Browsing by Subject "dorsal root ganglion"
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Item Open Access A Novel Approach to Percutaneous Lumbar Surgeries via Kambin's Triangle - A Radiographic and Surgical Planning Analysis with Nerve Segmentation Technology.(World neurosurgery, 2023-06) Tabarestani, Troy Q; Sykes, David AW; Kouam, Romaric W; Salven, David S; Wang, Timothy Y; Mehta, Vikram A; Shaffrey, Christopher I; Wiggins, Walter F; Chi, John H; Abd-El-Barr, Muhammad MObjective
While Kambin's triangle has become an ever more important anatomic window given its proximity to the exiting nerve root, there have been limited studies examining the effect of disease on the corridor. Our goal was to better understand how pathology can affect Kambin's triangle thereby altering laterality of approach for percutaneous lumbar interbody fusion (percLIF).Methods
The authors performed a single-center retrospective review of patients evaluated for percLIF. The areas of Kambin's triangle were measured without and with nerve segmentation. For the latter, the lumbosacral nerve roots on 3D T2 MRI were manually segmented. Next, the borders of Kambin's triangle were delineated ensuring no overlap between the area and the nerve above.Results
15 patients (67.5 ± 9.7 years, 46.7% female) were retrospectively reviewed. 150 Kambin's triangles were measured. The mean areas from L1-S1 were 50.0 ± 12.3 mm2, 73.8 ± 12.5 mm2, 83.8 ± 12.2 mm2, 88.5 ± 19.0 mm2, and 116 ± 29.3 mm2, respectively. When pathology was present, the areas significantly decreased at L4-L5 (p = 0.046) and L5-S1 (p = 0.049). Higher spondylolisthesis and smaller posterior disc heights were linked with decreased areas via linear regression analysis (p < 0.05). When nerve segmentation was used, the areas were significantly smaller from L1-L5 (p < 0.05). Among 11 patients who underwent surgery, none suffered from postoperative neuropathies.Conclusion
These results illustrate the feasibility of pre-operatively segmenting lumbosacral nerves and measuring Kambin's triangle to help guide surgical planning and determine the ideal laterality of approach for percLIF.Item Open Access Response of Midbrain Pain Receptors in a Rodent Model of Radiculopathy(2012) Hwang, Priscilla YIntroduction: Intervertebral disc herniation may contribute to nerve root compression or inflammatory processes that are associated with radicular pain and motor deficits. Molecular changes at the affected dorsal root ganglion (DRG), spinal cord, and even midbrain, have been documented in rat models of radiculopathy or nerve injury. The objective of this study was to evaluate gait mechanics and the expression of key pain receptors in the midbrain of rats after induced radiculopathy in order to test the hypothesis that DRG injury can promote molecular changes in the midbrain. Materials and Methods: Radiculopathy was induced by harvesting tail nucleus pulposus (NP) and placing upon the right L5 DRG in Sprague-Dawley rats. Tail nucleus pulposus (NP) was harvested and discarded in sham-operated rats. At 1 and 4 weeks after surgery, DRGs were sectioned and tested for immunoreactivity to astrocytes and microglial. Also at 1 and 4 weeks after surgery, midbrains were sectioned and tested for immunoreactivity to serotonin (5HT2B), mu-opioid (μ-OR), and metabotropic glutamate (mGluR4 and 5) receptor antibodies. Quantitative analysis was performed on all midbrain immunostained images and compared to naïve controls. Cerebral spinal fluid was also extracted at 1 and 4 weeks after surgery for monocyte-chemoattractant protein (MCP-1) assessment. Results: NP-treated animals placed less weight on the affected limb 1 week after surgery and experienced mechanical hypersensitivity over the entire time of the study. Astroctye activation was observed at the DRG 4 weeks after surgery. An increased expression of 5HT2B was observed in NP-treated rats at 1, but not at 4 weeks. Increased expression of μ-OR and mGluR5 was observed in the periaqueductal gray (PAG) region of NP-treated rat midbrains at 1 and 4 weeks post-surgery. By contrast, increased expression levels of mGluR5 in the PAG region of sham animals reverted to naïve levels by 4 weeks after surgery. No changes were observed in expression levels of mGluR4 in either sham or NP-treated animals at any point in this study. MCP-1 levels were higher in NP-treated animals at 4 weeks compared to sham animals. Conclusion: These observations support the hypothesis that the midbrain responds to injury at the DRG with a transient and adaptive change in receptors regulating pain mechanisms.
Item Open Access SHANK3 Deficiency Impairs Heat Hyperalgesia and TRPV1 Signaling in Primary Sensory Neurons.(Neuron, 2016-12-21) Han, Qingjian; Kim, Yong Ho; Wang, Xiaoming; Liu, Di; Zhang, Zhi-Jun; Bey, Alexandra L; Lay, Mark; Chang, Wonseok; Berta, Temugin; Zhang, Yan; Jiang, Yong-Hui; Ji, Ru-RongAbnormal pain sensitivity is commonly associated with autism spectrum disorders (ASDs) and affects the life quality of ASD individuals. SHANK3 deficiency was implicated in ASD and pain dysregulation. Here, we report functional expression of SHANK3 in mouse dorsal root ganglion (DRG) sensory neurons and spinal cord presynaptic terminals. Homozygous and heterozygous Shank3 complete knockout (Δe4-22) results in impaired heat hyperalgesia in inflammatory and neuropathic pain. Specific deletion of Shank3 in Nav1.8-expressing sensory neurons also impairs heat hyperalgesia in homozygous and heterozygous mice. SHANK3 interacts with transient receptor potential subtype V1 (TRPV1) via Proline-rich region and regulates TRPV1 surface expression. Furthermore, capsaicin-induced spontaneous pain, inward currents in DRG neurons, and synaptic currents in spinal cord neurons are all reduced after Shank3 haploinsufficiency. Finally, partial knockdown of SHANK3 expression in human DRG neurons abrogates TRPV1 function. Our findings reveal a peripheral mechanism of SHANK3, which may underlie pain deficits in SHANK3-related ASDs.