in the substance of that structure itself. That the vessels thus injected belong more especially to the cartilage is evident from the fact, that bone is only supplied with such looped and dilated branches when close to articular cartilage; when in its over-action that structure requires more nutriment, the vessels become engorged, and pour forth more plasma than can pass through the tubular structure of the lamella; this material becomes either pus or false membrane; the action, in fact, spreads to the bone, which now becomes inflamed, the bony plate supporting the articular lamella is detached from the rest of the bone, and adheres to the cartilage, which it causes to feel rough and gritty, like sand-paper.
Thus, as said above, the action, begun in the synovial membrane, passes to the cartilage, thence to the bone; in the synovial membrane it was inflammatory, in the bone inflammatory; it cannot, in its passage through the cartilage, have changed its nature twice-that is, once from inflammation in the synovial membrane, to something else in the cartilage, and once from that something else, back again to inflammation in the bone. It is more consonant with reason to admit at once the inflammatory nature of the action in articular cartilage.
Ulceration, even of this active type, may go considerable lengths without producing any distinct symptoms; this is by no means an argument against its inflammatory nature; it was shown above that hyperemia and hyperesthesia are but secondary conditions of inflam
mation. When, therefore, the inflammation reaches a point to produce the hyperemic condition above described, then certain symptomsstarting of the limb, "soreness of the bone," "gnawing of the bone,"* &c. &c., come on. These pains are obscure, and described variously by different patients; but they are not, as is generally supposed, symptomatic of commencing ulceration of cartilage, but of that action having already proceeded to a point when the bone is affected. Whether the attack have been more or less acute-i.e., the time since the commencement of the disease is immaterial, for whenever in synovitis that particular set of pains comes on, we shall find the cartilages destroyed over a greater or smaller surface, throughout, or nearly throughout, their entire thickness. I have some reason to believe, that when the articular lamella gives way, there is, at all events for a time, mitigation of these painful symptoms; but this is a point which requires more investigation, and the rarity of cases in which a strumous joint can be so early examined renders it very difficult to determine the fact by direct proof.
This view of the different diseases to which ulceration of cartilage is due, will explain why ulceration of cartilage is sometimes a painful disease; why at other times we find, after death, erosions, which gave during life no symptoms of their presence. Such excavations are frequently seen in the dissecting-room or in the dead-house, and may, by proper examination, be distinguished as belonging to two classes-firstly, to degenerative disease; secondly, to an inflammatory disease. The former of these gives rise to no hyperæmia in the cancellous structure, and therefore to no symptoms whatever; the latter is of a slow inflammatory form, causes a slight, variable, and very chronic engorgement of the cancellous structure, and in all probability gives rise to those obscure pains and stiffness in the joints which are often accompaniments of old age.
To recapitulate shortly The results of a careful examination of the anatomy, physiology, and pathology of articular cartilage lead to the following conclusions :—
1st. That although in the articular cartilage itself there are no vessels, there are situated immediately within the articular lamella a set of arteries destined to supply that cartilage with nutriment.
2ndly. That the articular lamella is composed of a finely tubular structure, which allows the nutrient fluid to find its way to the cartilage in finely divided streams.
3rdly. That the cartilage has no other source of nutriment.
4thly. That the diseases of cartilage must not be estimated or named by the alterations which the hyaline structure undergoes, but by those which take place in the cells.
5thly. That a certain number of these diseases are degenerative, but the larger number decrease or increase in the generative activity of the cells; the last of these attends all inflammatory diseases of the joints, and is itself inflammation.
So described frequently by patients.
6thly. That the hyperemia of this inflammation is situated in the vessels immediately beneath the articular lamella, and it is this hyperemia which gives rise to the symptoms usually supposed to be produced by ulcerating cartilage.
7thly. That simple degenerative diseases of the cartilage, as they produce no hyperemia, produce no symptoms.
Series of Clinical Cases (with Observations) illustrating the Views recently put forward by Dr. Brown-Séquard, as regards certain points connected with the Physiology of the Nervous System. By JOHN W. OGLE, M.D. Oxon, F.R.C.P., Assistant-Physician to St. George's Hospital, Secretary to the Pathological Society of London.
I DESIGN by the relation of the following clinical cases, which, with one exception, are selected from the records of medical experience in St. George's Hospital, to assist in rendering human pathology instrumental in elucidating the truthfulness of some of the ingenious and profound generalizations based mainly on experiment, and brought forward of late years by Dr. Brown-Séquard.
The members of the medical profession in England are now fully conversant with, and fully appreciate, most of the special researches of that dexterous experimental physiologist respecting the blood, muscle, animal heat, and the nervous system in general; and therefore any formal enunciation of his varied deductions would here be quite superfluous and misplaced. I will consequently, by way of premise to the cases which I shall detail, merely content myself with bringing before the mind of the reader, in a manner as concise as the intentions of this communication permit, those conclusions from facts observed by Brown-Séquard connected with the minute organization of the nervous system, the certainty of which I purpose to illustrate by the cases which I shall adduce, and which are in direct opposition to the conclusions arrived at by other physiologists, French, German, or English.
These cases will, I think, tend most materially to corroborate the following deductions ascertained by Brown-Séquard :
(a) That the posterior columns of the spinal cord do "NOT" form, as was thought by Longet and many other observers, the means for the entire (en totalité) conduction of sensitive impressions to the brain; but
(b) That these columns form a medium to a slight extent only for the passage of sensitive impressions; such conduction along the spinal cord chiefly occurring in the central or grey matter of the cord, into which part the fibres of the posterior sensitive roots of the nerves, by means of transverse, ascending, and chiefly descending fibres, find their way almost immediately after gaining the cord, via the posterior columns, the posterior grey cornua, and, in part, the lateral columns. And that if there be any fibres conducting sensitive impressions ascending
from the trunk or limbs along the entire length of the cord, their number must be very inconsiderable.
(c) That the fibres conveying sensitive impressions to the brain do not at any rate decussate at a point higher up in the cerebro-spinal axis than the pons Varolii.
(d) That the decussation of fibres conveying sensitive impressions must be of necessity not only at a part below the level of the upper margin or central part of the pons Varolii, but even for the most part, if not entirely, below the medulla oblongata itself. That is to say, this crossing or interlacement of sensory nerves must take place in the spinal cord itself, and that not in any particular spot, but in every portion of the cord almost immediately after the entrance therein of the afferent fibres.
(e) That all the motor or efferent fibres decussate at a distinct point immediately below the pons Varolii-that is to say, at the anterior pyramids and the neighbouring parts, contrary to the views of Valentin, Cruveilhier, Longet, Foville, &c.
Having thus enumerated in a succinct manner the various physiological positions which I purpose to illustrate and strengthen in this pathological communication, I will, without further circumstance or digression, proceed to narrate my cases, the true interpretation of which at the time of their occurrence, and upon the old theories then commonly in acceptance, could obviously not have been apparent. CASE I.-Dislocation of some of the vertebra, and projection of bone into the anterior surface of the spinal cord, the posterior columns remaining entire; perfect loss of sensibility and power of movement in the lower limbs. History.-P. S―, aged sixty-two, was brought into St. George's Hospital, having fallen a height of eleven feet, and received a scalp wound. He was for ten minutes stunned by the fall, but after admission walked into the ward, complaining only of pain at the neck. He had a slight cough. Nothing fresh was complained of until three days afterwards, when he felt numbness in the legs and tottered in walking. Sensibility of the skin to pinching and pricking was everywhere perfect. Seven days after the accident he had to such a degree lost power in the legs, that he scarcely was able to move them; still, sensibility of the skin remained as before. The bowels were constipated, and the catheter had to be used, the urine, too, becoming purulent. Stiffness also of the arms came on, and nine days after the accident he could with difficulty move them; they were also much flexed. All power also of voluntary movement below the diaphragm had disappeared. Eleven days after the accident the soft parts over the larger trochanter of the right femur began to slough, and two days later his cough was attended by dyspnoea. On the thirty-second day after the accident all sensibility of the skin, as well as all power of movement in the legs, was found to be lost: the respiration was chiefly abdominal. After some difficulty in swallowing, the patient died September 27th.
Post-mortem examination.-Dislocation forwards of the sixth cervical vertebra was found to exist, so that the body of the seventh vertebra projected for at least half an inch into the spinal canal behind. The dura mater opposite the sixth and seventh cervical vertebræ was thickened, and a slight amount of recently-formed soft fibrin existed at this spot between the bone and the theca