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number of cases; the only authority of weight who opposes this view
is Charcot, and his opposition is abundantly neutralized by a number
of carefully-studied American and European cases.
145 The coincidences among these three cases were remarkable. All three were
Germans, all three musicians, two had lost an only son. In all, the emotional
manifestations were pronounced from the initial to the advanced period of the
disease.

146 A Bohemian cigar-maker was startled by the sudden firing of a pistol-shot in a

dark hallway, and on arriving at the factory, and not fully recovered from the first fright,
he was again startled by the sudden descent of an elevator and the fall of a heavy
case from it close to where he stood. From the latter moment he trembled, and his
tremor continued increasing till the last stage of his illness was reached. This was my
shortest duration, four years, and of nuclear oblongata paralysis type.

Hysterical and other obscure neuroses have been claimed to act as

predisposing causes. But, inasmuch as it is well established that
sclerosis is not a legitimate sequel of even the most aggravated
forms of true hysteria,147 and, on the other hand, that disseminated
sclerosis, particularly in the early stages, may progress under the
mask of spinal irritative or other neuroses, it is reasonable to
suppose that cause and effect have been confounded by those who
advanced this view. According to Charcot, the female sex shows a
greater disposition to the disease than the male. Erb, who bases his
remarks on the surprisingly small number of nine cases, is inclined to
account for Charcot's statement on the ground that it was at a
hospital for females that Charcot made his observations. On
comparing the figures of numerous observers, it will be found that in
the experience of one the females, and of the other the males,
preponderate. In my own experience the males far exceed the
females both in private and in dispensary practice. Of 22 cases with
accessible records, only 7 were females.
147 Charcot's observation of lateral sclerosis in hysterical contracture, although made
so long ago, has not been confirmed, and the most careful examinations in equally
severe and protracted cases have proven altogether negative.
Syphilis has also been assigned as a cause. The connection is not
as clear as in tabes. In the few cases where there appears to be a
direct causal relation the lesion is not typical. There are sclerotic foci,
but in addition there is a general lesion, particularly of the posterior
columns of the cord, such as is found with paretic dementia. And it
has been noted that periendymal and subendymal sclerosis is more
frequent with the cases of alleged syphilitic origin than with those of
the typical form.

DIFFERENTIAL DIAGNOSIS.—In view of what has been already stated

regarding the numerous clinical types found in disseminated
sclerosis, it is easily understood why the diagnosis of this disease is
becoming more and more uncertain: every new set of researches
removes some one or several of the old and cherished landmarks;
and it may be safely asserted that only a minority of the cases show
that symptom-group which was formerly claimed as characteristic of
all. The discovery of a series of cases by Westphal,148 in which the
typical symptom-group of Charcot was present, but no sclerosis
deserving the name found after death, as well as the interesting
experience of Seguin, who found well-marked disseminated
sclerosis in a case regarded as hysterical intra vitam, illustrates the
increasing uncertainly of our advancing knowledge. It was believed
within a few years that the presence of cranial nerve-symptoms was
a positive factor in determining a given case to be one of
disseminated sclerosis, but in the very cases described by Westphal
such symptoms were present notwithstanding the lesion was absent.
Up to this time, however, no case has been discovered in which,
optic-nerve atrophy being present in addition to the so-called
characteristic symptoms of intention tremor, nystagmus, and
scanning in speech, disseminated foci of sclerosis were not found at
the autopsy. This sign may be therefore regarded as of the highest
determining value when present; but as it is absent in the majority of
cases, its absence cannot be regarded as decisive. The presence of
pupillary symptoms also increases the certainty of the diagnosis
when added to the ordinary and general symptoms of the disorder
related above.
 148 Archiv für Psychiatrie, xiv. p. 128.

Although the difference between the tremor of typical disseminated

sclerosis and that of paralysis agitans is pathognomonic, yet the
existence of a group of cases of disseminated sclerosis, as well as of
one of cases of paralysis agitans without tremor, renders an exact
discrimination in all cases impossible. It is a question, as yet,
whether the form of paralysis agitans without tremor described by
Charcot, and which is marked by pains in the extremities, rigidity,
clumsiness, and slowness of movement, general motor weakness, a
frozen countenance, impeded speech, and mental enfeeblement, is
not in reality a diffuse or disseminated sclerosis.

The diagnosis of this disease, while readily made in a large number

of cases on the strength of the characteristic symptoms detailed,
may be regarded as impossible in a minority which some good
authorities incline to regard as a large one.

Diffuse Sclerosis.

SYNONYMS.—Chronic myelitis, Diffuse myelitis, Simple or Diffuse

spinal sclerosis, Chronic transverse myelitis, Sclerosis stricte sic
dicta (Leyden, in part), Gray degeneration.

The various forms of sclerosis thus far considered were at one time
considered as varieties of chronic myelitis, and under different
names, founded on leading symptoms, were considered to be
merely local, and perhaps accidental, variations of one and the same
morbid process. More accurate clinical and pathological analysis has
separated from the general family of the scleroses one clearly
demarcated form after another. Tabes dorsalis, disseminated
sclerosis, amyotrophic lateral sclerosis, and the combined forms of
sclerosis have been successively isolated. Still, a large number of
cases are left which cannot be classified either with the regular
affections of the cord, limited to special systems of fibres, or with the
disseminated form last considered. They agree with the latter in that
they are not uniform; they differ from it in that they are not
multilocular. Not a few modern authors have neglected making any
provisions for these cases, while others treat of them in conjunction
with acute myelitis, of which disease it is sometimes regarded as a
sequel. The term diffuse sclerosis is here applied to those forms of
chronic myelitis which follow no special rule in their location, and to
such as are atypical and do not correspond in their symptomatology
or anatomy to the more regular forms of sclerosis. In regional
distribution the foci of diffuse sclerosis imitate those of acute myelitis:
they may be transverse, fascicular, or irregular.

MORBID ANATOMY.—In typical cases the lesion of diffuse sclerosis

constitutes a connecting-link between that of the disseminated form
and posterior sclerosis. Its naked-eye characters are the same.
There is usually more rapid destruction of the axis-cylinders, more
inflammatory vascularization, proliferation of the neuroglia-nuclei,
and pigmentary and hyaline degeneration of the nerve-cells, than in
the disseminated form.

Syphilitic inflammation of the cord extends along the lymphatic

channels, including the adventitial spaces, and leads to a diffuse
fibrous interstitial sclerosis. In one case in which I suspected syphilis,
though a fellow-observer failed to detect it after a rigid search, I
found a peculiar form of what would probably be best designated as
vesicular degeneration, according to Leyden, though associated with
a veritable sclerosis. The lymph-space in the posterior septum
showed ectasis; the blood-vessels were sclerotic, and each was the
centre of the mingled sclerotic and rarefying change. It appears that
while the interstitial tissue hypertrophied, the myelin of adjoining
nerve-tubes was pressed together till the intervening tissue
underwent pressure atrophy. The result was, the myelin-tubes
consolidated, some axis-cylinders perished, others atrophied, a few
remained, and, the myelin undergoing liquefaction, long tubular
cavities resulted, running parallel with the axis of the cord, and
exposed as round cavities on cross-section (Fig. 32). The changes in
the cells of the anterior horn in the same cord (Fig. 33) illustrate one
of the common forms of disease to which they are subjected in the
course of sclerotic disease.
FIG. 32.

FIG. 33.
The so-called myelitis without softening, or hyperplastic myelitis of
Dujardin-Beaumetz, which is ranked by Leyden and Erb among the
acute processes, properly belongs here. It is characterized by a
proliferation of the interstitial substance, both of its cellular and
fibrillar elements. The nerve-elements proper play no part, or at best
a very slight or secondary one. In the sense that this affection occurs
after acute diseases and develops in a brief period it may be called
an acute myelitis, but both in its histological products and its clinical
features it approximates the sclerotic or chronic inflammatory
affections of the cord. As far as the clinical features are concerned,
this is particularly well shown in the disseminated myelitis found by
Westphal after acute diseases, such as the exanthematous and
continued fevers.

CLINICAL HISTORY.—Impairment of motion is the most constant early

feature of chronic myelitis; in the transverse form it may be as
absolute as in the severest forms of acute myelitis; as a rule,
however, it is rather a paresis than a paralysis. The patient is usually
able to walk, manifesting the paraparetic gait: he moves along
slowly, does not lift his feet, drags them along, makes short steps; in
short, acts as if his limbs were heavily weighted. This difficulty of
locomotion is preceded and accompanied by a tired feeling before
other sensory symptoms are developed. Rigidity of the muscles, like
that found in disseminated sclerosis, is a common accompaniment,
and may even preponderate over the paresis to such an extent as to
modify the patient's walk, rendering it spastic in character. In such
cases the muscles feel hard to the touch, and the same exaggerated
reflex excitability may be present as was described to be
characteristic of spastic paralysis.

If, while the leg is slightly flexed on the thigh, the foot be extended,149
so as to render the Achilles tendon and the muscles connected with
it tense, and the hand while grasping the foot suddenly presses the
latter to still further extension, a quick contraction occurs, which, if
the pressure be renewed and kept up, recurs again and again, the
succession of the involuntary movements resembling a clonic
spasm. This action is termed the ankle-clonus or foot-phenomenon.
Gowers has amplified this test of exaggerated reflex excitability by
adding what he calls the front-tap contraction. The foot being held in
the same way as stated above, the examiner strikes the muscles on
the front of the leg; the calf-muscles contract and cause a brief
extension movement of the foot. It is believed that the foot-clonus
and the front-tap contraction are always pathological, but a few
observers, notably Gnauck, leave it an open question whether it may
not occur in neurotic subjects who have no organic disease. Gowers
considers the foot-clonus found in hysterical women as spurious,
and states that it differs from the true form in that it is not constant,
being broken by voluntary contractions, and does not begin as soon
as the observer applies pressure. But I have seen the form of clonus
which Gowers regards as hysterical in cases of diffuse sclerosis.
With regard to the front-tap contraction, its discoverer150 admits that
it may be obtained in persons in whom there is no reason to suspect
organic disease. It is significant only when unequal on the two sides.
149 By extension the approximation of the dorsal surface to the tibial aspect of the leg
—what some German writers call dorsal flexion—is meant.
 150 Gowers, The Diagnosis of the Diseases of the Spinal Cord, 3d ed., p. 33.

In severe cases contractures are developed in the affected muscular

groups, being, as a rule, preceded by the rigidity, increased reflex
excitability, and the thereon dependent phenomena above detailed.
These contractures may be like those of spastic paralysis, but
usually the adductors show the chief involvement, and sometimes
the leg becomes flexed on the thigh and the thigh on the abdomen in
such firm contraction that the patient, albeit his gross motor power is
not sufficiently impaired, is unable to move about, and is confined to
his bed, his heel firmly drawn up against his buttock. It is stated by
Leyden that the contracted muscles occasionally become
hypertrophied—an occurrence I have not been able to verify. As a
rule, some muscular groups are atrophied, though the limbs as a
whole, particularly in those patients who are able to walk about, are
fairly well nourished.

Pain in the back is a frequent accompaniment of diffuse sclerosis. It

is not pronounced, but constant.

The drift of opinion to-day is to regard pain in the spinal region as not
pathognomonic of organic spinal affections. It is true that pain is a
frequent concomitant of neuroses, and that it is more intense and
characteristic in vertebral and meningeal disease; but in denying a
significance to pain in the back as an evidence of diffuse disease of
the cord itself, I think many modern observers have gone to an
extreme. It is particularly in diffuse sclerosis that a dull heavy
sensation is experienced in the lumbo-sacral region; and in a
number of my cases of slowly ascending myelitis and of tabes
dorsalis the involvement of the arms was accompanied by an
extension of the same pain, in one case associated with intolerable
itching, to the interscapular region. It cannot be maintained that the
pain corresponds in situation to the sclerotic area. It is probably, like
the pain in the extremities, a symptom of irradiation, and
corresponds in distribution to that of the spinal rami of the nerves
arising in the affected level.
As the posterior columns are usually involved in transverse myelitis,
the same lancinating and terebrating pains may occur as in tabes
dorsalis. As a rule, they are not as severe, and a dull, heavy feeling,
comparable to a tired or a burning sensation, is more common. A
belt sensation, like that of tabes, and as in tabes corresponding to
the altitude of the lesion, is a much more constant symptom than
acute pains.

Cutaneous sensibility is not usually impaired to anything like the

extent found in advanced tabes. It is marked in proportion to the
severity of the motor paralysis; where mobility is greatly impaired,
profound anæsthesia and paræsthesia will be found; where it is not
much disturbed, subjective numbness, slight hyperæsthesia, or
tingling and formication may be the only symptoms indicating
sensory disturbance; and there are cases where even these may be
wanting.

The visceral functions are not usually disturbed. In intense

transverse sclerosis of the upper dorsal region I observed gastric
crises, and in a second, whose lesion is of slight intensity, but
probably diffused over a considerable length of the cerebro-spinal
axis, there is at present pathological glycosuria. The bladder
commonly shows slight impairment of expulsive as well as retaining
power, the patients micturating frequently and passing the last drops
of urine with difficulty. Constipation is the rule. The sexual powers
are usually diminished, though rarely abolished. As with sclerotic
processes generally, the sexual functions of the female, both
menstrual and reproductive, are rarely disturbed.

It is not necessary to recapitulate here the symptoms which mark

diffuse sclerosis at different altitudes of the cord. With this
modification, that they are less intense, not apt to be associated with
much atrophic degeneration, nor, as a rule, quite as abruptly
demarcated in regional distribution, what was said for acute myelitis
may be transferred to this form of chronic myelitis. The progress of
diffuse sclerosis is slow, its development insidious, and the history of
the case may extend over as long a period as that of diffuse
sclerosis. Sooner or later, higher levels of the cord are involved in
those cases where the primary focus was low down. In this way the
course of the disease may appear very rapid at one time, to become
almost stationary at others. Of three deaths which occurred from the
disease in my experience, one, in which there were distinct signs of
involvement of the oblongata,151 occurred from sudden paralysis of
respiration; a second from a cardiac complication, which, in view of
some recent revelations concerning the influence of the tabic
process on the organic condition of the valves of the heart, I should
be inclined to regard as not unconnected with the sclerosis; and in a
third, from bed-sores of the ordinary surgical variety. The malignant
bed-sore is not of frequent occurrence in this disease.
151 On one occasion the patient had momentary anarthria, followed a day later by two
successive periods of anarthria, lasting respectively about twenty seconds and one
minute, one of which was accompanied by diplopia of equally brief duration.

PROGNOSIS.—The disease may, as in the instances cited, lead to a

fatal termination, directly or indirectly, in from three to twenty years.
The average duration of life is from six to fifteen years, being greater
in cases where the sclerotic process is of slight intensity, even
though it be of considerable extent, than where it is of maximum or
destructive severity in one area, albeit limited. I am able to say, as in
the case of tabes dorsalis, that a fair number of patients suffering
from this disease whom I have observed for from two to six years
have not made any material progress in an unfavorable sense in that
time. One cure152 occurred in this series, of a patient manifesting
extreme contractures, atrophies, bladder trouble, and ataxiform
paresis, where the cause was plainly syphilis, and the histological
character of the lesion is somewhat a matter of conjecture in
consequence. Diffuse sclerosis of non-syphilitic origin—and this may
apply also to established sclerosis in syphilitic subjects—is probably
as unamenable to remedial treatment as any other sclerotic
affection.
152 The patient went, under direction of Leonard Weber and R. H. Saunders, to Aix-
la-Chapelle, where this happy result was obtained after mixed treatment had
 practically failed.

The same rules of DIAGNOSIS applicable to transverse myelitis of

acute onset apply, level for level, to the diagnosis of transverse
myelitis of insidious development, the history of the case often
furnishing the only distinguishing point between the acute and the
chronic form.

The main difference between the diffuse sclerosis and acute myelitis,
clinically considered, consists in the gradual development of
symptoms in the former as contrasted with their rapid development
in the latter disease. Acute myelitis is established within a few hours,
days, or at most, in the subacute forms, a few weeks; chronic
myelitis requires months and years to become a clearly-manifested
disorder. It is the essential correspondence of the symptoms of both
conditions, intrinsically considered, which renders it impossible to
distinguish clinically and in the absence of a history of the case
between some cases of acute myelitis in the secondary period and
the processes which are primarily of a sclerotic character.

It is unusual to find the degeneration reaction in myelitis of slow and

gradual development. Sometimes there is diminished reaction to
both the faradic and galvanic currents, or the so-called middle form
of degeneration reaction is obtained from atrophied muscles, the
nerve presenting normal or nearly normal irritability, and the muscle
increased galvanic irritability and inversion of the formula.

Among the less reliable or accessible points of differentiation

between the residua of acute myelitis and the chronic form is the
history of the onset and the age of the patient at the time of the
onset. Myelitis in young subjects is more likely to be of the acute
kind; in older persons it is more apt to be chronic.

In the diagnosis of diffuse sclerosis the question of differentiation

from neuroses not based on ascertainable structural disease, such
as are called functional, will be most frequently raised. In
differentiating between organic and functional spinal disorders all
known exact signs of organic disease must be excluded before the
case can be considered as appertaining to the latter group.
Symptoms of hysteria, nervous exhaustion, and spinal irritation
frequently coexist with diffuse sclerosis as well as with the
disseminated form; and this is not surprising, for, instead, as seemed
at one time to be believed, of the neurotic taint granting comparative
immunity against organic disease, it is the reverse, and it is not at all
uncommon to find a strongly-marked neurotic diathesis in the family
history of sufferers from diffuse sclerosis. That ordinary hysteria,
epilepsy, and what is vaguely called nervousness are common
features in the ancestral record of the hereditary forms of spinal
disease has already been stated in considering those affections.

One of the commoner forms of the grave phase of hysteria is

paraplegia.153 Often muscular atrophy—which ensues from disuse—
exaggeration of the deep reflexes, and retention of urine are added
to the paraplegia and heighten the resemblance to an organic
affection. Its development, though sometimes sudden, often
occupies weeks or months, and may be preceded, exactly as in
chronic myelitis, by weakness in the legs, and not infrequently by
combined ataxia and weakness. It is much more difficult to
discriminate here than is generally held or than is enunciated in
textbooks. The sufferer from hysterical paraplegia does not always
give other indications of the hysterical neurosis, and even if she did
show a globus and tenderness at certain points, it is a question
whether it could be called a scientific diagnosis which determined the
case to be one of functional trouble on these signs alone. More than
one error has been committed in this respect. In chronic myelitis
retention of urine is less common than incontinence, which is the
reverse of hysterical paraplegia. Pupillary symptoms do not occur
with the latter affection. If there be sensory anæsthesias, they are
bizarre in character or distribution, and do not usually harmonize with
the distribution of the paralysis. In most cases moral influences can
be exerted so as to increase the power of movement far beyond
what would be possible in an organic disease; and while an electrical
examination will not always yield positive results in chronic myelitis,
yet no case of chronic myelitis with complete or nearly complete
paraplegia but will show at least quantitative changes of such extent
as to prove beyond doubt that the case is of an organic character.
153 I have observed for two years a stationary brachial diplegia, of undoubted
hysterical origin, although the patient had never shown any ordinary hysterical
manifestations, and had had no other hysterical symptom than chromatopsia, and that
only for a short period. From its long duration, constancy, and the resulting atrophy of
disuse it had been regarded as a case of peculiarly limited chronic myelitis.

There is one point in which spinal and cerebral disease involving the
motor tract differs in the majority of cases, which may be utilized in
distinguishing obscure affections of the former from those of the
latter kind. In cerebral paralysis of any standing the superficial
reflexes, such as the cremaster and abdominal reflexes, are usually
diminished or abolished, while the deep or tendon reflexes are
exaggerated. In spastic conditions due to spinal disease—say
sclerosis of any kind affecting the lateral column and leaving the
motor nuclei of the anterior cornua unaffected—the deep reflexes
are similarly increased, but the cremaster reflex is increased also.154
This feature of the superficial reflexes is significant in the case of
cerebral disease only when unilateral.
154 Attention has been called, I believe, by Westphal, to the fact that the cremaster
reflex may not be demonstrable when reflex excitability is at its highest, because the
cremaster muscle is already in extreme spastic contraction.

The initial period of diffuse sclerosis is sometimes confounded with

rheumatism—an error less pardonable than in the case of tabes,
inasmuch as in diffuse sclerosis the pains are not usually
premonitory, but associated with motor paresis. It is erroneous to
regard a pain as rheumatic because it is aggravated or relieved by
changes in the weather. There are many subjects of myelitis who
regard themselves as veritable barometers, and with more justice
than most rheumatic patients.

In some cases of chronic alcoholism there are motor weakness and

a gait much like that of diffuse sclerosis.155 It is to be remembered
that the solar tickling reflex is very often abolished in alcoholic
subjects, and profound diminution of the normal cutaneous
sensibility of the leg and feet usually coexist. But unless there is
peripheral neuritis—which is an exceptional and, when present, well-
marked affection—the absence of profound nutritive changes of the
muscle, the presence of the alcoholic tremor, the absence of
sphincter and bladder trouble, and the great variation of the
symptoms from week to week, and even from day to day, serve to
distinguish the alcoholic spinal neurosis from myelitis.
155 Wilks' alcoholic paraplegia.

The Secondary Scleroses.

In studying the lesions underlying the symptoms of organic spinal

disease, the occurrence of fascicular scleroses, secondary to such
disease and due to the destructive involvement of nerve-tracts, was
repeatedly noted. Türck may be regarded as the discoverer of these
degenerations, and the reliability of this old observer may be inferred
from the fact that one bundle of fibres liable to individual
degeneration still goes by his name, and that, as far as he was able
to discriminate between the various paths which secondary
degenerations follow through the cerebro-spinal fibre-labyrinth, his
statements have not been materially modified by more recent
investigators, such as Bouchard, Vulpian, and Westphal.

The discovery by Meynert that the great cerebro-spinal tracts attain

the white color which they owe to the development of myelin around
their component axis-cylinders with advancing maturity, and that the
tracts of noblest, and therefore most intelligent, function were the last
to show this sign of maturity, was greatly extended by Flechsig, who
found that each tract receives its myelin at a definite period of intra-
uterine life, the lowest or the nerve-roots first; then the short or
intersegmental or—as the physiologist may call them—the automatic
tracts; then the long or controlling tracts; and last, the associating
tracts of the cerebral hemispheres which mediate the complex
relations underlying mental action. It was this discovery which gave a
new impulse to the study of the secondary affections of the cord and
brain. The accuracy with which secondary degeneration follows the
lines marked out by the normal course of the tract is as great,
diminishing when the tract diminishes, changing its position or
direction and decussating where the latter changes its direction or
position or decussates, that it constitutes not alone an interesting
subject for pathological study, but has become one of the most
reliable guides of the cerebral anatomist. It is of great importance to
the pathologist to be able to differentiate between the primary
disease and its secondary results, and, as the controversy
concerning the so-called system diseases shows, even the most
studious observers are uncertain in this direction in many cases.

MORBID ANATOMY.—Secondary degeneration manifests itself by a

discoloration of the affected nerve-tract, which accurately
corresponds in area to the normal area of that tract. The more recent
the degeneration the less pronounced is this change. In advanced
cases the color may be a dark gray, in moderately old ones a reddish
or yellowish gray, and in those of very recent origin no change may
be visible to the naked eye. It is claimed, however, that even here a
loss of translucency of the white substance, giving it a sort of
cheese-like opacity, may be detected. On hardening the specimen
containing the degenerated tract in Müller's fluid or a simple
bichromate salt solution, the affected area, instead of appearing dark
on section in contrast with the gray substance—which in such
preparations appears yellowish or a light brown—contrasts with the
former by its lighter tinge. This contrast is observable even in cases
where the naked eye was unable to detect the change in the fresh
specimen. It can be sometimes found as early as the tenth day after
the primary lesion, and is apparently simultaneously developed in
the whole length of the nerve-tract affected.

The minute changes characterizing secondary degeneration begin in

the essential conducting elements, the axis-cylinder, which exhibits a
finely granular or molecular disintegration, and disappear. According
to Homén, it shows an initial swelling and a failure to stain properly
before this. The myelin then follows suit: it becomes fragile, forms
variously-shaped globules, and also disappears, and together with
this a nuclear proliferation is noticed in the interstitial substance; fatty
granule-cells are observed in large numbers, and manifest a
tendency to accumulate in the perivascular districts. These cells are
not permanent; their gradual diminution is accompanied by a
proliferation of the interstitial tissue, which ultimately appears as a
pure connective substance composed of fine fibrillæ arranged in
undulating bundles. The entire process may be not inaptly compared
to an hypertrophy of the interstitial substance resulting from
overfeeding of its cellular elements by the morbid pabulum furnished
through the disintegration of the nervous substance proper.

The disappearance of the nerve-tubes, and the formation of a new

tissue in their place, which, like all tissues of the same character,
undergoes shrinkage, leads to considerable deformity in the shape
of the part which is the site of secondary degeneration. This is seen
in the accompanying figure, where in an old-standing secondary
degeneration of one interolivary layer the corresponding half of the
medulla is greatly reduced in diameter as compared with the other
side (Fig. 34), and the entire raphé is distorted. When one side of the
cord is the site of such a change a similar asymmetry results.

FIG. 34.
 Secondary Degeneration of Interolivary Layer: D Ds D, degenerated
area; r, the distorted raphé.

According as the original lesion is incompletely or completely

destructive, a larger or fewer number of axis-cylinders may be found
preserved in the sclerotic tissue. It is not yet determined whether in
some instances these fibres may not represent an admixture from
another source than are comprised in the mainly affected tract.

Secondary degenerations are classified as ascending and

descending. An ascending degeneration is one which is found
situated brainward of the primary lesion; a descending one is found
caudad of the lesion. It was once maintained that the direction of the
secondary degeneration was constant for each individual tract. This
seems to be true for a few. Some tracts, particularly in the brain,
degenerate on both sides of the lesion, as I showed with regard to
the interolivary layer.

The best studied form of secondary degeneration is that of the

voluntary motor conduit known as the pyramid tract. Beginning in the
so-called motor area of each cerebral hemisphere, the Rolandic loop
passes into the anterior part of the posterior half of the internal
capsule, to be thence continued through the crus, pons, and the
pyramids of the oblongata to the decussation or crossing-point of the
pyramids. Here the greater part of the tract crosses into the opposite
lateral column, occupying the position described in the section on
Spastic Paralysis. A smaller part remains on the same side of the
continuous interpyramidal and ventro-spinal fissure, constituting the
direct fasciculus of Türck.

The crossed-pyramid tract diminishes as it passes caudad in the

cord, giving off its fibres to the lateral reticular processes of the cord,
whence—whether interrupted by cells (Von Monakow) or not—they
probably reach the great cells in the gray substance from which the
anterior rootlets spring. The direct fasciculus probably terminates in
a similar way, and perhaps makes good, as it were, its failure to
participate in the gross decussation at the level of the foramen
magnum by decussating in detail along its entire length. It is usually
exhausted before the lumbar cord is reached, whereas the crossed
tract in the lateral column continues down as low as the origin of the
sacral nerves. A destructive lesion anywhere in the course of the
pyramid tract, whether it be in the motor area of the cortex, in the
loop of Rolando, in the internal capsule, the pons, or the cord itself,
will provoke descending degeneration; that is, sclerosis of so much
of the tract as lies below the lesion. Thus such degeneration is found
with porencephalic defect of the motor area. I found it in a paretic
dement who had extensive cortical destruction following a
submeningeal hemorrhage. It has been observed after focal lesion of
the pons (Homén, Schrader), and after transverse lesions of the
cord, either myelitic, traumatic, or as the result of compression by
vertebral disease. As a rule, the cells in the anterior horn are not
involved, and some observers question whether this ever occurs. I
have never found such involvement, although in its gross dimensions
the anterior horn as a whole appears atrophied. This atrophy I have
been able to account for satisfactorily by the disappearance of many
of the fibres which run into the gray substance from the reticular
processes.
While the distribution of degeneration in the cord is rather uniform,
varying only in harmony with the ascertained individual variations in
the relative preponderance of the crossed and uncrossed parts of
the pyramid tract, there is much more variation in the cerebral
distribution of the degeneration according to the extent of the original
lesion. Thus, if the entire capsule be destroyed, the greater part of
the crus is involved. If only the posterior division in its anterior part
be destroyed, the degeneration is in the crus, limited to that part
which runs a subpial course on the crural demi-cylinder, occupying
from a fifth to a third of its surface-area. Still more limited
degenerations are described, but as yet are too few in number to
base other than tentative conclusions on them. Among these is one
occupying a thin strip on the inner side of the crus, which
degenerates after lesions near the genu of the capsule, and probably
represents the tract which governs the cranial nerve-nuclei. An
excellent observation by Von Mannkopf shows that the course of the
motor fasciculus is subject to some individual variation even within
the capsule.

A number of forms of secondary degeneration are described,

involving intracerebral tracts, such as those connecting the cerebrum
and cerebellum. The degeneration of the visual tract, from the optic
nerve to the occipital lobe, observed by Richter and Von Monakow,
with some conflict of opinion between these observers, is often as
perfectly demonstrative of the course of the optic fasciculi as
degeneration of the pyramid tract is demonstrative of the course of
the voluntary innervation of the muscles moving the limbs.

The secondary degenerations following lesion of the pons varolii are

acquiring special interest in view of their relation to special nerve-
tracts of the spinal cord of hitherto unknown function. The purest
instance of an isolated degeneration of other than the pyramid tract
is the case illustrated in the accompanying diagrams. It involved the
interolivary layer, was both ascending and descending, being traced
above into the subthalamic region, and below decussating into the
opposite side of the oblongata, to terminate in the nuclei of the