We will pass over the cases in which an influenzal otitis or an empyema of the accessory cavities of the nose gives rise to a secondary purulent meningitis (Ewald, Baumler). Of much more importance is the primary fulminating influenzal meningitis occurring at the height, or as a rule at the very beginning, of the influenza attack. We may term it the meningitic form of influenza. The specific bacilli probably enter into the cranial cavity from their primary focus, the nasal cavity, through the lymph channels communicating with the subarachnoidal space, a phenomenon which is supposed by many to account for the transmission of epidemic cerebrospinal meningitis. But the germs can probably also be disseminated by the blood channels. In the pus of suppurative meningitis there are mostly only the ordinary pyogenic cocci and the ubiquitous diplococcus lanceolatus to be found, but Pfuhl and Hogerstedt have also found the specific influenza bacilli.
[In the case mentioned above of general influenzal infection, the bacillus of influenza was found in the cerebrospinal fluid and the cerebral abscesses, as well as in the blood. E. Frankel also found only Bacillus influenzae in two cases of meningitis.-Ed.]
Such cases of primary purulent influenzal meningitis have been described by Furbringer, Kelsch and Antony, Maillart, Rendu, Kuskow, Revilliod, Mackay, Gotz, Pel, Lennmalm, Edgren, and Koster. In our lectures of 1890 we reported four such highly acute fatal cases, together with the postmortem examination. The relation of the basal to the superficial meningitis in our cases was 1:3.
In very acute influenzal meningitis, just like in the fulminating cases of epidemic cerebrospinal meningitis, there may be no macroscopic evidence of pus, while, on the other hand, there may be occasionally a copious purulent exudate, with no less acute course of the affection.
The manifestations vary according to whether the convexity of the brain, as is the rule (intense headache, early stupor, the rigidity of the neck), or the base of the brain is affected. In the latter case the differentiation between influenzal and epidemic cerebrospinal meningitis is often impossible, for both begin suddenly with chill and high fever, and cervical rigidity sets in at once; in both, herpes labialis is seen, although this is far more frequent in epidemic than in influenzal meningitis.
The certain diagnosis of epidemic meningitis, as a recent case of ours illustrated, can be established only by the demonstration of the highly characteristic specific Meningococcus intracellularis (Weich selbaum, Jager) in the cerebrospinal fluid obtained by lumbar puncture. The influenza bacillus has not yet been found in the fluid obtained by lumbar puncture, nor has it or the Diplococcus intracellularis been found in the contents of the herpetic vesicles.
The differential diagnosis between influenza meningitis and epidemic cerebrospinal meningitis is easy when the influenza meningitis is accompanied or ushered in by the typical symptoms of influenza, that is, by coryza or diffuse bronchitis, or when pneumonia associates itself with the process; for such manifestations as were taught us by the epidemic of 1885-1886 never occur in true epidemic cerebrospinal meningitis. More especially, we never met with secondary pneumonia in this affection.* On the other hand, a differential diagnosis between cases of pneumonic meningitis in those in which the meningitis arises first and the pneumonia follows, and an influenzal meningitis with the same manifestations, is hardly possible. Of course, the demonstration of the influenza bacillus in the sputum of such patients would prove the influenzal nature of the meningitis. Unfortunately, however, the majority of cases of primary influenza meningitis run their course without any symptoms in the respiratory tract, without bronchitis and expectoration, thus preventing the possibility of demonstrating the influenza bacilli intra vitam. Lumbar puncture has not yet been tried for this purpose.
(I see from the reports of Heubner and Furbringer ** that Finkel stein anticipated me in 1895 in the demonstration of the Meningococcus intracellularis in the fluid obtained by lumbar puncture in Heubner's clinic.***)
Influenzal meningitis can be confounded only with tubercular meningitis when the patient comes under observation with the meningitis fully developed, and, as is often the case, in hospital patients without any exact history of the nature and character of the beginning of the disease. Tubercular meningitis never begins suddenly, as is the rule in influenzal meningitis, with rigor and pyrexia, is never accompanied by herpes, and initial delirium, often present in influenza meningitis, is absent in the insidiously developing tuberculous form of meningitis.
Caution is necessary in diagnosing influenzal meningitis, as influenza, by its toxins alone or by causing hyperemic changes in the meninges, is often accompanied by violent headache, vomiting, bradycardia, and stiffness of the neck,-the latter often merely as a sequel of violent occipital neuralgia,-and may in many respects simulate the symptom complex of meningitis. (Compare the remarks below on Pseudomeningitis.)
In considering purulent meningitis occurring in influenza we have finally still to note the variety which is observed as a sequel of croupous influenza pneumonia (Sokolowski, Kundrat, Gmeiner). Etiologically, it is to be considered on the same basis with the pneumonic meningitis occasionally occurring in genuine croupous pneumonia.
* Compare our work upon epidemic cerebrospinal meningitis, " Centralbl. f. allg. Gesundheitspflege," 1893, xii.
** "Deutsch. med. Wochenschr.," July 2, 1896. *** "Charite Annalen," 1895, Bd. xx, p. 297.
The interesting reports of Krannhals on " Zur Casuistik meningitis iihnlicher Krankheitsbilder " undoubtedly show that influenza may give rise to areas of hemorrhagic leptomeningitis-for so I interpret the cases described by the author-without any serous or purulent exudate in the meninges. These observations complete those described by us in which there were areas of hemorrhagic encephalitis, by showing that a similar process, probably also due to the dissemination of the germs by emboli, may also be located in the soft envelop of the brain with a relatively small affection of the cerebral cortex beneath. Here, too, the process is to be considered as nothing else than a hemorrhagic inflammation. That it is only a short step from this condition to the occurrence of a seropurulent or a purulent exudate is shown by one of our cases of hemorrhagic encephalitis, where there existed simultaneously a hemorrhagic leptomeningitis with small streaks of purulent exudate enveloping isolated pial vessels.*