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Support Center Support Center. External link. In contrast, the 3 cases reported by Chan et al. Thus, there are obviously contradictions in the definition and management of VZV meningoradiculitis.
It appears from the literature that clinicians tend to prescribe IV antiviral treatment to patients with VZV radiculitis after performing CSF investigations, even if this choice does not clearly influence the prognosis.
If meningoradiculitis comprises clinical meningitis with peripheral nerve root involvement, then it should be treated, as with any other VZV-CNS complication, using IV antiviral drugs after spinal tap and other necessary investigations [ 2 , 6 , 12 ]. Alternatively, we suggest considering radiculitis without obvious meningitis symptoms to be a VZV peripheral nervous system complication [ 15 ]. Such patients should therefore be exempt from CSF workup and, as for most cases in everyday clinical practice contrary to published cases , orally treated with acyclovir with generally good outcome [ 2 , 3 ].
What diagnostic value therefore should inflammatory CSF with direct or indirect markers of VZV viral activity in the CSF be given in VZV radiculitis, taking into account that inflammatory markers in the CSF are similar in patients with herpes-related clinical meningitis or encephalitis to those with meningoradiculitis see above [ 12 , 14 , 16 ]?
Moreover, mild inflammation in the CSF is reported in up to half of all patients with HZ and the presence of viral activity in the CSF does not necessarily establish a causal relationship with neurological symptoms [ 3 ].
Thus, CSF inflammation should not be used apart from the clinical context as a discriminating criterion between peripheral and central nervous system complications of VZV and should not solely determine the choice of the antiviral treatment route. In the cases published, clinicians perhaps over-treated patients by prescribing IV acyclovir without clinically evident VZV-related CNS symptoms associated with the radiculitis.
This was most probably done to prevent severe neurological complications even if, as stated above, this reasoning cannot be fully justified. None of the frequently reported immunosuppressive states inflammatory rheumatic diseases, immunosuppressive treatments, HIV infection, etc. Similarly, he had signs of alcohol abuse witnessed by macrocytosis, thrombopenia and increased serum IgA [ 19 — 21 ] , another condition that impairs CMI [ 21 ].
So in this case, in the absence of any other evident cause of immunosuppression, age and alcoholism were considered the factors lowering CMI and precipitating HZ. Nonetheless, clear guidelines do not exist for the choice of antiviral treatment in the context of such subtle immunosuppression. Reactivation of VZV was most probably precipitated by age- and alcohol-induced cell-mediated immunosuppression.
He was diagnosed with meningoradiculitis and treated with IV acyclovir, despite the absence of clinical meningitis. In available published cases, we did not find a consensual definition or management scheme for meningoradiculitis.
The presence of CNS symptoms or abnormal CSF findings did not allow discrimination of severe from benign cases and these patients were generally IV treated. However, well-designed clinical trials are needed to review severity criteria for patients with VZV-associated meningo -radiculitis, to study the efficiency of oral versus IV antiviral treatment and establish clear guidelines for management. Mild elevation of inflammatory markers in the CSF is not specific or sensitive enough to establish a diagnosis of meningitis without evocative clinical symptoms.
Patients with isolated VZV radiculitis should be exempt from CSF investigations and be given oral antiviral treatment, unless they are subject to any condition or pathology decreasing immunity, in particular CMI, in which case CSF workup and IV antiviral therapy may be necessary. VL and LW collected data, drafted and reviewed the manuscript. DF contributed to data collection, discussed results, diagnoses and management, and reviewed the manuscript.
GP contributed to the study design, discussed infectious diagnoses and results. J-AG contributed to discussion of neurological diagnoses and treatment, and reviewed the manuscript. DG participated in data collection, significantly participated in neurological diagnoses, discussion and reviewed the manuscript. JNC designed the study, discussed neurological diagnoses and treatment, wrote and reviewed the manuscript. All authors read and approved the final manuscript.
Written informed consent was obtained from the patient for publication of this Case Report and any accompanying images. A copy of the written consent is available for review by the Editor-In-Chief of this journal.
Vincent Luisier and Lalensia Weber contributed equally to this work. Vincent Luisier, Email: moc. Lalensia Weber, Email: moc. Daniel Fishman, Email: hc. Didier Genoud, Email: hc. Joelle Nsimire Chabwine, Phone: , Email: hc. National Center for Biotechnology Information , U. BMC Res Notes. Published online Sep Author information Article notes Copyright and License information Disclaimer.
Corresponding author. Received May 5; Accepted Sep This article has been cited by other articles in PMC. Associated Data Data Availability Statement The dataset supporting the conclusions of this article are included within the article.
Abstract Background The varicella zoster virus affects the central or peripheral nervous systems upon reactivation, especially when cell-mediated immunity is impaired.
Case presentation We report the case of an alcohol-dependent elderly Caucasian man presenting with left lower limb zoster paresis and mild cerebral spinal fluid inflammation, with favorable outcome upon IV antiviral treatment. Conclusion From this case report we suggest that varicella zoster virus-associated meningoradiculitis should necessarily include meningitis symptoms with the peripheral neurological deficits and cerebral spinal fluid inflammation, requiring intravenous antiviral treatment.
Background Varicella zoster virus VZV is an exclusively human virus primarily causing chickenpox [ 1 ]. Case presentation A year-old Caucasian man was admitted to the Emergency Room, addressed by his general practitioner for a 3-day history of progressive lower left limb weakness. We discuss interpretation of liquor inflammation in the absence of clinical meningitis and implications for the antiviral treatment route.
Conclusion: From this case report we suggest that varicella zoster virus-associated meningoradiculitis should necessarily include meningitis symptoms with the peripheral neurological deficits and cerebral spinal fluid inflammation, requiring intravenous antiviral treatment.
In the absence of cell-mediated immunosuppression, isolated zoster paresis does not necessitate spinal tap or intravenous antiviral therapy.
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