Why doesn't Horner syndrome include Cranial Nerve (CN) 3 extraocular movements?

From the Guidelines

Horner syndrome does not include Cranial Nerve (CN) 3 extraocular movement deficits because it results from disruption of the sympathetic pathway to the eye, not the oculomotor nerve (CN 3) pathway. The presentation of oculomotor palsy, which affects CN 3, is characterized by diplopia, ptosis, and difficulty reading due to accommodative deficiency, as noted in a 2024 study on adult strabismus preferred practice pattern 1. In contrast, Horner syndrome classically presents with ptosis, miosis, and anhidrosis on the affected side due to interruption of sympathetic innervation. Key differences between the two conditions include the involvement of extraocular muscles, with CN 3 palsy causing outward and downward deviation of the eye, diplopia, and pupillary dilation, whereas Horner syndrome spares extraocular movements. Some of the key features of CN 3 palsy, as described in the 2024 study, include an incomitant deviation, with the eye abducted, infraducted, and incyclotorted as a result of preserved lateral rectus muscle and superior oblique muscle function 1. The distinct neural pathways involved in Horner syndrome and CN 3 palsy explain why extraocular movements are not affected in Horner syndrome. The sympathetic pathway, which is disrupted in Horner syndrome, begins in the hypothalamus, descends through the brainstem and spinal cord, exits at T1, travels up the sympathetic chain to the superior cervical ganglion, and then follows the carotid artery to the eye. In contrast, CN 3 is a parasympathetic and somatic motor nerve that controls most extraocular muscles and upper eyelid elevation via the levator palpebrae superioris. The separate neural pathways involved in these conditions are crucial in understanding why Horner syndrome does not include CN 3 extraocular movement deficits. The clinical presentation and underlying pathology of Horner syndrome and CN 3 palsy are distinct, with different effects on extraocular movements and other ocular functions.

From the Research

Horner Syndrome Characteristics

• Horner syndrome is characterized by a triad of symptoms, including:
  • Ipsilateral miosis (pupillary constriction)
  • Ptosis (eyelid drooping)
  • Anhidrosis (reduced sweating on the affected side of the face) 2, 3, 4, 5
• The syndrome results from the interruption of sympathetic innervation to the eye and ocular adnexae 5

Cranial Nerve 3 Extraocular Movements

• Horner syndrome does not typically involve Cranial Nerve (CN) 3 extraocular movements, as CN 3 is responsible for controlling most of the eye's movements, including adduction, abduction, elevation, and depression, and is not directly affected by the sympathetic nervous system pathway involved in Horner syndrome 2, 3, 4, 5
• The symptoms of Horner syndrome are related to the disruption of the sympathetic nervous system, which affects the pupil, eyelid, and facial sweating, but not the extraocular muscles controlled by CN 3 6

Pathophysiology and Etiology

• Horner syndrome can result from disruption of the sympathetic nervous system at any point along its course, from the hypothalamus to the orbit 2, 3, 4, 5
• The etiology of Horner syndrome can be varied, including congenital, traumatic, infectious, or neoplastic conditions, and may involve the cervical sympathetic chain 4