The Experts below are selected from a list of 204 Experts worldwide ranked by ideXlab platform
Thomas Brandt - One of the best experts on this subject based on the ideXlab platform.
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Prevalence and distribution of HSV‐1, VZV, and HHV‐6 in human Cranial Nerve Nuclei III, IV, VI, VII, and XII
Journal of Medical Virology, 2020Co-Authors: Diethilde Theil, Anja K E Horn, Tobias Derfuss, Michael Strupp, V Arbusow, Thomas BrandtAbstract:The etiology of idiopathic Cranial Nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding Nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in Nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) Nuclei] and in Nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) Nuclei] of five human brainstems. Samples of the Cranial Nerve Nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic Cranial Nerve palsies. HSV-1 was distributed at random in all Cranial Nerve Nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic Cranial Nerve palsies result from viral reactivation in the brainstem Nuclei. J. Med. Virol. 74:102–106, 2004. © 2004 Wiley-Liss, Inc.
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prevalence and distribution of hsv 1 vzv and hhv 6 in human Cranial Nerve Nuclei iii iv vi vii and xii
Journal of Medical Virology, 2004Co-Authors: Diethilde Theil, Anja K E Horn, Tobias Derfuss, Michael Strupp, V Arbusow, Thomas BrandtAbstract:The etiology of idiopathic Cranial Nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding Nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in Nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) Nuclei] and in Nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) Nuclei] of five human brainstems. Samples of the Cranial Nerve Nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic Cranial Nerve palsies. HSV-1 was distributed at random in all Cranial Nerve Nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic Cranial Nerve palsies result from viral reactivation in the brainstem Nuclei. J. Med. Virol. 74:102–106, 2004. © 2004 Wiley-Liss, Inc.
Diethilde Theil - One of the best experts on this subject based on the ideXlab platform.
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Prevalence and distribution of HSV‐1, VZV, and HHV‐6 in human Cranial Nerve Nuclei III, IV, VI, VII, and XII
Journal of Medical Virology, 2020Co-Authors: Diethilde Theil, Anja K E Horn, Tobias Derfuss, Michael Strupp, V Arbusow, Thomas BrandtAbstract:The etiology of idiopathic Cranial Nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding Nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in Nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) Nuclei] and in Nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) Nuclei] of five human brainstems. Samples of the Cranial Nerve Nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic Cranial Nerve palsies. HSV-1 was distributed at random in all Cranial Nerve Nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic Cranial Nerve palsies result from viral reactivation in the brainstem Nuclei. J. Med. Virol. 74:102–106, 2004. © 2004 Wiley-Liss, Inc.
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prevalence and distribution of hsv 1 vzv and hhv 6 in human Cranial Nerve Nuclei iii iv vi vii and xii
Journal of Medical Virology, 2004Co-Authors: Diethilde Theil, Anja K E Horn, Tobias Derfuss, Michael Strupp, V Arbusow, Thomas BrandtAbstract:The etiology of idiopathic Cranial Nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding Nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in Nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) Nuclei] and in Nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) Nuclei] of five human brainstems. Samples of the Cranial Nerve Nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic Cranial Nerve palsies. HSV-1 was distributed at random in all Cranial Nerve Nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic Cranial Nerve palsies result from viral reactivation in the brainstem Nuclei. J. Med. Virol. 74:102–106, 2004. © 2004 Wiley-Liss, Inc.
Haim Sohmer - One of the best experts on this subject based on the ideXlab platform.
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contribution of the eighth Nerve and Cranial Nerve Nuclei to the short latency vestibular evoked potentials in cats
Otolaryngology-Head and Neck Surgery, 1997Co-Authors: Gang Li, Josef Elidan, Yulia Meyler, Haim SohmerAbstract:Abstract The object of this study was to assess the contributions of the vestibular Nerve and various Cranial Nerve Nuclei to the short-latency vestibular evoked potentials in cat. The following Nuclei were investigated: vestibular Nuclei and the third, sixth, and tenth Cranial Nerve Nuclei. In unilateral labyrinthectomized cats, we performed suboccipital craniectomy and partial cerebellectomy to place bipolar electrodes into the neural structures under investigation. The surface-recorded vestibular evoked potentials (far field) were compared with the potentials recorded intraCranially in response to the same acceleration impulses. The exact locations were later confirmed histologically. Reversible lesions also were induced by injection of lidocaine 2%. The results indicate that the first wave of the vestibular evoked potentials originates in the vestibular Nerve, and the second wave is mainly generated in the superior and medial vestibular Nuclei. The third, sixth, and tenth Cranial Nerve Nuclei apparently contribute to the later waves of the vestibular evoked potentials, particularly waves 3 and 4. (Otolaryngol Head Neck Surg 1997;116:181-8.)
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the contribution of Cranial Nerve Nuclei to the short latency vestibular evoked potentials in cat
Acta Oto-laryngologica, 1995Co-Authors: Josef Elidan, Gang Li, Haim SohmerAbstract:The object of this study was to assess the contributions of various Cranial Nerve Nuclei to the short latency vestibular evoked potentials (VsEPs) in cat. The following Nuclei were investigated: vestibular Nuclei, and 3rd, 6th and 10th Cranial Nerve Nuclei. In unilateral labyrinthectomized cats, suboccipital craniectomy and partial cerebellectomy were carried out in order to place bipolar electrodes into the neural structures under investigation. The surface recorded VsEPs (far-field) were compared with the potentials recorded intraCranially in response to the same acceleration impulses. The exact locations were later confirmed histologically. Reversible lesions also were induced by injecting of lignocaine 2%. The results indicate that the 2nd wave (P2) is mainly generated in the superior and medial vestibular Nuclei. The 3rd, 6th and 10th Cranial Nerve Nuclei apparently contribute to the later waves of the VsEPs, particularly P3 and P4
Michael Strupp - One of the best experts on this subject based on the ideXlab platform.
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Prevalence and distribution of HSV‐1, VZV, and HHV‐6 in human Cranial Nerve Nuclei III, IV, VI, VII, and XII
Journal of Medical Virology, 2020Co-Authors: Diethilde Theil, Anja K E Horn, Tobias Derfuss, Michael Strupp, V Arbusow, Thomas BrandtAbstract:The etiology of idiopathic Cranial Nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding Nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in Nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) Nuclei] and in Nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) Nuclei] of five human brainstems. Samples of the Cranial Nerve Nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic Cranial Nerve palsies. HSV-1 was distributed at random in all Cranial Nerve Nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic Cranial Nerve palsies result from viral reactivation in the brainstem Nuclei. J. Med. Virol. 74:102–106, 2004. © 2004 Wiley-Liss, Inc.
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prevalence and distribution of hsv 1 vzv and hhv 6 in human Cranial Nerve Nuclei iii iv vi vii and xii
Journal of Medical Virology, 2004Co-Authors: Diethilde Theil, Anja K E Horn, Tobias Derfuss, Michael Strupp, V Arbusow, Thomas BrandtAbstract:The etiology of idiopathic Cranial Nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding Nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in Nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) Nuclei] and in Nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) Nuclei] of five human brainstems. Samples of the Cranial Nerve Nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic Cranial Nerve palsies. HSV-1 was distributed at random in all Cranial Nerve Nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic Cranial Nerve palsies result from viral reactivation in the brainstem Nuclei. J. Med. Virol. 74:102–106, 2004. © 2004 Wiley-Liss, Inc.
V Arbusow - One of the best experts on this subject based on the ideXlab platform.
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Prevalence and distribution of HSV‐1, VZV, and HHV‐6 in human Cranial Nerve Nuclei III, IV, VI, VII, and XII
Journal of Medical Virology, 2020Co-Authors: Diethilde Theil, Anja K E Horn, Tobias Derfuss, Michael Strupp, V Arbusow, Thomas BrandtAbstract:The etiology of idiopathic Cranial Nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding Nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in Nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) Nuclei] and in Nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) Nuclei] of five human brainstems. Samples of the Cranial Nerve Nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic Cranial Nerve palsies. HSV-1 was distributed at random in all Cranial Nerve Nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic Cranial Nerve palsies result from viral reactivation in the brainstem Nuclei. J. Med. Virol. 74:102–106, 2004. © 2004 Wiley-Liss, Inc.
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prevalence and distribution of hsv 1 vzv and hhv 6 in human Cranial Nerve Nuclei iii iv vi vii and xii
Journal of Medical Virology, 2004Co-Authors: Diethilde Theil, Anja K E Horn, Tobias Derfuss, Michael Strupp, V Arbusow, Thomas BrandtAbstract:The etiology of idiopathic Cranial Nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding Nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in Nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) Nuclei] and in Nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) Nuclei] of five human brainstems. Samples of the Cranial Nerve Nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic Cranial Nerve palsies. HSV-1 was distributed at random in all Cranial Nerve Nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic Cranial Nerve palsies result from viral reactivation in the brainstem Nuclei. J. Med. Virol. 74:102–106, 2004. © 2004 Wiley-Liss, Inc.