Herpes zoster and central retinal artery occlusion

Hall, Scott; Carlin, Lane; Es, Roach; Wt, McLean

doi:10.1002/ana.410130226

Cited by 25 publications

(8 citation statements)

References 4 publications

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“…Rare presentations of monocular visual loss exemplify the capacity for VZV to infect small arteries. The first reported case of monocular loss of vision was that of a patient who developed occlusion of the ipsilateral central retinal artery 2 weeks after trigeminal-distribution zoster 6. The second case was that of a patient who developed sudden monocular visual loss 5 months after ipsilateral ophthalmic-distribution zoster 7.…”

Section: Clinical Features and Diagnosismentioning

confidence: 99%

Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment

Gilden

Cohrs

Mahalingam

et al. 2009

The Lancet Neurology

495

451

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Vasculopathies caused by varicella zoster virus (VZV) are indicative of a productive virus infection in cerebral arteries after either reactivation of VZV (shingles) or primary infection (chickenpox). VZV vasculopathy can cause ischaemic infarction of the brain and spinal cord, as well as aneurysm, subarachnoid and cerebral haemorrhage, carotid dissection, and, rarely, peripheral arterial disease. VZV vasculopathy in immunocompetent or immunocompromised individuals can be unifocal or multifocal with deep-seated and superficial infarctions. Lesions at the grey-white matter junction on brain imaging are a clue to diagnosis. Involvement of both large and small arteries is more common than that of either alone. Most patients have a mononuclear cerebrospinal fluid pleocytosis, often with red blood cells. Cerebrospinal fluid pleocytosis and rash are absent in about a third of cases. Anti-VZV IgG antibody in the cerebrospinal fluid is found more frequently than VZV DNA. In recent years, the number of recognised VZV vasculopathies has grown, and accurate diagnosis is important for the effective treatment of these disorders.

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Section: Clinical Features and Diagnosismentioning

confidence: 99%

Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment

Gilden

Cohrs

Mahalingam

et al. 2009

The Lancet Neurology

495

451

View full text Add to dashboard Cite

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“…However, since VZV can affect both large and small arteries resulting in ischemic or hemorrhagic strokes, clinical presentations may vary and include headache, mental status changes, aphasia, ataxia, hemisensory loss, hemianopia and even monocular visual loss [27,28]. Many patients experience transient ischemic attacks with protracted neurological symptoms and signs.…”

Section: Clinical Features and Diagnosismentioning

confidence: 99%

Virus Vasculopathy and Stroke: An Under-Recognized Cause and Treatment Target

Nagel¹,

Mahalingam²,

Cohrs³

et al. 2010

IDDT

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While arteriosclerotic disease and hypertension, with or without diabetes, are the most common causes of stroke, viruses may also produce transient ischemic attacks and stroke. The three mostwell studied viruses in this respect are varicella zoster virus (VZV), cytomegalovirus (CMV) and human immunodeficiency virus (HIV), all of which are potentially treatable with antiviral agents. Productive VZV infection in cerebral arteries after reactivation (zoster) or primary infection (varicella) has been documented as a cause of ischemic and hemorrhagic stroke, aneurysms with subarachnoid and intracerebral hemorrhage, arterial ectasia and as a co-factor in cerebral arterial dissection. CMV has been suggested to play a role in the pathogenesis of arteriosclerotic plaques in cerebral arteries. HIV patients have a small but definite increased incidence of stroke which may be due to either HIV infection or opportunistic VZV infection in these immunocompromised individuals. Importantly, many described cases of vasculopathy in HIV-infected patients were not studied for the presence of anti-VZV IgG antibody in CSF, a sensitive indicator of VZV vasculopathy. Unlike the well-documented role of VZV in vasculopathy, evidence for a causal link between HIV or CMV and stroke remains indirect and awaits further studies demonstrating productive HIV and CMV infection of cerebral arteries in stroke patients. Nonetheless, all three viruses have been implicated in stroke and should be considered in clinical diagnoses. Keywords Virus vasculopathy; VZV; HIV; CMV VIRAL CAUSES OF STROKEStroke is a common cause of mortality and morbidity worldwide [1]. While established risk factors, such as hypertension, diabetes, obesity and hypercholesterolemia have been identified and are targets for stroke prevention, viral infections have also emerged as risk factors for stroke. Identification of viruses that directly cause stroke, as evidenced by direct invasion of cerebral arteries corresponding to areas of infarction, would provide therapeutic targets for stroke prevention. Varicella zoster virus (VZV), human immunodeficiency virus (HIV) and cytomegalovirus (CMV) have all been associated with stroke. However, VZV is The incidence and prevalence of stroke caused by VZV is unknown, although estimates in children reveal that varicella accounts for 7 to 31% of arterial ischemic stroke [18,19], with 1 in 15,000 cases of varicella associated with stroke [18]. In transient cerebral arteriopathy of childhood, stroke is preceded by varicella in 44% of cases [20]. In adults, VZV vasculopathy is more common in immunocompromised than in immunocompetent individuals. In immunocompromised adults, VZV infection of the central nervous system (CNS) was detected in 1.5 to 4.4% of autopsy cases [21][22][23]. In postmortem studies of HIVinfected individuals, VZV vasculopathy occurred more frequently late in the course of infection when there was significant CD4+ depletion [24,25]. CLINICAL FEATURES AND DIAGNOSISIn adults, the typical clinical presentation of stroke...

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“…14 Visual loss due to occlusion of the central retinal artery two weeks after zoster in a trigeminal distribution has also been described. 15 Detection of intrathecal antibody to VZV during vasculopathy suggests that stroke is related to VZV. Humans produce more than three times their total volume of cerebrospinal fluid daily, a turnover rate that would render antiviral antibody undetectable in cerebrospinal fluid within days after zoster unless infection was protracted.…”

Section: A B Cmentioning

confidence: 99%

Two Patients with Unusual Forms of Varicella–Zoster Virus Vasculopathy

et al. 2002

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NFECTION of cerebral arteries by varicellazoster virus (VZV) can produce unifocal or multifocal vasculopathy. Unifocal large-vessel vasculopathy (granulomatous arteritis) usually affects elderly immunocompetent persons, whereas multifocal vasculopathy occurs primarily in persons who are immunocompromised. 1 Unifocal large-vessel infarcts may follow zoster in a trigeminal distribution and are presumed to result from transaxonal transport of virus from trigeminal afferent fibers that innervate vessels of the anterior circulation. 2 Similarly, smaller infarcts in deep white and gray matter may reflect transport of VZV from trigeminal or cervical afferent fibers to smaller branches of vessels of the posterior circulation. 2,3 We encountered two patients with unusual forms of VZV vasculopathy. Detection of VZV antibody in cerebrospinal fluid and reduced ratios of the concentration of anti-VZV IgG in serum to that in cerebrospinal fluid, in conjunction with normally high ratios for total IgG and albumin, verified the viral cause of their vascular disease. CASE REPORTS Patient 1In April 2001, zoster in a left sacral (S2) distribution developed in Patient 1, a 71-year-old man with chronic lymphocytic leukemia that was in remission. Despite treatment with oral valacyclovir (1000 mg three times daily for seven days), zoster spread to the right S2 dermatome. Lesions resolved in three to four weeks. In May 2001, bitemporal headaches developed, along with mild confusion, foot numbness, and unsteady gait. Vibratory sensation was reduced in the toes, ankle jerks were absent, and gait was mildly I wide-based. The white-cell count was 12,100 per cubic millimeter, with a normal differential count. Magnetic resonance imaging (MRI) of the brain and magnetic resonance angiography were normal (Fig. 1B). Two cerebrospinal fluid examinations revealed extensive mononuclear pleocytosis, an elevated protein level, and a normal glucose level (Table 1). Polymerase-chain-reaction (PCR) analysis of the cerebrospinal fluid revealed no amplifiable VZV DNA.Headaches, confusion, and imbalance resolved within two months. On October 15, 2001, the patient noted that he had difficulty finding words, numbness of the left hand, weakness of the left leg, and urinary urgency. Neurologic examination revealed halting speech, a flattened left nasolabial fold, mild weakness of the left side, an extensor plantar response on the left, and bilateral grasp reflexes. A complete blood count, electrolyte values, a blood-chemistry panel, and urinalysis were normal. MRI of the brain revealed an infarction in the right pericallosal distribution (Fig. 1A). Magnetic resonance angiography revealed occlusion of the anterior cerebral artery on the right side and stenosis on the left side (Fig. 1C). A third sample of cerebrospinal fluid (Table 1) was acellular, but the protein level, the total IgG level, and the rate of IgG synthesis were elevated, with three to four oligoclonal bands. PCR analysis revealed no amplifiable herpes simplex virus (HSV) or VZV DNA or antibody to...

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Herpes zoster and central retinal artery occlusion

Cited by 25 publications

References 4 publications

Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment

Varicella zoster virus vasculopathies: diverse clinical manifestations, laboratory features, pathogenesis, and treatment

Virus Vasculopathy and Stroke: An Under-Recognized Cause and Treatment Target

Two Patients with Unusual Forms of Varicella–Zoster Virus Vasculopathy

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