OPTIC ATROPHY
GASTRIC CRISES
EPILEPTIC MANIFESTATIONS
Chart 2
Peripheral neurosyphilis: The lesions of the cranial nerves were characteristically asymmetrical. Whereas the left third nerve looked entirely normal, the right third nerve had its diameter reduced two-thirds. On the other hand, the fourth nerves were equal and apparently normal. The sensory portion of the left fifth nerve was normal; the right fifth nerve was normal. The right sixth nerve agreed with the right third nerve in being atrophic, and was in fact reduced to a mere thread without contained nerve fibres at a point 2 mm. from its superficial origin. Although the right third nerve was atrophic, it was the left seventh and eighth nerves which had become atrophic; the process had spared the right seventh and eighth nerves. The remainder of the cranial nerves were grossly normal, except that the optic nerves had an outer zone of a translucent nature. So far, no spirochetes have been demonstrated in any portion of the nervous system of this case, but such asymmetrical and focal cranial nerve lesions are perhaps due to local spirochetal infection, punctuating (as it were) the diffuse process.
How much of the transient blindness, deafness, and ocular paralysis can be explained on the anatomical findings in these nerves? Possibly a portion of the phenomena can be so explained. Thus, the mechanical conditions of pressure inside and outside these nerves, both in their peripheral course and in their passage through the membranes, can be readily understood to differ during the acute and subacute inflammation, during the process of repair in the pial tissues, and during the process of overgrowth of neuroglia tissue about the superficial origins of the nerves. Of course, the majority of lesions of these nerves were entirely extinct at the time of the autopsy, and their history could be surmised only from the appearances in the left eighth nerve. Here occurred a sharply marked focal area of gliosis with apparently total destruction of nerve fibres and related with a lymphocytosis of the investing membrane (one of the few areas of lymphocytosis found anywhere in this case).
If it were not for the pre-infective history, the hysterical dysphasia and dypsnea, the youthful obsessions, the migrainous tendency, and the psychopathic inheritance, we might be tempted to try to explain the transient blindness, the deafness, and ocular palsies on the basis of mechanical and toxic variations in the conditions of the peripheral cranial nerves. The existence of a trace of lymphocytosis in the left eighth nerve leads to the hypothesis that treatment might still be effective in this particular region (see below in discussion of spinal symptoms).
Spinal neurosyphilis: Not only the spinal cord but also the posterior and anterior nerve roots exhibited severe lesions. These lesions were both meningeal and parenchymatous. The meningeal process differed in its intensity in different parts of the spinal cord, being severest in the thoracic region. At one point in this region, the dura mater was so firmly attached to the pia mater that the line of demarcation between the two membranes was hard to make out. In fact, it seems clear that there could have been no free intercommunication between the spinal fluid above these adhesions of dura to pia mater and the spinal fluid below the adhesions. Accordingly, it seems that lumbar puncture, had it been practised in this case, would have failed to show features representative of the whole cerebrospinal fluid system. Moreover, since at no point in this region of adhesions or in the pia mater of the spinal cord below this point, were found any lymphocytes, it seems clear that the ordinary lumbar puncture would have failed to reveal a pleocytosis. Whether this fluid would have yielded a positive globulin and excess albumin test, it is now impossible to say; but it appears that the process in the lower part of the spinal cord was to all intents and purposes extinct.
However, there was one region of more severe inflammatory involvement. The spinal cord in the cervical region showed a lymphocyte infiltration of its vessels amounting to a mild myelitis (meaning, thereby, an inflammatory process of the spinal cord remote from the pia mater). Moreover, in this region, there was, besides the perivascular infiltration of the substance, also an infiltration of the overlying membranes themselves, especially in and near the posterior root zones.
The lessons of this finding are several: The inflammatory process in this case does not appear to have been entirely extinct! Can we not suppose that treatment might still have benefited this local inflammation (perivascular infiltration of the cervical spinal cord substance and overlying lymphocytic meningitis)? Can we not also picture the gradual ascent of the inflammatory lesions from lower segments to higher segments and possibly conceive of the gradual elevation of the zone of hyperæsthesia manifested in this case as following the gradual displacement upward of the lymphocytic process? Are there spirochetes in this tissue? So far none have been discovered, possibly through inaccuracies of available technique. To the neuropathologist, however, the lesion looks like a local reaction to organisms.