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SECONDARY DEGENERATIONS
—OF THE—
SPINAL   COED,
    CH. BOUCHARD.



TRANSLATED FROM THE FRENCH BY




  EDWARD  R.  HUN,  M. D.
/^>3?y
^",^Jt,/Ja^ 
 
SECONDARY DEGENERATIONS
—OP THE—
SPINAL   COED,
CH. BOUCHARD
      HI
TRANSLATED FROM THE  FRENCH BT
EDWARD  R. HUN,  M. D.
.....-%
\ > .' \  -.3
/W;a,-
          UTICA, N. Y.
ROBERTS, BOOK AND JOB PRINTER, 60 GENESEE STREET.
              1869. 

fat ns--H-i+ 
SECONDARY  DEGENERATIONS
       OP  THE  SPINAL CORD.
  Comparatively recent observations in nervous diseases
have proved that when a nerve fibre  is injured in any
part of its  course, it undergoes certain degenerative
changes in that  portion which  is cut off from its con-
nection with the nervous centre, from which it derives
its supply of nerve force.  In other words the alteration
commences at the seat of the lesion and proceeds in the
direction of the transmission of nervous force.  If, there-
fore, we have any disease interesting the brain or upper
part of the spinal axis, by which  certain fasciculi of
nerve tubes are destroyed, we can trace these degenerated
tubes  throughout their  course  along the spinal cord,
observing with accuracy whether they terminate in the
gray matter of the cord or pass off in the  anterior roots
of the raehidian nerves.  In the same manner lesions af
the posterior roots, or lower segments of the cord result
in such alterations of the posterior columns as to admit
of our tracing the injured tubes in a centripetal direc-
tion.
   It being well  proved that the ultimate nerve fibres
do not anastomose with one another, but  continue their
course distinct  and separate from their peripheral to
their central extremity, we  have a  reliable method of
studying each individual nerve  throughout its passage
along the cord, as well as of investigating its relations
to the central ganglia, by carefully observing the altera-
tions which are secondary to primary lesions of the nerve:
tissue.
   This power of following a nerve tube along its course; 
4
is of inestimable value in  investigating  into  the pa-
thology and physiology of the nervous system; and ac-
curate observations  of cases will doubtless result  in a
great advance in our  knowledge of  this complex and
difficult subject.
  I have  translated the  following work  of  Bouchard
upon secondary degenerations of the  cord,  in  hope that
it will  lead  those who have opportunities of meeting
with such cases to keep careful records of the symptoms
and  post  mortem appearances, which, when  tabulated
and compared with  one another will  doubtless serve to
elucidate some  of the  difficult problems which are so
continually presented to us by the nervous system.
  Albany, Nov. 22d,  1868.            E. R. HUN.
  Besides the lesions proper of the spinal cord which
result from a primitive alteration of its tissue, there are
others which occupy, as a rule, the whole length of the
raehidian axis, which develop very rapidly and  almost
at the same time throughout this whole extent, and
follow either primitive lesions  limited  to  one  point of
the cord itself, or lesions of the brain, or lastly altera-
tions of the posterior roots.
  These secondary degenerations  of the cord take no
part in the proceedings of the primary lesion.   They
have their own physiology and pathological anatomy,
their special course, the same in every case, whatever be
the nature  of the diseases  of which they are the con-
sequence.   They result from that property common to
all  nerve  tubes which, injured at  one point of their
course, become altered throughout all that portion which
has thus lost its relations to the parts from which  they
take their  origin, and which exert  a preponderant in-
fluence on their nutrition. 
5
  Thus interpreted, these alterations of the cord  well
deserve the name of secondary degenerations, and differ
essentially from other affections also described as second-
ary, but which are  only the radiations to the cord  of a
process developed in a neighboring part, such as myelitis
or sclerosis consecutive to spinal meningitis; such also
as those diffused scleroses of the cord so frequent  in
general paralysis,*  and  of which M. Magnan  has de-
monstrated the relations with the  cerebral lesions pe-
culiar to that disease.
   I should say, at the commencement, that these second-
ary degenerations of the cord very often escape even  a
careful examination.   Notwithstanding when the at-
tention is drawn  to this  point  we  not  infrequently
discover them with the naked eye.  In all cases, certain
anatomical processes which I shall explain hereafter,  al-
ways enable  us to recognize them easily.  This research,
I think, should  not be any  longer neglected, for the
secondary degenerations have  their  own symptoms in-
dependent of those of the primary disease; they  may
persist after the disappearance of that disease,  and  then
betray themselves  by permanent functional  disorders
which, if one was  not forewarned, might  be attributed
to another cause; lastly, they tend to elucidate certain
points  still very obscure in the physiology, and above
all, in the normal anatomy of the spinal cord.
   Was it not for the difficulty of proving them in the
absence of the means which we employ at this day, one
would have the right to feel astonished that the second-
ary degenerations of the spinal cord had not struck the
observers who have studied the lesions of this nervous
centre before the present time.  Their  discovery is  in
fact of recent date.  In  going  over the ancient works
  * Etudes cliniques et  anatomo-pathologiques sur la paralysie
generate; prix de l'Academie de Medicine, 1865. 
6
on this subject, I have found  but one fact which is
connected with it:  it is given in the Sepulcretum.*   It
is in reference to an atrophy of the left half of the cord
in a  case of a considerable lesion of the right hemisphere.
But  the author of this observation, to which I shall refer
again, Wepfer, knew not how to interpret it.  Not only
he did not know that a hemiplegia of the left side can
be due to a lesion  of the right  hemisphere, but still
more, did  not attribute any importance to the lesion
of the  cord because  the  arm alone was  paralyzed.*)*
Morgagui,J who has commented at length upon the ob-
servation of Wepfer from a point  of view different from
that which we now  occupy, appears to have noticed the
relation which exists  between  the lesion of the  brain
and  that of the cord.  He  says, indeed, in the few lines
which he devoted to this last alteration,  that the lesions
of the right hemisphere,  " diminuerent aussi pendant
longtemps  Vafflux  des esprits dans la partie gauclie  de
la moelle epiniere?\
  It is in  fact  to Mr. Cruveilhier that the honor of
having discovered the descending  secondary alterations
consecutive to cerebral lesions, is due.  He has followed
them in the peduncles, in the pons  and in the  bulb,
but  he has not recognized  them in the cord.  I wish to
cite  this passage according to the text.§  " The  atten-
tion of observers cannot be drawn too much to  the  ap-

  *Theophili Boneti  Sepulcretum, lib.  1, sec.  15, obs. 4, p. 360:
Lugduni, 1700.
              f Ibid., Scholies de l'observation.
  I Recherches anatomiques sur le siege et les causes des maladies,
traduct. de Desormeaux et Destouet, t. 11, lettre xi., No. 10, p. 116.
  | Thus diminished for a long  time the afflux  of the spirits  into
the left half of the spinal cord.
     § Cruveilhier Anatomie pathologique, liv.  xxxii., p. 15. 
7
preciation  of  the influence of  hemorrhage and other
lesions of  the brain  on the condition of the cord, and
reciprocally of the influence of lesions of the  cord OB
the condition  of the brain.  I can give this as a positives
fact that the lesions  of the cord do not exert any in-
fluence upon the brain, but that the lesions of the brain
have a very marked action on the cord, both with refer-
ence to its functions and its organization.  Thus, often
coincident with apoplectic cicatrices, a result  of the al-
most complete destruction of the optic thalamus, I have
found the anterior pyramid of the same  side, and  con-
sequently of the side opposite to the hemiplegia, atro-
phied.  This  atrophy continued in the prolongation of
the pyramid  across the pons, and even in  front of the
pons in the inferior layer of the anterior peduncle.  I
have  not followed this pyramid downward below thg
decussation.   Finally, I have  never found, even in the*
oldest hemiplegias, the corresponding half of the cord
atrophied, or  at  least the difference between the right
and left halves of the cord has not struck me, by which
I do  not mean to say that, a difference which escaped
me may not become appreciable to the eyes of a more
attentive observer, whose ideas  are directed especially
to this point."
   This observation has given to L. Turcke* the results-
which M. Cruveilhier had foreseen.   In  a first memoir,
presented in 1851 to the Academy of Sciences of Vienna,
he showed the  alterations of the cord consecutive to
different cerebral lesions, and also to certain partial de^
structions of  the tissue of the cord itself; and he drew
from  these facts rigorous deductions  concerning the

  * Ueber secundare Erkrankung  einzelner Ruckenmarksstrangaf
und ihrer Fortsetzungen zum Gehirne, dans Compte rendu de la
section de mathematiques et sciences naturelles de  l'academie dea
sciences de Vienne, Mars, 1851. 
8
structure and distribution of medullary fibres as well as
some physiological consequences much more contestible.
Two years later, in a new communication,* he analysed
thirteen cases of secondary degeneration in consequence
of cerebral lesions, and twelve others resulting from prim-
itive alterations of the cord.  Finally, in 1855, he inci-
dentally came  upon  this question  in another memoir.f
Notwithstanding their importance, the works of Tlircke
have not attracted great attention.  We find them very
summarily mentioned in the  treatise of Rokitansky; J
they are not even spoken of in that of M. Lebert.  .At the
same time that Turcke published in Germany the result
of his researches, analogous discoveries  were  made in
France and  in Holland. |   MM. Charcot and  Turner§
presented to the society  of biology an example of de-
cussating atrophy of the cerebrum and cerebellum, and
noted also a  descending atrophy which followed the
cerebral peduncle, the pons, the anterior pyramid of the
atrophied cerebral  hemisphere and  the  antero-lateral
column  of the cord on the opposite side.   Some years
later M. Turner^f reproduced this fact in  his thesis,  re-
  * L. Tiircke, Compt. rend. de. l'Acad. des Sciences de Vienne, t.
xi.,  p. 93, juin, 1853.
  f  L. Turcke, Beobachtungen tiber das Leitungsvermogen  des
menschlichen Rttckenmarckes.  Ibid., t. xvi., p. 329, Mai, 1855.
  J  Lehrbuch de  Pathologischen  Anatomie, t. 11, p. 485, 3e edit.
  ||  Schroeder Van de Kolk, Waarneming van ene atrophie van het
linker halfrond der hersenen met gel'ijktijdige atrophie  du  regter-
zijde van  het ligehaam.  Verh. der Eerste  kl. van het Nederl.
Institunt, 1852;  Derde Reeks., D. V., p. 31.
  § Exemple d'atrophie cerebrale avec atrophie et deformation dans
une moitie du corps (Compt. rend, de la Societe de biologie, 1852,
p. 19).
  •*J De l'atrophie partielle ou unilaterale du cervelet, de la moelle
allongee et de la moelle epiniere consecutive aux destructions, avec
atropie d'un des hemispheres du cerveau.   (Theses de Paris, 1856.) 
9
porting with it two analogous ones.   Similar facts had
already been given by Rokitansky.
   It would  seem  that these facts should have had a
place in the discussion relative to the alterations which
divided nerves may undergo.  These two  questions, so
to speak, contemporary, and which could  have thrown
light upon  one another,  were nevertheless developed
almost independently.  At the same time that Turcke
communicated the result of his first researches, at Vienna,
Waller* published at Bonn, at London, and at Paris, his
experiments on the degeneration of divided nerves.  In
point of fact his observations did not bear upon the ele-
ments of the nervous centres; but the laws of the degen-
eration of nerve fibres such as he has formulated  them
seem to me  rigorously applicable to our subject. It was
also at this time when MM. Philippeaux and Vulpianf
made  known  their researches on the regeneration  of
nerves, that the study of the secondary degenerations of
the nervous centres was undertaken in France.  In the
 case published by M. Gubler, J an alteration of this nature
 commencing at the primary lesion of the brain descended

   *We cannot  say that Waller discovered an alteration  of the
 posterior columns of  the cord as a result of the lesion of the poste-
 rior "root.  He has certainly observed that, when these roots are
 divided, they degenerate between the  point of  section and  the
 cord, and even  that  the  alteration advances for a short distance
 into the substance of the posterior columns; but what he saw here
 was only an  alteration of the intermedullary portion of the roots.
 Augustus Waller, Nouvelle methode  anatccnique pour l'investiga-
 tion du systeme nerveux (lettre a l'academie des sciences  du 23
 Novembre, 1851:) Bonn, 1852.
   f Sur la Regeneration des nerf separes des centres nerveux. (Me-
 moires de la societe de biologie, 1859, p. 343.)
   I Du Ramollissement cerebral atrophique envisage comme lesion
 consecutive a d'autres affections encephaliques (Arch. gen. de med^
 t. 11, p. 31, Annee, 1859. 
                         10

across the peduncle  to  the  pons.   It was not followed
further, and the condition of the cord is not noted; but
already at this time an observation, cited by M. Gubler,
had been  presented to  the society of  biology  by M.-
Charcot.  In  this case the descending lesion was not-
only manifest in the peduncle, the pons, and the ante-
rior pyramid of the same side, but it continued  in the
anterodateral  column of the opposite side of the cord.
  Since this time, a large number of  cases have been
gathered at the Hospital of the Salpetriere by M. Charcot
and by M. Vulpian,  and have been, during the course of
the year 1862, the object of important communications;
made by those physicians to the Society  of Biology.  In
1863, M. Cornil*  had  occasion  to  observe with M.
Charcot some similar facts.   He says that in six cases of
old hemiplegia from cerebral lesion, they could discover
five times the descending alteration in the mass  of the
brain,  in the peduncle  in the pons, in  the anterior
pyramid.   He adds that  they find the  same alteration
in the cord, but  he  does  not fix either  the seat or the
extent of this alteration.  The same year Leydenf pub-
lished a remarkable case of secondary  degeneration of
the cord consecutive to  compression by Pott's disease,
and M. Cornil communicated to the medical  society of
observation an analogous case  found in the service of

  * A typographical error makes it appear that  M. Cornil said
that the secondary lesion occupied the anterior pyramid of the side
opposite to that of the cerebral lesion.  It is on the contrary always
on the side of the diseased hemisphere that we  find  the pyramid;
altered.
  Cornil.  Note sur les lesions  des nerfs et des muscles liees a la
contracture tardive et  permanente des  membres  dans les hemi-
plegies.  (Societe de Biologie, 1863.)
  f Die graue degeneration der hinteren Riickinmarcksstraenge:
Berlin, 1863. 
II
M. le Dr. Charcot.  In 1864, M. Laucereaux* compared
the atrophy of the optic nerves in cerebral amaurosis to
these descending degenerations of the cord, of which he
gave some new observations.   I  had  also at the same
time an  opportunity to meet frequently with  these
secondary lesions as  a consequence of diseases of the
brain or of primitive lesions of the  cord, in the service
of M. Charcot.  I communicated several cases of them to
the  Anatomical Society and to the Society of Biology.
Some  of these  observations have been published, f  I
gathered,  in  1865, some  new  cases at the St. Eugenie
Hospital in the service of M. Triboulet;  and two cases
to which I shall have to return, have been presented at
the  Society of Biologie, one by M. Cornil, the other by
M. Charcot.
                PATHOLOGICAL  ANATOMY.
   The secondary alterations of the spinal cord are never
observed except in the fasciculi of the white substance.
The gray substance has always been found intact.   We
could, indeed, foresee that this degeneration would only
affect  the conducting elements,  and that it could not
attack the  elements which  possess in a higher degree a
peculiar activity, nutritive and functional, and which we
  * De l'Amaurose liee a la degenerescence des nerfs optiques dans
les cas d'alteration des hemispheres cerebraux (Archives gen. de
Med., t. 1, p. 47:  1864.)
  f Bouchard, Rapport sur une observation de compression  de la
moelle.  (Bulletins de la societe anatomiques, juillet, 1864.)
  Aphasie sans lesion de la troisieme circonvolution frontale gauche.
(Compte rendu de la societe de biologie, 1864, p. 111.)
  De l'Ataxie locomotrice progressive au point de vue de ses lesions
anatomiques et de ses rapports avec  diverses maladies peu connues
de la moelle epiniere.  (Journal  de Medecine de Lyon, Novembre,
1864.
  Trousseau, Clinique Medicale de l'Hotel Dieu de Paris, t. 11, p.
604:  1865, observation de Egris  Valentine. 
12
rightly consider as nervous centres.  These degenerations
have been observed  in the white substance of the an-
terior part of the cord and in that of the posterior part.
When a white fibre is wounded by whatever  cause, in
one part of its course, either in the cord itself or in its en-
cephalic prolongations, the secondary  alteration  super-
venes as a rule, only on one side of the primitive lesion,
either above, or  below, but it extends  throughout the
whole length of this portion to its central or peripheral
extremity.   Hence, the names of ascending degeneration
and descending degeneration.   Only the injured fibres are
altered, and they are altered in their whole extent from
the point of the  lesion.  Now  as the white  fasciculi of
the cord receive  on their way new fibres which cannot
participate  in  the  degeneration,  it  results  that the
secondary alteration will undergo a relative diminution
according as we  go further from the point primitively
affected.  As, on the other hand, the fibres which exist
at this point, and degenerate, have not  all the  same des-
tination, but are lost from time to time in the  gray sub-
stance, it also results that, in following the degeneration
from its origin to its termination, we will find that it
undergoes a diminution not only relative, but  even ab-
solute.  Let us see now in what this defeneration con-
sists, and by what characters we can recognize it.
   Here is the place to recall briefly the effects  produced
by the section of nerves.   These experimental studies
have given results which offer the greatest analogy with
those which we  are  about to study.   We know since
the works of Waller* and  of MM. Philippeaux and
Vulpianf that the nerves, the  connexions of which with
the nervous centres are destroyed, present at the end of

                      * Loc. cit.
f Loc. cit. 
13
twenty-four hours, a diminution of their peculiar excita-
bility.  This enfeeblement extends  from the centre to
the periphery, gradually augments, and finally all activ-
ity entirely disappears by the end of the fourth day.
At this  period  the elements of the nerves which had
not yet offered any appreciable alteration of their struc-
ture, commence  to present marked modifications which
bear witness to  a serious disturbance produced in their
nutrition.   After the fifth day the medullary substance
of the tubes is, so to speak, coagulated, and at the same
time fissures form in its thickness and divide it into un-
equal  and irregular blocks; this is what we call  the
segmentation of the nerve tubes.   Very soon afterwards,
these fragments of medullary substance are seen to be
studded with fatty granulations, which go on multiply-
ing, and which take the place of the former throughout
the whole length of the tube.  At the end of a certain
time these fatty granulations are reabsorbed, and we see
only the neurilema withered and  shrivelled upon itself.
What becomes of the axis-cylinder while this retrograde
vpork  is going on ?  This is a point which  has not yet
been completely cleared up.  Let us add that the tubes
thus  destroyed can become regenerated; but they do
not reform in situ but  are only the expansion, the bud-
ding forth of tubes which remain healthy  above the
point cut.*  It  is at the end of fifteen days, at the soon-
est, that we can find the first indications of  excitability
in the regenerated  nerve;  at first in the parts nearest to
the section, then at points successively more and more
distant.
  * This opinion, which appears generally admitted by physiologists,
is not  absolute.  M. Vulpian has shown,  indeed, that in certain
animals, by choosing young subjects, we can  obtain, without any
influence of the centres regenerations of the hypoglossal and of the
lingual nerve. 
14
  Similar researches would be applicable to secondary
degenerations of the nervous centres; but experiments
have not as yet, so far as I know, been employed in this
special study.  Besides,  the  pathological facts do not
allow us to follow so easily the evolution of this morbid
process.  The cerebral or spinal disease kills the patient
before the alteration of the involved tubes  can become
evident, or on  the  other hand death comes when the
degeneration is complete, or when the fatty granulations
have  already been reabsorbed.   I have  nevertheless,
twice made observations  during the passage from the
state  of segmentation to the granular condition.   I
ought to mention here that, if we can come to conclusions
from the analogy of what is known of the nerves to that
which ought to take place in the spinal fasciculi, it is
best to do so  with an  extreme reserve, for the factg
known up to this day, and those which I have observed,
indicate that the same alterations present in these two
classes of organs marked  differences, above all as regards
their course and terminations. The white tissue of the
cord seems to be much more  delicate than  that of the
nerves; and  a  compression which, applied to a nerve,
would pass unperceived  and would be, at any rate, in-
capable of altering its structure, suffices to produce in
the spinal cord a secondary degeneration.  Besides the
work of  destruction of the tubes  requires in the cord
mu^ch more time than in the nerves; the granular con-
dition lasts a much longer time; and finally if the re-
generation of medullary fasciculi is possible, as I think
it is, it advances much more slowly than  that of the
nerves.
  L. Turcke, who seems to have been the first to submit
secondary degenerations  to a microscopic examination,
has not given the details relative to the  condition of the
nerve tubes.   He  only  points out the presence of  a 
15
great number  of  granular  bodies and  free molecular
granulations in the diseased tissue which are thus trans-
formed in situ.  We cannot adopt this manner of seeing
it, and we think that we have, at least at the commence-
ment, not a disease of tissue but an alteration of element.
In two cases of recent compression of the cord (one of a
duration of fifteen days and the other of six weeks) I
was able to see, by examining the degenerated fasciculi in
a fresh condition, that a certain number of  tubes were
clearly in a state of segmentation; fissure,  more or less
deep, divided  the neurilema transversely.   At certain
points  of  the  preparation, these  fragments were infil-
trated with fatty  granulations; others had been already
partly  destroyed  by the retrograde work which gave
the  tubes a  separated and  notched appearance.  Inde-
pendently of the fatty granulations  contained in the
altered tubes, a large number were free  among  the ele-
ments, and at certain points they  were agglomerated in
 a mass, in such a manner  as to form what  are known
 under the name of the granular corpuscles of Gluge.
   In these cases, a fine section, made perpendicular to the
 axis after  a maceration of some hours in  alcohol, showed
 in  the diseased fasciculi a large number of granular
 bodies scattered about under the form  of black spots.
 All about these  collections, the  tissue  had a  healthy
 appearance,  but the vessels presented on  their surface
 lines of fatty molecular granulations or even a complete
 envelope which rendered them black and opaque under
 the microscope. In more advanced cases, where there were
 descending alterations, as a result of cerebral softening
 dating from six months to one or two  years, I found,
 by  lacerating the tissue of the diseased fasciculi while
 in a fresh condition, that the nerve tubes were healthy
 or slightly varicose, and that they were  separated from
 one another by a small quantity of amorphous material, 
16
which was  usually  soft, transparent and, as it  were,
gelatinous, enclosing numerous fatty granulations, gran-
ular corpuscles  in  greater or  less number, and  also
nuclei analogous to those which exist normally in  the
gray  substance  of the nervous  centres, and  which M.
Robin has  described under  the name of myelocytes.
These nuclei were never very numerous;  but they were
the more abundant  in proportion as the  alteration was
of older date.   The appearance of the sections  made
after some hours' maceration  in alcohol,  did  not  mate-
rially differ  from that which  I have described for  the
first cases.   We saw in the midst of a tissue which  ap-
peared almost healthy, granular bodies in variable num-
bers,  and the vessels had a more or less atheromatous
appearance.   But the sections obtained from the  same
cord, after a maceration of some weeks in a weak solu-
tion of chromic acid, showed a notable difference between
the healthy  and diseased parts.  Examined under a low
power, the preparation showed  in  the altered portions
bright striae or transparent points disseminated between
the tubes which, by their opacity, contrasted with  the
spaces occupied  by the amorphous substance described
above, and which alone allowed the light to pass easily.
.In  the normal  parts, the  tubes pressed  against one
another, everywhere resisted the passage of light, and
gave a uniform and sombre shade to the section.
  Finally, in a case of compression of the cord, dating
back for thirteen years, an examination made in the fresh
state showed in  the diseased fasciculi a soft, transparent
and abundant amorphous matter, studded with myelo-
cytes ; and in the midst of it a few tubes, non-granular,
but varicose.  The fatty molecules were few in number,
the granular corpuscles were found only here  and  there
and the vessels were almost normal.  The fine sections
made after maceration in chromic acid,  and examined 
17
with a low power, at once made evident the diseased
parts, which contrasted in the clearest manner, by their
transparency, with the healthy parts, which  preserved
their uniform dark tint.  Besides,  in  the altered parts
we saw scattered about in the  transparent amorphous
substance black dots representing the sections of tubes
which had not been destroyed.   I should  add that the
connective tissue which had thus taken the place of the
nerve  tubes had produced, owing to the contractility
with which it is  endowed, a particular deformity of the
cord consisting in a longitudinal depression of the sur-
face at the points nearest to the altered fasciculus.
   By comparing  these different alterations, and by con-
sidering their chronological succession, we can, I think,
determine  the morbid process in  secondar}^  degenera*
tions.
   Three principal facts arise from  the preceding state-
ment : 1st, the atheromatous appearance of the capillaries
and the formation of granular corpuscles in  the tissue
which has  degenerated; 2nd, the alteration,  and after-
wards the disappearance, of a greater or less number of
the nerve tubes; 3rd, the formation of a connective tissue
which takes the  place  of the tubes.  Only two inter.
pretations seem to me possible.   We may suppose that
an irritation produced at the point of the primitive lesion
is propagated with rapidity through  the whole length
of the injured fasciculus, but in one direction only, viz.:
that of its physiological conductibility; that there hence
results a slow inflammation, exactly limited to the parts
whose functional  activity is no longer called in use, and
which cannot spread to contiguous  parts; and that this
inflammation gives rise to a morbid production of con-
nective tissue which unites the nerve  tubes, vitiates
their nutrition, and at last causes  their disappearance.
  Under this  hypothesis we might,  with M.  Robin,
       B 
18
consider the corpuscles of Gluge  as  leucocytes which
have undergone the granulo-fatty alteration.*  Under
another hypothesis which I hope to make more worthy
of acceptance, the tubes injured in one  point of  their
course are primarily altered in all that  portion which
has lost its connection with their centre of origin,  with-
out  there being any trouble of nutrition in the tissues
which they pass through.   Every thing then goes  on as
it does in the peripheral end of a  divided  nerve.  The
substance of the  tubes is  changed into fatty granules
which are diffused  through the tissue, some isolated,
others accumulated in masses, (granular corpuscles,f) or
in lines along the vessels, (atheromatous appearance of
the capillaries.)  The nutritive activity of  the tissue is
stimulated to action by this foreign substance which in-
filtrates it, absorption commences and causes  it to dis-
appear little by little, while at the same time prolifer-
ation of the connective tissue fills up the vacancies.
  The first hypothesis seems to me liable to very grave
objections.  Independently of the fact that there is some-
thing strange in imagining an inflammation which should
develope itself on one side only of the primary lesion,
and always on the same side, which should spread rapidly
through the whole length of a  spinal fasciculus without
manifesting itself by any symptom, and which, in this
sudden extension, should limit itself to  a  very narrow
band without encroaching upon contiguous  parts, which
notwithstanding have intimate nutritive relations  with
the diseased parts, by their nervous and vascular con-
nection, we should suppose that the microscope should

  *It is seldom,  except  in inflammatory softening, that we  can
attribute to leucocytes the origin of granular corpuscles.
  f It may be that certain granular corpuscles are the result  of the
granulo-fatty transformation  of drops of the white substance of
Schwann. 
                         19

show proliferation of the connective tissue before show-
ing the alteration of the tubes.  Now this is contrary
to what we observe.  The first lesions which we see are
the segmentation and the retrograde alteration of the
tubes;  the morbid production of connective tissue  is
secondary, and occurs much later.
   On the other hand, if the increase of connective tissue
was the initial phenomenon causing as its consequence
the disappearance of the tubes, secondary degeneration
would  be nothing more than  a sclerosis, and should
have the character  of sclerosis.   We know that, in this
latter  affection, the proliferation of connective  tissue
strangles  the nervous elements,  vitiates their nutrition,
and causes their atrophy and  disappearance; but this
disappearance  has  an  entirely special  character: the
white  substance  of Schwann  diminishes  in thickness,
generally in an unequal manner, so as  to give to the
tubes a varicose appearance; this substance may be en-
tirely  absorbed in  some parts where the axis-cylinder
remains bare; we can then trace it  to a point where  it
disappears in a sheath of medullary substance still in-
tact ; then it reappears further on; finally the absorption
of the medullary matter of the  tubes becomes complete,
and we can see the  axis-cylinders remaining in the midst
of the sclerosed mass, parallel to one another, and similar
in  appearance to the fibres of subcutaneous cellular
tissue, from which they are  easily distinguished by the
action of certain re-agents.  Then, there is direct atrophy
of the medullary substance  of  the tubes; in secondary
degenerations there is no atrophy of this substance;  it
disappears by the necessary intermediation of a process
entirely different from  atrophy, by a retrograde trans-
formation, and, before being absorbed, it loses its usual
appearance, its cohesion, and even its chemical constitu-
tion.   I may add, that I have never been able to find 
20
the denuded axis-cylinders in the case of secondary de-
generation,  and no observer has remarked their per-
sistence,  which we often find  in  cases  of sclerosis.
Finally, a new differential character is, that the sclerosed
tissue  is almost always  studded with  a considerable
number of amylaceous bodies;  these bodies are totally
absent, or  only exist in small  quantities in parts at-
tacked by secondary degeneration.
  It is not that I do not comprehend the analogy which
exists  between  the proliferation of connective tissue
which is observed at an  advanced period  of secondary
degenerations, and the new morbid product which prim-
itively  constitutes sclerosis;  but we  will see  what
essentially  different parts this hypergenesis takes, in the
two cases, with regard to the disappearance of the nerve
tubes.
  Here is the place to make an important remark: in
a nerve  attacked by secondary degeneration, all the
tubes are not altered;  some preserve their structure and
their functions almost intact; these are  those which,
already existing at the  part  primarily injured,  have
been respected by the  injury,  or  those which  have
emerged from the gray substance beyond the primary
seat of alteration.  These tubes, after the disappearance
of those which normally surround them, become isolated
in the midst  of the  connective  tissue which is under-
going proliferation, and which by its contact cannot fail
to  modify their vitality.   In fact they become varicose,
just as is  seen in  sclerosis.   It  is on account of  these
considerations that I have, in a former work,* described
secondary degenerations  under the  name of secondary

  * De l'Alaxie  locomotrice progressive au point de vue  de ses
lesions anatomiques et de ses rapports  avec diverses maladies peu
connues de la moelle epiniere.  (Journal de Medicine de Lyon,
Novembre, 1864.) 
21
sclerosis or false sclerosis, in contradistinction to primi-
tive sclerosis or true sclerosis.
  To finish with the processes  of secondary degenera-
tions, I ought yet to say a few words about the vascular
alterations  observed in  the diseased tissue.   I have al-
ready pointed out the atheromatous appearance of the
capillaries; it is observed almost constantly, but in very
variable degrees, and this fact, added to other characters
indicated further on, seem to justify  the  comparison
which M. Gubler* has made between secondary degen-
eration  and chronic cerebral  softening.  The  yellow,
depressed patches which are  so  often met with on the
surface of the brains of old persons, present in a peculiar
degree  all the  histological alterations  which we have
described, but in a much more marked form.   It is not
probable that the morbid process, although producing
similar results, is the same in the two cases.  Although
pathological anatomy and experiment have thrown light
upon certain points of the pathogeny of cerebral soften-
ing, the mode of formation of these yellow patches is far
from being: understood.   As for the atheromatous con-
dition of the capillaries which  is found  so constantly
and to so great an extent in this affection, we know not
whether it  is the product  or the  cause of the  disease.
In  secondary degeneration, this condition  of the vessels
seems to me to be consecutive to the  alteration of the
surrounding tissues.
  And first, it is not  the result of senile  degeneration,
for I have succeeded in  finding it in  a very advanced
degree  in very young children, as a result  of compres-
sion of the cord by Pott's disease.f  The fatty condition

     * Loc. cit.  (Archives gen. de Med., t. 11, p. 31: 1859.
  fl should protect myself against the charge  which might be
brought against me of having described, as atheroma of the capil-
laries in children, a condition of the vessels of the brain usual at 
09
of the capillaries is only the consequence and the index
of an  alteration of nutrition of  that  portion of the
tissue which has lost its physiological  activity; there-
fore it is  only the indirect consequence.  I could with
difficulty  comprehend  that a capillary vessel should be-
come  fatty  only because the neighboring nerve tubes
do not perform their functions; but if the neighboring
nerve tubes are greatly modified  in  their structure, it
may be that the abnormal materials  of disassimilation
which they give up to the capillaries, may produce  a
secondary trouble in the vitality  and structure  of the
latter.  Besides, the alteration with which we are occu-
pied, does not  seem to me  to have  advanced to this
degree.  If I am not deceived, there  is only an athero-
matous appearance,  and  not a fatty  transformation of
their substance.  During the early period of secondary
degeneration  in young  subjects,  the  abundant fatty
granulations appear to me to envelope the vessels rather
than  infiltrate them;  they seem to be external  to the
membrane proper of the capillary vessel, which latter
does not  appear to be perceptibly modified.   I have
even  demonstrated in  several cases that they were ac-
cumulated  between that  membrane  proper and its
envelope of connective  tissue, in that intermediate space
to which  M. Robin has called attention.   I do not deny
that these facts should be examined into: for the inter-
pretation which I  propose is  founded  upon  only a
limited number of cases.  At all  events it seems to me
to give a satisfactory explanation of the facts observed,

that period of life, a condition characterized by the presence  along
the capillaries of little  refracting beads and  granulations which
are evidently situated in the lymphatic  interspaces described by
M. Robin, and which, by their disposition in lines or their accumu-
lation at certain points, principally in the  angles of bifurcation,
may resemble in a superficial  examination, the atheromatous alter-
ation. 
23
and of their evolution, since the atheromatous appear-
ance, very marked at a certain period, seems afterwards
to diminish, so that when the connective tissue is com-
pletely formed,  the granular corpuscles  and molecular
granulations have in a great measure disappeared from
the diseased  part.   This theory of the  atheromatous
alteration of the capillaries of the nervous centres could
not be peculiar to secondary degenerations, for it enters
into that general law expressed by Billroth, as follows :*
"The fatty  degeneration of the capillaries of the brain,
or rather their  envelopment  in fat, is the consequence
not  the cause, of a  defect of nutrition  in the  central
nervous tissue."
   One  could  object to the theory which I  have just
given  of the  primitive granular fatty degeneration  of
the nerve tubes of the cord  that, in nerves where this
alteration  has been studied to better advantage, the
observed phenomena differ materially from those which
I have described above.  This is because, in the nerves,
each primitive fibre is contained in a solid and resisting
envelope, which is wanting to the tubes in the nervous
centres.   In  the  nerves, the fatty  granules resulting
from the transformation of the substance of Schwann
remain imprisoned in this envelope, and cannot distri-
bute themselves in the surrounding tissue as they do in
the cord.   This  anatomical peculiarity seems to me
sufficient to explain the differences of appearance which
the same alteration presents according  as it is in one
tissue or another.
   It would still  remain to  study the regeneration of
nerve tubes in the  spinal fasciculi which recover their

   *Theodor Billroth, Uebereine eigenthumliche gelatinose Degen-
ration  du Kleinhirnrinde nebst einigen Bemerkungen  iiber die
Beziehungen der Gefasserkrankungen zur kronischeu Encephalitis
(Archiv-der Heilkunde Dritter Jahrgang, p. 47.) 
24
functions after having been affected by secondary degen-
ation.  But the materials  for this study are completely
wanting;  and, in a  general way, we may say that  the
regeneration of spinal fibres has never been established
by  any  direct observation.   On one  occasion, MM.
Charcot and Vulpian thought they preceived the traces
of reproduction of the nerve tubes in a case of sclerosis
of the posterior columns.   This appearance  has never
even been mentioned among the results  of secondary
degenerations; and if I said above that I believed in
the regeneration of the  nerves  of the cord after these
alterations, it  was because I relied upon  clinical con-
siderations which I shall treat of hereafter.
  I should now point out  the methods of investigation
applicable to  anatomical  study of secondary degenera-
tions.
  Direct inspection often allows us to seize upon certain
peculiarities which may put us upon the track of this
alteration. Thus in descending degenerations, a result
of some old brain affection, it is not uncommon to find
the peduncle of the diseased side smaller than  that of
the other; we then  remark, after  having removed it
envelopes, that its color is changed, it presents on  its
inferior aspect a line of a  yellowish gray in the course
of its fibres, of greater or less  size, situated  sometimes
at its internal, sometimes at its middle and sometimes at
its  external part, according to the  location which  the
primitive alteration occupies in  the hemisphere.   In
these cases it is  not uncommon  for the  pons to pre-
sent a more or less marked flattening  on the same side.
The medulla  oblongata,  deprived  of its membranes,
also shows a  marked difference between the two  an-
terior pyramids.  The pyramid of the diseased side is,
like the peduncle, small and yellowish.  This atrophy of
the pyramid renders the olivary body of the same side 
25
more protuberant, and might lead us to think there was
a disease of this organ.
  As a general rule, the consistency of the degenerated
parts is not changed; but in one case M. Gubler noticed
a softening of this»tissue.
  As for the cord, an external  examination rarely fur-
nishes any indications, unless it be in very extensive
and very old  alterations  of  a hemisphere, and more
particularly in  cases  of cerebral  agenesis.   We then
find a diminution in size of that half  of the cord oppo-
site to the diseased hemisphere.  In cases of the same
kind, if the atrophy of one half of the cord is not evi-
dent, we  observe sometimes  a  slight  deformity of the
organ consisting  in a longitudinal depression in one
of its lateral parts, a little in advance of the  posterior
roots.   This lesion, however, cannot be well traced un-
less the cord has been previously hardened.
   Seen through  its membranes, the cord  does  not pre-
sent any  modification of  color  at  the situation of the
altered fasciculi;  even when the membranes are detached
without affecting its tissue, its  color appears to be nor-
mal.  But, if we make  a section of the organ in  a
direction perpendicular to its axis, we  can often see that
certain portions  of the  white  columns  have  not the
same appearance as the healthy parts. It is sometimes
a yellowish gray tint, sometimes a  semi-transparent,
bluish gray tint,  like that of milk diffused  in water; and
sometimes again it has the gelatinous grayish coloration
of sclerosis.  The yellowish color is principally observed
in cases of defeneration with an abundance of granular
bodies, that is to say in cases of not very  long  standing.
Nevertheless, and I should insist  upon  this  point, an
examination of the diseased tissue of  the  cord with the
naked eye is usually incapable  of leading us to suspect
even quite marked alterations. 
26
  After this preliminary inspection, and before submit-
ting the cord to any preparation, it is best to examine
with the microscope some portions of its tissue, removed
with small curved scissors, from the parts supposed to
be diseased.  These fragments  teased out in a drop of
water, should be examined with a power of from 150
to 300 diameters.  We thus recognize the condition of
the tubes, the atheromatous appearance of the capillaries,
the granular corpuscles, the molecular granulations and
the starch bodies.  We then replace  the water of the
first preparation  by a few drops of a weak solution  of
carmine whose alkalinity has  previously been  neutral-
ized by acetic acid.  The  amorphous matter interposed
between the tubes then becomes plainer, nuclei appear,
and  the capillaries are made more visible.   All these
details may be made still  more precise by the addition
of a drop  of acetic acid, after having taken the precau-
tion to remove  the excess of carmine  by washing with
pure water.  It is often more expeditious to replace the
carmine by an aqueous solution of       with or with-
out the addition of acetic acid.
   After these primary investigations, the cord is placed
in alcohol at 36° C, and after a few hours it will have
accquired  a sufficient degree of firmness to enable us to
make quite thin sections perpendicularly to its surface.
By treating these sections with acetic acid, compressing
them slightly between two glass slides, we can ascertain,
with a power of from 80 to 120 diameters, at what pre-
cise  points  the granular  corpuscles and atheromatous
vessels  are  situated.   This preparation cannot  give
other indications; but we can  renew the first examina-
tions which I have mentioned  above, on the portions of
the  cord  thus  treated with alcohol; the nerve tubes
then have sharper outlines, and the observation is less
impeded by the beads of the white substance of Schwann 
27
which are constantly formed in preparations made with
the fresh cord.
  The cord is then placed in a solution of chromic acid,
and, by the end of two  or  three weeks it will usually
have  acquired a sufficient degree of firmness.  Then it
is not very rare for the greenish yellow color of its sec-
tion to present, at the points  of degeneration, a lighter
tint than  at  the  healthy parts; and we can often map
out exactly the space occupied by the degeneration, by
pouring upon the surface of the  section a few drops of
a concentrated solution  of carmine.   By washing  this
surface, at the end of a minute, with a camel's hair pen-
cil  dipped in water,  the  diseased parts  only  remain
colored with  a lighter or darker  tint  of violet,  accord-
ing as the connective tissue of new formation is more
or less abundant.
  The examinations of these sections show also  the de-
formities  which  the  cord  may have undergone,  and
allow us to measure very exactly the dimensions of each
fasciculus,  by appreciating  the differences which may
exist on one side  or the other.
  Finally it is best to remove from these hardened cords
some very thin  slices which, treated first by  caustic
soda, then by glycerine,  show in the  clearest manner,
even  to the  naked eye,  the altered parts.  The  latter
appear as  clear, transparent  patches, plainly contrasting
with the surrounding tissue which remains opaque ;  and
under the microscope, they seem  studded  with  a vari-
able number of  black points, representing the  tubes
which have not been attacked by the degeneration.
  If we wish a preparation of the whole structure which
will also serve for a study of the elementary alterations
in detail, the section must first be placed in a weak solu-
tion of carmine, made neutral by acetic acid; at the end
of a few hours, when we  consider it sufficiently colored, 
28
we wash  it  with water, then with  absolute  alcohol,
finally we treat it with rectified essence of turpentine,
and finish the preparation in Canada balsam.
  This mode of preparation is also applicable to long-
itudinal sections.   We see in them the varicose condition
of the tubes, which, although comprised in the diseased
parts, have  been  respected by the degeneration,  but
have been surrounded and then deformed by the  con-
nective tissue of new formation.
  Thus far, I have studied the  secondary degenerations
in themselves, without considering the varieties of situ-
ation which these alterations may present in the different
columns of the  cord.  The anatomical facts are general;
they are applicable to all cases, whatever  be the direc-
tion in which the degeneration is produced, ascending
or descending, whatever be the nature or location of the
primitive lesion to which they  succeed.
   I am now going to commence the especial study of
these degenerations, and demonstrate in what direction
these lesions are produced, to what columns and what
portions of columns they are limited, according as the
primary disease is situated in such or such a part of the
nervous system.  I shall study successively the secondary
degenerations of  the spinal  cord, in  consequence of
primitive lesions,  1st, of the cerebral hemispheres; 2d,
of the cerebral peduncles; 3d, of the pons; 4th, of the
medulla oblongata; 5th, of the cord itself; 6th, of the
spinal roots.  At a future time we shall without  doubt
form a seventh class for ascending: degenerations of the
cord in consequence of primitive lesions of the ganglia
of the posterior roots; but I do not know that any ob-
servation is in existence at this day which can enter into
that division. 
29
I. SECONDARY DEGENERATIONS AS A RESULT OF PRIMITIVE
       LESIONS OF THE CEREBRAL  HEMISPHERES.
  These  degenerations' are the first which were  dis-
covered.   It is to these that the observation given in
the Sepulcretum refers; these are those the  existence of
which M. Cruveilhier suspected;  it is these which are
referred to in the first exact works published upon  this
subject by L. Turcke, by MM. Charcot and Turner, and
by Schroeder Van de  Kolk.  Up to this time a certain
number of observers have proved facts of this kind; but
we may say that the  subject, as yet very incompletely
known in an  anatomical,  is not at all understood in a
clinical point of view.
   We will point out hereafter the symptomatic pecul-
iarities which  may be referred to these degenerations.
As to the precise seat of  the alteration, the numerous
facts which  we  have gathered during the last  three
years, both  at the Salpetriere, in the  service of M.
Charcot,  or at  the hospital Sainte-Eugenie, in wards of
M. Triboulet, seem to us to fully confirm the ideas ad-
 vanced in 1851, by L. Turcke.
   But before entering into the details of this anatomical
study, some preliminary questions should be decided.
   And first, Do all morbid conditions of the  hemispheres
 determine secondary  degenerations?   Thus proposed,
 the question ought to be answered in the  negative.   I
 have  never found a trace of this alteration in simple
 cases of compression by tumors  of the membranes, by
 effusions into the arachnoid, or by thick false membranes
 of the dura mater, with meningeal hemorrhages.  Even
 very extensive superficial  lesions of the convolutions do
 not produce any descending degeneration.  This lesion
 is met with, neither in acute meningeal encephalitis, nor
 in tuberculous meningitis, nor in the diffused meningeal
 encephalitis of general paralysis, nor in the majority of 
30
superficial softenings of the convolutions either red or
yellow.  But certain lesions of the peripheral portions
of the brain which interest the deep layers of the gray
cortical substance, and destroy them, such as  the yel-
low patches, and which encroach even upon  the subja-
cent white tissue, may give rise to  secondary degenera-
tions which are usually not very marked.*  As a general
rule these degenerations result from lesions of the central
portions of the hemispheres.   It is above all in  cases of
hemorrhages or of softening of the corpora striata that
they  easily reveal themselves  to the observer.  Still it
is not necessary that the lesion should occupy exclusively
the centre  of the ganglia of gray substance.  There is a
remark verified a number  of times  by M. Charcot  and
M. Vulpian, that the most manifest  secondary degener-
ations succeed primary lesions which have destroyed to
a greater or less extent the little white bandsf interposed
between the  two corpora striata (capsule interne de
Burdach.)   Lesions of the optic thalami also produce
descending degenerations, which however are generally:
less marked than those which  are  consecutive to de-
struction of the corpora striata.  Finally, I have observed
recently, with M. Charcot, a case of secondary alteration
of the cord connected with the  existence of  depots of
cellular infiltration in the centrum ovale.  We  see that
a certain degree  of vagueness  reigns over this  subject,
and that the intensity of secondary degeneration, com-
pared with the extent of the primitive lesion and with
the exact situation of this lesion, deserves to be  studied

  * See the observation already cited of Egris Valentine, where I
have seen evident descending degeneration result from  a yellow
patch spread over several convolutions, with integrity of the corpora-
striata and the optic thalami, as well as of the expansions of the
peduncles.  (Troussean, Clinique Medic, loc cit.)
                 f Taenia semi-circularis. 
31
in a more precise manner.  This will be the surest way
of knowing what relative quantity of nerve tubes each
part of the brain sends directly to the  spinal cord, and
what location these tubes  occupy in the substance of
the raehidian axis.
   Thus far, the labors of M. Turcke have only determined
with exactitude the distribution of the descending de-
generation in consequence of cerebral lesions; and if the
results at which he has arrived are incomplete, as much
in regard to  the process  of this degeneration as to that
of the final evolution which it undergoes, we  ought to
acknowledge that he has determined with certainty the
location Avhich the  lesion occupies in  the  cord.   More
recent  works have  added nothing to his  description,
and the numerous facts which I have been able  to col-
lect, have all conformed to  the localization which he
had indicated.  A single fact anterior  to his researches
bore witness to the correlation which may exist between
atrophies of  the cord and lesions of the brain; but this
fact had not been understood.  I would speak  of the
observation  of Wepfer, which I have mentioned  before.
It concerned a young girl with paralysis of the left arm,
who had in the right hemisphere two  cavities as large
as eggs and filled with a turbid  liquid.   The  corpus
striatum and a portion of the corpus callosum were ulcer-
ated.   It is said, in  the  observation that the cord did
not fill the  raehidian cavity which contained a good
 deal of sanguinolent serum.  The  author adds:  " Quae
 (the cord) firma et nitida  erat,  sinistra  tamen pars
dextra minor videbatiw?  The history of secondary de-
generations  of the cord was limited to this phrase,  be-
fore the works  of Turcke.  However,  Rokitansky* had
remarked, after a considerable loss of substance  of the
 hemispheres by hemorrhage or inflammation, an atrophy
* Patholog. Anat., Ire edit., t. e, p. 715. 
                         32

of the peduncle, of the pons Varolii, of the  medulla
oblongata and of the spinal cord.
  Thus, there exists an intermediate  step between the
alteration of the cord  and the primitive lesion of the
hemisphere.  The degeneration is above  all marked in
the peduncle and  in  the medulla  oblongata.   It was
that which attracted  the  attention of M. Cruveilhier,
and  that which he has  described with  exactitude.  I
should say that the succinct description which he has
given of it is a resume of a long observation of facts
which have not been  published.  A  single case  of de-
scending degeneration as  the result of lesion of one
hemisphere is  given  in  his  Atlas  of pathological an-
atomy ;* it is so incomplete that it  could not have ena-
bled this author to  give the excellent description of sec-
ondary degenerations of the medulla oblongata to which
I have  already referred.   The observation to which I
allude is that of Jeanne Hamel, who died  at  the Sal-
petriere, the third  of January, 1833, at  the age of 72
years. This woman had a left incomplete hemiplegia, a
paraplegia with rigidity, and showed some defects of
intellect.   Death was the result of an acute red soften-
ing of the convolution.  They found in the midst of the
cerebral substance  several little cicatrices  of former
effusions  and  linear   induration in  the substance of
the  left peduncle.   The  pons  was  a little deformed,
the  median  line prominent,  the lateral portions de-
pressed ; it contained in its substance, on the right side,
a little  cellular cavity;  the  cord was indurated.  We
might ask if any one of these lesions is  the result of a
secondary  degeneration.   The  induration  of the left
peduncle could not be considered as a descending alter-
tion, from the  fact  that it was indurated; besides it  is
not stated whether there were marks of disease  in the
Anatomic Patholog., 32 livrais., p. 15. 
33
left  hemisphere;  finally  in  this  case  the hemiplegia
should have been in the right and not in the left side.
The cellular cavity of the pons was only the trace of a
primary softening.   The flattening of the  pons on the
left side could, alone, be attributed to a secondary de-
generation of its longitudinal  fibres; but  did this de-
generation have its  primitive cause in  the hemisphere
or in the peduncle?  As for the cord,  its induration,
which was  indicated  by the paraplegia, could not in
any manner be considered as the result of a descending
alteration.
   I have already indicated the characters of descending
degeneration in the medulla oblongata.   As this is not
the object of this work, I will not here enter into fuller
details, and I pass to the  examination of the situation
which the secondary degeneration consecutive to lesions
of the hemispheres occupies in the spinal cord.
   The alteration which, in the bulb, is  limited to the
anterior pyramid  of the side corresponding to the pri-
mary lesion of the brain, penetrates the cord  following
the distribution which normal anatomy indicates; it fol-
lows the  decussation of the pyramids, and occupies in
the cord the side opposite to the primitive lesion.  In all
cases where a secondary alteration of the bulb is mani-
fest we find an alteration of  the  same nature in the
antero-lateral column of the cord on the opposite side.
But this  alteration does  not  spread  throughout the
whole thickness of the antero-lateral column; it occupies
a  precise  location  in it, it is limited to the posterior
portion of the lateral column between the postero-lateral
fissure and the ligamentum denticulatum.   It is at this
point that Tlircke found the granular corpuscles; it  is
there also that the lesion has always seemed  to me to
be located.   In cases of considerable and very advanced
degeneration, where a large number of tubes  have dis-
       c 
34
appeared and have been replaced by connective tissue,
we  see  the antero-lateral  column, healthy in the re-
mainder of its structure, present a spot as if colored by
carmine at this exact point which in their sections con-
trasts by its transparency with the surrounding tissue,
and  looks  like a hole cut  by a  punch.  All around
the medullary is normal and we always find a little
band of healthy white  substance which  separates the
altered  portion from the pia mater.  This is the reason
why even in  cases  of very considerable degeneration
the external examination of the cord does not allow us
to perceive any modification in the color of  the altered
column, while we can do so in true sclerosis of the lateral
columns when the  diseased tissue, being in direct con-
tact with the meninges, is recognizable from its peculiar
gray tint.  However, in  hardened cords, we can some-
times see at  this point  a deformity of the organ, a de-
pression of its surface which forms an abnormal furrow
in advance of the  line of attachment of the posterior
roots.   The alteration of the posterior  portion of the
lateral  column, more marked in the  cervical region,
 diminishes as it recedes from  the bulb; but we can in
 most instances follow it throughout a great extent of the
 cord, sometimes even to the inferior part of the lumbar
 enlargement.
   We  know  that  at the  inferior part of the bulb the
 decussation of the pyramids is not complete, but that  a
 portion of the fibres which compose  each pyramid ap-
 proach the median line so as to form the internal  part
 of the anterior column of the same side.  This anatomi-
 cal fact would lead us to expect that in certain second-
 ary degenerations  we should observe,  as a result of  a
 lesion  of a  single  hemisphere,  a degeneration of the
 posterior part of the opposite lateral column, and of the
 internal part of the corresponding anterior column; that 
35
is to say a lesion of both sides of the cord.  This is what
we see in reality.   Out of six cases of secondary degen-
eration consecutive to lesions  of  the brain, L. Tiirck
has seen,  in three, the alteration of the internal part of
the anterior  column  accompanying that of the lateral
column of the opposite side.  I have had occasion to
observe this  double degeneration with M. Charcot; but,
in a greater number of autopsies, I have only once been
able to see the condition of sclerosis which succeeds to
the destruction of the tubes, in  the anterior column of
the side of the cerebral lesion.*   In this case the altera-
tion formed  a narrow little band,  clearly distinct from
the healthy tissue, applied  to the  expansion which  the
membranes send into the anterior  sulcus, and reaching
in front, the  inner surface of the pia mater, and behind,
the anterior face of the commissure.  Perhaps my atten-
tion has not been sufficiently fixed upon this question;
at all events, this alteration of the anterior column  seems
to me to be rare, besides it  is always accompanied by
an alteration of the same nature, and more pronounced,
of the posterior portion of the lateral column of the op-
posite side.  In order that  it should  occur, the altera-
tion of the  anterior pyramid must be  extensive and
must interest its external portion.   Secondary degener-
ation of the  internal  portion of the anterior columns,
as a result of lesions of the hemispheres, does not extend
through the whole leno;th  of  the cord.   In  the case
which I have seen, it could not be recognizedat the mid-
dle of the dorsal region; but Tiirck says, that, in two
cases, he has been  able  to find  the granular corpuscles
as far as  the level of insertion of the roots of the last
intercostal nerves.

  * I am indebted to MM. Charcot and Vulpian  for the communi-
cation of an analogous observation gathered by them in 1862. 
36
II. SECONDARY DEGENERATIONS AS A RESULT OF PRIMITIVE
        LESIONS OF THE  CEREBRAL PEDUNCLES.
  The absence of proper documents will oblige  us to
make this  a  brief chapter.   A single  observation  has
been published up to this day;  still it may be disputed
whether it was secondary degeneration.   It  had refer-
ence to a fibrous tumor of the left cerebral  peduncle in
an epileptic.   The case was  presented to the Society of
Biology by MM. Cornil and Thomas.*  The tumor  had
produced an atrophy of the peduncle, and this atrophy
extended to the pons and to the anterior pyramid of the
same side.  The tissue of the atrophied parts presented
no analogy to that of the  tumor; it was in every respect
similar to that of parts affected by sclerosis,  the  poste-
rior columns of those suffering from ataxy, for example;
no granular corpuscles were met with.  It may be that
this was not a secondary  degeneration  at the period of
proliferation of connective tissue, but a sort  of chronic
inflammation of the peduncle occasioned  by the tumor,
an  inflammation which  would be propagated  in  the
direction of the fibres of  the part, just as is usually ob-
served in primary sclerosis.  At all events, the condition
of the cord has not been  given in the observation.
  I  have  recently seen,  in  an autopsy made  at  the
Salpetriere, two symmetrical points  of softening in the
cerebral peduncles, the pons was flattened on each  side
of the median line, and the anterior pyramids presented
the atrophy and the yellowish  gray color characteristic
of secondary degeneration;  but a microscopic examina-
tion was not made, and the cord was not examined.
III. SECONDARY DEGENERATIONS  AS A RESULT OF PRIMITIVE
                 LESIONS OF THE PONS.
   Observations are still more completely wanting on
this subject.   A single case, although very incomplete,
      * Comptes-rendus de la Societe de Biologie, 1864, p. 46. 
37
seems to us worthy of being mentioned.   I borrow it
from the Atlas of Pathological Anatomy of M. Cruveil-
hier.*  Marie Duffet, aged  57 years, died  at  the  Sal-
petriere, June 3,1834.  Was hemiplegic on the right side;
motion was entirely lost on this side, and there was an
incomplete loss of sensibility.   The members of the left
side were not possessed of their natural power of motion.
At the autopsy the brain  was found  to be  healthy;
but in the pons was discovered an old apoplectic depot
implicating both sides, more  extensive superficially on
the right, but deeper on the left. The anterior pyramids
were atrophied, especially the left.
   The plate which  represents this lesion being inexact,
I cite word for word the correction of the author: " The
anterior pyramids were atrophied to such  a degree that,
in my notes taken at the time of the examination, I have
written: ' No anterior pyramid on the left side, the right
anterior pyramid atrophied.'  On this account I ought
to correct the figure, which, having been finished in my
absence, resembles  the normal condition a great deal
too much."
   Finally it is said in the observation that the cord was
healthy.
   Although incomplete, this observation at least proves
that the intensity of the secondary degeneration  is the
more pronounced as the primitive lesion  is nearer the
bulb.
IV. SECONDARY DEGENERATIONS AS A RESULT  OF PRIMARY
                LESIONS OF THE BULB.
   In proportion as  the primitive lesion  approaches the
spinal cord, the secondary degeneration of this nervous
centre ouo-ht to become more marked and more compli-
cated : every deep lesion of the peduncle, of the pons or
* 21 livraison, pi. v., fig. 3. 
38
of the bulb ought to produce an alteration not only of
the tubes which have their  origin in the altered part,
but  also of those  which, commencing higher up,  pass
through that part and are there injured in one point of
their course.  This increasing complication of secondary
degeneration could not have been treated of in the pre-
ceding paragraphs, since in none of the cases of primary
alteration of the peduncles or of the pons Varolii which
we have mentioned, has the condition of the cord been
studied.  It is  not so  in primary lesions of the bulb;
but these cases  are rare, for the alterations of this  part
of the nervous centres generally produce death before
the  degeneration has had time to become  developed.
We  have not  found in the authors any  observation
which can instruct us with regard to the  disposition of
descending degenerations consecutive to primary lesions
of the raehidian bulb.   The description  which we will
give of them rests solely upon two observations, of which
one was taken by us at the hospital Sainte-Eugenie, the
other was sent to us by M. Charcot.
  The first case regarded a little girl of five years, affected
by cervical arthritis.  An abscess produced by caries of
the axis  softened in front of the dura mater, and lifted
this  membrane  even in the interior of the cranium for
two  centimetres in front of the occipital foramen.   The
bulb was compressed and  flattened from before back-
wards by this collection of fluid, and, besides, an inflam-
mation, which, had caused adhesions anteriorly between
the arachnoid and dura mater, had implicated even  the
tissue of the bulb, the superficial portion of which was
the seat of a red inflammatory softening.  Death, which
was the result of this inflammation, occurred about fifteen
days after the commencement of the paralytic symptoms
which we could attribute to the compression.   Several
sections made at different parts of the cord at points 
39
which were  neither compressed nor inflamed, showed,
in the fresh  condition, numerous granular corpuscles
throughout  the whole  of the  antero-lateral  columns
accumulated  especially in the posterior half of the lat-
eral columns.  The capillaries  presented  in a marked
degree the atheromatous appearance; there was not as
yet any proliferation of the the elements of connective
tissue.  The  posterior columns were perfectly healthy.
  In the second case, the bulb was compressed by a dry
arthritis;  the new formations of bone narrowed consid-
erably the occipital foramen, and a marked thickening
with increased length of the odontoid process diminished
still more the free space  occupied by the bulb.  The
compression  was exerted  especially upon the anterior
and left lateral  portion of this organ; the point most
compressed appeared to be the inferior part of the left
pyramid, immediately above the decussation.  The com-
mencement of trouble dated back one year,  therefore
there was an abundant production of connective tissue
in place of portions of the cord secondarily degenerated.
These anatomical specimens have been  presented to the
Society of Biology, by M. Charcot, and we owe  to  his
kindness the opportunity of renewing upon this cord,
preserved in chromic acid, the examination which had
been made by him in the fresh condition, at the time of
the autopsy, and  afterwards upon thin  sections, after
hardening the oro;an.
  In the fresh condition there was seen  by the  naked
eye, thoughout the whole extent of the raehidian axis,
a gray coloration of the posterior  portion of the  right
lateral column, in  the seat of election of secondary de-
generations consecutive to cerebral lesions.  This gray
tissue was composed of varicose tubes, an amorphous
transparent granular matter, numerous oval or  spherical
nuclei and amyloid bodies.   The sections made from the 
40
hardened cord showed at this point a diminution of the
tubes; but this transparent spot due to the accumula-
tion of  connective tissue  of  new  formation, did  not
resemble a simple hole, it reached the inner face of the
pia mater; besides, the neoplastic production continued
along the  surface of  the  antero-lateral columns and
penetrated into the anterior sulcus, thus showing a de-
struction of the more  superficial tubes of these columns
on both  sides.  Finally at  the posterior portion of the
left lateral column a rarefaction of the  tubes could be
seen as  on the right side but less  considerable.  This
degeneration of the  left lateral column was not recog-
nizable   in  sections  made in the  fresh  condition.  I
should add that, on both  sides, but above all  on the
right, the proliferation of connective tissue of the pos-
terior and  external portion of the lateral columns  had
implicated for a very short distance the contiguous por-
tion of the posterior columns, between the extremity of
the posterior cornua and the collateral posterior sulcus.
These different lesions manifested the characters which I
have pointed out, only in the cervical region; below the
brachial enlargement,  only the alteration of the lateral
columns was  visible,  and  at the inferior part  of the
dorsal region, only  the degeneration of  the posterior
part of the right lateral column could be found, which
was then seen with  the same  characters as those of de-
generations of cerebral origin; that  is  to  say that  the
transparent portion occupied by the connective tissue
formed a circular hole separated from the meninges by
a little band of healthy medullary tissue.
   We see that in these two cases the seat of the lesion
does not appear to be the same; however, w^e  observe
that the degeneration was not limited  to the posterior
parts of the lateral columns, but that it extended in
the substance of the antero-lateral  columns.  The only 
41
difference is  that, in  the recent case,  we found some
granular corpuscles in  the substance  of the anterior
column and of the anterior part of the lateral column,
while in the case of  longer duration we did find that
there was, in these parts, an accumulation of connective
tissue which had undergone proliferation only  at the
surface.  But we must  remember  that  the new forma-
tion consecutive  to   destructions of tubes,  becomes
developed  and is apparent only in those cases where a
considerable  number  of nervous elements has been de-
stroyed at the same point, while the degeneration of a
few isolated tubes suffices to produce granular corpuscles.
The alteration of the  substance of the anterior portions
of the antero-lateral columns may therefore be manifest
in a recent case, and not be appreciable in a case of
longer duration.   This  remark is  applicable to  a very
large number of cases  of secondary degenerations.  It
is very seldom that, in cases where death occurs dur-
ing the first  few months after  the commencement of a
very limited  lesion of the brain, we do  not find in the
cord granular corpuscles or atheromatous capillaries;  on
the contrary  it is often the case that we cannot find any
proliferation  of connective tissue at the seat of election
in even more extensive cerebral lesions when death takes
place at a period when the granular  corpuscles  have
had time to disappear.  The study of degenerations con-
secutive to primary lesions of  the cord  itself is  about
to furnish  us new arguments in  support of this mode
of considering the subject.
  I should still  say a word or  two about the  very lim-
ited alteration  noticed in the posterior  columns  of
the cervical region in the last  observation.  Are there
some tubes which arise  from the bulb, and, following a
downward course, occupy the most external part of the
posterior columns? in  other words, are there,  in the 
42
posterior columns,  some whose centre of nutrition  is
situated higher up in the bulb or beyond it?  All the
known facts up to this day and those which Ave will
discuss in the two following paragraphs contradict this
hypothesis, and perhaps in this case we have an instance
of the propagation to neighboring parts of a formative
irritation, the seat of which was in the lateral columns.
  In  conclusion, we may say, after these two  observa-
tions, that  secondary alterations of the cord  depending
on primitive lesions of the bulb, affect the whole of the
antero-lateral columns with a  greater intensity at the
surface than in the deeper parts, but that the degenera-
tion implicates the  greatest number  of  tubes in the
posterior part of the lateral columns.
V. SECONDARY DEGENERATIONS  CONSECUTIVE TO PRIMITIVE
             LESIONS OF THE SPINAL CORD.
  The secondary degenerations of the cord  which fol-
low a lesion at a given point  of this nervous  centre
have  been  observed under  very varied  circumstances;
but it is more especially as a  result of compressions of
the cord by tumors of the meninges, by purulent col-
lections in the raehidian canal, by  fractures of the
vetrebral column, and above all by Pott's disease, that
they have been studied.  They have  also been seen  to
follow diseases of the tissue of the cord as partial scle-
roses; but  these  last facts, I should  say, are still very
obscure.  If the original disease of the cord is acute, it
seldom gives time for the degeneration to be produced;
if on the other hand it  is chronic, the alteration of the
tubes, even in the locality of the lesion, advances slowly,
and the portion which is  external to this locality may
then gradually become atrophied, in such a manner that
the production of the secondary lesion does  not appear
to  be absolutely identical with  that which we have
formerly indicated. 
43
  Every lesion of the cord  at  one point of its course
destroys, by descending degeneration, not only the fibres
which come directly  from the  different  parts  of the
brain, but also those which have arisen from the  gray
substance of the cord above or at  the level of the part
injured.   The descending  degeneration  then presents
the  greatest complications.   On the other hand, the
posterior columns, injured at one point of their  course,
degenerate on one side of the point primitively altered.
This alteration of tubes whose  centre of nutrition is at
their inferior extremity,  gives rise to ascending degener-
ations which we will constantly find in  the posterior
columns, and sometimes in a certain part of the lateral
columns.
  I  shall first study  the descending alterations:  they
have the greatest  analogy to  those which result  from
primitive lesions of the bulb.  This descending degener-
ation has been observed quite a large number of times
by  L. Tiirck.  His first memoir*  contains  three  cases
of it; two years later he reported in detail twelve new
cases.f   In the majority of the cases it was connected
with compressions of the cord by Pott's disease.   Below
the  primary lesion, the  posterior columns were  always
found perfectly normal; the  degeneration affected ex-
clusively the antero-lateral  columns which were  seen
to be studded throughout their entire  substance  with
granular bodies, accumulated principally at the posterior
part of the lateral  columns.   Passing from the point
primitively injured, and approaching the cauda equina,
it was found that the alteration of the anterior columns,
and  of the anterior part of the lateral columns, dimin-
  *Ueber secundare Erkrankung, etc. (Comptes-rendus de PAcad.
des Sciences de Vienne, Mars, 1851.)
  f Ueber secundare, etc. (Comptes-rendus de PAcad. des Sciences
de Vienne, Juin, 1853.) 
44
ished in intensity and disappeared entirely at about the
fourth insertion of nerves below the point compressed;
but, at  this level the granular bodies  still existed in
abundance in the posterior and external part of the lat-
eral columns, and in some cases could be found even at
the inferior part of the cord.
  Ten years later, Leyden reported a fine case of second-
ary degeneration of the cord by Pott's disease, in a little
girl aged three  years and nine  months.*  Below the
point compressed the antero-lateral columns were the
seat of a gray degeneration, especially at the periphery;
the posterior columns were healthy.  Leyden seems to
me not to have understood the process of secondary de-
generation which has reached the exaggerated produc-
tion of connective tissue, and he was  wrong when he
wished to support upon this fact a theory concerning the
nature of the process of the gray degeneration of the
posterior columns in  locomotor ataxy.  In this case of
secondary degeneration, the transparent material inter-
posed between the tubes did not contain many nuclei,
and did not offer a trace of amyloid bodies; peculiari-
ties which connect this case with degenerations of long
standing, such as we have described, and which separate
it from the medullary sclerosis, such as we find in  ataxy.
During the  same year, M. Cornil sent to the  medical
society of observation an example of compression  of the
cord, found in the service of M. Charcot.  He says  that
he found the inferior  segment of the cord normal.   But
an  examination was only made of a few morsels of med-
ullary tissue, and  perhaps if he  had made sections of
the inferior portion of the organ, an abnormal produc-
tion of connective tissue in the posterior  portions of
the lateral  columns  might  have been recognized in
  * Die graue degeneration der hinteren Riickenmarksstrange, p.
117; Berlin, 1863. 
45
place of granular bodies which had disappeared.  How-
ever, in another case, seen the next year by the same
author, the descending degeneration, such  as  Tiirck
had observed it, was indicated in the most exact man-
ner.   The compression, in this case, had been produced
by a fracture of the vertebral column;  and in the notes
which M. Cornil was kind enough to  give us, it is said
that in the inferior segment the posterior columns were
found perfectly healthy, but that the antero-lateral col-
umns  enclosed all through their substance  numerous
granular corpuscles, especially at the posterior part of the
lateral columns.
   About the same time, M. de Lacrousille showed to the
anatomical society an epithelial tumor of  the raehidian
arachnoid which  had compressed the cord  and deter-
mined a paraplegia whose commencement dated back
thirteen years.  The patient had been observed in the
service of M. Vulpian.  In a report which I was deputed
to make before the  Anatomical Society upon this pre
 sentation, I pointed out the following results to which
 an examination of this cord conducted me.  The com
 pression which was situated above the lumbar enlarge-
 ment had reduced the cord to such a degree that the
 meninges seemed to touch one another.  Below the point
 compressed the cord was notably diminished in size,
 but the atrophy did not exclusively affect  the antero-
 lateral columns.   The examination was not made in the
 specimen in the fresh condition.  In sections obtained
 after hardening it in chromic  acid, a  considerable rare-
 faction of the tubes was  seen at the  posterior  part of
 the lateral  columns, forming  a  transparent spot which
 in width came in  contact with the  meninges.   This
 lesion diminished in extent as it went further from the
 point compressed, but it could be traced to the  inferior
 part of the lumbar enlargement.  The methods of pre- 
46
 paration employed did not allow of any search for the
 existence of granular bodies, which, considering the long
 duration of the lesion, had probably disappeared.  As
 for the atrophy of the anterior columns and of the an-
 terior portion of the  lateral columns, it apparently re-
 sulted from the disappearance of a large number of nerve
 tubes,  which disseminated through these fasciculi, had
 allowed the tissue to  contract upon itself without  leav-
 ing any  empty  space between the elements which re-
 mained.
   The following  year I had an opportunity of taking
 at the hospital Sainte-Eugenie, in the service of M. Tri-
 boulet, the observation of a little girl of  thirteen years,
 affected with caries of the vertebras at  the lower part
 of the dorsal region.  Death occurred about six weeks
 after  the commencement of the paralytic symptoms
 which  were the result of the compression of the cord by
 an intra-rachidian abscess.  The portion situated below
 the point compressed  showed a perfect integrity of the
 posterior columns, but numerous granular bodies were
 found through the  substance of the  antero-lateral col-
 umns, especially at the posterior portion of the lateral
 columns which, at the lower end of the organ appeared
 to be  the  only ones  altered.  No hypergenesis  of the
 elements of connective tissue was found.
   M. Charcot has communicated  to me an observation
 of compression of the cord  by caries of the vertebrae,
 taken  in "1865, at the Salpetriere, in which these de-
 scending lesions  present  the  same  characters.   The
 paraplegia  became complete only three days  before
 death; nevertheless granular bodies were already to be
found in the lower segment of the cord.
  Finally, I have recently had  an  opportunity of  ob-
 serving at the Salpetriere, in the service of M. Charcot
a case of compression  of the cord produced by a cancer- 
47
ous tumor developed  in the  posterior lamina  of the
first dorsal vertebra.   Besides this, a collection  of pus
had softened in the raehidian canal and slightly com-
pressed the cord on its posterior aspect, outside of the
dura mater from  the  situation of the tumor to  a point
about  one inch above the lumbar enlargement.   The
patient died five and  a half months after the commence-
ment of the paraplegia.  All  the columns were altered
in the  compressed portion; but below, in the  lumbar
enlargement, the posterior  columns were healthy, while
the lateral columns contained a considerable number of
granular bodies, and a finely granular amorphous ma-
terial,  in which was  found a large number  of myelo
cytes and other very elongated nuclei, resembling embryo-
plastic nuclei.  In the anterior columns  also granular
bodies were found, relatively much less numerous; be-
sides there were  seen, between the nerve tubes, some
myelocytes and embryo-plastic  nuclei as  in the lateral
columns, but  in reality much  less abundant.
   From all these facts, it is clearly evident that, in cases
 of primitive lesion of the  cord, the descending second-
 ary degeneration occupies  exclusively the antero-lateral
 columns; that the posterior columns always  remain in-
 tact ;  that, in the  antero-lateral columns, the principal
 and most extensive alteration is limited to the posterior
 portion of the lateral columns; and  that the  anterior
 columns and  the anterior portions of the lateral  columns
 also degenerate, but that, in these fasciculi, the  desfener-
 ation  rapidly diminishes,  so  as to  disappear  entirely at
 a short distance from the part originally injured.
    Let us proceed now to the study of ascending  degener-
 ations of the  cord consecutive to primary lesions of that
 onran.  These degenerations  have been observed eleven
 times by Tiirck.  They implicate the posterior  columns
 and the posterior portion  of the lateral columns.  - The 
48
anterior  columns above  the point primitively injured
have always been found healthy.
  The alteration of the posterior  columns, which may
occupy the entire surface of the  section immediately
above  the  lesion, gradually becomes  narrower in pro-
portion as it approaches the bulb, and leaves, at its ex-
ternal  portion, the medullary tissue  perfectly healthy.
The granular bodies are become more and more limited
to a zone which rests upon the posterior sulcus and upon
the posterior  surface of the cord. In the cervical region,
they are  only found in the smaller  fasciculi, and the
lesion disappears at the level of the floor of the fourth
ventricle.
  In the lateral  columns, the granular  bodies occupy
the same situation as in the descending degenerations;
but their number progressively diminishes as they ap-
proach the bulb.  At this  level,  in  place of affecting
the anterior pyramid of the opposite side, as is observed
in descending degeneration, they continue their course
in the restiform body of the same side, pass upwards
behind the olivary, and can once more be found at the
insertion of the restiform body to the  cerebellum, with-
out having undergone any decussation in the substance
of the medulla oblongata.
  In the case of compression of the cord in a little girl,
which  I have  reported above  from Leyden,  there was
also  an ascending degeneration, but  this lesion  impli-
cated only the posterior columns;  the nerve tubes were
diminished in number and separated by a transparent
material, just as in *in the gray degeneration of  the pos-
terior cord in persons affected by ataxy.  In the case
presented by M. Cornil to the medical society of  obser-
vation, it is said that  they found above the point com-
pressed some granular bodies in the  posterior columns
and in the neighboring portion  of  the lateral columns. 
49
In the second  case of M. Cornil, they also found that
the posterior columns, above the lesion, presented a very
large number of granular bodies, and they also found
some of them in the antero-lateral columns, principally
in the course of the vessels.
   In the patient of M. Vulpian, who has been the subject
of a  communication to the Anatomical Society, I  have
found one of the most manifest ascending degenerations
occupying exclusively the posterior columns. Numerous
sections, made at different levels  above the point  com-
pressed, gave  me  the following  results: Immediately
above the lesion, we find the tubes diminished in num-
ber  throughout the  whole substance of the  posterior
columns;  a little higher up, we find upon each side a
little band of healthy tissue applied  upon  the internal
face  of the posterior cornua;  the  alteration occupies  all
the  remainder  of the posterior  columns, and j>resents
altogether  the  figure of  a trapezium, the two parallel
bodies being formed,  one  in  front, by the gray commis-
sure, another, behind, by the meninges, the  two others
being j>arallel to the posterior cornua.  In proportion
as we depart from the primitive  lesion, these  two last
borders approach one another more, at the same time
that the little  bands  of healthy tissue, situated at the
external parts of the posterior columns, increase in thick-
ness.  At length  these two borders  end by uniting in
front at the junction of the commissure with the posterior
sulcus.   At this point, the  altered  portion  appeared
upon the section like  the figure of an isosceles triangle,
the  base  of which was  behind  on  the meninges, the
summit on the middle of the commissure, and the pos-
terior sulcus formed the perpendicular dropped from the
summit to the middle of the base.   A little higher up,
the lesion still preserved its triangular form, but it con-
tinued growing more  contracted;  the base which rested
       D 
50
upon the posterior part of  the  organ,  diminished m
lengthy and the summit left the commissure so as to
approach little by little the base, following down the
posterior sulcus; at length the alteration terminated at
the level of the fourth ventricle.   In this patient, the
lateral columns presented no abnormal appearance.
  In the little girl of thirteen years of whom I made an
examination at the hospital Sainte-Eugenie, the granular
bodies were seen only in the posterior  columns above
the tumor.
  In the observation of recent compression by vertebral
caries, which was communicated  to me by M. Charcot,
the granular bodies were also only found in the poste-
rior columns above the point compressed.
  It is not the same in the case of paraplegia from cancer
of the vertebral column, recently observed by M. Charcot;
the ascending defeneration affected  at the same time
the posterior  columns and the posterior  part  of the
lateral columns; it was  characterized by the presence
of granular bodies,  of isolated  fatty granulations, in
large numbers and by the  atheromatous appearance of
the vessels in these parts.
  We may conclude from an analysis of the preceding
facts, that  ascending degenerations of the  cord  are  de-
veloped consecutive  to primary injuries  of that organ,
and these  secondary  degenerations  principally affect
the posterior columns; that in these columns they grad-
ually diminish in intensity, become limited  little  by
little to the internal and posterior fasciculi, and terminate
in a point at the floor  of the fourth ventricle.
  The alteration of the posterior part of the lateral
columns  is not mentioned  in all the observations.  It
may be remarked, in this connection, that  in  the  cases
of  Tiirck,  in which this  alteration  was  present, the 
51
primary lesion  was located quite high up the cord, at
least above the middle of the dorsal res-ion.
  In  one of the observations which  I have taken, the
cord was compressed just above the lumbar enlargement,
and the lateral columns were  intact.   In another case
this lesion was wanting, and the injury was located be-
low the middle of the dorsal region.   In  the only case
where I have found the lesion of the lateral columns, the
compression was due to an alteration  of the first dorsal
vertebra.   It would appear that the height  of the  pri-
mary lesion is not without influence on the alteration or
integrity of the lateral cord from  ascending  degenera-
tion.  At all events this  degeneration is of frequent
occurrence and continues upward in the restiform bodies.
Let us add in conclusion, that the anterior columns  and
the anterior part of the lateral columns are never altered
by ascending degeneration.

VI.  SECONDARY  DEGENERATIONS CONSECUTIVE  TO PRIMARY
           LESIONS  OF THE POSTERIOR  ROOTS.
  Another  ascending  degeneration of the  cord is ob-
served as a  result of primary lesions  of the posterior
roots; but we  know of only  one case which  demon-
strates this alteration: it was  found in the ward of M.
Trousseau, and the anatomical preparations  have been
presented to the  society of biology by M. Cornil.   An
intra-rachidian   tumor  compressed the cauda  equina
without  touching  the  cord;  the nervous alteration
implicated equally the anterior and the posterior roots;
but as far as regards the secondary degenerations of the
spinal cord, we may neglect the alteration of the anterior
roots, which, according  to  the results of Waller's ex-
perience,  degenerate only  in  the direction  of the peri-
phery.  The posterior roots,  on the contrary,  injured
above the ganglia which are  annexed to them, should 
52
degenerate in the centripetal direction.   This is what
was  found  in reality.   Besides,  the cord  presented
throughout its whole lens;th a diminution of  the  tubes
of the posterior columns.  This rarefaction implicating
the whole of the posterior columns at the level of the
lumbar enlargement diminished gradually in  intensity
as it ascended, and became confined to the internal and
posterior portions of the posterior fasciculi.   However,
the form of the alteration upon sections made at different
levels was not identical, with that which we have indi-
cated for ascending degenerations from primary lesions
of the cord itself.  In  place  of being, as in the latter
case, bounded laterally by two diverging straight lines,
nearer one another in front than behind, the degenera-
tion  from injury of the cauda equina was circumscribed
by the arc of a circle, the convexity of which was turned
forward towards the commissure, and the two extremities
of which  rested upon the posterior face of the cord.
The  degeneration disappeared at the level of the floor
of the fourth ventricle.
  Before coming to the study of the functional troubles
by which secondary degenerations of the cord betray
themselves, we may deduce  from the facts already de-
monstrated  some conclusions relative both to the in-
timate nature of the process of these  degenerations and
their proximate causes, and to the  normal structure of
the spinal cord.
OF THE PROXIMATE CAUSE OF SECONDARY DEGENERATIONS.
  We  have  already  demonstrated that  inflammation
plays no part in the production of secondary degenera-
tions of the white fibres of the cord;  it only supervenes
consecutively, if  we may give the name of  inflamma-
tion  to that slow production of connective tissue which
produces, so  to  speak, the cicatrization  of the degen-
erated column.  We have established the fact that the 
53
first alteration affects the nerve tubes which undergo
a granulo-fatty transformation analogous to that which
has been observed in the peripheral portion  of divided
nerves.   We have shown the analogy of this destruction
of the nervous elements of the cord with that which is
observed in cerebral softening from vascular obstruction,
and we can now affirm the identity of the  destructive
process in secondary degenerations, and in degenerations
of the nervous centres depending on arrest of the arterial
circulation.  In both cases there are found, after the first
few days,  granular bodies and a great abundance of
fatty molecular  granulations; the  origin of these ele-
ments appears to be, in the softening as well as  in the
secondary  degenerations, a destructive alteration of the
nerve tubes.  Some months since, I had an opportunity
of observing with M. Charcot, in  two cases  of recent
cerebral softening, the granulo-fatty infiltration of the
cylinders  of  myeline of several  tubes  taken from the
 very seat  of the softening,  and presenting  the  same
 characters as those which  I had been  able to find at
 the commencement of secondary degenerations.   But,
 when it is the result of a loss of the supply of blood,
 this destructive process seems to  progress with  more
 rapidity;  it is for  this reason that MM. Prevost and
 Cotard* have, in their  experiments, been able to find
 numerous fatty granulations thirty-seven  hours, and
 granular bodies three days, after the obliteration of a
 cerebral artery.  They have  also seen an atheromatous
 condition  of  the capillaries developed  in points where
 they artificially produced a softening by cutting off the
 supply of blood.  I have recognized in man, in a cer-
 tain number  of softenings  from arterial obliteration,
 that this atheromatous condition of the capillaries is, as
   * Societe  de biologie, Janvier, 1866.  (Gaz. Med. de Paris, 1866,
 passim.) 
54
in secondary  degenerations, only an  atheromatous  ap-
pearance;  the fatty  granulations  are,  outside of  the
proper wall of the vessel, accumulated between that mem-
brane  and the  lymphatic sheath.   Finally, as the last
analogy, let us state  that, in softening from a defective
supply of blood, as well as in secondary degenerations,
a proliferation of connective tissue  usually follows  the
destruction of the nervous elements, in that period of
cicatrization of which M.  Durand-Fardel has given so
excellent a description.
  Thus the same disturbance of nutrition producing a
necrobiotic destruction of nerve tubes may be produced
under the influence of two different causes, the loss of
the supply of blood and the loss of nutritive action.
  By the loss of nutritive action,  we understand  the
cessation of the influence which the  elements of the gray
substance exercise on the nutrition  of the nerve tubes,
thus admitting the conclusions to which his experiments
on the degenerations  of the nerves  have  conducted A.
Waller.   We know that according to this physiologist,
each tube of the peripheral nerves has at one of its extrem-
ities a nervous cell, which, independently of  its special
properties of innervation, has the function  of presiding
over the nutrition of the nerve tube which departs from
it, and even of  contributing by a peculiar influence to
the reproduction of this tube, when it becomes degener-
ated at some  point of its course.*  These cells Waller
has designated  under the name of neurogenotrophes;
we now call them more simply a-llulex-trophiqiies, (nu-
tritive cells.)

  * We should perhaps say with more precision at this time, that
the centres exert a certain influence on the restoration and not on
the  regeneration of nerve tubes.  It seems  to result from the re-
searches of M. Schiff,  and of MM. Philipeaux and Vulpian,  that
the return of the functions of a divided nerve is produced, not by
the production of new tubes in the midst of the debris  of the de- 
.).)
  I cannot here refrain from examining an opinion which
would tend to throw doubt upon the existence of these
nutritive  cells, or rather to deny the  nutritive action
which the nervous cells can exert upon the nerve tubes
which arise from them. Under this hypothesis, the fatty
degeneration of the nerve tubes could only be attributed
to functional inertia.  Reciprocally, if we admit that
functional inactivity is capable of producing  degenera-
tion of nerve fibres,  it is useless to accord to the central
elements  any influence whatever  upon the nutrition  of
the  tubes;  this property would be  superfluous,  and
for the cord, would  cease to be  demonstrable.  Let us
consider,  then, whether the facts  known up to this day
permit us to admit  that the nerve tubes can degenerate
from the  sole fact of functional inactivity.
   If we  cut a mixed nerve,  the central  extremity re-
mains healthy; on the contrary the peripheral end de-
generates, and the  alteration implicates all the fibres,
sensor and motor.   If we consider only the motor fibres,
the degeneration affects in truth only the trunk of those
fibres, which no longer receives  any impulse  from the
brain or the cord, which are consequently in  a state  of
functional  inactivity.  It is the same when we divide
the anterior roots;  the extremity attached to the cord,
and  which  receives  from it motor excitation,  remains
healthy;  the peripheral extremity, which no longer par-
ticipates  in this excitation, degenerates.  Thus far noth-
ing proves that the functional  inactivity may not  be
 the cause of the degeneration.
   In the section of a mixed nerve, we have said, all the

 generated  tubes, as Waller thought, but rather by the reforming
 of the white substance of Schwann in the sheath of old tubes,
 around the axis-cylinder which, according to the same experiments,
 may remain  for  a  long time, notwithstanding that it undergoes
 alterations which we are far from understanding. 
56
 fibres, and in particular the  sensitive  fibres, degenerate
 in  the peripheral end;  nevertheless,  in  this  portion
 separated from the centre, they continue to undergo the
 excitations of contact, of temperature,  <fcc.;  they receive
 impressions which they cannot transmit to the  centres;
 but the proper activity of the nerve tubes is put in play,
 notwithstanding which these tubes  degenerate.   On
 the contrary, the central end, which is certainly removed
 from all peripheral excitation, which is in the most com-
 plete  functional  inactivity,  remains  healthy.   Now
 make a  section  in the middle of the posterior  roots,
 and the degeneration affects the central extremity, the
 one which  is attached to  the cord,  and  which is in
 functional inactivity, and is entirely absent in the peri-
 pheral extremity which is in connection with the inter-
 vertebral  ganglion,  and  which  continues to  receive
 external  excitations.  Thus,  of  the  sensor fibres, the
 degeneration  attacks  sometimes  those which  are  in
 functional inactivity, and sometimes those whose  phys-
 iological  activity continues to be provoked, and vice
 versa. The functional inactivity then  exercises no in-
 fluence over the degeneration of sensor fibres.  The de-
 generation affects only those portions which have lost
 their relations with  the ganglia of the posterior roots,
 the central or medullary extremity of the posterior roots,
 and the peripheral ends of nerves.
  The condition  of integrity of a sensor fibre is  there-
 fore neither in the fibre itself, nor in its peripheral ex-
 tremity which receives the excitations, nor in the  cord:
 it is in the intervertebral ganglion, or, according to the
 opinion of M. Schiff, near this ganglion.
  If the functional inactivity is without influence upon
the degeneration  or the  integrity of  the sensor fibres,
we  may, without pushing the analogy, admit that  it is
the same for the motor fibres.  We then have the right 
57
to state that the condition of integrity of a motor fibre
is in the cord.
   For ease of expression, we may translate these two
propositions  in the following  manner: in nerves, the
motor fibres  have  their nutritive cells in the cord, the
sensor fibres have their nutritive cells in the ganglia of
the posterior roots.*
   If the integrity of the tubes of the peripheral nerves is
due to the nutritive centres  and not to the alternations
of activity and repose, we are right in supposing that it
is the same for the tubes of the cord, and that the degener-
ations which we have studied are  due, not  to  the func-
tional inactivity,  but to the suppression of the action of
the nutritive elements.  Here experimental demonstra-
tion is impossible.   In truth, in the cord, contrary to
that which we have seen for the sensor fibres of the
peripheral nerves, the degeneration of  the tubes is pro-
duced  always in  the direction of their physiological
activity.   The  antero-lateral columns, which conduct
centrifugal excitations, degenerate below the point in-
jured, that is to say, in the portion which is no longer
excited;  the posterior columns, whose conductibility is
centripetal, alter above the point injured, in the portion
which is thus reduced to functional inactivity.
   But, to place  a  column of the cord in a state of in-
action, it is  not necessary to  produce a lesion of  the

   * This word nutritive cells expresses more than  our actual knowl-
edge allows us to affirm, and perhaps it would be preferable to
speak only of the nutritive elements, or still better of the nutritive
centres. It is not demonstrated, in fact, that all the nerve tubes owe
to their connection with a nerve cell all the nutritive activity neces-
sary to the integrity of their structure.  As regards the posterior
roots, in particular,  all of whose fibres have their nutritive centre in
the intervertebral ganglia, it is well established that a certain num-
ber of these fibres only traverse the ganglion without  contracting
any relation with the  bipolar cells. 
58
column itself; we equally produce a functional inactiv-
ity of the fibres of the cord having a centripetal current,
by destroying in the  peripheral  nerves  the elements
which connect mediately with them.  This experiment is
realized in  amputations.  Now, never, as a result of an
amputation of the thigh, which nevertheless places in
the most absolute inactivity all the fibres which  were
intended to  transmit to the  cord,  and thence to the
brain, the excitations coming from the lower limb, never,
I say, has a degeneration been found of  the posterior
part of the  lumbar enlargement, nor of any point of the
posterior columns.  This observation has already been
made by L.  Tiirck.  In these cases, the fibres which
remain inactive during long years preserve the integrity
of their structure, because they have not lost their con-
nection with their nutritive cells.
   We can conclude then from  all this discussion, that
in the cord as in the nerves, the nerve tubes are placed
under the dependence of the nutritive  elements.  The
direction in which the degeneration will  be produced,
as a  result  of a lesion of a column, will indicate to us at
which extremity of the tubes the  nutritive elements are
situated.   We are now in a condition to draw from the
facts just studied some conclusions relative to the normal
structure of the spinal cord.
              ANATOMICAL DEDUCTIONS.
   In the secondary  degenerations which follow primary
lesions of the brain, of the  cord, and of the spinal roots,
the extent, form, situation and course of these  degener-
ations indicate in the most  exact manner the normal
distribution  of the  nerve  fibres which have been  de-
stroyed at  the point  primarily injured;  and permit us
also  to study very exactly the intimate structure of the
white columns of the spinal cord, ftieir origins and their
terminations, where  the  scalpel  and  the microscope
« 
50
could only after great labor afford results less precise,
often even very uncertain.  L. Tiirck,  first, sought to
draw from the anatomo-pathological facts which he ob-
served some deductions relative  to normal anatomy;
but  he is rather anxious  to  deduce from it, by an in-
terpretation which I do not think sufficiently strict, the
direction of the physiological conductibility of different
fasciculi  of the cord.   M. Gubler*  also understood all
the advantage that normal anatomy could derive from
these facts, when he said in one of the conclusions of his
memoir: " Thus the  lines of softening in both directions
(ascending  and descending) studied by attentive ob-
servers, will serve to determine  the situation and the
arrangement of the  sensor and motor fibres in the col-
umns as well as in the nervous centres.  Here pathology
will still  afford light to anatomy and to physiology."
Besides, this method is not new: it is only the appli-
cation to the cord of a process employed by Waller in
the study of the peripheral nerves, and which he himself
designated under the name of a  "new  method for the
anatomical investigation of the nervous system."  It is
by this method that we have been able to study the
distribution and anastomosing filaments of  the  nerves.
I think I may say that there would be every advantage
in artificially producing secondary degenerations of the
spinal cord, so as to  make an  experimental  application
of the Wallerian method to the cord.
   We have already seen that lesions of different parts,
and even of parts very high up in the brain, determine
secondary degenerations which can be traced throughout
the whole length of the  spinal cord: these degenerations
also exist  exclusively in  the antero-lateral columns. We
may therefore conclude that there are tubes in the whole
  * Du ramollissement cerebral atrophique, (Arch. Gen. de Med.,
1859, t. 11, 6e conclusion.) 
60
extent of these columns which have their nutritive cells
in different parts of the brain.  On the other hand, the
descending degenerations diminish  in intensity as they
depart from the bulb; then  the  cerebral tubes which
are prolonged into the cord have not  all the same des-
tination, but leave, in their  course, the  antero-lateral
columns, so that only a very  restricted number of them
remain at the inferior portion of these columns.   These
fibres  which  abandon  the   antero-lateral columns  do
not escape by the roots; for in no  case of secondary
degeneration has an alteration of the spinal roots been
noticed; we  are then obliged to  admit that they pass
into and terminate in the gray substance.
   The descending degenerations from  lesions of the
brain are  not disseminated throughout the whole  sub-
stance of the antero-lateral  columns; they sometimes
affect the  internal  portion of  the anterior column on the
same  side as  the primitive lesion, and this  alteration of
the anterior column disappears in the dorsal region; on
the other hand, they always  affect the posterior portion
of the lateral column  of the  opposite  side, and the de-
generation continues as far as the inferior extremity of
the cord.  We conclude that  the decussation of the pyr-
amids is  not complete;  that some fibres, those of the
external portion, which  more rarely becomes  degener-
ated,  gain the internal portion of the anterior column,
applying  itself to  the anterior sulcus, losing itself from
point to point in the gray substance, and that the longest
of these cerebral fibres do not go further than  the mid-
dle of the dorsal res-ion.   This collection of fibres which
the brain sends to the  cord without decussation, and
which is  situated at  the internal part of the  anterior
column,  we  will  call the direct  or internal cerebral
fasciculus.  As  a  second conclusion, we may state that
the great majority of fibres  which the brain  sends to 
61
the cord decussate below the pyramids so as to become
located at the posterior part of the  lateral column of
the  opposite  side;  that  they  preserve  this position
throughout the whole of their descending course; that
they insensibly become lost  in the gray substance, but
that some of them are sufficiently long to attain  the in-
ferior extremity of the raehidian axis.  This collection
of fibres which pass from the brain to the lateral column
of the  opposite side, we will call the decussating  or  ex-
ternal  cerebral fasciculus.
   We  have now built up only a small part of the antero-
lateral columns; the study of degenerations consecutive
to primary lesions of the cord will enable us to complete
the description.   We have stated that, when the cord
is compressed at one point, the antero-lateral columns
degenerate below the compressed portion, and that the
alteration, though of but  slight extent in the anterior
columns, and in  the anterior part of the lateral columns,
is on the contrary very pronounced in the posterior and
external portion of these latter fasciculi, and that in this
situation it extends to the inferior extremity of the cord.
Among  the tubes which  degenerate  below the point
compressed, there are some which come from the brain,
and these are  the ones of which we have spoken above.
The direct cerebral fasciculi and the decussating cerebral
fasciculi are in truth  compressed  at one point of their
course, as is the remainder of the cord, and ought to de-
generate in their inferior portion.   It results from this,
that at the internal part of the anterior columns,  and at
the posterior part of the lateral columns, the descending
degeneration will implicate the fibres of encephalic origin.
As it is only in this situation that there are any cerebral
fibres, the degeneration of the remaining portion  of the
antero-lateral  columns interests tubes  of another class,
tubes which do  not come from the brain.  The degener- 
62
ation of these latter tubes follows a descending direction;
they therefore have their nutrition cell above the  point
of compression.  This  nutritive  centre is not in  the
brain,  but it is above the point compressed; it is con-
sequently in the gray substance of the cord above  the
point compressed.
  There  are, then, in the  antero-lateral columns, inde-
pendently of the fibres of encephalic  origin, other  de-
scending fibres, medullary  fibres proj3er,  which  arise
from the gray substance of the cord itself.   In order to
understand the  distribution of these  latter fibres,  we
must recall, in an exact manner, the situation occupied
in the cord by the fibres of encephalic origin. To render
the description less obscure, I think  I  should  insist
more  particularly upon the form and position of  the
decussating cerebral fasciculus. The study of secondary
degenerations,  consecutive to  primary lesions  of  the
brain, has shown us that it is almost  cylindrical, and
located in  the  substance of the lateral column at its
posterior part, in front  of the  line of insertion of  the
posterior roots,  in the  angle formed by the meninges
and the external face of the posterior cornu.  It does
not come in contact with the pia mater, but is separated
from  it by other white fibres, in  such a manner that,
when it has been destroyed by secondary degeneration,
the sections of the cord show at  the posterior  part of
the lateral column a hole, as if cut with a punch, in  the
healthy medullary substance, a  narrow band of which
separates it from the meninges.  In  secondary degener-
ations from lesions of the cord itself, this hole is larger;
it has increased in front and on the outside, has come in
contact with  the pia mater, and is thus transformed into
a depression.  This is because the degeneration impli-
cates not only the fibres of encephalic  origin, but also
the medullary fibres  proper.  And as the depression 
63
which  maps out the degeneration on  sections of the
cord, passes  on towards the inferior extremity of the
raehidian axis, gradually becoming narrower, we may
conclude that certain medullary fibres descend, following
the posterior part of the lateral columns, and become
lost in the gray substance after going a long distance.
We  have  already seen that these  fibres  have  their
superior extremity in the gray substance of the cord it-
self; they then establish relations between parts of the
gray axis separated by quite long distances.  We will
designate these fibres by the name of long commissural
fibres.
   In compressions of the cord, the descending degener-
ation  does  not invade only the internal  part of the
anterior columns, and the posterior and external part of
the lateral columns; the granular bodies are met with
in the whole thickness of the antero-lateral column, but
their number  diminishes insensibly  as  we go further
from the point compressed, and they disappear entirely
at quite a short distance below the primary lesion.  The
fibres  which thus degenerate  through the whole  sub-
stance  of the  antero-lateral columns, after a short de-
scending course, are  lost in the gray substance  of the
cord.   They do not come from the brain, but they have
their nutritive cell above the point of compression; they
then arise from the gray substance of the cord, in which
they  also terminate at  a  short distance below their
 origin.  I will denominate them the  short commissural
fibres.
   Still  this is not all: we have seen that in compres-
 sions which act upon the cord above the middle of the
 dorsal region  a slight ascending  degeneration  of the
 posterior part of the lateral  columns is observed; that
 this degeneration pursues  its  course in the restiform
 bodies,  and even in the  inferior peduncles of the  cere- 
64
bellum.   We must therefore admit that this posterior
part of the lateral columns, where we  have already ad-
mitted the existence of two kinds of descending fibres,
encephalic and medullary, contains also fibres of a third
class, but in very small numbers: these should be fibres
which have their nutritive cell at their inferior extrem-
ity.   This nutritive cell we can only suppose to  be in
two points; either in the gray substance of the cord, or
in the ganglia of the posterior roots.   But we have seen
that lesions of the posterior  roots, which suppress  the
nutritive  action of the ganglia for the cord, do not de-
termine ascending degenerations of the lateral columns;
we should then admit that the gray substance  of the
cord sends along the posterior part of the lateral  col-
umns some fibres which reach the cerebellum by  the
restiform  bodies and the inferior cerebellar peduncles.
In several cases of secondary degenerations, a vain search
has been made for the trace of  tubes which should go
from the restiform bodies, across the deep portion of the
pons, in the direction of the optic thalami.
  In conclusion, the antero-lateral columns enclose en-
cephalic fibres disposed in two fasciculi, at each extrem-
ity, at the internal part  of the anterior column  and at
the posterior part of the lateral column.   Besides, they
are for the most part formed  by descending medullary
fibres proper, which establish  relations between the dif-
ferent levels of the gray substance, commissural  fibres,
quite short in the anterior columns and in the anterior
part of the lateral columns, much longer in the posterior
part of these same columns.   Finally,  there exists also
in this posterior portion of the white anterior substance
of the cord, some  ascending fibres which establish rela-
tions between the raehidian axis and the cerebellum.
  L. Tiirck, to whom belongs  the  discovery of ascend-
ing degenerations of the lateral columns, concluded from 
65
this that these columns contained in their posterior por-
tion, fibres with a centrifugal and  fibres with a centri-
petal current.   It  is possible that  the lateral columns
may conduct centripetal impressions:  certain physiolog-
ical facts, upon which I may not insist, would tend in-
deed to make us think so.   However this may be, this
opinion  cannot be legitimately deduced  from the ex-
amination of secondary degenerations.  We can  affirm
only one thing, which is that some  of the fibres of the
lateral columns have  their  nutritive  centres at  their
superior, and some at their inferior, extremity.  But the
degeneration of a tube  is  not necessarily produced in
the direction of its  physiological  conductibility: thus
the sensor fibres of the peripheral nerves, the functional
activity of which is exerted in the centripetal direction,
have their nutritive elements at the superior extremity;
so that the nutritive influence  acts in an  inverse direc-
tion to the physiological conductibility.
   Let  us now say a few words about the  origin of the
anterior roots, before passing to the study of the posterior
columns.  An experiment of Waller, already mentioned,
proves that these roots have their nutritive centre in the
cord.  We have seen elsewhere that in compressions of
the cord the anterior roots never degenerate either above
or below the point primarily injured; from this we may
conclude that  they arise from  the gray substance at a
point very near their emergence, and that  they run only
a  very short course along the antero-lateral column.
   The constitution of the posterior columns seems to be
less  complex than that of the  antero-lateral columns;
but, in fact, their  degenerations are not so completely
known.  From the special point of view which we take
in this research, we can obtain our information from
only two sources: from the study of compressions of the
cord, and from that of the lesions of the roots.
       E 
66
  Waller,  in  his experiments  upon  division  of  the
posterior roots, had already remarked that, while  the
end  attached  to  the ganglion remained healthy,  the
medullary end degenerated;  and that " this disorgani-
zation could be traced for a short distance in the fibres
of the posterior  column of the cord,  in the ascending
direction."*  Independently  of these fibres, which are
at once, or after a short course, lost in the gray substance,
the posterior roots send others which pass through  the
columns for a  much greater distance, and which are de-
monstrated in the  case  of  compression of the  cauda
equina, which we have  borrowed  from M.  Cornil.   In
this case, there was an ascending degeneration of the
whole length  of  the posterior columns, and the altera-
tion, very pronounced in the lumbar enlargement, grad-
ually diminished in intensity so as to terminate in a
narrow band,  spread out  under the  meninges at  the
superior portion of  the  posterior pyramids.   There are
then some fibres which pass from the posterior roots of
the lower part of the cord along the posterior columns,
and are lost from point to point in the gray substance,
some of them terminating only at the floor of the fourth
ventricle.   These fibres represent  only a small part of
those which the posterior roots bring to the cord;  the
remainder pass at once into the gray substance without
aiding in the formation  of the posterior columns. This
fact is plainly established by microscopic anatomy  and
by physiology, but  could not have  been deduced from
the study of secondary degenerations.
  The ascending radical fibres which  we have  just
pointed out, do not by themselves alone constitute the
posterior columns.   In fact, in this case of ascending
degeneration from compression of the  posterior roots, a
  * A. Waller, Nouvelle methode anatomique  pour l'investigation
du systeme nerveux: Bonn, 1852.  Appendice: 8e conclusion. 
67
section of the cord made at the lumbar enlargement, at
a point where it had not yet received  any healthy pos-
terior root,  showed, upon the  section of the posterior
column, quite a large number of tubes, disseminated
through the midst of the sclerosed  mass, which had
taken the place of the radical fibres.  These new tubes
did not come from  the roots; they did not have their
nutritive  cell at their  superior extremity,  since  we
know that compressions of the cord do  not determine
a descending degeneration  in  the  posterior columns:
we  must  then  admit that  they had their origin in
the gray  substance of the inferior part of the cord.
The same may be  said  of other ascending fibres orig-
inating at different  levels of the cord.  We can demon-
strate this proposition by comparing the form of  the
ascending degeneration in cases  of compression of  the
roots, and in that of compression of the cord itself.
When the degeneration is consecutive to  a lesion of the
roots, it is mapped out on the sections by a part of an
ellipse, the convexity of  the  curve being in front; and,
its two extremities resting on the posterior aspect of the
cord, the tissue external to this line is perfectly healthy.
When there is  compression of the  cord itself, these
ascending radical fibres are injured at one point of their
course and degenerate above the seat of compression;
but the figure  which  the degeneration presents, upon
sections of the cord, is no longer the same.  In place of
a segment of an ellipse, we have a triangle, the base of
which is on the posterior face of the cord and the apex
towards the commissure.  This is because the degener-
ation also implicates other fibres which have their
nutritive centre  at their  inferior extremity in the gray
substance of the cord.  These are the medullary fibres
proper, like those which we have pointed out in  the
antero-lateral columns.  In a case of compression of the 
68
cord above the lumbar enlargement,  I  have seen the
degeneration pass on retaining its same triangular form
as far as  the superior extremity of the posterior pyra-
mids;  the  medullary  fibres  proper  of  the  posterior
columns therefore terminate in the gray substance after
an ascending course of variable length.  Some of them
extend from the lumbar enlargement as  far as the floor
of the fourth ventricle.  They  have  their origin and
their termination in the gray substance;  they therefore
deserve the name of the posterior commissural fibres.
  Ascending  radical fibres and posterior commissural
fibres are intimately mingled in the posterior columns
without producing any confusion in their reciprocal dis-
tribution, since  the form of  the degeneration  differs
through the whole length of the cord, according as it
implicates the former or the latter.
  In the two cases of degeneration from compression of
the roots or from lesion of the cord, the degenerated part,
as it nears the bulb, becomes more and more limited to
the posterior and internal portion of the posterior  col-
umns.  We may therefore conclude that all  the fibres
of the posterior columns tend towards the posterior and
internal portion of these columns, and are there located
after they have run the greater part of their course.
Then they probably curve forward  and outward so as
to terminate in the gray substance.
   The distribution which I have just indicated is  only
exact for the  fibres which come from the lower half of
the cord.  Of these fibres those  which are prolonged as
far as the superior part of the cervical region, are all
situated in the substance  of  the small fasciculi and of
the posterior pyramids.  The fibres which  originate in
the upper half of the cord do not appear to mingle with
 the preceding, so that  the  sensor nerves of the lower
 limb and those of the upper limb should remain isolated 
69
from one  another, separated by the intermediate pos-
terior furrows.  Indeed, in a case of compression of the
cord at the upper part of the  dorsal region, L. Tiirck
has seen the degeneration occupy the external portion
of the posterior  columns.   Unfortunately, he  did not
make sections through the substance of the bulb nor
that of the pons, so  that  the anatomo-pathological de-
monstration of the continuation of a part of the posterior
columns through the restiform bodies, is completely
wanting.
  To recapitulate, the posterior columns are formed
from fibres which come directly from the posterior roots,
from commissural fibres, and probably also, at the upper
part, from fibres  which, following the lateral  portions,
reach the  brain  by the restiform  bodies  where  they
form  relations with the ascending fibres of the lateral
columns.
  As a conclusion from all that  precedes, we state, exclu-
sively upon a basis of pathological anatomy,  that we
may consider the cord as essentially constituted  by a
gray axis, the different parts of which can doubtless com-
municate  with each other even  in the gray substance
itself, but whose  relations are also  established  through
its  whole length by commissural fibres, some anterior
and others posterior.  This gray axis should receive at
its  anterior part, and throughout its whole extent, fibres
which come directly from the  brain, it should receive
at its posterior part and  throughout its whole length,
fibres which come from the ganglia of the posterior roots;
these latter  fibres being of two classes,  some, direct,
plunge  immediately into the gray substance, the others
ascending, only  get there after a longer or  shorter
course.   Then from the gray axis two classes  of fibres
should  be given off; some should proceed towards the
brain along  the  posterior part  of the  lateral  columns, 
70
and perhaps also along the external part of the posterior
columns; the  others should leave the  cord  at a point
very near their origin, and should  go to the  periphery
along the anterior roots.
  Thus considered, the  cord may  be represented as
formed of intrinsic parts, the gray  axis and the anterior
and  posterior commissural  fibres, and extrinsic  parts,
some afferent and others  efferent.  The extrinsic afferent
parts should have two origins, one encephalic and the
other peripheral.  The extrinsic  afferent parts,  of en-
cephalic  origin, should  only exist in the antero-lateral
columns, and should establish  relations of each of these
columns with the two cerebral hemispheres; with the
hemisphere of the same side by the direct or internal en-
cephalic fasciculus, and with the hemisphere of the oppo-
site side by the decussating or external encephalic fasci-
culus.  The extrinsic  afferent parts of  peripheral  origin
should come from  the spinal ganglia by the posterior
roots, and should divide  into two  series  of fibres, some
plunging directly into the gray axis, the others also
arriving at the gray substance after having assisted in the
formation of the posterior columns.  The extrinsic effer-
ent parts should also have two destinations: some should
pass up to the encephalic  destination by the antero-
lateral column, so as  to  reach the cerebellum; others,
arising probably from the upper half of the gray axis,
should reach the pons by the external part of the pos-
terior columns.  The  others with  a  peripheral destina-
tion should emerge at once from the cord by the anterior
roots so as  to terminate in the muscles.
  Thus the  cord would form a necessary intermedial
organ  for all impressions which reach the  brain from
the  periphery, and for all impulses which  go  to the
periphery from the brain; no fibre would go directly
from the brain to the muscles, or from the tegumentary
surface to the brain. 
71
  This structure of the cord, based entirely upon path-
ological anatomy, is  in perfect harmony with a large
number of facts already established by the scalpel and
by the microscope, and affords them complete  confirma-
tion ;  or rather, this  harmony testifies in  favor of the
excellence of the method we have pursued.
  The results at which we have arrived  determine cer-
tain questions which were as yet doubtful; besides they
seem to us to establish several new facts.
  What we have said about the incomplete decussation
of the pyramids has been known for a long time, and it
was known in what parts  of the antero-lateral column
the fibres, which come from the pyramids, were located;
but the terminations of these fibres were not so precisely
determined.
  The commissural fibres of the antero-lateral columns
had already been admitted by  Todd  and  Schrceder
Vander Kolk; however we do not think that their dis-
tinction into two classes, according to their length and
the special location of each of them, had been pointed
out.
  Notwithstanding the works of L. Tiirck, already pub-
lished for  some time, only very vague ideas  were held
about the ascending fibres of the lateral  columns.
  In conformity with the first opinion given by Schrceder
Vander Kolk, we have shown that certain fibres of the
posterior roots assist a great deal in the formation of the
posterior columns; but we think that M. Dean has  ex-
aggerated their importance in considering the posterior
columns as exclusively formed by these roots.   We
have, in fact, proved that there are in these  columns a
large number of commissural fibres admitted by Todd,
by Gratiolet, and by several other anatomists.
  As regards the fibres which pass from the  cord to the
brain along the posterior columns, pathological anatomy 
72
has not yet given  us  sufficient information; however,
we may say that, up to this  day, other methods of in-
vestigation have not led to a greater degree of certainty:
we are as yet reduced to physiological deductions.

                  SYMPTOMATOLOGY.
   The clinical study of the secondary degenerations of
the spinal cord has  not yet  been undertaken; and we
may say that it was impossible to study them, when we
only knew the first period of these alterations.  When
a nerve is destroyed at one point of its course, in such
a manner as to suppress the relations of the centre with
the periphery, the function  of this nerve is abolished,
and if it still possesses some activity of its own, it cannot
display it by any manifestation either of sensation  or of
movement.  We understand,  from this, that the  sub-
stance of the injured elements may become disintegrated
without there being any new symptom in the paralyzed
parts.   We may then  state, a priori,  that the work of
degeneration which is going on in a column of the  cord
does  not   actually  betray itself by any  symptomatic
modification.  Clinical observation fully justifies  this
presumption.  In fact, while the lateral column of the
paralyzed  side  commences  to  show manifest signs of
degeneration by the sixth day, following the commence-
ment of the apopleptic attack, we do not see  the symp-
toms present any notable changes at that period; the
primary contraction which is  very  rare in cerebral
softening,  and  uncommon  in hemorrhage, is  usually
earlier, and is  observed from  the  commencement of
the symptoms, or during the first few days.  In every
case, this symptom, which may exceptionally appear at
the period when the secondary degeneration is produced,
finds its explanation  in  the cerebral lesions which we
may, with good reason, consider as complications, and 
73
it should not be referred to the deuteropathic alteration
of the spinal cord.
  It is not the same for the contraction which comes on
at a later period, a symptom almost necessarily consecu-
tive to old cerebral lesions, and to which attention does
not seem to us to have been sufficiently attracted.  This
contraction of the paralyzed parts which we almost  in-
variably find in cases of hemiplegia  of long  duration,
seems to us to have been wrongly referred to  a chronic
irritation of the brain, due to a contraction of the cica-
trice of the primary seat of disease, or to the progressive
march of an imaginary encephalitis.   The cause of this
permanent, tardy contraction seems to us to be in the
cord.   Certainly we cannot refer it to the granulo-fatty
alteration of the tubes, an alteration which, as we  have
said above, cannot reveal  itself by any symptom; be-
sides, at the time when this contraction commences, the
tubes injured in the brain are already destroyed through-
out their  whole  extent.   But the tubes of encephalic
origin are mingled in the cord with other tubes which
arise from the gray substance  of the cord  itself. These
medullary tubes proper are then plunged into the midst
of a tissue which, after a considerable  period from the
commencement  of apopleptic  symptoms, is the seat of
quite an abundant proliferation of connective tissue.  It
is to the irritation of the medullary tubes by this neo-
plastic formation, it is to this secondary sclerosis, that
we think we should refer the later contraction in  cases
of hemiplegia.
  If this  hypothesis is  correct, we should meet  with
analogous  symptoms in all those diseases, whatever be
their nature and their location, which are  accompanied
by descending degeneration, with secondary production
of connective tissue  in the lateral columns; and these
symptoms  should closely resemble those produced  by 
74
primary sclerosis of these columns.  We are  thus led
to seek what are, in these different pathological condi-
tions, the common symptoms which can be referred to
this  common cause, primary or secondary sclerosis of
the lateral columns.
  It  is principally in the modifications which supervene
on the part of the motor apparatus that we shall find
these symptoms  common to the different diseases which
are accompanied by secondary degeneration of the spinal
cord.  We must understand that these  researches are
not  free from difficulties, not  only on account  of the
complication of facts, which hinders their interpretation,
but especially because much obscurity still reigns upon
this  point of the symptomatology of paralyses.
  Of all the modifications which  the  condition  of the
muscles may present in cases of hemiplegia, the contrac
tion  is without contradiction the most important;  it is
also  the one which has principally attracted the atten-
tion  of observers.  Early or tardy, temporary or perma-
nent, it has always been regarded as an index of an irri-
tation going on in the nervous  centres.   In accordance
with Lallemand and MM. Cruveilhier, Bouilland, An-
dral, Durand, Fardel, Todd has especially insisted upon
the  semiological importance of  this symptom, and has
made it the basis of a division of cases of hemiplegia.
He admits three classes of them, according to the condi-
tions of the muscles.  In the first, the paralyzed limbs
remain flaccid and relaxed; in  the second  there is
early rigidity of these muscles,  and the rigidity makes
its appearance at  the very  moment of the  apopleptic
attack, or a  short  time  after.   Finally,  in the third
category, the majority  of hemiplegic cases  enter,  in
which the paralyzed muscles, flaccid at the commence-
ment, are attacked  at a later period, and progressively,
by a rigidity which becomes permanent. 
75
  This distinction which Todd  has established and so
strongly insisted upon, between the early rigidity and
the tardy contraction is no less important in a path-
ogenetic than  in a clinical point  of  view.  "If the
paralysis had been accompanied by rigidity, says the
English  author,* I should have been led to the con-
clusion  that the cerebral  lesion was of  an irritating
nature.   This rigid state of the paralyzed limb (when
it comes on at the same  time as, or very soon after, the
paralysis) is generally seen when some  superficial part
is affected, as the meninges or the surface  of the brain,
or when there is a  growth from the skull,  or a tumor in
the hemispheres, or in some cases of inflammatory soften-
ing, or in some  conditions keeping up a constant irri-
tation;   but when there  is a  simple  rupture  of the
fibres of a deep-seated part of the  brain, as  the  corpus
striatum, with or without  pressure, there is no irritation,
and the paralyzed muscles are quite  lax."  And in
another  place :f " In the majority of  cases the early
rigidity  is  due  to an apoplectic clot.   My idea as to
its  cause is, that it depends upon a state  of irritation,
propagated from the torn brain to the point of implanta-
tion of the nerves of the affected muscles.   But, you will
ask, why is it that in some cases of clot, the hemiplegia
will be accompanied with  complete relaxation of mus-
cles, while  in  other cases  the rigidity of which  I  have
spoken exists ?   The answer to this question is  as fol-
lows : In the cases where  there is  no rigidity, the clot
lies in the midst of softened brain,  and has  not  in any
degree encroached upon sound brain; but when rigidity
exists, the clot has extended beyond the bounds of the
  * Clinical lectures on paralysis, certain diseases of the brain, and
other affections of the nervous system, by Robert Bentley Todd:
lee.  v. p. 100; London, 1856.
          f R. B. Todd Lectures, 10 and 11 passim. 
76
white softening, and has  torn up, to a  greater or less
extent, sound brain.    *     *     *     This form of
hemiplegia  sometimes occurs in surgical practice, m
consequence of a blow on the head, with  depression of
bone, or from considerable hemorrhage within the cra-
nium, such as results from injury of the  middle menin-
geal artery, or one or more of its branches.   The paralysis
of the  opposite side  is then accompanied by rigidity.
      *      *      Sometimes  inflammation of the pia
mater, or arachnoid, causes an accumulation of fluid in
the sub-arachnoid  spaces,  and then there is paralysis
and rigidity.    *     *     *    An affection of the
brain, of an irritating character, may give rise to this
form of hemiplegia."  All these  assertions of  Todd are
based upon observations where autopsies were made; it
is with  justice that he states the encephalic seat and the
irritating  nature of the cause of early contractions in
certain  hemiplegias.   Besides,  this  opinion  does not
materially  differ from that of French pathologists.  For
a long  time we have considered contractions in  hemi-
plegia as a sign of encephalitis; and, besides this too
absolute belief, a  certain number of facts, several of
which have been long known, have led us to admit that
the hemorrhage  determines  immediate  contractions,
when the seat of disease, breaking up the convolutions,
reaches the meninges, or when it bursts into the cavity
of the ventricles.   Then,  is it not to an inflammation
which is developed about  the seat of disease, that we
should  refer the muscular rigidity which comes on a few
days after the apoplectic attack?
   According to this opinion, which nothing now  seems
to contradict, the muscular rigidity would result  either
from the irritation of the peripheral end  of  the  fibres
lacerated by the traumatic cause, or by the hemorrhage,
or by the  softening, or else from the irritation of the 
77
fibres which surround the primary seat  of disease, and
which have preserved their integrity.   According to the
first hypothesis, as the lacerated fibres are  destroyed
after the sixth day, they should rapidly cease to be  the
seat of any phenomena of excitation.   It would then be
to these temporary contractions of the  commencement
that we could apply the opinion of M. Gubler* concern-
ing the part  of atrophic  softening in the cessation of
phenomena of excitation, and in particular of rigidity.
   If we may, strictly, consider secondary degenerations
as capable of putting an end to the muscular rigidity
of the commencement,  they play  an entirely different
part with reference to the later contractions; not, I re-
peat, that  we can consider the contraction as  the symp-
tomatic expression of the  work of granulo-fatty destruc-
tion of the tubes of the cord, nor  even  that we  can
attribute to the granules resulting  from this destruction
the power of  irritating  the neighboring  tubes.   The
muscles remain flaccid and inert while this  process of
atrophy is going on; they only become  rigid at a later
period, when the hypergenesis of nucleated elements
commences to appear in the degenerated column.
   The later contractions  of paralyzed muscles in cases
 of hemiplegia, are surely those whose clinical history is
 most imperfect; not that they have escaped  notice, but
 their  varieties,  the  date  of their commencement,  and
 the deformities (often characteristic) which they  pro-
   * Du Ramollissement cerebral atrophique (Archesis  gen. de med.,
 1859.) M.  Gubler thus expresses the seventh conclusion of his
 Memoir:  Clinical observation has as yet taught us nothing of the
 particular symptoms of secondary atrophic softenings; but we can
 forsee that after them we will observe a cessation of the phenomena
 of excitation, such as contraction, provided that the long duration
 of the primary affection has not given rise to such changes in the
 condition of the muscles as  are opposed to the mobility of the
 parts. 
78
duce, have as yet been only very incompletely pointed
out.  These  contractions  are, however, very frequent,
and we  may say that they are the rule in  cases of
hemiplegia of long duration.  Out of thirty-two cases,
the analyses  of which will be given  further on, I only
once  found  the  flaccid hemiplegia.  I do  not propose
to trace out  a complete study of these  contractions:  I
will only endeavor to point out the most  marked fea-
tures of their history, taking as a basis the numerous
facts which  the  clinique of the Salpetriere can furnish.
   When we  examine  a patient suffering  from an old
hemiplegia, we usually see the forearm of the paralyzed
side is semi-flexed  upon the arm, and we  are assured
that this position is invariably maintained against the
influence of gravity by the tension of the muscles of the
anterior part of  the arm.  The  biceps in particular,
even in cases of very long  duration where it has under-
gone  a notable  atrophy, makes  a more  or less marked
prominence, and  it is evident to the touch  that  it is
stretched like a cord between its insertions.  If we tell
the patient to extend  the arm, he succeeds with great
difficulty, even in those cases where voluntary motion
is not entirely lost, in increasing by a few  degrees the
angle formed by the arm and the forearm, and then he
is usually obliged to perform this movement  mechanic-
ally, by  pulling  upon the  paralyzed hand with the
member  of the healthy side. If the observer himself
tries to produce this movement of extension  at the elbow
joint, he finds a variable resistance, which in some cases
cannot be overcome.  Usually, however, he succeeds in
extending the forearm, at least within certain limits,
and he experiences during  this movement  the same
sensations as when the limbs of  a  dead body in the
state  of rigidity  are made to move.  The  old cases of
hemiplegia, in which the articulations of the  paralyzed 
79
arm are movable and loose, like those of a corpse when
the rigidity has been overcome, are entirely exceptional.
It is  to  these  latter that  we give the name of flaccid
hemiplegias.  We will regard all others as rigid, what-
ever may be the degree  of resistance produced  by the
muscles, and whatever may be  the number  of muscles
affected.
   In  hemiplegias of long  duration,  it  is  very  rare  to
find all the muscles of one half the body paralyzed; it
is equally rare to find voluntary motion injured  to the
same degree in all  the  affected muscles;  it is also ex-
ceptional to find all the  paralyzed muscles rigid.  The
contraction in cases  of hemiplegia is never general; but
it does not  affect indifferently such and such a muscle,
or such  and such a group  of muscles;  on the contrary
it presents a certain regularity in its  determination.
   I do not  know that it has ever been  observed in the
muscles of the trunk, and it may be said to be limited to
the muscles of the extremities.   However, there  is per-
haps an exception to be made for the muscles of the
face.   Certain  facts  have  led me to  think that the
muscles of  the face, paralyzed at the time of the apo-
plectic attack, may afterwards undergo retraction, and
produce a deviation of the features of the  side of the
face opposite to that where the  deviation primarily ex-
isted.  There  are the cases in which  the observations
made at the commencement of the affection indicated a
facial paralysis  on  the same  side  as  the  hemiplegia,
with deviation of the features  of the healthy side, and
where, upon examining the patients some years later, I
found that the features were, on the contrary, retracted
 on the same side as the paralysis, thus  simulating  an
 alternate paralysis.*  As  for  the muscles of the  orbit
   * See Bouchard, Aphasie sans lesion de la troisieme circonvolu-
tion frontale  gauche, dans comptes-rendus de la Societe de biologie, 
80
and neck, the contraction of which so often turns the
face and the eyes toward the side of the diseased hemis-
phere at the moment of the attack, we do not see that
they are ever  affected with a permanent  contraction at
a later period.*
  Thus limited to the extremities, the muscular rigidity
is not observed in the same degree in the superior  and
in the inferior.
  It is always  less marked and more  limited in the
pelvic than  in the thoracic extremities; it may be absent
in the former, while it  exists to a more or less marked
extent in the latter, while the reverse is not true.
  Out of 31 cases of hemiplegia with rigidity, the con-
traction affected the muscles of the  upper extremity 31
times, and the muscles  of the  lower extremity only 14
times.   Even  in the thoracic extremity, the rigidity is
not always observed  in all  the muscles;  and those
which are rigid  are not always  so to the same  extent.
Thus  we rarely see the  shoulder elevated—10 times in
31 cases—and when it droops, which is more common—
15 times in 31  cases—this result is  due rather to the
force of gravity than to muscular traction.   We do not
usually find any great  difficulty in giving  to  the arm
those  different movements which the articulation of the
shoulder permits; but,  abduction is often quite limited.
In  its habitual  attitude, the  arm  of hemiplegics is
nearly always in a state of adduction, which  the action
of gravity is often sufficient to explain.  Rarely, indeed,
the arm is so strongly pressed  against  the  thorax that
p. Ill, annee 1864.  In this observation,  there  was no lesion of
the pons capable of explaining the alternate hemiplegia, but there
was a very pronounced secondary degeneration.
  * M. Vulpian has insisted  upon this symptom, which M. Cruveil-
hier had already noticed, and M. Prevost  has made it the subject
of an interesting memoir:  De la Deviation conjuguee de la face
et des yeux dans les hemiplegies.  (Gazette hebdom., 1865.) 
81
it may be necessary to attribute it to the contraction
of the pectoralis  magnus;  however, this latter cause,
though very evident in some cases, should usually be
associated to a certain extent with the action of gravity;
for, besides  abduction being impeded, the humerus is
frequently—18 times out of 31—in a more  or less pro-
nounced state of rotation inward.*
  While the muscles of the regions of which I have just
mentioned are contracted in only a slight degree, or even
not at all, the muscles of  the arm, of the forearm and
of the hand,  are  always completely  or  partially con-
tracted, and, in every case, it is in those parts that  the
tardy rigidity is the most pronounced.
  The contracted muscles, triumphing over those which
are only paralyzed, produce  special  and permanent at-
titudes of the  limbs;  but those remarkable deformities
which we find in old cases of hemiplegia, result not only
from the predominant action of the paralyzed and con-
tracted muscles over those which are attacked by flaccid
paralysis; more frequently, indeed, the deformities  are
the result of the contraction of antagonistic groups of
muscles.  This is easily demonstrated for the muscles of
the arm  and forearm.
  The joints which the contraction has placed in a fixed
position communicate to the observer a notable resist-
ance, whatever be the direction  in  which he tries to
move them.   The elbow,  for example, which is  usually
semi-flexed in  cases of hemiplegia, is sometimes as difficult
to put in a  condition  of complete flexion as in that of
extension.
  Often, however,  the forearm presents in both direc-
tions a very limited degree of mobility, compatible with
  * We shall see that, out of 31 cases of rigid hemiplegia, I have
12 times seen the arm in adduction, once in abduction, and 19 times
in an indifferent position.
       F 
82
some very restricted voluntary or communicated move-
ments;  but if  we try to increase  the  movement, we
suddenly experience the resistance  which I have  men-
tioned above.   These movements which we endeavor to
produce  are  alike  painful  in  flexion  and  extension.
Finally we can determine by the touch that the antag-
onistic muscles are equally contracted.  While the'biceps
is stretched like  a  cord, we  feel the triceps hard and
rigid.
  We might suppose that this contraction  of antago-
nistic groups of muscles was  only a spasm, a reflex con-
vulsion provoked by  the pain induced  by the motions
which we give to the paralyzed limbs, something similar
to the muscular  retractions  in  arthritis or arthralgia.
But in these cases the inhalation of chloroform suddenly
puts an end to the spasm and restores their  entire free-
dom of motion to the joints; while  I  have convinced
myself, with M. Charcot, that this  is not the case with
rigid hemiplegias.  Several  patients  having been put
under the  influence  of chloroform,  we  have seen that
while all the other muscles became  relaxed, the con-
tracted muscles preserved a  marked rigidity, to a less
degree, however, than when the patients were not under
anaesthetic influence, but sufficient to prevent complete
extension or flexion,  and to reduce to  their primary
position the limbs whose attitudes  had been modified.
If we continued the action of chloroform for a longer
time, we then saw one of the antagonistic groups  yield
a little to the more powerful traction of the opposing
muscles, and produce a slight change  in the position of
the articulation;  then this   change once produced  re-
mained, even after the patient came out from under the
influence of the anaesthetic, and the limb gradually re-
turned to its former position, but not until several hours
after the cessation of the inhalations. 
83
  The permanent vicious  attitudes in hemiplegias of
long duration are then for the most part the result of
the opposing action of antagonistic groups of muscles
contracted in a relatively greater or less degree.  Hence
it  is that the  position of the limb is generally inter-
mediate between those which would be produced by the
isolated action  of these groups of muscles, more or less
flexed  or  more or less extended, according as the con-
traction is stronger in the  flexors  or  extensors.  This
fact is  made evident by a symptom which we can pro-
duce at will in  certain hemiplegics, and particularly in
those having a  unilateral atrophy of the brain resulting
from an affection of that organ, dating back from infancy.
The usual attitude of these patients consists in a flexion
of the forearm  with pronation and flexion of the hand
and fingers.   If by force we extend the fingers, we see
that at a certain  point  they  come spontaneously and
suddenly as the movement of a  spring into a condition
of forced extension, at the same time that the flexion in-
creases in the radio-corpal articulation, and the limb re-
mains  in this new posture  for an indefinite period.  If
we then induce flexion, we at  first  experience a certain
amount of resistance, then suddenly again the flexion of
the fingers is spontaneously completed, and the hand is
slightly straightened;  thus the primitive attitude is re-
produced.  Out of 14  patients in  the service of M.
Delasiauve, suffering from cerebral atrophy, I have ob-
served this  symptom twice, and I  have found it  once
with M. Charcot in one of his  patients who had cerebral
softening dating back thirteen years.
  The vicious  attitudes produced  by  permanent con-
traction  in  hemiplegics are very  variable;  they  are
principally remarkable in the upper extremity.  If we
consult the  table in  which are noted the 31 cases of
rigid hemiplegia upon which this description  is based, 
84
we see, as I have said  above, that the shoulder is ele-
vated 15 times, lowered 10 times, in an indifferent posi-
tion 6  times;  that the  arm is  adducted 12 times,  ab-
ducted once, in an indifferent position 18 times; that it
is rotated inward 18 times, and that 13 times it does
not show any tendency to  rotation in either direction.
We see, besides, that the elbow is flexed 27 times, ex-
tended 3 times, in an indifferent position once; that the
forearm is  pronated 24 times,  supinated 7 times; that
the hand is flexed 16 times, extended 15 times, in an in-
different position 10 times; finally that  the fingers  are
flexed 28 times, extended 3 times.
  The  hand being always in a determined  position  of
pronation or of supination, and the fingers being always
either permanently  flexed or extended, we may arrive
at the  following conclusion: that of all the muscles of
the economy, those of the forearm are most often gener-
ally affected  with permanent  contraction in cases of
hemiplegia; hence the precept that we should examine,
in cases of softening or hemorrhage of the brain, dating
back for some time,  whether the movements of rotation
which we give to the radius are  equally easy in both
directions,  and whether the fingers can be completely
straightened or flexed without difficulty.
  Many  of these partial  attitudes which I have just
pointed out are habitually grouped  together  and pro-
duce deformities of the whole  region, the various ele-
ments  of which do not appear related to  one another
according to invariable rules, but  in which it  is never-
theless possible, amid very numerous exceptions, to re-
cognize certain general types.   In order  to characterize
these types, we should take as a starting point the par-
tial deformities, which  are never  absent, that is to  say
the condition of pronation or supination of the forearm,
and the state of flexion or extension of the fingers.  We 
85
may thus artificially create four varieties, which, accord-
ing to our observations,  are  distributed in the follow-
ing manner:  out of 31 cases of rigid  hemiplegia, we
find 22  times pronation with flexion  of the  fingers,
twice pronation with  extension of the  fingers, 6 times
supination with flexion of the  fingers, once supination
with extension of the  fingers.   Adding  now thejcondi-
tion of extension or of flexion of the articulation of the
elbow, we should double the  number of these varieties,
but clinically we have only  been able  to find the six
following varieties:

Flexion of the elbow, pronation and flexion of the fingers, 18 times.
              "   pronation and exten. of the fingers, 2  "
              "   supination and flexion of the fingers, 6  "
              "   supination and exten. of the fingers, 1  "
Extension of the elbow, pronation and exten. of the fingers, 3  "
Indifferent position of the  elbow, pronation and  flexion of
    the fingers,.................................... 1  "-

   An examination of  this table shows that there is no
need of  thus multiplying the varieties, and that for the
clinique we should recognize one great type,  the type
of flexion characterized by the simultaneous  flexion of
the elbow and the Angers, or, in the absence of rigidity
in the elbow joint, by the simple  flexion of the fingers.
We will also place in this type of flexion, the cases in
which the fingers being extended the  flexion of the
elbow is so pronounced,  that the angle formed by the
arm and the forearm is less than 135 degrees.
   Another type much less frequent will be characterized
by the  complete  extension of the elbow, whatever  be
the condition of  the fingers, or 1 >y the extension of the
fingers, provided that  the angle of flexion of the elbow
be more than 135 degrees.
   By consulting the table in which the angles of flexion
of the elbow are indicated, we  will see that the type of 
86
flexion is observed 26 times, while we only meet with
the type of extension 5 times.
  The condition of pronation or of supination  of the
forearm adds two varieties for each of these types : thus
clinically, we may admit four forms of deviation of the
upper extremity in hemiplegias with tardy contraction,
and these forms are observed in the following order of
frequency:
    Flexion with pronation,......................20 times.
      "    "  supination,..................... 6  "
    Extension with pronation,.................... 4  "
       "     "  supination,................... 1  "
  We will describe only the first form, which is by far
the most frequent.   In  this  form we  have seen the
shoulder lowered 9 times and elevated 7 times; in four
cases  only, was the shoulder of  the diseased side on the
same  horizontal line as the other.  The arm is  usually
drawn to the body, either by its weight, or by a slight
contraction of the pectoralis magnus; it is in this form
that we  have met the  only case  of abduction  of the
arm which we have observed.  In the 20 cases in which
there  was flexion and pronation, we have 11  times seen
the hand flexed with the fingers; once the hand flexed
while the fingers  were  extended;  once  the hand  ex-
tended while the fingers were flexed; finally, the fingers
were flexed 7 times while the hand was in an indiffer-
ent position.   In the case where the flexion of the elbow
was most pronounced, the angle formed by the forearm
with the arm was 30 degrees.
  In  this form  of flexion with pronation which  we
usually meet in hemiplegics, the arm is  drawn  toward
the trunk, and, owing to the rotation of the humerus,
the forearm is applied against the body;  the hand,
usually flexed as well as the fingers, is, according to the
degree of flexion of the elbow, pressed  against the ab- 
87
domen or against the thorax, and the parts in contact
vary according to the degree of pronation of the fore-
arm.  In a first degree, the hand is in contact with the
trunk by its palmar surface; in the second degree, by
its  radial edge; in the third, by its  dorsal aspect; in
the latter  case, the elbow is more or less carried for-
ward.
  In the type of extension, we can still find these three
degrees of pronation.   The third was not shown by any
of the patients referred to  in the table, but it was very
marked in the  case of  a woman in the service of M.
Charcot, who has recently died from an old softening.
In  this woman, the left  forearm was  completely ex-
tended, the hand flexed at  a right angle, and the fingers
firmly folded up in the palm.   The movement of  rota-
tion had carried the  hand directly outward, the ulnar
edge was in front, the radial behind, and this deformity
had been increased by a rotation of the arm which had
brought the olecranon  directly in front.  In the case of
this woman, whose medulla oblons;ata I have shown to
the Anatomical  Society,  the descending degeneration
had advanced  to  an  extent which we rarely find: the
secondary sclerosis of the cord was visible as far as the
inferior extremity of  the left  lateral  column, and  I
should add that the sclerosis reached the meninges to-
wards the middle of the dorsal region, instead of form-
ino- a little band, completely  surrounded by healthy
white substance.  I was then too absolute in stating in
a former part of this work, that no fibre of the decus-
sating  encephalic  fasciculus came in  contact  with the
pia mater.   In this woman, besides, the flexion of the
fingers was such, that the nails in growing cut the skin
of the palmer surface.  This occurrence, which is not
very rare, and which has already been noticed by Todd,*
*Loc. cit., lecture x. 
88
produces very painful  ulcerations which secrete an  in-
fectious discharge; great care should therefore be taken
of the hands and nails; it is prevented by permanently
placing in the palm of the hand a  roll of bandage,
which is  sufficiently held there  by the  contraction of
the fingers.
  I should  say in conclusion of what has reference to
the deformities of the  hand, that when the hemiplegia
commences, before the complete development of the indi-
vidual, and above all in infancy, the hand which is usu-
ally flexed,  instead  of showing  the  flexed  joints  by
sharp angles, presents on the  contrary upon its  dorsal
portion a regularly convex surface  which continues
without interruption from the forearm to the last pha-
langes. This peculiar form is doubtless the result of
an  atrophy  of the osseous  tissue and of the articular
prominences; an  atrophy in  which the  subcutaneous
cellular tissue does not participate.  This character is
sometimes sufficient, in the absence of any history, to
distinguish a former softening in  the adult from unilat-
eral cerebral atrophy consecutive to some lesion which
has destroyed a more or less considerable portion of one
hemisphere  during infancy.*
  I shall pass more  rapidly over the  tardy contraction
of the lower extremity in hemiplegics, and the deformi-
ties which are its consequences.  I  shall only state that
out of 32 cases of hemiplegia of long duration I have
found muscular rigidity in the  pelvic extremity only
14 times; the hip was rigid 10 times, 4 times flexed, 6
times extended.  The  flexion was 3 times accompanied
by abduction;  the extension was 4 times accompanied
by  abduction.  The knee was found  flexed 10  times;

  * Consult upon this subject a memoir presented by M. Cotard to
the Society of Biology in 1865 :  Note sur quelques eas d'atrophie
cerebrale; de l'attitude des membres paralyses dans cette affection. 
89
22 times the limb was in the axis of the thigh without
any appreciable rigidity.  These 10 cases of flexion of
the knee coincided 5 times with extension of the hip, 4
times with flexion and once with relaxation of the coxo-
femoral articulation.  The foot was found rigid and out
of its proper position 11 times, 9 times presenting the
type of talipes equinus and twice that of talipes talus.
Of the 9 cases of talipes equinus, 5 were accompanied
by flexion of the knee. The  2 talipes talus  coincided
with  a  considerable degree of flexion in  the femoro-
tibial articulation.
   At what  period and in what manner is this tardy
contraction developed in hemiplegics \
   This is a question which has scarcely been proposed,
and which is far from having  been decided.   Todd,
who has distinguished so carefully between the preco-
cious  and the tardy  rigidity, says that he has  met
with the latter one year after the apoplectic attack, and
he quotes from M. Andral a case where the contraction
came  on three months after the commencement  of the
hemiplegia.   We may see that in  one  patient,  whose
case is referred to in the table, the flexor muscles of the
fingers were rigid at the end of four months, but in her
case the rigidity had already existed for some time.  We
have had an opportunity, in the case of this woman, to
follow the development of the disease from its com-
mencement,  and her case is interesting in more than one
respect.  She was suddenly attacked  at the age of 66
years, with  apoplexy with complete loss of conscious-
ness and left hemiplegia, without having presented any
prodromic symptoms.   The following day the intelli-
gence had entirely returned, the paralyzed muscles were
flaccid and there was no fever.  The temperature of the
rectum varied from morning to  evening between 100°
and 98.9°.   At  the end of eight days the fever came 
90
on; the temperature went up to 101.1° ; there was ex-
citement with  delirium, and   the  paralyzed muscles
became rigid.   Two days after, the temperature  came
down to 99.6°; the intelligence was restored and the
muscles had become flaccid again.  From this time the
general symptoms  disappeared, but the paralysis re-
mained.  Three weeks  after the commencement of the
illness the fingers were semi-flexed, but could be easily
extended: however, forcible extension appeared a little
painful.  Two months after the attack the flexion of the
fingers was more pronounced, and quite a marked resist-
ance was experienced when we tried  to  extend them,
an  operation which seemed  to produce  considerable
pain; the forearm was slightly pronated,  and resisted
slightly any movements of supination which we commu-
nicated to it; it presented a very slight amount of flex-
ion ; we were able to increase this flexion without hurt-
ing the patient, but when we  afterwards extended it,
we observed that  after having  easily reduced it to its
former position we  experienced a sudden resistance, of
such a kind that the extension could only be completed
by an effort which was painful to the patient.  At this
time there were no cerebral symptoms and no fever.
   In this case we see a precocious contraction connected,
as the delirium  and fever indicate, with slight symptoms
of secondary encephalitis;  then ^ve see  a contraction
become insensibly  developed, traces of  which we can
barely find at the end of three  weeks, and which is no
longer doubtful at the end of three months.   It is this
latter contraction, which  has since increased  while the
cerebral functions have returned more and more to their
normal condition, that we think should be referred to
the sclerosis secondarily developed in the  place  of the
degenerated fibres of the lateral column.
   This case also shows that if the muscles  of the fore- 
91
arm are the ones usually affected by tardy contraction,
it commences likewise in them.  This contraction comes
on gradually and insensibly; this is the reason why we
can hardly ever obtain from the patients information of
any value concerning the time of the appearance of this
symptom.  They know that at first their limb did not
offer any resistance to the movements communicated  to
it,  and that  at  a later  period  it  was fixed  in one
permanent attitude which  could  only be altered  by
a certain degree  of force, but the transition  between
these two conditions has been so  gradual that usually
it is impossible for them to tell, even approximatively,
the time of the commencement of the contraction. The
determination of this time is almost as  difficult for the
physician who is watching the development of the dis-
ease ;  so that he had better not give the result of  his
observations  except  after  quite long intervals, the
changes undergone by the muscles from  day to da}^ being
entirely inappreciable.   In the preceding case, the con-
traction was evident at the end of two months,  but it
already existed before this time, and I may state that,
having inquired into this question of a certain number
of patients, I think I may conclude  from  their  replies
that while the limb was flaccid during  the  first month,
it already presented a vicious attitude during the third
month.   It would then appear that the permanent con-
traction  habitually commences in the course  of the
second month.  It is plain that new investigations are
necessary to determine this point, as yet obscure, in the
symptomatology of hemiplegias.
  The contraction commences in the muscles of the fore-
arm ; generally the fingers are  flexed and the forearm is
pronated;  then, in most cases, the elbow becomes flexed,
and, while  the fingers curve more and more, the flexion
of the elbow progressively increases  in such a manner, 
92
that for a long time the attitude of the limb is changed,
showing it more every day.
  I have remarked that in the patient of whom I  have
just spoken the straightening of  the contracted parts
was painful from the commencement, even when a slight
effort sufficed to overcome the resistance of the muscles,
and then these explorations resulted in  momentarily in-
creasing the rigidity.  On the contrary, when  the con-
traction is  final, the muscles which we  extend  by force
oppose during a considerable time the movements which
we communicate to the limbs.
   Sometimes,  upon lifting  the contracted arm  of a
hemiplegic by the end of the fingers, we see the entire
limb agitated by a rapid trembling similar to that which
we produce by the same proceeding in  the  inferior  ex-
tremities of patients suffering from compression of the
cord.   I have only met with this symptom in the thoracic
extremity in  hemiplegia, and I think that we may con-
sider it as an exception.
   When the contraction has reached its complete devel-
opment, it may notwithstanding present  momentary
variations in its intensity under the influence of certain
circumstances, such as  emotions or pains along the
course of the nerves of the limb; in young women having
hemiplegia, we sometimes see the contraction  increase
during the menstrual period.
   I have already spoken of the action of chloroform
upon contracted muscles; I  shall also say some words
of electricity.   The  induced currents which usually
produce in the flaccid muscles  of hemiplegias of short
duration, slighter contractions than  in  the  normal con-
dition,  produce on the  contrary a marked and  some-
times an exaggerated effect upon the  muscles affected
with permanent rigidity, even when they have under-
gone a certain  amount  of atrophy.   But when this 
93
atrophy affects unequally the different muscles of a limb,
we can see, as I have found in one case, that by apply-
ing the poles to the muscles which act against the devi-
ation, this deviation,  far from diminishing, on the con-
trary increases.   In this case,  no doubt, the  currents
traverse the  atrophied muscles and  influence their an-
tagonists  so  as to increase their already predominant
power.
   Once  established, the tardy contraction may last for
long years, often during the whole life of the individual,
but sometimes it seems to diminish.   Then however, the
muscles cannot undergo a sufficient amount of extension,
and the articulations  present certain alterations which
hinder any complete straightening, and the vicious at-
titudes remain; they are then passive.   One might also
ask whether we  can hope for a cure of the hemiplegia
when the  muscles are already affected by tardy contrac-
tion.  I  do not know any fact which can encourage this
hope, and the patients sometimes are deluded with re-
ference to this subject.
   Voluntary motion is not always totally abolished in
the paralyzed limbs of hemiplegics, but the contraction
limits and renders more  difficult the muscular actions
which are still under the  influence of the will.  If the
rigidity diminishes, then these movements recover more
liberty,  and  such  a patient who is always  to remain
impotent  imagines that he sees in this modification the
commencement of his cure.
   Some symptoms which have a very great analogy to
these which we have just studied are observed in certain
diseases of the cord which are accompanied by second-
ary sclerosis  of the lateral columns, and especially in
cases of compression of that  organ.   During the first
period which correspond to  the granulo-fatty degenera-
tion of the tubes, the  paralyzed muscles remain flaccid; 
94
then, at a more or less advanced period, the contraction
appears, the muscles  atrophy and the lower limbs' as-
sume permanent attitudes which  it is difficult to over-
come.   In some  cases,  however, the muscles remain
flaccid and the limbs are swollen  with an elephantiasic
oedema; this is  on account of the softening of the in-
ferior portion of the cord.   The phenomena of  excita-
bility, on the contrary, are observed in those cases where
the autopsy reveals a secondary descending sclerosis.  I
need not insist in detail upon these symptoms, which
have been very well described, especially by MM. Louis,
Cruveilhier, and Brown-Sequard,* nor upon the charac-
ters of the  contraction, for it is in every respect identical
with that of patients suffering from hemiplegia. I think
that, in order to explain  these  facts, it is not necessary
to consider that there is  an accumulation of nervous in-
flux in the inferior part of the  cord; we  have here an
irritation  of  this  inferior extremity, as M. Brown-Se-
quard thinks; but this irritation has its  anatomical
cause.
  A woman in the wards of M. Charcot, suffering from
an ulcerated cancer of the breast,  the commencement of
which dated back for six  years, was suddenly  seized
with violent, lancinating pains in the lower extremities;
for two  months,  however,  the  patient  had enough
strength  to be able to walk with the assistance of a
cane.  At  the end of this time, she became unable to
stand and was obliged to keep her bed;  her legs were
flaccid and inert.   About seventy days after  the time
when she became bedridden, her limbs commenced to be-
come flexed, and this flexion, slightly pronounced at first,

  * Louis,  Recherches d'Anatomie Patholog.   Cruveilheir, An-
atomic Patholog. du corps humain.  Brown-Sequard, Lectures on
the diagnosis and treatment of the principal forms of paralysis of
the lower extremities: London, 1861. 
95
progressively increased.  The legs were strongly flexed
upon the thighs, the thighs were in a state of adduction
with  a certain  amount of flexion.   A considerable
amount of resistance was experienced when we  endeav-
ored to extend the contracted limbs, and these attempts
were very painful to the patient. The sensibility was
preserved; there was a certain degree of hyperaasthesia
and some pains in the lumbar regions, with a very pain-
ful feeling of constriction around the abdomen and at
the base of the lungs.  Although purulent  during the
last few days of life the urine remained acid until death.
The patient died the eighteenth of January, 1866, about
six months after the commencement  of  the paralytic
symptoms.   The autopsy  showed that the cord  was
compressed" by  a  cancerous tumor of the  first dorsal
vertebra and  by a purulent effusion in the canal, ex-
tendino* from the seventh cervical to  the tenth dorsal
vertebra.  Independently of the ascending degeneration,
in the cervical region, we found throughout the whole
substance of the lateral columns  of the lumbar enlarge-
ment, a considerable number of myelocytes and embryo-
plastic nuclei.  The  muscles of the posterior portion
of the thigh showed no transverse stria?, either by direct
or oblique light; the primitive fibres were studded with
 numerous fatty granules, (resisting the action of acetic
 acid;)  the nuclei of  the  sarcolemma were extremely
 numerous.
   In this case  also, the contraction  commenced about
 two months after the debut of the paralysis, precisely
 at the period when the proliferation of connective tissue
 becomes developed in the secondarily degenerated col-
 umns.   In another case of compression of the  cord, by
 Pott's disease which I examined at the hospital Sainte-
 Euo-enie with M.  Triboulet, death having  taken place
 one3 month and a half after the commencement  of the 
96
 paralysis, I noticed that the muscles were flaccid all the
 time, and at the autopsy I found only a fatty degenera-
 tion of the lateral columns below the seat of the lesion
 without any hypergenesis of the elements of connective
 tissue.
   We see that the permanent contraction which is com-
 mon to  hemiplegias and  to  compressions of the cord,
 presents in both  cases the greatest analogy as  regards
 symptomatology; it is connected with an anatomical
 condition of the cord common to both  these affections,
 and does not become developed in  either case until  the
 time when the secondary sclerosis of the lateral columns
 commences.  I should add that the permanent  contrac-
 tion of the extremities is seen to have the same characters
 in primary sclerosis of the lateral columns, as is shown
 by a remarkable  case communicated by M. Charcot* to
 the Medical Society of the hospitals, as well as in certain
 cases  of diffused  sclerosis of the  cord, affecting in a
 greater or less degree these  same lateral columns,  ex-
 amples of which are to be found  in  a recent work pre-
 sented by M.  Vulpian,f to the same society.    Why
 then, since in all these cases we observe common symp-
 toms and common lesions, do we refer the contraction,
 in paraplegias, to the lesion of the cord; in hemiplegias,
 to a lesion of the  brain ?
  This cerebral origin of the tardy contraction is not
 proved;  it was  admitted  at a time  when  we  were
 ignorant of the secondary alterations  of the cord, and
 when we considered softening as a chronic encephalitis.
 It is based therefore upon a double error.
  If we admit that the tardy contraction in  hemiplegia
results from a secondary sclerosis of the lateral columns,

  *Hysterie avec contracture sclerose des  cordes lateraux, 1864.
  f Note sur les scleroses en plaque de la moelle epiniere, 1866. 
97
 we shall have a  reason for certain facts which would
 otherwise  appear inexplicable.  Thus, in compressions
 of the cord, the contraction of the inferior extremities is
 stronger than in hemiplegias, because in the hemiplegia
 the secondary sclerosis is only developed in the sitnation
 of one portion of the decussating encephalic fasciculus,
 while in the compression of the cord it occupies not only
 this entire fasciculus, but a certain number of long; com-
 missural fibres besides.  Thus, also, in hemiplegias, the
 superior extremity is most often contracted,  and is so to
 a greater degree than the lower extremity, because the
 decussating encephalic fasciculus is richer  in nervous
 fibres in the cervical region than in  the  lumbar region,
 where it terminates in a point; the sclerosis, which is
 substituted for this  fasciculus  throughout its whole
 length, will therefore be more developed at the level of
 the origin of the nerves of the arm than at the point of
 departure of the nerves of the pelvic extremity.  Thus,
 also,  may we not  say that if the thoracic extremity is
 strongly contracted, while the head is not  perceptibly
 deviated, that it is because the  rotator muscles of the
 head are partly supplied with  nerves from the spinal
 accessory which arises from the lateral portions of the
 bulb and from the  superior  extremity of the  cord at
 points which are not influenced, by the secondary sclerosis,
 since, in this region, it is limited to  the internal part of
 the anterior pyramids?  But it might be objected  that
 all  hemiplegias are not  accompanied by contraction.
 We can answer this objection by stating that there are
 certain cerebral lesions, as for example superficial lesions
 of the convolutions, which  are capable of producing
hemiplegia, and which do  not determine secondary de-
generation.
  We might  refer  the  tardy contraction to other
causes, such as an  alteration  in the structure of  the
       a 
98
muscles due to the prolonged inertia,  but we find com-
plete hemiplegias which always remain flaccid;  or to an
atrophy of the  muscles, resulting either from rest or
from some other cause,  but the contraction is  found in
9 out of 31 cases, without  there having been any atro-
phy of the muscles, and in one case I have found a  cer-
tain amount of atrophy of the muscles of the arm, with-
out any contraction.  There are  in reality alterations in
the  structure  of contracted muscles  coinciding with a
fawn-colored appearance of their tissue;  the transverse
striae are often less  marked than usual,  sometimes  ab-
sent, the substance of the primitive  fasciculi is more
or less granular,  studded  with fatty and pigmentary
granules;  the nuclei of  the sarcolemma increase  in
number; 16 times out of 30  the size of the muscles di-
minishes.*  If these alterations are the proximate cause
of the  contraction, of which we  have no proof, nothing
authorizes us to  consider them as developed without  the
action of the central nervous  system.f
  Independently of the contractions,  one quite impor-
tant symptom seems to me  to  be attributable to  de-
  * Out of 30 cases of hemiplegia with contraction, I have 5 times
observed an increase in size of the paralyzed limb, but this hyper-
trophy no doubt depended  upon the cedema of the subcutaneous
tissue rather than upon an alteration of the muscles.
  f M. Charcot has  called my attention to a very curious peculiar-
ity of paralyzed and contracted muscles in hemiplegias of long du-
ration :  this is the absence of post mortem rigidity.  At the autopsy
the limbs of the healthy side present a perfect rigidity; on the  con-
trary the muscles which were contracted  during life are entirely
flaccid.   However, numerous examinations made at different hours
after death have  shown that usually the diseased muscles do not
escape the post mortem rigidity, which is manifest in them almost
immediately after death, and only for a very short time.  The ab-
sence of cadaveric  rigidity is seen also in infantile paralysis.  It
would be curious to  find out whether putrefaction is  developed
more rapidly in the paralyzed limbs. 
99
scending  degenerations,  and  more  especially to  the
secondary sclerosis of the bulb.  I refer to the epilepti-
form attacks and to those which are evidently epileptic,
which we  often  meet with  in subjects attacked with
hemiplegia during infancy, and which are not infrequent
in old persons suffering from softening, and in which we
find at the autopsy considerable  atrophy of a peduncle,
of the pons and of the bulb.  I must confess that  this
hypothesis does not as yet appear to me  susceptible of
a rigorous  demonstration;  but  it seems  to me  to be
true,  because in one patient suffering from an intense
sclerosis of the bulb  from compression of  that organ,
the epileptic fits  were very strong  and very frequent,
and because when we saw him  sometimes, a  few mo-
ments previous to an  attack, the  contraction markedly
increased in the paralyzed limb.
   We very often  see in cases of hemiplegia an increase
in the size of the nerves, with vascularity and increased
thickness of the envelope  of connective tissue, often
also with a deposit of fatty globules in its interstices.
I  do not  know whether this kind  of hypertrophous
neuritis, to which M. Charcot, and after him M. Cornil,*
have called attention, depends upon  secondary  degener-
ation of the cord, or whether it is not solely the result
of inertia;  at all events, it  seems to be connected with
those pains, often quite  severe, already pointed out by
Remak, which the hemiplegics feel in the paralyzed  arm,
pains which are increased by pressure along the  course
of the nerve, and which are often alleviated by the ap-
plication of a blister, as M. Charcot has  several times
proved.
   As for the alterations  of  nutrition, such  as the  atro-

   * Note sur les lesions des nerfs et des muscles liees a la contrac-
ture tardive et  permanente  des membres dans les hemiplegies.
(Comptes-rendus de la Societe de Biologie,  1863.) 
100
phy of the compact tissue of bone, the squamous con-
dition of the skin,  &c, I  doubt whether they can be
referred  to  the secondary degeneration  of  the cord.'"'
This  degeneration, besides, does not  modify in any re-
spect the phenomena of calorification which we observe
on the side of the paralyzed limbs.   The paralyzed hand
is always the warmer, even at a time  very distant from
the commencement of the symptoms,  and we sometimes
find considerable variations in the temperature of the
two sides of the body.f
  The examination of five patients, made with this ob-
ject in view, has furnished me with the following results:
Age.	Date of commencement.	Paralyzed hand.	Healthy hand.
70 years.	Several years.	95.3°	89.6°
42 "	14 months.	95c	89.9°
72 "	12 years.	99.3°	98.6W
65 "	5 "	97.8°	97.5°
51 "	14 months.	97.1°	95°
  Thus far I have only spoken of the symptoms of de-
scending degeneration; the secondary ascending scleroses
do not appear to betray themselves by a single symptom.
We  might however  imagine that this  sclerosis of the
posterior columns could  determine the  phenomena of
motor ataxy in the upper extremities, but it is not so;
and this is explained by the separation which the inter-

  * As for the articular  alterations, which are of frequent occur-
rence, they depend evidently only upon the immobility, and differ
in no respect from those which are produced by that cause, outside
of any influence of the nervous system.  Upon this subject con-
sult Teissier, Memoires sur les  effets  de  I'immobilite  longtemps
prolongee des articulations.  Lyons, 1844.

  f According to M. Routier,  there should be a  dimunition of the
temperature  of the paralyzed side immediately after the attack.
The elevation of the temperature only comes on at the end  of
twelve or twenty-four hours.  (A. Routier, Theses.   Paris, 1846.) 
101
mediate posterior sulcus establishes between the centri-
petal fibres of the pelvic and those of the thoracic ex-
tremities.   Even in cases of compression of the cord in
the cervical region,  when  the  secondary sclerosis also
affects the external fasciculus of the posterior column, it
is probable that we should not find symptoms of ataxy.
In fact, ataxy supposes the  destruction  of a  certain
number of nerve tubes, and secondary sclerosis does not
appear to destroy the healthy tubes which are plunged
into its interior; it  only deforms them and may exalt
their activity, but does not annihilate them.
  In conclusion, I will state that these  cases which I
have gathered  at Sainte-Eugenie, with M.  Triboulet,
and two others which I have studied at the Salpetriere
with M. Charcot, warrant me in affirming that a cure is
possible, even when the columns of the cord seem to
have undergone secondary degeneration.  In these  five
cases there was  complete paraplegia due to the compres-
sion of the cord by Pott's disease.  In  four cases, sensi-
bility and motion have returned in all their integrity;
in only one, motion, without having recovered its entire
liberty, nevertheless allows the patient to walk.  In this
case the paraplegia was flaccid; in the others it was ac-
companied with contraction.  We may therefore  con-
clude  that the nerve tubes of the cord may be regener-
ated like those of the peripheral nerves, not only in the
child but also in the adult, and even when the degener-
ated fasciculi have already been the seat of a hyper-
genesis of nuclear elements. 
 
SECONDARY DEGENERATIONS OF THE SPINAL CORD.

                 EXPLANATION  OF THE PLATE.

  Fig. 1.  Secondary degeneration of the mesocephale in an old
softening of the right hemisphere.  Atrophy and gray color of the
right peduncle.  Flattening of the Pons Varolii on the right side.
Atrophy and gray color of the right anterior pyramid.  Gray dis-
coloration in the left lateral column below the bulb.

  Fig. 2.  Histological lesions in  the first stage of secondary degen-
erations.
       a. Granular bodies.
       b. Vessel with fatty granulations accumulated in the lym-
     phatic sheath.
       c. The same granulations, but more numerous, in the lym-
     phatic sheath at the point of bifurcation.

  Fig. 3.   Histological  lesions in the later  stages  of secondary
degenerations.
       a.  Myelocyte.
       b. Vessel with numerous nuclei and very few fatty granula-
     tions in the sheath.
       c. Amyloid body.
  Fig. 4.  Section of the cord in the dorsal region in a case of old
secondary degeneration of the posterior columns.
       ac  and a'c. The posterior columns.
       be and 5V. The portion of these columns  where the  tubes
     are scanty, separated by the connective tissue of new forma-
     tion.
  Fig. 5.  Sections  of the  cord  in a case  of  old lesion of the  left
hemisphere.  The parts colored black indicate the points of loca-
tion of the secondary degeneration.
       a.  Cervical enlargement.
       b.  Dorsal region.
       c. Lumbar enlargement.
  Fig. 6.  Descending degeneration in a case  of compression of the
cord at the upper part of the dorsal region. 
104
       a.  Section made a few centimeters below the compression.
       b. Inferior portion of the dorsal region.
       c. Lumbar enlargement.
  Fig. 7.  Ascending degeneration in a case of compression of the
cord at the lower part of the dorsal region.
       a. Section made a few centimeters below the compression.
       b. Superior portion of the dorsal region.
       c. Middle of the cervical enlargement.
       d. Superior portion of the cervical enlargement.
  Fig. 8.  Secondary degeneration  in a case of compression of the
cauda equina.
       a. Inferior portion of the lumbar enlargement.
       b. Superior portion of the lumbar enlargement.
       c.  Middle of the dorsal region.
       d. Middle of cervical enlargement. 
SECONDARY DEGENEKATIONS  OF  THE  SPINAL  COED.          Cn. Bouchakd.
left.
left.
right.
right.
right.

right.

left.
right.

right.

right.
left.
left.
right.
right.
right.
left.
left.
right.
right.
left.

right.
left.
right.
left.
left.
right.
left.
left.
left.
left.
right.
right.
m
©   a
feeble.
quite strong.
quite strong.
flaccid.
strong.

very feeble.

very feeble.
feeble.

Triceps rigid

very strong.
strong.
feeble.
very elev.
lowered.
lowered.
very strong.
quite strong.
feeble.
feeble.
strong in the
  fingers.
quite strong.
quite strong, lowered.
strong.      elevated
lowered.
lowered.
lowered.
lowered.

lowered.
elevated.
lowered.
elevated.
lowered.
lowered.
ARM.
ADDUCTION.
slight.
slight.
slight.
very slight.

very slight.
quite strong.
elevated.
strong.
feeble.
quite strong.
feeble.
very feeble
except the
  fingers.
feeble.
quite strong.
quite strong.
feeble.
quite strong.
strong.
very feeble.
slight.
slight.
abduct.
elevated. '......
elevated, adduct.
lowered,  j......
elevated. ......
elevated.
lowered.
elevated.
lowered.
elevated.
adduct.
adduct.

adduct.
rotat'n.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
inward.
  (1)
CIRCTTM
30 | 30
19  20
24 | 25
32 | 34
    (3)

27 | 29

17 | 17
24 | 24
21 | 23
FOREARM.
flex'n.  rotat'n. CIRfU'M
THIGH.
100'
135'
 45'
(2)
70'
135'
150'
110'
extens.
26  90°
14  70°
2(> 130°
28:120°
24!  30°
lGJextens.
27 extens.
21,150°
20 130°
18!  90°
17j  30°

24 135 °
22 150°
25 135°
24 135°
20'
pron. 1st.
pron. 1st.
supina.

pron. 2d.

i pron. 1st.

sup. slight.
pro. slight.

pron. 1st.

pron. 1st.
pron. 2d.
sup. slight.
pron. 1st.
supina.
proD. 1st.
pron. 1st.
pron. 1st.
 26|flex. slight.
 20|..........
 22lext. slight.
 27!..........
... flex, strong.
flex, strong,
flex, slight.
flex, strong,
24
25 flexion very
     slight.
18
20
19 | 21
pron.  2d., 18
pron.  1st, j 18
pron.  2d. 16

pron.  1st. 123
pron.  2d. 21
pron.  2d. 21
pron.  1st. 21
pron.  2d. 17
flexion.
flex, strong.
ext. slight.
flex, of the
 1st phal.
flex, quite
  strong.
extension.
flex, of the
 1st phal.
flex, strong.
flexion.
flexion.
extens. very
  slight.
pron.  2d.
supina.
supina.
supina.
pron. 1st.
pron.  2d.
pron. 1st.
21
22;flexion.
23 j ext. slight.
23 flexion.
23 flex, slight.
20 flexion.
22.........
flexion.
flexion.
flexion.
flexion.
flexion.
flexion.
flexion.
extens. very
   slight.

flexion.
flexion.
very slight
 flexion.
flex, slight.
flexion.
flexion.
flex, slight.
flexion.
flexion.
flexion.
flexion.
flexion.
flex, slight.
extension.
flexion.
exten.
exten.
exten.
exten.
flexion
flexion
flexion
exten.
flexion
exten.
abduct,  semi-flexed, equin. slight.
abduct.
abduct.
abduct.
abduct.
flexion.
flexion.
very flexed,
flexion.
flexion.
flex.
ab. slight flex, slight.
abduct,  flexion.
equin. slight.
equin. very
  slight.
equin. quite
  marked.
equinus.
slight talus.
equin. slight.
talus.
equin. slight.
equinus.
equinus.
     Nota.—In this table, comprising the analyses of 32 old cases of hemiplegia, the blanks indicate an indifferent position of the
articulations owing to muscular flaccidity.
     (1) In  the columns giving the circumference of the arm and that of the forearm, the  numbers indicate centimetres, the first
refering to  the paralyzed and the second to the healthy arm.
     (2) In  this case all the  articulations were in an indifferent position; it is the only case  of flaccid hemiplegia.
     (3) Neither the circumference of the arm nor that of the forearm are indicated, as it was  imposible to know whether the par-
alyzed limb was atrophied,  the patient having suffered amputation of the non-paralyzed limb. 
 
 Archives ^enerdies de xnedeciaeH0 de Septenibre 1866,pa^e 3oo .
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