Test Bank for College Algebra with Modeling and

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MULTIPLE CHOICE. Choose the one alternative that best completes the statement or answers the question.

Find a point-slope form for the equation of the line satisfying the conditions.
1) Slope -2, passing through (6, 4)
A) y - 4 = 2x - 6
B) y - 4 = -2x + 6
C) y = -2(x - 6) - 4
D) y = -2(x - 6) + 4
Answer: D

2) Slope -9, passing through (-5, -4)

A) y = 9(x - 5) + 4
B) y = -9(x + 5) - 4
C) y = -9(x - 5) + 4 D) y + 4 = 9x + 5
Answer: B

3) Passing through (5, -6) and (-2, -2)

A) y= (x + 5) + 6 B) y = -6(x + )+5

C) y = 6(x - )-5

D) y = - (x - 5) - 6
Answer: D

Write an equation in slope-intercept form for the line shown.

4)
 A) y = -6x + 6
B) y = 6x + 6
C) y = 6x - 6
D) y = -6x - 6
Answer: A

Full file at https://testbankuniv.eu/College-Algebra-with-Modeling-and-Visualization-6th-Edition-Rockswold-Test-Bank

5)

A) y = x + 1
B) y = -x + 1
C) y = x - 1
D) y = -x - 1
Answer: A

6)
 D) y = 2x
Answer: D

7)

A) y = x-3
B) y = 3x + 3
C) y = 3x - 3
 D) y = x+3
Answer: D

8)

A) y = 2x

B) y = x
C) y = -2x

D) y = - x
Answer: B

3
 9)

A) x
=
3
B) x
=
-
3
C
)
y
=
3
D) y = -3

Answer: D

Match the equation to its graph.

10) y = 2x + 4
A)
 4

C)
 Answer: A

11) y = 5x - 3
A)

5
 B)

Answer: B
12) y = -2x + 4
A)
 Answer: A

13) y = -2x - 6
A)

D)
 Answer: D

14) y = -5x
A)
 D)

Answer: B

15) y = -6
A)
 C)

Answer: B

16) y = 2(x - 2) + 5
A)

B)
Answer: D
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cords of three dogs, and in each instance produced changes which
he interpreted as comparable to the myelitis of human pathology. But
the inflammation thus provoked was not of the cord-substance alone;
it also involved the membranes, and the inflammatory foci were in
several instances purulent. Now, pus never85 forms in ordinary
myelitis. An abscess of the cord never occurs where a septic agency
can be excluded. In six dogs whose spinal cords I wounded in the
dorsal and lumbar regions by aseptic methods, and who survived
from two to seven days, I never found purulent or indeed any active
inflammatory process, as that term is ordinarily understood, but
exactly such passive and necrotic or reactive changes as occur in
the acute myelitis of human pathology.
83 Klinik der Rückenmarkskrankheiten, ii. p. 115.

84 Cited by Leyden.

85 In the textbooks and encylopædias, without an exception, the statement that pus
may be a product of myelitis is made. This is true of traumatic cases and of such
depending on septic and zymotic causes alone. I am unable to find a single carefully
observed case of the occurrence of pus in simple myelitis in the literature.

Owing to the advance of clinical and anatomical knowledge made

within the past fifteen years many forms of spinal disease classed
with the inflammations have been recognized as distinct pathological
entities, no longer to be confounded with simple acute myelitis,
ordinarily so called. Special forms of acute spinal paralysis, notably
acute poliomyelitis anterior of children and the corresponding chronic
affection among adults, have become separated in this way, and are
accordingly treated of in separate parts of this volume.86
86 For other and practical reasons the traumatic and compression forms of myelitis
are also assigned a separate place.

Some dispute exists as to the propriety of making a distinction

between acute and chronic myelitis, since an acute myelitis, if the
initial attack be recovered from with life, presents a similar condition
clinically as chronic myelitis; and this quiescent or slowly-progressing
condition may extend over many years. The term acute with
reference to inflammation of the spinal cord refers only to the active
period of the disease. Just as an embolic softening of the brain is an
acute affection, but may be followed by a chronic paralysis or
aphasia, so the acute myelitic process may be followed by a chronic
paraplegia. It is improper to call the latter a chronic myelitis. It is
merely a protracted symptomatic sequel of the acute process. The
latter is distinguished from chronic myelitis both clinically (by the
rapidity of its onset) and anatomically (by the early dissolution of
nerve-elements in the focus of disease). Limited in this sense, acute
myelitis, excluding the special clinical forms already adverted to, is
rather a rare disease.

MORBID ANATOMY.—The most recognizable change noted in an acute

myelitic focus is one of consistency: the spinal substance is
softened. In some cases the softening is so slight that the observer
may doubt whether he has a pathological or cadaveric softening to
deal with, the dorsal cord, which is most apt to be the site of an
acute transverse myelitis, being precisely the part which is most apt
to show the latter change even in fairly well-preserved bodies. In
extreme cases the softening may be so intense that the cord-
substance, completely fluidified, runs out of the meningeal sac,
leaving the latter a collapsed membranous cylinder to mark the place
where the cord once was. Where the cord-substance is sufficiently
firm to permit of sections being made through it, the normal outline of
the gray and white substance is found obliterated, either presenting
the appearance as if the gray and white matter had been stirred up
together or of a more uniform color-change. The color may be either
white, reddish, yellowish, or chocolate-like. It depends upon the
participation of the blood-vessels in the change. If there be much
hyperæmia, there will be developed what is known as red softening;
if there be much extravasation and commingling of blood with the
diffluent cord-tissue, a chocolate color will mark the diseased area;
and similarly one and the same focus may present different tints in
different parts according to the age and intensity of the process and
the more or less advanced retrogressive metamorphosis of the
extravasated fluid. As already stated, the purulent form of softening
or abscess does not occur in ordinary myelitis.

There is considerable variation in the extent of the affected areas of

acute myelitis. In the typical and severe transverse form the whole
thickness of the cord may be disorganized, and the disorganization
may extend in the length of the cord, so as to involve the level of exit
of from two to five pairs of nerves. In less furibund cases the area of
absolute softening is confined to the gray substance and its
immediate neighborhood, the submeningeal white substance being
but slightly affected or escaping. Sometimes several foci of intense
softening are scattered through a short length of the cord and
connected by less severely involved areas of softening or œdema.
Leyden distinguishes three types of distribution—the transverse, the
longitudinal, and the disseminated insular or multiple form. He
includes under the longitudinal type the so-called central softening of
Albert, but undoubtedly many cases of syringo-myelia have passed
under this designation. The submeningeal form of softening which,
with Ollivier, he states to occur in association with spinal meningitis,
must be a very rare affection, as it is difficult to find a well-
established case recorded. The longitudinal form shows the same
predilection for the gray substance which the acute myelitic process
generally does, but I have seen a finely demarcated fascicular
myelitis limited to the lateral column in a paretic negro. In this case
the pyramid tract and the contiguous area in front of it were so
intensely softened that for a length of twelve centimeters a hollow
canal ran through the cord in the place previously occupied by the
diseased substance. In recent cases of myelitis the diseased area is
usually found surrounded by a transition zone in which, the morbid
change gradually becoming less intense, the consistency is firmer,
and which merges into that of the normal cord. In cases where death
occurs after a few weeks a more abrupt demarcation is usually
found; this is due to the reactive changes occurring in the
neighborhood. The connective tissue becomes firmer, and thus the
softening centre becomes surrounded by a sclerosing capsule.
Ultimately, the centre undergoes complete disintegration and
absorption, and a cavity is left behind filled with a clear fluid; in short,
a cyst surrounded by a firm capsule represents the residua of
disease. In cases where the softening at the centre of the focus does
not proceed so rapidly nor reach so high a degree as to result in
liquefaction, the less vulnerable elements, the blood-vessels and
supporting tissues, survive the death of the ganglionic and
conducting substance; the connective elements hypertrophy, and
thus a firm sclerotic patch is formed, indicating the location of the
previously softened field.

It seems to be generally admitted, with Hayem, that the blood found

exuded in the hemorrhagic form of myelitis does not necessarily
indicate an active determination, but is rather, like some forms of so-
called red softening of the brain, the result of capillary rupture or
necrosis in the midst of the disintegrated tissue, now rendered
incapable of supporting the vessels. The existence of a purely white
form of myelitic softening shows that a textural change is the primary
occurrence, and that the participation of hyperæmia or congestion is
not an essential feature of myelitis. The assumption of an initial
inflammatory congestion is made rather on theoretical grounds than
on the basis of observation. It is simply incredible that, as Ross87
claims, white softening should be a third stage, preceded by red and
yellow softening as a first and a second stage! How the extravasated
blood, which pathologists generally allow to leave long-lasting traces,
manages to disappear, and how blood-vessels in the midst of
necrotic or œdematous surroundings suddenly acquire such
contractile energy as to produce a total emptying of their contents
while the perishable nerve-elements remain behind, are problems
which should be solved before attempting to assign to a condition
which is often found to be a primary phase of myelitis the position of
a late and regressive stage. Erb admits that red softening, to which
he also assigns the position of a first stage, is very rarely seen, only
traumatic and rapidly fatal cases of central myelitis offering
opportunities of examining it. None of the various forms of exudation
claimed to occur at this period under the names of vitreous, colloid,
or hyaline deposit have been confirmed in any recently well-studied
case.88 The great mass of authorities, however, still agree in
regarding the minute changes of the initial stage of myelitis to
correspond to those of ordinary inflammation. The vessels are
described as injected, the adventitial spaces as crowded with the
formed elements of the blood, and the vascular walls and the
neuroglia infiltrated with granule-cells and fatty granular matter. By
some, inflammatory changes of the neuroglia are described, but I am
unable to find a single case in which these were determined in early
fatal cases. As far as our observation goes, the hypertrophy of the
neuroglia is a later occurrence.
87 A Treatise on Diseases of the Nervous System, 1882, vol. ii. p. 280. The author
states no authority, nor does he advance his own observations in support of this
statement.

88 Baumgarten's case of hyaline exudation, Archiv der Heilkunde, vol. xvii. 276, was
an infectious myelitis and associated with anthrax.

As to the nervous elements themselves, they are always found

affected. The nerve-cells appear inflated, their processes fragile,
sometimes suddenly swollen in their course, at others very thin and
brittle. Multiplication of the nuclei of the large multipolar cells has
been described. It must be an unusual occurrence, as it has been
confirmed by but a few of the numerous observers who have
examined into this question. The protoplasm of the nervous
elements loses its normal striation and fine molecular granulation; it
becomes either coarsely granular or hyaline. The axis-cylinders, both
in their intracinereal and their intramyelinic course, show changes
similar to those of the cell-processes in the gray matter. Particularly
frequent are swellings in their course, the diameter of the cylinder
being so much increased as to almost equal that of the myelin tube.
This increase in diameter is regarded as an inflammatory swelling by
some, as secondary to disturbed nutrition by others; it precedes
disintegration: the substance becomes granular, fragile, and in the
end dissolves. In the mean time the myelin loses its continuity,
irregular segments of it fusing into round and oval masses.89
89 Many of the bodies represented as granule and colloidal cells are in reality round
spheres of myelin, whose resemblance to a nucleated cell is sometimes heightened
by their occasional inclusion of a fragment of an axis-cylinder which has not yet lost
 its power of imbibing carmine and other dyes. Where softening has proceeded
farthest, there the spherical and other forms of myelin are found crowding the field,
and mingled with them are blood-corpuscles, fragments of blood-pigment, granular
detritus, and bodies known as fatty granular cells. A number of bodies of very different
origin have received this name, some of them, like the fragments of myelin alluded to,
not even meriting the name of cells. Others, however, are veritable formed histological
elements, either leucocytes or cellular ingredients of the neuroglia, which, having fed
on the products of myelin disintegration, have become enlarged and coarsely
granular. The longer the duration of the process the more numerous are these bodies,
showing that they are not the coarse and essential factor of the inflammation, but an
accompaniment, subserving some conservative process, inasmuch as they either
remove effete material or contribute to the permanent organization of the cicatricial or
atrophic tissue.

The period now reached by the morbid process may be regarded as

a sort of interregnum. The necrotic tissues have not yet disappeared
on the one hand, the products of inflammation have not yet
organized themselves on the other. It is in this period that the
ganglionic elements are described as undergoing certain changes in
outline and in appearance. Above all, one change has interested
observers, which, consisting in the development of what appear to
be spherical vacuoles in the interior of the cell, is termed
vacuolization. I can compare it to nothing so nearly as to the
appearance which is produced by the formation of gas-bubbles in a
putrefying albumen or other semifluid substance.

This vacuolization of ganglion-cells is now regarded as a cadaveric

change. It is not agreed, as yet, whether its occurrence in myelitis is
so frequent as to suggest its ante-mortem occurrence as a veritable
feature of the disease. I have been struck by this change in the
neighborhood of wounds artificially produced in dogs, even in the
fresh specimen. It must be remembered, however, that under these
circumstances, the nutrition of the cell being destroyed and exposure
to the macerating effect of the cerebro-spinal and pathologically
exuded fluids occurring, a cadaveric change may take place intra
vitam.
The influence of phosphorus and alkaloid as well as metallic poisons
on the cord has been experimentally studied by a number of
observers. Unfortunately, Popow, Tschisch, and Danillo—who
described as characteristic a resulting change in the staining
reaction of the cells, the development of vacuoli in them, and an
atrophy of their processes—had not made a sufficient number of
examinations of normal cords under like methods of preparation to
recognize which of these deviations is without the physiological
confines. Kreyssig90 demonstrated the existence of all these
conditions in the cords of perfectly healthy animals preserved in
chromic acid;91 and Schultze confirms him, and expresses a
surprise, which must be shared by all reflecting investigators, that
poisons of so widely different a character should have an identical
effect on the cord-substance, as is claimed by the writers named.
90 Virchow's Archiv, cii.

91 He attributes the remarkable difference in staining of nerve-cells of the same

ganglionic group and in the same section to the sudden transferral of the hardened
specimens to strong alcohol, which seems to be the custom in some German
laboratories. He claims that uniformity in staining is effected if the specimen be
transferred from the chromic preparation to weak alcohol, then to stronger, and thus
by gradual increase of the strength to strong spirit. Possibly, instead of approximating
the real structural indications by this method, Kreyssig may obliterate them. In
specimens which alcohol is not permitted to touch before staining is completed, very
deeply and very lightly stained cells will be found almost side by side. The shorter the
hardening process, the more perfect the staining method, the more likely are these
differences to be found. It is reasonable to assume that the difference in dye-
absorbing power indicates slight differences in the cell-protoplasm, marking the
nutritive state of the latter and occurring within physiological limits.

If life be prolonged and the conservative processes assert

themselves, the disintegrated material disappears, and as the white
color of the greater area of the cord was due to the myelin, and the
latter has now become destroyed within the diseased area, the latter
presents a grayish color. This phase is often termed gray softening.
The consistency is, however, much firmer than in the previous stage.
Trabeculæ of connective tissue form, enclosing in their meshes a
large number of neuroglia-nuclei and sometimes spaces filled with
fluid. According as condensation and retraction or rarefication
preponderate the process will terminate either in the formation of a
sclerotic focus or of a cyst. Occasionally an irregular spongy tissue
containing several small cysts results.

Charcot claims that a restitution of anatomical continuity, and

therefore of physiological potentiality, may occur in a myelitic cicatrix.
But the experiments of Kahler92 and Homén93 prove that when a
nerve-tract is once destroyed within the spinal cord all hope of
restoring that tract in structure, and thus to restore its functions, is at
an end. Unlike the fibres of the peripheral nerves, those of the spinal
cord and brain do not seem capable of regeneration.94 If a
restoration of function is to occur at all, it must occur through other
channels than those destroyed—in other words, by vicarious action.
92 Prager medizinische Wochenschrift, 1884, No. 31.

93 Contribution expérimentale à la Pathologie et à l'Anatomie pathologique de la

moelle épinière, Helsingfors, 1885, abstracted in Centralblatt für die medizinisches
Wochenschriften, 1886, No. 16.

94 According to the first observer, this is probably due to structural differences. The
extramedullary fibres have a sheath and annular constrictions which are absent in the
intramedullary.

In a large number of cases myelitis is a limited affection; that is, its

ravages remain confined to the area originally involved. But
occasionally the morbid process involves the next segments above
or below, extending with specially great rapidity through the anterior
gray horns. Exceptionally, the entire cord may thus become the site
of a generalized myelitis. There is one segment of the cord which
may be regarded as possessing an acquired vulnerability when a
myelitic focus is in its neighborhood, and that is the lower end. It
seems that while the results of a transverse myelitis in the middle
dorsal cord may remain stationary for ten or more years, those of a
transverse myelitis at the upper lumbar level do not; on the contrary,
the entire cord below the lesion appears to be doomed to undergo
the same degeneration by contiguity. This is the only occurrence
which seems to deserve the name of a descending myelitis: an
ascending extension is more frequently noted in other parts of the
cord, but the frequency of both the so-called ascending and
descending types has been unduly magnified by the inclusion of the
secondary degenerations, which are constant sequelæ of all
complete destructive transverse lesions of the cord, but which are
rather passive phenomena, and probably influence the clinical
progress of the case but little, except under such conditions as are
potent in that chronic form of myelitis which underlies tabes dorsalis.

CLINICAL HISTORY.—The symptoms of acute myelitis usually

correspond to those of any more or less completely transverse lesion
of the cord, and accordingly vary with the altitude of the upper level
of the lesion. In a general way, they may be stated as consisting of—

First, paralysis of movement in the parts supplied from the nerves

given off below the level of the lesion. The reason for this can be
easily recognized in those cases where the pyramid tract, which
conveys voluntary impulses centrifugally, is interrupted by the
softening.

Second, paralysis of sensation in the parts supplied by the same

nerves. This is equally explained by the pathological interruption of
the centripetal impressions normally conveyed brainward.

Third, alterations in the nutrition of the parts supplied by the nerves

arising in the affected level.

Fourth, abolition of those reflexes which are translated in the level of

the lesion.

Speaking crudely, then, the symptoms of a transverse myelitis fall

into two natural groups. The one which includes the first and second
categories enumerated are symptoms due to interruption of cerebral
functions; the other, which comprises the last two categories, being
due to abolition or perversion of spinal functions. There is a third
group comprising certain constitutional symptoms.

Aside from those variations due to the distribution, extent, and

intensity of the lesion there are others which depend on the rapidity
of its invasion. There are three types in this respect—the
apoplectiform, the ordinary acute, and the subacute. The term
apoplectiform has been used in two different senses, one being
clinical, and referring to the rapidity of onset of the symptoms; the
other anatomical, and referring to the nature of the lesion. It is,
however, doubtful if a distinction in the latter sense is practically
valuable. The presence of a blood-clot in a myelitic focus is itself
secondary to the softening, and the intensity and rapidity of the
process must have shown itself in the development of the latter.95
The term ought, therefore, to be used in a clinical sense only.
95 I am able to recall but a single case in which, even clinically speaking, a primary
hemorrhage into the cord-substance was plausible. In this instance a sudden arrest of
menstruation had occurred nearly simultaneously with a combined strain and
exposure in a young girl.

The constitutional symptoms of acute myelitis—which, however, are

often absent—are its most distinctive features in one sense.
Disorders of motion and sensation and perversions of nutrition are
signs common to all destructive affections of the cord, whether of a
traumatic, neoplastic, or a chronic inflammatory character. But fever,
headache, and delirium,96 associated with gastric and visceral
disturbances of acute development, are not found to be initial and
intrinsic symptoms with them as with acute myelitis. In their absence
the mode of onset is characteristic. A high degree of paralysis, motor
or sensory, is developed with a rapidity unequalled in any chronic
affection of the cord. Sometimes there is a prodromal period in which
formication, numbness, and disorders of movement are observed in
the same part of the body which are destined to become paralyzed
at a later stage of the malady. Within a few hours, days, or at most
weeks, complete paraplegia may become developed. The prodromal
symptoms may include any form of disturbed sensation. Lancinating
pains, tingling, a feeling of the limbs falling asleep, peculiar and
indescribable sensations attending the acts of micturition and
defecation or of placing the feet violently on the ground, are
common. Occasionally they are found in one limb only, although
motor and sensory paralysis may ultimately occupy the symmetrical
member as completely as the one first involved. In some cases it has
been noted that the patient is unable to lie down, or, if lying, to
occupy the dorsal recumbent position. This feature has been utilized
to support the theory of an initial congestion, which is supposed to
be relieved or aggravated according as the cord is kept elevated or
depressed.
96 These symptoms are to be regarded as actual parts of the myelitic symptoms only
when they accompany the prodromal or initial periods. The later complications,
uræmia and septicæmia, the latter arising from pyelitis, cystitis, or decubitus, often
lead to constitutional disturbance which is not due to the myelitis as such.

In most cases of transverse myelitis, when the anterior cornua are

destructively involved, we possess in the electrical tests valuable
and unerring means of determining the altitude and extent of the
lesion. Whenever we find the atrophy of a paralyzed muscle
accompanied by qualitative electrical changes in myelitis, we must
conclude that the cell-group from which that muscle receives its
nerve-supply is destructively involved.97 These changes are
particularly well demonstrable when the cervical or lumbar
enlargements are affected. They are not as readily ascertainable in
the case of a transverse myelitis in the upper dorsal region, on
account of the situation of the muscles supplied by the upper dorsal
nerves, and the consequent difficulty of application of the necessary
tests.
97 The proposition, originally, I believe, made by myself, that there are distinct cell-
groups in the spinal cord which are constant with certain animal species, and
correspond in relative development to ventral, dorsal, and appendicular muscular
groups (“Architecture and Mechanism of the Brain,” Journal of Nervous and Mental
Diseases, April, 1880), appears to be confirmed in a general way by the researches
and cases of Edinger, Kahler-Pick, Dejerine-Major, Genzmer, Von Monakow, Sahli,
 Prévost-David, F. Schultze, Remak, and Parrot-Joffroy; for the knowledge of the first
and last of which I am indebted to the review of the subject by Starr (“Localization of
the Functions of the Spinal Cord,” American Journal of Neurology and Psychiatry,
August, 1883).

The disturbance of the deep reflexes with very few exceptions

affects the same peripheries as are represented in the destroyed
and impaired gray nuclei. Thus, if the lower part of the lumbar
enlargement be affected, the reflexes of the Achilles tendon and the
gluteal muscles will disappear; if the upper lumbar enlargement, the
knee-jerk disappears.98 Disease of the lower part of the cervical
enlargement is in like manner associated with absence of the wrist-
tendon reflexes, while the disappearance of the elbow-tendon reflex
suggests a higher involvement at the levels of the fifth and sixth
cervical nerve-roots.
98 The disappearance of the knee-jerk and similar reflexes was originally supposed to
be a phenomenon exclusively pertaining to spinal disease and to a destructive lesion
anywhere in the track of the centripetal and centrifugal nerves connected with that
segment of the cord in which the reflex is supposed to be translated. But aside from a
number of physiological observations99 which prove that cerebral conditions may
influence the intensity of the jerk, there are pathological ones which show that it may
be permanently abolished in disease of the pons and cerebellum, and temporarily
abolished or diminished immediately after capsular and ventricular hemorrhage. The
associated symptoms in the former case, and the history of the onset and total
hemiplegia in the latter, serve to distinguish them from destructive spinal lesions
should the occasion for discriminating between them ever arise; which is not likely.

99 S. Weir Mitchell and M. J. Lewis found that voluntary effort increases the jerk at
first, but if continued diminishes its excursiveness (The Medical News, 1886, Feb.
13th and 20th).

In complete transverse acute myelitis of the cervical region high

fever is a constant symptom. In unilateral myelitis of this region
flushing of the face and unilateral sweating are produced, together
with iridoplegia, sometimes preceded by dilatation, owing to initial
irritation and succeeding paralysis of the sympathetic branches
originating at this level of the cord.
Just as the disturbed reflexes and the belt sensations enable us to
distinguish at what levels of the cord the myelitis is situated, so the
distribution of the motor and sensory paralysis affords corroborative
evidence of such location and additional proof of its extent and
intensity.

Transverse myelitis at and above the level of origin of the phrenic

nerve is almost immediately fatal, through its interference with the
innervations required in respiration. In the upper part of the cervical
enlargement it produces complete paraplegia of motion and
sensation in the trunk and all four extremities. In the lowest part of
the cervical enlargement it produces paralysis of the same parts, but
the serratus magnus and scapular muscles escape. The nuclei of
origin of the muscles moving the upper extremity are situated so that
those which are farthest removed from the axis of the body when the
arms are extended are situated lowest in the cord. The sensory
paralysis is distributed in harmony with the motor paralysis; that is,
when there is paralysis of motion in the hand and forearm the
anæsthesia or subjective numbness is also in the hand and forearm.
The same correspondence is not found in affections of the lumbar
enlargement, for anæsthesia of the gluteal region accompanies
paralysis of the crural muscles when the lesion is low down at the
level of the lower lumbar and upper sacral nerves. The distribution of
the anæsthesia, in other words, is not by segments of the limb, but
by surfaces. The gluteal, posterior femoral, gastrocnemial, and outer
pedal surfaces are affected together with the muscles moving the
foot, while the thigh and inner side of the leg and foot become
anæsthetic, with lesion of the upper part of the lumbar enlargement
accompanying paralysis of the quadriceps and deep muscles. It is
not difficult to understand this discrepancy when we bear in mind the
different plan of distribution followed by the brachial plexus as
compared with the lumbar and sacral plexuses. It is not, in my
experience, found that the anæsthesia affects that surface which
covers the part moved by the paralyzed muscle; which is
characteristic of associated paralysis and anæsthesia from cortical
disease.
One of the most dreaded occurrences in acute myelitis is the
malignant bed-sore. The ordinary decubitus which results from the
protracted sojourn of the patient in bed, coupled with the prominence
of his trochanters and sacrum resulting from general or atrophic
emaciation, is also common, but is comparatively benign and easy to
prevent or to manage when established. The malignant bed-sore, on
the other hand, is a spontaneous occurrence, due to the same
obscure but undeniable trophic influences exerted for good by the
normal and for evil by the diseased nerve-centres, which play so
large a part in the symptomatology of tabes dorsalis. It cannot be
avoided; it is not due to pressure alone, or, as some have claimed, to
the macerating influence of the dribbling and decomposing urine.
The development of this lesion is exceedingly rapid, and it may be
regarded as a sort of local gangrene. The skin shows a livid color;
vesicles appear, then burst; the part becomes denuded; and within a
few days a deep ulcer with a dark border and base appears,
discharging a sanious fluid. The subsequent history is that of a rapid
extension and destruction of the neighboring tissues, even down to
the bone, and if situated over the sacrum opening into the spinal
canal through the necrotic arches of the sacral vertebra, thus leading
either to general septicæmia or to putrid infection of the spinal
meningeal sac. Occasionally, gangrenous spots coexist on other
parts of the body, notably the lower extremities, where neither
pressure nor maceration can be accused of playing a part, proving
that the process is primarily due to the spinal affection.

Acute central myelitis, as described by Dujardin-Beaumetz, Hayem,

Hallopeau, and Erb, usually runs its course very rapidly. Indeed, all
of these observers speak of it as the most violent and quickly fatal
variety of spinal inflammation. I have, however, seen one case with
T. A. McBride at the Presbyterian Hospital in which all the
characteristic symptoms of acute central myelitis were markedly
developed and present in their characteristic groupings, and yet the
patient had been suffering from progressing symptoms of myelitis for
one year and a half before that time.100 Usually, complete
anæsthesia and paralysis of the lower half of the body occur in this
form. But the most characteristic feature is a rapidly progressive
atrophy not only of the paralyzed muscles, but also of some which
are still partially under the dominion of the will. With this there is
extreme vesical and rectal trouble, the sphincters being paralyzed.
As a rule, the deep and superficial reflexes are destroyed—they are
always diminished—and trophic disturbances of a malignant type,
such as acute decubitus, joint-changes, and œdema, are common.
The paraplegia is characterized by the flaccid condition of the limbs;
the contractures and spastic symptoms found with other forms of
myelitis are entirely absent, and qualitative electrical changes,
beginning with disappearance of farado-muscular contractility, are
found in the atrophying muscles. There are marked constitutional
symptoms with this form; the tendency to an ascent of the process
and successive involvement of one segment after another of the
gray matter is great, and a fatal issue, as far as known, is inevitable.
100 At the time the patient had undergone such a profound change in appearance that
I failed to remember him, and it was only by accident I learned that I had seen him in
private consultation with his family attendent, F. A. McGuire, a year previous. On the
latter occasion I had made the diagnosis of subacute myelitis chiefly limited to the
posterior columns; there were ataxia, both static and locomotor, slight incontinence,
belt sensation, and ocular symptoms, with abolition of the deep reflexes in the lower
limbs.

DIAGNOSIS.—The principles governing the determination of the

affected region of the cord in acute myelitis are exactly the same as
those detailed in the later sections on Chronic Myelitis or Sclerosis,
the acuteness of the onset, and the relapses which sometimes
occur, and the predominance of irritative spasms—which, however,
is an inconstant criterion—serving to distinguish between the acute
and chronic form of spinal inflammation. In the present state of our
knowledge it is impossible to always differentiate between acute
central myelitis and syringo-myelus—a condition in which the
formation of a periendymal neoplasm, and its subsequent breaking
down in the axis of the cord, lead to the formation of a tubular
cavity.101 The neoplasm in this instance is classified among the
gliomatous new formations. The symptoms depend, exactly as do
those of myelitis, on the distribution of the destructive lesion. In some
cases the posterior cornua and columns are chiefly involved, and
extreme anæsthesia is found; in others the anterior columns are
affected, and the symptoms of a poliomyelitis or an imperfect
transverse myelitis may be imitated.102
101 This cavity, unlike that of hydro-myelus, is not a dilatation of the central canal, but,
lying to one side of it, is excavated in the cord-substance.

102 Repeated fractures have been noted in cases marked by profound analgesia. It is
believed that they are not always due to trophic changes, but may be the result of
muscular action, exaggerated on account of the patient's inability to gauge his efforts.
Still, in the majority of cases the presence of positive trophic disturbances of the skin
seems to indicate the probability of some textural change facilitating the fracture.

As a rule, the sensory disturbance in syringo-myelus is out of

proportion to the muscular atrophy developed; that is, it involves a
far more extensive province. It is usually of a peculiar character:
some forms of sensation are involved but slightly, or even escape,
and others may be nearly destroyed. Commonly, it is the pain and
temperature-sense which suffer most, while the cutaneous space
and pressure, as well as the muscular sense, are not materially
disturbed. These peculiarities are not commonly found in cases of
myelitis, and when present, and particularly when the paralytic or
sensory affections involve all four extremities alike, they suggest the
existence of syringo-myelus. As yet we are unable to make more
than a probable diagnosis between the two diseases.

DURATION AND PROGNOSIS.—The duration of the disease varies.

Cases of the apoplectiform variety are mentioned, in which the
process reached its height in a few minutes, or where the patient,
having retired in good health the night before, awoke finding himself
paralyzed in the lower half of his body. Death may terminate such a
case in a few days or weeks. In another class of cases, complicated
by serious involvement of the bladder, the fatal termination is often
precipitated by putrid cystitis, pyelitis, or uræmic poisoning, and even
in cases which have passed the dangers of the early period in safety
these ominous complications may develop with the usual result
many years after the beginning of the illness. In a number of cases
the first period, that in which the morbid process becomes
developed, is followed by one of comparative quiescence, in which
the paralyses of sensation and motion then established remain
stationary for months and years. A number of authors, Erb, Leyden,
Strümpell, and Ross, speak of such a case as one in which chronic
myelitis has followed an acute myelitis. It seems improper to use the
terms acute or chronic in this way. As it is generally understood that
the term acute applies to myelitis in which disintegration of the
nerve-elements predominates over interstitial proliferation, and in
which the secondary sclerosis is rather like the cicatrix of an acute
inflammation and necrosis, it should not be confounded at any
period, no matter how similar the clinical signs may be, with a
process which is essentially an interstitial one from the start. If
chronic amaurosis results from an acute glaucoma, we do not
change the latter designation to chronic glaucoma.

In cases where the symptoms at the acme indicate rather an

involvement of the peripheral than the central paths of the cord, and
in which an incomplete motor and sensory paralysis develops, the
patients often regain a considerable amount of motor power and
sensation, so that they may reach a good age, suffering at most from
a paresis of some one muscle or muscular group, occasional bladder
trouble, and pains. It has been laid down as a rule that where
paraplegia and other signs remain stationary for years, there is no
hope of even partial recovery. The following remarkable and well-
attested case proves that this rule is not without exceptions:

Isidor K——, æt. forty-four years, worker in tobacco. After over-

exertion in the fall of the year 1879 he had numbness, tingling,
dorsal pain, and paresis rapidly developed, which induced him to
consult the physicians at the clinic of the University of the City of
New York. After some slight improvement a relapse occurred, and
several others followed, usually provoked by over-exertion, till he
became completely paraplegic. He was, according to his account,
several times exhibited to a medical class by William A. Hammond,
and remembers that this authority spoke of a possible ascent of the
affection and ensuing involvement of the arms. His bladder was at
no time seriously disturbed. For four years and three months he was
totally paraplegic; his lower extremities were without life; and for the
greater part of the time he could not move his toes. The limbs were
cold and pale, but underwent little atrophy. The only exercise
obtained during this time was in a roller carriage. His sexual power
was abolished throughout the whole four years and over. Nothing
can be learned as to his reflexes in this period.103 The paralysis of
sensation was as complete as that of motion, and the lower limbs
never perspired. The arms remained free. There was a dorsal belt
sensation.
103 Hammond has no notes of the case, having discontinued the clinic, and Ludwig
Weiss, the physician in charge, saw him only occasionally in behalf of a benefit
society.

On July 23, 1884, shortly before mid-day, while lying on the bed, in
which he had lain a helpless cripple for over four years, except when
lifted into the roller carriage, he felt a sudden rush of warmth.
Surprised at this first sensation he had felt for years in limbs which
had been quasi-foreign appendages, he raised up the bed-clothes
and saw that they changed color. There was some tingling for about
three minutes, and a perspiration broke out in the affected members.
With this he found he could move his feet: half alarmed, half exulting,
he sent for his physician, L. Weiss, who found that the patient could
stand and walk with considerable freedom. I was then consulted, and
found the patient presenting a picture of incomplete transverse
myelitis. He could walk, turn about, stand with closed eyes with slight
swaying, and his knee-phenomenon was of short excursiveness, but
exceedingly spasmodic, and this symmetrically so. He was carefully
watched, and against the advice of his physician engaged in
peddling cigars, and subsequently took a position as attendant at the
pauper asylum on Ward's Island. Here he was on his feet fully twelve
hours a day, and his motion, which had continued improving until it
was to all practical intents and purposes normal, aside from a slight
stiffness, again became impaired, and a joint trouble in the
metacarpo-phalangeal articulation of the right little toe, which had
troubled him a week after his partial recovery, recurred.104 On
January 15th of the present year I again examined him. His knee-
phenomenon was greatly exaggerated, cutaneous sensations
scarcely impaired, gait paraparetic, but he could walk great
distances, and claimed to suffer less from the exertion than from the
tenderness accompanying the joint trouble referred to. There had,
therefore, occurred, without any assignable cause—for the patient
was not under treatment for a year or more before the event—an
almost instantaneous restoration of sensation, locomotion, and
sexual power; all of which faculties, notwithstanding the infraction of
every medical direction given, remained established for two years,
with prospects of so continuing a longer period.
104 This was a trophic joint trouble.

TREATMENT.—Most of the therapeutic propositions relating to the

treatment of the acute myelitic process are based on the theory that
it is of a congestive character or associated with congestion.
Accordingly, the internal administration of such drugs as ergotin,
which diminish the calibre of the blood-vessels, and local measures,
such as depletion, wet cupping, and counter-irritation, intended to act
in the same way by derivation, are unanimously recommended by
authorities. The suggestion of Hammond, that the patient occupy a
ventral or lateral, and not the dorsal, position, is based on, and
entirely consistent with, this same view. It is difficult to say what
effect is attributable to these measures. Remarkable spontaneous
changes—retrogressions as well as advances of the morbid process
—occur equally under expectant as under active treatment. I have
never seen any improvement in the active phase of simple myelitis
which I felt confident I could attribute to any special remedy
employed with a view of acting directly on the morbid process.
Indeed, improvement has been claimed by Jewell as a result of the
use of strychnia—a drug which under the very dogmas governing the
orthodox treatment of the disease might be expected to do positive
damage.105
105 Jewell gives very large doses of this alkaloid. L. C. Gray, in a discussion held
before the American Neurological Association, cited numerous observations directly
 conflicting with those of Jewell. I cannot, in view of a recent observation in a typical
case of acute anterior poliomyelitis, in which by accident the toxic effects of strychnia
were obtained, consider this dispute as at all settled. In direct connection with the
toxic symptoms the abolished patellar jerk returned in an exaggerated form; motion
also returned, and rapid improvement ensued.

In relapses of acute myelitis which had been brought on by chilling of

the feet I have obtained good results by derivation to the lower
extremities, and on many grounds think that the morbid process in
the cord, if it can be affected at all, can be affected by treating the
periphery where the symptoms are noted more readily than by
applying the cautery or bleeding over the proven site of the disease.
Exposure of the dorsal region to cold has not yet been noted as a
cause of acute myelitis, whereas such exposure of the lower
extremities is a frequent one. This seems to show that the spinal
cord is more vulnerable to influences affecting its nervous
distribution than to those which are topographically nearer. If this is
true as regards morbid influences, it may be urged that it is plausible
as regards remedial influences if these are to drive out the disease
tendency by the same door it entered.

Rest is imperative during the active progress of the disease. It may

be stated as a canon that the earlier the patient takes to his bed, and
the more thoroughly he obeys the injunction to attempt no motion of
the affected members, the better, cæteris paribus, will the result
obtained be. Countless cases are on record where a relapse was
directly traceable to a walk undertaken prematurely or carried farther
than was wise. As convalescence or partial restitution advances,
gradually increasing exercise is to be attempted, not waiting for the
danger-signal of a tired feeling to discontinue it; for that feeling,
developed, means positive harm already done. It is therefore
necessary to allow the returning function to be utilized only within
small limits at first, and extending them slowly.

In all cases of severe myelitis where the formation of bed-sores is to

be apprehended the water-bed should be employed. Owing to the
low temperature which the rubber sac constituting it has, it is