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Managing the Patient with Oculomotor Nerve Palsy

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REVIEW CURRENT OPINION Managing the patient with oculomotor nerve palsy Karthikeyan A. Sadagopana and Barry N. Wassermanb Purpose of review To provide clinically relevant information regarding the evaluation and current treatment options for oculomotor nerve 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 subarachnoid hemorrhage, polycythemia, sphenoiditis, neurobrucellosis, interpeduncular fossa lipoma, metastatic pancreatic cancer, leukemia, and lymphoma. Surgical studies have focused on modifications and innovations regarding strabismus surgery for this condition. New globe 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 oculomotor nerve palsy 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 pupil and accommodation. Strabismus surgery can be challenging but also rewarding with appropriate selection and staging of procedures. Keywords aberrant regeneration, ptosis, 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 eyelid 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 diplopia may be revealed in cranial aneurysms and head injury, 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 Ophthalmology 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 www.co-ophthalmology.com Volume 24 Number 5 September 2013 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Management of oculomotor nerve palsy Sadagopan and Wasserman 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 amblyopia. associated with a pupil-sparing palsy, myasthenia gravis 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 aneurysm, 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. Multiple sclerosis 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 stroke [7], sellar chordoma [8], nonaneurys- Pupillary involvement has diagnostic implications and mal subarachnoid hemorrhage [9], and radiation can yield photophobia, anisocoria, 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 extraocular muscles, 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- atherosclerosis, 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, diabetes 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 orbit 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. 1040-8738 ß 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins www.co-ophthalmology.com 439 Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. Pediatrics and strabismus 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
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