The Experts below are selected from a list of 121371 Experts worldwide ranked by ideXlab platform

Albert C. Ludolph - One of the best experts on this subject based on the ideXlab platform.

  • Communicating Hydrocephalus Following Eosinophilic Meningitis Is Pathogenic for Chronic Viliuisk Encephalomyelitis in Northeastern Siberia
    2016
    Co-Authors: Er Storch, Jan Kassubek, Hayrettin Tumani, Vsevolod A. Vladimirtsev, Andreas Hermann, Vladimir L. Osakovsky, Vladimir A. Baranov, Vadim G. Krivoshapkin, Albert C. Ludolph
    Abstract:

    Background: Viliuisk encephalomyelitis (VE) is an endemic neurological disease in Northeast Siberia and generally considered to be a chronic encephalomyelitis of unknown origin actually spreading in the Sakha (Yakutian) Republic. Methodology and Principle Findings: In search for the pathophysiology and causative agent of VE, we performed a cross-sectional study on clinical, serological and neuroimaging data on chronic VE patients during two medical expeditions to three villages within the Viliuiski river basin in the Republic of Sakha in 2000 and to the capital Yakutsk in 2006. The severity of the core clinical picture with predominant sensory ataxia, gait apraxia, lower limb spasticity, cognitive impairment and bladder dysfunction correlated with the degree of MRI findings showing enlargement of inner ventricular spaces as in communicating hydrocephalus. Laboratory studies revealed transient eosinophilia during the preceding acute meningitis-like phase, but no ongoing inflammatory process in the CSF. We found immune reactions against Toxocara canis in the majority of chronic VE patients but rarely in controls (P = 0.025; Fisher’s exact test). Histological analysis of subacute to subchronic VE brain samples showed eosinophilic infiltrations with no signs of persistent Toxocara canis infection. Conclusions and Significance: Our data showed that pressure by the communicating hydrocephalus as a Mechanical Factor is the major pathogenic mechanism in chronic VE, most likely triggered by eosinophilic meningitis. There are no signs for a

  • communicating hydrocephalus following eosinophilic meningitis is pathogenic for chronic viliuisk encephalomyelitis in northeastern siberia
    PLOS ONE, 2014
    Co-Authors: Alexander Storch, Jan Kassubek, Hayrettin Tumani, Vsevolod A. Vladimirtsev, Andreas Hermann, Vladimir L. Osakovsky, Vadim G. Krivoshapkin, Vladimir Baranov, Albert C. Ludolph
    Abstract:

    Background Viliuisk encephalomyelitis (VE) is an endemic neurological disease in Northeast Siberia and generally considered to be a chronic encephalomyelitis of unknown origin actually spreading in the Sakha (Yakutian) Republic. Methodology and Principle Findings In search for the pathophysiology and causative agent of VE, we performed a cross-sectional study on clinical, serological and neuroimaging data on chronic VE patients during two medical expeditions to three villages within the Viliuiski river basin in the Republic of Sakha in 2000 and to the capital Yakutsk in 2006. The severity of the core clinical picture with predominant sensory ataxia, gait apraxia, lower limb spasticity, cognitive impairment and bladder dysfunction correlated with the degree of MRI findings showing enlargement of inner ventricular spaces as in communicating hydrocephalus. Laboratory studies revealed transient eosinophilia during the preceding acute meningitis-like phase, but no ongoing inflammatory process in the CSF. We found immune reactions against Toxocara canis in the majority of chronic VE patients but rarely in controls (P = 0.025; Fisher's exact test). Histological analysis of subacute to subchronic VE brain samples showed eosinophilic infiltrations with no signs of persistent Toxocara canis infection. Conclusions and Significance Our data showed that pressure by the communicating hydrocephalus as a Mechanical Factor is the major pathogenic mechanism in chronic VE, most likely triggered by eosinophilic meningitis. There are no signs for an ongoing inflammatory process in chronic VE. The past eosinophilic reaction in VE might be caused by Toxocara ssp. infection and might therefore represent the first hint for an initial cause leading to the development of chronic VE. Our data provide a framework for future studies and potential therapeutic interventions for this enigmatic epidemic neurological disease potentially spreading in Sakha Republic.

Isabel C N Sacco - One of the best experts on this subject based on the ideXlab platform.

  • the effects of plantar fasciitis and pain on plantar pressure distribution of recreational runners
    Clinical Biomechanics, 2011
    Co-Authors: Ana Paula Ribeiro, Francis Trombinisouza, Vitor Daniel Tessutti, Fernanda Rodrigues Lima, Silvia Maria Amado Joao, Isabel C N Sacco
    Abstract:

    article i nfo Article history: Received 14 May 2010 Accepted 20 August 2010 Background: Plantar fasciitis is the third most frequent injury in runners. Despite its high prevalence, its pathogenesis remains inconclusive. The literature reports overload as the basic mechanism for its development. However, the way that these plantar loads are distributed on the foot surface of runners with plantar fasciitis and the effects of pain on this Mechanical Factor has not yet been investigated. Therefore, the aim of this study was to evaluate and compare the plantar pressure distributions during running in runners with symptom or history of plantar fasciitis and runners without the disease. Methods: Forty-five recreational runners with plantar fasciitis (30 symptomatic and 15 with previous history of the disease) and 60 runners without plantar fasciitis (control group) were evaluated. Pain was assessed by a visual analogue scale. All runners were evaluated by means of the Pedar system insoles during running forty meters at a speed of 12(5%) km/h, using standard sport footwear. Two-way ANOVAS were employed to investigate the main and interaction effects between groups and plantar areas. Findings: No interaction effects were found for any of the investigated variables: peak pressure (P = 0.61), contact area (P = 0.38), contact time (P = 0.91), and the pressure-time integral (P =0 .50). Interpretation: These findings indicated that the patterns of plantar pressure distribution were not affected in recreational runners with plantar fasciitis when compared to control runners. Pain also did not interfere with the dynamic patterns of the plantar pressure distributions.

Alexander Storch - One of the best experts on this subject based on the ideXlab platform.

  • communicating hydrocephalus following eosinophilic meningitis is pathogenic for chronic viliuisk encephalomyelitis in northeastern siberia
    PLOS ONE, 2014
    Co-Authors: Alexander Storch, Jan Kassubek, Hayrettin Tumani, Vsevolod A. Vladimirtsev, Andreas Hermann, Vladimir L. Osakovsky, Vadim G. Krivoshapkin, Vladimir Baranov, Albert C. Ludolph
    Abstract:

    Background Viliuisk encephalomyelitis (VE) is an endemic neurological disease in Northeast Siberia and generally considered to be a chronic encephalomyelitis of unknown origin actually spreading in the Sakha (Yakutian) Republic. Methodology and Principle Findings In search for the pathophysiology and causative agent of VE, we performed a cross-sectional study on clinical, serological and neuroimaging data on chronic VE patients during two medical expeditions to three villages within the Viliuiski river basin in the Republic of Sakha in 2000 and to the capital Yakutsk in 2006. The severity of the core clinical picture with predominant sensory ataxia, gait apraxia, lower limb spasticity, cognitive impairment and bladder dysfunction correlated with the degree of MRI findings showing enlargement of inner ventricular spaces as in communicating hydrocephalus. Laboratory studies revealed transient eosinophilia during the preceding acute meningitis-like phase, but no ongoing inflammatory process in the CSF. We found immune reactions against Toxocara canis in the majority of chronic VE patients but rarely in controls (P = 0.025; Fisher's exact test). Histological analysis of subacute to subchronic VE brain samples showed eosinophilic infiltrations with no signs of persistent Toxocara canis infection. Conclusions and Significance Our data showed that pressure by the communicating hydrocephalus as a Mechanical Factor is the major pathogenic mechanism in chronic VE, most likely triggered by eosinophilic meningitis. There are no signs for an ongoing inflammatory process in chronic VE. The past eosinophilic reaction in VE might be caused by Toxocara ssp. infection and might therefore represent the first hint for an initial cause leading to the development of chronic VE. Our data provide a framework for future studies and potential therapeutic interventions for this enigmatic epidemic neurological disease potentially spreading in Sakha Republic.

Ana Paula Ribeiro - One of the best experts on this subject based on the ideXlab platform.

  • the effects of plantar fasciitis and pain on plantar pressure distribution of recreational runners
    Clinical Biomechanics, 2011
    Co-Authors: Ana Paula Ribeiro, Francis Trombinisouza, Vitor Daniel Tessutti, Fernanda Rodrigues Lima, Silvia Maria Amado Joao, Isabel C N Sacco
    Abstract:

    article i nfo Article history: Received 14 May 2010 Accepted 20 August 2010 Background: Plantar fasciitis is the third most frequent injury in runners. Despite its high prevalence, its pathogenesis remains inconclusive. The literature reports overload as the basic mechanism for its development. However, the way that these plantar loads are distributed on the foot surface of runners with plantar fasciitis and the effects of pain on this Mechanical Factor has not yet been investigated. Therefore, the aim of this study was to evaluate and compare the plantar pressure distributions during running in runners with symptom or history of plantar fasciitis and runners without the disease. Methods: Forty-five recreational runners with plantar fasciitis (30 symptomatic and 15 with previous history of the disease) and 60 runners without plantar fasciitis (control group) were evaluated. Pain was assessed by a visual analogue scale. All runners were evaluated by means of the Pedar system insoles during running forty meters at a speed of 12(5%) km/h, using standard sport footwear. Two-way ANOVAS were employed to investigate the main and interaction effects between groups and plantar areas. Findings: No interaction effects were found for any of the investigated variables: peak pressure (P = 0.61), contact area (P = 0.38), contact time (P = 0.91), and the pressure-time integral (P =0 .50). Interpretation: These findings indicated that the patterns of plantar pressure distribution were not affected in recreational runners with plantar fasciitis when compared to control runners. Pain also did not interfere with the dynamic patterns of the plantar pressure distributions.

Vadim G. Krivoshapkin - One of the best experts on this subject based on the ideXlab platform.

  • Communicating Hydrocephalus Following Eosinophilic Meningitis Is Pathogenic for Chronic Viliuisk Encephalomyelitis in Northeastern Siberia
    2016
    Co-Authors: Er Storch, Jan Kassubek, Hayrettin Tumani, Vsevolod A. Vladimirtsev, Andreas Hermann, Vladimir L. Osakovsky, Vladimir A. Baranov, Vadim G. Krivoshapkin, Albert C. Ludolph
    Abstract:

    Background: Viliuisk encephalomyelitis (VE) is an endemic neurological disease in Northeast Siberia and generally considered to be a chronic encephalomyelitis of unknown origin actually spreading in the Sakha (Yakutian) Republic. Methodology and Principle Findings: In search for the pathophysiology and causative agent of VE, we performed a cross-sectional study on clinical, serological and neuroimaging data on chronic VE patients during two medical expeditions to three villages within the Viliuiski river basin in the Republic of Sakha in 2000 and to the capital Yakutsk in 2006. The severity of the core clinical picture with predominant sensory ataxia, gait apraxia, lower limb spasticity, cognitive impairment and bladder dysfunction correlated with the degree of MRI findings showing enlargement of inner ventricular spaces as in communicating hydrocephalus. Laboratory studies revealed transient eosinophilia during the preceding acute meningitis-like phase, but no ongoing inflammatory process in the CSF. We found immune reactions against Toxocara canis in the majority of chronic VE patients but rarely in controls (P = 0.025; Fisher’s exact test). Histological analysis of subacute to subchronic VE brain samples showed eosinophilic infiltrations with no signs of persistent Toxocara canis infection. Conclusions and Significance: Our data showed that pressure by the communicating hydrocephalus as a Mechanical Factor is the major pathogenic mechanism in chronic VE, most likely triggered by eosinophilic meningitis. There are no signs for a

  • communicating hydrocephalus following eosinophilic meningitis is pathogenic for chronic viliuisk encephalomyelitis in northeastern siberia
    PLOS ONE, 2014
    Co-Authors: Alexander Storch, Jan Kassubek, Hayrettin Tumani, Vsevolod A. Vladimirtsev, Andreas Hermann, Vladimir L. Osakovsky, Vadim G. Krivoshapkin, Vladimir Baranov, Albert C. Ludolph
    Abstract:

    Background Viliuisk encephalomyelitis (VE) is an endemic neurological disease in Northeast Siberia and generally considered to be a chronic encephalomyelitis of unknown origin actually spreading in the Sakha (Yakutian) Republic. Methodology and Principle Findings In search for the pathophysiology and causative agent of VE, we performed a cross-sectional study on clinical, serological and neuroimaging data on chronic VE patients during two medical expeditions to three villages within the Viliuiski river basin in the Republic of Sakha in 2000 and to the capital Yakutsk in 2006. The severity of the core clinical picture with predominant sensory ataxia, gait apraxia, lower limb spasticity, cognitive impairment and bladder dysfunction correlated with the degree of MRI findings showing enlargement of inner ventricular spaces as in communicating hydrocephalus. Laboratory studies revealed transient eosinophilia during the preceding acute meningitis-like phase, but no ongoing inflammatory process in the CSF. We found immune reactions against Toxocara canis in the majority of chronic VE patients but rarely in controls (P = 0.025; Fisher's exact test). Histological analysis of subacute to subchronic VE brain samples showed eosinophilic infiltrations with no signs of persistent Toxocara canis infection. Conclusions and Significance Our data showed that pressure by the communicating hydrocephalus as a Mechanical Factor is the major pathogenic mechanism in chronic VE, most likely triggered by eosinophilic meningitis. There are no signs for an ongoing inflammatory process in chronic VE. The past eosinophilic reaction in VE might be caused by Toxocara ssp. infection and might therefore represent the first hint for an initial cause leading to the development of chronic VE. Our data provide a framework for future studies and potential therapeutic interventions for this enigmatic epidemic neurological disease potentially spreading in Sakha Republic.