Imaging in Strabismus
Mays A. El-Dairi, MD
DIAGNOSTIC CONSIDERATIONS
Strabismus is a common presentation for intracranial pathology. Before deciding on surgery in strabismus, it is important to rule out an active neurological cause and manage it. Below is an overview of the indications and type of neuroimaging to consider before strabismus surgery. Additionally, imaging modalities such as UBM, AS-OCT, and MRI may also play a role in identifying the location of extraocular muscle insertions and the presence of a slipped muscle in reoperations.
INDICATIONS FOR IMAGING
Apparent Congenital Strabismus
Esotropia: Neuroimaging is indicated in patients with the following findings:
Abduction deficit.
Facial palsy (rule out Moebius syndrome or brainstem abnormality)
Optic neuropathy.
A mild duction lag in an infant is very difficult to see on simple duction testing. Check duction lag monocularly using a patch and doll’s head maneuver, and/or check saccades with an OKN drum.
Bilateral partial facial palsies are difficult to see in an infant. Check for decreased facial expressions. If an infant’s facial expressions are less animated than the parents, consider hypotonia or facial palsy.
Exotropia: The presence of a vertical component, ptosis, or anisocoria should alert the examiner to the possibility of a third cranial nerve palsy. A mild third nerve palsy in a child can present with intermittent fusion giving the false diagnosis of intermittent exotropia. Children with a homonymous visual field defect will frequently develop an intermittent or constant exotropia that enlarges their functional field. Pediatric patients with exotropia should have careful visual acuity and visual field testing (Fig. 57.1). Consider formal visual fields testing and OCT if visual acuity is not normal. The presence of a visual field deficit or optic neuropathy should warrant neuroimaging.
 FIGURE 57.1. A, B. A 6-year-old boy with a long-standing history of intermittent exotropia presented with worsening control of his eye alignment. His visual acuity was 20/50 OD and 20/30 OS. Dilated fundus examination was notable for mild bilateral optic nerve pallor. Figure A shows a left homonymous hemianopia. Figure B is his MRI imaging which revealed a lobulated mass lesion involving the optic chiasm, right greater than left extending along bilateral optic pathways (Courtesy of Tammy Yanovitch, MD MHSc). |
Check visual fields monocularly in all patients with exotropia, use saccades to check for duction lag, perform prism alternate cover testing in the six cardinal positions of gaze, and look for fundus torsion on examination. A bilateral fourth nerve palsy may look like a V-pattern esotropia (see below).
Fourth nerve palsy: Imaging is indicated if bilateral or associated with other findings. In the case of a bilateral fourth nerve palsy (V-pattern esotropia with alternating hypertropia and bilateral fundus excyclotorsion), pay special attention to the fourth ventricle. Fourth nerve palsy with a contralateral Horner syndrome is suggestive of a central fourth nerve palsy (see below). A typical isolated fourth nerve palsy with a large vertical fusional amplitude, inferior oblique overaction, and facial asymmetry does not warrant imaging even if noted later in life as these findings indicate that the etiology is likely congenital.
Acquired Strabismus
Trauma: Image if suspect orbital or intracranial pathology that requires intervention (orbital fracture, hemorrhage, or entrapment). Strabismus surgery should be delayed until full possible recovery (at least 6 months) unless there is entrapment of an extraocular muscle.
 FIGURE 57.2. CT scan of the orbits, coronal view. Soft tissue window. There is a minimally displaced “trapdoor” or “greenstick” fracture of the left orbital floor. The left inferior rectus is only minimally visualized in this image, as it is caught within the bony fracture and likely compressed at this level. Comparison can be made to the right orbit with the inferior rectus muscle running above the orbital floor (Courtesy of Jason Liss, MD). |
Children are at particular risk of muscle entrapment with inferior orbital wall fractures because their orbital floor is more apt to greenstick and then bounce back (“trap-door fracture”), entrapping the inferior rectus muscle (Fig. 57.2). They may present with a “white-eyed blow-out fracture” (history of trauma with little evidence of soft tissue injury). Nausea and vomiting are common with this type of fracture, and their association with limitation to elevation should make one very suspicious of muscle entrapment.
Acute peripheral cranial mononeuropathy (isolated): An isolated cranial neuropathy in a patient with vasculopathic risk factors such as systemic hypertension, diabetes mellitus, cigarette smoking, hyperlipidemia, and radiation injury is probably ischemic and does not require neuroimaging acutely (reminder: ask giant cell arteritis [GCA] symptoms and check erythrocyte sedimentation rate [ESR], C-reactive protein [CRP] if GCA is suspected). However, the patient should be seen again in 3-4 weeks, and imaged if no improvement of motility examination and duction lag.
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