❖ Complete oculomotor nerve palsy: Every intraocular and almost every extraocular muscle is affected, with loss of both accommodation and pupillary light reaction. The failure of the parasympathetic fibers in the oculomotor nerve produces mydriasis. Ptosis is present because the levator pal-pebrae is also paralyzed. The paralyzed eye deviates in extorsion and depression as the function of the lateral rectus and superior oblique is preserved. Patients do not experience diplopia because the ptotic eyelid covers the pupil.
❖ Partial oculomotor nerve palsy:
- External oculomotor nerve palsy (isolated paralysis of the extraocular muscles supplied by the oculomotor nerve; see Fig. 17.1) is characterized by deviation in extorsion and depression. If the ptotic eyelid does not cover the pupil, the patient will experience diplopia.
- Internal oculomotor nerve palsy is isolated paralysis of the intraocular muscles supplied by the oculomotor nerve. This is characterized by loss of accommodation (due to paralysis of the ciliary muscle) and mydriasis (due to paralysis of the sphincter pupillae). Patients do not experience diplopia as there is no strabismic deviation (see also tonic pupil and Adie syndrome).
Combined cranial nerve palsies. The third, fourth, and sixth cranial nerves can be simultaneously affected, for example in a lesion at the apex of the orbi tal cavity or in the cavernous sinus. Clinical suspicion of combined lesion may be supported by a corneal sensitivity test as the ophthalmic division of the trigeminal nerve, which provides sensory supply to the cornea, courses through the cavernous sinus. Where there is loss of corneal sensitivity, whether the lesion is located in the cavernous sinus must be determined.
Diagnosis of ophthalmoplegia: Examination of the nine diagnostic positions of gaze (see Chapter 1). The patient is asked to follow the movements of the examiner's finger or a pencil with his or her eyes only. The six cardinal directions of gaze (right, upper right, lower right, left, upper left, lower left) provide the most information; upward and downward movements are performed with several muscles and therefore do not allow precise identification of the action of a specific muscle. Immobility of one eye when the patient attempts a certain movement suggests involvement of the muscle responsible for that movement.
The Bielschowsky head tilt test is performed only where trochlear nerve palsy is suspected (see symptoms).
Measuring the angle of deviation. Measuring this angle in the nine diagnostic directions of gaze provides information about the severity of the palsy, which is important for surgical correction. This is done using a Harms tangent
— Measuring the angle of deviation with the Harms tangent table. -
Fig. 17.18 The patient sits at a distance of 2.5 meters from the table and fixates on the light in the center. The examiner evaluates the nine diagnostic positions of gaze. The grid provides the coordinates for measuring the horizontal and vertical deviations, and the diagonals are used to measure the angle of deviation at a head tilt of 45 degrees (Bielschowsky head tilt test in trochlear nerve palsy). A small projector with positioning cross hairs mounted on the patient's forehead permits the examiner to determine the patient's head tilt with a relatively high degree of precision. The tilt of the image (paralytic strabismus often leads to image tilting) can also be measured with the Harms tangent table. To do so, the fixation light in the center of the table is spread into a band of light.
table (Fig. 17.18). In addition to the vertical and horizontal graduations of the Maddox's cross, the Harms table also has diagonals. These diagonals permit the examiner to measure the angle of deviation even in patients with a compensatory head tilt, such as can occur in trochlear nerve palsy.
Differential diagnosis: Table 17.4 shows the most important differences between paralytic strabismus and concomitant strabismus.
Treatment of ophthalmoplegia: Surgery for paralytic strabismus should be postponed for at least one year to allow for possible spontaneous remission. Preoperative diagnostic studies to determine the exact cause are indicated to permit treatment of a possible underlying disorder, such as diabetes mellitus. Severe diplopia may be temporarily managed by alternately patching the eyes until surgery. Alternatively, an eyeglass lens with a prism correction for the paralyzed eye may be used to compensate for the angle of deviation and eliminate diplopia. Eyeglasses with nonrefracting lenses may be used for patients who do not normally wear corrective lenses. Prism lenses may not always be able to correct extreme strabismus. If surgery is indicated, care
Table 17.4 Differential diagnosis between concomitant strabismus and paralytic strabismus
Differential criterion Concomitant strabismus Paralytic strabismus
Onset At an early age, initially only At any age, sudden onset.
Hereditary,uncorrected refractive error, perinatal injury.
Disease of or injury to ocular muscles, supplying nerves, or nuclei.
None; image suppressed (except in late strabismus with normal sensory development).
Diplopia is present.
Compensatory head None. posture
Depth perception Not present.
Only present when patient assumes compensatory head posture (see symptoms).
Usually unilaterally reduced visual acuity.
No change in visual acuity.
Angle of deviation
Constant in every direction of gaze.
Variable, increasing in the direction of pull of the paralyzed muscle.
must be taken to correctly gauge the angle of deviation. The goal of surgery is to eliminate diplopia in the normal visual field, i.e., with head erect, in both near and distance vision. It will not be possible to surgically eliminate diplopia in every visual field.
Procedure: The antagonist of the respective paralyzed muscle can be weakened by recession. Resecting or doubling the paralyzed muscle can additionally reduce the angle of deviation.
Strabismus surgery for ophthalmoplegia is possible only after a one-year regeneration period.
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