Treatment of acquired partial oculomotor nerve palsy with dexamethasone – A case report

Abstract

Introduction/importance

Oculomotor nerve palsy is an acquired condition caused by injury to the third cranial nerve. Patients present classically with their eye in a “down and out” positioning, ptosis and abnormalities in most extraocular movements causing diplopia. Ocular dysfunction may be due to a variety of different etiologies, such as aneurysm, microvascular disease, trauma, and viral infections. Clinical prognosis is usually quite good and is often self-limiting.

Case representation

We present a case of an otherwise healthy 40-year-old male who awoke one morning with moderate diplopia, unable to focus with binocular vision and developed eyelid ptosis two days later. He was previously infected with the Omicron variant of COVID-19; however, a rapid test could not confirm it. No intracranial or vascular pathology were identified on CT head, CT angiogram, or MRI. Repeat COVID-19 PCR test was negative. He was assessed by a neuro-ophthalmologist and was diagnosed with left partial oculomotor nerve palsy presumed secondary to viral microvascular injury. COVID-19 infection seemed likely given the history but could not be confirmed. The specialist recommended monitoring the patient without any treatment, with no recommendation of corticosteroid use.

Clinical discussion

Cranial neuropathy guidelines for viral palsies involving the 7th or 8th cranial nerve are treated with corticosteroids. After considering the risks, the patient elected treatment with a left eye patch and a dexamethasone taper. Full return of function in all extremes of gaze was restored less than 2 months after onset.

Conclusion

Given the complete and timely recovery, it may be reasonable to consider corticosteroids for all cranial neuropathies.

Highlights

• •Corticosteroid use was effective and led to full recovery of oculomotor nerve palsy.
• •Viral infections can cause oculomotor nerve palsies but adequate treatment guidelines are not yet established.
• •Oculomotor nerve palsies are caused by many different etiologies and clinicians must consider these when treating patients.

1. Introduction

Oculomotor nerve palsy is an ocular pathology due to injury to the third cranial nerve. The resulting damage can present as somatic dysfunction to the extraocular muscles and/or autonomic dysfunction leading to damage of the ciliary and pupillary sphincter muscles [1]. Clinical symptoms of the resulting oculomotor nerve palsy depend on the affected oculomotor pathway and can be divided into complete or partial palsy. Patients with complete oculomotor palsy present with complete ptosis, “down and out” eye deviation, inability to adduct, infraduct or supraduct the eye, a dilated pupil with sluggish reaction, and diplopia [2]. Partial oculomotor palsy can present with variable eye duction movements and varying degrees of ptosis and pupillary dysfunction [1]. Oculomotor nerve palsy can result from multiple different etiologies including: aneurysm, microvascular disease, trauma, viral infections, encephalitis, meningitis, vasculitis, and systemic lupus erythematosus [3]. It has been shown that the most common causes of unilateral oculomotor nerve palsy were caused by intracranial aneurysms (29.8 %), diabetic peripheral neuropathy (26.5 %), painful ophthalmoplegia (9.9 %), trauma (5.8 %), pituitary lesions (5.0 %), cavernous sinus disease (5.0 %), brainstem infarction (2.5 %), brainstem encephalitis (0.8 %), and other unknown causes (14.9 %) [4].

Prognosis for oculomotor palsy is typically good, seeing as natural improvement of symptoms occur within a few months. Clinical course and prognostic factors of acquired ocular palsy show that most patients affected by oculomotor palsy recovered within roughly 4 months [4]. It was also shown that the group with a vascular etiology has the best recovery rate and shortest recovery time, whereas the neoplastic group has the longest recovery time.

Clinical management for oculomotor palsy depends on many factors. In cases of oculomotor palsy causing diplopia, occlusion of one eye with a patch or opaque contact lenses can be helpful [5]. The majority of complete or partial oculomotor palsies that are pupil sparing are a secondary ischemic process and these patients notice an improvement after 4 weeks with resolution of symptoms in 12 weeks [6].

Coronavirus disease (COVID-19) is a viral infection leading to severe acute respiratory syndrome and pneumonia [7]. Although acquired oculomotor nerve palsy due to COVID-19 is very rare, some case reports have shown acquired cranial nerve neuropathy [[8], [9], [10], [11], [12], [13], [14], [15], [16]]. Treatment has ranged from supportive, to the use of corticosteroids, the use of hydroxychloroquine and azithromycin, and intravenous immunoglobulin. In the these identified patients, COVID-19 symptoms were mild and neurological symptoms resolved in many patients without any specific interventions. To our knowledge, corticosteroid use for partial oculomotor nerve palsies has not been fully investigated due to the limited amount of case reports [[12], [13], [14]]. Thus, it remains unknown if corticosteroids have the capacity to improve clinical symptoms directly since other cases have shown full recovery without steroid treatment. Here we report an additional case of acquired partial oculomotor nerve palsy treated successfully with corticosteroids to add to the current state of the literature.

2. Case presentation

A 40-year-old healthy male otolaryngologist awoke on the morning of August 9th, 2022 with moderate diplopia, correctable with effortful focus. He had an unremarkable medical history and was free of any medications. He had a prodrome of sore throat and diarrhea 5 days prior. He had been infected with Omicron on January 5th, 2022 with mild rhinitis symptoms. His wife had been infected with COVID-19 two weeks prior, suffering from laryngitis and a sore throat. His COVID-19 rapid test was negative. He was fully vaccinated with three doses of the Pfizer COVID-19 vaccine.

On August 11th, he was unable to focus with binocular vision and eyelid ptosis had developed. He presented to the local emergency department where a CT head, CT angiogram, and MRI were performed. There was no intracranial or vascular pathology identified (see Fig. 2). Repeat COVID-19 PCR test was negative. He was assessed on August 12th by neuro-ophthalmology and was found to have a left partial oculomotor nerve palsy presumed to be secondary to viral microvascular injury. COVID-19 infection seemed likely given the delayed onset and clinical history but could not be confirmed by testing. The treatment recommendation was to watch and wait with no evidence or recommendation for corticosteroid use.

Fig. 2.

A) T2-weighted brain MRI in the axial view and B) Gadolinium-enhanced T1-weighted brain MRI in the coronal view. No oculomotor muscular atrophy and is free of any masses, lesions, infarction, hemorrhages, or oculomotor nerve impingement.

After considering the risks, he elected treatment with a left eye patch and dexamethasone 8 mg PO TID for 7 days, with a taper over 5 days of 6 mg TID, 4 mg TID, 2 mg TID, 2 mg BID, and 2 mg OD then stop. He instituted daily visual tracking exercises including smooth pursuit exercises (see Fig. 1). By day 7, partial left eye mobility began to return. Functional binocular vision was present by day 14 after onset. He was able to function without the left eye patch on day 20. He was able to return to work on August 29th with mild diplopia on extreme right gaze only. This mild gaze dependent diplopia was no longer detected subjectively on October 7th. Normal ophthalmologic exam was confirmed on November 3rd with no objective residual weakness.

Fig. 1.

Clinical progression of left oculomotor nerve palsy treated with dexamethasone. NOTE: severe ptosis in the left eyelid and brow, the lack of medial abduction in the affected eye on rightward gaze, and how the affected eye reaches further medially throughout recovery.

3. Discussion

This case report details the experience of a patient with an acquired, partial oculomotor nerve palsy. In the setting of viral infection, the underlying pathophysiology of partial oculomotor nerve palsy is thought to be due to microvascular injury. Viral palsies involving the 7th or 8th cranial nerves are treated with corticosteroids to presumably reduce edema and regain function [17,18]. While the evidence is equivocal, it is often the only tool available.

Our patient elected to use corticosteroids. Eye movements were recorded daily. Return of function of the extraocular muscles occurred 14 days after onset and after 12 days of dexamethasone use. Near complete function was restored 20 days after onset to the point where he had normal depth perception and no longer needed to patch the left eye. Full return of function in all extremes of gaze was restored on day 52, less than 2 months after onset. Three other case reports of unilateral oculomotor nerve palsy in the literature have been treated with corticosteroids [[12], [13], [14]] and will be discussed further.

Firstly, a previously healthy 10-year-old boy developed acute, unilateral diplopia and ptosis due to confirmed COVID-19 infection. He was prescribed prednisone 2 mg/kg/day for 10 days and complete recovery was achieved in 7 days [12]. Seeing as the clinical presentation of cranial nerve palsies is confounded by children's ability to repair and regenerate damaged tissues [19], perhaps the authors opted to use corticosteroids to expedite the recovery process to preserve long-term function. Our patient elected for corticosteroid treatment instead of supportive therapy as well and nearly achieved full return of function in 2–3 weeks. The young patient had a positive COVID-19 contact 5 days before the onset of symptoms, whereas our patient had a presumed much longer incubation period and could explain the longer recovery time when compared.

Secondly, a previously healthy 46-year-old male who presented with acute, unilateral diplopia, strabismus and ptosis due to confirmed COVID-19 infection one day after symptom onset [13]. The patient was treated with 1 g/day of oral methylprednisolone for 3 days and showed full recovery after two weeks. Our patient had restored oculomotor function 12 days after initiating corticosteroid treatment as well and shows that significant improvement of symptoms can be achieved in a relatively short timeframe. These two cases showing similar recovery times supports the use of corticosteroids without any major reported adverse events.

Thirdly, a 60-year-old woman with a history of rheumatic fever and Crohn's disease was infected with COVID-19 and presented initially with absent extraocular symptoms that required no treatment [14]. She awoke 6 weeks later with diplopia and a fixed, dilated pupil, and was diagnosed with an oculomotor nerve palsy presumably as a complication of the COVID-19 infection. She was prescribed oral prednisone 60 mg with a slow taper. Her pupil size and diplopia gradually improved over a few weeks and eventually showed full recovery. Our patient had a similar delayed onset of oculomotor nerve palsy symptoms and recovery timeframe, which increases the likelihood of the etiology being infectious given that neuro-imaging ruled out any structural, vascular or traumatic causes for both patients.

The direct action of the COVID-19 virus has the capacity to induce local inflammation of the oculomotor nerve and cause oculomotor dysfunction. There are very few cases of COVID-associated oculomotor neuropathies treated with corticosteroids to formulate treatment decisions on given the novelty of the virus. Seeing as full recovery was attained in all four cases using corticosteroids, the role of corticosteroid in reducing local inflammation of the oculomotor nerve and restoring function quickly cannot be dismissed.

4. Conclusion

Partial oculomotor nerve injury recovery usually occurs within 3–4 months without any specific treatment. Whether corticosteroids sped the patient's recovery is unknown but recovery was faster using the pharmaceutical intervention. Given the inclusion of corticosteroids in the current viral 7th and 8th cranial neuropathy guidelines [17,18], the corticosteroids may have played an important role in hastening the recovery timeframe and restoring significant function in a short time. The role of COVID-19 in other cranial neuropathies including anosmia, sudden hearing loss, and facial weakness has been demonstrated, and perhaps steroids should be considered for all cranial neuropathy cases given these highlighted cases. There are very few reports in the literature on the use of steroids for partial oculomotor nerve palsies, and while this is but one case, the outcome was full and expedient recovery and highlights the effectiveness of treating acquired, unilateral oculomotor nerve palsies with corticosteroids.

Ethics statement

According to our local REB regulations, “If more than three patients are included in the project, it becomes a case series, is considered research, and requires REB review and approval.” Our case report includes one patient and thus, we deemed that it was not necessary to receive REB approval.

Consent

Written informed consent was obtained from the patient for publication and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

Scare guidelines

The work has been reported in line with the SCARE criteria [20].

Sources of funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Author contribution

Cory Tremblay: study design, data collection, data analysis, writing the paper.

Dr. Matthew Brace: study design, data collection, data analysis, writing the paper.

Guarantor

Cory Tremblay & Dr. Matthew Brace.

Declaration of competing interest

The author(s) declare that the ideas in the submitted article are our own. We have no potential conflicts of interest to declare.