THE SPINAL CORD IN A CASE OF 
PERNICIOUS AN/EMIA. 
READ AT THE ANNUAL MEETING OF THE AMERICAN NEUROLOGICAL ASSOCIATION, JUNE 2, I 896. 
BY 
C. EUGENE RIGGS, A.M., M.D., 
ST. PAUL, MINN. 
Reprinted from the International Medical Magazine for September, 1896. NOTE. 
On page I, line 2, read Dr. Gottfried Stamm. 
Through an oversight, the credit which should have been given in 
the text to Dr. L. B. Wilson, for his efficient services in preparing the 
plates, was omitted. 
Owing to my absence from home, and consequent inability to 
correct the proofs, the technique of the preparation of the specimens 
was inadvertently included in the following article. 
In addition to the references already made, I desire to call atten- 
tion to Dr. James Hendrie Lloyd's "The Spinal Cord in Pernicious 
Anaemia" (Journal of Nervous and Mental Disease, April, 1896,) and 
Dr. James Taylor's (M. R. C. P., London,) "On Nervous Symptoms and 
Morbid Changes in the Spinal Cord in Certain Cases of Profound 
Anaemia" (Volume 78, Medico-Chirurgical Transactions). THE SPINAL CORD IN A CASE OF PERNI- 
CIOUS ANEMIA. 
Mrs. B., aged forty-five, was referred to me in September, 1895, by Dr. 
Goetfried Starm. She was paraplegic and exceedingly anaemic; the para- 
plegia was, however, not complete; she could move her limbs, although 
unable to walk or stand. Her disease seemed to date from some nervous 
shock three years previous, when one of her children had been injured at 
school and died from the effects; she had never been the same person since. 
Two years before I saw her she had been previously sick with an ill- 
defined trouble, which, I am informed by Dr. E. J. Abbott, her physician 
at the time, presented many of the clinical symptoms, but none of the 
physical signs, of an acute tuberculosis. In July, 1895, the loss of power 
in the legs was first observed. Her temperature during her illness fluctu- 
ated between normal and 100° F. 
After her death I was told that at one time she was supposed to have 
suffered from Bright's disease. Examination of the urine, however, while 
she was under my care at the hospital was entirely negative. She com- 
plained especially at night of a sensation as if, as she expressed it, her bones 
were going through her flesh. 
Examination showed that tactile sense was markedly diminished over 
both lower extremities and over the trunk as high as the ensiform cartilage, 
being most marked over the area supplied by the anterior crural nerve. 
Temperature sense was normal, while that of pain was diminished. She 
complained of distressing parsesthesia, especially in the area of lessened 
tactile sensibility; it was present in the upper extremities as well. Rectus 
clonus was marked in both legs; patellar reflexes were exaggerated. At 
my first examination I succeeded in obtaining ankle clonus; later it became 
barely appreciable. There was no ataxia either of the extremities or of the 
trunk ; no lightning pains. 
Superficial reflexes: Plantar diminished; gluteal diminished, abdominal 
epigastric, dorso-lumbar absent; interscapular present. 
On October 21 a blood-count was made by Dr. Charles L. Greene 
which showed 2,264,000 cells per cubic millimetre, representing a count 
of eighty squares. Haemoglobin thirty per cent., adherent poikilocytes, 2 
C. EUGENE RIGGS, M.D. 
microcytes, and megalocytes. On November 27 another blood-count was 
made, showing 1,340,000 cells per cubic millimetre. The post-mortem 
examination, by Dr. A. W. Dunning, was made about six hours after death. 
Subject was found extremely white and but little emaciated ; calvarium nor- 
mal in thickness and easily removed; meninges not unusually adherent. On 
removal of the cerebellum there was found a necrotic area the size of the end 
of the little finger, located upon the posterior surface of the petrous portion 
of the right temporal bone, just below the attachment of the tentorium 
cerebelli. The forceps were thrust into this aperture to the depth of three- 
quarters of an inch in a forward and outward direction into the mastoid 
process. The spinal cord was removed by dividing the pedicles, thus ex- 
posing the spinal canal anteriorly. Within this canal in the mid-dorsal 
region was found a considerable extravasation of blood, together with a 
quantity of apparently serous effusion. The thorax was filled with serum ; 
the pericardium was distended, and the abdomen also contained a large 
quantity of serum. The blood-vessels were everywhere empty and color- 
less. The heart was pale and flabby, with a small clot of blood in each 
ventricle; liver was enlarged ; the spleen was dark and also enlarged. The 
pancreas was enlarged and extremely fibrous; the intestines were thin- 
walled and pale; the lungs normal in size and apparently healthy. 
MICROSCOPICAL EXAMINATION. 
The upper three segments of the spinal cord were attached to the brain 
when received in the laboratory, and, together with the brain, were hardened 
in four per cent, formalin. 
In hardening, these three segments were somewhat flattened dorso-ven- 
trally by the weight of the brain partiallyresting on them. The remainder 
of the cord was hardened in Muller's fluid and alcohol. This portion was 
slightly twisted at the level of the D. 6. 
(All the segments were then separated, embedded in celloidin, soaked en 
bloc in copper acetate solution, cut, stained in Weigert's haematoxylin, decol- 
orized in potassium ferricyanide and sodium biborate solution, cleared in 
clove oil, and mounted in xylol-balsam.) 
On examination with low power the following degenerations were ob- 
served : 
1. Anterior Pyramidal Tract.-1The area of degeneration was greatest at 
the level of the C. 6, much less at the level of the C. 5, and showed only as 
a trace on the right side in the C. 4. Below the D. 7 it became gradually 
reduced in size till it finally disappeared as a trace on the right side at the 
level of the D. 8. 
2. Direct Cerebellar Tract.-The area of degeneration appeared as a 
trace at the level of the D. 10, gradually increased in extent to the level of 
the D. 4, and continued thence without materially changing in size to the 
C. 1. The area was greatest on the left side throughout the whole extent 
of the cord. THE SPINAL CORD IN A CASE OF PERNICIOUS ANAEMIA. 
3 
3. Cross Pyramidal Tract.-The area of degeneration appeared as a 
trace in the C. 2, gradually increased in extent to the level of the D. 8, and 
decreased from there to the L. 3, where it disappeared. It was greatest in 
the left side throughout. 
4. Column of Lissauer.-1The area of degeneration extended from the 
C. 1 to the D. 6, and was greatest at the C. 6. 
5. Column of Burdach.-The area of degeneration extended from the 
C. 1 to the L. 3, being greatest at the level of the D. 6. The degeneration 
was most marked at the median and posterior margins of the column. 
5(a). Posterior External Field of Posterior Column.-The area of degen- 
eration extended from the C. 1 to the D. 7, being greatest at the C. 5. 
6. Column of Goll.-The area of degeneration extended from the C. 1 
to the end of the column, being greatest at the D. 6 and the C. 3. From 
the C. 4 downward the posterior median aspect of the column was less 
degenerated than the other portions, and from the L. 2 downward the area 
in the right side was wider than on the left. 
All other columns were normal throughout their entire extent. 
Examination of the degenerated areas with high power showed axis 
cylinders and medullary sheaths in various stages of disintegration. Many 
of them were granular and others fatty. The degenerated columns, espe- 
cially in the mid-dorsal region, were shrunken and contained an excess of 
connective tissue. 
The gray matter appeared normal throughout. 
The arteries wherever present showed a thickening of the endothelium, 
and here and there an inward projecting growth of new connective tissue. 
The Liver.-(The liver was hardened in alcohol, embedded in celloidin, 
cut, stained in lithium carmine, treated with potassium ferrocyanide and 
acid alcohol, cleared in clove oil, and mounted in balsam.) 
Examination showed areas of fatty infiltration and degeneration, and an 
enormous deposit of haemosiderin and haematoidin, both in the liver cells 
and in their trabeculae. The pigment was mostly in the centre zone, but 
extended in some lobules through the middle zone, even lining the walls 
of the capillaries. 
Spleen.-The spleen was treated as the liver. The only pathological 
change observed was a scattered deposit of the same pigments found in the 
liver. 
Arteries.-(Portions of arteries from the circle of Willis were hardened 
in alcohol, embedded in celloidin, cut, stained in lithium carmine, cleared 
in xylol, and mounted in balsam.) 
Examination showed thickening of the middle coat. 
No apparent relation existed between the areas of degeneration and the 
mid-dorsal clot noted at the post-mortem. The points of origin of degen- 
eration were widely separated, some lying in the upper cervical and others 
in the lower lumbar. None of the columns, except possibly the left direct 4 
THE SPINAL CORD IN A CASE OF PERNICIOUS ANJEMIA. 
cerebellar and the right direct pyramidal, had all their fibres involved, 
supposing their sectional areas to be correctly figured in the standard 
atlases. 
Taken as a whole, it would seem that the scleroses were certainly not 
systemic in their origin, but probably were of vascular origin. 
This view is held by Nonne, and quoted by Marie, in the Revue Neuro- 
logique for November, 1895. 
Nonne examined cords in seventeen cases of pernicious anaemia, in 
seven of which the findings were negative; in three the lesions were clearly 
defined in the neighborhood of vessels, and in the last seven there were 
medullary lesions of pronounced type. The first two of these groups 
showed no distinctive clinical symptoms; not even in all the cases of the 
third group were they present, and when found consisted mainly of the loss 
of the knee-jerk, a slight ataxia, and some troubles of sensation. 
Nonne concludes further that the pathological characteristics are small 
patches of degeneration, beginning in the cervical cord, showing predilec- 
tion for the root-zones of the posterior columns, as well as for the anterior 
and lateral columns. 
The findings in this case would seem to bear out Nonne's conclusions. 
Osler also quotes Lichtheim, Morris Lewis, and Burr as reporting cases 
of sclerosis of the posterior column. He further notes the constant and 
peculiar distribution of haemosiderin in the liver. International 
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