The actual cause of the neuritis is still a matter of doubt. It is possible that the same cause is not present in every case. Still, sufficient evidence is to hand to justify the probability that neuritis is dependent on the general increase of intracranial pressure--there is, at any rate, a close relationship between the two. The cerebro-spinal fluid is forced into and dammed up within the vaginal sheaths of the optic nerve, leading, in the first instance, to an œdema, and later on, to compression of the lamina cribrosa and interference with the circulation. The increase of intraventricular pressure may also act directly on the optic tracts and chiasma--the anterior boundaries of the third ventricle--the pressure being then transferred directly to the nerve tracts. Furthermore, the great intensity, great frequency of occurrence, and rapid development of optic neuritis when the tumour is subtentorial in position may be explained on the hypothesis that the rigid enclosure of the cerebellum permits of the ready application of pressure to the veins of Galen or to the iter, thus leading to an increase of intraventricular pressure, this pressure being then transferred to the optic region. The alternative theory states that the old tissue destruction and the new tissue formation sets free certain toxic substances which act on the optic nerve-fibres, leading to œdema and inflammation. Paton, however, comes to the conclusion that ‘the nature of the tumour does not play any part in determining the onset of neuritis except in so far as the nature determines its localization’. Whatever be the localizing value of optic neuritis, it is generally accepted that it commences in the upper nasal quadrant. Visual acuity is but little impaired in the earlier stages of optic neuritis, but so soon as atrophic changes develop, diminution in the field of vision occurs. The pupillary changes associated with tumours of the brain are closely connected with these fundus changes. In the early stages, the pupils may be contracted with the object of protecting the inflamed surfaces exposed to light, whilst, when atrophy develops, the pupils may steadily dilate, becoming fully dilated and fixed as the atrophic changes become fully developed. These pupil changes must therefore be taken into consideration in estimating the value of pupillary changes in general. =Vomiting.= Vomiting is dependent on stimulation of the medullary vomiting centre, or on irritation of the dura mater in the immediate neighbourhood of the tumour. The dura is supplied by branches of the fifth cranial nerve, the stimulus being referred to the vagus centre in the floor of the fourth ventricle.