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 hyperæmia[69] 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
{804} pathological hyperæmias, even if the phenomena of both were
similar; which is not the case.
[Footnote 68: _Diseases of the Nervous System_, 7th ed., p. 392.]
[Footnote 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
circumstances[71] 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.
[Footnote 70: Clark, _St. Louis Med. and Surg. Journ._, cited from
Hammond, _loc. cit._]
[Footnote 71: E. Leyden, _Archiv für Psychiatrie_, ix. p. 316.]
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 {805} 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.
[Footnote 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]
[Footnote 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 {806} 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.
How far the spinal cord is liable to suffer from arterial spasm is as
yet a matter of conjecture. It is supposable that just as a powerful
psychical impression provokes a sudden spasm of the cerebral arteries,
so a peripheral irritation may provoke a spasm of the spinal arteries.
In this way the reflex paralyses, motor and vaso-motor, are explained
by many writers.
The subject of reflex palsy has been so much confused by improper
cataloguing—if it can be so called—that some of the best authorities
have become sceptical as to its occurrence. Among the chief sources of
error has been the attributing to irritation of the genital organs
various convulsive, psychical, and paralytic disorders. Adherence of
the prepuce and its excessive length were charged with being
responsible for idiocy, imbecility, epilepsy, and every form of
paraplegia and panplegia. It was further claimed that instances of
complete cure of each of these {807} affections had followed the
removal of the exuberant or adherent prepuce. I cannot find a single
instance recorded where such a cure was effected in any of our large
medical centres, so as to prove convincing to critical colleagues. On
the contrary, L. C. Gray[74] has shown that various surgical
procedures have been needlessly resorted to on this erroneous theory
in cases of organic diseases of the spinal cord. I have seen two
unfortunate children suffering from the worst forms of anterior
poliomyelitis, one afflicted with pseudo-hypertrophic paralysis, and
several hydrocephalous and microcephalous idiots, whose prepuces had
been sacrificed to the theory alluded to—it is needless to add without
any result, good or bad.
[Footnote 74: _Reflex Irritation from Genital Irritation_. In this
paper written communications from all or nearly all neurologists in
the United States—certainly including all those of national fame and
large experience—are cited, in which they testify to never having seen
a case of this character cured by operations on the penis (_Annals of
Anatomy and Surgery_, Jan. and Feb., 1882.)]
The possibility of a reflex paralysis occurring from genital
irritation in the male cannot be denied; among the lower animals a
ligature around the spermatic cords sometimes produces paraparesis,
and paraplegia is a common complication of renal and vesical troubles
in others. But analogous observations in man are rare, and becoming
rarer with our increasing acumen in diagnosis. In females peculiar
reflex disturbances are found associated with uterine and ovarian
derangements. In one case of retroflexion, with possible dislocation
of the ovary, referred to me by H. J. Boldt, there is a remarkable
vaso-motor paralysis of the right arm during each menstrual period:
this member becomes greatly enlarged, of a purplish-blue color, and
cold. Equally remarkable are the reflex disturbances resulting from
the presence of worms in the intestinal canal. Every form of spinal
and cerebral paralysis, even aphasia, has been observed in connection
with helminthiasis. Such disorders yield as rapidly as they are
developed to the exhibition of vermifuges.
Special interest has been aroused by the discovery laid down in the
joint treatise of J. W. Mitchell, Morehouse, and Keen of reflex
paralysis following injuries, observed in the War of the Rebellion.
The cases cited by them appear singular on first sight. The paralysis
is often observed in parts of the body which are not only remote from
the seat of injury, but have no direct connection, physiologically or
otherwise, with it. The hand may be injured and the opposite leg
paralyzed.
Since Mitchell, Morehouse, and Keen first announced the existence of
this peculiar form of reflex paralysis a careful search has been made
by military surgeons engaged in other campaigns for like results.
Notably was this done in the Franco-Prussian War. A number of
confirmatory instances have been collected, some of which rival in
singularity those related by the discoverers of the affection. In one
case a unilateral paralysis agitans followed a punctured wound of the
opposite shoulder, and in another reflex aphasia followed a gunshot
wound of the lumbar region.[75] A discrimination is to be made between
such cases where the paralysis, anæsthesia, or neuralgia is an
immediate result of the injury, and those where they follow after
weeks or months. In the latter instance we have not true reflex
disorders to deal with, an ascending {808} neuritis having been found
in the few cases which could be carefully followed up.[76]
[Footnote 75: _Sanitäts Bericht über die deutschen Heere im Krieg
gegen Frankreich_, 1870-71, vol. vii.—abstracted in _Neurologisches
Centralblatt_, 1886, p. 207.]
[Footnote 76: In a case of Mollenhauer's, vesical paralysis and
paresis of the right leg occurred six years ago (1880) in a veteran of
our civil war who had a gunshot wound of the right hand, with signs,
which are still present, of occasional exacerbation of brachial
neuritis. Prodromal signs of paresis were noticed at intervals since
his return from the campaign. The bladder trouble and paresis are now
apparently stationary. Such a case can be accounted for only on the
assumption of an organic cord-change secondary to a neuritis.]
The theory that the reflex paralysis from utero-ovarian, intestinal,
and surgical affections, when acutely produced, is due to central
anæmia, is as acceptable as any other would be in the absence of
decisive observations.
Spinal anæmia will but rarely present itself as a subject for special
and separate treatment. When not associated with an intrinsically
grave condition, such as aortic obstruction, dysentery, fatal
hemorrhage, or typhoid fever, it is an exceedingly benign affection,
rapidly yielding to tonic and restorative measures combined with rest.
Embolism, Thrombosis, Hemorrhage, and Abscess of the Spinal Cord.
Although the spinal cord is a segment of the same central organ as the
brain, nourished in a similar way, and subject to the same
physiological and pathological laws, lesions of the vascular
apparatus, which play so important a part in brain pathology, play a
comparatively insignificant one in that of the spinal cord. Embolic,
thrombic, and primary hemorrhagic lesions of the cord are so rare that
their possible existence has even been denied. A primary thrombosis of
the cord has not yet been satisfactorily demonstrated to occur
independently of syphilitic lesions; and when it occurs the ensuing
tissue-changes, as described by Heubner, Julliard, and Greiff, are
usually in the background as compared to the gummatous, sclerotic, or
meningitic changes which coexist. The clinical as well as the
anatomical picture is accordingly either one of a myelitis or
meningitis, as the cases of Charcot-Gombault, Heubner, McDowell,
Wilks, Wagner, Zambaco, Homolle, Winge, Moxon, Schultze, Westphal,
Julliard, and Greiff show. (See Myelitis and Spinal Meningitis.)
With regard to the occurrence of hemorrhage into the substance of the
spinal cord (hæmato-myelia), it is so rare an occurrence that I can
recall but a single case in which I entertained the diagnosis of this
lesion; and in that very case I am unable to declare that it was not a
hemorrhagic myelitis. Aneurismal changes of the spinal arteries are
comparatively of rare occurrence, and as other predisposing causes to
primary vascular rupture are rare in the cord, the probability of its
occurrence is very much diminished. Hebold,[77] in a young girl who
had developed severe cerebro-spinal symptoms during a period of nine
months following an erysipelatous disorder, found the upper dorsal
cord, on section, dotted with numerous reddish and round points. These
points corresponded to {809} aneurismal dilatations of the vessels. As
there were other inflammatory and vascular lesions in the same
subject, the author referred their causation to a general
constitutional vice, the result either of the phlegmonous or of a
tuberculous disorder.
[Footnote 77: _Archiv für Psychiatrie_, xvi. 3. Rupture of miliary and
other aneurisms in the meninges has been reported by Astley Cooper,
Traube, and others. It is remarkable that such cases are more and more
rarely recorded from year to year in inverse ratio to the accuracy of
our spinal autopsies. I have never found a miliary aneurism below the
uppermost cervical level of the cord. On the other hand, I have found
extensive spinal hemorrhage in cases where the vessels of the cord
proper were fairly healthy.]
It is claimed that suppression of the menses, over-exertion, lifting
heavy weights, and concussion are causes of spinal hemorrhage. The
same causes are also mentioned for acute hemorrhagic myelitis; and it
is a question whether the supposed hemorrhage is an initial lesion or
secondary to congestive or anæmic softening.[78]
[Footnote 78: I have never found vascular ruptures, although carefully
searching for them, in the spinal cord of persons dying instantly
after falls from a great height, or, as in one case which I was
fortunately able to secure the cord of, where the subject had been
violently thrown down. Where hemorrhages have been found under these
circumstances they were, as far as I am able to learn from the cases
recorded, meningeal.]
The symptoms attributed to spinal hemorrhage are the same, taking the
same locality of the cord, as those of a very rapidly-developed
transverse myelitis. It is unnecessary to enumerate these here in
anticipation of the next section. They are described as being much
more sudden. This suddenness is the only diagnostic aid on which we
can rely.[79] The fate of the patient is said by Erb to be decided
within a few days. If he survive the immediate consequences of the
hemorrhage, he is apt to recover, as to life, altogether, with such
permanent atrophies, paralyses, and anæsthesias as are entailed by the
destruction of the tracts and gray substance involved in the
hemorrhage. The treatment recommended for this condition consists of
rest, either in the lateral or prone position, local depletion and
derivation to the intestinal canal, as well as the internal use of
ergotin. The local application of ice, which is also advised, is
probably based on illusory views.[80] After the immediate danger is
past the case is to be treated as one of myelitis—a very safe
recommendation in view of the probability that it was a case of
myelitis from the beginning.