THE SPINAL CORD IN POTT’S DISEASE. 
BY 
CHARLES W. BURR, M.D., 
PATHOLOGIST TO THE ORTHOPEDIC HOSPITAL AND INFIRMARY FOR NERVOUS 
DISEASES, PHILADELPHIA, AND TO THE STATE HOSPITAL FOR THE 
INSANE, NORRISTOWN. 
FROM 
THE MEDICAL NEWS, 
November n, 1893. [Reprinted from The Medical News, November io, 1893.] 
THE SPINAL CORD IN POTT'S DISEASE} 
By CHARLES W. BURR, M.D., 
PATHOLOGIST TO THE ORTHOPEDIC HOSPITAL AND INFIRMARY FOR 
NERVOUS DISEASES, PHILADELPHIA, AND TO THE STATE 
HOSPITAL FOR THE INSANE, NORRISTOWN. 
In considering the pathology of the nervous 
symptoms of caries of the spine we need pay but 
little attention to the morbid anatomy of the bone- 
disease. We may define Pott’s disease pathologi- 
cally as an osteitis, usually tuberculous, of the bodies 
of one or more vertebrae, resulting in caseous 
necrosis and caries. Rarely the primary cause is 
syphilis and not tuberculosis. The bone-disease 
may be secondary to inflammation in neighboring 
structures. Finally, sometimes in septicemia sec- 
ondary abscesses occur in the vertebrae. It is a curi- 
ous fact, and one for which so far as I know no sat- 
isfactory explanation has been given, that this osteitis 
is most likely to occur in the dorsal region. The 
explanation sometimes offered that this region is the 
most exposed to injury does not explain, for the 
causal relation of trauma to Pott’s disease has not 
as yet been positively proved. 
The conditions mimicking Pott’s disease—malig- 
1 Read at the October meeting of the Orthopedic Section of 
the College of Physicians, Philadelphia. 2 
nant tumors of the vertebrae and aortic aneurism— 
we may dismiss without further mention. 
The first question for our consideration is : Upon 
what do the nervous symptoms depend ? Are they 
caused directly by the angular curvature and the 
consequent narrowing and angulation of the canal? 
In the great majority of cases, no. It is, of course, 
true that if a carious vertebra suddenly breaks down 
and fragments of bone are driven forcibly against 
the cord, or if the odontoid ligament gives way, 
we will find sudden, severe, and even fatal nervous 
symptoms; but ordinarily, even if the diameter 
of the vertebral canal be diminished by the sud- 
den breaking down of a vertebra, the cord slips 
behind the projecting bone and escapes very serious 
compression. In by far the greater number of cases 
the nervous symptoms are due to inflammatory 
changes in the dura causing pressure upon, and 
later, organic changes in the cord and nerves. So 
soon as the osteitis has progressed far enough to 
cause a breaking down of the posterior surface of 
the body of a vertebra and ulceration of the poste- 
rior common ligament, and consequent communica- 
tion with the loose tissue filling up the epidural 
space, inflammatory changes due to direct contiguity 
of tissue arise in the latter and soon appear on the 
external surface of the dura, ending in a pachy- 
meningitis. When this process has progressed far 
enough to produce pressure upon the cord this 
organ, according to Hoffa,1 becomes edematous 
1 Albert Hoffa: Transactions American Orthopedic Associa- 
tion. Fifth Session. Washington, 1891. 3 
from the interference with the flow of lymph and a 
stasis of the fluids of its tissue. The retained lymph 
acts not only mechanically but also as a poison, 
producing at first softening of the cord with, at the 
same time, an increase of the connective tissue, 
which, when sufficient, causes sclerosis. The same 
is true of the peripheral nerves at their points of 
exit from the dura. Edema is of necessity present. 
As to the poisonous effect of retained lymph we 
need further investigation. 
As the time at which communication is established 
between the diseased bone and the canal is, as one 
might say, accidental, or, rather, depends not so 
much upon the amount of bone-tissue diseased as 
upon the situation of disease in the body and the 
direction of its progress, it follows, as is well-known, 
that nervous symptoms, spasmodic abdominal pain, 
numbness or tingling in the extremities, alteration 
of the knee-jerk, paralysis, or indeed all of the symp- 
toms referable to the cord, may precede deformity 
or, indeed, any sign of bone-disease. The reverse 
is also true. There may be severe bone-disease and 
marked angularity without nervous symptoms. 
The liability to nervous symptoms varies with the 
region of the spine affected. Bouvier1 found only 
five paraplegias among thirty-eight cases of lumbar 
caries; Coudroy de Laureal only one paraplegia 
among fifty-nine similar cases. Among fifty-six 
cases of dorsal caries, on the contrary, Bouvier 
observed thirty-eight cases of paraplegia, and Cou- 
droy nineteen cases among seventy-seven in the same 
1 Quoted by Mary Putnam Jacobi. Keating’s Cyclopedia of 
the Diseases of Children, vol. iv, p. 646. 4 
locality. The reason of this greater frequency of 
paraplegia in dorsal disease is not difficult to find. 
The dorsal region is the most liable to severe de- 
formity, and to abscesses with pent-up pus, and is 
normally the narrowest part of the spinal canal. 
The inflammation of the dura may be either 
simple or purulent. If simple, the external surface 
of the dura is reddened, with here and there patches 
of lymph. So long as this condition persists there are 
few or no severe nervous symptoms. If the inflamma- 
tion be purulent, there is pus, caseous material, and 
organized inflammatory products. The thickening 
varies much, sometimes amounting to half an inch, 
and may surround the cord, or occupy one side, or be 
irregularly distributed, with nodular or even fungoid 
growths scattered here and there. Adhesion to the 
bone soon takes place. Commonly, the thickening 
and adhesion occur first and are greatest in the ante- 
rior portion of the dura, and hence motor cord- 
symptoms usually precede sensory ones. The pachy- 
meningitis is usually confined to the neighborhood 
of the diseased bone, but may extend far beyond 
its limits. Ordinarily, the inner surface of the dura 
and the pia-arachnoid escape inflammatory changes 
till late in the disease, even though the cord is 
seriously disabled. This being so, we are able to 
say that the changes in the cord are not due to a 
tuberculous process in it, but to the mechanical 
effect of pressure and possibly the irritant effect of 
retained lymph, as mentioned. When the pachy- 
meningitis invades the inner surface and the pia- 
arachnoid, another element is added to the destruc- 
tive process. 5 
The pressure of the thickened dura affects not 
only the spinal cord but also the peripheral nerves 
at their points of passage through it, producing 
Gowers’ “ root symptoms ” and “ cord symptoms.” 
Which set of symptoms predominate will, of course, 
depend upon whether pressure is greatest on the 
nerve-roots or on the cord, and also upon which 
part of the periphery of the cord is most involved. 
As a fact, “ root symptoms ” vary much in inten- 
sity. There may be simply pain in the course and 
distribution of the affected nerves or spots of anes- 
thesia, sometimes painful areas, muscular wasting 
and palsy and, curiously enough, sometimes herpes 
zoster. The cord symptoms, as I have said, will 
vary with the varying portions of the transverse 
area affected, and of.course with the variation in the 
longitudinal position of the disease. 
These symptoms are too well known to need 
repetition. In disease of the three upper cervical 
vertebrae, however, there is at times a curiously an- 
omalous distribution of symptoms. Instead, as might 
be expected, of paralysis of all four extremities, 
there may be palsy of the arms, without any affec- 
tion of the legs. According to Brown-Sequard the 
explanation is that the motor tracts for the arms are 
more superficial than those for the legs, and hence 
are earlier involved in a lesion advancing from the 
periphery. On the other hand, Vulpian maintains 
that just the opposite is true, or in other words, that 
in the cervical region the nerve-fibers for the arms 
have already entered the gray matter of the cord, 
while those for the legs are still in the lateral col- 
umns. He claims on this very account that the 6 
arm-fibers will be more compressed, owing to the 
less density of the gray matter as compared with 
the white. 
At autopsy in an advanced case the nerves are 
found much decreased in size, being sometimes mere 
threads. Under the microscope we find an increased 
amount of connective tissue, with an absence of 
many nerve-fibers, and sometimes with enlarged axis- 
cylinders. It is not strictly true to call this condi- 
tion an inflammation. It is rather a degeneration. 
The cord ordinarily shows gross disfigurement at the 
seat of meningitis and curvature. It may be flattened, 
cylindrical, or indented. Angulation may be so 
marked as to persist after the removal of the cord 
from the canal, even in cases which at the time of 
death presented no symptoms. I know of no case 
in which there was complete severance of the cord. 
Shaffer1 refers to an autopsy in which a portion of 
the eighth dorsal vertebra was found impinging 
directly upon the cord, through which it had so 
nearly cut its way that only a slender thread 
remained. 
On microscopic examination in severe cases a 
peculiar interstitial myelitis is found. The newly 
formed connective tissue, which at first contains 
cells, later becomes changed into a dense reticulum, 
which much increases the hardness of the cord. 
The nerve-fibers are to a greater or less extent com- 
pletely degenerated, though usually some are left 
with narrowed myelin-sheaths, and a few may be 
normal. The anterior part of the cord is likely to be 
1 Transactions American Orthopedic Association, vol. iv, 
p. 156- 7 
most affected. The gray matter cannot be distin- 
guished from the white, and the ganglion-cells have 
lost their processes and are shrunken and atrophied. 
Scattered everywhere are found masses of myelin, 
granule-corpuscles, and corpora amylacea. The 
walls of the small vessels are often thickened by a 
growth of spindle-cells arranged concentrically 
around the lumen, making it smaller or obliterating 
it entirely. This cutting off of the blood-supply 
of course increases the damage to the cord. The 
changes are greatest at the point of greatest pressure, 
but extend for variable distances up and down the 
cord. Above and below the transverse myelitis are 
found the usual ascending degeneration in the pos- 
terior columns and descending degeneration in the 
lateral pyramidal tracts. But secondary cord-changes 
in this disease do not always follow the usual law. 
According to Gowers and Charcot there may be an 
ascending inflammation of the lateral pyramidal 
tracts with consequent symptoms referable to the 
arms. Anomalous symptoms are also produced 
occasionally by inflammatory foci scattered here and 
there through the cord or even the medulla. Again, 
if the nerve-roots are affected before the cord the 
piessure-neuritis may invade the cord, causing 
streaks of sclerosis in the posterior columns. In 
the cases in which there is a sudden paraplegia not 
caused by the direct pressure of a dislocated piece of 
bone, hemorrhage has occurred either in the 
inflamed membranes or, more rarely, in the cord. 
The processes by which the cord regains its func- 
tions are not altogether clear. The nerve-fibers 
that suffer from pressure insufficient to cause organic 8 
change, and even those in which the myelin-sheaths 
are greatly narrowed, will of course resume their 
functions on removal of the pressure. But can a 
nerve-fiber in the spinal cord, if completely degen- 
erated in a part of its course, be regenerated? In 
peripheral nerves regeneration certainly sometimes 
takes place. Quite as certainly it does not happen 
in the spinal cord if the destructive lesion is sudden. 
Apparently, however, if the lesion be a slowly in- 
creasing one, as ordinarily it is in Pott’s disease, 
axis-cylinders may regenerate. It is also, curious 
that there may be complete restoration of function 
in a cord the transverse area of which at the seat 
of former disease is half or less than half that of 
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