Hunter Tod,[53] reporting on 100 cases treated at the London Hospital, found that in children under 10 years of age temporo-sphenoidal abscess occurred in 87 per cent. cases, and cerebellar in 13 per cent., whereas in adults cerebral abscess occurred in 65 per cent. and cerebellar in 35 per cent. The development of temporo-sphenoidal and cerebellar abscesses in the same case was observed in 5 per cent. cases.
Pathology.
Insomuch as chronic middle ear disease forms the main predisposing factor in the development of abscess of the brain, the pathology of brain abscess in general may be considered by discussing the main features peculiar to otitic abscess in particular.
As the result of chronic middle ear disease, the mucous lining of the middle ear and its accessory cavities becomes destroyed, the antrum filled with cholesteatomata, and the middle and external ears with granulations. The discharge of pus, previously free, is obstructed, partial or complete blockage occurring. The destruction of the mucous lining allows of invasion of the surrounding bone, the veins become thrombosed and filled with bacteria, and the cancellous spaces blocked with granulations. Further erosion of the bone results, both in the upward direction towards the tegmen tympani and in the backward towards the lateral sinus groove and cerebellum. The veins of the tegmen communicate freely with those of the temporo-sphenoidal lobe, whilst those ramifying in the mastoid region either communicate with the lateral sinus itself or with the anterior cerebellar venous system. Infection may therefore spread (1) upwards to the temporo-sphenoidal lobe, or (2) backwards to the lateral sinus and cerebellum. In the former case, meningitis or temporo-sphenoidal abscess develops: in the latter instance, meningitis, lateral sinus thrombosis, or cerebellar abscess.
For the formation of a brain abscess it is, of course, essential that the brain membranes overlying the main site of osseous erosion should be sealed off in such a manner as to prevent a general infection of the meningeal region, the dura becoming adherent to the eroded tegmen, &c. It is œdematous and throws out granulations, both on its parietal and visceral aspects. The parietal granulations aid in the further erosion of the bone, whilst the visceral may, according to Macewen,[54] even indent the brain. By means of thrombosed veins, perivascular lymphatics, and minute arterioles, a channel of infection is now opened up between the site of osseous erosion and the temporo-sphenoidal and cerebellar lobes.
Fig. 74a. Diagram to show Extension of Disease from Tympanic Cavity, in Middle Ear Suppuration. 1, Perforation through tympanic membrane; 3, Perforation through Shrapnell’s membrane; 4, Fistula through outer wall of attic (roof of external meatus); 5a, Extradural abscess; 5b, Meningitis; 5c, Temporo-sphenoidal abscess; 6, Bulb of jugular (thrombosis); 11, Internal ear; 12, 12a, 13, Route of infection through internal ear giving rise to extradural abscess, meningitis, and cerebellar abscess. (After Hunter Tod.)
Fig. 74b. Diagram to show Surgical Anatomy for Operations for Otitic Intracranial Lesions. 1, Attic; 2, Antrum; 3, Point for opening temporo-sphenoidal abscess (just above and along the tegmen tympani); 4, External semicircular canal; 5, Lateral sinus; also shows area of bone removed in mastoid operation; 6, Bulb of jugular vein; 7, Facial nerve; 8, Point for opening cerebellum behind lateral sinus; 9, Point for opening cerebellum in front of lateral sinus (between sinus behind and external semicircular canal in front). (After Hunter Tod.)
In any case the abscess usually develops in the white substance of the brain, just beneath the grey matter, and in close relation to the primary source of infection.