The most common stimulus for pupillary constriction is exposure of the retina to light. Reflex pupillary constriction is also part of the act of convergence and accommodation for near objects (near synkinesis).
The pathway for the pupillary light reflex consists of three parts (Fig. 13-9). There is an afferent limb, fibers of which originate in the retinal receptor cells, pass through the bipolar cells, and synapse with the retinal ganglion cells. In addition to stimulating rod and cone photoreceptors, light also drives pupillary constriction by stimulating special intrinsically photosensitive retinal ganglion cells (ipRGC) that contain melanopsin and directly signal the presence of light (Hattar). The light reflex fibers course through the optic nerve and chiasm and then leave the optic tract just rostral to the lateral geniculate body and enter the rostral midbrain, where they synapse in the pretectal nucleus. From here, the special intercalated neurons pass ventrally to the ipsilateral Edinger-Westphal nucleus and, via fibers that cross in the posterior commissure, to the contralateral Edinger-Westphal nucleus as well (Fig. 13-9). The effector arm of the reflex consists of an efferent two-neuron pathway from the Edinger-Westphal nucleus that synapses in the ciliary ganglion, from which the short ciliary nerves innervate the sphincter to cause pupillary constriction. Following initial constriction, the pupil may normally dilate slightly in spite of a light shining steadily in one or both eyes.
Alterations of the Pupils
The pupils tend to be large in children and small in the aged, sometimes markedly miotic but still reactive (senile miosis). An asymmetry of the pupils of 0.3 to 0.5 mm is found in 20 percent or more of normal individuals (Lam). Normally the pupil constricts under a bright light (direct reflex), and the other unexposed pupil also constricts (consensual reflex). With complete or nearly complete interruption of the optic nerve, the pupil will fail to react to direct light stimulation; however, the pupil of the blind eye will still show a consensual reflex, that is, it will constrict with illumination of the healthy eye. Contrariwise, lack of direct and consensual light reflex with retention of the consensual reflex in the opposite eye places the lesion in the efferent limb of the reflex arc, that is, in the homolateral oculomotor nerve or its nucleus. A lesion of the afferent limb of the light reflex pathway will not affect the near responses of the pupil, and lesions of the visual pathway caudal to the point where the light reflex fibers leave the optic tract will not alter the pupillary light reflex (Fig. 13-9).
The “relative afferent pupillary defect,” or Marcus Gunn pupillary sign, exposes a retrobulbar optic neuropathy. It is best identified by the “swinging-flashlight test,” in which each pupil is alternately exposed to light at 1-s intervals; the pupils both show a poor constriction or even paradoxical dilatation when light is shined on the side of an optic neuropathy. It is best to assess in a dimly lighted room with the patient fixating on a distant target.
Hippus, a rapid fluctuation in pupillary size, is common in metabolic encephalopathy but otherwise has no particular significance and is occasionally seen in normal persons. To distinguish hippus from the Marcus Gunn afferent pupillary defect one carefully observes the first movement of the pupil as the light is repeatedly moved to the affected eye; in hippus, half of the initial responses will be dilation and half, constriction, whereas in a deafferented pupil all the initial movements are dilation.