Sometimes, diseases can affect the sympathetic control of the pupil. For instance, interruption of the sympathetic innervation of the head and neck leads to a condition called Horner's syndrome. This syndrome is characterized by abnormal pupillary constriction (miosis), drooping of the upper eyelid (ptosis) due to paralysis of the superior tarsal muscle, and loss of sweating (anhidrosis) on the face. In certain animals like rats, cats, and dogs, enophthalmos (retraction of the eye into the orbit) may also occur, but in humans, true enophthalmos does not occur. However, there is an apparent enophthalmos, which is an illusion created by partial closure of the eyelid due to ptosis. Horner's syndrome can be caused by a lesion that destroys the sympathetic preganglionic neurons in the upper thoracic spinal cord, interrupts the cervical sympathetic chain, or damages the lower brainstem in the region of the reticular formation, through which pathways descend to the spinal cord to activate sympathetic preganglionic neurons. In the last case, there is also a loss of sweating on the side of the body ipsilateral to the lesion.

The size of the pupil is reduced by the pupillary light reflex and during accommodation for near vision. In the pupillary light reflex, light that reaches the retina is processed by retinal circuits that excite W-type retinal ganglion cells. These cells respond to diffuse illumination. Some of the W-type cells' axons project through the optic nerve and tract to the pretectal area, where they synapse in the olivary pretectal nucleus. This nucleus contains neurons that also respond to diffuse illumination. Activity of neurons in the olivary pretectal nucleus causes pupillary constriction through bilateral connections with parasympathetic preganglionic neurons in the Edinger-Westphal nuclei. This reflex leads to contraction of the pupillary sphincter muscles in both eyes, even when light is shone into only one eye.

The accommodation response, which is important for focusing on near objects, involves pupillary constriction, increasing the curvature of the lens, and convergence of the eyes. This response is triggered by information from M cells of the retina that is transmitted to the striate cortex through the geniculostriate visual pathway. The specific stimuli that trigger accommodation are believed to be a blurred retinal image and disparity of the image between the two eyes. After the information is processed in the visual cortex, signals are transmitted to the middle temporal cortex, where they activate neurons in a visual area called MT. Neurons in area MT transmit signals to the midbrain, which activate parasympathetic preganglionic neurons in the Edinger-Westphal nuclei, resulting in pupillary constriction. Simultaneously, signals are transmitted to the ciliary muscle, causing it to contract. The contraction of the ciliary muscle allows the lens to round up and increase its refractive power. (Convergence is a somatic response mediated by neurons in the oculomotor [cranial nerve III] nucleus of the midbrain.)
Sympatheticcontrolofthepupilissometimesaffectedbydisease.Forexample,interruptionofthesympatheticinnervationoftheheadandneckresultsinHorner’s syndrome. Thissyndromeischaracterizedbythetriadofmiosis(abnormalpupillaryconstriction),ptosis(causedbyparalysisofthesuperiortarsalmuscle),andanhydrosis(lossofsweating)ontheface.Enophthalmos (retractionoftheeyeintotheorbit)alsooccursinsomeanimals(rats,cats,anddogs,amongothers),butinhumansnotrueenophthalmosoccurs;however,thereisanapparentenophthalmos,anillusioncreatedbypartialclosureoftheeyelidfromtheptosis.Horner’ssyndromecanbeproducedbyalesionthat(1)destroysthesympatheticpreganglionicneuronsintheupperthoracicspinalcord,(2)interruptsthecervicalsympatheticchain,or(3)damagesthelowerbrainstemintheregionofthereticularformation,throughwhichpathwaysdescendtothespinalcordtoactivatesympatheticpreganglionicneurons.Inthelastcase,thereisalsoalossofsweatingonthesideofthebodyipsilateraltothelesion.
Pupil size is reduced by the pupillary light reflex and during accommodation for near vision. In the pupillary light reflex, light that strikes the retina is processed by retinal circuits that excite W-type retinal ganglion cells (see
Chapter 8). These cells respond to diffuse illumination. The axons of some of the W-type cells project through the optic nerve and tract to the pretectal area, where they synapse in the olivary pretectal nucleus. This nucleus contains neurons that also respond to diffuse illumination. Activity of neurons of the olivary pretectal nucleus causes pupillary constriction by means of bilateral connections with parasympathetic preganglionic neurons in the Edinger-Westphal nuclei. The reflex results in contraction of the pupillary sphincter muscles in both eyes, even when light is shone into only one eye.
The accommodation response, which is important for focusing on near objects, involves pupillary constriction, increasing the curvature of the lens, and convergence of the eyes. This response is triggered by information from M cells of the retina that is transmitted to the striate cortex through the geniculostriate visual pathway (see ). The specific stimuli that trigger accommodation are thought to be a blurred retinal image and disparity of the image between the two eyes. After the information is processed in the visual cortex, signals are transmitted directly or indirectly to the middle temporal cortex, where they activate neurons in a visual area known as MT. Area MT neurons transmit signals to the midbrain that activate parasympathetic preganglionic neurons in the Edinger-Westphal nuclei, which results in pupillary constriction. At the same time, signals are transmitted to the ciliary muscle that cause it to contract. The ciliary muscle contraction allows the lens to round up and increase its refractile power. (Convergence is a somatic response mediated by neurons in the oculomotor [cranial nerve III] nucleus of the midbrain.)