Pure spinal hyperæmia rarely presents itself for treatment. The form due to over-exertion is recovered from by rest in a very short time; that due to suppressed discharges, by the re-establishment of the latter or by the application of leeches to the lumbo-sacral and iliac region. Ergotin is recommended by Hammond in very large doses. It is a question whether this drug may not exert a bad effect in protracted cases where its use has to be continued for a long time.72 In using it, it is well to bear in mind that imperfect nutrition of nerve-elements is perfectly compatible with an increased blood-amount.

72 A young physician, who for a long period took ergotin in twelve-grain doses for the relief of symptoms regarded as congestive, acquired a tolerance of the drug such as I have not seen recorded anywhere, and in addition presents some obscure signs of cerebellar disease and initial optic-nerve atrophy.

Strychnia has been given with benefit in the caisson disease—another evidence, as this drug is theoretically contraindicated in true hyperæmia, that this disease is not, as Hammond and the majority of authors with him regard it, essentially a congestive affection. The treatment of those numerous cases in which signs of venous fulness accompany spinal exhaustion and irritation is detailed in the articles dealing with those affections.

Spinal Anæmia.

Anæmia of the cord-substance proper, like hyperæmia, is practically inseparable from the corresponding condition of the membranes. The influence of a reduced blood-amount on the functional activity of the spinal cord is more susceptible of exact demonstration than the corresponding nutritive disturbance of the brain. As the functions of this segment of the nervous axis are far simpler than those of the higher organ, there is more unanimity among observers as to the interpretation of their disordered states. In Stenon's experiment, and the more elaborate modifications made by those who have followed his method, it is found that interference with the supply of arterial blood to the spinal cord is followed by abolition of the function of the gray matter; if the supply be still further diminished, the functions of the white tracts become eliminated; next the peripheral nerves, and ultimately the muscles themselves, lose their normal excitability. On the re-establishment of the circulation these various parts regain their functional capacity in the inverse order of its suspension—the muscles first, next the nerves, then the white substance, and last the gray substance of the cord. The initial symptoms of some cases of myelitis from refrigeration correspond more nearly to such a result of artificial anæmia of the cord than they do to anything that is customarily regarded as hyperæmia.73

73 I have seen distinct pallor of the spinal meninges on dipping the posterior extremities of a dog, whose cord had been exposed, into water. It is to be remarked, however, that other observers, notably Hammond, have either obtained different results or interpreted the consequences of refrigeration differently.

No one has gone farther than Hammond in erecting a theoretical anatomical framework which elaborately provides for the accommodation of various symptoms of spinal anæmia. He describes anæmia of the posterior columns, and sharply discriminates between it and anæmia of the antero-lateral columns. It is a question whether the conducting tracts of these columns are seriously affected in their functions by anæmia as long as the centres of innervation are well nourished. Undoubtedly, it is the gray substance of the cord which is most vulnerable to the influence of disturbed circulation and nutrition, as Stenon's experiment has shown; and a glance at the distribution of the blood-vessels will show that a partial anæmia or hyperæmia, limited to special cornua in any considerable length of the cord, is an exceedingly improbable occurrence. With regard to isolated anæmia of the white columns, it is to be admitted that the posterior are most vulnerable to malnutrition. But it is doubtful whether this vulnerability is so great as to allow of an exclusively posterior anæmia, or whether a protracted anæmia of this kind could exist for years as a purely symptomatic—or, as some designate it, functional—disorder.

Hammond candidly states that in specifically locating the lesions in these affections he is aware that post-mortem examinations are wanting to support them, and admits that what he calls anæmia of special parts of the cord is the spinal irritation of most authors, and in part the reflex paraplegia of others.

The most clearly-established form of cerebral anæmia is the one which is indicated by the ischæmic paraplegia of Jaccoud and the paraplegia following profuse hemorrhages. The former is produced by all causes which, by obstructing the flow of arterial blood in the abdominal or thoracic aorta, cut off the proper blood-supply to the cord, which the latter receives through the intercostal and upper lumbar arteries. Aneurism, compression by tumors, and embolism of the aorta produce this result. The consequence is paraplegia corresponding in all features of its development to the phenomena observed in Stenon's experiment. These features, already detailed, suffice to show that it is not the anæmia of the peripheral nerves and muscles that is chiefly responsible for the paraplegia, but the insufficient irrigation of the gray and white substance of the cord itself. The same is true of the paraplegia following hemorrhage which has been noted after uterine, renal, and enteric hemorrhages. Both affections are exceedingly rare.

The influence of general anæmia on the functions of the spinal cord is not susceptible of accurate study. The cerebral enlargement of the nervous axis is so much more unfavorably situated than the cord that it suffers first and most when general anæmia is present. The consequence is that the signs of cerebral anæmia mask those of spinal anæmia. It is supposed, however, by many authorities that the effect of anæmia on the cord may be regarded as an auxiliary factor in the production of hysterical and neurasthenic symptoms.