Treatment: Borofski was put on antisyphilitic treatment consisting of 0.6 gram of salvarsan twice a week and potassium iodid, together with intramuscular injections of mercury salicylate. The convulsions then ceased. After four months Borofski returned to work, and he has remained at work for a year. He has never regained his former health.
Fifteen months after beginning of treatment the laboratory tests were again made (there had been more than 60 injections of salvarsan), and the cell count and gold sol reactions were found to be negative. Globulin and albumin were also in smaller amounts than in the original examination. However, the W. R. of the serum and the spinal fluid remained positive.
Head and Fearnsides state that cases of cerebrospinal syphilis should return negative spinal fluid tests after six months of treatment. Upon this criterion of Head and Fearnsides, Borofski would not be a case of cerebrospinal syphilis; but it is probably impossible to separate various forms of neurosyphilis into categories on any such grounds.
1. Shall case David Borofski be regarded as one of paretic neurosyphilis (“general paresis”)? He has returned to work and has remained at work, though without regaining his former health. In any event, however, he does not offer the typical picture of inevitable decline and death presented by the typical case of Pietro Martiro (15) presented in our discussion of systematic diagnosis. However, we could not upon laboratory grounds, or even upon the ground of clinical observation, distinguish Borofski from Martiro; Borofski has greatly improved; Martiro is dead. Borofski developed his obvious neurosyphilis only two years after the original infection. The conservative syphilographer might, accordingly, reply that David Borofski is not a typical case of paretic neurosyphilis (“general paresis”) either in the length of the incubation period for his neurosyphilitic symptoms, or in his outcome.
2. What is the cause of such convulsions as those developed by David Borofski? Evidence from clear cases of general paresis with convulsions leads to the hypothesis that such convulsions as those developed by Borofski are not necessarily based upon frank destructive lesions such as would be produced by the plugging of terminal arteries. They may well be produced through the activities of minor lesions, only demonstrable by microscopic methods, either through properly disposed cell losses or by the pressure of exudate, or even by endotoxins or other substances derived from the bodies of dead or living spirochetes.
3. Aside from the well-known syphilitic epilepsy due to meningitis, is there a non-meningitic epilepsy (such a disease as Fournier formerly described under the term parasyphilitic epilepsy)? We dismiss from discussion the so-called symptomatic epilepsies which are the result of a gross organic disease of the brain substance or its membranes, and which do not differ so far as we are aware from organic epilepsy produced by other gross lesions of an identical size and structure. These symptomatic epilepsies may be partial, or even may present the appearance of generalized epilepsy. We may also leave out of account those epileptic pictures which are produced in general paresis itself, and which may be viewed as nothing but partial phenomena of general paresis. The kind of so-called “parasyphilitic” epilepsy that Fournier described is a kind of epilepsy that cannot be distinguished from genuine epilepsy, in which the sole disease-phenomenon throughout a long period of time consists of epileptic convulsions. It appears that these “parasyphilitic” imitations of genuine epilepsy occur in individuals with a very long post-infective “incubation period,” but that there are some cases in which the epilepsy appears, on the contrary, in the very earliest stages of syphilis. The attacks are a little less common than those of idiopathic epilepsy; they have the same apparently causeless beginning; are associated with complete amnesia; and are followed by characteristic dazed states. The patient’s intelligence, however, suffers little. Now and then a case reacts well to antisyphilitic treatment energetically pushed. (Spontaneous long remissions in non-syphilitic epilepsy must be remembered.) Petit mal attacks occur sometimes between the more severe attacks. In short, it would appear that there is a group of syphilitic epilepsies in which the brain shows no gross structural lesions, which accordingly do not exhibit any Jacksonian appearances, and which last a comparatively long time without changing their character, and often without being especially altered for the better by any form of antisyphilitic treatment. This condition is sometimes known as a post-syphilitic epileptic neurosis. Nonne had been able to collect up to 1902 some 12 cases from his own service.
4. Would it be proper to call Borofski a case of taboparesis? Absent knee-jerks in a victim of paretic neurosyphilis should not be used to suggest a diagnosis of taboparesis. This question of terminology has been discussed above, under Sullivan (16).
5. What is the mechanism by which the amnesia of a case like Borofski is produced? The answer runs in the same terms as the answer to the questions concerning the cause of convulsions. The amnesia in general paresis has surprising functionality. A study of autopsied cases of general paresis has shown that amnesia is practically as common in cases without marked destruction of brain tissue as in cases with atrophy of classical extent and depth. The clinical recovery in this case was practically complete in respect to memory. We must regard the amnesia as not due to the destruction of storage cells bearing the so-called neurograms (Morton Prince).
6. What is the explanation of the persistently positive W. R.’s of the serum and spinal fluid associated with diminished globulin and albumin tests, a negative gold sol reaction, and normal cell count? See discussion under Case Martha Bartlett (21).
7. How atypical is the early development of paretic symptoms in David Borofski? C. B. Craig has collected, in 100 cases of brain syphilis (a list including both paretic and non-paretic cases), some data on this point. The shortest period reported by Craig was in a case in which the neurosyphilitic symptoms appeared one month after infection. Craig found three cases where symptoms appeared in six months, and six cases within a year. The longest post-infective period of Craig’s list was thirty years. Our case of Chatterton (73) developed symptoms 33 years after infection and Washington (66), forty years after infection. Nonne casts some doubt on statements to the effect that tabetic symptoms may occur three to four months after infection. It seems to be admitted that pupillary anomalies and reflex changes may occur in the early secondaries and may recover under antisyphilitic treatment. Nonne’s case of longest post-infective interval, like that of Craig, was one of 30 years.