The bodies of its preganglionic sympathetic afferent neurons are located in the lateral horn of the spinal cord.

Post-ganglionic efferents then leave the SCG and join the internal carotid nerve plexus of the internal carotid artery, accompanying first this artery and subsequently its branches to reach the orbit and ultimately innervate the dilator pupillae muscle to mediate pupillary dilatation.

The internal carotid plexus carries the postganglionic axons of the SCG to the eye, lacrimal gland, mucous membranes of the mouth, nose, and pharynx, and numerous blood vessels in the head.

[8] The SCG provides sympathetic innervation to the eye and lacrimal gland, regulating vasoconstriction in the iris and sclera, pupillary dilation, widening of the palpebral fissure, and the reduced production of tears.

[9] The SCG innervates blood vessels of the skin mediates vasoconstriction, regulating body heat loss.

The SCG is connected with vestibular structures, including the neuroepithelium of the semicircular canals and otolith organs, providing a conceivable substrate for modulation of vestibulo-sympathetic reflexes.

Horner's syndrome is a disorder resulting from damage to the sympathetic autonomic nervous pathway in the head.

[7] Lesion or significant damage to the SCG results in a third order neuron disorder (see Horner's Syndrome: Pathophysiology).

In the late 19th century, John Langley discovered that the superior cervical ganglion is topographically organized.

When left to their own accord, the fibers reinnervated the SCG and the initial autonomic reflexes were recovered, though there was limited recovery of pineal gland function.

These ganglia are studied as synaptic connections show many similarities to the central nervous system (CNS) and are also relatively accessible.