Pupillary constriction is a parasympathetic function and pupillary dilation is a sympathetic function (“wide eyed with fear”). The pupils constrict in response to light and accommodation, and dilate in response to darkness and adrenergic states. Pupillary asymmetry is referred to as anisocoria, and can be caused by a variety of neurologic and ophthalmologic conditions. Changes in pupil size can also be caused by medications. Miosis refers to an abnormally constricted pupil, and mydriasis refers to an abnormally dilated pupil (mnemonic: mydriasis is a longer word than miosis, and mydriasis refers to the larger pupil size [i.e., dilated]).
Pupillary constriction in response to light requires transmission of light information from the retina to the brain (afferent pathway), and signals from the brain to constrict the pupils (efferent pathway) (Fig. 10–1). The afferent pupillary light reflex fibers travel through the optic nerves, optic chiasm, and optic tracts, and then separate from the optic tracts to proceed to the pretectal nuclei of the dorsal midbrain (note the separation of light reflex afferents from visual pathway fibers at this point; the visual pathway fibers in the optic tracts proceed to the lateral geniculate nuclei; see Fig. 6–1). In the dorsal midbrain, the pretectal nuclei communicate with the Edinger-Westphal nuclei, which give rise to the efferent pupillary constrictor fibers that travel in the oculomotor nerves (CN 3). These parasympathetic pupillomotor fibers of CN 3 synapse in the ciliary ganglion in the orbit, and short ciliary neurons arising from the ciliary ganglion innervate the pupillary constrictor muscles of the iris. Each pretectal nucleus projects bilaterally to both Edinger-Westphal nuclei so that both pupils constrict equally in response to light input from either side. For example, light shined in the left eye causes constriction of both the left pupil (direct response) and the right pupil (consensual response) and vice versa.
Impaired pupillary constriction to light can be caused by dysfunction in the afferent pathway (most commonly CN 2 dysfunction) or the efferent pathway (CN 3 dysfunction).
If CN 2 is not functioning properly on one side (e.g., optic neuritis), no light will enter on that side, and so there will be neither a direct (ipsilateral) nor a consensual (contralateral) response to light shined on the affected pupil. However, since CN 2 is functioning on the unaffected side and both CN 3s are functioning, both pupils will constrict in response to light shined in the unaffected eye.
For example, if there is a lesion of CN 2 on the right (and the right CN 3, left CN 2, and left CN 3 are all intact), there will be no (or minimal) pupillary constriction in either eye when light is shined in the right eye, but both pupils will constrict when light is shined in the left eye (Fig. 10–2). In the swinging flashlight test in this situation, one would note bilateral pupillary constriction when light is shined in the left eye, but bilateral pupillary dilation (back to normal size) when light is shined in the right eye, since that light is not “seen” on the right due to right optic nerve dysfunction. The apparent dilation of the right eye after swinging the flashlight from the left pupil to the right pupil is due to the fact that the right pupil had constricted when light was shined in the left eye, and is returning to normal size since it does not “see” the light when the flashlight returns to the right eye. This is called a relative afferent pupillary defect (RAPD or Marcus Gunn pupil), which is most commonly caused by lesions of CN 2 (i.e., optic neuropathy; see “Monocular visual loss” in Chapter 6), but can also occur with severe unilateral or asymmetric retinal disease, or rarely with lesions in the optic chiasm, optic tract, or dorsal midbrain. An optic tract lesion as the cause of an RAPD results in contralateral hemianopia (see Ch. 6) and contralateral RAPD. A dorsal midbrain lesion as the cause of an RAPD will not cause any visual loss (since visual information proceeds to the lateral geniculate nucleus en route to the visual cortex, not the midbrain).
FIGURE 10–2
The swinging flashlight test and relative afferent pupillary defect. When light is shined in the right pupil (A), there is minimal reaction of the pupils on both sides. When light is shined in the left pupil (B), both pupils constrict. When the light is returned to the right pupil (C), the right pupil appears to dilate as compared to (B) whenit returns to its normal size. When light is returned to the left pupil (D), both pupils constrict. This patient has a right optic neuropathy. Reproduced with permission from Martin T, Corbett J: Practical Neuroophthalmology. New York: McGraw-Hill Education; 2013.
If there is CN 3 dysfunction on one side and all else is working, the pupil on the side of the dysfunctional CN 3 will not respond to light in either eye since its pupillary constrictors cannot be activated. However, since CN 2 on the side of CN 3 dysfunction is still intact, light shined in the pupil on the side of CN 3 dysfunction will be seen and will signal the constriction of the contralateral pupil. For example, if there is left CN 3 dysfunction, light shined in either eye will cause right-sided pupil constriction, but the left pupil will not constrict in response to light shined in either eye since CN 3 is not working on that side to “transmit the message” to the left pupil to constrict no matter which eye has light shined in it.
CN 3 also controls several extraocular movements and eyelid elevation in addition to pupillary constriction (see Ch. 11). Therefore, a complete CN 3 palsy will cause multiple eye movement abnormalities in addition to pupillary dilation/lack of response to light. However, since the pupillary constrictor fibers run on the medial exterior of the nerve, they can be compressed in isolation without causing eye muscle weakness (e.g., by posterior communicating artery aneurysm, tumor, or uncal herniation). See Chapter 11 for further discussion of CN 3 palsy.
The pathway for pupillary dilation begins in the hypothalamus, travels in the dorsolateral brainstem, and descends to the lower cervical/upper thoracic spinal cord before traveling upward to the eye by way of the lung apex, and then along the internal carotid through the neck and cavernous sinus en route to the orbit (Fig. 10–3). This pathway has three components:
First-order neurons travel from the hypothalamus through the brainstem to the intermediolateral column (ciliospinal center of Budge).
Second-order (preganglionic) neurons travel from the spinal cord over the lung apex to the superior cervical ganglion.
Third-order (postganglionic) neurons travel from the superior cervical ganglion to the eye, traveling alongside the internal carotid artery in the neck and cavernous sinus.
FIGURE 10–3
The sympathetic pathway for pupillary dilation. Reproduced with permission from Aminoff M, Greenberg D, Simon R: Clinical Neurology, 9th ed. New York: McGraw-Hill Education; 2015.
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