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Show TournaI of Clinical Neuro-ophthalmolog.y 6(2): 113-115. 1986. Herpes Zoster Maxillaris with Delayed Occipital Infarction J. Michael Powers, M.D. '<) 1986 Raven Press, New York A case of occipital infarction following herpes zoster involving the maxillary division of the trigeminal nerve is presented. Herpes zoster ophthalmicus is followed occasionally by an angiitis and cerebral infarction, usually manifest as a hemiplegia. Cerebral angiitis has not been reported previously following herpes zoster involving the maxillary or mandibular divisions. Patients with herpes zoster involving any trigeminal division may be at risk for delayed stroke. The distribution of rash and angiitis in this case supports the hypothesis that the virus extends directly to the large vessels adjacent to the gasserian ganglion, instead of being transmitted along intracranial nerves. From the Prentice Eye Institute, St. Luke's Medical Center, Phoenix, Arizona. Address correspondence and reprint requests to J. Michael Powers, M.D., 525 North 18th St., Suite 602, Phoenix, AZ 85006, U.S.A. 1/3 The syndrome of herpes zoster ophthalmicus with delayed contralateral hemiplegia is being recognized with increasing frequency. A patient with ipsilateral occipital infarction following herpes zoster of the maxillary division of the trigeminal nerve is reported. CASE REPORT A 68-year-old man presented with a left homonymous hemianopic scotoma. He had been in excellent health aside from glaucoma of 15 years' duration. There was no history of hypertension, cardiac disease, or diabetes mellitus. There were no symptoms suggestive of past transient ischemic attack or stroke. Yearly physical examinations, including extensive cardiovascular testing, were consistently normal. In September 1984, he developed herpes zoster involving the right maxillary nerve distribution. The rash extended from near the tragus to the nose. The rash and associated pain slowly cleared over 3 months. In early January 1985, the patient began experiencing recurring transient visual distortions to the left of fixation. On the third day, he developed independent spells of left face and arm numbness. Upon awakening on the fourth day, he noted a persistent opaque cloud to the left of fixation. There were no subsequent motor or somatic sensory symptoms. Neurological examination performed 8 days after onset of the fixed visual deficit demonstrated a congruous homonymous hemianopic paracentral scotoma sparing the macula and extending above and below the horizontal meridian. The remainder of the neurological and general physical examination was unremarkable. A computed tomographic (CT) scan following contrast enhancement revealed a dense, homogeneous lesion in the right occipital lobe, adjacent to 1/4 ,. M. POWERS the falx (Fig. 1). This region was isodense on the precontrast CT scan, consistent with an infarction of 2-3 weeks' age. A selective right vertebral arteriogram demonstrated normal vertebral, basilar, and left posterior cerebral arteries. The right posterior cerebral artery showed marked bead-like segmental narrowing beginning 2 cm beyond its origin (Fig. 2). More distally, the artery was occluded completely. Bilateral carotid arteriograms were normal. The complete blood count and panel of serum chemistries were normal. The cholesterol was 214 mg/dl and triglycerides 191 mg/dl. The Westergren sedimentation rate was 1 mm/h. An antinuclear antibody (ANA) was positive at 20 dilutions with a speckled pattern. When repeated 2 months later, the ANA was no longer positive. Throughout his hospitalization and 3 months of observation, the patient remained normotensive with no evidence of systemic vascular disease. He was treated with aspirin, 325 mg daily, and noted a gradual reduction in the size and density of the homonymous scotomata, with no subsequent episodes suggestive of cerebral ischemia. DISCUSSION Cerebral infarction following herpes zoster ophthalmicus is associated with a distinctive angiographic pattern indicative of vasculitis (1). The large arteries at the base of the brain are affected most, especially the Ml segment of the middle cerebral artery and the Al and A2 segments of the FIG. 1. CT scan demonstrating contrast enhancing infarction in the medial right occipital lobe. , eli" Nellro-ophthalnlOl, Vol. 6, No.2, 1986 FIG. 2. Selective right vertebral arteriogram showing bead·like segmental narrowing of the proximal right posterior cerebral artery (small arrow) with complete occlusion distally (large arrow). anterior cerebral artery (1). Pathological examinations have demonstrated a necrotizing segmental cerebral arteritis with viral inclusions present in the vessel walls (2,3). The present case is of interest because a stroke has not been reported previously following herpes zoster affecting the maxillary division of the trigeminal nerve. The arteriogram demonstrated the pattern of segmental stenosis with beading considered characteristic of herpetic vasculitis. In the absence of evidence of atherosclerosis or other vascular disease, the diagnosis of herpetic cerebral angiitis appears reasonably certain. This case addresses two persisting questions regarding the mechanism of herpetic angiitis. Why has cerebral angiitis not been reported following maxillary and mandibular division herpes zoster? To what extent is the distribution of the cerebral infarction related to the distribution of the herpes zoster? Herpetic angiitis with stroke remains an uncommon complication of herpes zoster. Three current reviews identify 35 cases of stroke following herpes zoster ophthalmicus (4-6). The ophthalmic division is involved with herpes zoster much more frequently than the maxillary and mandibular divisions. Thomas and Howard (7) reviewed 1,210 cases of herpes zoster and found restricted in- HERPES ZOSTER MAXILLARIS U5 volvement of the first trigeminal division in 158, second division involvement in 16, and third division in 10. Thus, the ophthalmic division was involved 10 times as often as the maxillary division. The absence of reports of delayed stroke following second and third division herpes zoster simply may reflect the relative infrequency of involvement of the lower trigeminal divisions. If this is true, all patients with trigeminal herpes zoster would be at risk for development of angiitis and stroke. The mechanism of herpetic angiitis has not been established. Pathological studies document the presence of inflammation in the trigeminal ganglion. The virus may extend directly from the gasserian ganglion to the adjacent large vessels (8). MacKenzie et al. (1) recently proposed that the virus reaches the arteries by transmission along the intracranial branches of the ophthalmic nerve. Most strokes following herpes zoster ophthalmicus consist of a contralateral hemiplegia due to angiitis and infarction in the middle cerebral artery distribution. The portions of the middle and anterior cerebral arteries which are affected most commonly by the angiitis are also the portions innervated by the intracranial branches of the ophthalmic nerve. The first division also supplies the parieto-occipital dura, the falx, and tentorium cerebelli (1). Bourdette et al. (4) reported a case of occipital infarction following herpes zoster ophthalmicus, indicating that other vessels supplied by the ophthalmic nerve can develop angiitis. The maxillary and mandibular divisions of the trigeminal nerve also have an intracranial component, combining to form the middle meningeal nerve which innervates the middle fossa. In the current case, the maxillary division was affected by rash, but the infarction was in the territory supplied by the ophthalmic division. Linnemann and Alvira (3) reported a case of brainstem infarction following herpes zoster ophthalmicus. These examples demonstrate that the distribution of the angiitis does not correspond necessarily to the division with the cutaneous involvement. It is possible that herpes zoster limited to one division of the trigeminal nerve could produce infection of the entire gasserian ganglion, with potential for virus transmission along any of the intracranial nerve branches. This appears unlikely, since the angiitis usually is restricted to the large vessels in proximity to the ganglion. The lack of correspondence between the segments involved by the rash and the angiitis supports the hypothesis that the herpes virus extends directly from the gasserian ganglion to the adjacent arteries at the base of the brain. REFERENCES 1. MacKenzie R. A., Forbes G. S., Karnes W. E.: Angiographic findings in herpes zoster arteritis. Ann Neural 19:458-464, 1981. 2. Doyle P. W., Gibson G., Dolman C L.: Herpes zoster ophthalmicus with contralateral hemiplegia: identification of cause. Ann Neural 14:84-85, 1983. 3. Linnemann C C, Alvira M. M. Pathogenesis of varicellazoster angiitis in the CNS. Arch Neural 37:239-40, 1980. 4. Bourdette D. N., Rosenberg N. L., Yatsu F. M. Herpes zoster ophthalmicus and delayed ipsilateral cerebral infarction. Neurology 33:1428-32, 1983. 5. Chan C, Huffaker G. Herpes zoster ophthalmicus with contralateral hemiparesis. I Clin Neuro-ophthallllol 3:111-4, 1983. 6. Hilt D. C, Buchholz D., Krumholz A., et al. Herpes zoster ophthalmicus and delayed contralateral hemiparesis caused by cerebral angiitis: diagnosis and management approaches. Ann Neuro/14:543-53, 1983. 7. Thomas J. E., Howard F. M.: Segmental zoster paresis-a disease profile. Neurology (Mi/llleap) 22:459-66, 1972. 8. Kuroiwa Y., Furukawa T. Hemispheric infarction after herpes zoster ophthalmicus: computed tomography and angiography. Neurology 31:1030-32, 1981. 1Clin Neuro-ophthalmol, Vol. 6, No.2, 1986 |
