Paralytic Strabismus
Jared E. Duncan, MD
PREOPERATIVE CONSIDERATIONS
Paralytic strabismus refers to a group of eye muscle impairments that results from innervation interruption to the third, fourth, and/or sixth cranial nerves. Common causes include motor nerve palsies and disorders of the neuromuscular junction (eg, ocular myasthenia gravis [MG]). Important preoperative considerations include determination of the goals of surgery and the appropriate workup of acute insults to the cranial nerves. Elucidation of these factors is facilitated by a thorough preoperative examination that focuses on more than just motility patterns.
Important Historical Elements to Consider
Visual symptoms: Is the patient diplopic? Is the diplopia monocular or binocular? Is it horizontal, vertical, or torsional?
Timing: Are the patient’s symptoms acute? Are they fatigable? Worse at end of the day?
Other symptoms: Does the patient have associated symptoms like headaches, scalp pain/tenderness, nausea/vomiting, or other motor/sensory deficits?
Eye Examination Pearls in the Patient With Paralytic Strabismus
Look carefully for pupillary changes (afferent pupillary defect, anisocoria), deficits in confrontational visual fields (indicative of possible postchiasmal pathology), and eyelid ptosis. The presence of one or more of these will usually necessitate the need for further workup.
Perform a thorough yet focused sensorimotor examination.
Diagnosis will usually require cover testing in primary gaze, horizontal gazes, vertical gazes, and head tilts. Another measurement in primary gaze with near fixation is also helpful. Surgical planning may require the use of cover testing in all nine positions of gaze and head tilts. The presence of incomitance is highly suggestive of muscle paresis or restriction.
Carefully evaluate versions and ductions
Look carefully at force generations (see Chapter 42): indicates residual function of paralytic muscle and guides surgical planning. Force generations can be graded on a scale of mild (>50% function), moderate (25%-50% function), or severe (<25% function to none at all).1
Role of Imaging and Neurologic Workup in Patients With Paralytic Strabismus (See Chapter 57)
The most important factors for determining the need for workup in a patient with paralytic strabismus are timing (acute vs. chronic), age, associated symptoms, and to a lesser extent, past medical history (particularly, a history of cancer).
When indicated workup should include neuroimaging, with MRI being the preferred modality. Referral to an internist or pediatrician is also imperative, as many patients will have cardiovascular or neurologic risk factors. Blood work for MG may also be indicated.
Maintain a high index of suspicion for giant cell arteritis (GCA) in adult patients ≥50 years of age. Erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and a platelet count are imperative in patients who present with symptoms of GCA.
Blood testing for MG (antiacetylcholine receptor antibody test) is frequently falsely negative. If index of suspicion is high, single-fiber EMG remains the gold standard for diagnosis. A trial of pyridostigmine or oral steroids may also be diagnostic.
MG can mimic any form of paralytic strabismus. If in doubt, repeat examination on a different day and/or time may be helpful. Fluctuation in motility measurements may be observed.
Features of GCA include: (1) abrupt onset headache, (2) scalp tenderness, (3) jaw and tongue claudication, (4) visual symptoms, (5) constitutional symptoms, (6) polymyalgia symptoms, and (7) limb claudication.
Improvement and/or resolution of ptosis and/or diplopia after applying an ice pack to the eyelid for 2 minutes or after a rest period of 15-20 minutes supports a diagnosis of MG.
Most clinicians prefer to conduct a workup in all patients who present with nontraumatic, acute onset third, fourth, and sixth nerve palsies.2
A lower threshold for imaging patients includes age <60, presence of associated ocular signs/symptoms (optic disc edema, ptosis, pupillary changes, visual field deficits), and presence of systemic signs/symptoms (headache, weakness, focal neurologic deficits including presence of multiple cranial nerve palsies).
Timing of Surgical Intervention in Patients With Paralytic Strabismus
Surgery must be delayed in patients who present acutely or who have an unstable medical condition that prevents elective surgery.
Although opinions vary, it is common to wait a minimum of 6 months before offering surgery in cases of acute-onset paralytic strabismus. In general, patients with vascular or idiopathic etiologies tend to recover more quickly and more frequently than those with traumatic etiologies of acute palsy. Pediatric patients may require earlier intervention to prevent the development of amblyopia in the nonfixating eye. Ensure appropriate penalization (eg, patching) in pediatric cases where surgical management is delayed.
Interim elimination of diplopia can be achieved with the use of occlusion or temporary (eg, Fresnel) prism (see Chapter 56).
Consider botulinum toxin injection to the antagonist prior to surgery (see Chapter 55).
In acute sixth nerve palsies secondary to head trauma, botulinum toxin may give temporary relief of diplopia and reduce muscle contractures of the antagonist. It can be particularly helpful in sixth nerve palsies that are severe, bilateral, and/or in children. One disadvantage of botulinum toxin injection is that it may diffuse and cause a vertical deviation that can take longer to resolve than the initial nerve palsy.
Determine Realistic Preoperative Goals for Surgical Repair of Paralytic Strabismus
The goal of treatment is to produce the largest field of binocular vision possible. Restoration of full muscle function is not typically possible. This goal should be discussed in detail with the patient prior to surgical intervention.
OPERATIVE CONSIDERATIONS
Surgical Planning
Strengthening the paralytic muscle should only be performed on muscles with mild to moderate function on forced-generation testing.
Resect, plicate, or “tuck” the paretic muscle.
Strengthening the paralytic muscle often needs to be paired with a weakening procedure of the antagonist muscle.
Whenever possible look to create a matching deficit in the uninvolved eye.
Often helps to satisfy the goal of achieving largest field of binocular vision.
Accomplished by weakening yoke muscle of the paretic muscle in uninvolved eye.
Example: In a left sixth nerve palsy, weaken the medial rectus muscle of the right eye.
Long-standing cases of paralytic strabismus may result in contracture of the paralytic muscle’s antagonist. Therefore, there may be an additional restrictive component to the strabismus.
Perform intraoperative forced ductions to identify restriction (see Chapter 42).
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