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.

Magnetic resonance imaging findings of redundant nerve roots of the cauda equina

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.

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.

A Case of Acute Cauda Equina Syndrome for Combined Lumbar Ossification of the Posterior Longitudinal and Yellow Ligament

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.

THE EXPRESSION OF BCL-2, BAX AND CASPASE-3 IN NEURON OF THE SPINAL CORD ANTERIOR HORN AFTER CAUDA EQUINA ACUTE COMPRESSION

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.

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.

Mobile Schwannoma of the Cauda Equina for Which Intraoperative Myelography Was Useful in Locating

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.

Enlarged cauda equina nerve roots in Cerebrotendinous Xanthomatosis

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.

Plexiform neurofibroma of the cauda equina with follow-up of 10 years:A case report

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.

Spinal canal decompression for hypertrophic neuropathy of the cauda equina with chronic inflammatory demyelinating polyradiculoneuropathy:A case report

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.

Post-traumatic cauda equina nerve calcification:A case report

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.

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.

Cauda equina arachnoiditis–a rare manifestation of West Nile virus neuroinvasive disease:A case report

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.

Ischemic <i>Cauda equina</i>Syndrome Due to Spinal Embolization as a First Manifestation of an Infrarenal Abdominal Aortic Aneurysm

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.

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 with urinary retention as a postoperative complication of lumbar spine surgery:A case report

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.

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.

Microsurgical dorsal root entry zone coagulation for chronic neuropathic pain due to spinal cord and/or cauda equina injuries

Chronic pain is a major problem for patients suffering from spinal cord injury （SCI）.The prevalence of SCI-related pain ranges from 48% to 94% depending on the method of data acquisition and type of pain considered.1 SCI-related neuropathic pain is classified into three subtypes：above-,at-,and below-lesion-level pain.After SCI,it is believed that the dorsal horn of the injured spinal cord expressed increased electrical activity.2 Thus,the neurosurgical procedures for coagulation in the dorsal root entry zone （DREZ） have proved to be most effective in chronic neuropathic pain due to SCI.The aim of this study was to describe the effect and safety ofmicrosurgical DREZ coagulation in treating chronic SCI-related neuropathic pain.

尺胫针结合丹鹿通督片加麦肯基疗法对腰椎间盘突出症合并马尾神经损伤患者的临床研究

目的:探讨尺胫针结合丹鹿通督片加麦肯基疗法对腰椎间盘突出症合并马尾神经损伤患者的疗效及对镇痛效应和致疼因子及ERK、p-P38表达的影响。方法:90例腰椎间盘突出症合并马尾神经损伤患者随机分为对照组与研究组,每组各45例。对照组患者采用丹鹿通督片结合麦肯基疗法进行治疗,研究组在丹鹿通督片结合麦肯基疗法治疗的基础上给予尺胫针治疗,连续治疗4周后统计临床疗效。比较对照组和研究组治疗前后Frankel脊髓损伤评分、VAS疼痛评分、血清前列腺素E2(PGE2)、5-羟色胺(5-HT)以及一氧化氮(NO)等致疼因子表达水平以及血清细胞外调节蛋白激酶(ERK)和磷酸化-P38丝裂原活化蛋白激酶(p-P38MAPK)表达水平。结果:研究组治疗总有效率91.11%(41/45)显著高于对照组的73.33%(33/45),差异具有统计学意义(P<0.05);治疗结束后研究组下肢放射性疼痛、麻木无力、大便无力和排尿不畅评分低于对照组,差异具有统计学意义(P<0.05);治疗结束后研究组Frankel脊髓损伤评分高于对照组,差异具有统计学意义(P<0.05);研究组VAS,评分低于对照组,差异具有统计学意义(P<0.05);治疗结束后研究组血清PGE2、5-HT以及NO含量低于对照组,差异具有统计学意义(P<0.05);治疗结束后研究组血清ERK、p-P38MAPK表达水平低于对照组,差异具有统计学意义(P<0.05)。结论:尺胫针结合丹鹿通督片加麦肯基疗法对腰椎间盘突出症合并马尾神经损伤患者疗效更佳,有助于修复马尾神经损伤,降低致疼因子的表达,从而减轻患者腰腿疼痛症状,其机制可能与影响ERK、p-P38MAPK的表达有关。

腰椎MRI评估马尾神经前根横截面积在脊髓性肌萎缩Ⅱ型和Ⅲ型的应用价值

目的:探讨腰椎MRI评估马尾神经前根横截面积在脊髓性肌萎缩(SMA)Ⅱ型和Ⅲ型的应用价值。方法:根据发病年龄及能达到的最大运动里程碑,将26例基因确诊的SMA儿童分为SMAⅡ型组16例和SMAⅢ型组10例,以双下肢肌力评定标准,将其分为轻度组13例和中重度组13例,同时收集性别、年龄匹配的26例健康儿童作为对照组(NC)。以腰椎MRI正中矢状面T_(2)WI快速自旋回波序列脊髓圆锥下方10 mm的横轴面图像作为测量平面,分别测量各组左、右马尾神经前根的最大横截面积(MCA),进行组内与组间比较。结合双下肢肌力组别,进行左、右马尾神经前根MCA比较分析,同时评价两者相关性。结果:SMAⅡ型组[左侧(0.942±0.141)mm^(2)vs.(1.313±0.217)mm^(2),t=-5.729,P<0.01;右侧(0.907±0.185)mm^(2)vs.(1.309±0.194)mm^(2),t=-5.984,P<0.01]和Ⅲ型组[左侧(1.047±0.150)mm^(2)vs.(1.588±0.255)mm^(2),t=-5.779,P<0.01;右侧(1.065±0.148)mm^(2)vs.(1.603±0.253)mm^(2),t=-5.799,P<0.01]儿童马尾神经前根的MCA均较其性别、年龄匹配的NC组纤细。不同肌力组别SMA儿童同侧马尾神经前根MCA之间差异具有统计学意义(P均<0.01)。SMA儿童左、右马尾神经前根MCA与双下肢肌力之间存在较强正相关(左侧r=0.763,右侧r=0.813)。结论:马尾神经前根纤细是SMA儿童特征性影像学标志。腰椎MRI可定量测量SMAⅡ型和Ⅲ型儿童马尾神经前根横截面积,MCA与双下肢肌力呈正相关。