A man in his mid-fifty’s seeks attention from an eye specialist after experiencing a sever migraine. The man notes his left eyelid drooping, along with a constricted pupil (Beck, 1988, p. 234). The man is later diagnosed with oculosympathetic palsy, also known as Horner’s syndrome (Kanski, 1990, p.65). The main ocular symptoms in Horner’s are a unilateral ptosis and miosis of the effected eye. This syndrome is caused by a disruption of the sympathetic nervous system, and can arise from a multitude of etiologies (Kanski, 1990, p.65). This paper aims to explain and explore the various causes, clinical features, and diagnostic tests an eye-care professional can utilize in diagnosis of Horner’s syndrome.
The sympathetic pathway is a part of the autonomic nervous system and is responsible for preparation of the fight-or-flight response of the body (Remington, 1998, p. 253). The pathway of the sympathetic nervous system originates from the hypothalamus, where it then travels to the lateral gray matter of the spinal chord. The pathway extends from the thoracic to the upper lumbar column segments. The portions of interest responsible for innervation of ocular structures are found in segments T-1 to T-3 (Remington, 1998). The sympathetic nerve fibers that innervate ocular structures are composed of preanglionic fibers and exit the ventral root of the spinal chord, ascending to the superior cervical ganglion. The superior cervical ganglion synapses with postganglionic fibers, which form the sympathetic carotid plexus around the internal carotid artery. The nerve then branches into many routes, with some extensions traveling alongside the trigeminal nerve to ultimately innervate the; iris and ciliary muscles, smooth muscles of the lids, choroidal and ciliary blood vessels and the lacrimal gland (Remington, 1998).
In the case of Horner’s syndrome, there is a lesion or obstruction along the sympathetic pathway in one of the three branches of the neural arc inhibiting communication between structures (Beck, 1988, p.236). A lesion involving the first branch is easily diagnosed, and is frequently accompanied by significant neural defects. The second neural branch passes along the ciliospinal centre of Budge to the superior cervical ganglion (Kanski, 1990, p. 64). These lesions are usually from neck trauma or neck surgery (Beck, 1988). The third branch travels along the internal carotid artery, and enters the skull via the cavernous sinus. Lesions of the third branch are associated with carotid trauma and cavernous sinus lesions (Kanski, 1990, p. 64; Beck, 1988, p.236). Lesions do not have to occur along the central nervous system for the development of Horner’s syndrome. Conditions such as; apical pulmonary disease, aortic aneurisms, migraines, metastasis, goiter and a multiple of other causes can inhibit signals from the sympathetic pathway to the ocular structures (Cogan, 1948, p.178).
Horner’s syndrome can be congenital, in which the damage...