Benefit has been claimed from the energetic use of mercury, chiefly in the form of calomel, by older writers; and recently Handfield Jones has endorsed its administration, attributing to it a remission in a case in which it was employed. It must be remembered, however, that remissions occur spontaneously in this disease, and that the purgative action of calomel may act well for the time being in an affection so apt to be associated with hyperæmia and increased cerebral pressure as is an abscess of the brain.63 In the nature of the case, even this latter momentarily beneficial effect is at the best temporary.
63 Brain, October, 1884, p. 398.
The prophylaxis of cerebral abscess can be carried out only in cases due to cranial and aural affections. The importance of treating all scalp and cranial injuries under aseptic64 precautions is recognized by all surgeons. It is generally admitted that the trephining of a bone suspected to be the site of an ostitic or necrotic process involves fewer risks than the allowing it to remain. Similar principles govern the treatment of the inflammatory involvement of the mastoid cells often complicating otitis media. If trephined at all, these should be trephined at the earliest moment. It was a belief among the older aurists that the sudden cessation of an aural discharge was of evil augury, and that cerebral complications were more apt to follow under such circumstances than when the ear discharged freely. Von Tröltsch, Politzer, Gruber, and Toynbee have opposed the exclusive application of the old dogma. In so far as the older ear-surgeons regarded a profuse aural discharge as an encouraging sign, in this respect they were of course wrong. But their observation of the frequent concurrence of cerebral sequelæ with suppression of discharge is, I think, borne out by a large number of cases. It does not apply, however, to the suppression of discharge by the rational employment of aseptic injections.
64 This term is used in its widest sense here.
Spinal Hyperæmia.
The spinal cord is found to vary considerably in color in different individuals. To some extent this difference is influenced by the position occupied by the body after death, but not as markedly as in the case of the brain. Thus it will be paler in a body which has been kept in the prone than in one which has been kept in the supine position.65 It is usually found more injected in persons who have died of febrile affection than in those who have died of exhausting diseases; notably is this the case with typhus fever and with subjects who die with congestive malarial chill. But the most intense congestion, where the gray substance instead of having the normal rosy hue appears like a blood-soaked sponge, and the white substance instead of the tint to which it owes its name has a pink shade, is found in subjects dying in convulsive disorders complicated by asphyxia, such as epileptic status, tetanus, and certain toxic disorders.
65 I have not seen it noticed anywhere, but it is a fact readily demonstrable in any autopsy made in a well-preserved body that when a short segment of cord is observed at the moment of section the section surface appears pale; but if it be again examined after a few moments, it will show a reddish tinge, marked as a faint injection would be; this tinge distinctly deepens under the eye. I have observed this in specimens which were not held in the hand, so that the influence of pressure can be excluded. Nor do I believe that the elasticity of the tissues is such as to account for the phenomenon.
In attempting to apply the fact that varying degrees of vascular injection are found on post-mortem examinations of the spinal cord to the elucidation of certain clinical phenomena, we encounter the same difficulties and sources of error that confronted us in the study of nutritive brain disorders. The majority of writers have therefore contented themselves with making a careful clinical study of the mostly subjective signs of disorders which, once designated as spinal anæmia and hyperæmia, are now classified under the non-committal titles of spinal irritation and exhaustion (neurasthenia), as in this volume. A number of these disorders, like the so-called anæmic paralysis of Bouchut, Leroy d'Etiolles, Beroliet, Baimer, and Brandis, would to-day be considered as hysterical or reflex; and a few of the instances cited by their contemporaries as cases of spinal hyperæmia have been since demonstrated to resemble the initial phases of organic diseases of the cord.
The causes of active spinal hyperæmia are either direct, as when the spinal centres are overtasked by muscular strain either through over-exertion or through toxic convulsions, surprised by violent shocks, such as concussion accidents, or collateral, as when a physiological discharge (menstruation) or a pathological one (hemorrhoidal flux) is suddenly checked. A few cases are reported where carbonic-oxide-gas poisoning provoked spinal hyperæmia. But, like the alleged cases of spinal hyperæmia after continued and exanthematic fevers, they were probably cases of incipient or established myelitis. Hammond claims that surface chilling exerts the same congesting influence on the cord which he claims for the brain; but no definite observations have been made in this direction.
Passive spinal hyperæmia has been attributed to obstructive cardiac and chronic pulmonary affections. In such cases, as with most causes acting on the circulation of blood in the nerve-centres, the coexisting cerebral congestion usually masks the spinal. It is a question how far the intense hyperæmia of the cord found in some cases of tetanus, strychnia-poisoning, and the condition called hydrophobia66 is primary and an indication of neural hyperexcitability, and how far it is secondary to the asphyxia attending the last phases of these convulsive states. The weight of opinion is in favor of an acceptation of the latter as the chief or only factor.