INTERVERTEBRAL DISK DISEASE

Having commentedupon the site of orrgm of the intraocular fluid, and discussedin some degreeits mode of exit, we may now mention certain facts establishedexperimentally, and collate these with the observed symptoms and signs of glaucoma. In so doing we may producethe hypothesis which seemsmost likely to unlock its secrets. This, then, is an attempt to bridge the gap between the laboratory and the clinician. Though the nature of progress is to reduce this gap, only in completed acts of research,of course, can it. be abolished, and the problem of glaucoma falls far short of this distinction. It has been known for some time that there is a regular daily variation of the tension of the normal eye, averaging from one to two milhmetres of mercury (Schiotz); the tension usually rises to 8 a.m. and falls through the remainderof the day. Experimental evidence has made it likely that the underlying cause of this is a rhythmic alteration in the capillary pressureof the eye. The vascular eventsduring this variation are seen to be as follows. The pressure,both systolic and diastolic, in the anterior ciliary arteries remains constant, but the venous pressureshows changescomparablewith those of the intraocular pressure, and it is observed t hat these venous changesprecede the alteration in tension of the eye. As the venouspressureis readily reflected in the pressurein the capillary circulation, it seemsunlikely that this variation in the venouspressure is itself primary, and presumably it dependson events in the capillary bed. In primary simple glaucoma, the intraocular base pressure of the eye may remain normal. but the variations run riot, and it is as if in this state of wide oscillations the eye has lost some power of vascular control. At first and fc,r a long period the tension is able to return to normal, but It eventually remains high and the base pressurerises also. When such a stateof irreversibility has been reached, one might expect some similar irreversible state to have developedin the capillaries. Indeed, in such eyes as have come to examination,widespreadsclerosis of the capillaries Is seen. The suggestionis that while the sclerosis is confined to the posterior segmentof the eye, the Intraocular tension is not greatly disturbed. When the areas of sclerosis are considerable enough to affect the overlying retina, its nervous elementsperish, with the production of scotomata. The nerve fibres degeneratecentripetally to the optic disk. The optic nerve shows areas of disappearanceof nerve fibres without compensatingincrease In glial substance,so that empty lacunreare formed and cupping occurs. Similar lacunasor cavernsmay occur far up the nerve where raised Intraocular tension could not account for them, and the picture is one commonly seen in any highly differentiated organ when the blood supply is cut off. Cuppingis primarily due to this process,though, of course, a raised intraocular tension will increaseit. A similar picture is seenin lacunar atrophy of the brain, when the cerebral cortex degenerates in the sameway in the condition of senile vascularsclerosis.