The Experts below are selected from a list of 270 Experts worldwide ranked by ideXlab platform

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

  • reactivation of type 1 herpes simplex virus and varicella Zoster virus in an immunosuppressed patient with acute peripheral facial weakness
    Journal of the Neurological Sciences, 2012
    Co-Authors: Jean Tsai, Randall J Cohrs, M Nagel, Ravi Mahalingam, Scott D Schmid, Alexander Choe, Donald H Gilden
    Abstract:

    We describe a 26-year-old man treated with azathioprine for myasthenia gravis who developed acute left-sided peripheral facial weakness. Brain magnetic resonance imaging (MRI) revealed enhancement in the left geniculate ganglion and in the intracanalicular and tympanic segments of the facial nerve. Analysis of cerebrospinal fluid (CSF) and serum revealed intrathecal synthesis of anti-varicella Zoster virus (VZV) IgG antibody. Although previous analyses of saliva, blood mononuclear cells, serum antibodies, middle ear fluid, and auricular and geniculate zone skin scrapings have shown that a small but definite proportion of patients with idiopathic peripheral facial palsy ("Bell's palsy") have the Ramsay Hunt syndrome Zoster Sine Herpete (RHS ZSH), this is the first confirmation of RHS ZSH by intrathecal synthesis of anti-VZV IgG antibody. In addition, herpes simplex virus (HSV)-1 DNA was found in saliva of the patient on 3 consecutive days. Simultaneous reactivation of two alphaherpesviruses (HSV-1 and VZV) in our immunosuppressed patient underscores the need to consider opportunistic infection as a cause of facial weakness.

  • subclinical reactivation of varicella Zoster virus in all stages of hiv infection
    Journal of the Neurological Sciences, 2011
    Co-Authors: Marius Birlea, Scott D Schmid, Donald H Gilden, G Arendt, Eser Orhan, William J Bellini, Christian Schmidt, Randall J Cohrs
    Abstract:

    Analysis of 200 paired serum and cerebrospinal fluid (CSF) samples from 180 HIV-positive individuals, 136 of whom had AIDS, revealed intrathecal synthesis of antibodies specific for varicella Zoster virus (VZV) in 28 (16%) individuals, measles virus in 15 (8%), herpes simplex virus-1 (HSV-1) in 1 (0.6%), and HSV-2 in none. Of the 28 subjects with a positive VZV antibody specificity index, only 1 had Zoster rash at the time of serum and CSF sampling; of the total 180 HIV-positive subjects, 146 (81%) had no history of Zoster. Based on an estimated 33.4 million HIV-positive individuals worldwide, subclinical reactivation of VZV in even less than 16% of HIV-positive people suggests the possibility that millions of people have active VZV infection of the central nervous system. In cases of VZV vasculopathy, myelopathy and even Zoster Sine Herpete, the CSF is often positive for anti-VZV antibody, but negative for VZV DNA. To rule out VZV infection of the nervous system, CSF must be tested for VZV DNA and anti-VZV IgG and IgM antibody.

  • Zoster Sine Herpete virologic verification by detection of anti vzv igg antibody in csf
    Neurology, 2011
    Co-Authors: D T Blumenthal, Randall J Cohrs, M Nagel, Ravi Mahalingam, E Shachamshmueli, Felix Bokstein, D S Schmid, Donald H Gilden
    Abstract:

    Classic Zoster Sine Herpete (ZSH) is defined clinically as dermatomal distribution pain without rash. ZSH was designated as a nosologic entity based on virologic confirmation in 3 men over age 60 with chronic thoracic-distribution radicular pain, with amplifiable varicella Zoster virus (VZV) DNA found in CSF of the first 2 patients1 and in blood mononuclear cells (MNCs) in the third patient.2 Herein, we describe a patient who developed radicular pain without rash in the same dermatome as his initial cervical-distribution Zoster episode, but with a remarkably prolonged interval between episodes, and in whom ZSH was virologically confirmed by the detection of anti-VZV immunoglobulin G (IgG) antibody in CSF with serum/CSF ratios indicative of intrathecal antibody synthesis. ### Case report. In 2008, a 77-year-old man developed right C8-distribution Zoster; he was not treated with an antiviral agent or steroids and his rash and pain resolved completely. One year later, …

  • neurological disease produced by varicella Zoster virus reactivation without rash
    Current Topics in Microbiology and Immunology, 2010
    Co-Authors: Donald H Gilden, Randall J Cohrs, Ravi Mahalingam, M Nagel
    Abstract:

    Reactivation of varicella Zoster virus (VZV) from latently infected human ganglia usually produces herpes Zoster (shingles), characterized by dermatomal distribution pain and rash. Zoster is often followed by chronic pain (postherpetic neuralgia or PHN) as well as meningitis or meningoencephalitis, cerebellitis, isolated cranial nerve palsies that produce ophthalmoplegia or the Ramsay Hunt syndrome, multiple cranial nerve palsies (polyneuritis cranialis), vasculopathy, myelopathy, and various inflammatory disorders of the eye. Importantly, VZV reactivation can produce chronic radicular pain without rash (Zoster Sine Herpete), as well as all the neurological disorders listed above without rash. The protean neurological and ocular disorders produced by VZV in the absence of rash are a challenge to the practicing clinician. The presentation of these conditions varies from acute to subacute to chronic. Virological confirmation requires the demonstration of amplifiable VZV DNA in cerebrospinal fluid (CSF) or in blood mononuclear cells, or the presence of anti-VZV IgG antibody in CSF or of anti-VZV IgM antibody in CSF or serum.

  • vzv vasculopathy and postherpetic neuralgia progress and perspective on antiviral therapy
    Neurology, 2005
    Co-Authors: Donald H Gilden, Randall J Cohrs, Ravi Mahalingam
    Abstract:

    Two serious complications of varicella-Zoster virus (VZV) reactivation are vasculopathy and postherpetic neuralgia (PHN). Clinical-virologic analyses have proven that VZV vasculopathy is caused by chronic active virus infection in cerebral arteries. Conclusive evidence that PHN is caused by persistent or productive VZV infection is less compelling because human ganglia are not accessible during life for pathologic and virologic examination. However, the notion that PHN may reflect a smoldering VZV ganglionitis is supported by 1) the detection of VZV DNA and proteins in peripheral blood mononuclear cells of many patients with PHN; 2) studies of multiple patients with Zoster Sine Herpete, which indicate a productive VZV ganglionitis; and 3) a favorable response of some patients with Zoster Sine Herpete and PHN to antiviral treatment. Few studies have used antiviral therapy to manage PHN with conflicting results. Larger, double-blind studies, which give IV antiviral drug, are needed.

Ravi Mahalingam - One of the best experts on this subject based on the ideXlab platform.

  • reactivation of type 1 herpes simplex virus and varicella Zoster virus in an immunosuppressed patient with acute peripheral facial weakness
    Journal of the Neurological Sciences, 2012
    Co-Authors: Jean Tsai, Randall J Cohrs, M Nagel, Ravi Mahalingam, Scott D Schmid, Alexander Choe, Donald H Gilden
    Abstract:

    We describe a 26-year-old man treated with azathioprine for myasthenia gravis who developed acute left-sided peripheral facial weakness. Brain magnetic resonance imaging (MRI) revealed enhancement in the left geniculate ganglion and in the intracanalicular and tympanic segments of the facial nerve. Analysis of cerebrospinal fluid (CSF) and serum revealed intrathecal synthesis of anti-varicella Zoster virus (VZV) IgG antibody. Although previous analyses of saliva, blood mononuclear cells, serum antibodies, middle ear fluid, and auricular and geniculate zone skin scrapings have shown that a small but definite proportion of patients with idiopathic peripheral facial palsy ("Bell's palsy") have the Ramsay Hunt syndrome Zoster Sine Herpete (RHS ZSH), this is the first confirmation of RHS ZSH by intrathecal synthesis of anti-VZV IgG antibody. In addition, herpes simplex virus (HSV)-1 DNA was found in saliva of the patient on 3 consecutive days. Simultaneous reactivation of two alphaherpesviruses (HSV-1 and VZV) in our immunosuppressed patient underscores the need to consider opportunistic infection as a cause of facial weakness.

  • Zoster Sine Herpete virologic verification by detection of anti vzv igg antibody in csf
    Neurology, 2011
    Co-Authors: D T Blumenthal, Randall J Cohrs, M Nagel, Ravi Mahalingam, E Shachamshmueli, Felix Bokstein, D S Schmid, Donald H Gilden
    Abstract:

    Classic Zoster Sine Herpete (ZSH) is defined clinically as dermatomal distribution pain without rash. ZSH was designated as a nosologic entity based on virologic confirmation in 3 men over age 60 with chronic thoracic-distribution radicular pain, with amplifiable varicella Zoster virus (VZV) DNA found in CSF of the first 2 patients1 and in blood mononuclear cells (MNCs) in the third patient.2 Herein, we describe a patient who developed radicular pain without rash in the same dermatome as his initial cervical-distribution Zoster episode, but with a remarkably prolonged interval between episodes, and in whom ZSH was virologically confirmed by the detection of anti-VZV immunoglobulin G (IgG) antibody in CSF with serum/CSF ratios indicative of intrathecal antibody synthesis. ### Case report. In 2008, a 77-year-old man developed right C8-distribution Zoster; he was not treated with an antiviral agent or steroids and his rash and pain resolved completely. One year later, …

  • neurological disease produced by varicella Zoster virus reactivation without rash
    Current Topics in Microbiology and Immunology, 2010
    Co-Authors: Donald H Gilden, Randall J Cohrs, Ravi Mahalingam, M Nagel
    Abstract:

    Reactivation of varicella Zoster virus (VZV) from latently infected human ganglia usually produces herpes Zoster (shingles), characterized by dermatomal distribution pain and rash. Zoster is often followed by chronic pain (postherpetic neuralgia or PHN) as well as meningitis or meningoencephalitis, cerebellitis, isolated cranial nerve palsies that produce ophthalmoplegia or the Ramsay Hunt syndrome, multiple cranial nerve palsies (polyneuritis cranialis), vasculopathy, myelopathy, and various inflammatory disorders of the eye. Importantly, VZV reactivation can produce chronic radicular pain without rash (Zoster Sine Herpete), as well as all the neurological disorders listed above without rash. The protean neurological and ocular disorders produced by VZV in the absence of rash are a challenge to the practicing clinician. The presentation of these conditions varies from acute to subacute to chronic. Virological confirmation requires the demonstration of amplifiable VZV DNA in cerebrospinal fluid (CSF) or in blood mononuclear cells, or the presence of anti-VZV IgG antibody in CSF or of anti-VZV IgM antibody in CSF or serum.

  • vzv vasculopathy and postherpetic neuralgia progress and perspective on antiviral therapy
    Neurology, 2005
    Co-Authors: Donald H Gilden, Randall J Cohrs, Ravi Mahalingam
    Abstract:

    Two serious complications of varicella-Zoster virus (VZV) reactivation are vasculopathy and postherpetic neuralgia (PHN). Clinical-virologic analyses have proven that VZV vasculopathy is caused by chronic active virus infection in cerebral arteries. Conclusive evidence that PHN is caused by persistent or productive VZV infection is less compelling because human ganglia are not accessible during life for pathologic and virologic examination. However, the notion that PHN may reflect a smoldering VZV ganglionitis is supported by 1) the detection of VZV DNA and proteins in peripheral blood mononuclear cells of many patients with PHN; 2) studies of multiple patients with Zoster Sine Herpete, which indicate a productive VZV ganglionitis; and 3) a favorable response of some patients with Zoster Sine Herpete and PHN to antiviral treatment. Few studies have used antiviral therapy to manage PHN with conflicting results. Larger, double-blind studies, which give IV antiviral drug, are needed.

  • another case of virologically confirmed Zoster Sine Herpete with electrophysiologic correlation
    Journal of NeuroVirology, 1996
    Co-Authors: Catherine Amlielefond, Ravi Mahalingam, Glenn A Mackin, Michelle Ferguson, Roy R Wright, Donald H Gilden
    Abstract:

    A third virologically-confirmed case of thoracic-distribution Zoster Sine Herpete is reported. Electromyography (EMG) of paraspinal muscles demonstrated frequent fibrillation potentials restricted to chronically painful thoracic root segments. Treatment with intravenous acyclovir and oral famciclovir were ineffective. These findings suggest the usefulness of EMG of muscles corresponding to painful dermatomes, combined with virologic studies, to support the diagnosis of Zoster Sine Herpete.

Yasushi Furuta - One of the best experts on this subject based on the ideXlab platform.

  • Case Report A Case of Associated Laryngeal Paralysis Caused by Varicella Zoster Virus without Eruption
    2016
    Co-Authors: Keishi Fujiwara, Yasushi Furuta, S Fukuda
    Abstract:

    Copyright © 2014 Keishi Fujiwara et al.This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. We report a patient with significant weakness of the left soft palate, paralysis of the left vocal cord, and left facial nerve palsy. Although the patient showed no herpetic eruption in the pharyngolaryngeal mucosa and auricle skin, reactivation of varicella Zoster virus (VZV) was confirmed by serological examination. She was diagnosed with Zoster Sine Herpete. After treatment with antiviral drugs and corticosteroids, her neurological disorder improved completely. When we encounter a patient with associated laryngeal paralysis, we should consider the possibility of reactivation of VZV even when no typical herpetic eruption is observed. 1

  • A Case of Associated Laryngeal Paralysis Caused by Varicella Zoster Virus without Eruption
    Hindawi Limited, 2014
    Co-Authors: Keishi Fujiwara, Yasushi Furuta, S Fukuda
    Abstract:

    We report a patient with significant weakness of the left soft palate, paralysis of the left vocal cord, and left facial nerve palsy. Although the patient showed no herpetic eruption in the pharyngolaryngeal mucosa and auricle skin, reactivation of varicella Zoster virus (VZV) was confirmed by serological examination. She was diagnosed with Zoster Sine Herpete. After treatment with antiviral drugs and corticosteroids, her neurological disorder improved completely. When we encounter a patient with associated laryngeal paralysis, we should consider the possibility of reactivation of VZV even when no typical herpetic eruption is observed

  • quantitation of varicella Zoster virus dna in patients with ramsay hunt syndrome and Zoster Sine Herpete
    Journal of Clinical Microbiology, 2001
    Co-Authors: Yasushi Furuta, S Fukuda, Fumio Ohtani, Hirofumi Sawa, Yukio Inuyama
    Abstract:

    Varicella-Zoster virus (VZV) reactivation causes facial nerve palsy in Ramsay Hunt syndrome (RHS) and Zoster Sine Herpete (ZSH) with and without Zoster rash, respectively. In the present study, we analyzed the VZV DNA copy number in saliva samples from 25 patients with RHS and 31 patients with ZSH using a TaqMan PCR assay to determine differences in the viral load between the two diseases. VZV copy number in saliva peaked near the day of the appearance of Zoster in patients with RHS. Consequently, VZV DNA was less frequently detected in patients with RHS who exhibited facial palsy several days after the appearance of Zoster. These findings suggest that the VZV load in saliva samples reflects the kinetics of viral reactivation in patients with RHS. In addition, VZV DNA was equally detected in saliva from patients with RHS and ZSH, and there was no significant difference in the highest viral copy number between patients with RHS and those with ZSH. The VZV load does not appear to reflect a major difference between RHS and ZSH.

  • early diagnosis of Zoster Sine Herpete and antiviral therapy for the treatment of facial palsy
    Neurology, 2000
    Co-Authors: Yasushi Furuta, S Fukuda, Fumio Ohtani, Yasushi Mesuda, Yukio Inuyama
    Abstract:

    The effect of antiviral agents on recovery from facial palsy in patients with Zoster Sine Herpete (ZSH; varicella Zoster virus reactivation without Zoster) has not been evaluated because ZSH is difficult to diagnose early after onset. In this study, all 13 patients who received acyclovir-prednisone treatment within 7 days of onset, as confirmed by a positive PCR result, showed complete recovery. PCR-based early diagnosis of ZSH and antiviral therapy elicited an excellent outcome for recovery from facial palsy due to ZSH.

  • detection of varicella Zoster virus dna in patients with acute peripheral facial palsy by the polymerase chain reaction and its use for early diagnosis of Zoster Sine Herpete
    Journal of Medical Virology, 1997
    Co-Authors: Yasushi Furuta, S Fukuda, Seigo Suzuki, Tsuyoshi Takasu, Yukio Inuyama, Kazuro Nagashima
    Abstract:

    Varicella-Zoster virus (VZV) reactivation without cutaneous vesicles (Zoster Sine Herpete) has been demonstrated in 8 to 25% of patients with acute peripheral facial palsy (APFP) by serological methods. To make an early diagnosis of Zoster Sine Herpete, VZV DNA in oropharyngeal swabs from patients with APFP was examined by the polymerase chain reaction (PCR). VZV DNA was detected in oropharyngeal swabs from 6 of 36 (17%) patients with APFP by PCR. VZV DNA was detected in the oropharyngeal swabs from the six patients at their initial visit (2 to 4 days after the onset of APFP), while the anti-VZV IgM and IgG antibody titers were not increased significantly. In contrast, VZV DNA was undetectable in the oropharyngeal swabs at the time when the VZV specific antibody response appeared. These results indicate that detection of VZV DNA in oropharyngeal swabs by PCR is more useful than currently available serological assays for the early diagnosis of Zoster Sine Herpete in patients with APFP.

Yukio Inuyama - One of the best experts on this subject based on the ideXlab platform.

  • quantitation of varicella Zoster virus dna in patients with ramsay hunt syndrome and Zoster Sine Herpete
    Journal of Clinical Microbiology, 2001
    Co-Authors: Yasushi Furuta, S Fukuda, Fumio Ohtani, Hirofumi Sawa, Yukio Inuyama
    Abstract:

    Varicella-Zoster virus (VZV) reactivation causes facial nerve palsy in Ramsay Hunt syndrome (RHS) and Zoster Sine Herpete (ZSH) with and without Zoster rash, respectively. In the present study, we analyzed the VZV DNA copy number in saliva samples from 25 patients with RHS and 31 patients with ZSH using a TaqMan PCR assay to determine differences in the viral load between the two diseases. VZV copy number in saliva peaked near the day of the appearance of Zoster in patients with RHS. Consequently, VZV DNA was less frequently detected in patients with RHS who exhibited facial palsy several days after the appearance of Zoster. These findings suggest that the VZV load in saliva samples reflects the kinetics of viral reactivation in patients with RHS. In addition, VZV DNA was equally detected in saliva from patients with RHS and ZSH, and there was no significant difference in the highest viral copy number between patients with RHS and those with ZSH. The VZV load does not appear to reflect a major difference between RHS and ZSH.

  • early diagnosis of Zoster Sine Herpete and antiviral therapy for the treatment of facial palsy
    Neurology, 2000
    Co-Authors: Yasushi Furuta, S Fukuda, Fumio Ohtani, Yasushi Mesuda, Yukio Inuyama
    Abstract:

    The effect of antiviral agents on recovery from facial palsy in patients with Zoster Sine Herpete (ZSH; varicella Zoster virus reactivation without Zoster) has not been evaluated because ZSH is difficult to diagnose early after onset. In this study, all 13 patients who received acyclovir-prednisone treatment within 7 days of onset, as confirmed by a positive PCR result, showed complete recovery. PCR-based early diagnosis of ZSH and antiviral therapy elicited an excellent outcome for recovery from facial palsy due to ZSH.

  • detection of varicella Zoster virus dna in patients with acute peripheral facial palsy by the polymerase chain reaction and its use for early diagnosis of Zoster Sine Herpete
    Journal of Medical Virology, 1997
    Co-Authors: Yasushi Furuta, S Fukuda, Seigo Suzuki, Tsuyoshi Takasu, Yukio Inuyama, Kazuro Nagashima
    Abstract:

    Varicella-Zoster virus (VZV) reactivation without cutaneous vesicles (Zoster Sine Herpete) has been demonstrated in 8 to 25% of patients with acute peripheral facial palsy (APFP) by serological methods. To make an early diagnosis of Zoster Sine Herpete, VZV DNA in oropharyngeal swabs from patients with APFP was examined by the polymerase chain reaction (PCR). VZV DNA was detected in oropharyngeal swabs from 6 of 36 (17%) patients with APFP by PCR. VZV DNA was detected in the oropharyngeal swabs from the six patients at their initial visit (2 to 4 days after the onset of APFP), while the anti-VZV IgM and IgG antibody titers were not increased significantly. In contrast, VZV DNA was undetectable in the oropharyngeal swabs at the time when the VZV specific antibody response appeared. These results indicate that detection of VZV DNA in oropharyngeal swabs by PCR is more useful than currently available serological assays for the early diagnosis of Zoster Sine Herpete in patients with APFP.

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

  • reactivation of type 1 herpes simplex virus and varicella Zoster virus in an immunosuppressed patient with acute peripheral facial weakness
    Journal of the Neurological Sciences, 2012
    Co-Authors: Jean Tsai, Randall J Cohrs, M Nagel, Ravi Mahalingam, Scott D Schmid, Alexander Choe, Donald H Gilden
    Abstract:

    We describe a 26-year-old man treated with azathioprine for myasthenia gravis who developed acute left-sided peripheral facial weakness. Brain magnetic resonance imaging (MRI) revealed enhancement in the left geniculate ganglion and in the intracanalicular and tympanic segments of the facial nerve. Analysis of cerebrospinal fluid (CSF) and serum revealed intrathecal synthesis of anti-varicella Zoster virus (VZV) IgG antibody. Although previous analyses of saliva, blood mononuclear cells, serum antibodies, middle ear fluid, and auricular and geniculate zone skin scrapings have shown that a small but definite proportion of patients with idiopathic peripheral facial palsy ("Bell's palsy") have the Ramsay Hunt syndrome Zoster Sine Herpete (RHS ZSH), this is the first confirmation of RHS ZSH by intrathecal synthesis of anti-VZV IgG antibody. In addition, herpes simplex virus (HSV)-1 DNA was found in saliva of the patient on 3 consecutive days. Simultaneous reactivation of two alphaherpesviruses (HSV-1 and VZV) in our immunosuppressed patient underscores the need to consider opportunistic infection as a cause of facial weakness.

  • subclinical reactivation of varicella Zoster virus in all stages of hiv infection
    Journal of the Neurological Sciences, 2011
    Co-Authors: Marius Birlea, Scott D Schmid, Donald H Gilden, G Arendt, Eser Orhan, William J Bellini, Christian Schmidt, Randall J Cohrs
    Abstract:

    Analysis of 200 paired serum and cerebrospinal fluid (CSF) samples from 180 HIV-positive individuals, 136 of whom had AIDS, revealed intrathecal synthesis of antibodies specific for varicella Zoster virus (VZV) in 28 (16%) individuals, measles virus in 15 (8%), herpes simplex virus-1 (HSV-1) in 1 (0.6%), and HSV-2 in none. Of the 28 subjects with a positive VZV antibody specificity index, only 1 had Zoster rash at the time of serum and CSF sampling; of the total 180 HIV-positive subjects, 146 (81%) had no history of Zoster. Based on an estimated 33.4 million HIV-positive individuals worldwide, subclinical reactivation of VZV in even less than 16% of HIV-positive people suggests the possibility that millions of people have active VZV infection of the central nervous system. In cases of VZV vasculopathy, myelopathy and even Zoster Sine Herpete, the CSF is often positive for anti-VZV antibody, but negative for VZV DNA. To rule out VZV infection of the nervous system, CSF must be tested for VZV DNA and anti-VZV IgG and IgM antibody.

  • Zoster Sine Herpete virologic verification by detection of anti vzv igg antibody in csf
    Neurology, 2011
    Co-Authors: D T Blumenthal, Randall J Cohrs, M Nagel, Ravi Mahalingam, E Shachamshmueli, Felix Bokstein, D S Schmid, Donald H Gilden
    Abstract:

    Classic Zoster Sine Herpete (ZSH) is defined clinically as dermatomal distribution pain without rash. ZSH was designated as a nosologic entity based on virologic confirmation in 3 men over age 60 with chronic thoracic-distribution radicular pain, with amplifiable varicella Zoster virus (VZV) DNA found in CSF of the first 2 patients1 and in blood mononuclear cells (MNCs) in the third patient.2 Herein, we describe a patient who developed radicular pain without rash in the same dermatome as his initial cervical-distribution Zoster episode, but with a remarkably prolonged interval between episodes, and in whom ZSH was virologically confirmed by the detection of anti-VZV immunoglobulin G (IgG) antibody in CSF with serum/CSF ratios indicative of intrathecal antibody synthesis. ### Case report. In 2008, a 77-year-old man developed right C8-distribution Zoster; he was not treated with an antiviral agent or steroids and his rash and pain resolved completely. One year later, …

  • neurological disease produced by varicella Zoster virus reactivation without rash
    Current Topics in Microbiology and Immunology, 2010
    Co-Authors: Donald H Gilden, Randall J Cohrs, Ravi Mahalingam, M Nagel
    Abstract:

    Reactivation of varicella Zoster virus (VZV) from latently infected human ganglia usually produces herpes Zoster (shingles), characterized by dermatomal distribution pain and rash. Zoster is often followed by chronic pain (postherpetic neuralgia or PHN) as well as meningitis or meningoencephalitis, cerebellitis, isolated cranial nerve palsies that produce ophthalmoplegia or the Ramsay Hunt syndrome, multiple cranial nerve palsies (polyneuritis cranialis), vasculopathy, myelopathy, and various inflammatory disorders of the eye. Importantly, VZV reactivation can produce chronic radicular pain without rash (Zoster Sine Herpete), as well as all the neurological disorders listed above without rash. The protean neurological and ocular disorders produced by VZV in the absence of rash are a challenge to the practicing clinician. The presentation of these conditions varies from acute to subacute to chronic. Virological confirmation requires the demonstration of amplifiable VZV DNA in cerebrospinal fluid (CSF) or in blood mononuclear cells, or the presence of anti-VZV IgG antibody in CSF or of anti-VZV IgM antibody in CSF or serum.

  • vzv vasculopathy and postherpetic neuralgia progress and perspective on antiviral therapy
    Neurology, 2005
    Co-Authors: Donald H Gilden, Randall J Cohrs, Ravi Mahalingam
    Abstract:

    Two serious complications of varicella-Zoster virus (VZV) reactivation are vasculopathy and postherpetic neuralgia (PHN). Clinical-virologic analyses have proven that VZV vasculopathy is caused by chronic active virus infection in cerebral arteries. Conclusive evidence that PHN is caused by persistent or productive VZV infection is less compelling because human ganglia are not accessible during life for pathologic and virologic examination. However, the notion that PHN may reflect a smoldering VZV ganglionitis is supported by 1) the detection of VZV DNA and proteins in peripheral blood mononuclear cells of many patients with PHN; 2) studies of multiple patients with Zoster Sine Herpete, which indicate a productive VZV ganglionitis; and 3) a favorable response of some patients with Zoster Sine Herpete and PHN to antiviral treatment. Few studies have used antiviral therapy to manage PHN with conflicting results. Larger, double-blind studies, which give IV antiviral drug, are needed.