Browsing by Subject "neuropathic pain"

Now showing 1 - 5 of 5
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    Capturing the Perceived Phantom Limb through Virtual Reality
    (Office of the Vice Chancellor for Research, 2015-04-17) Lau, Jonathan; Huynh, Denver; Albertson, Steven; Beem, James; Qian, Enlin
    Phantom limb is the sensation amputees may feel where the missing limb (occasionally an organ) is still attached to the body and is still moving as it would if it were there. Between 50-80% amputees report neuropathic pain, also known as phantom limb pain (PLP). Recent studies suggest that providing sensory input to the stump or amputation area may modulate how PLP can be related to neuroplastic changes in the cortex. However, there is still little understanding of why PLP occurs and there are no fully effective, long-term treatments available. Part of the problem is the difficulty for amputees to describe the sensations of their phantom limbs due to the lack of a physical limb as well as phantom limbs that are in positions that are impossible to attain. This project aims to develop an effective 3D tool with the Maya 3D animation software and the Unity game engine. The tool will then be used for those with phantom limb syndrome to communicate the sensations accurately and easily through various hand positions using a model arm with a user friendly interface. The 3D model arm will be able to mimic the phantom sensation, being able to go beyond normal joint extensions of a regular arm. This way we can have a true 3D visual of how the amputee with phantom limb feels if it is abnormal. Testing the effectiveness of the tool will involve a pilot study with able-bodied volunteers. The non-dominant limb of the volunteers will be hidden behind a blind. After putting their limb in a random position, they will attempt to capture the limb on the 3D model. The actual position and captured position will be compared to determine the reproducibility and accuracy of the virtual limb. By taking advantage of computer graphics, virtual reality and computerized image capture technologies we are hoping to achieve a far less challenging way to quickly and accurately capture the position and striking feelings of the phantom limb sensation.
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    Early-onset treadmill training reduces mechanical allodynia and modulates calcitonin gene-related peptide fiber density in lamina III/IV in a mouse model of spinal cord contusion injury
    (Lippincott, Williams, and Wilkins, 2016-03) Nees, Timo A.; Tappe-Theodor, Anke; Sliwinski, Christopher; Motsch, Melanie; Rupp, Rüdiger; Kuner, Rohini; Weidner, Norbert; Blesch, Armin; Department of Neurological Surgery, IU School of Medicine
    Abstract: Below-level central neuropathic pain (CNP) affects a large proportion of spinal cord injured individuals. To better define the dynamic changes of the spinal cord neural network contributing to the development of CNP after spinal cord injury (SCI), we characterized the morphological and behavioral correlates of CNP in female C57BL/6 mice after a moderate T11 contusion SCI (50 kdyn) and the influence of moderate physical activity. Compared with sham-operated animals, injured mice developed mechanical allodynia 2 weeks post injury when tested with small-diameter von Frey hair filaments (0.16 g and 0.4 g filament), but presented hyporesponsiveness to noxious mechanical stimuli (1.4 g filament). The mechano-sensory alterations lasted up to 35 days post injury, the longest time point examined. The response latency to heat stimuli already decreased significantly 10 days post injury reaching a plateau 2 weeks later. In contrast, injured mice developed remarkable hyposensitivity to cold stimuli. Animals that underwent moderate treadmill training (2 × 15 minutes; 5 d/wk) showed a significant reduction in the response rate to light mechanical stimuli as early as 6 days after training. Calcitonin gene-related peptide (CGRP) labeling in lamina III-IV of the dorsal horn revealed significant increases in CGRP-labeling density in injured animals compared with sham control animals. Importantly, treadmill training reduced CGRP-labeling density by about 50% (P < 0.01), partially reducing the injury-induced increases. Analysis of IB4-labeled nonpeptidergic sensory fibers revealed no differences between experimental groups. Abnormalities in temperature sensation were not influenced by physical activity. Thus, treadmill training partially resolves signs of below-level CNP after SCI and modulates the density of CGRP-labeled fibers.
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    Enhancing excitatory activity of somatosensory cortex alleviates neuropathic pain through regulating homeostatic plasticity
    (Nature Publishing group, 2017-10-06) Xiong, Wenhui; Ping, Xingjie; Ripsch, Matthew S.; Chavez, Grace Santa Cruz; Hannon, Heidi Elise; Jiang, Kewen; Bao, Chunhui; Jadhav, Vaishnavi; Chen, Lifang; Chai, Zhi; Ma, Cungen; Wu, Huangan; Feng, Jianqiao; Blesch, Armin; White, Fletcher A.; Jin, Xiaoming; Anatomy and Cell Biology, School of Medicine
    Central sensitization and network hyperexcitability of the nociceptive system is a basic mechanism of neuropathic pain. We hypothesize that development of cortical hyperexcitability underlying neuropathic pain may involve homeostatic plasticity in response to lesion-induced somatosensory deprivation and activity loss, and can be controlled by enhancing cortical activity. In a mouse model of neuropathic pain, in vivo two-photon imaging and patch clamp recording showed initial loss and subsequent recovery and enhancement of spontaneous firings of somatosensory cortical pyramidal neurons. Unilateral optogenetic stimulation of cortical pyramidal neurons both prevented and reduced pain-like behavior as detected by bilateral mechanical hypersensitivity of hindlimbs, but corpus callosotomy eliminated the analgesic effect that was ipsilateral, but not contralateral, to optogenetic stimulation, suggesting involvement of inter-hemispheric excitatory drive in this effect. Enhancing activity by focally blocking cortical GABAergic inhibition had a similar relieving effect on the pain-like behavior. Patch clamp recordings from layer V pyramidal neurons showed that optogenetic stimulation normalized cortical hyperexcitability through changing neuronal membrane properties and reducing frequency of excitatory postsynaptic events. We conclude that development of neuropathic pain involves abnormal homeostatic activity regulation of somatosensory cortex, and that enhancing cortical excitatory activity may be a novel strategy for preventing and controlling neuropathic pain.
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    Neuropathic pain after spinal cord injury: the impact of sensorimotor activity
    (Wolters Kluwer, 2017-03) Nees, Timo A.; Finnerup, Nanna B.; Blesch, Armin; Weidner, Norbert; Neurological Surgery, School of Medicine
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    Sustained relief of ongoing experimental neuropathic pain by a CRMP2 peptide aptamer with low abuse potential
    (Wolters Kluwer, 2016-09) Xie, Jennifer Y.; Chew, Lindsey A.; Yang, Xiaofang; Wang, Yuying; Qu, Chaoling; Wang, Yue; Federici, Lauren M.; Fitz, Stephanie D.; Ripsch, Matthew S.; Due, Michael R.; Moutal, Aubin; Khanna, May; White, Fletcher A.; Vanderah, Todd W.; Johnson, Philip L.; Porreca, Frank; Khanna, Rajesh; Anesthesia, School of Medicine