Cauda equina syndrome caused by the application of DuraSeal^(TM) in a microlaminectomy surgery:A case report

BACKGROUND The management of dural tears is important.While a massive dura can be repaired with absorbable suture lines,cerebrospinal fluid leakage can be attenuated by dural sealant when an unintended tiny durotomy occurs intraoperatively.DuraSeal is often used because it can expand to seal tears.This case emphasizes the need for caution when DuraSeal is used as high expansion can cause complications following microlaminectomy.CASE SUMMARY A 77-year-old woman presented with L2/3 and L3/4 lateral recess stenosis.She underwent microlaminectomy,foraminal decompression,and disk height restoration using an IntraSPINE~? device.A tiny incident durotomy occurred intraoperatively and was sealed using DuraSeal ^(TM).However,decreased muscle power,urinary incontinence,and absence of anal reflexes were observed postoperatively.Emergent magnetic resonance imaging revealed fluid collection causing thecal sac indentation and central canal compression.Surgical exploration revealed that the gel-like DuraSeal had entrapped the hematoma and,consequently,compressed the thecal sac and nerve roots.While we removed all DuraSeal ^(TM) and exposed the nerve root,the patient’s neurological function did not recover postoperatively.CONCLUSION DuraSeal expansion must not be underestimated.Changes in neurological status require investigation for cauda equina syndrome due to expansion.

Apoptosis of lumbar spinal cord neurons in cauda equina syndrome rats

Objective To explore the law of apoptosis of lumbar spinal cord neurons in cauda equina syndrome (CES). Methods Cauda equina of rats was compressed by a piece of silica gel stick. From day 1 to day 28,the lumbar spinal cord specimens were harvested and assessed by Nissl’s staining and TUNEL staining. Results Compression of cauda equina caused lesion and apoptosis of neurons in lumbar spinal cord,and the extent of apoptosis reached the peak on 7th day after compression. Conclusion Apoptosis of neurons in lumbar spinal cord might be one of the reasons why patients with CES get poor prognosis.

Non-Classical Hodgkin＇s Lymphoma Presenting As Cauda Equina Syndrome a Rare presentation： One Case Report

Nodular lymphocyte predominant Hodgkin＇s disease occurs in 5% of all cases of Hodgkin＇s disease. It occurs more commonly in male. Only 5% of all Hodgkin＇s lymphoma cases develop spinal cord compression and in only 0.2% cases, spinal cord compression occurs as the initial presentation. So our case is rare both in the form of the unique variety of Hodgkin＇s disease and also in the form of presentation.

Cauda equina syndrome： a review of clinical progress

Objective To review the literature on the clinical progress in cauda equina syndrome （CES）, including the epidemic history, pathogenesis, diagnosis, treatment policy and prognosis. Data sources All reports on CES in the literature were searched in PubMed, Ovid, Springer, Elsevier, and the Chinese Biomedical Literature Disk using the key terms ＂cauda equina syndrome＂, ＂diagnosis＂, ＂treatment＂, ＂prognosis＂ and ＂evidence-based medicine＂. Study selection Original milestone articles and critical reviews written by major pioneer investigators about the cauda equina syndrome were selected. Results CES is rare, both atraumatically and traumatically. CES is variable, depending on the etiology of the syndrome. Males and females are equally affected. The incidence of The most common cause of CES is herniation of a lumbar intervertebral disc. CES symptoms may have sudden onset and evolve rapidly or sometimes chronic ally. Each type of CES has different typical signs and symptoms. Low back pain may be the most significant symptoms, accompanied by sciatica, lower extremities weakness, saddle or perianal hypoesthesia, sexual impotence, and sphincter dysfunction. MRI is usually the preferred investigation approach. Patients who have had CES are difficult to return to a normal status. Conclusions The diagnosis of CES is primarily based on a careful history inquiry and clinical examination, assisted by elective radiologic investigations. Early diagnosis and early surgical decompression are crucial for a favorable outcome in most CES cases.

Changes in compressed neurons from dogs with acute and severe cauda equina constrictions following intrathecal injection of brain-derived neurotrophic factor-conjugated polymer nanoparticles

This study established a dog model of acute multiple cauda equina constriction by experimental constriction injury （48 hours） of the lumbosacral central processes in dorsal root ganglia neurons. The repair effect of intrathecal injection of brain-derived neurotrophic factor with 15 mg encapsulated biodegradable poly（lactide-co-glycolide） nanoparticles on this injury was then analyzed. Dorsal root ganglion cells （LT） of all experimental dogs were analyzed using hematoxylin-eosin staining and immunohistochemistry at 1,2 and 4 weeks following model induction. Intrathecal injection of brain-derived neurotrophic factor can relieve degeneration and inflammation, and elevate the expression of brain-derived neurotrophic factor in sensory neurons of compressed dorsal root ganglion Simultaneously, intrathecal injection of brain-derived neurotrophic factor obviously improved neurological function in the dog model of acute multiple cauda equina constriction. Results verified that sustained intraspinal delivery of brain-derived neurotrophic factor encapsulated in biodegradable nanoparticles promoted the repair of histomorphology and function of neurons within the dorsal root ganglia in dogs with acute and severe cauda equina syndrome.

p75 neurotrophin receptor signal pathway influence on apoptosis in anterior horn neurons of the spinal cord in a rat model of cauda equina compression injury

BACKGROUND： Studies have demonstrated that cauda equina compression results in apoptosis of motor neurons in the spinal cord. The combination of p75 neurotrophin receptor （p75NTR） and precursor of nerve growth factor （pro-NGF） expression initiates the apoptotic pathway and induces neuronal apoptosis. However, few reports have focused on the p75-mediated mechanism of neuronal apoptosis following cauda equine compression injury OBJECTIVE： To determine apoptosis of spinal cord neurons and activation of the pro-NGF-p75NTR-JNK（c-Jun N-terminal kinase） signal pathway in rats following cauda equina compression, and to verify experimental outcomes. DESIGN, TIME AND SETTING： A randomized, controlled, in vivo experiment was performed at the Medical Experimental Center of Xi＇an Jiaotong University between April and November in 2008. MATERIALS： Streptavidin-perosidase kit was purchased from Wuhan Boster, China; in situ end labeling detection kit was provided by Promega, USA; type AEG-220G electron microscope was purchased from Hitachi, Japan. METHODS： A total of 48 healthy, adult, female, Sprague Dawley rats were randomly assigned to three groups： normal （n = 6）, sham-surgery （n = 6）, and compression （n = 36）. The compression group was randomly assigned to six subsets at 1,3, 5, 7, 14, and 28 days, respectively, with 6 rats in each subset. A cylindrical silica gel stick was implanted into the rats to compress 75% of the vertebral canal in the compression group; in the sham-surgery group, only vertebral resection was performed; and no procedures were performed in the normal group. MAIN OUTCOME MEASURES： At 1,3, 5, 7, 14, and 28 days following compression, L2-3 spinal cord segments were processed for immunohistochemistry, in situ cell apoptosis detection, and transmission electron microscopy observation. Nissl staining was used to observe neuronal survival in the L2 spinal cord segment. Immunohistochemistry was applied to detect expressions of pro-NGF, p75NTR, and JNK in the L2 segment. TUNEL fluorometric method was used to observe apoptosis of neurons in the L2 segment. RESULTS： In the normal and sham-surgery groups, little neuronal apoptosis was observed in the L2-3 spinal cord segment. At 3 days after compression injury, pro-NGF, p75NTR and JNK expression was observed in the spinal cord. Expression levels reached a peak at 7 days, and then gradually decreased. In the compression and sham-surgery groups, neurons primarily expressed pro-NGF and p75NTR. The number of JNK-positive neurons in the compression group was dramatically increased compared with the sham-surgery group （P〈 0.05）. A few neurons were apoptotic in the spinal cord 1 day after compression injury. The number of apoptotic neurons gradually increased and reached a peak at 7 days, and subsequently decreased. Apoptosis was still detectable at 28 days. There was a positive correlation between p75NTR expression and neuronal apoptosis （r= 0.75, P〈 0.05）. CONCLUSION： Following cauda equina compression injury, apoptosis of spinal cord neurons was observed. The compression-induced neuronal apoptosis was associated with p75NTR expression in the L2-3 spinal cord segment.

Mechanical properties of nerve roots and rami radiculares isolated from fresh pig spinal cords

No reports have described experiments designed to determine the strength characteristics of spinal nerve roots and rami radiculares for the purpose of explaining the complexity of symptoms of medullary cone lesions and cauda equina syndrome. In this study, to explain the pathogenesis of cauda equina syndrome, monoaxial tensile tests were performed to determine the strength characteristics of spinal nerve roots and rami radiculares, and analysis was conducted to evaluate the stress-strain relationship and strength characteristics. Using the same tensile test device, the nerve root and ramus radiculares isolated from the spinal cords of pigs were subjected to the tensile test and stress relaxation test at load strain rates of 0.1, 1, 10, and 100 s-1 under identical settings. The tensile strength of the nerve root was not rate dependent, while the ramus radiculares tensile strength tended to decrease as the strain rate increased. These findings provide important insights into cauda equina symptoms, radiculopathy, and clinical symptoms of the medullary cone.

Adenovirus-mediated short hairpin RNA interference against p75 neurotrophin receptor in pheochromocytoma cells

Previous studies have confirmed that motor neuron apoptosis in the anterior horn of the lumbosacral spinal cord is positively correlated with p75 neurotrophin receptor （p75NTR） expression in rat models of cauda equina syndrome. This study used adenovirus to carry a short hairpin RNA （shRNA） for p75NTR gene silencing, to reduce p75NTR expression in the damaged phase and to decrease motor neuron apoptosis. Three p75 siRNA template oligonucleotide segments （shRNA） were designed, and cloned into the 1.0 CMV shuttle vector. HEK293 cells were cotransfected with shuttle vector （carrying shRNA） and an adenovirus vector framework expressing enhanced green fluorescent protein. Thus, this study successfully obtained adenovirus carrying p75shRNA. The obtained viruses were named Ad.shRNA1, Ad.shRNA2, and Ad.shRNA3. The recombinant adenoviruses were separately used to infect cultured pheochromocytoma cells （PC12）. Forty-eight hours later, p75NTR mRNA and total protein were analyzed from the PC12 cells. Compared with the negative controls, RNA interference rates were separately 98.49 ± 0.68%, 95.08 ± 1.79% and 96.60 ± 1.14% at the mRNA level, and 72.89 ± 2.17%, 58.83 ± 1.15% and 59.88 ± 0.44% at the protein level in the Ad.shRNA1, Ad.shRNA2, and Ad.shRNA3 groups, respectively. Thus, recombinant adenovirus shRNA-mediated gene silencing successfully suppressed p75NTR expression.