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Recovery of Ocular Motor Cranial Nerve Palsy After Herpes Zoster Ophthalmicus

Chhabra, Manpreet S. MD; Golnik, Karl C. MD, MEd

Journal of Neuro-Ophthalmology: March 2014 - Volume 34 - Issue 1 - p 20–22
doi: 10.1097/WNO.0b013e3182a59c69
Original Contribution

Objective: To report the course of ocular motor cranial nerve palsy due to herpes zoster.

Methods: A retrospective chart review identified patients with ocular motor cranial nerve palsy occurring at the time of herpes zoster ophthalmicus. Patients were seen by a single neuro-ophthalmologist from 1994 to 2012.

Results: Twenty-one patients were identified; 3 were excluded because of incomplete follow-up. Nine (50%) had complete recovery and 8 (44%) had partial recovery but no diplopia in primary gaze (mean time = 10 weeks). One patient with complete ophthalmoplegia had persistent diplopia in primary position for recovery.

Conclusion: Ophthalmoplegia secondary to herpes zoster ophthalmicus has good long-term prognosis for recovery.

Department of Ophthalmology (MSC, KCG), University of Cincinnati, Cincinnati Eye Institute, Cincinnati, Ohio; and the Virdi Eye Clinic (MSC), Rock Island, Illinois.

Address correspondence to Karl C. Golnik, MD, MEd, Department of Ophthalmology, University of Cincinnati, 260 Stetson Street, Suite 5300, Cincinnati, OH 45267, E-mail:

Supported by Research to Prevent Blindness.

Presented in part as a poster at the AAO Annual Meeting in Chicago in 2012.

The authors report no conflicts of interest.

Infection with herpes zoster, commonly known as shingles, is caused by varicella zoster virus (VZV) in individuals who have already been exposed to the virus, either wild type or via vaccination (1). The initial VZV infection usually occurs in childhood, and once it resolves, the virus is not eliminated and remains in the body and can cause zoster later in life. There are reports of at least 1 million cases of herpes zoster annually in the United States (1–5).

Herpes zoster ophthalmicus (HZO) refers to the involvement of the ophthalmic division of the fifth cranial nerve (6). Patients acutely develop a rash that evolves through papular, vesiculobullous, pustular, and crusting stages over days to 3 weeks with associated periocular pain. Ocular involvement is variable and is observed in 20%–70% of HZO cases (1–6). It can cause follicular conjunctivitis, epithelial and/or interstitial keratitis, dendritic keratitis, uveitis, scleritis or episcleritis, chorioretinitis, optic neuropathy, and ocular motility disorders.

A thorough review of the English literature involving the words “zoster,” “ophthalmoplegia,” and “nerve palsies” showed only multiple isolated case reports of incomplete and complete ophthalmoplegia after HZO. Patients typically want to know their prognosis for resolution of diplopia. We report our single institution consecutive patient experience of the recovery of ocular motor cranial nerve palsies due to HZO.

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This study was approved by the Institutional Review Board at the University of Cincinnati. We performed a retrospective chart review of all patients with ocular motor cranial nerve palsy presenting within a month of developing HZO. These patients were initially seen by an optometrist or a general ophthalmologist and referred to and eventually seen by a single neuro-ophthalmologist (K.C.G.) at the same institution.

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We found 21 patients of which 3 were excluded because they were only seen on initial visit. The mean age of the patients was 75 years (range: 41–91 years). Mean interval between the onset of HZO and ophthalmoplegia was 8.6 days with range 1–15 days. All patients were already on oral antivirals (acyclovir or valacyclovir) at the time of referral. Seven patients were also treated with a short course of oral prednisone.

The mean time period for follow-up to resolution was 10 weeks (range: 2 weeks to 8 months). Sixth nerve involvement (6 patients) was most common followed by third (5 patients) and fourth (3 patients) nerve palsies. Four patients had multiple ocular motor cranial nerve involvement; third and sixth in 2 patients, third and fourth in 1 patient, and 1 patient had complete ophthalmoplegia due to involvement of all 3 ocular motor cranial nerves.

Nine patients (50%) recovered completely (Table 1). Eight patients (44%) had incomplete recovery but had resolution of diplopia in primary gaze. The one patient with complete ophthalmoplegia had mild improvement but persistent diplopia in primary gaze for 6 months after which he was lost to follow-up.



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There are reports of ocular motor cranial nerve palsies in 5%–31% of the cases of HZO (6–8). Multiple mechanisms have been postulated for the involvement of ocular motor cranial nerves after HZO. Wyss (9) proposed that thromboplebitis is responsible for extraocular muscle paresis. Edgerton (10) postulated that contiguous inflammation in the cavernous sinus or the superior orbital fissure from the trigeminal to ocular motor cranial motor nerves is responsible. Kreibig (11) believed the cause to be myositis as well as perineuritis and perivasculitis. Naumann et al (12) evaluated the histopathology of 21 enucleated eyes affected by herpes zoster after HZO and proposed that occlusive vasculitis is responsible for the ocular motor cranial nerve palsy.

In 1948, Edgerton (8) reviewed 40 cases of unilateral ophthalmoplegia in the setting of HZO. He included a number of his own patients, 4 of which had ophthalmoplegia. Three of these 4 patients recovered completely in 2 weeks to 12 months. Archambault et al (13) described 6 cases of ophthalmoplegia after HZO. The third nerve was involved in 4 patients, fourth nerve in 5, and sixth nerve in 3 cases. Five patients (83%) recovered from diplopia over 3 weeks to 12 months. Chang-Godinich et al (14) reported 3 cases of complete ophthalmoplegia associated with HZO and reviewed 13 additional cases of complete ophthalmoplegia reported from 1968 to 1997. Recovery was documented in 9 of these patients ranging from 1 to 18 months. Cases of isolated sixth (15–17) and fourth (18) nerve palsies also have been described.

Our series of patients with ophthalmoplegia associated with HZO appears to be the largest from a single institution. Only 1 patient with complete ophthalmoplegia had persistent diplopia in primary gaze at a 6-month follow-up. It is possible that our follow-up duration was too short to witness recovery in this patient because patients reported by Chang-Godich et al (14) required up to 18 months to recover. It is also possible that our patients with incomplete recovery (diplopia in eccentric gaze) could have recovered completely over a longer period of time. Nevertheless, our report shows that patients with ophthalmoplegia after HZO have a good prognosis with almost all recovering from diplopia at least in primary gaze.

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