* A LECTURE 
ON 
» 
THE LOCALIZATION OF DISEASES IN THE 
SPINAL CORD, 
DELIVERED BEFORE THE 
ANATOMICAL AND SURGICAL SOCIETY OF BROOKLYN, 
EDWARD C. SEGUIN, M. D., 
CLINICAL PROFESSOR OF DISEASES OF THE MIND AND NERVOUS SYSTEM, 
COLLEGE OF PHYSICIANS AND SURGEONS, NEW YORK. 
REPRINTED FROM THE ANNALS OF THE SROOKLVN, 
VOL. 11, I/ 
BROOKLYN. N. Y. 
2 8 MADISON STREET. 
1880. THE LOCALIZATION OF DISEASES IN THE 
SPINAL CORD. 
EDWARD C. SEGUIN, M. D.> 
CLINICAL PROFESSOR OF DISEASES OF THE MIND AND NERVOUS SYSTEM- 
COLLEGE OF PHYSICIANS AND SURGEONS, NEW YORK.* 
I HAVE designed this lecture as a pendant to Dr. Gray’s 
discourse upon the new anatomy of the spinal cord and 
its intra-cranial expansion. In the last fifteen years advances 
in the normal and pathological anatomy and the physiology 
of the nervous centres have progressed hand in hand, one 
illustrating and confirming the other. 
At the beginning of this century, and from that time until 
some fifteen years ago, though great progress was achieved 
in the clinical description of spinal diseases, from Ollivier to 
Brown-Sequard ; and though we have acquired some knowl- 
edge of the pathological anatomy of the points involved, 
almost no attempt had been made to localize the lesions of 
various diseases in definite sections of the spinal cord. The 
admirable spinal localization of the present day, we owe to 
the accumulated labors of Cruveilhier, Tiirck, Goll, Charcot, 
Leyden and Erb. 
I shall offer you to-night a brief review of this localization 
* Delivered before the Society, April X2th, 1880. 
Reprinted from the Annals of the Anatomical and Surgical Society, 
Brooklyn, Vol. ii, No. 12, 1880. 2 
EDWARD C. SEGUIN. 
of diseases in the spinal cord, as founded upon normal anat- 
omy, physiology and pathological anatomy. Such a study 
will be facilitated by admitting as practically correct a some- 
what rough division of the spinal cord into two unequal 
regions, one including the posterior columns and the posterior 
gray matter, serving for the transmission of centripetal or 
sensory impulses, and the second, much larger, including the 
anterior gray horns, the anterior columns and the antero- 
lateral columns, serving for the transmission of motor, cen- 
trifugal impulses. The former region is the Eesthesodic sys- 
tem of the spinal cord, the latter the kinesodic system. The 
accompanying wood cut illustrates the limits of these two 
systems, on a transverse section of the spinal cord. 
FIG, I. 
DIAGRAM OF TRANSVERSE SECTION OF THE SPINAL CORD 
a. Anterior median fissure, p. Posterior median septum, i. Columns of Goll. 2. Col- 
umns of Gerlach. 3. Direct cerebellar fasciculi. 4. Crossed pyramidal columns. 5. Lateral 
columns. 6. Anterior columns. 7. Direct pyramidal columns. 8. Posterior gray horns. 
0. Anterior gray horns. Stippled part—Gray matter. Shaded part—Aisthesodic system. 
Unshaded part—Kinesodic system. 
The following table embodies the principal localized 
lesions of the spinal cord which give rise to definite symptom- 
groups, and which we are able to diagnosticate: 
LOCALIZED SPINAL DISEASES. 
A. Systematic diseases of the spinal cord: 
I. Diseases of the sesthesodic system— SPINAL LOCALIZATION. 
3 
a. Sclerosis of the posterior columns (progress- 
ive locomotor ataxia). 
b. Ascending degeneration. 
2, Diseases of the kinesodic system— 
a. Degeneration of anterior ganglion cells (pro- 
gressive muscular atrophy). 
b. Inflammation of anterior gray horns (atrophic 
spinal paralysis of adults and children). 
c. Sclerosis of the lateral columns (tetanoid 
paraplegia). 
d. Descending degeneration, 
oc.—of spinal origin; 
ft.—of cerebral origin. 
B. Focal affections of the spinal cord (injuries, tumors, 
foci of softening, myelitis transversa, clots, etc.): 
a. In lumbar enlargement. 
b. In lower dorsal region. 
c. In upper dorsal region. 
d. In lower cervical enlargement. 
e. In upper cervical region. 
f. At the cauda equina. 
It will be impossible to do more this evening than to con- 
sider the first of the two great divisions—viz., that of sys- 
tematic lesions. 
At the present time there is only one disease of this class 
—viz., posterior spinal sclerosis or progressive locomotor 
ataxia. The lesion consists, roughly speaking, in sclerosis of 
the posterior columns of the spinal cord. Since 1873 closer 
analysis at the hands of Charcot and Pierret has shown that 
the primary and essential sclerosis occupies only the external 
part of these columns—that which is adjacent to the pos- 
terior gray horns, and which histology teaches us is traversed 
by fibres of the posterior roots on their way to the gray 
matter of the cord. In most cases which come to the post- 
mortem table the median fasciculi of the posterior columns 
i. Diseases of the sesthesodic system: 4 
EDWARD C. SEGUIN'. 
or the columns of Goll are likewise sclerosed, but this altera- 
tion is is to be looked upon as secondary, as a form of 
ascending degeneration, and probably as wholly disconnect- 
ed with the symptoms. Almost always sclerosis of the ex- 
ternal part of the posterior columns, or columns of Burdach, 
commences in the lumbar enlargement and advances upward. 
Ultimately, in old cases, the whole of the posterior columns 
as high as the medulla oblongata is sclerosed and degener- 
ated, atrophied and hardened. Another part of the lesion 
of locomotor ataxia is a sclerosis and degenerative change 
in the posterior roots extending to the ganglia on these roots 
and even involving them. In uncomplicated cases of loco- 
motor ataxia, the anterior and antero-lateral columns, and 
the whole of the gray matter of the spinal cord, are healthy. 
The symptoms of the disease are chiefly of a sensory sort, 
and there is never any true paralysis in uncomplicated cases. 
The chief symptom in some respects, the initial symptom in 
the vast majority of cases, is a peculiar, almost pathogno- 
monic neuralgia, which usually has its seat in the lower ex- 
tremities alone, and sometimes affects the upper extremities 
and trunk, very rarely the head. The diagnosis of locomo- 
tor ataxia depends so much upon this symptom and its 
exact appreciation that I need no other apology for stating 
its characteristics with some fulness. 
a. The pains are vagrant; they occur in innumerable 
spots in the affected parts, so much so that patients who 
have long had them are unable to enumerate the localities 
in which they have suffered; or, rather, they can hardly 
name a region which has escaped. 
b. The pains do not occur in the course or distribution of 
recognized nerve trunks and filaments; they are local pains, 
and this peculiarity may serve (with d) to distinguish between 
the pain of sclerosis and true neuralgia (sciatica, etc.). 
c. The seat of the pain is commonly in an area of skin SPINAL LOCALIZA TION. 
5 
varying in size from that of a pea to that of a small hand. 
In many cases pains are referred to the muscles, to the 
vicinity of the bones, and even to articulations and viscera. 
d. The pains are paroxysmal in a completely irregular 
manner; they may occur every few moments for hours in 
one spot, or be altogether wanting for weeks; or at times a 
single pain in a given region is the signal that the disease is 
not cured. It seems probable that the atmospheric disturb- 
ance (low barometer) which precedes a storm causes an in- 
crease in this symptom, or even calls it forth. 
e. The pains are sudden, and vary in severity from the 
sensation caused by the penetration of a small knife-blade 
to that we may imagine to result from tearing through the 
tissues with a hook or large knife; or, the sensation is like 
an electric pain in suddenness. Perhaps most of the suffer- 
ing in such cases is in the shape of stabbing pains in an 
ovoid or round area of skin (foot, thigh, arm, or shin) re- 
peated every few seconds for hours, or even a whole day. 
The pain is often such as to make the strongest-willed man 
writhe and shriek. The seat of pain becomes hyperalgesic 
—i. e., painful to the lightest touch ; yet firm pressure may 
give relief. From their suddenness and electric character 
the pains of locomotor ataxia are often called fulgurating, or 
terebrating. 
The ratio7iale or physiology of these characteristic pains 
is found in the morbid anatomy. As described above, there 
is in this disease a sclerosis of the connective tissue in the 
posterior columns of the spinal cord, and chiefly in their lat- 
eral portions—i. e., those portions which are traversed by 
fibres of the posterior roots. Irritation of these sensory 
nerve fibres is produced by the advancing sclerosis, and 
probably varies in degree according to changes in the circu- 
lation in the diseased spinal cord. 
It should be borne in mind that fulgurating pains usually 6 
EDWARD C. SEGUTN. 
precede ataxia by three or four years; but this neuralgic 
period may be shorter (a few weeks) or much longer, perhaps 
indefinite (in a case of my own, twenty-nine years). 
Other sensory symptoms of posterior spinal sclerosis are 
numbness and ansesthesia. The numbness often goes hand in 
hand with the pains, and is probably due to the same cause 
—viz., irritation of the posterior roots and their intra-spinal 
expansion. It usually affects the feet first, and seems to 
ascend. When the upper extremities are involved, the numb- 
ness first shows itself in the finger tips. 
Anasthesia is present in a large majority of cases; prob- 
ably in all which enter the second period—viz., the ataxic 
period. It may progress to such an extent as to make 
the patient perfectly unaware of any excitation applied to 
the legs (or hands); and to render him ignorant of the posi- 
tions and existence of the limbs without the aid of sight or 
touch, the patient “ loses his legs in bed.” The ansesthesia 
is caused by the actual destruction or great compression of 
the sensory fibres already referred to. 
Destruction of the myeline and pressure on the axis cylin- 
ders by the sclerosed interfibrillar tissue may also explain a 
singular symptom—viz., the retardation of sensations—i. e., 
the occurrence of a measurable time (10 to 120 seconds) be- 
tween the pricking of a part and the acknowledgment of the 
pain by the patient. 
Other symptoms of scelerosis of the posterior columns 
are motor to all appearances, yet in reality depend upon in- 
terference of the disease with the spinal sensory apparatus. 
First. Diminished reflexes, pupillary, cutaneous, tendinous 
and visceral. For example, in many cases the pupils are 
small (may be unequal), and do not appreciably respond to 
light and shade, though they do change under accommodat- 
ive efforts. 
Again, if we tap the ligamentum patellae in a patient SPINAL LOCALIZA TION. 
7 
suffering from fulgurating pains, or in one who has entered 
the ataxic stage, we observe that the quadriceps extensor 
femoris does not contract and cause a movement of the leg 
(the knee being semi-bent) as in health. This is known tech- 
nically as absence of the patellar reflex, a new and most 
important symptom of posterior spinal sclerosis, one which 
in my experience hardly ever fails, and which deserves 
to be ranked as at least equal in importance with the fulgu- 
rating pains. Reflexes from cutaneous surfaces are also 
diminished or lost. The visceral reflex actions by which we 
micturate, defecate, and produce the sexual orgasm are like- 
wise progressively impaired ; and thus we find these patients 
impotent as a rule, and presenting constipation and slow, im- 
perfect micturition as symptoms. 
This reduction in reflexes is caused by disease of the intra- 
spinal sensory parts connected with the various organs and 
parts we test; the arc for reflex actions is impaired in the 
posterior columns of the spinal cord or in corresponding re- 
gions of the spinal tract. 
The ataxic movement of the legs (and of the arms in some 
cases) which are characteristic of the second stage of the 
disease, appear at a variable period after the beginning of 
the neuralgic stage (three months to ten years or more) and 
is essentially characterized by an irregular, asynergic action 
of the muscular groups which serve to produce a given 
movement. The legs are jerked forward and outward, and 
the heel brought forcibly down in the attempt to walk; the 
fingers and arms oscillate and perform unnecessary excur- 
sions in trying to reach a given point, or accomplish a given 
action. Later, the irregularity of movement is so great that 
the patient is confined to bed. 
We are not yet agreed upon a theory of ataxia, but these 
hypotheses are deserving of consideration. 
a. That interference with sensory intra-spinal tracts dimin- 8 
EDWARD C. SEGUIN. 
ishes the muscular tonus (chiefly produced in an unconscious 
reflex way), and that this atony varying in different mus- 
cles gives rise to the inharmonious movements. 
b. The anaesthesia affects the muscles as well as the super- 
ficial parts, and thus diminution or loss of the “ muscular 
sense” is caused and the patients can no longer guide their 
contractions. 
c. The sclerosis of the posterior columns affects other 
fibres besides common sensory ones—viz., those arciform or 
longitudinal commissural fibres described by Lockhart Clarke, 
and which seem to unite, for the purpose of harmonious 
action, the spinal centres for the various muscles of a group, 
or of a limb. If these commissural fibres be destroyed by 
sclerosis, we obtain ill-combined, asynergic muscular move- 
ments in the attempt to step. 
There are many other symptoms in the course of posterior 
spinal sclerosis, but those just analyzed are the characteristic 
ones—the ones which are logically related to the lesion. 
Under the head of diseases of the aesthesodic region we 
must also place the lesion of the posterior columns known 
as ascending degeneration. This lesion is limited to the 
posterior median columns, or columns of Goll, and dimin- 
ishes in extent the higher we examine the spinal cord. We 
find this ascending degeneration above a spot in the spinal 
cord where it is compressed, or destroyed, and it is also met 
with in progressive locomotor ataxia. Prof. Charcot and 
others teach that this extension of sclerosis from the columns 
of Burdach to the columns of Goll is a non-essential feature of 
locomotor ataxia, and is secondary. At any rate sclerosis or 
degeneration of the posterior median columns alone does not, 
as far as we know to-day, give rise to any special symptoms; 
hence I can give you no clinical picture to accompany the 
pathological statement. We know only that the lesion exists SPINAL LOCALIZA TION. 
9 
in a living patient by learning the pathological state of the 
cord from other symptoms present. 
2. Diseases of the kinesodic system, including the anterior 
gray horns, the anterior columns, the antero-lateral columns, 
and the postero-lateral columns (or crossed pyramidal fas- 
ciculi). 
There are, as indicated in the table, several very definite 
and distinct affections of those parts. 
a. Degeneration of ganglion cells in the anterior horns. 
In this disease the protoplasm of these cells is very slowly 
transformed into granulo-fatty material, the cell processes 
are broken off, the nucleus and nucleolus destroyed, and in 
later stages there remains of the cell only a small mass of 
granules, or its place in the tissues may be vacant. These 
changes take place with extreme slowness, and the symptoms 
are correspondingly gradual in their appearance. For rea- 
sons which we do not understand, this granular degeneration 
may be limited to a few groups of ganglionic cells, or may 
involve a large number of the cells from the medulla oblong- 
ata to the end of the cord. We are not acquainted with 
the lesion above the medulla, although there is no reason 
why the nuclei of the fifth, sixth, seventh, fourth and third 
cranial nerves should not suffer. I wish to lay particular 
stress upon the slowness of the degeneration because of its 
harmony with symptoms, and its contrast with allied states. 
Degeneration of anterior ganglion cells is externally ex- 
pressed by muscular atrophy—usually progressive muscu- 
lar atrophy. This singular disease shows itself often first in 
peripheral muscles, in hands and feet, in other cases it at- 
tacks the shoulder, arm and thigh muscles. Indeed, it may 
commence in any muscular group. Yet there are certain 
characteristic peculiarities in this wasting. 
i. It is very gradual; fasciculi after fasciculi in the muscles 
undergo a diminution in size, lose their faradic contractility, 10 
EDWARD C. SEGUIN. 
and disappear, while adjacent fasciculi remain normal. There 
is no paralysis of a muscle, but a partial and gradual death 
of its constituents. 
2, The atrophy affects, in the vast majority of cases, 
symmetrical and homologous parts. For example, both 
shoulders may be wasted, or the arms and thighs, or the 
forearms and legs. Unilateral muscular wasting is presum- 
ably not progressive muscular atrophy. 
3. The muscles which are undergoing the early changes 
of this wasting are the seat of what are called fibrillary con- 
tractions. These are produced by the involuntary rapid 
contraction of fasciculi of muscular fibres in a muscle. 
Sometimes a patient is covered with them. Some years 
ago these fibrillary contractions were held to be patho- 
gnomonic, but I can assure you that this is not so, as they 
may be observed in lead palsy, in conditions of neurasthenia, 
in simple paralysis. Indeed, many years ago, Prof. Schiff, 
now of Geneva, showed that muscles separated from their 
motor nerves were prone to show fibrillary contractions. 
The electrical reactions are diminished, but not altered in 
quality; and the reduction or loss of reaction (to faradism) 
is in direct proportion to the wasting. In partly-atrophied 
muscles some fasciculi look well and contract well, while 
their neighbors are thin, and rise but feebly under faradism. 
Uncomplicated degeneration of ganglion cells is unaccom- 
panied by numbness, anaesthesia, or vesical symptoms, 
though aching pains may be present in the affected regions. 
b. Inflammation of the anterior gray horns; myelitis 
anterior in adults and in children. 
Autopsies have shown that the lesion in this disease in- 
volves the anterior and central gray matter of the spinal 
cord, and that there may also be present, as secondary con- 
ditions, atrophy and degeneration of the antero-lateral 
columns (not distributed as in regular descending degenera- SPINAL LOCALIZA TION. 
11 
tion). The ganglion cells of the affected anterior horns are 
found in various states of change swollen, containing 
vacuoles, filled with granulo-fatty matter, or shrunken and 
almost destroyed. Besides, the neuraglia round about these 
cells is always more or less altered. In some cases the lesion 
might be designated as a diffused central myelitis with de- 
struction of anterior ganglion cells. It need hardly be added 
that there exists an absolute anatomical relation between 
the level at which the changes occur in the spinal cord and 
the distribution of symptoms at the periphery. 
The symptoms of myelitis anterior are chiefly motor, very 
much as in group (a); but the morbid process being com- 
paratively or absolutely rapid, they appear in a strikingly 
acute or sub-acute form. 
First. Paralysis.—ln some few cases this appears with 
almost apoplectic rapidity (suggesting haemorrhage in the 
cord); in the majority the paralytic phenomena are complete 
in one or two days. Often we learn from the mother of a 
child who has myelitis anterior (infantile spinal paralysis) 
that she put the child to bed well, or simply a little feverish, 
and that the next morning both legs, or one extremity, or 
all the limbs were limp and paralyzed. In a minority of 
cases (adults) the muscular groups in the limbs lose power 
slowly, and a week or several weeks elapses before the 
patient is obliged to lie a-bed. It is important to contrast 
this paralytic loss of power, affecting a whole limb, or a 
whole muscular group, with the atrophic failure of power, or 
the fascicular atrophy described under the head of “ Pro- 
gressive Muscular Atrophy.” 
Second. > Atrophy of muscles.—The palsied muscles in 
myelitis anterior always undergo, in the course of the first 
four or five weeks, marked and even extreme atrophy. This 
wasting, even in the most sub-acute forms of myelitis 
anterior, is rapid as compared with the most rapid forms of 12 
EDWARD C. SECU IN. 
progressive muscular atrophy. Besides, in the former disease, 
the atrophy, like the paralysis, always affects a whole muscle, 
or a muscular group, or the muscular apparatus of one or 
more limbs, en masse, and is not, as in the latter affection, 
fascicular in distribution. Fibrillary contractions in wasting 
muscles are common in progressive muscular atrophy, and 
very rare in myelitis anterior. 
Third. Remarkably distinct evidences of the degeneration 
reaction to electricity are obtained from the second to the 
tenth week. The nerve-trunks supplying the paralyzed 
muscular groups lose their excitability to faradism and 
galvanism, and these wasting muscles react only to galvanism, 
and that their reaction formula is altered from the normal; 
in general terms, we may say that An cc = Kacc, or even 
An c c > Ka c c ; and all contractions are slow and wavelike. 
Fourth. The distribution of the paralysis is important for 
diagnosis and prognosis. In myelitis anterior the bladder 
and rectum are never paralyzed, and it is exceedingly rare 
to observe paralysis of the respiratory muscles, and of those 
which serve for deglutition. On the other hand, muscles 
supplied by the cranial nerves may be paralyzed. 
Fifth. An important symptom not usually referred to is 
abolition of reflexes in the paralyzed parts, especially the 
tendon reflexes. For example, if the muscles of the thigh 
(quadriceps extensor femoris) be paralyzed, no patellar ten- 
don reflex can be obtained, just as in posterior spinal sclero- 
sis. The mechanism is in both affections the same, but in 
either case different portions of the spinal arc serving for 
reflexes are injured ; in posterior spinal sclerosis the centrip- 
etal (sensory) portion of the arc is destroyed ; in myelitis the 
anterior (motor) portion. At an early stage of myelitis an- 
terior, and in cases (infantile) where much fat serves to 
obscure atrophy, this negative symptom acquires great 
value. SPINAL LOCALIZATION. 
13 
Sixth. Sensory symptoms are very slightly developed in 
myelitis anterior. In some cases a degree of numbness or 
other parsesthesia is experienced in the paralyzed limb for a 
few hours or days. In others severe neural pains are experi- 
enced. I style these neural because they apparently are in 
the course of nerve trunks or large branches, and are not in 
spots or patches like the fulgurating pains of posterior 
spinal sclerosis. Although the suffering in some few cases of 
myelitis anterior may be very severe, yet it is only careless 
observers who could mistake these pains for those of loco- 
motor ataxia. Anaesthesia is never present in myelitis ante- 
rior. When it is observed in any marked degree the case 
should be designated as diffused central myelitis. 
Seventh. Fever is present in a majority of cases in chil- 
dren and adults. Other peculiar symptoms are vomiting, 
oedema of the extremities, hyperaesthesia of affected parts, 
delirium. These rare symptoms occur in the first stage of 
the disease. In the atrophic stage the patient’s general 
health is usually good. 
c. Sclerosis of the lateral columns has been recently de- 
scribed by Erb (1875) and Charcot (1876) as probably an in- 
dependent or protopathic lesion of the spinal cord. To the 
symptom-group characteristic of this lesion, Prof. Charcot 
has given the name of spasmodic tabes, Prof. Erb that of 
spastic spinal paralysis. I have proposed the name of teta- 
noid paralysis or paraplegia, which seems to me most 
expressive. 
The pathological anatomy of this affection is not as yet 
well established; it is doubtful if the lateral columns gen- 
erally are sclerosed, or whether the lesion is limited to their 
posterior positions, as in descending degeneration (vide infra). 
The lesion is always (?) bi-lateral. Another uncertain point is 
whether the lateral sclerosis is primary or secondary—i. e., 
due to a focus of disease centrally placed above the begin- 14 
EDWARD C. SEGUIN'. 
ning of the sclerosis. It seems to me that the weight of 
evidence is in favor of the latter view. 
The symptoms of tetanoid paraplegia consists in slowly 
increasing paresis in the legs (and arms rarely) with tendency 
to contracture and increase in all reflexes. The loss of 
power is exceedingly slow. The patellar tendon reflex is 
increased very early in the disease, and becomes greatly ex- 
aggerated. The skin of the feet form the starting point of 
reflex muscular contractions when the patient is awake. 
Except at the close of the disease the affected limbs are 
relaxed in sleep. As a result of this increase of reflex 
action, there is a peculiar attitude and gait. The legs tend to 
cross one another, or actually do so from over-action of the 
adductors. The heel is drawn up, or at any rate raised, by 
over-action of the gastrocnemii and solei; the legs in step- 
ping are stiffened, their muscles sensibly hardened. The 
extremities are in a tetanoid condition. In later stages, in 
bed-ridden patients, the legs may be fixed in semi-flexion 
and adduction. These symptoms indicate clearly that the 
proper spinal activity, its reflex and automatic activity, is in- 
creased. 
Another motor disturbance, due to increased reflex action, 
is precipitate micturition and defecation. The patient must 
hurry, as from increased reflex action the bladder and rectum 
are apt to contract suddenly and involuntarily upon their 
contents. We have here an example of incontinence through 
spasm—a condition to be carefully distinguished from para- 
lytic incontinence. The muscles in parts affected with teta- 
noid paralysis retain their volume, nutrition, and normal 
electrical reactions. 
Sensory symptoms are practically wanting in this disease ; 
there is no anaesthesia, and seldom numbness. 
If there were time I should like to draw a contrast- 
ing picture between this condition and sclerosis of the SPINAL LOCALIZATION. 
15 
posterior columns; you can, however, easily do it for 
yourselves. 
In little children we not very rarely meet with the symp- 
toms of tetanoid paralysis involving the legs alone, or all the 
limbs. The child cannot stand or walk because of the spas- 
modic condition of the legs and the apparent absence of 
cerebral stimulus ; no anaesthesia is present. In some cases 
we find microcephaly and idiocy conjoined. Prof. Erb was 
the first to describe these infantile forms (1877), and he is 
disposed to think that pathological researches will show as 
lesions, sclerosis or want of proper development in the pos- 
tero-lateral colums. I incline to the view that in these teta- 
nized children the entire motor tract, from its cortical (cere- 
bral) starting point to its distribution in the spinal cord, is 
more or less incompletely developed. The operation of cir- 
cumcision is still gravely advocated as a cure for infantile 
tetanoid paralysis, but we have no recent and uncontradicted 
statements of cures; besides, in my experience, Jewish chil- 
dren fully circumcised from birth frequently come to my 
clinic with these symptoms. 
A combination of b and c is recognized under the name of 
amyotrophic lateral sclerosis (Charcot). 
In this affection the lesions proper to b and c respectively 
are found in the spinal cord—viz., destruction of the anterior 
ganglion cells, and sclerosis (degeneration, probably) of the 
postero-lateral (or crossed pyramidal) columns. 
The symptoms correspond. We have a paralysis with 
atrophy in the upper and lower extremities, followed by 
contractions, with increased reflex in the non-atrophied and 
non-paralyzed muscles. 
d. Descending degeneration: a. Of spinal origin. This 
takes place when the physiological continuity of the spinal 
cord is interrupted. For example, after division of the cord 
with a knife, after great pressure from a tumor, or from a 16 
EDWARD C. SEGUIN. 
displaced vertebra’, or from a focus of transversely localized 
myelitis, we observe these changes. They differ completely 
above and below the seat of pressure or of section. Above 
the lesion we find an alteration almost limited to the pos- 
terior median columns (columns of Goll) extending indefi- 
nitely upward toward the apex of the fourth ventricle. The 
degenerated tissue appears in transverse sections as a wedge- 
like area with its base resting on the pia mater and its apex 
not quite reaching the posterior commissure (see Fig. i). 
Careful examination often shows on each side of the cord 
another tract of altered nerve tissue—viz., a portion of the 
postero-lateral columns lying posteriorly to the crossed pyra- 
midal column, and extending to the pia mater and the pos- 
terior gray horn—the so-called ascending cerebellar fascicu- 
lus (Flechsig). 
Below the lesion dividing the spinal cord the degenera- 
tions are found chiefly in two locations. First, in the crossed 
pyramidal columns (see fig. i); and, second, in the anterior 
columns, or, physiologically, the direct pyramidal columns. 
In these columns the descending degeneration extends to 
the lowermost portion of the cord. A more complete de- 
scription of these columns will be gitfen in the next section. 
The symptoms of the ascending degenerative changes, if 
there be any, are now unknown. As regards descending 
changes, they very probably are expressed by a more or less 
defined tetanoid state of the paralyzed limbs. In some cases 
this is well marked, and constitutes the spinal epilepsy of 
Brown-Sequard, or may resemble the symptom-group (c) at- 
tributed to the primary (?) lateral sclerosis. No sensory 
symptoms accompany either ascending or descending degen- 
eration. 
j3. Descending degeneration of cerebral origin: 
In this condition the foci of disease are found above the 
decussation of the anterior pyramids; by far the greater SPINAL LOG A LIZA TION. 
17 
number within the cerebral hemispheres. The nature of 
the lesion is, of course, immaterial, providing it be a 
desrtuctive one. Such, for examples, are clots in the motor 
regions of the brain (more especially involving the anterior 
two-thirds of the internal capsule), patches of softening in- 
volving the motor convolutions or tumors in similar loca- 
tions. Usually such a lesion is uni-lateral, but once in a 
while bi-lateral lesions exist, and we must be prepared for 
the existence of bi-lateral symptoms. 
From the focus of disease in these motor convolutions, or 
in the associated fasciculi of the corona radiata, the internal 
capsule (directly or indirectly involved), in general terms 
from the central part of the motor tract described to you by 
Dr. Gray, we can trace the degenerative changes with the 
naked eye (after six or eight weel«) to near the end of the 
spinal cord, through certain well-known columns or fasciculi 
of the cerebro-spinal apparatus. Let us take an example: 
A patch of softening involving the motor convolutions 
bounding the fissure of Rolando in the right hemisphere, 
now known to be the source of direct innervation for the 
left upper and lower extremities. Beneath the patch there 
is an altered bundle of fibres of the corona radiata, extend- 
ing downward in the anterior (or middle) portion of the inter- 
nal capsule ; thence into the right crus cerebri, the right 
inferior half of the pons, the right anterior pyramid of the 
medulla oblongata. At the base of the brain, in the crus, 
pons, and medulla the degeneration is superficially evidenced 
by an atrophy of the parts and cord. Below the medulla 
oblongata the changes are to a considerable degree invisible 
to the naked eye, but appear upon transverse sections of 
the spinal cord. On examining such sections we find 
changes in different localities in the two halves of the spinal 
cord. In the immense majority of subjects, the evident, the 
principal change, or secondary degeneration, is found in the 18 
EDWARD C. SEGUIN, 
left posterior lateral column, or, more strictly speaking, the 
crossed pyramidal column, so called because it is the contin- 
uation across the median line of the anterior pyramid which 
has (partially) decussated at the point known as the pyra- 
midal decussation. The exact location of this bundle (in 
the transverse section) varies somewhat at different levels in 
the spinal cord. In the upper cervical region it lies deep in 
the lateral columns, and as we examine sections made lower 
down we find it more posteriorly and laterally. It is always 
in the posterior-lateral column, to use a rough anatomical 
term, and never quite reaches to the periphery of the cord ; 
it diminishes in size (area) from above downward, and is 
quite lost to the naked eye in the lower lumbar enlargement. 
In this crossed pyramidal column (see fig. i), I repeat, the 
principal descending degeneration is found. The other, 
smaller descending lesion, in our supposed case, is found in 
the right half of the spinal cord—i. e., on the same side as 
the original disease and the intra-cranial degeneration-paths. 
This second spinal degeneration involves the anterior col- 
umn of the cord, strictly speaking—i. e., that fasciculus 
which lies between the anterior median fissure and the 
anterior gray horn—the so-called column of Tiirck (see fig. 
i). This column embraces those fibres of the anterior pyra- 
mid which have not crossed the median line; hence the 
better name for this fasciculus is the direct pyramidal col- 
umn. In our supposed case we find the right anterior col- 
umn more or less altered throughout the length of the cord. 
To sum up; Below the pyramidal decussation the second- 
ary degeneration is found both in the crossed and the direct 
columns derived from one of the pyramids—the right in our 
hypothetical case. 
A most important law, discovered and abundantly proved 
by Prof. Flechsig, of Leipzig, is that of variability in the 
■byramidal decussation. He found that in most of his speci- SPINAL LOCALIZA TION. 
19 
mens the crossing took place as above described, the great 
majority of- pyramidal fibres from the anterior pyramid cross- 
ing the median line and going to form the crossed pyramidal 
column, while a smaller number remained uncrossed and 
constituted the direct pyramidal column. But in one of his 
foetuses this was reversed—i. e., the direct pyramidal column 
was much larger than the crossed column. In several 
instances he found a degree of equality between the two 
columns derived from a pyramid. He concludes—and I 
entirely agree with him—that we must look upon the old 
law of decussation of motor fibres as liable to rare but 
remarkable variations. One result of such reversal of the 
law of decussation in a given individual would be to cause 
the paralysis from a cerebral lesion to appear on the same 
side of the median line. Although Brown-Sequard has 
written on the subject of paralysis from cerebral disease 
since the publication of Flechsig’s great work (1876), he 
ignores these facts, which are alone sufficient to maintain 
the accepted hypothesis of cerebral motor action, and also 
to completely refute his iconoclastic theories, since, if we 
admit that sometimes the pyramidal distribution is chiefly 
direct, we must deny the value of three 
hundred cases of paralysis on the same side as the cerebral 
lesion. As long ago as January, 1878, I made use of this 
argument, which to my mind is convincing. 
To return to the subject of descending degeneration; 
Its symptoms consist in increased reflexes (from tendons 
especially) and contracture, in the wholly or partially paral- 
yzed parts; arm and leg, rarely the face. It is useless to 
further describe this condition which we all see so often in 
uncured cases of hemiplegia. I would, however, call your 
attention to one important fact which I believe I was the 
first to notice and draw a conclusion from—viz., that during 
sleep in a warm bed the affected limbs are wholly or par- 20 
EDWARD C. SEGUIN. 
tially relaxed, and contract at once upon waking or upon 
exposure to the cooler air. I need hardly add that the con- 
tracture, like the paralysis, in hemiplegia, is greatest in peri- 
pheral parts. 
The classic theory of the physiology of contracture in 
hemiplegia is that it is due to the secondary degeneration— 
i. e., actively caused by the lesion of the postero-lateral 
column. Seven years ago (see Archives of Scientific and 
Practical Medicine, vol. I, p. 106, 1873) I rejected this 
hypothesis, and suggested a different one, which I have 
since elaborated and taught in my clinical lectures at the 
College of Physicians and Surgeons, New York. This hy- 
pothesis, which I intend shortly to publish in detail, is 
briefly that the spasm is due, not to direct irritation from 
the sclerosed (?) tissue in the postero-lateral column, but to 
the cutting off of the cerebral influence by the primary 
lesion, and the consequent preponderance of the proper or 
automatic spinal action—an action which is mainly reflex. 
This theory explains the phenomena observed in cases of 
primary spinal diseases with descending degeneration (a) 
and can be reconciled with results of experiments on 
animals (increased reflex power of spinal cord after a section 
high up, Brown-Sequard’s; inhibitory power of encephalon 
on spinal cord, Setchenow). 
Want of time will prevent us from considering the focal 
affections of the spinal cord, classed in the table under sec- 
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