Radiology Resident Case of the Week
Etiology/Pathophysiology:
As of a recent case report in the Journal of Neuroimaging, there have been 60 reported cases of delayed ipsilateral cerebral infarction and contralateral hemiparesis following herpes zoster ophthalmicus (HZO). The average time delay between the HZO and the onset of neurologic symptoms is seven weeks (2).
There remains some debate about the pathophysiologic mechanism for the development of ipsilateral cerebral infarcts following HZO, however, most individuals now agree that it is local spread of the virus from the gasserian ganglion to the carotid artery. There is contiguous spread to the ipsilateral ACA and MCA via a perivascular plexus supplied by the ophthalmic division of the trigeminal nerve (3). This would correlate with the imaging findings in this patient as the area of severe ICA stenosis is within the supraclinoid portion just distal to the origin of the ophthalmic artery. The presence of segmental narrowing in the P2 segment of the right PCA as well as mild narrowing in the supraclinoid portion of the left ICA in this patient may be secondary to spread along perivascular plexuses about the circle of Willis even though the right posterior communicating artery is not appreciated on angiography.
Cases of bilateral and more diffuse vascular changes suggests that some cases may result from CSF or hematogenous spread.
Pathology:
The inflammatory process leading to obliteration of the intracerebral vessels is often referred to as a "granulomatous angiitis". A main histologic feature is an arteritis with fibrinoid necrosis of the media (4-5). The supposition of direct virus invasion has been supported by the presence of viral particles in smooth muscle cells of the vessel wall.
Miscellaneous:
The outcome of cerebral angiitis following HZO is extremely variable with complete recovery not uncommon. However, progressive demise in neurologic status is equally common with a reported mortality rate of 25% (2).
Treatment regimens have consisted of steroid therapy most often long term prednisone, however, anticoagulant therapy has also been employed. No consistent successful treatment regimen has been established (6)..
Imaging:
Cerebral angiogram: A focal area of severe narrowing is seen in the supraclinoid portion of the right internal carotid artery just distal to the origin of the ophthalmic artery. An area of mild tapering is also seen in the supraclinoid portion of the left ICA. Evaluation of the posterior circulation via a left vertebral artery injection shows areas of marked tapering of the proximal portion of the right P2 segment of the posterior cerebral artery.
MRI: A large area of high T2 signal intensity and low T1 signal intensity is seen in the white matter adjacent to the frontal horn of the right lateral ventricle and within the right centrum semiovale. An associated relative flow void is seen in the right internal carotid artery correlating with the region of severe tapering on the cerebral angiogram.
DDx:
post herpetic cerebral angitis with associated right cerebral white matter ischemia.
Key references:
1. Patrick JT, Russell E, Meyer J, et al. Cervical (C2) herpes zoster infection followed by pontine infarction. J Neuroimaging 1995;5:192-93.
2. Hilt DC, Buchholz D, Krumholz A, et al. Herpes zoster ophthalmicus and delayed contralateral hemiparesis caused by cerebral angiitis: Ann Neurol 1983;14:543-553.
3. O' Donohue JM, Enzmann DR. Mycotic aneurysm in angiitis associated with herpes zoster ophthalmicus. AJNR 1987;8:615-619. 4. Gasperetti C, Song SK. Contralateral hemiparesis following herpes zoster ophthalmicus. J Neur, Neurosurg, Psychiatry 1985; 48: 338-341.
5. Chan C, Huffaker G. Herpes zoster ophthalmicus with contralateral hemiparesis. J Cllin neuro-ophthalmol 1983;3:111-114.
6. Bourdette DN, Rosenberg NL, Yatsu FM. Herpes zoster ophthalmicus and delayed ipsilateral cerebral infarction. Neurology 1983;33:1428-32.
ACR Code:
17.2065
Keywords:
herpes zoster ophthalmicus, cerebral infarction, angiitis
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