The Surgery of the Skull and Brain

by Louis Bathe Rawling

The state of irritation subsides or merges into that of cerebral compression.

Compression.

Its pathology. A compression force—whether foreign body, blood extravasation, abscess or tumour—must act on the brain substance or on the fluid constituents of the skull. The brain, however, is itself incompressible. It may be squeezed like a sponge, but its actual structure is unalterable. Consequently, the compressing force exercises its main influence on the fluid contents, driving out the cerebro-spinal fluid, depleting the cerebral veins and emptying the arterioles, producing in other words a state of brain anæmia.

Experimentally, it has been ascertained that from 3 to 6 per cent. of the cranial capacity can be taken up by a foreign body without producing compression symptoms—probably owing to the escape of cerebro-spinal fluid into the spinal canal, and the recession of the medulla and cerebellum into the foramen magnum. Furthermore, it would appear that the incidence of compression symptoms is associated with depletion of those cerebral veins which are in closest relation to the compression force. As this force increases—for example, in middle meningeal hæmorrhage—the pressure exercised on the surrounding regions increases proportionately, to the level of the capillary pressure, and even to that of the smaller arteries. A state of cerebral anæmia results, first localized to the region primarily involved, then invading more widely and finally affecting both supra- and infra-tentorial spaces.

With regard to the continuity of pressure between these three spaces, there is but little pressure discontinuity between the two supra-tentorial spaces, whilst, between the supra- and infra-tentorial regions, there is less ready communication.

A slight degree of compression in the supra-tentorial space will act on the corresponding space only, greater degrees will involve all three. On the other hand, a rise of infra-tentorial pressure is not of necessity associated with a corresponding elevation in the other two regions. For example, a cerebellar tumour readily affects the medullary centres, whilst the higher cortical regions are for the time being totally unaffected. Again, a tumour situated in the frontal pole does not necessarily produce any of those symptoms of cerebral compression which are regarded as referable to an increase of subtentorial pressure—slow pulse, vaso-motor disturbances, subnormal pressure, and deep rhythmical respiration.

Returning once more to the vascular effects of a localized compression, it is obvious that whilst the compressing force is producing a surrounding anæmia—depleted veins and arterioles—yet that the neighbouring but more distant brain is venously engorged—from venous retardation. Insomuch, moreover, as the venous tension and cerebro-spinal pressure are equal, it is obvious that, as the result of venous engorgement, there is some surrounding serous transudation into the perivascular, pia-arachnoid, and cerebral regions. The brain bordering on the anæmic area is therefore œdematous, the œdema diminishing and fading away in direct proportion to the distance of the area involved from the primary focus of compression.

If the compression force is of a progressive nature, the engorged area becomes in turn anæmic, and still more distant regions become engorged and œdematous. This state is known as that of progressive œdema. Its complete development is largely dependent on brain infection—abscess of the brain, &c.

The rapidity with which the symptoms of compression develop are largely dependent on the producing cause. Thus, three examples may be cited:—

(1) Compression of slow development, requiring weeks or months before typical symptoms are observable—e. g. tumour formation.