A patient with cervical ligamentum flavum haematoma: case report.

INTRODUCTION: Ligamentum flavum haematoma (LFH) is an extremely rare entity, found mostly in the lumbar and thoracic ligamentum flavum and seldom in the cervical ligamentum flavum. Cervical LFH can cause paralysis in patients. We describe a case of LFH in the cervical spine that accepted surgical treatment. CASE PRESENTATION: A 70-year-old man with incomplete spinal cord injury presented with sudden paralysis of his left limbs for 10 days and hemi-hypaesthesia below the level of the right clavicle. Magnetic resonance imaging (MRI) showed a space-occupying lesion in the left ligamentum flavum between the C4 and C5 laminae. The preliminary diagnoses were concluded to be incomplete spinal cord injury, spinal epidural lesions, and cervical spinal stenosis. After a posterior C3-C6 laminectomy with lateral mass screw instrumentation, the muscle strength and sensation recovered partially. The lesion was greyish black and located in the ligamentum flavum. A pathological examination identified it as a haematoma of the ligamentum flavum. The patient was discharged 15 days after the operation and commenced rehabilitation. DISCUSSION: The LFH was mainly caused by slight trauma during gentle activities and contributed by many factors. MRI is an essential tool but pathological diagnosis is the gold standard. Most LFH patients can be treated surgically.

The Development of Spinal Endoscopic Ultrasonic Imaging System with an Automated Tissue Recognition Algorithm.

STUDY DESIGN: Preclinical experimental study. OBJECTIVE: To develop an intraoperative ultrasound-assisted imaging device, which could be placed at the surgical site through an endoscopic working channel and which could help surgeon recognition of different tissue types during endoscopic spinal surgery (ESS). SUMMARY OF BACKGROUND DATA: ESS remains a challenging task for spinal surgeons. Great proficiency and experience are needed to perform procedures such as intervertebral discectomy and neural decompression within a narrow channel. The limited surgical view poses a risk of damaging important structures, such as nerve roots. METHODS: We constructed a spinal endoscopic ultrasound system, using a 4-mm custom ultrasound probe, which can be easily inserted through the ESS working channel, allowing up to 10 mm depth detection. This system was applied to ovine lumbar spine samples to obtain ultrasound images. Subsequently, we proposed a two-stage classification algorithm, based on a pretrained DenseNet architecture for automated tissue recognition. The recognition algorithm was evaluated using accuracy and consistency. RESULTS: The probe can be easily used in the ESS working channel and produce clear and characteristic ultrasound images. We collected 367 images for training and testing of the recognition algorithm, including images of the spinal cord, nucleus pulposus, adipose tissue, bone, annulus fibrosus and nerve roots. The algorithm achieved over 90% accuracy in recognizing all types of tissues with a Kappa value of 0.875. The recognition times were under 0.1 s using the current configuration. CONCLUSION: Our system was able to be used in existing ESS working channels and clearly identified at-risk spinal structures in vitro. The pretrained algorithms could identify six intraspinal tissue types accurately and quickly. The concept and innovative application of intraoperative ultrasound in ESS may shorten the learning curve of ESS and improve surgical efficiency and safety.

Bromocriptine protects perilesional spinal cord neurons from lipotoxicity after spinal cord injury.

Recent studies have revealed that lipid droplets accumulate in neurons after brain injury and evoke lipotoxicity, damaging the neurons. However, how lipids are metabolized by spinal cord neurons after spinal cord injury remains unclear. Herein, we investigated lipid metabolism by spinal cord neurons after spinal cord injury and identified lipid-lowering compounds to treat spinal cord injury. We found that lipid droplets accumulated in perilesional spinal cord neurons after spinal cord injury in mice. Lipid droplet accumulation could be induced by myelin debris in HT22 cells. Myelin debris degradation by phospholipase led to massive free fatty acid production, which increased lipid droplet synthesis, ß-oxidation, and oxidative phosphorylation. Excessive oxidative phosphorylation increased reactive oxygen species generation, which led to increased lipid peroxidation and HT22 cell apoptosis. Bromocriptine was identified as a lipid-lowering compound that inhibited phosphorylation of cytosolic phospholipase A2 by reducing the phosphorylation of extracellular signal-regulated kinases 1/2 in the mitogen-activated protein kinase pathway, thereby inhibiting myelin debris degradation by cytosolic phospholipase A2 and alleviating lipid droplet accumulation in myelin debris-treated HT22 cells. Motor function, lipid droplet accumulation in spinal cord neurons and neuronal survival were all improved in bromocriptine-treated mice after spinal cord injury. The results suggest that bromocriptine can protect neurons from lipotoxic damage after spinal cord injury via the extracellular signal-regulated kinases 1/2-cytosolic phospholipase A2 pathway.