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In the spinal cord, the central sympathetic tract makes contact with neurons at the lateral horns of the spinal cord at the C8 and T1 segments. These neurons constitute the second group of neurons. The area where these neurons are located is called the Budge ciliospinal center (Figure 187.1 [2]). Fibers from these neurons leave the spinal cord with the appropriate anterior roots and travel with the spinal nerve briefly. They exit the spinal nerve and form a bundle of fibers that give rise to the cervico-thoracic sympathetic trunk. The oculosympathetic fibers climb in this trunk adjacent to the carotid artery to make contact with neurons in the superior cervical ganglion (Figure 187.1 [3]). The neurons in this ganglion constitute the third group of neurons. Fibers from neurons in the superior cervical ganglion travel with the internal carotid through the cavernous sinus, enter the orbits, and innervate the muscles of Müller and the pupillary dilator muscle (Figure 187.1).

Figure 187.1. Oculosympathetic pathway is represented as a blue line. The pathway originates in the posterior hypothalamus; from there it travels ipsilaterally to the Budge ciliospinal center; from the Budge ciliospinal center it travels to the superior cervical ganglion; from the superior cervical ganglion it enters the skull and then the orbit. The facial sympathetic pathway takes a similar path until the superior cervical ganglion; from the superior cervical it travels with the external carotid artery.

Oculosympathetic system dysfunction manifest during wakefulness. The affected eye can not open as wide as the normal eye (Figure 187.2). A lesion in the oculosympathetic system may occur anywhere in its trajectory.


Figure 187.2.— Oculosympathetic lesion. [A] No facial asymmetry while crying. [B] Facial asymmetry is restricted to the upper quadrant and it is only present during quiet awake.

Oculosympathetic pathway damage produces Horner syndrome. The manifestations of Horner syndrome are ptosis, miosis, and anhydrosis. Brainstem lesions involve the central sympathetic tract and produce anhydrosis involving the face and body. The pathology of a brainstem lesion is usually not found. Lesions in the brachial plexus (Figure 187.1 [A]) are more common than brainstem lesions. They involve the cervico-thoracic sympathetic trunk. These lesions occur either at C8, T1, or T2 ventral roots or spinal nerves. Anhydrosis only involves the face. Horner syndrome due to brachial plexus injury results from trauma, but may also occur with congenital chickenpox or with involvement outside of the brachial plexus in the thoracic spine. Horner syndrome is usually associated with Klumpke palsy. Horner syndrome may also occur with congenital neuroblastomas. The cause of Horner syndrome is often not found. Neonates with Horner syndrome without an obvious cause should have an MRI of the brain and neck, and blood studies searching for the possibility of excessive catecholamine secretion.


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third neuron in the oculosympathetic pathway frequent site of injury superior cervical ganglion second neuron in the oculosympathetic pathway at the Budge center brachial plexus common carotid artery common carotid artery Budge ciliospinal center internal carotid artery external carotid artery internal carotid artery first neuron in the oculosympathetic pathway external carotid artery central sympathetic tract cavernous sinus pupil dilator muscle muscle of Muller muscle of Muller muscle of Muller Alfonso, 1984 Pause pointer on different areas of the figure for labels. Figure must be centered. pipillary dilator muscle muscle of Müller muscle of Müller superior orbital fisure naso-ciliary branch of the fifth cranial nerve naso-ciliary branch of the fifth craneal nerve cavernous sinus internal carotid artery foramen lacerum skull skull external carotid artery common carotid artery superior cervical ganglion first thoracic spinal nerve first thoracic root Budge ciliospinal center area fo the foramen magnum cervical spine medulla pons midbrain posterior hypothalamus