- Damage to the sympathetic chain is most commonly responsible for Horner's syndrome.
- Horner's syndrome is characterized by a classic triad of symptoms: ptosis (drooping of the upper eyelid), miosis (constriction of the pupil), and anhidrosis (loss of sweating) on the affected side of the face.

- The reason for this is that Horner's syndrome results from disruption of the sympathetic nerve supply to the eye and face.
- The sympathetic pathway begins in the hypothalamus, descends through the brainstem, and synapses in the cervical sympathetic chain, specifically at the superior cervical ganglion.
- Damage at any point along this pathway, but most commonly in the cervical region of the sympathetic chain, leads to the syndrome.

- In contrast, the oculomotor nerve (cranial nerve III) controls most of the extraocular muscles and the pupillary constrictor via parasympathetic fibers.
- Lesions here cause a different set of signs, such as a “down and out” eye and a dilated pupil.

- The trochlear nerve (cranial nerve IV) innervates the superior oblique muscle of the eye and does not contribute to sympathetic innervation.

- Similarly, the facial nerve (cranial nerve VII) is responsible for motor innervation to facial muscles and parasympathetic fibers to lacrimal and salivary glands, but not sympathetic pathways.

Therefore, damage to the sympathetic chain is the most common cause of Horner's syndrome.

Reference: Adams and Victor’s Principles of Neurology, 11th Edition, Volume 1, Chapter 8/Pages 150-152