Varicella-zoster virus claims yet another painful scalp—Giant cell arteritis

Kennedy, Peter G. E.; Lipton, Howard L.

doi:10.1212/wnl.0000000000001459

Cited by 6 publications

(5 citation statements)

References 5 publications

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“…The problem of false positive immunohistochemical detection of VZV antigens in these temporal arteries, due to antibody cross-reactivity, was highlighted in another study [ 32 ]. Further, it is not certain that direct causality has been demonstrated, as it is possible that VZV reactivation could result from the inflammatory process per se of GCA [ 33 ], although the authors thought that there was a cause-and-effect process, in that the VZV triggered the immunopathology [ 27 ].…”

Section: Giant Cell Arteritismentioning

confidence: 99%

The Spectrum of Neurological Manifestations of Varicella–Zoster Virus Reactivation

Kennedy

2023

Viruses

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Varicella–Zoster virus (VZV) is a pathogenic human alpha herpes virus that causes varicella (chicken pox) as a primary infection and, following a variable period of latency in different ganglionic neurons, it reactivates to produce herpes zoster (shingles). The focus of this review is on the wide spectrum of the possible neurological manifestations of VZV reactivation. While the most frequent reactivation syndrome is herpes zoster, this may be followed by the serious and painful post-herpetic neuralgia (PHN) and by many other neurological conditions. Prominent among these conditions is a VZV vasculopathy, but the role of VZV in causing giant cell arteritis (GCA) is currently controversial. VZV reactivation can also cause segmental motor weakness, myelitis, cranial nerve syndromes, Guillain–Barre syndrome, meningoencephalitis, and zoster sine herpete, where a neurological syndrome occurs in the absence of the zoster rash. The field is complicated by the relatively few cases of neurological complications described and by the issue of causation when a neurological condition is not manifest at the same time as the zoster rash.

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Section: Giant Cell Arteritismentioning

confidence: 99%

The Spectrum of Neurological Manifestations of Varicella–Zoster Virus Reactivation

Kennedy

2023

Viruses

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“…The problems of false-positive staining of human tissue sections with antibodies to VZV due to antibody cross-reactivity were also emphasised in another recent study [ 33 ], where caution was advised in interpreting such apparently positive staining. As well as the problems of possible nonspecific staining, the presence of VZV antigens in some normal TAs, and the varying positive detection rates in different studies, a critical issue is the one of a cause-and-effect relationship between the viral detection and the production of the human disease [ 34 ]. Gilden [ 30 ] considered a causal relation likely and that there may be a subgroup of patients with GCA in which VZV is a critical determinant in whom corticosteroids alone in the absence of antiviral therapy may actually be deleterious since it may allow an ongoing untreated viral infection to persist.…”

Section: Neurological Complications Of Vzv Reactivationmentioning

confidence: 99%

Clinical Features of Varicella-Zoster Virus Infection

Kennedy

Gershon

2018

Viruses

236

211

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Varicella-zoster virus (VZV) is a pathogenic human herpes virus that causes varicella (chickenpox) as a primary infection, following which it becomes latent in peripheral ganglia. Decades later, the virus may reactivate either spontaneously or after a number of triggering factors to cause herpes zoster (shingles). Varicella and its complications are more severe in the immunosuppressed. The most frequent and important complication of VZV reactivation is postherpetic neuralgia, the cause of which is unknown and for which treatment is usually ineffective. Reactivation of VZV may also cause a wide variety of neurological syndromes, the most significant of which is a vasculitis, which is treated with corticosteroids and the antiviral drug acyclovir. Other VZV reactivation complications include an encephalitis, segmental motor weakness and myelopathy, cranial neuropathies, Guillain–Barré syndrome, enteric features, and zoster sine herpete, in which the viral reactivation occurs in the absence of the characteristic dermatomally distributed vesicular rash of herpes zoster. There has also been a recent association of VZV with giant cell arteritis and this interesting finding needs further corroboration. Vaccination is now available for the prevention of both varicella in children and herpes zoster in older individuals.

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“…GCA is characterized pathologically by inflammation in and damage to the vessel wall of the temporal arteries (TAs) [31,32]. The condition may be strongly suspected on clinical grounds, with symptoms including headache, scalp tenderness, weight loss, malaise, and raised erythrocyte sedimentation rate, and the diagnosis is confirmed by a TA biopsy showing the typical inflammatory histopathological features.…”

Section: Giant Cell Arteritismentioning

confidence: 99%

Issues in the Treatment of Neurological Conditions Caused by Reactivation of Varicella Zoster Virus (VZV)

Kennedy

2016

Neurotherapeutics

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Varicella zoster virus (VZV) is a ubiquitous neurotropic human herpesvirus. Primary infection usually causes varicella (chicken pox), after which virus becomes latent in ganglia along the entire neuraxis. Decades later, virus reactivates to produce herpes zoster (shingles), a painful dermatomally distributed vesicular eruption. Zoster may be further complicated by postherpetic neuralgia, VZV vasculopathy, myelitis, and segmental motor weakness. VZV reactivation has also been associated with giant cell arteritis. This overview discusses treatment of various conditions that often require both corticosteroids and antiviral drugs. Treatment for VZV-associated disease is often based on case reports and small studies rather than largescale clinical trials. Issues that require resolution include the optimal duration of such combined therapy, more effective treatment for postherpetic neuralgia, whether some treatments should be given orally or intravenously, the widening spectrum of zoster sine herpete, and the role of antiviral therapy in giant cell arteritis.

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Varicella-zoster virus claims yet another painful scalp—Giant cell arteritis

Cited by 6 publications

References 5 publications

The Spectrum of Neurological Manifestations of Varicella–Zoster Virus Reactivation

The Spectrum of Neurological Manifestations of Varicella–Zoster Virus Reactivation

Clinical Features of Varicella-Zoster Virus Infection

Issues in the Treatment of Neurological Conditions Caused by Reactivation of Varicella Zoster Virus (VZV)

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