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.

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.

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.

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.

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.

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 (L7) 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 ofmotor neurons in the spinal cord. The combination of p75 neurotrophin receptor (p75NTR) andprecursor of nerve growth factor (pro-NGF) expression initiates the apoptotic pathway and inducesneuronal apoptosis. However, few reports have focused on the p75-mediated mechanism ofneuronal apoptosis following cauda equine compression injuryOBJECTIVE: To determine apoptosis of spinal cord neurons and activation of thepro-NGF-p75NTR-JNK(c-Jun N-terminal kinase) signal pathway in rats following cauda equinacompression, and to verify experimental outcomes.DESIGN, TIME AND SETTING: A randomized, controlled, in vivo experiment was performed at theMedical 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 endlabeling detection kit was provided by Promega, USA; type AEG-220G electron microscope waspurchased from Hitachi, Japan.METHODS: A total of 48 healthy, adult, female, Sprague Dawley rats were randomly assigned tothree groups: normal (n = 6), sham-surgery (n = 6), and compression (n = 36). The compressiongroup was randomly assigned to six subsets at 1,3, 5, 7, 14, and 28 days, respectively, with 6 rats ineach subset. A cylindrical silica gel stick was implanted into the rats to compress 75% of thevertebral canal in the compression group; in the sham-surgery group, only vertebral resection wasperformed; and no procedures were performed in the normal group.MAIN OUTCOME MEASURES: At 1,3, 5, 7, 14, and 28 days following compression, L_(2-3) spinalcord segments were processed for immunohistochemistry, in situ cell apoptosis detection, andtransmission electron microscopy observation. Nissl staining was used to observe neuronal survivalin the L_2 spinal cord segment. Immunohistochemistry was applied to detect expressions of pro-NGF,p75NTR, and JNK in the L_2 segment. TUNEL fluorometric method was used to observe apoptosis ofneurons in the L_2 segment.RESULTS: In the normal and sham-surgery groups, little neuronal apoptosis was observed in theL_(2-3) spinal cord segment. At 3 days after compression injury, pro-NGF, p75NTR and JNK expressionwas observed in the spinal cord. Expression levels reached a peak at 7 days, and then graduallydecreased. In the compression and sham-surgery groups, neurons primarily expressed pro-NGFand p75NTR. The number of JNK-positive neurons in the compression group was dramaticallyincreased compared with the sham-surgery group (P < 0.05). A few neurons were apoptotic in thespinal cord 1 day after compression injury. The number of apoptotic neurons gradually increasedand reached a peak at 7 days, and subsequently decreased. Apoptosis was still detectable at 28days. 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 wasobserved. The compression-induced neuronal apoptosis was associated with p75NTR expression inthe L_(2-3) spinal cord segment.

Cauda equina syndrome： a review of clinical progress

在尾 equina 症候群( CES )在临床的进步上考察文学的目的包括流行历史，致病，诊断，治疗政策和 prognosis.Data 在文学在 CES 上采购所有报告在 PubMed 被寻找，奥维德， Springer ， Elsevier ，并且用钥匙的中国生物医学的文学磁盘称为“尾 equina 症候群”，“诊断”，“treatment'”，预后“并且”基于证据的药“ .Study 选择原版里程碑文章和批评评论 wdtten 由男性和女性同等地被影响。CES 的发生是可变的，取决于症候群的病原学。CES 的最普通的原因是一个腰部的 intervertebral 磁盘的形成疝。CES 症状可以有突然的发作并且很快或有时发展长期的联盟者。CES 的每种类型有不同典型症状。腰骶部疼痛可以是最重要的症状，由坐骨神经痛，更低的极限软弱，僵绳或 perianal 伴随了感觉迟钝，性无能，和括约肌机能障碍。MRI 通常是比较喜欢的调查途径。有 CES 的病人是困难的把 CES 的诊断还给正常 status.Conclusions 首先基于小心的历史询问和临床的检查，被选任的放射线学的调查帮助。早诊断和早外科的解压缩为在大多数 CES 盒子中的有利结果是关键的。

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.

基于高通量转录组测序的牦牛和犏牛附睾尾部差异表达基因分析

【目的】探明牦牛和犏牛的附睾尾部差异表达基因(DEGs),筛选出与精子成熟和贮存密切相关的功能基因,为揭示犏牛精子发生及其成熟过程的分子机制打下理论基础。【方法】以牦牛和犏牛的附睾尾部为研究对象,通过Illumina 127-HiSeq 2000平台完成高通量转录组测序,经过滤、质量控制及拼接组装后,依据FDR<0.05且|log_(2)Fold Change|>1的筛选标准,通过EBSeq筛选出DEGs,然后进行GO功能注释分析和KEGG信号通路富集分析,并以实时荧光定量PCR验证高通量转录组测序数据的准确性。【结果】在牦牛和犏牛的附睾尾部共筛选获得76个DEGs,其中43个DEGs上调、33个DEGs下调;76个DEGs在COG、GO、KEGG、KOG、Nr、Pfam、Swiss-Prot和eggNOG等数据库中均有注释信息,尤其在COG和Pfam数据库中的注释率最高(达88.16%)。GO功能注释分析结果显示,DEGs被注释到生物过程(Biological process)、细胞组分(Cellular component)和分子功能(Molecular function)三大功能类别上;KEGG信号通路富集分析发现76个DEGs主要显著富集在3条信号通路上,分别是胆汁分泌通路(ko04976:Bile secretion)、ABC转运器(ko02010:ABC transporters)和cAMP信号通路(ko04024:cAMP signaling pathway)。随机选择8个DEGs(SERPINA1、MMP7、ATP2C1、ABCC1、NMT1、NAT1、CFTR和PRX)进行实时荧光定量PCR检测验证,结果显示这8个DEGs的表达模式与高通量转录组测序的结果基本一致,表明转录组数据准确可靠。【结论】在牦牛和犏牛的附睾尾部存在76个DEGs(43个DEGs上调,33个DEGs下调),显著富集在胆汁分泌通路、ABC转运器及c AMP信号通路上,与精子获能相关的DEGs有MMP7、IGFBP2和ABCC4基因,且这3个基因在犏牛附睾尾部呈下调表达,即精子获能失败可能是导致犏牛雄性不育的主要原因。

应激死亡无尾刺豚鼠的病理学观察

近年,圈养野生动物应激损伤的发病率呈上升趋势,严重影响圈养野生动物的饲养繁育工作。病理学作为一门研究疾病的分支学科,在应激损伤的诊断和治疗中具有重要的应用意义。该文以应激死亡的无尾刺豚鼠为例,采用病理学诊断技术进行描述讨论,为今后相关工作的开展提供基础资料。

Extensive Spinal Epidural Abscess: Cord Compression with Permanent Neurological Defects

Spinal epidural abscesses (SEA) are considerably rare and tend to present over two to five vertebral segments. Occasionally, there will be two or more noncontiguous areas of pyogenic collections [1]. Minimal cases have been reported to span the entire vertebral column;a meta-analysis estimates that 1% of all SEA are holospinal [2]. The triad of presenting symptoms includes fever, back pain (often midline), and neurologic defects [1] [2] [3]. Early detection is identified as a critical aspect of improved outcomes. Cases that do not present in this manner or with other masking symptoms can lead to delayed diagnosis, thus delaying treatment. In the event of cord compression, the occurrence of neurologic defects increases. Time from the onset of clinical manifestations to the operating room is crucial in reversing symptoms [2]. This article seeks to review a case of a 65-year-old male that presented to the emergency department (ED) due to a falling second to weakness and thigh pain. On presentation, he was also noted to have rhabdomyolysis causing acute kidney injury (AKI) with tubular necrosis. The patient was admitted to the hospital with a complex history of progressive leg weakness, pain in the lower back, incontinence, and elevated white blood cell count. Days into the admission, a magnetic resonance imaging (MRI) study was performed, which revealed a continuous posterior SEA from C4 to S2 with anterior mass effect causing spinal cord compression. Emergency neurosurgery was scheduled for laminectomies in the cervical, thoracic and lumbar spine to drain the abscess. Evaluation of this complex medical course, surgical approach to drainage of an incessant spinal column abscess, and sustained neurologic defects will be discussed.