Australas J. Dermatol 1993; 34: 113-114 CEREBRAL INFARCTION FOLLOWING THORACIC HERPES ZOSTER AJAY KUMAR AND LINDSAY MOLLISON Alice Springs SUMMARY Objective: To present a case of cerebral infarction following thoracic herpes zoster presenting as Gerstmann 's syndrome. Clinical features: A 61 year old male developed herpes zoster of T1-2 dermatomes. Four months later he developed a confusional state together with expressive aphasia, dyscalculia, dysgraphia and finger agnosia with no long tract signs. CT scan of head showed recent infarction of this left parietal lobe. He recieved a five day course ofacyclovir 800mgfour times daily and showed slow but steady improvement. Conclusion: Herpes zoster is uncommonly followed by cerebral infarction. Acyclovir may have a role in therapy of this complication. Key words: Herpes zoster, cerebral infarction, varicella-zoster virus. Four months after his herpes zoster he presented with gradual onset of a disabling confusional state along with difficulty with speech. Corticosteroids were stopped and he was referred to hospital. On admission he was found to be mentally alert but disoriented and had a marked expressive aphasia, dyscalculia, dysgraphia and finger agnosia. Psychomotor examination revealed a deficiency of short term memory. There were no long tract signs. Head CT scan showed recent infarction of his left parietal lobe. Full blood count, electrolytes and renal function tests were in the normal range. Liver function tests showed continuing resolution of cholestasis. ESR was 22 mm/hr. HIV and HTLV-1 antibodies were negative. Carotid doppler, study was normal. Lumbar puncture was not performed. He was given a five day course of oral acyclovir 800 mg four times daily and showed a slow but steady clinical improvement. INTRODUCTION Delayed cerebrovascular events are a well recognised complication of herpes zoster ophthalmicus (HZO). The most commonly reported syndrome is that of delayed contralateral hemiplegia.'^ Cerebrovascular events have been rarely described following segmental zoster.^** We describe a patient with thoracic zoster which was followed by expressive aphasia and CT scan evidence of ipsilateral parietal lobe infarction. CASE REPORT Two months after an episode of severe cholestatic hepatitis A infection complicated by renal failure and haemolytic anemia, a 61 year old man developed herpes zoster of his left Tl-2 dermatome. At this time he was an inpatient receiving prednisolone on a slowly reducing dose for cholestatis and haemolysis. The clinical presentation consisted of a vesicular rash confined to one shoulder, with associated pain. Prednisolone was continued and the rash resolved. Three weeks later with recovery of his renal and bone marrow function the patient was discharged: subsequently carbamezapine lOOmg three times a day was added with minimal benefit for post herpetic neuralgia. DISCUSSION Delayed cerebrovascular events following herpes zoster have been described in over fifty individuals following HZO'^ but in only three previous reports after truncal segmental zoster.^ •* Subsequent to resolution of cutaneous zoster lesions, after an interval ranging from zero to six months, cerebrovascular complications may develop. The most common finding has been contralateral hemiparesis. The presentation may be gradual or acute. Early alteration of mentation Ajay Kumur MBBS. Lindsay Mollison FRACP, Department of Medicine, Alice Springs Hospital. Address for correspondence: Dr Lindsay Mollison, Alice Springs Hospital, Gap Rd, Alice Springs, N.T. 0870, Australia. 113 AJAY KUMAR AND LINDSAY MOLLISON has been reported in a large number of these patients. This encephalopathy, often presenting as a toxic confusional state or delirium, probably indicates generalised bihemispherical involvement with other focal signs developing later in the clinical course.^ Patients present with aphasia, cranial nerve dysfunction, hemiparesis or hemisensory symptoms.' In the case we report, four months after developing Tl-2 left sided segmental zoster, the patient presented with an acute confusional state after which he developed expressive aphasia with additional features of Gertzmann*s syndrome, including dyscalculia, dysgraphia and finger agnosia. Although cerebral CT scan may show no abnormality, many reports have described findings consistent with infarcts in the distribution of the ipsilateral middle cerebral artery and its branches with lesions in the deep grey matter or internal capsule.^ Our patient's CT scan revealed a recent infarct in the ipsilateral middle cerebral artery territory in the parietal lobe. Cerebral angiography when performed has revealed segmental narrowing in the proximal middle cerebral and anterior cerebral arteries with stasis suggesting an arteritis.^ Although less frequently noted other abnormalities include aneurysm of the intracavernous internal carotid artery and intracranial carotid artery stenosis at the level of the siphon.' Angiography may worsen the patient's clinical condition.* Pathologically a thrombo-occlusive vasculopathy of the branches of the circle of Willis has been described.' The cause of the arteritis is unclear, but direct viral infection or an immune mechanism have both been proposed.* In some cases immunoperoxide histochemistry of the arterial wall has demonstrated Varicella-zoster virus antigens.* CSF abnormalities are seen, the most common being an increased number of mononuclear cells and raised protein.' 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