If an optic nerve lesion is present the affected pupil will not constrict to light when light is shone in the that pupil during the swinging flashlight test. It is important to be able to differentiate whether a patient is complaining of decreased vision from an ocular problem such as cataract or from a defect of the optic nerve. It is due to damage inoptic nerve or severe retinal disease. Relative Afferent Pupillary Defect (RAPD, Marcus Gunn Pupil)Īn RAPD is a defect in the direct response.
They synapse at the superior cervical ganglion where third-order neurons travel through the carotid plexus and enter into the orbit through the first division of the trigeminal nerve. Post synaptic neurons travel down all the way through the brain stem and finally exit through the cervical sympathetic chain and the superior cervical ganglion. Sympathetic innervation begins at the cortex with the first synapse at the cilliospinal center (also known as Budge's center after German physiologist Julius Ludwig Budge). Dilation is controlled by the dilator pupillae, a group of muscles in the peripheral 2/3 of the iris. Sympathetic innervation leads to pupillary dilation. The fibers enter the orbit with CNIII nerve fibers and ultimately synapse at the cilliary ganglion. The pathway of pupillary constriction begins at the Edinger-Westphal nucleus near the occulomotor nerve nucleus. The fibers of the sphincter pupillae encompass the pupil. A circular muscle called the sphincter pupillae accomplishes this task.
Parasympathetic innervation leads to pupillary constriction. The physiology behind a "normal" pupillary constriction is a balance between the sympathetic and parasympathetic nervous systems.
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