Strabismus Online Information Resource

Superior Oblique Palsy

The superior oblique is innervated by the fourth cranial nerve. Its actions from the primary position include intorsion, depression, and abduction of the eye. Superior oblique palsy (SOP) can be congenital or acquired. Congenital SOP is the most common paretic form of strabismus in children. Its etiology is unknown. It can remain unrecognized secondary to fusional mechanisms until late childhood. These mechanisms decompensate later in life either spontaneously or after trauma.

Causes of acquired SOP include head trauma, vascular problems, diabetes, brain tumors, cavernous/ superior orbital fissure syndromes, herpes zoster, and decompensated congenital palsy. Trauma is the most common cause of SOP.

Symptoms of SOP include vertical and torsional diplopia as well as difficulty reading. Signs on exam are head tilt, hypertropia and a positive Parks 3-step test. Facial asymmetry and large vertical fusional amplitudes are signs that indicate chronicity. Review photography to verify chronicity and avoid unnecessary neurologic evaluation

Parks 3-step test: e.g. LHT worse on gaze right and head tilt left; explained on basis of utricular stimulation; e.g. a tilt to the left will result in compensatory right cyclorotation of 5-6 degrees of both eyes; since the superior rectus and superior oblique are the intorters and the superior oblique is weak, then the superior rectus function is enhanced; since its main function is elevation, the LHT increases; head tilt away from the affected eye avoids stimulation of the intorters of the involved eye and the LHT diminishes.

Initially, the greatest vertical misalignment is in the field of action of the involved superior oblique muscle; later there is contracture of the ipsilateral direct antagonist, the inferior oblique muscle, causing the greatest vertical deviation in the elevated, adducted position; the contralateral inferior rectus and the ipsilateral superior rectus muscle can contracture, causing spread of comitance.

The deviation increases in gaze away from the paretic eye and on head tilt towards the paretic eye. When the paretic eye is the preferred eye for fixation, an inhibitional palsy of the contralateral antagonist occurs along with contracture of the contralateral inferior rectus; this can simulate a double elevator palsy.

Look for subjective excyclotorsion with BiMaddox rods, Bagolini lenses, red-green projection lights, visual field blind spots; look for objective excyclotorsion with ophthalmoscope.

The superior oblique tendon may be absent (e.g. Crouzon); it may be floppy (early onset palsy); it is often normal.

One should perform an exaggerated traction test.

Bilateral superior oblique palsy is usually post-traumatic; there is an LHT on right gaze, an RHT on left gaze, an LHT on tilt left and an RHT on tilt right. It may be very asymmetric or one side may be masked. Bilateral SOP can be difficult to detect. Its presence should be suspected if there is a chin-down position, lack of a head tilt, a V-pattern esotropia in downgaze, excyclotorsion greater than 10° in downgaze when measured by the double maddox rod test, bilateral fundus torsion on ophthalmoscopy, and a positive Bielschowsky test with head tilt in both directions.

SOP can be classified according to a grading system based on the gaze position or positions of greatest vertical misalignment: Knapp Classification

  • Class I: greatest hypertropia in opposite up oblique field
  • Class II: greatest hypertropia in opposite down oblique field
  • Class III: greatest hypertropia in entire opposite field
  • Class IV: greatest hypertropia in entire opposite field and across the lower field
  • Class V: greatest hypertropia across lower field
  • Class VI: bilateral SOP
  • Class VII: traumatic paresis combined with Brown's syndrome

The differential diagnosis of SOP includes myasthenia gravis, Graves' myopathy, orbital inflammatory disease, orbital injury to trochlea, dissociated vertical deviation, third cranial nerve palsy, skew deviation, and Brown's syndrome.

Treatment:

Early onset - if floppy redundant tendon --> tuck superior oblique +/- inferior oblique weakening

Childhood or adult onset - if inferior oblique overactive and primary position deviation not greater than 15 PD --> inferior oblique weakening only; if primary position deviation greater than 15 PD --> inferior oblique weakening + contralateral inferior rectus recession (especially if superior oblique is underactive; you get 3 PD of correction per mm inferior rectus recession; if hyper persists on gaze towards paretic eye and contralateral superior oblique is overactive --> add ipsilateral superior rectus recession. A patient undergoing surgery for a seemingly unilateral SOP should be aware of the possibility of a masked palsy in the "normal" eye. This would require further surgery when the palsy is unmasked after the first surgery. Every attempt should be made NOT to overcorrect or reverse the hypertropia with the operation. In fact a slight undercorrection is the safest post-op situation.

Bilateral palsy: Treatment must often address excyclotorsion as well as significant esotropia in downgaze. Bilateral superior oblique tuck and bimedial recession with infraplacement can be very effective. If the inferior oblique overacting, bilateral inferior oblique weakening should be done; if the SOP is asymmetric a unilateral inferior rectus recession (adjustable) might be indicated. With minimal hypertropia in primary position but debilitating torsional diplopia, one can do anterotemporal displacement of the anterior half of the superior oblique tendon (Harada-Ito procedure).