Physiology of Astigmatism

We know that the expression emmetropia is a conventional one and that in fact all normal human eyes have mild degrees of spherocylindrical errors (Shilo, 1997) or consist of a bitoric optical system, i.e. have principal meridians of relatively higher and lower powers at right angles. It is generally accepted that genetic factors have a significant role in determining ocular refractive status as well as astigmatism (Hammond et al., 2001) but many conditions and procedures such as surgery, suturing, wound healing, and ocular comorbidities modify the cylindrical status of the eye. Induced astigmatism and surgical correction of astigmatism are extensively addressed in other chapters of this book. Manifest astigmatism is the vectorial sum of anterior corneal toricity and internal astigmatism. A variety of factors change the magnitude and shift the meridians of these cylindrical components and the perceived subjective astigmatism throughout life. Astigmatism is an extremely dynamic phenomenon, and changes in the shape of optical interfaces, refractive index, optical aperture, eyeball-extraocular structures (eyelids and extraocular muscles) interaction, visual tasks, accommodation, binocularity, tear film status, and even body position induce and modify baseline ocular astigmatism. In this chapter we shall focus on factors that determine baseline, diurnal, functional, and dynamic aspects of ‘physiological astigmatism’.