Isolated, complete paralytic mydriasis secondary to herpes zoster ophthalmicus ============================================================================== * Craig N Czyz * Thomas S Bacon * Thomas P Petrie * Joshua D Justice * Kenneth V Cahill ## Abstract Herpes zoster ophthalmicus is a manifestation of herpes zoster when the ophthalmic division of the trigeminal nerve becomes involved. Ocular symptoms are varied and mainly due to inflammatory mechanisms. Total, external and/or internal ophthalmoplegias, as well as isolated third, fourth and sixth cranial nerve palsies have all been reported as complications. In a minority of cases, concurrent pupillary paralysis has been documented. The presentation of complete paralytic mydriasis as the sole cranial nerve complication following herpes zoster ophthalmicus infection is a rare finding. The postulated pathophysiologic aetiology is a partial third nerve palsy with the pupillary fibres for light and accommodation-convergence affected and motor fibres spared. The mechanism responsible for the postulated lesion is speculative. * HERPES ZOSTER * PUPILS * OPHTHALMOLOGY Herpes zoster affects 10%–20% of people over their lifetime. Herpes zoster ophthalmicus—involvement of the ophthalmic division of the trigeminal nerve—occurs in 15%–25% of cases, of whom half have ocular involvement and so risk ocular complications. Isolated, complete pupillary paralysis is perhaps the rarest of these sequelae. A 76-year-old woman reported 5 days of worsening sharp left-sided face and eye pain with photophobia. On examination, there was mild erythema and ptosis of the left upper eyelid. Corrected visual acuities were 6/18 (right) and 6/24 (left). Intraocular pressures were 20 mm Hg bilaterally. Pupils were equal and normally reacting with no relative afferent pupillary defect. Extraocular muscle function was normal, and visual fields were full. Slit lamp evaluation (left) showed conjunctival injection, small corneal epithelial defects and a pseudodendrite. There was a cataract but no anterior chamber inflammation. The iris was hazel coloured, flat and round. Dilated funduscopy showed normal macula and peripheral retina and clear, vitreous, flat, pink nerves bilaterally, with sharp margins and normal cup-to-disc ratio. We diagnosed keratoconjunctivitis and prescribed erythromycin ointment and ketorolac tromethamine drops. She was admitted for pain control and observation on suspicion of herpes zoster without cutaneous eruptions. A temporal artery biopsy was normal. On day 3, she developed a vesicular rash over her left upper face and was started on intravenous acyclovir. At follow-up 21 days after presentation, she reported a blurred vision and a foreign body sensation in the left eye, with continued left-sided head and face pain. Corrected visual acuity was 6/18 (right) and 6/30 (left). There were vesicular lesions on the left upper brow, left lower eyelid and nose (figure 1, top left). The left pupil was fixed at 7 mm diameter and unresponsive to direct or consensual light or accommodation. Slit lamp examination showed diffuse left conjunctival injection. There were no iris adhesions or transillumination defects. The cornea was clear and the anterior chamber contained trace inflammation. We prescribed erythromycin ointment and topical prednisolone 1%. At 6 months’ follow-up, her visual acuity had returned to baseline and the signs had resolved, apart from a persistently dilated (7 mm), non-reactive left pupil (figure 1 top right). The palsy was complete without transillumination defect or iris adhesions (figure 1 bottom left and right). ![Figure 1](http://pn.bmj.com/https://pn.bmj.com/content/practneurol/13/3/183/F1.medium.gif) [Figure 1](http://pn.bmj.com/content/13/3/183/F1) Figure 1 (Top left) Three-quarter view of patient at initial follow-up visit. The image shows left-sided resolving zoster lesions, conjunctival injection, reactive ptosis and a dilated, non-reactive pupil. (Top right) Frontal view of patient at 6-month follow-up visit. The zoster lesions and ocular symptoms have resolved though her left pupil remains dilated and non-reactive. The left upper lid appears ptotic; however, this is pseduoptosis due to the dilated pupil. (Bottom left) Slit lamp image of the left eye that illustrates the symmetry of the iris margin, lack of synechiae and absence of inflammatory remnants. (Bottom right) Slit lamp image of left eye displaying to retroillumination defects. ## Discussion Pupillary paralysis is one of the many ocular complications of herpes zoster ophthalmicus. Pupillary paralysis commonly accompanies total, external and/or internal ophthalmoplegias, as well as isolated third, fourth and sixth cranial nerve palsies. However, there have been only two previous cases presented with complete pupillary paralysis as the sole cranial nerve complication.1 ,2 The cause of the paralysis is either inflammatory or non-inflammatory. Having excluded localised iris abnormalities, the possible mechanisms include microinfarction from occlusive vasculitis, direct neuropathic damage, demyelination and compression due to orbital inflammation. All may play a role to a varying degree. Our patient's paralytic mydriasis probably resulted from  partial third nerve palsy, affecting pupillary fibres for light and accommodation-convergence, but sparing the motor fibres. Because of its rarity, patients presenting like this need further investigation to confirm the underlying cause. ### Practice points * Herpes zoster ophthalmicus complicates 15%–25% of cases of zoster. * Half of those with herpes zoster ophthalmicus develop complications, including total, external and/or internal ophthalmoplegia, isolated third, fourth and sixth cranial nerve palsies. * Isolated pupillary paralysis with herpes zoster is rare and requires exclusion of other causes. * Complete paralytic mydriasis is probably caused by a partial third nerve palsy, where pupillary fibres for light and accommodation-convergence are affected, but the motor fibres to external ocular muscles are spared. ## Footnotes * Patient consent Obtained. * Competing interest None. * Contributors CC was involved in direct patient care, concept, drafting and critically revising the manuscript. TB was involved in reviewing the pertinent literature and preparing the manuscript draft. TP was involved in drafting the manuscript and reviewing the pertinent literature. JJ was involved in direct clinical care of the patient and aiding in drafting the manuscript. KC was involved in critically revising the manuscript for important intellectual content. All authors read and approved the final manuscript. * Provenance and peer review Not commissioned. Externally peer reviewed. This paper was reviewed by Mark Willis, Cardiff, UK. ## References 1. Sen DK. ‘Isolated pupillary paralysis in a case of herpes zoster’. J Pediatr Ophthalmol Strabismus 1979;16:33–4. [PubMed](http://pn.bmj.com/lookup/external-ref?access_num=312315&link_type=MED&atom=%2Fpractneurol%2F13%2F3%2F183.atom) [Web of Science](http://pn.bmj.com/lookup/external-ref?access_num=A1979GG90400007&link_type=ISI) 2. Elliot. ‘Some observations on herpes zoster ophthalmicus’. Trans Ophthalmol Soc UK; 1918;38:351–62. ## Suggested Further Reading 1. 3. 1. Tasman W, 2. Jaeger E De Luis VP. Chapter 20: Varicella and herpes zoster ocular disease. In: Tasman W, Jaeger E , eds. Duane's ophthalmology. Philadelphia, PA: Lippincott Williams & Wilkins, 2006, vol 4. 2. 4. Assal F, Frank HG, von Gunten S, et al. ‘Internal ophthalmoplegia as a presenting sign of herpes zoster ophthalmicus’. Euro Neurol 2001;45:189–90. [PubMed](http://pn.bmj.com/lookup/external-ref?access_num=11306868&link_type=MED&atom=%2Fpractneurol%2F13%2F3%2F183.atom)