12/2/2023 0 Comments Pupil constriction reatment![]() ![]() The ipsilateral face is involved in lesions involving the second-order neurons. Anhidrosis with first-order neuron lesions affects the ipsilateral side of the body as the sympathetic supply from its central origin. Ipsilateral anhidrosis, another classic presentation, depends on the level of interruption of the sympathetic supply. The reaction of the pupils to light and accommodation is normal as those systems do not depend on sympathetic nerve supply. When disrupted, parasympathetic supply is uninhibited, and constriction of the pupil (miosis) ensues. The sympathetic nervous supply is responsible for pupil dilationupil (mydriasis). ![]() The lower eyelid may be slightly elevated owing to denervation of the lower lid muscle, which is analogous to the superior tarsal muscle. This explains the partial ptosis seen in Horner syndrome. The superior tarsal muscle is responsible for keeping the upper eyelid in a raised position after levator palpebrae superioris raises it. Denervation of this muscle causes ptosis, which is milder than oculomotor (CN III) palsy which supplies the levator palpebrae superioris. Superior tarsal muscle helps raise the upper eyelid and has a sympathetic nerve supply. The symptomology depends on the location of the lesion, and severity depends on the degree of denervation. The fibers then exit the cavernous sinus to enter the orbit via the superior orbital fissure and the ophthalmic branch (V1) of the trigeminal nerve (CN V) as the long ciliary nerves.Īs previously described, Horner syndrome is a consequence of sympathetic disruption. The remaining fibers ascend along the internal carotid artery in the carotid plexus to eventually enter the cavernous sinus, where they join the abducens nerve (CN VI). Third-order, postganglionic fibers branch off into the sudomotor and vasomotor fibers, which follow the external carotid artery and innervate the sweat glands and blood vessels of the face. Second-order preganglionic neurons exit at the T1 level of the spinal cord to enter the cervical sympathetic chain, where the fibers ascend to synapse in the superior cervical ganglion at the C3-C4 level. The first-order neurons originate from the hypothalamus and descend through the midbrain and pons uncrossed, terminating at the C8-T2 level of the spinal cord in the intermediolateral cell columns (ciliospinal center of Budge). The nerve supply is constituted by three different neurons, starting from the posterolateral hypothalamus and ending as the long ciliary nerves to supply the iris dilator and superior tarsal muscles (Muller muscle). Understanding the sympathetic innervation of the eye is vital to understanding the features of this syndrome. The condition was formally described and later named after Swiss ophthalmologist Johann Friedrich Horner in 1869. It was outlined more thoroughly by the French physiologist Claude Bernard in 1852, followed by several physicians who offered different interpretations. The syndrome was first described by Francois Pourfour du Petit in 1727 when considering results from an animal experiment involving resection of intercostal nerves and subsequent changes seen in the ipsilateral eye and face. The syndrome has several names, such as Bernard-Horner syndrome (French-speaking countries), Horner syndrome (English speaking countries), oculosympathetic palsy, and Von Passow syndrome (Horner syndrome in association with iris heterochromia). Therefore, treatment is centered around identifying and appropriate management of the underlying secondary cause. It is primarily acquired following damage to the sympathetic nerve supply, but rare cases of congenital forms have been seen. Horner syndrome is a rare condition classically presenting with partial ptosis (drooping or falling of upper eyelid), miosis (constricted pupil), and facial anhidrosis (loss of sweating) due to a disruption in the sympathetic nerve supply. ![]()
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