Traumatic cysts within the calvarium, whatever their situation, may be divided into two definite groups:—
1. Where the cyst possesses fibrinous walls (in which hæmatoidin cysts may be deposited) and contains a grumous material. These cysts are usually subdural in position, are dependent on the previous existence of a hæmatoma, and are known as ‘blood-cysts’.
2. Where the cyst—often of considerable size—is lined by a thin, shiny, membranous wall. The contained fluid is almost colourless, closely resembling cerebro-spinal fluid, but albuminous and having no sugar-reducing reaction. The fluid is at high tension, spurting out when the cyst is punctured. The cyst usually lies in relation to the arachnoid membrane. Hence the name, ‘arachnoid cyst’.
To account for the development of these ‘arachnoid cysts’ two theories have been advanced. Firstly, that they arise as the ultimate result of a long-continued circulatory disturbance of the vessels of the membranes or of the cortex, with consequent local cystic accumulation of cerebro-spinal fluid or serum; and secondly, that shrinking of the brain occurs in the region of an injury as the result of sclerotic changes in the cerebral substance, any contraction tending to lead to the formation of a vacuum which becomes filled with fluid derived from the surrounding membranes. According to this latter theory, arachnoid cysts are in reality ‘cysts ex vacuo’.
As regards symptomatology, little need be said. Occasionally ‘arachnoid cysts’ of considerable size have been discovered at post-mortem examinations which appeared to have exercised no local or general pressure effects during life. More often the cysts, whether ‘blood-cyst’ or ‘arachnoid cyst’, lead to the development of Jacksonian epilepsy, chronic headache, and the like, and are discovered during the exploratory operation carried out for such conditions. Occasionally they may be shelled out entire, but it is more usual for the surgeon to remain content with the removal of the parietal wall (see [p. 195]). The results obtained by surgical treatment are sufficiently gratifying.
TRAUMATIC ORBITAL ANEURYSM
(Pulsating Exophthalmos)
This condition was first investigated by Rivington in 1875. Since that date many other cases have been reported, and the following remarks are based on the examination of the records of 26 cases, 2 of which have come under my own care.
The nature of the trouble, the results obtained by operative treatment, and the direct evidence supplied by post-mortem examination furnish sufficient proof to justify the statement that the symptoms are dependent on the formation of an arterio-venous aneurysm, the internal carotid artery and the cavernous sinus intercommunicating by means of one or more fistulous channels. That such a lesion may arise from direct violence—the introduction of some sharp weapon along the upper and inner portion of the orbital cavity—-is readily comprehensible. Such injuries are, however, of rare occurrence, and the formation of the aneurysmal communication is usually the result of indirect violence—the application of severe blows to the antero-lateral and lateral aspects of the head.
In explanation, the following preliminary facts may be accepted:—
In the great majority of cases the blow was applied to the temporal region, the patient was rendered unconscious, bleeding freely from the ear, nose, and mouth, and remained under treatment for some considerable time. From these facts it may be assumed that the patient suffered from a fracture of the base of the skull—anterior or middle fossa, or both fossæ. Evidence has already been brought forward to show (1) that the majority of fractures involving both anterior and middle fossæ traverse the body of the sphenoid, and (2) that the cavernous sinus is very susceptible to injury. It was also demonstrated that the internal carotid artery is only liable to injury in that part of its intracranial course where it is embedded in the outer wall of the cavernous sinus. Two instances of such a lesion have been described in the section dealing with injuries to intracranial vessels (see [p. 148], and [Figs. 53] and [54]).