66 In a case of hydrophobia clinically as well marked as has been recorded, which I had the privilege of examining through the courtesy of Kretschmar, both brain and cord were found remarkably anæmic.
Over-exertion and sexual excesses are frequently followed by a sensation of fulness and tension in the sacral and lumbar regions, which may be relieved by lying prone, while it is aggravated while lying supine.67 From the location of this pain it is evident that it is not due to congestion of the cord or its membranes, but to fulness of the vertebral and spinal veins of the lower segment of the vertebral column. A similar sensation, which may be relieved by the same change in position or by a hemorrhoidal flux, is complained of by patients suffering from portal obstruction. The veritable symptoms of hyperæmia manifest themselves in the parts which receive their nervous supply from the affected districts. The reflexes are usually more active; paræsthesias of different kinds, such as formication, tingling, and creeping sensations, are common; and there is more or less motor weakness, the limbs feeling heavy and sometimes being the seat of an acute pain. As a rule, these symptoms are limited to the lower half of the body.
67 Although this fact has been questioned, I have no doubt whatever that it is true, from a large number of observations. In many subjects suffering from the results of excessive venery or masturbation, an intolerable, sometimes pulsating, feeling in the lumbo-sacral region is only relieved by raising the lower end of the trunk with the back up. This condition is influenced by a change of residence to a district having a different level above the sea, and consequently a different barometric condition.
There is very little question when these symptoms exist for any length of time, and become aggravated, that more subtle nutritive changes than are covered by the single term hyperæmia become responsible for them. In a pure hyperæmia the position-test of Brown-Séquard, which shows relief when the patient is upright or prone and aggravation when he is supine, particularly if the gravitation of blood to the cord be facilitated by raising the head and extremities, ought to yield constant results. But in some cases, particularly those of long-standing, the very opposite is noted: the patient's symptoms are aggravated by standing or sitting up, and relieved by lying down. Here there is probably exhaustion or malnutrition of the nerve-elements, rendering them abnormally sensitive to exertion. This view is supported by the fact that molecular disturbances, such as those which probably accompany simple concussion, predispose the patient to the development of the symptoms of spinal hyperæmia, and aggravate them if established previous to such accident.
Hammond,68 who in his chapter on Spinal Congestion and Anæmia follows rather the older authors, such as Ollivier, than the newer and either more cautious or more sceptical writers on the subject, describes the symptoms of congestion as comprising belt sensations, paraplegia, erections of the penis, muscular twitches, loss of expulsive power, and incontinence of the bladder, paralysis of the abdominal muscles, paralysis of the anal sphincter, loss or abolition of reflex excitability, diminution of electro-muscular contractility, and occasionally hyperæsthesia and shooting pains. It is not doubtful for a moment that if such a case were to occur in hospital experience it would be regarded as one of organic disease, and not incipient, but well-established organic disease of the cord. Those making the diagnosis would have their opinion strengthened if, as Hammond states, the process took place with great rapidity and had a tendency to extend itself and eventually involve the whole cord, or if, as Brown-Séquard is by him cited as stating, bed-sores occurred in addition. Although Hammond describes certain anatomical changes, such as increased development of blood-vessels and distension and injection of them, I am unable to find any cases recorded as spinal congestion during life, and carefully examined with a due regard to sources of error after death, in which such changes were found. It is true that after strychnine- and cocaine-poisoning an intense hyperæmia69 of the cord is found. In mammals it is of a far more pronounced character than in reptiles, and usually more marked in proportion to the existing asphyxia. That the characteristic toxic effects of these drugs is not to be sought for in their direct or indirect congesting influence is shown by the fact that exsanguinated frogs can be made to undergo strychnine tetanus when their blood is replaced by a saline solution according to the method of Salkowski. Little support, therefore, could be derived from a pretended analogy between toxic and pathological hyperæmias, even if the phenomena of both were similar; which is not the case.
68 Diseases of the Nervous System, 7th ed., p. 392.
69 It is true that in animals which are so organized that the congestion cannot be attributed to asphyxia, as I showed (Hammond Prize Essay of the American Neurological Association, 1878) in some experiments on strychnine, arterial congestion and small foci of hemorrhage were found in the upper cervical cord of frogs who had been kept in continuous strychnine tetanus for over seventy days.
The introduction of subaqueous caissons for workmen engaged in the building of bridges, in which those employed labor under abnormal atmospheric pressure, has led to the development of a previously-unknown cerebro-spinal affection known as the caisson disease, and in which, it is generally supposed, either congestion or hemorrhage of the spinal cord occurs in consequence of sudden changes of vascular pressure resulting from sudden diminution of the barometric pressure. Clinically, this affection has been studied in England, France, and above all in America in connection with the building of the East River Bridge and the one over the Mississippi at St. Louis.70 Experiments by Hoppe-Seyler, Bert, and I. Rosenthal have shown that a sudden diminution of pressure leads to hemorrhages in various tissues, and, according to the two first-named, a development of gas occurs in the vascular and other fluids of the body. A number of peculiar symptoms which do not specially interest us here occur in conjunction with the so-called caisson disease: these are—pain in the ear, with or without otitis sicca; peculiar pains in the joints, which occur on leaving the caisson, and are probably due to hyperæmia of the joint-surfaces and sudden increase of the intra-articular fluid; and retardation of the pulse-rate. In some cases cerebral hyperæmia is added, the patients tottering about as if drunk. The spinal symptoms consist of a paraplegiform affection. The paralysis is usually sudden; in some cases the patient a few minutes after stepping from the air-chamber falls down perfectly helpless as far as the lower half of the body is concerned. The expulsive power of the bladder is usually weakened, and there is anæsthesia to all forms of sensation in the affected limbs, as well as diminished electro-cutaneous sensibility. The patient often complains of a strange feeling, as if the lower half of his body were a foreign substance. With this the electro-muscular reactions are normal. In the majority of cases these symptoms disappear entirely in from three to ten days, but occasionally they remain longer; imperfect recovery of motion and sensation occurs, or, as happened in a few cases, one of which was carefully examined during life by Lehwess and after death by Leyden, death occurs as in myelitis. In the only case where an autopsy and careful microscopical examination were made under these circumstances71 peculiar fissures were found in the substance of the spinal cord, surrounded by areas of reactive myelitis and filled with granule-cells. The absence of any pigmentary relics of a hemorrhage induced Leyden to assume that the lacunæ were not of hemorrhagic origin. He inclines to the view that they were due to the escape of gas from the blood-plasma, and consequent multilocular inflation of the tissue. If his observation be confirmed, it constitutes a strong objection to the hyperæmia theory of the caisson disease. There is neither permanent hyperæmia nor congestive or hemorrhagic myelitis developed, as far as the limited material thus far studied permits a conclusion.
70 Clark, St. Louis Med. and Surg. Journ., cited from Hammond, loc. cit.
71 E. Leyden, Archiv für Psychiatrie, ix. p. 316.