In opposition to the pupillary constriction produced by cranial nerve III, the sympathetic system dilates the pupil. The dilator system functions by a reflex arc similar to the sphincter system. The afferent arm, however, is much less circumscribed than the light reflex. Afferent stimulation along pain and temperature pathways from the spinal cord generally causes pupillary dilatation that is abrupt in onset and lasts 20 to 60 seconds. More sustained dilatation often attends mental states involving fear, anxiety, or surprise. Because the sympathetic afferent pathways are anatomically ill defined, especially at rostral levels of the CNS, this discussion focuses on the efferent sympathetic pathways. Anatomical reports have shown sympathetic fiber degeneration in the upper brain stem after experimental lesions in the hypothalamus. These studies document widely dispersed fiber tracts in the upper midbrain and diencephalon but none in the pons or medulla. The descending system is most likely a polysynaptic one, despite the clinical use of "the central neuron" in the chain leading to the iris dilator. Clinical studies have documented that dorsolateral lesions throughout the brain stem often produce ocular sympathetic dysfunction ipsilaterally, whereas medial and ventral lesions do not. This is the basis for the widely accepted view that the polysynaptic central ocular sympathetic system is dorsolaterally disposed in the brain stem.
This pathway continues into the spinal cord to the C8 through T2 segmental levels, where the central fibers synapse with cells in the intermediolateral gray horns. This zone between C8 and T2 is commonly known as the cilio-spinal center of Budge and Waller.[5} The central pathways through the cervical spinal cord are located very superficially (near the pia) in the lateral columns. [6 The preganglionic cells from the ciliospinal center send axons to the paravertebral sympathetic ganglion chain by way of the C8-T2 ventral roots. These preganglionic fibers travel upward in the sympathetic chain through the stellate (combined upper thoracic and lower cervical ganglion) and the middle cervical ganglions. They synapse with postganglionic cells in the superior cervical ganglion, which is usually
Figure 9-2 A, Axial section of the orbits viewed from above. The eyes are shown in conjugate right gaze, which places the right eye in the abducted position and the left eye in the adducted position. The superior oblique muscle is shown with its tendon passing through the trochlea or pulley on the anterior medial orbital rim. The rectus muscles are the primary elevators and depressors when the eye is in abduction, and the obliques perform this function with the eye in a<B, A diagram showing the position of maximum action of the extraocular muscles of the two eyes as viewed from in front of the patient. Mr, medial rectus; LR, lateral rectus; SR, superior rectus, IR, inferior rectus; IO, inferior oblique; SO, superior oblique.
Figure 9-3 (Figure Not Available) A cross section through the midbrain showing the third cranial nerve nuclear complex. The subnuclei extend in rostrocaudally oriented columns, as depicted in this three-dimensional representation modeled on Warwick's schemata. The letters superimposed on each nuclear group indicate the muscle innervated as follows: LP, levator palpebrae; SR, superior rectus; IR, inferior rectus; IO, inferior oblique; MR, medial rectus. A right nuclear third nerve lesion is illustrated. Open triangles and dotted lines indicate lesioned neurons and their axons. Filled triangles and solid lines denote normal neurons and their axons. All of the outflow to the right third nerve is lesioned. Crossed outflow from the right SR and LP subnuclei gives rise to paresis of contralateral eye elevation and ptosis. The left ptosis is partial because there is still ipsilateral (uncrossed) outflow from left LP subnucleus to the left LP. The crossed pathway from left LP subnucleus to right LP is affected at the axonal level as the fibers course through the damaged right third nerve complex (transition of solid lines to dotted); thus right ptosis is complete. The contralateral elevator palsy and ptosis thus distinguish nuclear nerve palsy from fascicular palsy, in which the findings are limited to the ipsilateral eye (From Goodwin JA: Eye signs in neurologic diagnosis. in Weiner WJ, Goetz CG: Neurology for the Non-Neurologist, 3rd ed. Philadelphia, J.B. Lippincott, 1994, pp 298-348.)
Figure 9-4 Diagram of the cavernous sinus. Oculomotor (III), trochlear (IV) () and ophthalmic division of the trigeminal and abducens cranial (VI) nerves are indicatfFrom MillerNR: Walsh andHoyt's ClinicalNeuro-Ophthalmology, Vol2, 4th ed. Baltimore, Williams
found high in the neck, often under the angle of the mandible. This means that the common lesions that cause ocular sympathetic palsy (Horner's syndrome) interfere with preganglionic fibers as they course through the upper thorax and neck. Virtually all lesions producing postganglionic sympathetic dysfunction are intracranial and intraorbital, because the superior cervical ganglion is so near the base of the skull. The postganglionic axons at first travel in the adventitia of the carotid artery and those supplying vascular and sweat gland structures in the lower face travel with external carotid branches. The ocular sympathetics and those serving vasomotor and sudomotor function for the forehead travel with the internal carotid into the middle cranial fossa. A contingent of ocular sympathetic fibers takes a side path through the otic ganglion in the middle ear. This apparently explains the occasional occurrence of Horner's syndrome with middle ear infections. The main ocular sympathetic pathway, however, follows the carotid artery through its siphon region and then joins the first division (ophthalmic) of the trigeminal nerve, which carries it into the orbit. A sympathetic contingent passes through the parasympathetic ciliary ganglion, constituting the so-called sympathetic root of the ganglion, but no sympathetic synapses occur there. In the orbit, the ocular sympathetics innervate the iris dilator muscles together with small smooth muscles in the lids (Muller's muscle), which contribute to upper lid elevation and lower lid depression.
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