rarely preceded by the usual inflammatory symptoms of chilly
sensations, restlessness, headache, etc. A sharp rigor is the first
indication of disease in most cases. This is followed by fever, with
high temperature and a quick, full, hard pulse. Pain in the back
follows, either confined to a limited region or extending throughout
the whole extent of the spine, soon becoming acute, and aggravated by
any movement of the trunk or even of the limbs. There is usually but
little tenderness on pressure upon the spinous processes, and often
none at all. The pain extends around the body and throughout the
limbs. In the course of a few hours muscular contraction in the region
of the back, and also of the limbs, is observed. When the disease is
situated in the cervical region, the head is drawn backward, and
cannot be moved without severe pain. If it occupies a considerable
extent of the spine, the dorsal muscles become rigidly contracted and
the body is arched forward (opisthotonos), as in tetanus, so that the
patient may even rest upon his occiput and sacrum. Owing to the
implication of the muscles of respiration, more or less dyspnœa is
common, and may even cause death by asphyxia. There is no paralysis of
the limbs, unless there be complication of myelitis, but the patient
abstains as far as possible from any movement from dread of pain.
Reflex irritability is exaggerated. Retention of urine and
constipation are common, probably for the same reason. Hyperæsthesia
of the surface of the body in limited areas is sometimes noticed,
owing to the irritation of the posterior spinal roots. Provided the
extent of the inflammation be comparatively limited, recovery is
possible, though rare, at this stage of the disease.
When the course of the disease is unfavorable, symptoms of paralysis
appear, from compression of the cord by the products of inflammation.
The hyperæsthesia of the skin gives place to insensibility; the
muscles lose their reflex function and their reaction to electricity;
the bladder and rectum become paralyzed. The invasion of the medulla
by the disease, which is announced by paralysis of the muscles of the
œsophagus and of the tongue, is a fatal complication. The pulse and
the respiration become rapid and irregular from compression of the
vagus, the temperature rises to 106° or 108° F., and death ensues
through asphyxia or failure of the heart.
The course of acute spinal meningitis is rapid. It sometimes
terminates fatally within two or three days, and the average duration
of fatal cases is about a week, but exceptionally the disease may last
for several weeks or even months. Even then complete recovery may take
place, though permanent effects are usually left behind, such as
paresis or paralysis of the lower extremities, muscular contractions,
muscular atrophy, etc., from injury to the nerve-roots or the cord.
The mind is generally clear in the early stage; afterward there may be
delirium, especially along with cerebral complication.
MORBID ANATOMY.—It is rarely that the pia mater is the only tissue
involved in the inflammation. Frequently the inner surface of the dura
{751} is the seat of a fine injection, with delicate false membranes,
and the cord itself—at least its exterior portions—probably always
participates more or less in the congestion. The pia is reddened and
thickened, the surface showing small bloody extravasations, and the
space between its two layers is the seat of a fibro-purulent deposit.
The spinal fluid is turbid and flocculent. The seat and extent of the
morbid appearances vary in different cases; they are always more
abundant in the posterior than the anterior part of the cord, and may
be confined to a limited space or extend throughout its whole length.
It is remarkable that the region of the medulla oblongata is generally
free or only slightly affected; but since bulbar symptoms are often
prominent in grave cases, Leyden[6] accounts for it by supposing that
the exudation is washed away by the constant movement of the
cerebro-spinal fluid. If the cord be involved in the inflammation, it
is softened and injected, the nerve-sheaths are destroyed, and the
axis-cylinders swollen in places. The nerve-roots show hyperæmia,
infiltration of the interstitial tissue with round cells, and
destruction of the nerve-sheaths.
[Footnote 6: _Klinik der Rückenmarks-krankheiten_, von E. Leyden,
Berlin, 1874, vol. i. p. 407.]
DIAGNOSIS.—Spinal meningitis is easily recognized in most cases by its
sudden onset and the severity of its symptoms. The distinguishing
symptoms are sudden and acute pain in the back, extending around the
body and into the limbs, which is increased by every movement of the
trunk, rigidity of the back, hyperæsthesia of the skin, retraction of
the head, with difficulty of breathing and of swallowing. The diseases
from which it must be distinguished are muscular rheumatism (so
called), tetanus, and myelitis. In rheumatism of the dorsal muscles
the pain is confined to the back, does not extend to the limbs, and is
only excited by movement. The fever is moderate or absent; there are
no symptoms of spinal complication, such as cutaneous hyperæsthesia,
retraction of the head, paresis of the limbs, etc.; and the result is
uniformly favorable. Tetanus is almost always due to some well-marked
traumatic cause; the muscles of the jaw are usually first implicated
(trismus); and the attacks of general muscular spasm are easily
excited by peripheral irritation. Myelitis can be distinguished by the
absence of pain in the limbs and by paraplegia, but it must be borne
in mind that myelitis and spinal meningitis may coexist.
PROGNOSIS.—Acute spinal meningitis is always a grave disease, hence a
guarded opinion should be given even in apparently favorable cases.
General mildness of the symptoms, with no indication of extension to
the medulla oblongata, would afford ground for encouragement. The
unfavorable symptoms are those showing compression or inflammation of
the cord, such as paresis, paralysis, twitching of the limbs, muscular
contractions, cutaneous anæsthesia, etc. The extension of the disease
to the medulla, as shown by difficulty of swallowing, speaking, or
breathing, is almost necessarily fatal.
TREATMENT.—During the first stage of the disease an effort should be
made to reduce the hyperæmia of the membranes by the local abstraction
of blood. This is best effected by cupping along each side of the
spine and by the application of leeches to the anus; the bleeding
should be promoted by poultices. Free purging is likely to be of
service, and is best obtained by means of ten grains each of calomel
and jalap (for an {752} adult), followed by saline laxatives.
Counter-irritation to the back may be induced by the application of
blisters or by painting the skin with a strong tincture of iodine (one
or two drachms of iodine to an ounce of sulphuric ether). After the
effusion of lymph and pus, as shown by symptoms of compression of the
nerve-roots and cord, absorbents should be tried, of which the iodide
of potassium, in doses of five to ten grains, four times daily, is
most likely to be of benefit. Pain must be relieved by opium or
morphia and chloral hydrate. The latter, either alone or combined with
hyoscyamus and bromide of potassium, will be useful to allay spasmodic
twitching, opisthotonos, or muscular contraction. The patient should
be enjoined to lie on each side alternately, or on the face if
possible, in order to equalize the hyperæmia of the membranes and
cord. Liquid nourishment must be freely administered, such as milk,
broths, gruel, etc., together with wine and other stimulants in case
of exhaustion and threatening of collapse. During convalescence the
patient should be carefully protected against cold and fatigue, and
the strength must be supported by quinine and iron with suitable diet.
Chronic Spinal Meningitis.
SYNONYMS.—Chronic inflammation of the pia mater of the spinal cord,
Chronic spinal leptomeningitis.
Chronic spinal meningitis may follow the acute form, or it may arise
from chronic disease of the vertebræ or of the cord, especially
myelitis and sclerosis. It is most apt to accompany sclerosis of the
posterior columns, and it is often difficult to say in any particular
case whether the meningeal affection preceded or followed that of the
cord. Probably some cases of chronic myelitis, especially of the
disseminated form, owe their origin to chronic meningitis.[7] It has
been thought to follow blows on the back, and also to arise from
general concussion without traumatism, and has been considered as a
frequent result of accidents from railroad collisions, etc. This view
has been disputed by Herbert W. Page,[8] who says: “Of the exceeding
rarity of spinal meningitis as an immediate result of localized injury
to the vertebral column we are well assured.... And we know of no one
case, either in our own experience or in the experience of others, in
which meningeal inflammation has been indisputably caused by injury to
some part of the body remote from the vertebral column.” Chronic
alcoholism and syphilis, especially the latter, predispose to the
disease. In many cases no adequate cause can be assigned.
[Footnote 7: Leyden, _op. cit._, vol. i. p. 442.]
[Footnote 8: _Injuries of the Spine and Spinal Cord, without Apparent
Mechanical Lesion and Nervous Shock, in their Medico-legal Aspects_,
London, 1883, p. 128.]
SYMPTOMS.—Gowers[9] remarks that a large number of symptoms formerly
assigned to chronic spinal meningitis have nothing to do with that
pathological state, but are now known to be owing to alterations
within the cord which are frequently associated with it. The symptoms
which are really due to the meningeal inflammation—namely, those {753}
arising from interference with the nerve-roots in their passage
through the thickened membranes—do not differ essentially from those
of chronic pachymeningitis of the spine; the principal are pain in the
back, especially on movement, extending to the trunk and limbs,
hyperæsthesia of the skin in various regions within the domain of the
irritated sensory roots, with diminution or loss of the knee-jerk, and
areas of anæsthesia due to their more complete compression. The
compression of the motor roots gives rise to symptoms which are
similar to those of disease of the anterior cornua, consisting chiefly
of muscular wasting, with impairment of motion in corresponding
regions, without fever.
[Footnote 9: _The Diagnosis and Diseases of the Spinal Cord_, by W. R.
Gowers, M.D., 2d ed., Philada., 1881, p. 73.]
The anatomical appearances, which are most pronounced in the posterior
aspect of the cord, and diminish from below upward, are often of
considerable extent. The membrane is thickened, opaque, and often
adherent to the cord. On the inner surface are seen numerous small
bodies composed of proliferating connective tissue.[10] These,
according to Vulpian, are chiefly found in the lower dorsal and lumbar
region and on the cauda equina. The dura is very frequently involved
in the inflammation; it is thickened, and its inner surface is
adherent to the pia, often showing numerous miliary bodies similar to
those found in the pia.
[Footnote 10: Leyden, _op. cit._, vol. i. p. 144; A. Vulpian, _Mal. du
Syst. nerv._, Paris, 1879, p. 126.]
DIAGNOSIS.—Chronic spinal meningitis so rarely exists apart from
disease of the dura or of the cord that its separate diagnosis must be
mainly a matter of conjecture. Leyden justly says we must usually be
content to diagnosticate chronic meningitis without attempting any
further distinction, except in cases which originate in disease of the
vertebræ or of their neighborhood, and afterward penetrate into the
spinal canal, and which would probably give rise to pachymeningitis.
The diseases with which chronic meningitis of the spine is most likely
to be confounded are posterior sclerosis (locomotor ataxia) and
chronic degeneration of the anterior cornua (progressive muscular
atrophy).[11] From the former it is distinguished by the absence of
ataxia; from the latter, by the irregular distribution of the
symptoms; and from both, by the existence of limited areas of
anæsthesia and of extensive spinal pain. It must be remembered that
inflammation of the cord complicating that of the meninges, or
pressure upon the cord by the thickened membranes may give rise to
mixed symptoms. The latter is especially observed in syphilitic cases.
[Footnote 11: Gowers, _op. cit._, p. 74.]
PROGNOSIS.—Simple chronic spinal meningitis is rarely if ever fatal.
How far it is capable of amelioration or of cure is not, in the
present state of our knowledge, known. When complicated with disease
of the cord the prognosis will depend upon that of the latter.
Syphilitic chronic meningitis is to a certain extent amenable to
appropriate medication.
TREATMENT.—The treatment should have for its object (1st) to relieve
pain; (2d) to arrest the progress of the inflammation, and especially
to prevent it from extending to the cord; (3d) to promote the
absorption of the exudation. For the first object the internal or
hypodermic employment of morphia should be combined with external
applications, such as fomentations, liniments, ice, etc.
Counter-irritation by means of dry cupping, blisters, iodine, etc.,
with leeches, shampooing, and douches of hot water, may be of some use
in retarding the progress of the {754} inflammation, and should be
aided by the administration of mercurials and the preparations of
iodine. The biniodide of mercury would be useful for this purpose in
the dose of one-sixteenth to one-eighth of a grain three times daily,
its effect being carefully watched in order to prevent salivation. The
same means will also aid in favoring the absorption of lymph. In
syphilitic cases an appropriate specific treatment is indicated.
Spinal Meningeal Hemorrhage.
SYNONYMS.—Spinal meningeal apoplexy, Hæmatorrhachis.
Spinal meningeal hemorrhage may take place between the dura mater and
the walls of the vertebral canal, or between the dura and the pia
mater—_i.e._ into the arachnoid space.
ETIOLOGY.—Penetrating wounds, injuries to the vertebræ, fractures and
dislocations, and violent blows are apt to give rise to more or less
hemorrhage into the spinal canal. Violent convulsions, as in tetanus,
epilepsy, uræmic eclampsia, hydrophobia, may be followed by meningeal
hemorrhage, owing to the disturbance of the circulation from asphyxia;
and excessive muscular effort, as in lifting heavy weights, etc., has
been said to cause it. In cerebral meningeal hemorrhage and in
effusion into the substance of the brain the blood sometimes escapes
into the spinal canal. An aneurism of the aorta has been known to
communicate with the canal; such a case was reported by Laennec.[12]
In certain diseases with hemorrhagic tendency, as purpura and scurvy,
spinal extravasation is occasionally observed.[13]
[Footnote 12: _Traité d'Auscultation médiate_, 4th ed., Paris, 1837,
vol. iii. p. 443.]
[Footnote 13: A case of scorbutic spinal hemorrhage is reported in the
_British Med. Journal_, Nov. 19, 1881.]
SYMPTOMS.—These vary according to the conditions under which the
hemorrhage is produced and to the amount of bleeding. In traumatic
cases the signs of hemorrhage are often completely overshadowed by
those of the injury of the vertebræ, the membranes, or the cord, and
are undistinguishable. When a large amount of blood is suddenly
introduced into the spinal canal, it usually gives rise, by pressure
on the cord, to paraplegia, which, however, is sometimes of only short
duration. Thus in Laennec's case the bursting of an aneurism into the
spinal cavity was signalized by a sudden paraplegia, but in half an
hour the power of movement returned, though sensation did not. The
patient died in a few hours from hemorrhage into the left pleural
cavity. The amount of blood in the spinal cavity is not stated, and,
in fact, it would appear that the spine was not opened. When the
amount of blood is smaller the symptoms indicate irritation of the
spinal nerves and of the cord. Pain in the back is always present,
extending into the limbs, and is sometimes severe. Its seat
corresponds to that of the effusion. There may be a feeling of
tingling and numbness in the lower extremities, with anæsthesia or
hyperæsthesia of the skin and more or less paresis. A feeling of
constriction around the waist or the chest is sometimes complained of.
In slight effusions the symptoms may be limited to numbness and
formication of the extremities, with slight paresis. There is rarely
fever in the early stages, unless the amount of blood is {755}
sufficient to give rise to inflammatory conditions of the cord or
membranes. If the extravasation be moderate it is generally absorbed,
with relief to the symptoms, although slight numbness and paresis of
the extremities may continue for a long time.
PATHOLOGICAL ANATOMY.—In hemorrhage outside the dura the loose
cellular tissue between the membrane and the bony canal contains more
or less coagulated blood according to the circumstances of the case,
especially in the posterior region of the canal and covering the
nerve-roots. The dura is reddened by imbibition of the coloring matter
of the blood. When the amount of the effusion is large, as in
traumatic and aneurismal cases, or where cerebral hemorrhage has
extended into the spine, the cord may be compressed by it. Hemorrhage
into the arachnoid sac, except in cases of violence, etc., is usually
of limited amount, sometimes only in the form of drops of blood upon
the surface of the dura or pia. When more abundant it may surround the
cord more or less completely, but in most cases it is limited in
longitudinal extent, being confined to the space of one or two
vertebræ. The cord may be more or less compressed, reddened, and
softened. In all cases the spinal fluid is discolored and reddened in
proportion to the amount of the hemorrhage.
DIAGNOSIS.—When the complications are such that symptoms attributable
to hemorrhage are not observed, the diagnosis of spinal hemorrhage is
impossible. This may happen in the case of wounds and injuries of the
vertebræ and of the passage into the spinal canal of blood from an
apoplectic effusion of the brain. In the convulsions of tetanus,
epilepsy, etc. the amount of the hemorrhage is rarely sufficient to
give rise to distinctive symptoms. In idiopathic and uncomplicated
cases the chief diagnostic marks are suddenness of the attack; pain in
the back, usually at the lowest part; disturbances of sensation in the
extremities (anæsthesia, formication, etc.); paresis or paralysis of
the legs; the absence of cerebral or spinal inflammatory symptoms;
and, in many cases, the favorable course of the disease. Sometimes an
ostensible cause, such as scurvy, purpura, suppressed menstruation, or
hemorrhoidal flux, will aid in the diagnosis. The disease for which
spinal hemorrhage is most likely to be mistaken is acute myelitis, but
this is not sudden in its onset, is accompanied with fever, and gives
rise to paralysis both of motion and sensation, and to loss of control
over the sphincters, to bed-sores, etc. Hemorrhage of the cord would
be accompanied by paraplegia and loss of sensation in the lower
extremities and slight tendency to spasmodic manifestations; it is
fatal in the majority of cases, or else is followed by permanent
paralysis. Hysteria might be confounded with spinal hemorrhage, but
the history of the case and the transient duration of the symptoms
would clear up all obscurity.
PROGNOSIS.—In traumatic cases the hemorrhage is usually only one
element in the gravity of the situation, which depends chiefly upon
the character and extent of the original injury. In idiopathic and
uncomplicated cases the prognosis, which must always be doubtful, will
vary according to the severity of the symptoms as corresponding to the
amount of the effusion. The danger is greatest during the first few
days; if there should then be diminution of the more important
symptoms, an encouraging opinion may be given. The immediate effects
may, however, be {756} less grave than the remote, such as bed-sores,
cystitis, etc. Except in the very mildest cases the patient is likely
to be confined to bed for several weeks. In more severe ones the
convalescence may be very protracted, and permanent lameness, etc. may
result.
TREATMENT.—In the early stage absolute rest in bed, with cold
applications to the back and moderate purging, should be employed.
Large doses of ergot are recommended, but there is little evidence of
benefit from this medicine. In traumatic cases no rules for treatment
of the hemorrhage can be laid down. If the extravasation evidently
depends upon a constitutional diathesis, as in purpura, scurvy, etc.,
the remedies appropriate for these diseases should be employed,
especially tonics and astringents, such as the tincture of the
chloride of iron, in doses of from fifteen to thirty drops three times
daily, quinine, and the vegetable acids. Should there be evidence of
blood-pressure from suppressed discharge, as in amenorrhœa, arrested
hemorrhoidal flow, etc., leeches should be applied to the anus, and
blood may be taken from the region of the spine by cupping. In the
later stages an attempt may be made to aid the absorption of the
effused blood by the administration of the iodide of potassium or the
protiodide of mercury, and by the application of blisters or strong
tincture of iodine to each side of the spine. Pain must be relieved
and sleep obtained, when necessary, by means of opium, chloral
hydrate, or other anodynes. Electricity, rubbing, bathing, etc. will
be useful for combating the paralytic symptoms which may remain after
the disease itself is relieved.
{757}
SPINA BIFIDA.
BY JOHN ASHHURST, JR., M.D.
DEFINITION.—By the term spina bifida is meant a congenital
malformation of the vertebral column, consisting in the absence of a
part—commonly the spinous processes and laminæ—of one or more of the
vertebræ, and thus permitting a protrusion of the spinal meninges,
which, with their contents, form a tumor of variable size and shape,
usually in the lumbo-sacral region.
SYNONYMS, ETC.—Of the various names which have been proposed for this
affection, most are objectionable, as not expressing with sufficient
definiteness what is meant. Thus, hydrorachis (the term generally
employed by French writers), hydrorachitis, spinal hydrocele, etc.,
convey merely the notion of an accumulation of fluid within the spinal
canal, and are as applicable to simple serous effusions in that part,
whether occurring as a complication of hydrocephalus or as the result
of injury, as to the special affection under consideration. Again,
myelochysis—pouring out or protrusion of the spinal marrow—would imply
that the cord itself was necessarily involved in the tumor, which is
certainly not always the case. The terms schistorachis (cleft spine)
and atelorachidia (defective spine—a name suggested by Béclard) would
be preferable, and are really more accurate than the name spina
bifida, since, as a matter of fact, the spinous processes are, as a
rule, not bifid, but totally deficient. The latter term, however, has
the advantage of being more familiar, and may be retained simply as a
matter of convenience. It is said by Itard to have been first employed
by the Arabian physicians.
HISTORY.—Spina bifida does not appear to have been known to the
ancients, the earliest recorded observations of the affection being
found in the writings of Bauhinus (1560-1624), of Tulpius (1593-1674),
of Bonetus (1620-89), and of Ruysch (1638-1731). Good accounts of the
affection may be found in the _Dictionnaire des Sciences médicales_
(tome xxii., Paris, 1818), and particularly in Holmes's _Surgical
Treatment of the Diseases of Infancy and Childhood_ (2d ed., London,
1869), in Follin and Duplay's _Traité de Pathologie externe_ (tome
iii.), and in Treves's article on “Malformations and Injuries of the
Spine” in the _International Encyclopædia of Surgery_ (vol. iv., New
York, 1884).
ETIOLOGY.—There are two conditions essential to the formation of a
spina bifida: (1) an arrest of development, or at least a defective
closure, of the vertebral arches; and (2) a dropsical condition either
of the central canal of the spinal cord or of the subarachnoid spaces;
but which {758} of these is the antecedent condition it is, as justly
remarked by Erb, impossible to decide. Spina bifida often occurs as a
complication of hydrocephalus, and is itself often complicated with an
atrophic and deformed condition of the lower extremities—a
circumstance which led Tulpius to suggest that the malformation was
caused by a malposition of the fœtus in utero, an explanation which it
seems hardly necessary to waste time in considering. Salzmann observed
spina bifida in two children born of the same mother, and Camper
noticed it in twins.