Journal of Neuro-Ophthalmology, June 1983, Volume 3, Issue 2

Herpes zoster ophthalmicus with contralateral hemiparesis. A case report and review of the literature.

An 80-year-old man developed right herpes zoster ophthalmicus complicated by contralateral hemiparesis after right cataract extraction. Although herpes zoster ophthalmicus is a frequent occurrence among the elderly, the association with contralateral hemiparesis is probably overlooked by many ophthalmologists. A review of the literature has been made to outline the etiology of this problem and to make diagnosis more likely. The varicella virus probably spreads in a retrograde fashion from the gasserian ganglion toward the cavernous sinus to involve cranial nerves 3, 4, or 6. Involvement of the ipsilateral carotid arterial system by the progressive inflammatory reaction can result in the contralateral hemiparesis. Standard therapy includes topical steroids and topical antibiotics for the ocular and surface lesions. The efficacy of systemic steroids to minimize the hemiparesis is still in question.

]. Clin. Neuro-ophthalmol. 3: 111-114, 1983. Herpes Zoster Ophthalmiclls with Contralateral Hemiparesis A Case Report and Review of the Literature CLEMENT CHAN, M.D. GARY HUFFAKER, M.D. Abstract An SO-year-old man developed right herpes zoster ophthalmicus complicated by contralateral hemi­paresis after right cataract extraction. Although herpes zoster ophthalmicus is a frequent occurrence among the elderly, the association with contralateral hemi­paresis is probably overlooked by many ophthalmolo­gists. A review of the literature has been made to outline the etiology of this problem and to make diag­nosis more likely. The varicella virus probably spreads in a retrograde fashion from the gasserian ganglion toward the cavernous sinus to involve cra­nial nerves 3, 4, or 6. Involvement of the ipsilateral carotid arterial system by the progressive inflamma­tory reaction can result in the contralateral hemi­paresis. Standard therapy includes topical steroids and topical antibiotics for the ocular and surface lesions. The efficacy of systemic steroids to minimize the hemiparesis is still in question. Introduction Herpes zoster ophthalmicus is a frequent occur­rence among the elderly. An associated contralat­eral hemiparesis is probably more common than recognized. Few cases have been reported in the literature. Walsh and Hoytl cited only nine pub­lished cases. The purpose of this presentation is to alert the ophthalmologist to this association so that he will be prepared when confronted by a patient with zoster and associated motor impairment. Pro­posed mechanisms and therapeutic modalities are also considered. Case Report An 80-year-old, oriental male underwent right cataract extraction with intraocular lens implanta­tion on December 18, 1980. Two weeks after sur­gery, painful vesicles developed on the right side of the forehead and scalp. These lesions, lid swell­ing, and iritis were noted by his ophthalmologist From the Department of Ophthalmology, White Memorial Medical Center, Lorna Linda University, Lorna Linda, California. June 1983 6 days later. The diagnosis of herpes zoster ophthalmicus was made. The patient was placed on topical steroids and antibiotics (Pred Forte, Maxitrol drops, q.i.d.). Oral prednisone was also started, 60 mg/day for the first week with gradual tapering and discontinuance the following week. Diplopia was noted by the patient 2 weeks after the onset of the skin lesions. Four weeks after the onset, transient dysarthria lasting for 24 hours, left facial drooping, and left-sided hemiparesis oc­curred. He was admitted by his family physician to another facility with the diagnosis of cerebral vascular accident. One week later, he was transferred to the White Memorial Medical Center Rehabilitation Unit. On admission his vital signs were within normal limits (BP: 110/80, P: 88). Carotid pulses were strong, equaL and without bruits. The skin eruption was now in the cicatricial stage. He was unable to elevate his left arm and leg more than 30° from the supine position. Ambulation was not possible. Ophthalmoscopic examination showed oculomo­tor nerve paresis and iritis of the right eye. The former was demonstrated by limitation of vertical and medial gazes, levator weakness, and mydriasis. Laboratory data consisted of the following: normal electrocardiogram, negative serology and skin tests, and mildly elevated Westergren sed rate of 33 mm. A spinal tap was refused. A CT scan demonstrated a small low-density lesion, consist­ent with ischemia, in the right parietal-frontal re­gion. Topical steroid (pred Forte drops, t.i.d.) was continued for the iritis. The skin lesions continued to steadily resolve. By February 16, 1981, 2 weeks after the onset of the hemiparesis, improvement of the hemiparesis was evident by patient's ability to elevate his left extremities more than 45° above the horizontal. Left-sided motor strength had im­proved by 50% during isometric and isotonic ex­ercises. Oculomotor paresis also was almost com­pletely resolved. A vigorous physical therapy pro­gram was continued. The patient was able to am­bulate with support by March 16, 1981, 5 weeks from the onset of the paresis. 111 Zoster Ophthalmicus with Hemiparesis Discussion Macular, papular, and vesicular eruptions of herpes zoster ophthalmicus present along the skin surface supplied by the ophthalmic division of the trigeminal nerve. The frontal branch of the oph­thalmic division is almost always involved. The supraorbital portion of the frontal branch is fre­quently affected. If eruption occurs on the tip of the nose, ocular involvement is almost certain be­cause of nasociliary nerve involvement. I Ragoz­zino's2 epidemiological study showed that ocular involvement was present in 20% of those with herpes zoster ophthalmicus. The first known case of herpes zoster ophthal­micus associated with contralateral hemiparesis was reported by Dumery in 1866.3 In the subse­quent years, more cases have been documented in the literature (Table 1). Certain features of herpes zoster ophthalmicus are: 1. Occurs most frequently in patients past the age of 60. 2. Male to female ratio is 2:1. 3. Hemiparesis usually occurs 4-8 weeks after the skin eruption. 4. Some form of ocular complication is usu­ally present. s. Pleocytosis and elevated cerebrospinal fluid protein may be present. Mechanism The short time span between the appearance of the skin lesions and the oculomotor paresis and contralateral paresis strongly suggests their com­mon etiology. The"direct-spread" and the"arter­itis" theories have been offered by investigators as possible mechanisms. Cope and Jones4 suggested the direct spread of the inflammation from the trigeminal ganglion to the corticospinal tract. Anastasopoulos5 proposed that ganglionitis induces a secondary arteritis and thrombosis of the surrounding vessels. Involve­ment in the carotid cerebral artery territory would be expected to produce contralateral hemiparesis. This explanation accounts for the selective contra­lateral involvement, whereas, the "direct-spread" theory does not. Both histopathological and angiographic studies have lent support to the "arteritis" theory. Ko­lodnyll described autopsy cases associated with herpes zoster ophthalmicus and contralateral hemi­paresis under the entity of "granulomatous angiitis of the nervous system."18 The necrotizing angiitis was characterized by focal and segmental mono­nuclear and giant cell infiltration of small and medium sized arteries and veins. Similar granu­lomatous angiitis of the central nervous system was described by Rosenblum and Hadfield. 12 Carotid TABLE 1. Clinical Features of Herpes Zoster Ophthalmicus with Contralateral Hemiparesis Case Report P(aRreigsihst)R Age Eruption to Acute Ocular ComplicatiL)nS CSF PI eo- Miscellaneous L (Left) and Sex Paresis Paresis cytosis CompliGltions Dumery, 1866" L ?M 4 wks. Perrin, 1938" L 68M 3 wks. Gordon, 1945 7 R 26M 3 wks. 2 mos. Unequal pupils (+) Dvsphasia Hughes, 1951" L 70F 5 wks. 2 mos. (-) Dysarthria Cope, 1954' L 54F 5 wks. 1 mo. Unequal pupils (+) Dysarthri.~ Anastasopoulos, R 29M 4 wks. 1 mo. Unequal pupils, lid ptosis (-) Dysphasia 1958" Ocular paresis Laws, 1960" R 65F 14 wks. It mos. Keratitis Dysphasia Acers, 1963'" R 32M 3 wks. 2 mos. Keratitis, iritis (-) R 61M 4 wks. 3 mos. Corneal ulcer•• tion. conjunctivitis (-) Kolodny, 1968" L 96F 6 wks. 1 mo. Corneal ulceration, conjuncti- (+) vitis, proptosis, unequal pupils ocular palsy Rosenblum, 1972'" L 64M 5 wks. 1 mo. Eyes deviate to right (+) Psychosis Walker, 19731:1 R 7M 6 mos. 2 wks. Keratitis, unequal pupils (-) Dysphasia Gilbert, 1974\' L 73M one 6 days Conjunctivitis (-) Expressive .~phasia Victor, 1976\" L 58M 4 wks. 2 mos. Unequal pupils. conjunctivitis, (+) L homonymous Pratesi, 1977'" iridocyclitis, ocular palsy hemianopsia L 48M 10 wks. 1 mo. Unequal pupils, ocular palsy (-) L homonymous MacKenzie, 1981\7 L 70M 7 wks. Hemianopsia 4 wks. Uveitis, glaucoma Dysarthria R 67F 6 wks. Keratitis, uveitis (-) Dysphasia R 60 M 8 wks. L homonymous Unreactive pupil (+) Hemianopsia Chan, 1981 L 80 M 4 wks. Dysphasia 4 wks. Lid ptosis, unequal pupils, ocular Dysarthria palsy 112 Joumal of Clinical Neuro-ophthalmology angiography also demonstrated multiple vascular occlusions of the middle cerebral artery in their patient. Stasis and segmental narrowing of the middle and anterior cerebral arteries contralateral to the hemiparesis were shown by angiography in Walker's13 patient. These cases suggest vasculitis­induced cerebral ischemia to be an integral part of this syndrome. Recently, McKenziel7 modified the "arteritis" theory by proposing that the intracranial branch­ings of the ophthalmic nerve provide a direct route of travel by the virus to the cerebral arteries. He performed full-circle angiography on four patients with herpes zoster ophthalmicus and ipsilateral "hemispheric disturbance." The extracranial and contralateral intracranial circulations were normal. However, single or multiple "narrowings" were present either in the"A2 segment" of the proximal pericallosal artery, or the "Ml segment" of the middle cerebral artery on the ipsilateral side. The pattern of lesions corresponded closely with distri­butions of the ophthalmic nerve to the involved arteries. Further studies are necessary to confirm the validity of this proposal. Initially, the varicella virus probably spreads in a retrograde fashion from the gasserian ganglion toward the cavernous sinus to involve cranial nerve 3, 4, or 6, most commonly the oculomotor nerve. Further spread into the subarachnoidal space and the cerebrospinal fluid can result in myelitis or meningoencephalitis. Involvement of the ipsilateral carotid arteriClI system by the progressive inflam­matory reaction can result in the contralateral hemiparesis. Treatment Standard therapy for herpes zoster ophthalmicus includes topical steroids to alleviate the ophthalmic inflammatory reaction, and topical antibiotics to prevent secondary bacterial invasion. The use of systemic steroids is a controversial subject. A num­ber of reports demonstrated the efficacy of sys­temic steroids in reducing periorbital edema, 19 ocu­lar complications,2" and postherpetic neuralgia.~I-~:l Dosages varying between 50-120 mg!day of pred­nisone (or equivalent) up to 14 days with subse­quent tapering have been reported.19-~:l In the case of postherpetic neuralgia, at least two well-de­signed prospective studies~I. ~:! have demonstrated the efficacy of early systemic therapy (within 10 days from the onset of skin eruption) before irre­versible irritative fibrosis of the involved sensory ganglia occurs. Similar studies for patients with herpes zoster ophthalmicus with hemiparesis would be difficult due to its rarity. Various anec­dotal reports l4 • Ifi have suggested that improvement of hemiparesis accompanies systemic steroids; however, a causal relationship cannot be estab­lished. June 1983 Chan. Huff.1h.er References 1. Walsh, F,B" and Hoyt, W,F,: Idiopathic herpes zos­ter. In Clinical Neuro-ophthalmology, Vol. 2, F,B, Walsh, Ed, Williams & Wilkins Co., Baltimore, 1969, pp, 1351-1361. 2, Ragozzino, M,W" Melton, L.J., Kurland, L.T, Chu, c.p" and Perry, H,O,: Population-based study of herpes zoster and its sequelae. Medicine 61: 310­316, 1982, 3, Baudouin, E., and LantuejouI. P,: Les troubles mo­teurs dans Ie zona, Gaz. d, Hop, 92: 1293, 1919, 4, Cope,S., and Jones, AT.: Hemiplegia complicating ophthalmic zoster. Lancet 2: 898-899, 1954. 5. Anastasopoulos, G" Routsoni, K., and lerodiakonou, C.S,: Ophthalmic herpes zoster with contralateral hemiparesis. /. Neurol. Neurosurg, Psychiatry 21: 210-212,1958. 6. Perrin, M., et al.: Hemiplegie post-zonateuse. Rev, Med, de Nancy 6: 309-314, 1938, 7. Gordon, I.R.s., and Tucker, JT: Lesions of the cen­tral nervous system in herpes zoster, /. Neurol, Neu­rosurg, Psychiatry 8: 40-46, 1945, 8, Hughes, W.N.: A case report: Herpes zoster of the right trigeminal nerve with left hemiparesis, Neu­rology 1: 167-169, 1951. 9. Laws, H, W,: Herpes zoster ophthalmicus compli­cated by contralateral hemiplegia, Arch, Ophtha/­mol, 63: 273-279, 1960. 10. Acers, TE.: Herpes zoster ophthalmicus with con­tralateral hemiplegia, Arch, Ophthalmol. 71: 371­376,1964. 11. Kolodny, E,H" Rebeiz, 1.1.. Caviness, V.s., and Rich­ardson, E,P.: Granulomatous angiitis of the central nervous system. Arch. Neurol. 19: 510-524, 1968. 12. Rosenblum, W.L.. and Hadfield, M,e.: Granuloma­tous angiitis of the nervous system in cases of herpes zoster and lymphosarcoma, Neur%gy 22: 348-354, 1972, 13. Walker, R.J., Gammal, TE., and Allen, M.B.: Cranial arteritis associated with herpes zoster: Case report with angiographic findings, Neuroradiology 107: 109-110, 1973, 14, Gilbert, G.J.: Herpes zoster ophthalmicus and de­layed contralateral hemiplegia: Relationship of the syndrome to central nervous system granulomatous angiitis. l.AM.A 229: 302-304, 1974. 15. Victor, 0.1., and Green, W.R.: Temporal artery bi­opsy in herpes zoster ophthalmicus with delayed arteritis. Am. /. Ophtha/mol. 82: 6Z8-b30, 197b. 16, Pratesi, R" Freeman, F,R., and Lowry, J,l.; Herpes zoster ophthalmicus with contralateral hemiplegia. Arch, Neurol. 34: 640-641, 1977. 17, MacKenzie, R,A, Forbes, C.s., and Karnes. WE: Angiographic findings in herpes zoster arteritis, Ann, Neural. 10: 458-464, 1981. 18. Cravioto. H" and Feigin, I.: Noninfectious granu­lomatous angiitis with a predilection for the nervous system, Neur%gy 9: 590 -b08, 1959, 19, Carter, A,B., and Royds, J.E.: Treatment of ophthal­mic zoster with prednisone, Br. Med, /. 2: 74b-748, 1957 20. Scheie, H,G" and McLellan, Te.: Treatment of herpes zoster ophthalmicus with corticotropin and corticosteroids. Arch, Ophthalmol. 62: 579-586, 1959, 113 Zoster Ophthalmicus with Hemiparesis 21. Eaglstein, W.H., Katz, R., and Brown, J.A.: The effects of early corticosteroid therapy on the skin eruption and pain of herpes zoster. /.AM.A 211: 1681-1683,1970. 22. Elliott, F.A.: Treatment of herpes zoster with high doses of prednisone. Lancet 2: 610-611,1964. 1]4 23. Keczkes, K., and Basheer, AM.: Do corticosteroids prevent postherpetic neuralgia? Br. /. Dermatol. 102: 551-555, 1980. Write for reprints to: Clement Chan, M.D., Department of Ophthalmology, Lorna Linda University, Lorna Linda, California 92354. Journal of Clinical Neuro-ophtha!mo!ogy