Efferent arm of the pupillary light reflex (Fig. 4.26). The efferent fibers originate in the Edinger-Westphal nucleus and travel in the oculomotor nerve to the orbit. The parasympathetic preganglionic fibers branch off from the oculomotor nerve within the orbit and travel to the ciliary ganglion, whose ganglion cells constitute a synaptic relay station. The short postganglionic fibers emerge from the ciliary ganglion and then enter the globe to innervate the sphincter pupillae muscle (Fig. 4.26).
Lesions of the efferent pathway. If the oculomotor nerve or ciliary ganglion is damaged, the impulses from the Edinger-Westphal nucleus can no longer reach the sphincter pupillae muscle of the ipsilateral eye. The result is mydriasis with absence of the light reflex.
Other stimuli affecting the width of the pupils.The width of the pupils varies not only in response to the incident light but also in response to various kinds of stimuli arising outside the eye. Very painful stimuli, such as a deep pinch of the nuchal musculature, as well as heightened emotional arousal can induce pupillary dilatation. Themydriasis seen in these situations was long attributed to increased activity of the sympathetic nervous system, leading to contraction of the dilator pupillae muscle (which is discussed further below). Recent studies have shown, however, that decreased activity of the parasympathetic innervation of the pupil is probably the more important factor.
Anisocoria.The word “anisocoria” comes from the Greek and means, literally, inequality of the pupils (it is thus redundant to state, “The pupils are anisocoric”). A mild disparity of pupillary width is often noted in normal persons (physiological anisocoria), but a larger disparity should provoke suspicion of a (unilateral) intracranial mass compressing the oculomotor nerve. In clinical situations, it is important to remember that anisocoria is often produced by the instillation of dilating or constricting drugs into one eye (which should be avoided, for example, in comatose patients).
Sympathetic and Parasympathetic Innervation of the Eye
Parasympathetic innervation of the eye (Fig. 4.27). The parasympathetic innervation of the sphincter pupillae muscle and of the ciliary muscle was discussed above in connection with the pupillary light reflex and the accommodation reflex. Activation of the parasympathetic supply to the eye is manifested by pupillary constriction (miosis) and accommodation in response to a near object.
Sympathetic innervation of the eye(Fig. 4.27). The nuclear area from which the sympathetic innervation of the eye arises, the so-called ciliospinal center, is located in the lateral horn of the spinal cord from C8 to T2. The preganglionic fibers originate here and ascend to a relay station in the superior cervical ganglion, from which the postganglionic fibers emerge and then ascend together with the internal carotid artery and ophthalmic artery into the orbit, finally reaching and innervating the dilator pupillae, superior and inferior tarsal, and orbitalis muscles (Figs. 4.27 and 4.28). Other sympathetic fibers supply the sweat glands and blood vessels of the ipsilateral half of the face.
Afferent supply of the ciliospinal center: Afferent fibers from the retina travel to the hypothalamus (suprachiasmatic nucleus), in which the central sympathetic pathway arises. The pathway crosses the midline at the level of the midbrain and descends through the brainstem and cervical spinal cord to the ciliospinal center.
Horner syndrome(Fig. 4.28). A lesion affecting the central sympathetic pathway, the ciliospinal center, the superior cervical ganglion, or the postganglionic sympathetic fibers on their way to the eye produces a characteristic constellation of abnormalities, called Horner syndrome. The triad of ocular findings consists of: narrowing of the palpebral fissure (due to loss of function of the superior tarsal muscle), miosis (due to loss of function of the dilator pupillae muscle, resulting in a preponderance of the constricting effect of the sphincter pupillae muscle), and enophthalmos (due to loss of function of the orbitalis muscle). Anhidrosis and vasodilatation in the ipsilateral half of the face are seen when the sympathetic innervation of the face is also involved, either at the ciliospinal center or in the efferent fibers that emerge from it.