https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&id=36213062&retmode=xml&tool=Litmetric&email=readroberts32@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=pubmed&term=nerve+root&datetype=edat&usehistory=y&retmax=5&tool=Litmetric&email=readroberts32@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09https://eutils.ncbi.nlm.nih.gov/entrez/eutils/efetch.fcgi?db=pubmed&WebEnv=MCID_67957a9a57ad91ef34086a61&query_key=1&retmode=xml&retmax=5&tool=Litmetric&email=readroberts32@gmail.com&api_key=61f08fa0b96a73de8c900d749fcb997acc09
We aimed to study the mechanism of sacral nerve injury caused by sacral fractures and the relationship between nerve decompression and nerve function. First, we observed the anatomical features of lumbosacral nerve root region in Sprague-Dawley rats. Next, the rats were divided into the sham, 10 g, 30 g, and 60 g groups for electrophysiological studies on nerve root constriction injury. Then we studied the biomechanical properties of rat nerve roots, lumbosacral trunk, and sacrum. Finally, we established a finite element analysis model of sacral nerve roots injury in rats and determined the correlation between sacral deformation and the degree of sacral nerve roots injury. Anatomical study showed L5 constitutes sciatic nerve, the length of the L5 nerve root is 3.67 ± 0.15 mm, which is suitable for electrophysiological research on nerve root compression injury. After a series of electrophysiological study of L5 nerve roots, our results showed that nerve root function was almost unaffected at a low degree of compression (10 g). Nerve root function loss began at 30 g compression, and was severe at 60 g compression. The degree of neurological loss was therefore positively correlated with the degree of compression. Combining biomechanical testing of the lumbosacral nerve roots, finite element analysis and neuroelectrophysiological research, we concluded when the sacral foramina deformation is >22.94%, the sacral nerves lose function. When the compression exceeds 33.16%, early recovery of nerve function is difficult even after decompression. In this study, we found that the neurological loss was positively correlated with the degree of compression. After early decompression, nerve root function recovery is possible after moderate compression; however, in severe compression group, the nerve function would not recover. Furthermore, FEA was used to simulate nerve compression during sacral fracture, as well as calculate force loading on nerve with different deformation rates. The relationship between sacral fractures and neurological loss can be analyzed in combination with neurophysiological test results.
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http://dx.doi.org/10.3389/fbioe.2022.920991 | DOI Listing |
Biomedicines
January 2025
Second Department of Internal Medicine, Division of Nephrology, Kansai Medical University, Hirakata 573-1010, Japan.
: Charcot-Marie-Tooth (CMT) disease is an inherited peripheral neuropathy primarily involving motor and sensory neurons. Mutations in INF2, an actin assembly factor, cause two diseases: peripheral neuropathy CMT-DIE (MIM614455) and/or focal segmental glomerulosclerosis (FSGS). These two phenotypes arise from the progressive degeneration affecting podocytes and Schwann cells.
View Article and Find Full Text PDFBioengineering (Basel)
January 2025
School of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA 19104, USA.
Background: A brachial plexus avulsion occurs when the nerve root separates from the spinal cord during birthing trauma, such as shoulder dystocia or a difficult vaginal delivery. A complete paralysis of the affected levels occurs post-brachial plexus avulsion. Despite being reported in 10-20% of brachial plexus birthing injuries, it remains poorly diagnosed during the acute stages of injury, leading to poor intervention approaches.
View Article and Find Full Text PDFCureus
December 2024
Neurosurgery, Fluminense Federal University, Niterói, BRA.
Complex regional pain syndrome (CRPS) is a chronic pain condition characterized by significant sensory, motor, and autonomic dysfunction, often following trauma or nerve injury. Historically known as causalgia and reflex sympathetic dystrophy, CRPS manifests as severe, disproportionate pain, often accompanied by hyperalgesia, allodynia, trophic changes, and motor impairments. Classified into type I (without nerve injury) and type II (associated with nerve damage), CRPS exhibits a complex pathophysiology involving peripheral and central sensitization, neurogenic inflammation, maladaptive brain plasticity, and potential autoimmune and psychological influences.
View Article and Find Full Text PDFOsteoarthr Cartil Open
March 2025
Nantes Université, Oniris, CHU Nantes, INSERM, Regenerative Medicine and Skeleton, RMeS, UMR 1229, Nantes, F-44000, France.
Objective: This study aimed to describe the anatomical landmarks for intervertebral disc (IVD) percutaneous approaches (transpedicular TPA and transannular TAA) using CT scans in humans and dogs for regenerative medicine research.
Method: CT scans of 57 human (30 supine, 27 prone) and 49 canine (29 chondrodystrophic, 20 non-chondrodystrophic) lumbar spines were analyzed. Morphometric data, cutaneous landmarks, and approach angles were measured, with additional sections assessing nerve root distances from TPA routes.
World J Orthop
January 2025
Department of Orthopedics, The Third Medical Center, General Hospital of the Chinese People's Liberation Army, Beijing 100039, China.
Lumbar intervertebral disc degeneration is thought to be the main cause of low back pain, although the mechanisms by which it occurs and leads to pain remain unclear. In healthy adult discs, vessels and nerves are present only in the outer layer of the annulus fibrosus and in the bony endplate. Animal models, and histological and biomechanical studies have shown that annulus tear or endplate injury is the initiating factor for painful disc degeneration.
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