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M. De Vincentiis - One of the best experts on this subject based on the ideXlab platform.

  • Bell's palsy and autoimmunity
    Autoimmunity Reviews, 2012
    Co-Authors: Antonio Greco, Andrea Gallo, M. Fusconi, C. Marinelli, G.f. Macri, M. De Vincentiis
    Abstract:

    Abstract Objectives To review our current knowledge of the etiopathogenesis of Bell's palsy, including viral infection or autoimmunity, and to discuss disease pathogenesis with respect to pharmacotherapy. Systematic review methodology Relevant publications on the etiopathogenesis, clinical presentation, diagnosis and histopathology of Bell's palsy from 1975 to 2012 were analysed. Results and conclusions Bell's palsy is an idiopathic peripheral Nerve palsy involving the facial Nerve. It accounts for 60 to 75% of all cases of unilateral facial paralysis. The annual incidence of Bell's palsy is 15 to 30 per 100,000 people. The peak incidence occurs between the second and fourth decades (15 to 45 years). The aetiology of Bell's palsy is unknown but viral infection or autoimmune disease has been postulated as possible pathomechanisms. Bell's palsy may be caused when latent herpes viruses (herpes simplex, herpes zoster) are reactivated from Cranial Nerve Ganglia. A cell-mediated autoimmune mechanism against a myelin basic protein has been suggested for the pathogenesis of Bell's palsy. Bell's palsy may be an autoimmune demyelinating Cranial neuritis, and in most cases, it is a mononeuritic variant of Guillain–Barre syndrome, a neurologic disorder with recognised cell-mediated immunity against peripheral Nerve myelin antigens. In Bell's palsy and GBS, a viral infection or the reactivation of a latent virus may provoke an autoimmune reaction against peripheral Nerve myelin components, leading to the demyelination of Cranial Nerves, especially the facial Nerve. Given the safety profile of acyclovir, valacyclovir, and short-course oral corticosteroids, patients who present within three days of the onset of symptoms should be offered combination therapy. However it seems logical that in fact, steroids exert their beneficial effect via immunosuppressive action, as is the case in some other autoimmune disorders. It is to be hoped that (monoclonal) antibodies and/or T-cell immunotherapy might provide more specific treatment guidelines in the management of Bell's palsy.

Randall J Cohrs - One of the best experts on this subject based on the ideXlab platform.

  • review the neurobiology of varicella zoster virus infection
    Neuropathology and Applied Neurobiology, 2011
    Co-Authors: M Nagel, Subbiah Pugazhenthi, Randall J Cohrs
    Abstract:

    Varicella zoster virus (VZV) is a neurotropic herpesvirus that infects nearly all humans. Primary infection usually causes chickenpox (varicella), after which virus becomes latent in Cranial Nerve Ganglia, dorsal root Ganglia and autonomic Ganglia along the entire neuraxis. Although VZV cannot be isolated from human Ganglia, nucleic acid hybridization and, later, polymerase chain reaction proved that VZV is latent in Ganglia. Declining VZV-specific host immunity decades after primary infection allows virus to reactivate spontaneously, resulting in shingles (zoster) characterized by pain and rash restricted to one to three dermatomes. Multiple other serious neurological and ocular disorders also result from VZV reactivation. This review summarizes the current state of knowledge of the clinical and pathological complications of neurological and ocular disease produced by VZV reactivation, molecular aspects of VZV latency, VZV virology and VZV-specific immunity, the role of apoptosis in VZV-induced cell death and the development of an animal model provided by simian varicella virus infection of monkeys.

  • varicella zoster virus infection clinical features molecular pathogenesis of disease and latency
    Neurologic Clinics, 2008
    Co-Authors: Niklaus H Mueller, Randall J Cohrs, Donald H Gilden, Ravi Mahalingam, M Nagel
    Abstract:

    Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in Cranial Nerve Ganglia, dorsal root Ganglia, and autonomic Ganglia along the entire neuraxis. Years later, in association with a decline in cell-mediated immunity in elderly and immunocompromised individuals, VZV reactivates and causes a wide range of neurologic disease. This article discusses the clinical manifestations, treatment, and prevention of VZV infection and reactivation; pathogenesis of VZV infection; and current research focusing on VZV latency, reactivation, and animal models.

Jeffrey T. Vrabec - One of the best experts on this subject based on the ideXlab platform.

  • Quantitative analysis of herpes simplex virus in Cranial Nerve Ganglia
    Journal of NeuroVirology, 2004
    Co-Authors: Jeffrey T. Vrabec, Raye L. Alford
    Abstract:

    A susceptible individual exposed to herpes simplex virus (HSV) will develop latent infection in multiple Cranial Nerve Ganglia. There are a few quantitative studies of the viral load within the trigeminal ganglion, but none that investigate other Cranial Nerve Ganglia. In this study, human trigeminal, geniculate, vestibular (Scarpa’s) and cochlear (spiral) Ganglia were obtained from willed body donors. Real time quantitative polymerase chain reaction (PCR) analysis of the HSV DNA polymerase gene was performed on ipsilateral ganglion sets from the same individual. Viral load, expressed as HSV genomes per 10^5 cells, was significantly greater in the vestibular ganglion (mean ± SD, 176705 ± 255916) than in the geniculate (9948 ± 22066), cochlear (3527 ± 9360), or trigeminal (2017 ± 5578) Ganglia. There was not a significant correlation among Ganglia from the same individual. The results support the hypothesis that neuronal subpopulations have variable susceptibility to HSV infection.

  • prevalence of herpesviruses in Cranial Nerve Ganglia
    Acta Oto-laryngologica, 2001
    Co-Authors: Jeffrey T. Vrabec, Deborah A Payne
    Abstract:

    A number of Cranial Nerve disorders are known to result from viral infection or reactivation, including Bell's palsy, Ramsay Hunt syndrome and herpetic laryngitis. The consequences of these diseases are well established although the patient population at risk is not. Prevalence studies in the general population are an initial step toward defining individuals at risk. The aim of this study was to determine the prevalence of herpesvirus DNA in Cranial Nerve Ganglia in a random population sample. Qualitative molecular biologic analysis using polymerase chain reaction assay of the trigeminal, geniculate, vestibular, spiral and vagal Ganglia was used in 18 randomly selected fresh cadaver heads. Herpes simplex virus (HSV) DNA was detected in 42% of all Ganglia surveyed. Varicella zoster virus (VZV) DNA was detected in 44% of all Ganglia. The difference in the prevalence rate between viruses was not significant ( p = 0.63). At least 1 of the 2 viruses was found in 65% of all Ganglia. Both HSV and VZV can commonl...

Donald H Gilden - One of the best experts on this subject based on the ideXlab platform.

  • Update on Varicella Zoster Virus Vasculopathy
    Current Infectious Disease Reports, 2014
    Co-Authors: Maria A. Nagel, Donald H Gilden
    Abstract:

    Primary infection of humans with varicella zoster virus (VZV) causes varicella (chickenpox), after which the virus becomes latent in Cranial Nerve Ganglia, dorsal root Ganglia and autonomic Ganglia along the entire neuraxis. As VZV-specific cell-mediated immunity declines in elderly and immunocompromised individuals, VZV reactivates from one or more Ganglia and typically causes herpes zoster (shingles). Zoster may also be complicated by VZV vasculopathy due to productive virus infection of the cerebral arteries. In recent decades, the clinical spectrum of VZV vasculopathy has expanded to include not only transient ischemic attacks and ischemic and hemorrhagic stroke, but also multifocal VZV vasculopathy, with temporal artery infection mimicking giant cell arteritis, extraCranial vasculopathy, aneurysm with and without subarachnoid hemorrhage, arterial dissection and dolichoectasia, ischemic Cranial neuropathies, cerebral venous sinus thrombosis, spinal cord infarction and peripheral thrombotic disease.

  • the global epidemiology of herpes zoster
    Neurology, 2013
    Co-Authors: Barbara P Yawn, Donald H Gilden
    Abstract:

    Varicella-zoster virus (VZV) is a ubiquitous, highly neurotropic, exclusively human α-herpesvirus. Primary infection usually results in varicella (chickenpox), after which VZV becomes latent in neurons of Cranial Nerve Ganglia, dorsal root Ganglia, and autonomic Ganglia along the entire neuraxis. As humans undergo a natural decline in cell-mediated immunity (CMI) to VZV with age, VZV frequently reactivates to produce zoster, characterized by maculopapular or vesicular rash and dermatomal-distribution pain. Pain and rash usually occur within days of each other. Pain is severe and often burning. Colorful descriptions of zoster exist worldwide. In Arabic, Hezam innar means belt of fire; in Hindi, Baoisayaa daga means big rash; in Norwegian, Helvetesild means Hell's fire (also described as a bell of roses from Hell); and in Spanish, Culebrilla means small snake.1 The most common complication of zoster is postherpetic neuralgia (PHN), operationally defined as pain lasting for more than 90 days after rash. Zoster may be followed by multiple neurologic disorders (meningoencephalitis, myelitis, and vasculopathy, including VZV temporal arteritis) as well as ocular disease (acute or progressive outer retinal necrosis).

  • varicella zoster virus infection clinical features molecular pathogenesis of disease and latency
    Neurologic Clinics, 2008
    Co-Authors: Niklaus H Mueller, Randall J Cohrs, Donald H Gilden, Ravi Mahalingam, M Nagel
    Abstract:

    Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in Cranial Nerve Ganglia, dorsal root Ganglia, and autonomic Ganglia along the entire neuraxis. Years later, in association with a decline in cell-mediated immunity in elderly and immunocompromised individuals, VZV reactivates and causes a wide range of neurologic disease. This article discusses the clinical manifestations, treatment, and prevention of VZV infection and reactivation; pathogenesis of VZV infection; and current research focusing on VZV latency, reactivation, and animal models.

M Nagel - One of the best experts on this subject based on the ideXlab platform.

  • review the neurobiology of varicella zoster virus infection
    Neuropathology and Applied Neurobiology, 2011
    Co-Authors: M Nagel, Subbiah Pugazhenthi, Randall J Cohrs
    Abstract:

    Varicella zoster virus (VZV) is a neurotropic herpesvirus that infects nearly all humans. Primary infection usually causes chickenpox (varicella), after which virus becomes latent in Cranial Nerve Ganglia, dorsal root Ganglia and autonomic Ganglia along the entire neuraxis. Although VZV cannot be isolated from human Ganglia, nucleic acid hybridization and, later, polymerase chain reaction proved that VZV is latent in Ganglia. Declining VZV-specific host immunity decades after primary infection allows virus to reactivate spontaneously, resulting in shingles (zoster) characterized by pain and rash restricted to one to three dermatomes. Multiple other serious neurological and ocular disorders also result from VZV reactivation. This review summarizes the current state of knowledge of the clinical and pathological complications of neurological and ocular disease produced by VZV reactivation, molecular aspects of VZV latency, VZV virology and VZV-specific immunity, the role of apoptosis in VZV-induced cell death and the development of an animal model provided by simian varicella virus infection of monkeys.

  • varicella zoster virus infection clinical features molecular pathogenesis of disease and latency
    Neurologic Clinics, 2008
    Co-Authors: Niklaus H Mueller, Randall J Cohrs, Donald H Gilden, Ravi Mahalingam, M Nagel
    Abstract:

    Varicella zoster virus (VZV) is an exclusively human neurotropic alphaherpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in Cranial Nerve Ganglia, dorsal root Ganglia, and autonomic Ganglia along the entire neuraxis. Years later, in association with a decline in cell-mediated immunity in elderly and immunocompromised individuals, VZV reactivates and causes a wide range of neurologic disease. This article discusses the clinical manifestations, treatment, and prevention of VZV infection and reactivation; pathogenesis of VZV infection; and current research focusing on VZV latency, reactivation, and animal models.