In a cooperative patient, nonparalytic strabismus may be demonstrated by showing that each eye moves fully when the other eye is covered. Tropias and phorias can readily be detected by means of the simple “cover” and “cover–uncover” tests. When fusion is disrupted by covering one eye, the occluded eye will deviate; uncovering that eye results in a quick corrective movement designed to reestablish the fusion mechanism.
Clinical Effects of Lesions of the Third, Fourth, and Sixth Nerves
A complete third nerve palsy includes ptosis, or drooping of the upper eyelid (as the levator palpebrae is supplied mainly by this nerve), and an inability to rotate the eye upward, downward, or inward. This corresponds to the weaknesses of the medial, superior, and inferior recti and the inferior oblique muscles. The remaining actions of the fourth and sixth nerves give rise to a position of the eye described by the mnemonic “down and out.” The patient experiences diplopia in which the image from the affected eye is projected upward and medially. In addition, one finds a dilated, nonreactive pupil (iridoplegia), and paralysis of accommodation (cycloplegia) because of interruption of the parasympathetic fibers in the third nerve. However, the extrinsic and intrinsic (pupillary) eye muscles may be affected separately in certain diseases. For example, a lesion affecting the central portion of the oculomotor nerve, as occurs in diabetic ophthalmoplegia, typically spares the pupil, as the parasympathetic preganglionic pupilloconstrictor fibers lie near the surface. Conversely, compressive lesions of the nerve usually dilate the pupil as an early manifestation. After injury, regeneration of the third nerve fibers may be aberrant, in which case some of the fibers that originally moved the eye in a particular direction now reach another muscle or the iris; in the latter instance the pupil, which is unreactive to light, may constrict when the eye is turned up and in.
A lesion of the fourth nerve, which innervates the superior oblique muscle, is the most common cause of isolated symptomatic vertical diplopia. Although oculomotor palsy was a more common cause of vertical diplopia in Keane’s 1975 series, in instances where this is the sole complaint, trochlear palsy (and brainstem lesions) have predominated in our experience. Paralysis of the superior oblique muscle results in weakness of downward movement of the affected eye (Fig. 13-7E), so that the patient complains of special difficulty in reading or going down stairs. The affected eye tends to deviate slightly upward when the patient looks straight ahead and the upward deviation increases as that eye adducts on attempted horizontal gaze. In the presence of a third nerve palsy, one can assess the function of the fourth nerve by evaluating whether the eye intorts on attempted down gaze. Double vision from an isolated fourth neve palsy is worse with ipsilateral head tilt. Compensatory head tilting to the opposite shoulder (Bielschowsky sign) is especially characteristic of fourth-nerve lesions; this maneuver causes intorsion of the unaffected eye and ameliorates the double vision. Lesions affecting the trochlear nucleus (rather than the nerve itself) will cause paresis of the contralateral superior oblique muscle; here, the patient will tilt their head toward the side of the lesion to ameliorate the diplopia.
Bilateral trochlear palsies, as may occur after head trauma, give a characteristic alternating hyperdeviation depending on the direction of gaze (unilateral traumatic trochlear paresis is still the more common finding with head injury). A useful review of the approach to vertical diplopia is given by Palla and Straumann.