A second important group of paralyses in influenza is of cerebral origin. These paralyses, hemiplegias and monoplegias, are clinically differentiated from the above mentioned neuritic and nuclear varieties by their sudden apoplectiform onset, either at the very beginning or at the height of the influenza attack, with high fever and grave cerebral symptoms (delirium, early unconsciousness, coma, epileptiform convulsions, Jacksonian epilepsy, etc.). The clinical picture so frequently resembles apoplexy caused by cerebral hemorrhage or embolism accompanied by the hemiplegia that only the youth of the patient, the acute onset with rigors, the accompanying high fever, and the occurrence of such cases at the time of an influenza epidemic admit of differentiation from ordinary apoplexy. The differential diagnosis from ordinary apoplexy is easier if the influenza attack does not set in with the cerebral symptom complex described above, but typical manifestations of influenza precede the cerebral symptoms by one or more days.
In exceptional cases this apoplectiform attack may develop suddenly during convalescence from influenza, with a renewed rigor and high fever. These cases we regard as influenza relapses, with the difference, however, that the second attack appears in the form of an influenza encephalitis.
Cerebral apoplexy has been described as a symptom of influenza in England as far back as the epidemic of 1743, and in 1782 by Michell (Holland), by Bodel in 1800 (Dordrecht), and in 1833 by Escherich and D. Lombard (Geneva). The latter observer in particular called attention to the cases of "cephalalgia with hemiplegia"; so, too, Fife in the epidemic of 1837. All these observations, however, and particularly the erroneously quoted cases of Recamier (1837) concerning "apoplectiform influenza," have been so vaguely described that it is impossible to make an exact diagnosis. There are no accounts of any postmortem examinations in this period.
Another statistical note regarding the most recent epidemic may be mentioned. The general mortality statistics concerning the frequency of apoplexy in England and Germany show that there was no increase of this condition during the period of influenza in these countries, which is not surprising since influenza apoplexy is always exceedingly uncommon and must be regarded as a rarity. On the other hand, the Swiss statistics of F. Schmid, tabulated during the principal epidemic month, January, 1890, show well a remarkable increase of mortality from "stroke."
In my influenza lectures of the spring of 1890 I first called attention to these apoplectiform hemiplegias and monoplegias occurring in influenza, and at that time reported no fewer than eight cases.* Some of these cases terminated fatally, others recovered.
Anatomically, there was neither simple cerebral hemorrhage nor an extensive embolus or thrombus, but a focal " acute hemorrhagic encephalitis" which up to that time had not been described. In the first case the foci were situated principally in the cerebral cortex, and in the later cases frequently also in the central ganglia and particularly in the thalamus. Regarding its pathogenesis, I conjectured at that time (1890) that " the condition consisted of foci of capillary emboli due probably to a dissemination of the influenza germs," an opinion which later on was substantiated by the demonstration of the specific organism in these encephalitic areas (Pfuhl, and especially Nauwerck) .*
* Loc. cit., p. 29.
At the same time I pointed out that this variety of encephalitis is by no means pathognomonic of influenza. Such hemorrhagic encephalitic areas Klebs and I have observed occasionally in epidemic cerebrospinal meningitis during the epidemic of 1885-1886, in which cases these areas caused the hemiplegia which occurred in the course of the meningitis. Similar forms are occasionally met with in ulcerative endocarditis, and are doubtlessly due to capillary emboli.
During the years following the pandemic of 1889 we observed four more cases of acute hemorrhagic encephalitis, which were described by me,** and more exhaustively by Bucklers. *** In the absence of marked influenza symptoms and because they did not occur during the epidemic we did not venture to attribute these cases with certainty to influenza. I classed them pathologically with the disease described by Strumpell in October, 1890, under the title, " Primary Acute Encephalitis." Undoubtedly these "primary" cases are to be attributed to microparasitic infection and the formation of emboli by unknown microbes.
Our observations regarding acute hemorrhagic grippal encephalitis were corroborated by the case described by Virchow-Senator, and especially by the reports of Furbringer, Konigsdorf, and J. Schmidt, and the domain of " primary acute encephalitis" was extended further by H. Oppenheim.
We cannot discuss more in detail the pathologic anatomy of this acute encephalitis that so frequently sets in with apoplectiform manifestations. The foci are usually sharply defined, varying in size from that of a cherry stone to the size of a pigeon's egg; by the confluence of adjacent foci still larger areas may form. Sometimes only one area exists, but more frequently there are several (multiple encephalitis). It is nearly always situated in the gray matter, most frequently in the cerebral cortex and the central ganglia, and far less commonly in the pons and cerebellum. The encephalitic areas occasionally form wedges extending from the cerebral cortex or the central ganglia into the white matter of the hemispheres. Even in our earliest publication we called attention to the symmetric localization of the areas in both cerebral hemispheres. The encephalitic area in its typical form consists of innumerable dense aggregations of, as we expressed it, "flea bite like" dots of blood, between which the tissue is softened and of a gray to a grayish red color. By secondary hemorrhage into the softened center larger hemorrhagic areas may arise. Undoubtedly such "cerebral hemorrhages" in influenza have been regarded as primary apoplexies, while the true condition was secondary hemorrhage into the softened central encephalitic area.