BACKGROUND Cauda equina syndrome(CES)is characterized by a group of symptoms that may be caused by inflammation,spinal cord compression,venous congestion,or ischemia.This syndrome is commonly an indication for surgica...BACKGROUND Cauda equina syndrome(CES)is characterized by a group of symptoms that may be caused by inflammation,spinal cord compression,venous congestion,or ischemia.This syndrome is commonly an indication for surgical intervention but has not been determined as a postoperative complication following surgery for lumbar spine disease.CASE SUMMARY To report the case of a 54-year-old male patient who had CES following spinal surgery,with no obvious compression lesions found during re-exploration,suggesting that vascular insufficiency may have contributed to the condition.Furthermore,a series of urodynamic studies on bladder recovery patterns in such complications have also been investigated.CONCLUSION Postoperative CES requires urgent imaging and exploration to rule out compression;noncompressive cases,including vascular insufficiency may performed conservative management.展开更多
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...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.展开更多
BACKGROUND Redundant nerve roots(RNRs)of the cauda equina are often a natural evolutionary part of lumbar spinal canal stenosis secondary to degenerative processes characterized by elongated,enlarged,and tortuous nerv...BACKGROUND Redundant nerve roots(RNRs)of the cauda equina are often a natural evolutionary part of lumbar spinal canal stenosis secondary to degenerative processes characterized by elongated,enlarged,and tortuous nerve roots in the superior and/or inferior of the stenotic segment.Although magnetic resonance imaging(MRI)findings have been defined more frequently in recent years,this condition has been relatively under-recognized in radiological practice.In this study,lumbar MRI findings of RNRs of the cauda equina were evaluated in spinal stenosis patients.AIM To evaluate RNRs of the cauda equina in spinal stenosis patients.METHODS One-hundred and thirty-one patients who underwent lumbar MRI and were found to have spinal stenosis between March 2010 and February 2019 were included in the study.On axial T2-weighted images(T2WI),the cross-sectional area(CSA)of the dural sac was measured at L2-3,L3-4,L4-5,and L5-S1 levels in the axial plane.CSA levels below 100 mm^2 were considered stenosis.Elongation,expansion,and tortuosity in cauda equina fibers in the superior and/or inferior of the stenotic segment were evaluated as RNRs.The patients were divided into two groups:Those with RNRs and those without RNRs.The CSA cut-off value resulting in RNRs of cauda equina was calculated.Relative length(RL)of RNRs was calculated by dividing the length of RNRs at mid-sagittal T2WI by the height of the vertebral body superior to the stenosis level.The associations of CSA leading to RNRs with RL,disc herniation type,and spondylolisthesis were evaluated.RESULTS Fifty-five patients(42%)with spinal stenosis had RNRs of the cauda equina.The average CSA was 40.99±12.76 mm^2 in patients with RNRs of the cauda equina and 66.83±19.32 mm^2 in patients without RNRs.A significant difference was found between the two groups for CSA values(P<0.001).Using a cut-off value of 55.22 mm^2 for RNRs of the cauda equina,sensitivity,specificity,positive predictive value(PPV),and negative predictive value(NPV)values of 96.4%,96.1%,89.4%,and 98.7%were obtained,respectively.RL was 3.39±1.31(range:0.93-6.01).When the extension of RNRs into the superior and/or inferior of the spinal canal stenosis level was evaluated,it was superior in 54.5%,both superior and inferior in 32.8%,and inferior in 12.7%.At stenosis levels leading to RNRs of the cauda equina,29 disc herniations with soft margins and 26 with sharp margins were detected.Disc herniation type and spondylolisthesis had no significant relationship with RL or CSA of the dural sac with stenotic levels(P>0.05).As the CSA of the dural sac decreased,the incidence of RNRs observed at the superior of the stenosis level increased(P<0.001).CONCLUSION RNRs of the cauda equina are frequently observed in patients with spinal stenosis.When the CSA of the dural sac is<55 mm^2,lumbar MRIs should be carefully examined for this condition.展开更多
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 fact...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.展开更多
Acute cauda equina syndrome is known as a symptom of lumbar disc herniation, but to date, there have been no reports of cases caused by lumbar vertebral ligament ossification. We encountered a 61-year-old female patie...Acute cauda equina syndrome is known as a symptom of lumbar disc herniation, but to date, there have been no reports of cases caused by lumbar vertebral ligament ossification. We encountered a 61-year-old female patient with acute cauda equina syndrome associated with lumbar vertebral OPLL and OLF. The symptoms were improved by emergency laminectomy. One year after the surgery, the disturbances of gait and urination have been resolved.展开更多
Objective To explore the influence of the acute cauda equina compression on the lumbosacral spinal cord; To clarify the pathologic change of the motor neuron after acute cauda equina compression. Methods 27 canis fami...Objective To explore the influence of the acute cauda equina compression on the lumbosacral spinal cord; To clarify the pathologic change of the motor neuron after acute cauda equina compression. Methods 27 canis familiaris were randomly divided into 9 groups (3 in each): one for normal group, one for control group, and seven for compression groups. The control group and compressed groups was given operation and the sac made of silica gel was placed under the lamina of L5-6. Water was injected into the sac until their posterior legs paralysis in compressed groups, the animals had been compressed for 4, 8, 12, 24, 48, 72, 168 hours. The control group were not injected water. Cells apoptosis was investigated with the technology of TdT-mediated biotin dUTP nick end-labeling (TUNEL) staining. The Bcl-2 Bax and Caspase-3 protein was investigated by immunohistochemical method. Results TUNEL staining cells in anterior horn presented after compressed 8-12 hours, and at 72 hours the number of positive cells got to maximum, it decreased subsequently after 168 hours. The protein of Bax, Bcl-2 expressed a little in normal motor neuron. The caspase-3 protein didn't express in normal cell. They all reached the peak at 72 hours after compression. Conclusion The apoptosis of motor neuron occurred earlier after cauda equina acute compression. Bax protein restrained Bcl-2 protein then active caspase-3 and conduced apoptosis of motor neuron.展开更多
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 spina...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.展开更多
We report on a case of a mobile schwannoma of the cauda equina. The patient was a 24-year-old woman who visited our hospital with the chief complaints of low back pain and numbness of the right leg. A tumor was noted ...We report on a case of a mobile schwannoma of the cauda equina. The patient was a 24-year-old woman who visited our hospital with the chief complaints of low back pain and numbness of the right leg. A tumor was noted from the L2 midbody level to the L3 upper endplate on preoperative MRI and myelogram. During the surgery, a right L2 hemilaminectomy was performed, and the dura was incised, but no tumor was founded in the surgical field, and this was noted as a missing tumor. Intraoperative myelography showed that the tumor had moved to the adjacent vertebra on the caudal side. Myelography applied again to the caudal side of the mobile tumor. Then, the tumor had moved upward, and could be excised without an additional laminectomy.展开更多
CXT is a rare inherited autosomal recessive lipid storage disease due to the impaired metabolic pathway of cholesterol secondary to a deficiency in 27- sterol hydroxylase, an enzyme in the synthesis of chenodeoxycholi...CXT is a rare inherited autosomal recessive lipid storage disease due to the impaired metabolic pathway of cholesterol secondary to a deficiency in 27- sterol hydroxylase, an enzyme in the synthesis of chenodeoxycholic acid (CDCA), a primary bile acid. Abnormal bile acid synthesis leads to elevated plasma Cholestanol (a derivative of cholesterol) accumulation, especially in the lens, central nervous system (CNS) and tendons.展开更多
BACKGROUND Plexiform neurofibromas are extremely rarely found in the region of cauda equina and can pose a significant challenge in the diagnostic and management sense.To our knowledge,only 7 cases of cauda equina neu...BACKGROUND Plexiform neurofibromas are extremely rarely found in the region of cauda equina and can pose a significant challenge in the diagnostic and management sense.To our knowledge,only 7 cases of cauda equina neurofibromatosis(CENF)have been reported up-to-date.CASE SUMMARY We describe a case of a 55-year-old man with a 10 years history of progressive lower extremities weakness and bladder dysfunction.Before presenting,patient was misdiagnosed with idiopathic polyneuropathy.Lumbar spine MRI revealed a tortuous tumorous masses in the cauda equina region,extending through the Th12-L4 vertebrae.The patient underwent Th12-L3 Laminectomy with duraplasty.During the operation,the most enlarged electroneurographically silent nerve root was resected,anticipating inadequate decompression if nerve root was spared.The patient’s neurological condition improved post-operatively,but urinary retention became the major complaint.We provide a follow-up period of 10 years.During this time,the patient’s condition progressively worsened despite extensive decompression.The consequent MRI scans showed progressive enlargement of cauda equina roots and increasing lumbar stenosis,predominantly affecting L3-L4 segment.During the follow-up 8 years after the operation,the patient complained of worsening lower extremities sensorimotor function and neurogenic claudication.Subsequent MRI revealed lumbar spine stenosis at the level of L3-L4,requiring further decompression.The patient underwent a second surgery involving L4-L5 Laminectomy with duraplasty and L2-L5 transpedicular fixation.The post-operative period was uneventful.Latest follow-up 18 mo after the second surgery revealed substantial improvement in patient’s well-being.CONCLUSION CENF should be kept in mind during the differential diagnostic work-up for polyneuropathies.Management with an extensive decompression,duraplasty and primary spinal fixation represents a rational approach to achieve a sustained symptomatic improvement and superior overall outcome.展开更多
BACKGROUND Hypertrophic neuropathy of the cauda equina(HNCE)is a rare disease,especially in children.It can be caused by different etiological agents such as inflammation,tumor or hereditary factors.Currently,there is...BACKGROUND Hypertrophic neuropathy of the cauda equina(HNCE)is a rare disease,especially in children.It can be caused by different etiological agents such as inflammation,tumor or hereditary factors.Currently,there is no uniform standard for clinical treatment of HNCE.Furthermore,it is unclear whether spinal canal decompression is beneficial for patients with HNCE.CASE SUMMARY We report the case of a 13-year-old boy with enlargement of the cauda equina.The onset of the disease began at the age of 6 years and was initially marked by radiating pain in the buttocks and thighs after leaning over and weakness in the lower limbs when climbing a ladder.The child did not receive any medical treatment.As the disease slowly progressed,the child needed the help of others to walk,and he had a trendelenburg gait.He underwent spinal canal decompression and a nerve biopsy during his hospital stay.A diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy was made based on electrophysiological findings and pathological examination results.Immunoglobulin or hormone therapy was recommended during hospitalization,but his mother refused.After discharge,the boy’s mother helped him carry out postoperative rehabilitation training at home.His lower-limb muscle strength gradually increased,and he could stand upright and take steps.Six mo after surgery,the child was readmitted and began immunoglobulin therapy.Long-term oral steroid treatment was initiated after discharge.The movement and sensation of the lower limbs were further improved,and the boy could walk normally 1 year after surgery.CONCLUSION Spinal canal decompression can improve the clinical symptoms of HNCE caused by inflammation,even in children.When combined with specific etiological interventions,spinal cord decompression can lead to optimal outcomes.展开更多
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 o...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.展开更多
BACKGROUND Post-traumatic cauda equina nerve calcification is extremely rare in clinical practice,and its etiology,pathogenesis,treatment and prognosis are unclear.There are few studies and reports on Post-traumatic c...BACKGROUND Post-traumatic cauda equina nerve calcification is extremely rare in clinical practice,and its etiology,pathogenesis,treatment and prognosis are unclear.There are few studies and reports on Post-traumatic cauda equina nerve calci-fication,and this review reports a case of Post-traumatic cauda equina nerve calcification for reference.CASE SUMMARY A 52-year-old patient presented to our hospital with a history of lumbar spinal stenosis and a lumbar vertebral fracture caused by trauma.The patient's right lower limb had weakness in hip flexion,knee extension and plantarflexion with muscle strength grade 3,right ankle dorsiflexion and thumb dorsiflexion with muscle strength grade 0.The patient's skin sensation below the right knee plane disappeared.The patient's Computed tomography(CT)data showed signs of cauda equina nerve calcification and the terminal filaments in the plane of the third to fifth lumbar vertebrae.After treatment the patient's symptoms were slightly relieved.CONCLUSION We provide an extremely rare case of Post-traumatic cauda equina nerve calcification and offer a conservative treatment plan.However,the etiology,mechanism and treatment of Post-traumatic cauda equina nerve calcification are still unclear.This requires scholars to conduct more research and exploration in this area.展开更多
BACKGROUND Data regarding the neuroradiology features of the West Nile virus neuroinvasive disease(WNV NID)is rather scarce.To contribute to the knowledge of the WNV NID,we present a patient with a combination of ence...BACKGROUND Data regarding the neuroradiology features of the West Nile virus neuroinvasive disease(WNV NID)is rather scarce.To contribute to the knowledge of the WNV NID,we present a patient with a combination of encephalitis and acute flaccid paresis,with cauda equina arachnoiditis as the main magnetic resonance(MR)finding.CASE SUMMARY A 72-year-old female patient was admitted due to fever,headache and gait instability.During the first several days she developed somnolence,aphasia,urinary incontinence,constipation,and asymmetric lower extremities weakness.Cerebrospinal fluid analysis indicated encephalitis.Native brain computed tomography and MR were unremarkable,while spinal MR demonstrated cauda equina enhancement without cord lesions.Virology testing revealed WNV IgM and IgG antibodies in serum and cerebrospinal fluid,which confirmed acute WNV NID.The treatment was supportive.After two months only a slight improvement was noticed but cognitive impairment,loss of sphincter control and asymmetric inferior extremities weakness remained.The patient died after a month on chronic rehabilitation.CONCLUSION Cauda equina arachnoiditis is a rare,but possible neuroradiological feature in acute flaccid paresis form of WNV NID.展开更多
Spinal cord ischemia is an uncommon complication of an abdominal aortic aneurysm (AAA). We report the case of a 59-year-old man admitted for an acute ischemic Cauda equina syndrome secondary to a spinal cord embolizat...Spinal cord ischemia is an uncommon complication of an abdominal aortic aneurysm (AAA). We report the case of a 59-year-old man admitted for an acute ischemic Cauda equina syndrome secondary to a spinal cord embolization from an unknown partially thrombosed aortic aneurysm. The patient being at risk of further embolization, we achieved an emergency EVAR. The vascular post-operative course was uneventful. Neurologically, a post operative lumbar medullar MRI confirmed an ischemic Cauda equina syndrome and six months after the surgery, the patient still had a motor and sensory deficit in both lower limbs.展开更多
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 ...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.展开更多
文摘BACKGROUND Cauda equina syndrome(CES)is characterized by a group of symptoms that may be caused by inflammation,spinal cord compression,venous congestion,or ischemia.This syndrome is commonly an indication for surgical intervention but has not been determined as a postoperative complication following surgery for lumbar spine disease.CASE SUMMARY To report the case of a 54-year-old male patient who had CES following spinal surgery,with no obvious compression lesions found during re-exploration,suggesting that vascular insufficiency may have contributed to the condition.Furthermore,a series of urodynamic studies on bladder recovery patterns in such complications have also been investigated.CONCLUSION Postoperative CES requires urgent imaging and exploration to rule out compression;noncompressive cases,including vascular insufficiency may performed conservative management.
基金supported by grants from the Medical Scientific Fund and Intensive Research of Nanjing Military Area Command of Chinese PLA, No.Nan2007-13 and Nan 08Z003the Medical Scientific Fund and Research of Chinese PLA during the 12th Five-Year Plan Period,No.CWS11J260
文摘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.
基金This study was reviewed and approved by the Ethics Committee of the Tokat Gaziosmanpasa University Faculty of Medicine(No.19-KAEK-099).
文摘BACKGROUND Redundant nerve roots(RNRs)of the cauda equina are often a natural evolutionary part of lumbar spinal canal stenosis secondary to degenerative processes characterized by elongated,enlarged,and tortuous nerve roots in the superior and/or inferior of the stenotic segment.Although magnetic resonance imaging(MRI)findings have been defined more frequently in recent years,this condition has been relatively under-recognized in radiological practice.In this study,lumbar MRI findings of RNRs of the cauda equina were evaluated in spinal stenosis patients.AIM To evaluate RNRs of the cauda equina in spinal stenosis patients.METHODS One-hundred and thirty-one patients who underwent lumbar MRI and were found to have spinal stenosis between March 2010 and February 2019 were included in the study.On axial T2-weighted images(T2WI),the cross-sectional area(CSA)of the dural sac was measured at L2-3,L3-4,L4-5,and L5-S1 levels in the axial plane.CSA levels below 100 mm^2 were considered stenosis.Elongation,expansion,and tortuosity in cauda equina fibers in the superior and/or inferior of the stenotic segment were evaluated as RNRs.The patients were divided into two groups:Those with RNRs and those without RNRs.The CSA cut-off value resulting in RNRs of cauda equina was calculated.Relative length(RL)of RNRs was calculated by dividing the length of RNRs at mid-sagittal T2WI by the height of the vertebral body superior to the stenosis level.The associations of CSA leading to RNRs with RL,disc herniation type,and spondylolisthesis were evaluated.RESULTS Fifty-five patients(42%)with spinal stenosis had RNRs of the cauda equina.The average CSA was 40.99±12.76 mm^2 in patients with RNRs of the cauda equina and 66.83±19.32 mm^2 in patients without RNRs.A significant difference was found between the two groups for CSA values(P<0.001).Using a cut-off value of 55.22 mm^2 for RNRs of the cauda equina,sensitivity,specificity,positive predictive value(PPV),and negative predictive value(NPV)values of 96.4%,96.1%,89.4%,and 98.7%were obtained,respectively.RL was 3.39±1.31(range:0.93-6.01).When the extension of RNRs into the superior and/or inferior of the spinal canal stenosis level was evaluated,it was superior in 54.5%,both superior and inferior in 32.8%,and inferior in 12.7%.At stenosis levels leading to RNRs of the cauda equina,29 disc herniations with soft margins and 26 with sharp margins were detected.Disc herniation type and spondylolisthesis had no significant relationship with RL or CSA of the dural sac with stenotic levels(P>0.05).As the CSA of the dural sac decreased,the incidence of RNRs observed at the superior of the stenosis level increased(P<0.001).CONCLUSION RNRs of the cauda equina are frequently observed in patients with spinal stenosis.When the CSA of the dural sac is<55 mm^2,lumbar MRIs should be carefully examined for this condition.
基金the National Natural Science Foundation of China, No. 30672136
文摘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.
文摘Acute cauda equina syndrome is known as a symptom of lumbar disc herniation, but to date, there have been no reports of cases caused by lumbar vertebral ligament ossification. We encountered a 61-year-old female patient with acute cauda equina syndrome associated with lumbar vertebral OPLL and OLF. The symptoms were improved by emergency laminectomy. One year after the surgery, the disturbances of gait and urination have been resolved.
文摘Objective To explore the influence of the acute cauda equina compression on the lumbosacral spinal cord; To clarify the pathologic change of the motor neuron after acute cauda equina compression. Methods 27 canis familiaris were randomly divided into 9 groups (3 in each): one for normal group, one for control group, and seven for compression groups. The control group and compressed groups was given operation and the sac made of silica gel was placed under the lamina of L5-6. Water was injected into the sac until their posterior legs paralysis in compressed groups, the animals had been compressed for 4, 8, 12, 24, 48, 72, 168 hours. The control group were not injected water. Cells apoptosis was investigated with the technology of TdT-mediated biotin dUTP nick end-labeling (TUNEL) staining. The Bcl-2 Bax and Caspase-3 protein was investigated by immunohistochemical method. Results TUNEL staining cells in anterior horn presented after compressed 8-12 hours, and at 72 hours the number of positive cells got to maximum, it decreased subsequently after 168 hours. The protein of Bax, Bcl-2 expressed a little in normal motor neuron. The caspase-3 protein didn't express in normal cell. They all reached the peak at 72 hours after compression. Conclusion The apoptosis of motor neuron occurred earlier after cauda equina acute compression. Bax protein restrained Bcl-2 protein then active caspase-3 and conduced apoptosis of motor neuron.
基金supported by the National Natural Science Foundation of China (No.30672136)
文摘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.
文摘We report on a case of a mobile schwannoma of the cauda equina. The patient was a 24-year-old woman who visited our hospital with the chief complaints of low back pain and numbness of the right leg. A tumor was noted from the L2 midbody level to the L3 upper endplate on preoperative MRI and myelogram. During the surgery, a right L2 hemilaminectomy was performed, and the dura was incised, but no tumor was founded in the surgical field, and this was noted as a missing tumor. Intraoperative myelography showed that the tumor had moved to the adjacent vertebra on the caudal side. Myelography applied again to the caudal side of the mobile tumor. Then, the tumor had moved upward, and could be excised without an additional laminectomy.
文摘CXT is a rare inherited autosomal recessive lipid storage disease due to the impaired metabolic pathway of cholesterol secondary to a deficiency in 27- sterol hydroxylase, an enzyme in the synthesis of chenodeoxycholic acid (CDCA), a primary bile acid. Abnormal bile acid synthesis leads to elevated plasma Cholestanol (a derivative of cholesterol) accumulation, especially in the lens, central nervous system (CNS) and tendons.
文摘BACKGROUND Plexiform neurofibromas are extremely rarely found in the region of cauda equina and can pose a significant challenge in the diagnostic and management sense.To our knowledge,only 7 cases of cauda equina neurofibromatosis(CENF)have been reported up-to-date.CASE SUMMARY We describe a case of a 55-year-old man with a 10 years history of progressive lower extremities weakness and bladder dysfunction.Before presenting,patient was misdiagnosed with idiopathic polyneuropathy.Lumbar spine MRI revealed a tortuous tumorous masses in the cauda equina region,extending through the Th12-L4 vertebrae.The patient underwent Th12-L3 Laminectomy with duraplasty.During the operation,the most enlarged electroneurographically silent nerve root was resected,anticipating inadequate decompression if nerve root was spared.The patient’s neurological condition improved post-operatively,but urinary retention became the major complaint.We provide a follow-up period of 10 years.During this time,the patient’s condition progressively worsened despite extensive decompression.The consequent MRI scans showed progressive enlargement of cauda equina roots and increasing lumbar stenosis,predominantly affecting L3-L4 segment.During the follow-up 8 years after the operation,the patient complained of worsening lower extremities sensorimotor function and neurogenic claudication.Subsequent MRI revealed lumbar spine stenosis at the level of L3-L4,requiring further decompression.The patient underwent a second surgery involving L4-L5 Laminectomy with duraplasty and L2-L5 transpedicular fixation.The post-operative period was uneventful.Latest follow-up 18 mo after the second surgery revealed substantial improvement in patient’s well-being.CONCLUSION CENF should be kept in mind during the differential diagnostic work-up for polyneuropathies.Management with an extensive decompression,duraplasty and primary spinal fixation represents a rational approach to achieve a sustained symptomatic improvement and superior overall outcome.
基金Supported by the Yunnan Provincial Department of Science and Technology Kunming Medical University Application Foundation Research Joint Fund Project,No.202001AY070001-273the Epilepsy Research Fund of China Anti-Epilepsy Association,No.CQ-B-2021-04the Kunming Health Science and Technology Talent Training Project and“100 thousand”Project Training Plan,No.2021-SW(province)-23.
文摘BACKGROUND Hypertrophic neuropathy of the cauda equina(HNCE)is a rare disease,especially in children.It can be caused by different etiological agents such as inflammation,tumor or hereditary factors.Currently,there is no uniform standard for clinical treatment of HNCE.Furthermore,it is unclear whether spinal canal decompression is beneficial for patients with HNCE.CASE SUMMARY We report the case of a 13-year-old boy with enlargement of the cauda equina.The onset of the disease began at the age of 6 years and was initially marked by radiating pain in the buttocks and thighs after leaning over and weakness in the lower limbs when climbing a ladder.The child did not receive any medical treatment.As the disease slowly progressed,the child needed the help of others to walk,and he had a trendelenburg gait.He underwent spinal canal decompression and a nerve biopsy during his hospital stay.A diagnosis of chronic inflammatory demyelinating polyradiculoneuropathy was made based on electrophysiological findings and pathological examination results.Immunoglobulin or hormone therapy was recommended during hospitalization,but his mother refused.After discharge,the boy’s mother helped him carry out postoperative rehabilitation training at home.His lower-limb muscle strength gradually increased,and he could stand upright and take steps.Six mo after surgery,the child was readmitted and began immunoglobulin therapy.Long-term oral steroid treatment was initiated after discharge.The movement and sensation of the lower limbs were further improved,and the boy could walk normally 1 year after surgery.CONCLUSION Spinal canal decompression can improve the clinical symptoms of HNCE caused by inflammation,even in children.When combined with specific etiological interventions,spinal cord decompression can lead to optimal outcomes.
文摘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.
基金Supported by National Natural Science Foundation of China,No.82060879Natural Science Foundation of Gansu Province,No.20JR10RA356 and No.2022-0405-JCC-1430+2 种基金Lanzhou Science and Technology Plan Project,No.2022-3-30Paikouen-Spine Pathological Fracture Vertebral Body Strengthening Treatment Special Fund Project,No.BKJP2018004Local Projects Transferred by the Central Government in 2021,No.20210200111.
文摘BACKGROUND Post-traumatic cauda equina nerve calcification is extremely rare in clinical practice,and its etiology,pathogenesis,treatment and prognosis are unclear.There are few studies and reports on Post-traumatic cauda equina nerve calci-fication,and this review reports a case of Post-traumatic cauda equina nerve calcification for reference.CASE SUMMARY A 52-year-old patient presented to our hospital with a history of lumbar spinal stenosis and a lumbar vertebral fracture caused by trauma.The patient's right lower limb had weakness in hip flexion,knee extension and plantarflexion with muscle strength grade 3,right ankle dorsiflexion and thumb dorsiflexion with muscle strength grade 0.The patient's skin sensation below the right knee plane disappeared.The patient's Computed tomography(CT)data showed signs of cauda equina nerve calcification and the terminal filaments in the plane of the third to fifth lumbar vertebrae.After treatment the patient's symptoms were slightly relieved.CONCLUSION We provide an extremely rare case of Post-traumatic cauda equina nerve calcification and offer a conservative treatment plan.However,the etiology,mechanism and treatment of Post-traumatic cauda equina nerve calcification are still unclear.This requires scholars to conduct more research and exploration in this area.
基金Croatian Science Foundation,Project No. IP 2016-06-7456 CRONEUROARBOEuropean Union’s Horizon 2020 Research and Innovation Programme,No. 653316。
文摘BACKGROUND Data regarding the neuroradiology features of the West Nile virus neuroinvasive disease(WNV NID)is rather scarce.To contribute to the knowledge of the WNV NID,we present a patient with a combination of encephalitis and acute flaccid paresis,with cauda equina arachnoiditis as the main magnetic resonance(MR)finding.CASE SUMMARY A 72-year-old female patient was admitted due to fever,headache and gait instability.During the first several days she developed somnolence,aphasia,urinary incontinence,constipation,and asymmetric lower extremities weakness.Cerebrospinal fluid analysis indicated encephalitis.Native brain computed tomography and MR were unremarkable,while spinal MR demonstrated cauda equina enhancement without cord lesions.Virology testing revealed WNV IgM and IgG antibodies in serum and cerebrospinal fluid,which confirmed acute WNV NID.The treatment was supportive.After two months only a slight improvement was noticed but cognitive impairment,loss of sphincter control and asymmetric inferior extremities weakness remained.The patient died after a month on chronic rehabilitation.CONCLUSION Cauda equina arachnoiditis is a rare,but possible neuroradiological feature in acute flaccid paresis form of WNV NID.
文摘Spinal cord ischemia is an uncommon complication of an abdominal aortic aneurysm (AAA). We report the case of a 59-year-old man admitted for an acute ischemic Cauda equina syndrome secondary to a spinal cord embolization from an unknown partially thrombosed aortic aneurysm. The patient being at risk of further embolization, we achieved an emergency EVAR. The vascular post-operative course was uneventful. Neurologically, a post operative lumbar medullar MRI confirmed an ischemic Cauda equina syndrome and six months after the surgery, the patient still had a motor and sensory deficit in both lower limbs.
文摘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.
