Complications of Varicella Zoster Virus Reactivation
ABSTRACT Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in ganglionic neurons along the entire neuraxis. With advancing age or immunosuppression, cell-mediated immunity to VZV declines and virus reactivates to cause zoster (shingles), which can occur anywhere on the body. Skin lesions resolve within 1-2 weeks, while complete cessation of pain usually takes 4-6 weeks. Zoster can be followed by chronic pain (postherpetic neuralgia), cranial nerve palsies, zoster paresis, meningoencephalitis, cerebellitis, myelopathy, multiple ocular disorders and vasculopathy that can mimic giant cell arteritis. All of the neurological and ocular disorders listed above may also develop without rash. Diagnosis of VZV-induced neurological disease may require examination of cerebrospinal fluid (CSF), serum and/ or ocular fluids. In the absence of rash in a patient with neurological disease potentially due to VZV, CSF should be examined for VZV DNA by PCR and for anti-VZV IgG and IgM. Detection of VZV IgG antibody in CSF is superior to detection of VZV DNA in CSF to diagnose vasculopathy, recurrent myelopathy, and brainstem encephalitis. Oral antiviral drugs speed healing of rash and shorten acute pain. Immunocompromised patients require intravenous acyclovir. First-line treatments for post-herpetic neuralgia include tricyclic antidepressants, gabapentin, pregabalin, and topical lidocaine patches. VZV vasculopathy, meningoencephalitis, and myelitis are all treated with intravenous acyclovir.
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ABSTRACT: Infections of the nervous system have a significant impact on global mortality and morbidity. These infections are medical emergencies that are frequently diagnostically challenging. Incorporation of neuroimaging can be essential for early diagnosis and initiation of proper treatment. In this second part of this two-part review, we focus on diagnostic imaging features of selected fungal and viral nervous system infections.Current Infectious Disease Reports 04/2015; 17(4):474. DOI:10.1007/s11908-015-0474-9
Article: Infections of the Cerebellum[Show abstract] [Hide abstract]
ABSTRACT: Although the cerebellum can be affected by any infection that also involves other parts of the brain parenchyma, cerebrospinal fluid, or nerve roots, a limited range of infections targets cerebellar structures preferentially. Thus, a primarily cerebellar syndrome narrows infectious differential diagnostic considerations. The differential diagnosis of rapidly evolving cerebellar signs suggesting infection includes prescription or illicit drug intoxications or adverse reactions, inflammatory pseudotumor, paraneoplastic processes, and acute postinfectious cerebellitis. This article discusses the diagnosis and differential diagnosis of viral, bacterial, fungal, and prion pathogens affecting the cerebellum in patterns predictable by pace of illness and by involved neuroanatomic structures. Copyright © 2014 Elsevier Inc. All rights reserved.Neurologic Clinics 10/2014; 32(4). DOI:10.1016/j.ncl.2014.07.009 · 1.61 Impact Factor
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ABSTRACT: Increased understanding of the pathogenesis of immune-mediated neurologic conditions with concomitant development of new therapeutic agents modulating various aspects of the immune system has resulted in the use of innovative therapies in the treatment of these diseases. These novel immunomodulatory therapeutic regimens also augment the potential for complications, including severe adverse effects.In this review, the authors address practical issues regarding management of patients with neuroimmunological conditions treated with immunomodulatory therapies, including glucocorticoids, methotrexate, azathioprine, mycophenolate, cyclophosphamide, rituximab, tumor necrosis factor-α inhibitors, and intravenous immunoglobulins. Particular focus is placed on their infectious and noninfectious adverse effects, contraindications, safety monitoring, risk surveillance, and preventive strategies in clinical practice.Seminars in Neurology 09/2014; 34(4):467-78. DOI:10.1055/s-0034-1390395 · 1.78 Impact Factor