Paralytic Strabismus

Strabismus caused by weakness or paralysis of one or more extraocular muscles from damage to cranial nerves III, IV or VI, their nuclei, the neuromuscular junction, or the muscle itself.

• The deviation is incomitant: it varies with gaze direction, is greatest when the eye moves into the field of the paretic muscle, and differs depending on which eye fixates (secondary deviation exceeds primary deviation, because of greater effort to fixate with the paretic eye, in accordance with equal innervation to yoke muscles).
• Causes by age:
  • Congenital: congenital fourth nerve palsy, Duane syndrome, Moebius sequence, congenital third nerve palsy, congenital fibrosis of extraocular muscles.
  • Acquired adult: diabetes and hypertension (microvascular), trauma, tumour, aneurysm, giant cell arteritis, multiple sclerosis, stroke, meningitis, myasthenia gravis, thyroid eye disease (restrictive pattern mimicking palsy), Guillain-Barre and Miller Fisher syndrome, Wernicke encephalopathy.
  • Children: viral or post-viral sixth nerve palsy, raised intracranial pressure, brain tumour (pontine glioma), trauma, ophthalmoplegic migraine.
• Hering law and Sherrington law apply in palsy: yoke muscles receive equal innervation and antagonists relax.

• Diplopia: horizontal in sixth nerve, vertical or torsional in third and fourth, with the separation maximal in the direction of action of the paretic muscle; images are further apart in the paretic field.
• Compensatory head posture to move the eye into the area of least diplopia (face turn toward the paretic lateral rectus, chin elevation or depression, head tilt away from a fourth nerve palsy).
• Limitation of movement in the field of action of the weak muscle, overaction of the contralateral synergist (yoke muscle) and ipsilateral antagonist, then late contracture of the antagonist, producing spread of comitance.
• Third nerve: ptosis, mydriasis, abducted and depressed eye; sixth nerve: esotropia worse at distance, abduction deficit; fourth nerve: hypertropia, excyclotorsion.
• Associated: headache, pain (microvascular, aneurysm, giant cell arteritis), neurological signs.

• Detailed motility testing in nine positions with ductions and versions; Hess or Lees chart; prism cover tests in gaze positions; measurement of primary and secondary deviation; saccadic velocity (slow in paresis, normal in restriction); forced duction (free in paresis, restricted in restriction).
• Red glass and Maddox rod test, field of binocular single vision (Goldmann or Lancaster chart).
• Investigate cause: blood pressure, glucose and HbA1c, ESR, CRP, platelet count in patients over 50; thyroid function; acetylcholine receptor antibodies and ice pack test; neuroimaging (MRI brain and orbits, MR or CT angiography when pupil involved or painful); lumbar puncture with opening pressure when idiopathic intracranial hypertension is suspected.
• Neurological examination of other cranial nerves, fundus for papilloedema, and general examination.

• Treat the cause; observe microvascular palsies for 3 to 6 months (expect recovery in 80 to 90 percent).
• Temporary: monocular occlusion, Fresnel prisms; amblyopia treatment in children.
• Botulinum toxin to the antagonist (injection of 2.5 to 5 units into the medial rectus in sixth nerve palsy) in the first 3 to 6 months to prevent contracture.
• Surgery after at least 6 months of stable deviation:
  • Partial palsy: recess the antagonist and resect the paretic muscle (for sixth nerve, medial rectus recession 4 to 6 mm and lateral rectus resection 6 to 8 mm).
  • Complete palsy: muscle transposition (vertical rectus muscles to the lateral rectus, with or without augmentation sutures), with ipsilateral medial rectus recession or botulinum toxin.
  • Contralateral yoke muscle weakening (posterior fixation suture, recession) to balance versions.
  • Third nerve palsy: lateral rectus recession and medial rectus resection, superior oblique transposition; ptosis surgery last.
• Prisms (ground in) for small residual deviations; Bangerter filters for diplopia; lenses to reduce diplopia in primary position.
• Counselling: recovery time, driving restrictions, recurrence of diplopia.