In addition to the spinal meningitis, chronic and acute, as above described, there were extensive parenchymatous spinal lesions.

In the first place, the meningitis had affected practically all the posterior roots so that the explanation of the posterior column sclerosis of this case is clear. The meningitis had apparently been so marked, also, that all the fibres anywhere near the periphery of the spinal cord had been likewise destroyed. The posterior columns and the posterior root zones were markedly sclerotic; or as we say (having reference to the overgrowth of neuroglia tissue) gliotic. But there was as much sclerosis (gliosis) of the lateral columns (particularly in the posterior two-thirds) as there was in the posterior columns and root zones. In fact, the entire posterior half or two-thirds of the spinal cord markedly outstripped the anterior portions of the cord in the severity of the gliosis (sclerosis) shown.

But although we can explain the posterior column sclerosis, the sclerosis of the posterior root zones and the marginal sclerosis (Randsklerose) round the entire periphery of the cord, on the basis of long-standing effects of old meningitis, we cannot thus explain another finding, namely, the destruction of the fibres in the lateral columns. This, in fact, is explained through lesions (mentioned below) that affected the encephalon. The net result of all these lesions of the spinal cord was to leave only the gray matter and a small amount of surrounding fibres (belonging to short tracts uniting nearby segments) intact. Briefly stated, every long tract in the spinal cord appeared upon examination to be extensively degenerated. The genesis of this parenchymatous loss was, however, double, being in part due to a local meningeal process (sometimes known as “perimeningitis”) and in part due to a cutting off of the pyramidal tract fibres on both sides by lesions higher up in the nervous system.

Case I. Spinal Cord (Three Levels) Showing:
A. Marginal sclerosis—effect of old meningitis now extinct.
B. Posterior column sclerosis—effect of meningitis about posterior roots also now extinct.
C. Bilateral pyramidal tract sclerosis—effect of cerebral thrombotic lesions.
Note distortion of tissues in B and C, partly artificial (tissues in places diffluent).

ANATOMICAL FORMULAE
MENINGOVASCULOPARENCHYMATOUS INVOLVEMENT
M, V, P, or Combinations Applied to the Classification of Head and Fearnsides
I.SYPHILIS MENINGOVASCULARIS
CEREBRAL FORMSM or V or MV[[3]]
HEMIPLEGIAV
AFFECTION OF THE CRANIAL NERVESM
MUSCULAR ATROPHYM
LATERAL AND COMBINED DEGENERATIONSM
EPILEPSYM or V
II.SYPHILIS CENTRALIS
DEMENTIA PARALYTICAMVP or VP
TABES DORSALISMP
MUSCULAR ATROPHYP
OPTIC ATROPHYP
GASTRIC CRISES(M? or) P?
EPILEPTIC MANIFESTATIONSP?
Chart 3

Can we offer any explanation of the partial return of knee-jerks after their temporary total loss at a certain period of the disease? We may assume that the knee-jerks were functionally lost about a year before the death of the patient through the partial or even almost complete destruction of the entering posterior root fibres at that level of the spinal cord which is directly related with the knee-jerk. The later partial return of the knee-jerks apparently requires us to suppose the maintenance of some fibres and collaterals by which a functional connection can be effected between the fibres of the posterior roots and the anterior horn cells which innervate the quadriceps femoris. Let us now suppose that pari passu with the actual return of the knee-jerks, the destructive processes that are affecting both pyramidal tracts high up in the nervous system are now advancing. It is clear that, whatever inhibitory influence these pyramidal tracts have been exerting up to this time upon the knee-jerk reflex arc, that influence is now to be decidedly reduced in amount and possibly absolutely lost. Upon the loss of such inhibitory influences exerted from above, the few persisting connections of the posterior roots and anterior horn cells are now permitted to resume their functions.

Encephalic neurosyphilis: The lesions mentioned above as causing destruction of the pyramidal tracts of the spinal cord were symmetrically destructive and atrophic lesions of the gray matter of both corpora striata with atrophy of the anterior segments of the internal capsules. There was a degenerative process of the corpus callosum especially affecting the forceps minor of the tapetum. The ventricles were largely dilated, indicating a considerable destruction and atrophy of the white matter in general.

After the above discussion of the possible effects of pyramidal tract lesion in this case, it is unnecessary further to discuss the paraplegia produced by the cystic lesions of the corpora striata. The theorist might inquire how these cystic lesions are produced: whether by vascular blocking or by toxic effects of the accumulations of spirochetes. Evidence is lacking which would completely sustain either hypothesis. Still, we do know that lesions almost identical in appearance may be produced by the necrosis consequent to the plugging of nutritive vessels in an organ like the brain supplied with end arteries. Therefore, it is probable that most pathologists would believe these lesions of the corpora striata to be produced by vascular plugging of the nature of thrombosis.

It is worth while to note that there was a suggestion of foci of encephalitis made out upon the gross examination. The cortex in general showed strikingly few lesions. However, the convolutions did show in places numerous ill-defined areas of hyperemia and slight swelling. These areas were of irregular distribution and only a few mm. or cm. in diameter. No gross vascular lesions were demonstrable in connection with these focal areas. Microscopically, however, venous plugs of polymorphonuclear leucocytes were found, and the local hyperemias were found to be largely due to venous congestion. However, very few polymorphonuclear leucocytes were found outside the blood vessels.