Sensory nerve responses elicited by experimental ocular hypertension.

In order to clarify the neurophysiological mechanisms underlying the pain sensations that accompany certain forms of glaucoma, the responses of ocular sensory fibers to artificially induced intraocular pressure increases were studied in the cat. In lightly anesthetized animals, intraocular pressure elevations up to 120 mmHg did not evoke the sustained reflex changes in arterial pressure or heart rate that would be suggestive of strong nociceptive stimulation. Multiunit activity recorded from filaments of mixed ciliary nerves showed a sharp frequency increase (phasic response) at the onset of intraocular pressure elevations of 20 mmHg or more. In half of the nerves, the discharge stabilized at a higher firing frequency throughout the rise in pressure (tonic response). Corneal units fired phasically in response to intraocular-pressure elevations, and in one third of them this burst of impulses was followed by a low-frequency tonic discharge. Most of the fibers sensitive to light mechanical stimulation of the scleral surface discharged only phasically when intraocular pressure was raised to values of 60 mmHg or more, whereas high threshold scleral fibers were totally insensitive. Iridial fibers responded in all cases to ocular hypertension with a phasic response that became progressively tonic with higher intraocular-pressure values. It is concluded that mechanical deformation of the ocular structures resulting from intraocular-pressure elevations to pathological levels causes only transient excitation of most ocular sensory fibers. Hence, mechanical stimulation appears to be directly responsible only for the transient pain sensations during acute intraocular pressure increases experienced by glaucoma patients.