Clinical Note continued

suppressing the image from the abnormal eye. The patient may then no longer have double vision but will become psychically blind in the affected eye, and stereopsis (depth perception) will be compromised. The complaint of diplopia usually denotes a recent lesion.

Other symptoms of ophthalmoplegia demonstrated by a physical exam may include strabismus (the lack of parallelism of the ocular axes). Specifically, the affected pupil will be displaced laterally (lateral strabismus) and downward because of the unopposed action of the muscles innervated by cranial nerves IV and VI. Because there is loss of innervation to the levator pal-pebrae, the eyelid will be partially closed, a condition called ptosis. The pupil will be dilated (mydriasis) because of the loss of parasympa-thetic innervation to the sphincter muscle, leaving the unopposed action of the sympathetic innervation of the dilator muscles. The loss of parasym-pathetic innervation to the eye can also be demonstrated by testing for the pupillary light reflex and accommodation reflex, both of which will be absent in ophthalmoplegia. Because the parasympathetic fibers of the ocular motor nerve tend to lie near the outer surface of the nerve, they are the most vulnerable to compression lesions. Thus, a less severe compression would be reflected primarily in a fixed (unresponsive) and dilated pupil whereas a more severe lesion would cause the loss of all oculomotor nerve function.

Lesions of the oculomotor tract in the midbrain may involve surrounding structures. In the basal midbrain, a single lesion may compromise both the exiting oculomotor fibers and the surrounding motor pathways that transmit information from the motor cortex to muscles on the contralateral side of the body. This would result in ipsilateral ophthalmoplegia and contralateral hemiplegia (partial paralysis), a condition known as Weber's syndrome.

Ptosis can also be caused by loss of sympathetic innervation to the tarsalis muscle of the eyelid, a condition called Homer's syndrome. This condition can be distinguished from ophthalmoplegia because sympathetic neurons innervate pupillo-dilator muscles as well as the tarsalis muscle. A patient with Horner's syndrome would have ptosis (usually not as severe as with ophthalmoplegia) and the pupil would be constricted rather than dilated, as it would be with ophthalmoplegia.

Loss of input from cranial nerve IV can also cause diplopia, particularly when the patient tries to walk down stairs or read, activities that require downward gaze. A patient may also tilt his or her head slightly toward the side of the lesion in an attempt to adjust for the elevated and intorted position of the affected eye. Some loss of superior oblique muscle action may be compensated by actions of unaffected superior and inferior rectus muscles.

A marked medial strabismus can result from lesions of the abducens nerve caused by the loss of innervation to the lateral rectus muscles. A patient with medial strabismus tends to keep his head turned toward the side of the lesioned nerve to compensate for the position of the affected eye and thus avoid diplopia.

lesions are the most common cause of the pathologic appearance of spontaneous nystagmus.

Suggested Readings

Dowling JE. The retina: an approachable part of the brain. Cambridge,

MA: Belknap Press of Harvard University Press, 1987. Fuchs AF, Kaneko CRS, Scudder CA. Brainstem control of saccadic eye movements. Annu Rev Neurosci 1985; 8:307-337. Fukushima K, Kaneko CRS, Fuchs AF. The neuronal substrate of integration in the oculomotor system. Prog Neurobiol 1992; 39:609. Hubel DH. Eye, brain and vision, Scientific American library series

No. 22, New York: Freeman, 1998. Land EH. The retinex theory of color vision. Set Am 1977; 237(6): 108-128.

Lisberger SG, Morris EJ, Tychsen L. Visual motion processing and sensory-motor integration for smooth pursuit eye movements. Annu Rev Neurosci 1987; 10:97-129. Livingstone M, Hubel D. Segregation of form, color, movement, and depth: anatomy, physiology and perception. Science 1988; 240:740-749.

Nathans J. Rhodopsin: structure, function and genetics. Biochemistry 1992; 31:4923.

Palczewski K, Benovic J. G-protein-coupled receptor kinases. Trends

Biochem Sci 1991; 16:387. Rodieck RW. The vertebrate retina: principles of .structure andfunction.

San Francisco: Freeman, 1973. Stone J, Dreher B, Leventhal A. Hierarchal and parallel mechanisms in the organization of visual cortex. Brain Res Rev 1979; l: 345-394.

Stryer L. The molecules of visual excitation. Sci Am 1987; 235:42.

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