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REVIEW

CURRENT OPINION Managing the patient with oculomotor palsy

Karthikeyan A. Sadagopana and Barry N. Wassermanb

Purpose of review To provide clinically relevant information regarding the evaluation and current treatment options for palsies. We survey recent literature and provide some insights into these studies. Recent findings Recent case reports highlight emerging new causes of oculomotor cranial nerve palsies, including sellar chordoma, odontogenic abscess, nonaneurysmal , polycythemia, sphenoiditis, neurobrucellosis, lipoma, metastatic pancreatic cancer, leukemia, and lymphoma. Surgical studies have focused on modifications and innovations regarding surgery for this condition. New fixation procedures may include fixation to the medial orbital wall by precaruncular and retrocaruncular approaches, apically based orbital bone periosteal flap fixation and the suture/T-plate anchoring platform system. Summary Management of depends in part upon the underlying cause and anatomical location of the lesion. Careful clinical evaluation and appropriate imaging can identify a definitive cause in most cases. Surgical options depend on the number, extent, and severity of the muscles involved as well as the presence or absence of signs of aberrant regeneration. The clinician should also address issues that arise due to involvement of the and . can be challenging but also rewarding with appropriate selection and staging of procedures. Keywords aberrant regeneration, , pupil, strabismus, third nerve palsy

INTRODUCTION regeneration play a crucial role in surgical planning. Oculomotor nerve palsy significantly impacts Careful assessment and appropriate surgical plan, patients, and challenges the strabismus surgeon. coupled with realistic patient expectations, form the Also called third cranial nerve palsy, it may be basis of successful management. congenital or acquired. Most acquired causes in Patients may present with a variety of symptoms adults are due to ischemia and resolve completely and signs. Complete ptosis can prevent dip- in a few months. Congenital oculomotor nerve lopia in the initial period. If ptosis improves before palsy, as well as those occurring later due to intra- motility, intolerable may be revealed in cranial and head , may partially multiple, if not all, gaze positions. When the pupil recover, and sometimes present with signs of aber- is involved, light sensitivity and compromised rant regeneration. Patients may require neurosurgi- accommodation compound patient discomfort. cal intervention as well as strabismus surgery. Associated neurological findings including hemiple- Clinical evaluation and imaging assist in defining gia, tremor, and ataxia may further impact quality of the cause. Advances in neuroimaging may now life. Physical appearance may add considerable identify a definitive cause wherein conventional

imaging modalities fail. Management depends upon a factors including visual acuity, presence of amblyo- Pediatric and Ocular Genetics, Aravind Eye Care Sys- tem, Madurai, Tamil Nadu, India and bPediatric Ophthalmology, Wills Eye pia, and cause of the oculomotor nerve palsy. In Institute, Philadelphia, Pennsylvania, USA cases in which simple observation leads to resol- Correspondence to Karthikeyan A. Sadagopan, DNB, FRCS, Consultant ution, management involves supportive interven- Pediatric Ophthalmologist and Ocular Geneticist, Aravind Eye Hospital tions to optimize patient comfort and function in [Madurai] 1, Anna Nagar, Madurai - 625 020, Tamil Nadu, India. Tel: +91 the interim. When surgical intervention is needed, 944 458 2919/452 435 6100; fax: +91 452 253 0984 the extent and severity of extraocular muscle Curr Opin Ophthalmol 2013, 24:438–447 involvement and the presence of aberrant DOI:10.1097/ICU.0b013e3283645a9b

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In elderly individuals, headache and cranial KEY POINTS nerve palsy may occur prior to onset of herpes zoster  Managing oculomotor nerve palsy is challenging, and manifesting as oculomotor palsy. When diurnal depends on the cause, motility, and presence variation or fluctuations in clinical findings are of . associated with a pupil-sparing palsy, should be excluded (Fig. 1) [5]. Evaluation  Congenital oculomotor palsy, and acquired oculomotor for tuberculosis and sarcoidosis would, at a palsy due to trauma and intracranial , often recover incompletely, and show signs of aberrant minimum, require chest radiograph, skin testing regeneration. for the former and angiotensin converting enzyme level for the latter. Signs of increased intracranial  Prisms, occlusion, and botulinum toxin injection are hypertension warrant neuroimaging to rule out options during observational periods. space occupying lesions. If imaging is normal, a  Current surgical techniques for strabismus focus on lumbar puncture is considered to exclude idio- transposition procedures, globe fixation, and lateral pathic intracranial hypertension. rectus inactivation. should also be considered in the differential diag- nosis. Other causes that have been recently reported  Frontalis sling is currently the preferred option for & subsequent management of associated ptosis. include odontogenic abscess [6 ], cryptogenic mid- brain [7], sellar chordoma [8], nonaneurys-  Pupillary involvement has diagnostic implications and mal subarachnoid hemorrhage [9], and radiation can yield , , and treatment [10&&]. accommodative dysfunction. In children, ophthalmoplegic migraine with recurrent oculomotor palsy is rare but should be considered if there is a strong family history psychological distress. However, careful observation of migraine and if the onset of the palsy is for at least 6 months is essential, as some patients associated with nausea and vomiting. Laboratory will show partial or full spontaneous recovery. parameters and neuroimaging are usually normal Complete oculomotor nerve palsy is perhaps [11], though imaging abnormalities have been one of the most difficult challenges facing reported in patients with migraine [12]. Recurrent strabismus surgeons [1]. These cases are difficult palsy has also been reported as the presenting because multiple , as well as feature of neurofibromatosis [13&]. Idiopathic the levator muscle may be involved. Involvement intracranial hypertension usually causes abducent of four extraocular muscles induces horizontal, nerve palsies, but can also cause oculomotor palsy. vertical, and torsional strabismus. Surgery on Spontaneous intracranial hypotension has been multiple muscles raises concern about postopera- reported as a transient cause of oculomotor palsy tive anterior segment ischemia. Aberrant regener- [14&]. ation and pupil and accommodative dysfunction The diagnostic yield of imaging depends add to the complexity. upon patient age, presence of pupil involvement, and extent of extraocular muscle involvement [15]. Pupil-sparing oculomotor palsy in adults over SYSTEMIC ASSESSMENT 50 years of age with atherosclerotic risk factors When a patient presents with acquired complete or (hyperglycemia, hypertension, family history of partial third cranial nerve palsy, systemic investi- , hyperlipidemia, or heavy smoking) gations to identify a cause are of primary import- is most likely caused by microvascular ischemia and ance. In pupil-sparing palsy, and does not require imaging [16,17&]. MRI and mag- hypertension must be identified or excluded as netic resonance angiography (MRA) are required these affect both prognosis and anesthetic concerns. when aneurysm is suspected [18]; some studies Evolving pupil involvement must be carefully moni- have reported MRI findings with herpes zoster tored in the first few days after the onset of strabis- [19]. Conventional MRI studies may not reveal mus. The patient is warned to return immediately the cause of the oculomotor nerve palsy. Demer for increasing light sensitivity in the affected eye or and coworkers [20] reported that multipositional any new difficulty in reading. Patients and family high-resolution MRI (hrMRI) can demonstrate members are instructed to observe for anisocoria. structural abnormalities of the and oculomo- Patients are also warned to return if any new neuro- tor nerve in nonaneurysmal oculomotor nerve logical symptoms occur. Absence of pupil involve- palsy as well as various degrees of extraocular ment does not exclude an aneurysm [2,3&]. Pupil muscle atrophy and decreased contractility that might be involved also in diabetic etiology [4&]. could be of importance in surgical planning.

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After neostigmine test

FIGURE 1. Myasthenia gravis masquerading as oculomotor nerve palsy. A 30-year-old man presented with ptosis of the left eye and double vision. Ocular motility examination suggests a possible pupil sparing left oculomotor nerve palsy. The lower panel shows the same patient 5 min after neostigmine test, confirming a diagnosis of myasthenia gravis. There is dramatic improvement of the ptosis and adduction. Diurnal variation of symptoms and orbicularis weakness suggested myasthenia gravis. Reproduced with permission from [5].

OPHTHALMIC ASSESSMENT There will be limitation of movements in all fields of The primary position deviation, presence and gaze except abduction and intorsion. Incomplete severity of ptosis, extent and severity of limitation palsy implies either partial limitation (paresis) of of ocular motility, and pupillary involvement elevation, depression or abduction or even full should be documented. Versions and ductions movement in one or more of these directions. Multi- should be tested. Forced ductions and force gener- ple cranial nerve involvement must be excluded. ation tests are performed in adults and co-operative An examination of all cranial nerve functions is children to rule out restriction (that may mimic an useful, in particular abduction and, by having the oculomotor nerve palsy) and assess residual muscle patient attempt to look down and in, intorsion. The function, respectively. Total oculomotor nerve palsy latter may require slit lamp examination to see the implies involvement of all muscles innervated by subtle intorsion, especially in the presence of a the oculomotor nerve with pupillary involvement. complete oculomotor palsy.

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Divisional oculomotor nerve palsy implies strabismus. Strict control of diabetes and hyperten- selective involvement of the upper or lower division sion is essential. Hyperlipidemia, anemia, and of the oculomotor nerve. Intracranial aneurysms obesity should be adequately controlled. Systemic and orbital disease usually result in divisional steroids are not indicated in ischemic oculomotor oculomotor nerve palsy. Cryptococcal meningitis, palsies, and pose additional risk of inducing poor sphenoiditis, rhinocerebral , meta- metabolic control. Systemic steroids are used in static pancreatic cancer [21] and other rare causes granulomatous etiologies such as sarcoidosis and [22] have been reported to cause superior divisional neurocysticercosis as adjuvant to antihelminthic oculomotor nerve palsy. This subtype should be medications [26]. Antivirals are used in herpetic considered as differential diagnosis in children with oculomotor nerve palsy [27]. Oral acetazolamide congenital complicated ptosis, and in adults with is useful in patients with idiopathic intracranial acquired monocular elevation deficit and myasthe- hypertension. Neurosurgical intervention may be nia gravis. Inferior divisional oculomotor nerve required for or aneurysm. palsy is less common and is usually caused by orbital Pupil involvement in third cranial nerve palsy disease [23] or diabetes [24]. Congenital oculomotor results in anisocoria and in some cases, increased palsy may exist in isolation as a result of isolated light sensitivity. Pilocarpine can be used if there are congenital absence of the oculomotor nerve or its no other contraindications. Some patients are con- , or may be associated with other central cerned about the cosmetic appearance of anisocoria. nervous system abnormalities. Using pilocarpine prior to attending social events is Signs of aberrant regeneration must be ident- helpful. Diminished accommodation can also occur ified. Aberrant regeneration is often seen in congen- in pupil involving oculomotor palsy, and the clini- ital palsy but may also occur in acquired traumatic cian should consider near vision addition in optical and aneurysmal palsy. Aberrant regeneration does prescriptions. This becomes also important when not occur with diabetic or hypertensive microangi- patching children for amblyopia treatment. Per- opathy. Histopathologic, clinical, and experimental haps, the greatest cause of visual loss in children evidence suggests random misdirection of regener- with oculomotor palsy is amblyopia. If possible, ating motor within an injured oculomotor strabismus surgery is deferred until after amblyopia nerve [25]. Clinical presentation reveals anomalous management is complete. One indication for earlier eye movements on attempted adduction, elevation intervention is a large angle that fails and depression, with associated narrowing or wid- to spontaneously recover. Taping the lids to the ening of the palpebral fissure. Pupillary constriction forehead or crutch should be considered may be seen with attempted . The to manage significant ptosis during the time of pupil can be, smaller or larger than the unaffected patching. fellow eye. The aberrant regeneration involves both lid gaze dyskinesis and pupil gaze dyskinesis. Lid gaze dyskinesis includes widening (improvement of Observation the ptosis) of the palpebral fissure on attempted Strabismus surgery is usually deferred for a mini- adduction (Inverse ) and elevation mum of 6 months following the onset of oculomo- of the lid on depression (Pseudo von-Graefe’s tor palsy. If there is continuing improvement, sign). Pupil gaze dyskinesis includes constriction surgery can be delayed further. Most oculomotor of the pupil in the affected eye on attempted adduc- nerve palsy due to microangiopathy resolves com- tion (Pseudo-Argyll-Robertson pupil) or during pletely in the first few months. Congenital palsy depression. requires surgery. Delays in surgery can result in irreversible amblyopia and increasing difficulties with aberrant regeneration. Although oculomotor TREATMENT palsy due to trauma or intracranial lesion usually Treatment initially involves medical management requires surgery, spontaneous improvement can of systemic predisposing factors and conservative occur, especially after a tumor or aneurysm is measures to obviate symptoms followed later by removed. One study reported a spontaneous recov- surgical intervention in nonresolving oculomotor ery rate of only 30% following trauma [28]. Studies nerve palsy. have shown that larger deviations at presentation and delayed surgical intervention (beyond the optimal time for spontaneous recovery) have nega- Medical management tive prognostic effect on the surgical outcome [29]. Active systemic causes must first be addressed before While waiting for spontaneous improvement, proceeding to surgical interventions for the controlling diplopia by occluding one eye may be

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beneficial. Patches or clear adhesive tape on one rectus muscle toward the insertion of inferior rectus of a patient’s spectacles prevent diplopia, the muscle, with tenotomy of the ipsilateral superior latter often being more cosmetically acceptable. oblique was effective in managing such patients. Prisms have a limited role as the deviations are Paralysis of the upper division of the oculomotor often extremely large, incomitant, multivectorial, nerve results in ptosis due to involvement of and torsional [30&]. Prisms can be considered post- levator palpebrae superioris and limitation of operatively for small residual misalignment in elevation due to superior rectus involvement. A primary position and downgaze. Knapp procedure (transposition upward of the medial and lateral rectus to the corners of the superior rectus insertion) on the affected eye com- Botulinum toxin bined with a recession of the contralateral superior Botulinum toxin acts by inducing temporary para- rectus can be effective [33&&]. Patients with isolated lysis of the unopposed ipsilateral antagonist muscle, palsy may benefit from peri- reducing the deviation. The role of botulinum toxin osteal anchoring of the medial rectus with or with- is well established in acute palsy. out lateral rectus disinsertion [34&]. Vertical muscle The role of injecting botulinum toxin in a previously transposition has been used following medial rectus contractured muscle (i.e., a longstanding palsy) transection following sinus procedures [35,36,37]. is controversial. Botulinum toxin injection may Isolated inferior oblique palsies are rare and man- help shorten the duration of symptoms in acute aged by weakening procedures on the ipsilateral traumatic oculomotor nerve palsy [31]. It might also superior oblique (tenotomy or tenectomy) alone be useful when the patient is not a candidate for or coupled with contralateral superior rectus reces- neurosurgical intervention or strabismus surgery, sion [38]. When of the affected eye is for example, due to unstable associated medical the main ocular motility finding or when there is conditions. aberrant regeneration causing the eye to elevate in attempted depression, then resection and anterior transposition of the paretic inferior oblique can be Surgical management beneficial [39]. Meticulous preoperative examinations and appro- The presence of aberrant regeneration poses priate surgical designs are essential. The goals additional surgical challenges. A recess–resect and limitations of the surgery should be clearly procedure on the horizontal muscles of the ipsi- understood by the patient to avoid disappoint- lateral eye can be performed if there are minimal ment. In patients with partial oculomotor signs of aberrant regeneration [40] (Fig. 2a) [41]. palsy and sufficient motility, routine strabismus The surgeon can take advantage of the aberrant surgery may be successful in restoring functional, regeneration to correct both the strabismus and single . Patients with total oculo- the ptosis by performing a horizontal recess–resect motor palsy may have the more limited goal procedure on the contralateral normal eye with of primary gaze alignment. Surgical manage- appropriatemuscledisplacementforthevertical ment sometimes requires several staged proce- deviation [42] (Fig. 2b). Sometimes surgical inter- dures to avoid anterior segment ischemia, and to vention may not be required for partial oculomotor assess results prior to considering the further palsy or for its accompanying aberrant regeneration options. If needed, ptosis surgery is usually done (Fig. 2c). 4–6 months following strabismus surgery. Ptosis Complete third nerve palsy is more difficult to is best managed by frontalis sling procedures as manage as there is no residual muscle function. The the levator muscle is also paralyzed to a variable surgical goal is ocular alignment in primary position extent and shows variable response to levator and downgaze. It is very difficult to achieve binoc- resection. ularity in other gaze positions. An attempt to Surgical outcome is often better in partial ocu- remove all abducting forces is planned. There are lomotor nerve palsy than complete oculomotor several surgical options. nerve palsy. Isolated palsy of the inferior division of the oculomotor nerve is rare. The clinical pres- entation includes exotropia and hypertropia, pupil SUPERIOR OBLIQUE TENDON TRANSFER involvement, and fundus incyclotorsion due to Scott [43] first used this technique wherein unopposed action of the superior oblique. Kushner the superior oblique tendon is disinserted at its [32] reported that simultaneous transposition of the insertion, without fracturing the trochlea, short- to lie adjacent to the medial ened, and sutured to the upper border of rectus and simultaneous transposition of the lateral the medial rectus insertion to the with

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A1

A2

B1

B2

C

FIGURE 2. Management of aberrant regeneration. Surgery on the ipsilateral eye: Patient with left congenital oculomotor nerve palsy with minimal signs of aberrant regeneration. (Row A1) There is mild ptosis and a small angle exotropia of the left eye with the right eye fixing. There is minimal limitation of the left eye adduction. Note the aberrant regeneration manifesting as widening of the palpebral fissure (improvement in ptosis) in adduction. Row A2 shows the first postoperative day appearance after left eye lateral rectus recession. Surgery on the contralateral normal eye: Row B1 shows the preoperative appearance of right oculomotor nerve palsy 1 year after head injury, showing a large angle exotropia and moderate ptosis of the right eye. One can also observe the compensatory lid retraction in the normal left eye. Note that there is gross widening of the palpebral fissure in the right eye on adduction (aberrant regeneration). Row B2: postoperative appearance following a lateral rectus recession and medial rectus resection with vertical displacement, operated on the normal left eye. One can observe that the ptosis and strabismus of the right eye is corrected. Surgery on the left eye results in more innervation to the left lateral rectus in primary position, which by Herrings law results in more innervation to the right medial rectus in primary position and hence causes improvement of ptosis in the right eye. No surgical intervention: Row C shows a child with congenital oculomotor palsy of the left eye with minimal ptosis and minimal widening of the palpebral fissure on attempted adduction. There is minimal compensatory right eye lid retraction. The patient was orthotropic both for distance and near and had binocularity and . No surgery was required. Reproduced with permission from [41].

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nonabsorbable suture to hold the eye taught in thus totally eliminating abduction [45]. A com- adduction. Induced hyper deviations and paradoxi- promise is made regarding motility for purposes cal ocular movements often occur, and the of alignment. It is usually combined with a supra- procedure may result in exotropic drift with time. maximal resection of the ipsilateral medial rectus, An earlier alternative procedure involved fracturing superior oblique tendon transfer, or globe anchor- thetrochlea,butthisisseldomusedtoday.When ing procedures. the superior oblique is altered by tenotomy or by transposition to the medial rectus, all of its abducting force is inactivated (Fig. 3 A1, A2 and GLOBE ANCHORING PROCEDURES A3). This is often combined with conventional The globe can be anchored to the periosteum of lateral rectus recession and supramaximal medial the anterior lacrimal crest. Some flattening of the rectus resection. The lateral rectus recession can medial canthal area has been reported with this be substituted with its disinsertion and fixation to procedure [39]. Several materials have been used the lateral orbital periosteum. to anchor the globe, including periosteal flaps [46], superior oblique tendon [47], silicone bands [48], fascia lata [49], and 5–0 polyester sutures [39]. LATERAL RECTUS DISINSERTION AND Globe fixation may also include fixation to the PERIOSTEAL FIXATION medialorbitalwallretrocaruncular[50]orpre- Conventional recess–resect procedures on the caruncular [44] (Fig. 3 B1, B2 and B3). Such horizontal recti result in exotropic drift [44]. Even procedures may require traction sutures for a week, supramaximal recession of the lateral rectus and cause significant edema and discomfort in the will with time contract, and through posterior nasal bulbar and medial canthus. orbital connections, cause abduction. Lateral rectus Initial overcorrections of up to 10 prism diopters disinsertion and periosteal l fixation is a reversible of have been advocated to avoid later way of totally inactivating the lateral rectus and exotropic drift. Yonghong et al. [39] performed

A1 A2 A3

B1 B2 B3

C1

C2

FIGURE 3. Management of complete oculomotor nerve palsy. A1: Preoperative photograph of a patient with acquired right complete oculomotor nerve palsy with aberrant regeneration following head injury. Patient underwent right lateral rectus disinsertion and periorbital fixation combined with a supramaximal medial rectus resection and superior oblique tendon transfer to the medial rectus insertion in a single stage procedure. No deviation in primary position on first postoperative day (A2). A small exotropic drift is noted 1 month after surgery. This patient had an exotropic drift a year later (A3) requiring surgery on the left eye. Precaruncular globe anchorage: B1: preoperative photographs of right complete oculomotor nerve palsy, B2): after globe fixation by nonabsorbable sutures by precaruncular approach; and B3: ptosis management with crutch glasses. (C1) Top row shows preoperative photographs of complete oculomotor nerve palsy of the right eye with complete ptosis, exotropia, and limitation of adduction. (C2) The lower row shows postoperative photographs following a lateral rectus recession and medial rectus resection in the right eye followed by frontalis sling procedure for ptosis. Photo B courtesy of Dr Rohit Saxena, All India Institute of Medical Sciences, New Delhi.

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Oculomotor never palsy

Partial To t a l

Complete Divisional Isolated Incomplete

Aberrant regeneration Upper Lower Medial Superior Inferior Inferior rectus rectus rectus oblique Mild Moderate/severe Absent

Knapp Hemi tendon procedure No surgery Ipsilateral recess- Superior oblique transposition resects procedure tendon transfer of vertical recti Partial or procedure knapp/ Contralateral (combined with knapp recess–resect conventional procedure procedure with procedure) Te no t omy of sup e r i or Inverse appropriate oblique + knapp muscle procedure displacement Lateral rectus Full tendon transposition disinsertion with of superior rectus towards periosteal fixation medial rectus + Ipsilateral superior (substituted for lateral oblique weakening +/– rectus recession) Full tendon transposition contralateral superior of lateral rectus towards rectus recession inferior rectus Globe anchorage

Precaruncular/retrocaruncular Periosteal flaps

The suture/T-plate anchoring platform system

FIGURE 4. Surgical options in the management of oculomotor nerve palsy. The flow chart summarizes the surgical options for nonresolving oculomotor nerve palsy discussed in this article.

globe fixation for combined oculomotor and glasses (Fig. 3 C1 and C2). The various options in the superior oblique palsy. In our experience, results surgical management of nonresolving oculomotor of globe anchoring are improved when combined nerve palsy are shown (Fig. 4). with lateral rectus inactivation by disinsertion. Ahmed et al. [51] suggest that globe fixation with CONCLUSION orbital apex-based periosteal flaps shares a more natural direction of the muscle path, whereas Managing patients with oculomotor palsy poses medial canthus anchorage changes the natural several challenges. Most microvascular palsies course of the muscle. Their study had only two recover spontaneously. Traumatic and aneurysmal patients with isolated oculomotor nerve palsy cases may not recover completely, and often and only one had significant improvement. These develop signs of aberrant regeneration. Careful were performed in patients after multiple failed assessment of versions and ductions, followed by nonglobe fixation procedures. The suture/T-plate forced ductions and generations, and observation anchoring platform system[52]anchorstheglobe for aberrant regeneration will help plan the appro- by sutures to a titanium T-plate screwed to the priate surgical plan. There has been an increasing orbital wall. Benefits of this approach include trend to perform modifications of globe fixation reduced risk of anterior segment ischemia and fewer anchoring procedures. Surgical management is chal- re-operations, with likely longer durability of the lenging but potentially rewarding if appropriate system. The suture/T-plate anchoring platform sys- procedures are performed. tem often requires orbital surgeon involvement. Perhaps,theremaybearoleinthefutureforendo- Acknowledgements nasal approaches to globe fixation. Ptosis can be The authors sincerely thank Dr Rohit Saxena, for his managed by frontalis sling procedures or by crutch contribution of Fig. 3b.

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