The Experts below are selected from a list of 81 Experts worldwide ranked by ideXlab platform
Eelco F. M. Wijdicks - One of the best experts on this subject based on the ideXlab platform.
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Ultra-Early Aneurysmal Rebleeding and Brainstem Destruction
Neurocritical Care, 2012Co-Authors: Jennifer E. Fugate, Grant W. Mallory, Eelco F. M. WijdicksAbstract:Background Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, parenchymal hematoma, or seizures. Methods Case report. Results A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem parenchyma and ventricles. Conclusions Sudden clinical deterioration after SAH with coma and a fixed “blown” pupil may result from hemorrhage extension into the brainstem parenchyma rather than Oculomotor Nerve Injury from compression or stretch.
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Ultra-Early Aneurysmal Rebleeding and Brainstem Destruction
Neurocritical Care, 2011Co-Authors: Jennifer E. Fugate, Grant W. Mallory, Eelco F. M. WijdicksAbstract:Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, parenchymal hematoma, or seizures. Case report. A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem parenchyma and ventricles. Sudden clinical deterioration after SAH with coma and a fixed “blown” pupil may result from hemorrhage extension into the brainstem parenchyma rather than Oculomotor Nerve Injury from compression or stretch.
Shiting Li - One of the best experts on this subject based on the ideXlab platform.
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Electrical stimulation promotes regeneration of injured Oculomotor Nerves in dogs.
Neural Regeneration Research, 2016Co-Authors: Lei Du, Min Yang, Xuhui Wang, Shiting LiAbstract:Functional recovery after Oculomotor Nerve Injury is very poor. Electrical stimulation has been shown to promote regeneration of injured Nerves. We hypothesized that electrical stimulation would improve the functional recovery of injured Oculomotor Nerves. Oculomotor Nerve Injury models were created by crushing the right Oculomotor Nerves of adult dogs. Stimulating electrodes were positioned in both proximal and distal locations of the lesion, and non-continuous rectangular, biphasic current pulses (0.7 V, 5 Hz) were administered 1 hour daily for 2 consecutive weeks. Analysis of the results showed that electrophysiological and morphological recovery of the injured Oculomotor Nerve was enhanced, indicating that electrical stimulation improved neural regeneration. Thus, this therapy has the potential to promote the recovery of Oculomotor Nerve dysfunction.
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experimental study on the effect of electrostimulation on neural regeneration after Oculomotor Nerve Injury
Journal of Molecular Neuroscience, 2014Co-Authors: Chunmei Zhang, Min Yang, Youqiang Meng, Xuhui Wang, Zhen Li, Baohui Feng, Bo Ning, Shiting LiAbstract:The Oculomotor Nerve can regenerate anatomically and histologically after Injury; however, the degree of functional recovery of extraocular muscles and the pupil sphincter muscle was not satisfactory. Electrostimulation was one potential intervention that was increasingly being studied for use in Nerve Injury settings. However, the effect of electrostimulation on regeneration of the injured Oculomotor Nerve was still obscure. In this study, we studied the effects of electrostimulation on neural regeneration in terms of neurofunction, myoelectrophysiology, neuroanatomy, and neurohistology after Oculomotor Nerve Injury and found that electrostimulation on the injured Oculomotor Nerve enhanced the speed and final level of its functional and electrophysiological recovery, promoted neural regeneration, and enhanced the selectivity and specificity of reinnervation of the regenerated neuron, the conformity among the electrophysiological and functional recovery of extraocular muscles, and neural regeneration, and that the function of extraocular muscles recovered slower than electrophysiology. Thus, we speculated that electrostimulation on the injured Oculomotor Nerve produced a marked effect on all phases of neural regeneration including neuronal survival, sprout formation, axonal elongation, target reconnection, and synaptogenesis. We think that neural electrostimulation can be used in Oculomotor Nerve Injury.
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Oculomotor Nerve Injury induces nuerogenesis in the Oculomotor and edinger westphal nucleus of adult dog
Journal of Molecular Neuroscience, 2013Co-Authors: Chunmei Zhang, Min Yang, Youqiang Meng, Xuhui Wang, Zhen Li, Baohui Feng, Bo Ning, Shiting LiAbstract:Technical developments have extensively promoted experimental and clinical studies on cranial Nerve regeneration, but intracranial Nerve recovery is still an unexplored research area compared to peripheral Nerve repair. In this study, we researched whether neurogenesis occurs in adult Oculomotor (OMN) and Edinger–Westphal nucleus (EWN) or not after Oculomotor Nerve Injury. To assess cell proliferation in response to unilateral Oculomotor Nerve crush (ONC) in adult beagle dog, repetitive 5-bromo-2′-deoxyuridine (BrdU) intravenous injections were performed during 3 or 7 days before the dogs were euthanized 2 h after the last injection on days 3, 7, 14, and 28 post-ONC. The proliferating cell types were investigated with three cell phenotypic markers and confocal microscopy on serial sections throughout the whole extent of OMN and EWN. BrdU-positive nuclei were detected in bilateral OMNs and EWNs from 3 to 28 days after ONC with the peak value at 3 days. Confocal analysis revealed that partial BrdU-positive cells colocalized with nestin or βIII-tubulin or GFAP, and the number of every kind of double-labeled cell maintained an increased tendency from 3 to 28 days post-ONC. Neither single-labeled BrdU-positive nuclei nor double-labeled cells were detected in the subependymal layer of cerebral aqueduct (SELCA) of all unilateral ONC dogs; also, they were not observed in the OMNs, EWNs, and SELCA of intact and sham-operated dog. These findings demonstrate that ONC can trigger continual mitotic activity, proliferation of NSCs, neurogenesis, and astrogliogenesis in the OMN and EWN of adult dogs.
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A standardized method to create peripheral Nerve Injury in dogs using an automatic non-serrated forceps.
Neural Regeneration Research, 2012Co-Authors: Xuhui Wang, Min Yang, Youqiang Meng, Wenchuan Zhang, Baohui Feng, Xinyuan Li, Shiting LiAbstract:This study describes a method that not only generates an automatic and standardized crush Injury in the skull base, but also provides investigators with the option to choose from a range of varying pressure levels. We designed an automatic, non-serrated forceps that exerts a varying force of 0 to 100 g and lasts for a defined period of 0 to 60 seconds. This device was then used to generate a crush Injury to the right Oculomotor Nerve of dogs with a force of 10 g for 15 seconds, resulting in a deficit in the pupil-light reflex and ptosis. Further testing of our model with Toluidine-blue staining demonstrated that, at 2 weeks post-surgery disordered Oculomotor Nerve fibers, axonal loss, and a thinner than normal myelin sheath were visible. Electrophysiological examination showed occasional spontaneous potentials. Together, these data verified that the model for Oculomotor Nerve Injury was successful, and that the forceps we designed can be used to establish standard mechanical Injury models of peripheral Nerves.
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the differentiation of the newborn Nerve cells in Oculomotor nuclear after Oculomotor Nerve Injury
Neurological Sciences, 2011Co-Authors: Min Yang, Youqiang Meng, Xuhui Wang, Jun Zhong, Wenchuan Zhang, Massimiliano Visocchi, Shiting LiAbstract:Oculomotor Nerve Injury is a common complication of cranial trauma and craniotomy. For a long time, it has been generally considered that the Oculomotor Nerve is unable to regenerate and recover functionally after Injury. With the development of neuroradiology, microsurgery and neurohistology, it has been reported that the injured Oculomotor Nerve could be repaired by operation. However, the mechanisms of neural regeneration of the injured Oculomotor Nerve remain obscure. Therefore, by investigating the differentiation of the newborn Nerve cells in Oculomotor nuclear after Oculomotor Nerve Injury, the mechanisms of the neural regeneration of the injured Oculomotor Nerve was studied in the present paper. After animal model establishment, we found that the function of the injured Oculomotor Nerve could recover at some degree without treatment, at fourth week after the Nerve Injury. This result confirms that the injured Oculomotor Nerve per se has the potential to regenerate and repair. At the present study, by BredU stain, BrdU labeling cells were observed in Oculomotor nuclear at the fourth week post-operatively. It indicated that the Oculomotor nuclear per se has the ability of generating the cells, which will regenerate and differentiate after the Nerve Injury, without stimulation by exogenous agents. Immunofluorescence double staining was used in this study to show the differentiation of the newborn cells in Oculomotor nuclear after Oculomotor Nerve Injury. It is found that they could differentiate into neural progenitor cells, neuronal cells and neuroglial cells. It is suggested that the different differentiation of cells may play a role in the Nerve regeneration procedure.
Jennifer E. Fugate - One of the best experts on this subject based on the ideXlab platform.
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Ultra-Early Aneurysmal Rebleeding and Brainstem Destruction
Neurocritical Care, 2012Co-Authors: Jennifer E. Fugate, Grant W. Mallory, Eelco F. M. WijdicksAbstract:Background Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, parenchymal hematoma, or seizures. Methods Case report. Results A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem parenchyma and ventricles. Conclusions Sudden clinical deterioration after SAH with coma and a fixed “blown” pupil may result from hemorrhage extension into the brainstem parenchyma rather than Oculomotor Nerve Injury from compression or stretch.
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Ultra-Early Aneurysmal Rebleeding and Brainstem Destruction
Neurocritical Care, 2011Co-Authors: Jennifer E. Fugate, Grant W. Mallory, Eelco F. M. WijdicksAbstract:Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, parenchymal hematoma, or seizures. Case report. A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem parenchyma and ventricles. Sudden clinical deterioration after SAH with coma and a fixed “blown” pupil may result from hemorrhage extension into the brainstem parenchyma rather than Oculomotor Nerve Injury from compression or stretch.
Grant W. Mallory - One of the best experts on this subject based on the ideXlab platform.
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Ultra-Early Aneurysmal Rebleeding and Brainstem Destruction
Neurocritical Care, 2012Co-Authors: Jennifer E. Fugate, Grant W. Mallory, Eelco F. M. WijdicksAbstract:Background Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, parenchymal hematoma, or seizures. Methods Case report. Results A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem parenchyma and ventricles. Conclusions Sudden clinical deterioration after SAH with coma and a fixed “blown” pupil may result from hemorrhage extension into the brainstem parenchyma rather than Oculomotor Nerve Injury from compression or stretch.
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Ultra-Early Aneurysmal Rebleeding and Brainstem Destruction
Neurocritical Care, 2011Co-Authors: Jennifer E. Fugate, Grant W. Mallory, Eelco F. M. WijdicksAbstract:Early secondary neurologic deterioration after aneurysmal subarachnoid hemorrhage (SAH) may have many causes including rebleeding, hydrocephalus, parenchymal hematoma, or seizures. Case report. A 69-year-old woman presented with thunderclap headache and nausea. A head computed tomography (CT) showed SAH. On initial evaluation she was awake, alert, and confused without focal neurologic deficits. Two episodes of marked clinical deterioration occurred, manifesting as acute unresponsiveness and fixed anisocoria. Serial head CTs showed massive extension of hemorrhage into the brainstem parenchyma and ventricles. Sudden clinical deterioration after SAH with coma and a fixed “blown” pupil may result from hemorrhage extension into the brainstem parenchyma rather than Oculomotor Nerve Injury from compression or stretch.
Min Yang - One of the best experts on this subject based on the ideXlab platform.
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Electrical stimulation promotes regeneration of injured Oculomotor Nerves in dogs.
Neural Regeneration Research, 2016Co-Authors: Lei Du, Min Yang, Xuhui Wang, Shiting LiAbstract:Functional recovery after Oculomotor Nerve Injury is very poor. Electrical stimulation has been shown to promote regeneration of injured Nerves. We hypothesized that electrical stimulation would improve the functional recovery of injured Oculomotor Nerves. Oculomotor Nerve Injury models were created by crushing the right Oculomotor Nerves of adult dogs. Stimulating electrodes were positioned in both proximal and distal locations of the lesion, and non-continuous rectangular, biphasic current pulses (0.7 V, 5 Hz) were administered 1 hour daily for 2 consecutive weeks. Analysis of the results showed that electrophysiological and morphological recovery of the injured Oculomotor Nerve was enhanced, indicating that electrical stimulation improved neural regeneration. Thus, this therapy has the potential to promote the recovery of Oculomotor Nerve dysfunction.
-
experimental study on the effect of electrostimulation on neural regeneration after Oculomotor Nerve Injury
Journal of Molecular Neuroscience, 2014Co-Authors: Chunmei Zhang, Min Yang, Youqiang Meng, Xuhui Wang, Zhen Li, Baohui Feng, Bo Ning, Shiting LiAbstract:The Oculomotor Nerve can regenerate anatomically and histologically after Injury; however, the degree of functional recovery of extraocular muscles and the pupil sphincter muscle was not satisfactory. Electrostimulation was one potential intervention that was increasingly being studied for use in Nerve Injury settings. However, the effect of electrostimulation on regeneration of the injured Oculomotor Nerve was still obscure. In this study, we studied the effects of electrostimulation on neural regeneration in terms of neurofunction, myoelectrophysiology, neuroanatomy, and neurohistology after Oculomotor Nerve Injury and found that electrostimulation on the injured Oculomotor Nerve enhanced the speed and final level of its functional and electrophysiological recovery, promoted neural regeneration, and enhanced the selectivity and specificity of reinnervation of the regenerated neuron, the conformity among the electrophysiological and functional recovery of extraocular muscles, and neural regeneration, and that the function of extraocular muscles recovered slower than electrophysiology. Thus, we speculated that electrostimulation on the injured Oculomotor Nerve produced a marked effect on all phases of neural regeneration including neuronal survival, sprout formation, axonal elongation, target reconnection, and synaptogenesis. We think that neural electrostimulation can be used in Oculomotor Nerve Injury.
-
Oculomotor Nerve Injury induces nuerogenesis in the Oculomotor and edinger westphal nucleus of adult dog
Journal of Molecular Neuroscience, 2013Co-Authors: Chunmei Zhang, Min Yang, Youqiang Meng, Xuhui Wang, Zhen Li, Baohui Feng, Bo Ning, Shiting LiAbstract:Technical developments have extensively promoted experimental and clinical studies on cranial Nerve regeneration, but intracranial Nerve recovery is still an unexplored research area compared to peripheral Nerve repair. In this study, we researched whether neurogenesis occurs in adult Oculomotor (OMN) and Edinger–Westphal nucleus (EWN) or not after Oculomotor Nerve Injury. To assess cell proliferation in response to unilateral Oculomotor Nerve crush (ONC) in adult beagle dog, repetitive 5-bromo-2′-deoxyuridine (BrdU) intravenous injections were performed during 3 or 7 days before the dogs were euthanized 2 h after the last injection on days 3, 7, 14, and 28 post-ONC. The proliferating cell types were investigated with three cell phenotypic markers and confocal microscopy on serial sections throughout the whole extent of OMN and EWN. BrdU-positive nuclei were detected in bilateral OMNs and EWNs from 3 to 28 days after ONC with the peak value at 3 days. Confocal analysis revealed that partial BrdU-positive cells colocalized with nestin or βIII-tubulin or GFAP, and the number of every kind of double-labeled cell maintained an increased tendency from 3 to 28 days post-ONC. Neither single-labeled BrdU-positive nuclei nor double-labeled cells were detected in the subependymal layer of cerebral aqueduct (SELCA) of all unilateral ONC dogs; also, they were not observed in the OMNs, EWNs, and SELCA of intact and sham-operated dog. These findings demonstrate that ONC can trigger continual mitotic activity, proliferation of NSCs, neurogenesis, and astrogliogenesis in the OMN and EWN of adult dogs.
-
A standardized method to create peripheral Nerve Injury in dogs using an automatic non-serrated forceps.
Neural Regeneration Research, 2012Co-Authors: Xuhui Wang, Min Yang, Youqiang Meng, Wenchuan Zhang, Baohui Feng, Xinyuan Li, Shiting LiAbstract:This study describes a method that not only generates an automatic and standardized crush Injury in the skull base, but also provides investigators with the option to choose from a range of varying pressure levels. We designed an automatic, non-serrated forceps that exerts a varying force of 0 to 100 g and lasts for a defined period of 0 to 60 seconds. This device was then used to generate a crush Injury to the right Oculomotor Nerve of dogs with a force of 10 g for 15 seconds, resulting in a deficit in the pupil-light reflex and ptosis. Further testing of our model with Toluidine-blue staining demonstrated that, at 2 weeks post-surgery disordered Oculomotor Nerve fibers, axonal loss, and a thinner than normal myelin sheath were visible. Electrophysiological examination showed occasional spontaneous potentials. Together, these data verified that the model for Oculomotor Nerve Injury was successful, and that the forceps we designed can be used to establish standard mechanical Injury models of peripheral Nerves.
-
the differentiation of the newborn Nerve cells in Oculomotor nuclear after Oculomotor Nerve Injury
Neurological Sciences, 2011Co-Authors: Min Yang, Youqiang Meng, Xuhui Wang, Jun Zhong, Wenchuan Zhang, Massimiliano Visocchi, Shiting LiAbstract:Oculomotor Nerve Injury is a common complication of cranial trauma and craniotomy. For a long time, it has been generally considered that the Oculomotor Nerve is unable to regenerate and recover functionally after Injury. With the development of neuroradiology, microsurgery and neurohistology, it has been reported that the injured Oculomotor Nerve could be repaired by operation. However, the mechanisms of neural regeneration of the injured Oculomotor Nerve remain obscure. Therefore, by investigating the differentiation of the newborn Nerve cells in Oculomotor nuclear after Oculomotor Nerve Injury, the mechanisms of the neural regeneration of the injured Oculomotor Nerve was studied in the present paper. After animal model establishment, we found that the function of the injured Oculomotor Nerve could recover at some degree without treatment, at fourth week after the Nerve Injury. This result confirms that the injured Oculomotor Nerve per se has the potential to regenerate and repair. At the present study, by BredU stain, BrdU labeling cells were observed in Oculomotor nuclear at the fourth week post-operatively. It indicated that the Oculomotor nuclear per se has the ability of generating the cells, which will regenerate and differentiate after the Nerve Injury, without stimulation by exogenous agents. Immunofluorescence double staining was used in this study to show the differentiation of the newborn cells in Oculomotor nuclear after Oculomotor Nerve Injury. It is found that they could differentiate into neural progenitor cells, neuronal cells and neuroglial cells. It is suggested that the different differentiation of cells may play a role in the Nerve regeneration procedure.
