A study of pupil response components in human vision
The overall aim of the research described in this thesis was to investigate the basic mechanisms of the pupil of the eye in relation to human vision and brain function. It also evaluates the potential application of new research techniques to clinical studies that involve assessment of the visual function. Pupil response components were investigated in normal subjects and in patients with damaged visual pathways. A series of experiments were carried out to investigate the pupil response to periodic modulation of several stimulation parameters such as: luminance contrast, stimulus size, spatial and temporal frequency content, and colour. Much larger responses were found for square-wave as compared to sinusoidal luminance modulation. A model with two populations of neurones (sustained and transient) was developed to explain the non-linear combination of two response components in the light reflex. In contrast to these findings, responses to isoluminant coloured stimuli or sinusoidal gratings whose spatial average luminance is equal to that of the background do not depend of the temporal wave-form of the stimulation. Studies in patients with lesions to specific areas in the brain suggest that these responses are caused by a transient weakening of the steady central sympathetic inhibition to parasympathetic neurones innervating the sphincter muscle as a result of cortical processing of specific stimulus attributes such as colour and spatial structure. Pupil measurements in patients suffering from demyelinating neurological disorders such as multiple sclerosis and optic neuritis also confirm the existence of distinct pupil response components and reveal selective loss to chromatic and luminance pathways. The results indicate a preferential damage to thinner axons which are thought to predominantly mediate the chromatic responses. These studies suggest that the use of modern pupillometric techniques in neuro-ophthalmology can yield useful information on the extent of the damage and the progression of disease in lesions of the optic nerve.