A novel anatomo-physiologic high-grade spondylolisthesis model to evaluate L5 nerve stretch injury after spondylolisthesis reduction

L5 nerve palsy is a well-known complication following reduction of high-grade spondylolisthesis. While several mechanisms for its occurrence have been proposed, the hypothesis of L5 nerve root strain or displacement secondary to mechanical reduction remains poorly studied. The aim of this cadaveric study is to determine changes in morphologic parameters of the L5 nerve root during simulated intraoperative reduction of high-grade spondylolisthesis. A standard posterior approach to the lumbosacral junction was performed in eight fresh-frozen cadavers with lumbosacral or lumbopelvic screw fixation. Wide decompressions of the spinal canal and L5 nerve roots with complete facetectomies were accomplished with full exposure of the L5 nerve roots. A 100% translational slip was provoked by release of the iliolumbar ligaments and cutting the disc with the attached anterior longitudinal ligament. To evaluate the path of the L5 nerves during reduction maneuvers, metal bars were inserted bilaterally at the inferomedial aspects of the L5 pedicle at a distance of 10 mm from the midpoint of the L5 pedicle screws. There was no measurable change in length of the L5 nerve roots after 50% and 100% reduction of spondylolisthesis. Mechanical strain or displacement during reduction is an unlikely cause of L5 nerve root injury. Further anatomical or physiological studies are necessary to explore alternative mechanisms of L5 nerve palsy in the setting of high-grade spondylolisthesis correction, and surgeons should favor extensive surgical decompression of the L5 nerve roots when feasible.

Optimization of Loading Condition for Maxillary Molar Intrusion with Midpalatal Miniscrews by Using Finite Element Analysis

An anterior open bite is one of the most difficult malocclusions in orthodontic treatment. For such malocclusion, orthodontic miniscrew insertion into both buccal and palatal alveolar regions has been indicated for molar intrusion, but it involves a risk of tooth root injury. To solve the problem, a midpalatal miniscrew-attached extension arm (MMEA) is adopted. However, this method causes palatal tipping of the molar because intrusive loads were applied only from the palatal side. Currently, a transpalatal arch is added to avoi0d tipping movement, but it induces the patient’s discomfort. Hence, the objective of this study was to evaluate the loading conditions for maxillary molar intrusion without tipping movement, only by MMEA through finite element (FE) analysis. FE models of maxillary right first molar and surrounding tissues were created. Three hook positions of MMEA were set at 6.0 mm perpendicular intervals in the occluso-apical direction along the mucosal contour. An intrusive unit load was applied from the palatal side of the molar, and various counter loads were applied from the buccal side. An optimal counter load for molar intrusion without palatal tipping was observed in each hook position. In conclusion, an ideal maxillary molar intrusion can be achieved only by MMEA with an optimal counter load.

Early operative morbidity in 184 cases of anterior vertebral body tethering

Fusion is the current standard of care for AIS. Anterior vertebral body tethering (AVBT) is a motion-sparing alternative gaining interest. As a novel procedure, there is a paucity of literature on safety. Here, we report 90-day complication rates in 184 patients who underwent AVBT by a single surgeon. Patients were retrospectively reviewed. Approaches included 71 thoracic, 45 thoracolumbar, 68 double. Major complications were those requiring readmittance or reoperation, prolonged use of invasive materials such as chest tubes, or resulted in spinal cord or nerve root injury. Minor complications resolved without invasive intervention. Mean operative time and blood loss were 186.5 ± 60.3 min and 167.2 ± 105.0 ml, respectively. No patient required allogenic blood transfusion. 6 patients experienced major (3.3%), and 6 had minor complications (3.3%). Major complications included 3 chylothoracies, 2 hemothoracies, and 1 lumbar radiculopathy secondary to screw placement requiring re-operation. Minor complications included 1 patient with respiratory distress requiring supplementary oxygen, 1 superficial wound infection, 2 cases of prolonged nausea, and 1 Raynaud phenomenon. In 184 patients who underwent AVBT for AIS, major and minor complication rates were both 3.3%.

Anatomy of the L5 nerve root in the pelvis for safe sacral screw placement: a cadaveric study

OBJECTIVE Previous reports have focused on the complications of L5 nerve root injury caused by anterolateral misplacement of the S1 pedicle screws. Anatomical knowledge of the L5 nerve root in the pelvis is essential for safe and effective placement of the sacral screw. This cadaveric study aimed to investigate the course of the L5 nerve root in the pelvis and to clarify a safe zone for inserting the sacral screw. METHODS Fifty-four L5 nerve roots located bilaterally in 27 formalin-fixed cadavers were studied. The ventral rami of the L5 nerve roots were dissected along their courses from the intervertebral foramina to the lesser pelvis. The running angles of the L5 nerve roots from the centerline were measured in the coronal plane. In addition, the distances from the ala of the sacrum to the L5 nerve roots were measured in the sagittal plane. RESULTS The authors found that the running angles of the L5 nerve roots changed at the most anterior surface of the ala of the sacrum. The angles of the bilateral L5 nerve roots from the right and left L5 intervertebral foramina to their inflection points were 13.77° ± 5.01° and 14.65° ± 4.71°, respectively. The angles of the bilateral L5 nerve roots from the right and left inflection points to the lesser pelvis were 19.66° ± 6.40° and 20.58° ± 5.78°, respectively. There were no significant differences between the angles measured in the right and left nerve roots. The majority of the L5 nerves coursed outward after changing their angles at the inflection point. The distances from the ala of the sacrum to the L5 nerve roots in the sagittal plane were less than 1 mm in all cases, which indicated that the L5 nerve roots were positioned close to the ala of the sacrum and had poor mobility. CONCLUSIONS All of the L5 nerve roots coursed outward after exiting the intervertebral foramina and never inward. To prevent iatrogenic L5 nerve root injury, surgeons should insert the S1 pedicle screw medially with an angle > 0° toward the inside of the S1 anterior foramina and the sacral alar screw laterally with an angle > 30°.

Profiling sensory neuron microenvironment after peripheral and central axon injury reveals key pathways for neural repair

Sensory neurons with cell bodies in dorsal root ganglia (DRG) represent a useful model to study axon regeneration. Whereas regeneration and functional recovery occurs after peripheral nerve injury, spinal cord injury or dorsal root injury is not followed by regenerative outcomes. Regeneration of sensory axons in peripheral nerves is not entirely cell autonomous. Whether the DRG microenvironment influences the different regenerative capacities after injury to peripheral or central axons remains largely unknown. To answer this question, we performed a single-cell transcriptional profiling of mouse DRG in response to peripheral (sciatic nerve crush) and central axon injuries (dorsal root crush and spinal cord injury). Each cell type responded differently to the three types of injuries. All injuries increased the proportion of a cell type that shares features of both immune cells and glial cells. A distinct subset of satellite glial cells (SGC) appeared specifically in response to peripheral nerve injury. Activation of the PPARα signaling pathway in SGC, which promotes axon regeneration after peripheral nerve injury, failed to occur after central axon injuries. Treatment with the FDA-approved PPARα agonist fenofibrate increased axon regeneration after dorsal root injury. This study provides a map of the distinct DRG microenvironment responses to peripheral and central injuries at the single-cell level and highlights that manipulating non-neuronal cells could lead to avenues to promote functional recovery after CNS injuries or disease.

Nerve injury following ultrasound-guided nerve root block with 2% lidocaine for shoulder manipulation: a case report

Shoulder manipulation under ultrasound (US)-guided C5 and C6 nerve root block is effective for treating refractory adhesive capsulitis (AC). We herein report the development of cervical nerve root injury following manipulation under anesthesia (MUA) in a patient with AC. A 47-year-old woman underwent shoulder manipulation under US-guided C5 and C6 root block with 2% lidocaine for the management of AC-induced shoulder pain. For the procedure, 3 mL of 2% lidocaine (total of 6 mL) was injected around each C5 and C6 nerve root under US guidance. Seven days after the procedure, the patient visited a university hospital because of severe neuropathic pain (numeric rating scale score of 9) in the right anterior arm, lateral arm, and forearm areas. Sensory deficits in the corresponding C5 and C6 dermatomes and motor weakness of the right shoulder abductor, elbow flexor, and wrist extensor were observed. Electrophysiologic studies demonstrated C5 and C6 nerve root injury. The patient was diagnosed with right C5 and C6 nerve root injury following MUA, and lidocaine toxicity or ischemia was the suspected cause. Clinicians should be mindful of the possibility of this complication.

Dorsal Root Injury—A Model for Exploring Pathophysiology and Therapeutic Strategies in Spinal Cord Injury

Unraveling the cellular and molecular mechanisms of spinal cord injury is fundamental for our possibility to develop successful therapeutic approaches. These approaches need to address the issues of the emergence of a non-permissive environment for axonal growth in the spinal cord, in combination with a failure of injured neurons to mount an effective regeneration program. Experimental in vivo models are of critical importance for exploring the potential clinical relevance of mechanistic findings and therapeutic innovations. However, the highly complex organization of the spinal cord, comprising multiple types of neurons, which form local neural networks, as well as short and long-ranging ascending or descending pathways, complicates detailed dissection of mechanistic processes, as well as identification/verification of therapeutic targets. Inducing different types of dorsal root injury at specific proximo-distal locations provide opportunities to distinguish key components underlying spinal cord regeneration failure. Crushing or cutting the dorsal root allows detailed analysis of the regeneration program of the sensory neurons, as well as of the glial response at the dorsal root-spinal cord interface without direct trauma to the spinal cord. At the same time, a lesion at this interface creates a localized injury of the spinal cord itself, but with an initial neuronal injury affecting only the axons of dorsal root ganglion neurons, and still a glial cell response closely resembling the one seen after direct spinal cord injury. In this review, we provide examples of previous research on dorsal root injury models and how these models can help future exploration of mechanisms and potential therapies for spinal cord injury repair.