On version testing, Hering’s law may cause the superior oblique muscle to overact in the normal eye. If the surgeon is misled and performs superior oblique tenotomy on the normal eye, thereby converting a unilateral superior oblique palsy to a bilateral one, disabling torsional diplopia can result.
Whatever the approach, it is important to avoid overcorrection of a long-standing unilateral superior oblique muscle palsy in adult patients. Overcorrection can worsen with time and can cause disabling diplopia.
Bilateral superior oblique muscle palsy Surgical planning for treatment of bilateral superior oblique muscle palsy can be complex as surgery on both eyes is required and any asymmetry of the paralysis must be taken into account. The plan depends on several factors:
magnitude of inferior oblique overaction and superior oblique weakness degree of laxity of the superior oblique tendons
magnitude of cyclodiplopia and extorsion
presence and size of a hyperdeviation in primary position size of the V pattern
If the palsies are symmetric and both inferior oblique muscles are significantly overacting, weakening of both muscles is appropriate but may not be completely effective on its own. If the superior oblique muscles are lax or weak and cyclodiplopia or sizable extorsion is present, these muscles should be strengthened, using either tendon tucking or one of the variations of the Harada-Ito procedure.
If the paralysis is asymmetric, a hyperdeviation is usually present in primary position and the hyperdeviations on right and left gaze differ. There are several options for correcting this asymmetry, including symmetric oblique muscle surgery with a unilateral vertical rectus recession and asymmetric oblique muscle surgery tailored to correct more oblique muscle function in the eye with the worse palsy.
There are other, less common approaches to treating bilateral superior oblique palsy, including bilateral inferior rectus muscle recessions, which serve to add extra innervational drive on downgaze to help overcome the superior oblique deficits.
Any of these approaches should collapse a large V pattern, but if there is concern that some of the pattern may persist after one of the options is chosen, additional surgery may be necessary (see Chapter 10).
Inferior Oblique Muscle Palsy
Whether inferior oblique muscle palsy actually exists has been questioned. Most cases are congenital or posttraumatic. Some cases could be explained by a highly localized orbital lesion, but this is rare. It has recently been suggested that at least some cases, especially those with a history of head trauma or with additional neurologic findings, are a form of skew deviation, even if the diagnosis of inferior oblique muscle palsy is supported by results of the 3-step test (Fig 11-4). Other cases are thought to be explained by demonstrable abnormalities of the muscle.
Figure 11-4 Right inferior oblique muscle palsy. There is a small left hypertropia in primary position that increases in left gaze and with head tilt to the left, the 3-step pattern consistent with this diagnosis. This patient had no abnormal neurologic findings. Note convergence in straight upgaze, an important point of differentiation from Brown syndrome. (Courtesy of Edward
L. Raab, MD.)
In inferior oblique muscle palsy, the hypotropic eye is intorted, which may lead to subjective excyclodiplopia (image appears to tilt outward); in skew deviation, the hypotropic eye is extorted, a finding incompatible with the diagnosis of inferior oblique muscle palsy. These phenomena are analogous to those described in regard to superior oblique palsy. Cases in which the results of the 3- step test are not clear may represent asymmetric or unilateral primary superior oblique muscle overaction with secondary underaction of the inferior oblique muscle.
Clinical features
As with Brown syndrome (see Chapter 12), elevation is deficient in the adducted position of the eye. The features that distinguish inferior oblique muscle palsy from congenital Brown syndrome are listed in Table 11-3.
Management
Indications for treatment of inferior oblique muscle palsy are abnormal head position, vertical deviation in primary position, and diplopia. Management consists of weakening either the ipsilateral superior oblique muscle or the contralateral superior rectus muscle. The former procedure will aggravate the existing extorsion of the hypotropic eye if an undetected skew deviation is the true underlying abnormality.
Table 11-3