The Experts below are selected from a list of 243 Experts worldwide ranked by ideXlab platform

Masoumeh Jorjani - One of the best experts on this subject based on the ideXlab platform.

  • aromatase inhibition exacerbates Pain and reactive gliosis in the dorsal horn of the spinal cord of female rats caused by spinothalamic tract injury
    Endocrinology, 2014
    Co-Authors: Samar Ghorbanpoor, Ali Haerirohani, Luis M Garciasegura, Fariba Khodagholi, Masoumeh Jorjani
    Abstract:

    Central Pain Syndrome is characterized by severe and excruciating Pain resulting from a lesion in the Central nervous system. Previous studies have shown that estradiol decreases Pain and that inhibitors of the enzyme aromatase, which synthesizes estradiol from aromatizable androgens, increases Pain sensitivity. In this study we have assessed whether aromatase expression in the dorsal horns of the spinal cord is altered in a rat model of Central Pain Syndrome, induced by the unilateral electrolytic lesion of the spinothalamic tract. Protein and mRNA levels of aromatase, as well as the protein and mRNA levels of estrogen receptors α and β, were increased in the dorsal horn of female rats after spinothalamic tract injury, suggesting that the injury increased estradiol synthesis and signaling in the dorsal horn. To determine whether the increased aromatase expression in this Pain model may participate in the control of Pain, mechanical allodynia thresholds were determined in both hind paws after the intrathe...

  • Role of Microglia and Astrocyte in Central Pain Syndrome Following Electrolytic Lesion at the Spinothalamic Tract in Rats
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Kobra Naseri, Elham Saghaei, Fatemeh Abbaszadeh, Mina Afhami, Ali Haeri, Farzaneh Rahimi, Masoumeh Jorjani
    Abstract:

    Central Pain Syndrome (CPS) is a debilitating state and one of the consequences of spinal cord injury in patients. Many pathophysiological aspects of CPS are not well documented. Spinal glia activation has been identified as a key factor in the sensory component of chronic Pain. In this study, the role of glial subtypes in the process of CPS induced by unilateral electrolytic lesion of spinothalamic tract (STT) is investigated. Male rats received a laminectomy at T8–T9 and then unilateral electrolytic lesion centered on the STT. Thermal and mechanical thresholds as well as locomotor function were measured on days 0, 3, 7, 14, 21, and 28 post-injuries by tail flick, von Frey filament, and open field tests, respectively. To investigate the spinal glial activation following denervation in STT-lesioned groups, Iba1 and GFAP were detected by immunohistochemistry and Western blotting at the same time points. Data showed that STT lesion significantly decreased thermal Pain at day 3 in comparison with sham groups. Significant bilateral allodynia appeared in hind paws at day 14 after spinal cord injury and continued to day 28 ( P  

  • role of microglia and astrocyte in Central Pain Syndrome following electrolytic lesion at the spinothalamic tract in rats
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Kobra Naseri, Elham Saghaei, Fatemeh Abbaszadeh, Mina Afhami, Ali Haeri, Farzaneh Rahimi, Masoumeh Jorjani
    Abstract:

    Central Pain Syndrome (CPS) is a debilitating state and one of the consequences of spinal cord injury in patients. Many pathophysiological aspects of CPS are not well documented. Spinal glia activation has been identified as a key factor in the sensory component of chronic Pain. In this study, the role of glial subtypes in the process of CPS induced by unilateral electrolytic lesion of spinothalamic tract (STT) is investigated. Male rats received a laminectomy at T8–T9 and then unilateral electrolytic lesion centered on the STT. Thermal and mechanical thresholds as well as locomotor function were measured on days 0, 3, 7, 14, 21, and 28 post-injuries by tail flick, von Frey filament, and open field tests, respectively. To investigate the spinal glial activation following denervation in STT-lesioned groups, Iba1 and GFAP were detected by immunohistochemistry and Western blotting at the same time points. Data showed that STT lesion significantly decreased thermal Pain at day 3 in comparison with sham groups. Significant bilateral allodynia appeared in hind paws at day 14 after spinal cord injury and continued to day 28 (P < 0.05). Additionally, electrolytic spinal lesion attenuated locomotor function of injured animals after 7 days (P < 0.05). In both histological assessments and Western blotting, Iba1 increased at days 3 and 7 while increased GFAP occurred from day 14 to 28 after lesion. It appears that microglial activation is important in the early stages of Pain development and astrocytic activation occurs later. These events may lead to behavioral outcomes especially Central neuropathic Pain.

  • Estradiol attenuates spinal cord injury-induced Pain by suppressing microglial activation in thalamic VPL nuclei of rats.
    Neuroscience research, 2013
    Co-Authors: Elham Saghaei, Samar Ghorbanpoor, Kobra Naseri, Fatemeh Abbaszadeh, Mina Afhami, Ali Haeri, Farzaneh Rahimi, Masoumeh Jorjani
    Abstract:

    In our previous study we showed that Central Pain Syndrome (CPS) induced by electrolytic injury caused in the unilateral spinothalamic tract (STT) is a concomitant of glial alteration at the site of injury. Here, we investigated the activity of glial cells in thalamic ventral posterolateral nuclei (VPL) and their contribution to CPS. We also examined whether post-injury administration of a pharmacological dose of estradiol can attenuate CPS and associated molecular changes. Based on the results,in the ipsilateral VPL the microglial phenotype switched o hyperactive mode and Iba1 expression was increased significantly on days 21 and 28 post-injury. The same feature was observed in contralateral VPL on day 28 (P

Sergio Canavero - One of the best experts on this subject based on the ideXlab platform.

Vincenzo Bonicalzi - One of the best experts on this subject based on the ideXlab platform.

  • Central Pain Syndrome
    2018
    Co-Authors: Sergio Canavero, Vincenzo Bonicalzi
    Abstract:

    Central Pain Syndrome (CPS) is a neurological condition caused by damage specifically to the Central nervous system brain, brainstem, or spinal cord. This is the only up-to-date book available on the clinical aspects (including diagnosis and therapy) of CPS management. The authors have developed a complete reference source on Central Pain, which includes background material, the pathophysiology of the Syndrome, and diagnostic and therapeutic information. The Syndrome has been a medical mystery for 100 years with no effective cure; this book turns the concept of incurability of Central Pain on its head, providing a rational approach to therapy based on a scientific theory.

  • Central Pain Syndrome: Pathophysiology, Diagnosis and Management
    2007
    Co-Authors: Sergio Canavero, Vincenzo Bonicalzi
    Abstract:

    1. Introduction 2. Central Pain of brain origin 3. Central Pain of cord origin 4. Diagnosing Central Pain 5. Drug therapy 6. Neuromodulation 7. Pathophysiology 8. Piecing together the evidence.

  • Comprar Central Pain Syndrome | Sergio Canavero | 9780521866927 | Cambridge University Press
    2007
    Co-Authors: Sergio Canavero, Vincenzo Bonicalzi
    Abstract:

    Tienda online donde Comprar Central Pain Syndrome al precio 67,69 € de Sergio Canavero | Vincenzo Bonicalzi, tienda de Libros de Medicina, Libros de Anestesiologia, Dolor y Reanimacion - Dolor

  • comprar Central Pain Syndrome sergio canavero 9780521866927 cambridge university press
    2007
    Co-Authors: Sergio Canavero, Vincenzo Bonicalzi
    Abstract:

    Tienda online donde Comprar Central Pain Syndrome al precio 67,69 € de Sergio Canavero | Vincenzo Bonicalzi, tienda de Libros de Medicina, Libros de Anestesiologia, Dolor y Reanimacion - Dolor

  • Central Pain Syndrome: elucidation of genesis and treatment
    Expert review of neurotherapeutics, 2007
    Co-Authors: Sergio Canavero, Vincenzo Bonicalzi
    Abstract:

    Central Pain (CP), namely, Pain or allied symptoms that follow damage to the CNS, has remained an obscure neurological Syndrome with no explanation or effective treatment since Edinger's description in 1891. Once believed to be rare, CP is now known to affect several millions of people worldwide, making it at least as frequent as, for example, Parkinson's disease. It follows such common entities as stroke, spinal cord injury and multiple sclerosis, but also many other conditions, including neurosurgical procedures on the brain and spine. A disturbance of thalamocortical transmission is now acknowledged to be the main engine of CP. When drugs fail, neuromodulation, both electrical and chemical, provide relief to many drug nonresponders. A small stereotactic lesion deep in the subparietal white matter promises complete relief, without the ravages of neuroablation as performed widely in the past.

Elham Saghaei - One of the best experts on this subject based on the ideXlab platform.

  • Role of Microglia and Astrocyte in Central Pain Syndrome Following Electrolytic Lesion at the Spinothalamic Tract in Rats
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Kobra Naseri, Elham Saghaei, Fatemeh Abbaszadeh, Mina Afhami, Ali Haeri, Farzaneh Rahimi, Masoumeh Jorjani
    Abstract:

    Central Pain Syndrome (CPS) is a debilitating state and one of the consequences of spinal cord injury in patients. Many pathophysiological aspects of CPS are not well documented. Spinal glia activation has been identified as a key factor in the sensory component of chronic Pain. In this study, the role of glial subtypes in the process of CPS induced by unilateral electrolytic lesion of spinothalamic tract (STT) is investigated. Male rats received a laminectomy at T8–T9 and then unilateral electrolytic lesion centered on the STT. Thermal and mechanical thresholds as well as locomotor function were measured on days 0, 3, 7, 14, 21, and 28 post-injuries by tail flick, von Frey filament, and open field tests, respectively. To investigate the spinal glial activation following denervation in STT-lesioned groups, Iba1 and GFAP were detected by immunohistochemistry and Western blotting at the same time points. Data showed that STT lesion significantly decreased thermal Pain at day 3 in comparison with sham groups. Significant bilateral allodynia appeared in hind paws at day 14 after spinal cord injury and continued to day 28 ( P  

  • role of microglia and astrocyte in Central Pain Syndrome following electrolytic lesion at the spinothalamic tract in rats
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Kobra Naseri, Elham Saghaei, Fatemeh Abbaszadeh, Mina Afhami, Ali Haeri, Farzaneh Rahimi, Masoumeh Jorjani
    Abstract:

    Central Pain Syndrome (CPS) is a debilitating state and one of the consequences of spinal cord injury in patients. Many pathophysiological aspects of CPS are not well documented. Spinal glia activation has been identified as a key factor in the sensory component of chronic Pain. In this study, the role of glial subtypes in the process of CPS induced by unilateral electrolytic lesion of spinothalamic tract (STT) is investigated. Male rats received a laminectomy at T8–T9 and then unilateral electrolytic lesion centered on the STT. Thermal and mechanical thresholds as well as locomotor function were measured on days 0, 3, 7, 14, 21, and 28 post-injuries by tail flick, von Frey filament, and open field tests, respectively. To investigate the spinal glial activation following denervation in STT-lesioned groups, Iba1 and GFAP were detected by immunohistochemistry and Western blotting at the same time points. Data showed that STT lesion significantly decreased thermal Pain at day 3 in comparison with sham groups. Significant bilateral allodynia appeared in hind paws at day 14 after spinal cord injury and continued to day 28 (P < 0.05). Additionally, electrolytic spinal lesion attenuated locomotor function of injured animals after 7 days (P < 0.05). In both histological assessments and Western blotting, Iba1 increased at days 3 and 7 while increased GFAP occurred from day 14 to 28 after lesion. It appears that microglial activation is important in the early stages of Pain development and astrocytic activation occurs later. These events may lead to behavioral outcomes especially Central neuropathic Pain.

  • Estradiol attenuates spinal cord injury-induced Pain by suppressing microglial activation in thalamic VPL nuclei of rats.
    Neuroscience research, 2013
    Co-Authors: Elham Saghaei, Samar Ghorbanpoor, Kobra Naseri, Fatemeh Abbaszadeh, Mina Afhami, Ali Haeri, Farzaneh Rahimi, Masoumeh Jorjani
    Abstract:

    In our previous study we showed that Central Pain Syndrome (CPS) induced by electrolytic injury caused in the unilateral spinothalamic tract (STT) is a concomitant of glial alteration at the site of injury. Here, we investigated the activity of glial cells in thalamic ventral posterolateral nuclei (VPL) and their contribution to CPS. We also examined whether post-injury administration of a pharmacological dose of estradiol can attenuate CPS and associated molecular changes. Based on the results,in the ipsilateral VPL the microglial phenotype switched o hyperactive mode and Iba1 expression was increased significantly on days 21 and 28 post-injury. The same feature was observed in contralateral VPL on day 28 (P

Kobra Naseri - One of the best experts on this subject based on the ideXlab platform.

  • Role of Microglia and Astrocyte in Central Pain Syndrome Following Electrolytic Lesion at the Spinothalamic Tract in Rats
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Kobra Naseri, Elham Saghaei, Fatemeh Abbaszadeh, Mina Afhami, Ali Haeri, Farzaneh Rahimi, Masoumeh Jorjani
    Abstract:

    Central Pain Syndrome (CPS) is a debilitating state and one of the consequences of spinal cord injury in patients. Many pathophysiological aspects of CPS are not well documented. Spinal glia activation has been identified as a key factor in the sensory component of chronic Pain. In this study, the role of glial subtypes in the process of CPS induced by unilateral electrolytic lesion of spinothalamic tract (STT) is investigated. Male rats received a laminectomy at T8–T9 and then unilateral electrolytic lesion centered on the STT. Thermal and mechanical thresholds as well as locomotor function were measured on days 0, 3, 7, 14, 21, and 28 post-injuries by tail flick, von Frey filament, and open field tests, respectively. To investigate the spinal glial activation following denervation in STT-lesioned groups, Iba1 and GFAP were detected by immunohistochemistry and Western blotting at the same time points. Data showed that STT lesion significantly decreased thermal Pain at day 3 in comparison with sham groups. Significant bilateral allodynia appeared in hind paws at day 14 after spinal cord injury and continued to day 28 ( P  

  • role of microglia and astrocyte in Central Pain Syndrome following electrolytic lesion at the spinothalamic tract in rats
    Journal of Molecular Neuroscience, 2013
    Co-Authors: Kobra Naseri, Elham Saghaei, Fatemeh Abbaszadeh, Mina Afhami, Ali Haeri, Farzaneh Rahimi, Masoumeh Jorjani
    Abstract:

    Central Pain Syndrome (CPS) is a debilitating state and one of the consequences of spinal cord injury in patients. Many pathophysiological aspects of CPS are not well documented. Spinal glia activation has been identified as a key factor in the sensory component of chronic Pain. In this study, the role of glial subtypes in the process of CPS induced by unilateral electrolytic lesion of spinothalamic tract (STT) is investigated. Male rats received a laminectomy at T8–T9 and then unilateral electrolytic lesion centered on the STT. Thermal and mechanical thresholds as well as locomotor function were measured on days 0, 3, 7, 14, 21, and 28 post-injuries by tail flick, von Frey filament, and open field tests, respectively. To investigate the spinal glial activation following denervation in STT-lesioned groups, Iba1 and GFAP were detected by immunohistochemistry and Western blotting at the same time points. Data showed that STT lesion significantly decreased thermal Pain at day 3 in comparison with sham groups. Significant bilateral allodynia appeared in hind paws at day 14 after spinal cord injury and continued to day 28 (P < 0.05). Additionally, electrolytic spinal lesion attenuated locomotor function of injured animals after 7 days (P < 0.05). In both histological assessments and Western blotting, Iba1 increased at days 3 and 7 while increased GFAP occurred from day 14 to 28 after lesion. It appears that microglial activation is important in the early stages of Pain development and astrocytic activation occurs later. These events may lead to behavioral outcomes especially Central neuropathic Pain.

  • Estradiol attenuates spinal cord injury-induced Pain by suppressing microglial activation in thalamic VPL nuclei of rats.
    Neuroscience research, 2013
    Co-Authors: Elham Saghaei, Samar Ghorbanpoor, Kobra Naseri, Fatemeh Abbaszadeh, Mina Afhami, Ali Haeri, Farzaneh Rahimi, Masoumeh Jorjani
    Abstract:

    In our previous study we showed that Central Pain Syndrome (CPS) induced by electrolytic injury caused in the unilateral spinothalamic tract (STT) is a concomitant of glial alteration at the site of injury. Here, we investigated the activity of glial cells in thalamic ventral posterolateral nuclei (VPL) and their contribution to CPS. We also examined whether post-injury administration of a pharmacological dose of estradiol can attenuate CPS and associated molecular changes. Based on the results,in the ipsilateral VPL the microglial phenotype switched o hyperactive mode and Iba1 expression was increased significantly on days 21 and 28 post-injury. The same feature was observed in contralateral VPL on day 28 (P