* Compare the section on Bacteriology of Influenza, p. 585.
** "Deutsch. med. Wochenschr.," 1892, No. 2.
*** "Arch. f. Psyehiatrie unci Nervenkrankh.," 1892, Bd. xxiv.
The veins in the areas of hemorrhagic encephalitis occasionally become the seat of thrombi; the thrombus may then extend further into the superior cerebral veins and the longitudinal sinus, or from the veins of the corpus striatum and the optic thalamus into the choroidal veins, the vena magna Galeni, the straight and transverse sinuses. In such cases the differentiation between primary encephalitis or primary thrombosis with secondary hemorrhagic softening is only possible upon microscopic examination. Occasionally hemorrhagic leptomeningitis and pachymeningitis are combined with influenzal encephalitis; in rare cases streaks of purulent exudate extending along the pial vessels are found. Undoubtedly the process, when the inflammation is not very intense and affects only small areas, may undergo resolution. Several of our acute cerebral influenza hemiplegias recovered in a very short time. Whether they were actually encephalitis is always uncertain in such cases. In no instance was there a permanent paralysis with contractions similar to that following ordinary apoplexies. Neither have such cases come under our notice in the literature. But the course of the illness is not always so tumultuous or so definitely apoplectiform as we have noted in describing the typical condition. The encephalitic hemiplegia in exceptional cases develops gradually, insidiously, and without such acute cerebral symptoms, although dizziness and headache, disturbances of consciousness with epileptiform convulsions, or even somnolence and coma, are usually frequent.
It is obvious that the symptoms vary markedly according to the intensity of the process, the number and size and especially the position of the inflamed areas. As regards the focal symptoms, there may be either complete hemiplegia, pure aphasia without motor disturbances, or only paralysis of individual nerves, like the facial, hypoglossal and brachial monoplegia, or, more rarely, crural monoplegia.
The process occurs especially in the motor cortex as small, sharply defined foci, whence the monoplegia. On the other hand, no authentic case is known of acute influenzal encephalitis, situate on the floor of the third or fourth ventricle, and giving rise to an acute hemorrhagic superior or inferior polioencephalitis.* All the reported cases of nuclear oculomotor paralysis developed after influenza had run its course, generally some time after, without fever or marked cerebral manifestations; in other words, they were typical cases of degenerative neuritis and neuronucleitis.
If the influenzal encephalitis spares the motor centers and tracts, it may run its course without any motor or paralytic symptoms. In one such case in which there were high fever and early unconsciousness, followed by death during coma, we discovered inflamed areas at the apex of both frontal lobes and the right temporal lobe.
Posthemiplegic motor disturbances, unilateral tremor, hemiataxia, hemichorea, and hemiparalysis agitans but rarely succeed influenza hemiplegia. Permanent paralyses followed by contractures, as previously mentioned, we have never seen.
Of course we do not go so far as to assume that all or even the greater part of the cerebral hemiplegias and monoplegias observed in influenza are caused by encephalitis. Very often other processes, e. g., small extravasations of blood, emboli, and thrombi, may have occurred or transitory toxic influences on certain cerebral centers, or conditions of cerebral hyperemia, produced these results (Helweg, Kohts).
The cases of Erlenmeyer (Jacksonian epilepsy with unconsciousness and convulsions in the left arm), those of R. Gross (apoplectiform hemiplegias with or without aphasia and recovery already in twenty four to forty eight hours), the cases of Eichhorst, Stembo (motor aphasia with brachial hemiplegia), those of Remak (brachial monoplegia with anesthesia), those of Drasche (brachial monoplegia), those of Bilhaut (cortical epilepsy), of Prentis (three cases of postinfluenzal cerebral apoplexy), the cases ef Herzfeld (left sided hemiplegia with paralysis of the abducens, pupillary immobility, nystagmus, and aphasia), of Warfvinge,-(1) hemiparesis, followed by chorea; (2) hemiplegia with aphasia; (3) Jacksonian epilepsy, with fatal termination by excessive increase of the attacks,-and finally the cases of "isolated motor aphasia without paralytic symptoms" described by Brakenridge, Warfvinge, and Goudet, may have had different causes from encephalitis and may in part have been due (especially the last described anatomic changes) to neuritis.** On the other hand, the case described by Revilliod as " cerebellitis," with softening, and also a well described case by Duck
* Compare, furthermore, p. 647, the case of Macdonald. ** Compare section on Neuritis, p. 640.
(Rimpar), may, without doubt, be attributed to hemorrhagic encephalitis. An observation made by Kohts, as he himself surmises, and perhaps also the case of Macdonald, described as a capillary hemorrhagic inferior polioencephalitis, fall into this category. Also Jennings' case (meningeal hemorrhage, hemorrhagic area of softening in the left temporal and frontal lobes) may be classified under encephalitis. Both of the cases observed by Straumann (fever, coma, death) may be most readily classified under the above described form of "acute encephalitis without motor manifestations or motor paralysis."
The proof of the existence of an "acute focal hemorrhagic influenza encephalitis" in our most recent epidemics may be considered an advance in the pathology and anatomy of influenza, especially since Nauwerck and Pfuhl have added to these clinical observations by demonstrating the presence of the influenza bacilli in these areas.
We still must consider two other inflammatory cerebral affections caused by influenza.
Purulent encephalitis, abscess of the brain, frequently accompanied by purulent meningitis, most frequently arise from a purulent otitis, from suppurative processes in the accessory sinuses of the nose, in the frontal sinus (Redtenbacher), and from the antrum of High more. Pulmonary abscesses, pleural empyema, and, as Arzel believed in one case, purulent bronchitis and influenzal tonsillitis, may give rise to metastatic suppurating areas in the brain.
Influenza may also give rise to a primary purulent encephalitis (Bristowe, Leichtenstern, German army reports); and the mostly non purulent hemorrhagic encephalitis may, under certain conditions, result in suppuration. Such a mixed form of hemorrhagic purulent encephalitis is seen in the case of Senator-Virchow. Abscess of the brain as a direct consequence of infection by the influenza bacilli has been proved by the detection of the specific organism in the pus by Pfuhl. That this bacillus possesses pyogenic properties and can give rise to an abscess through necrotic action upon the tissue is seen in the fact that the organism is capable by itself of bringing about suppuration in the most typical manner (R. Pfeiffer) in catarrhal pneumonia and in abscess of the lung, without mixed infection with the common pyogenic cocci.