Dose-response study of spinal hyperbaric ropivacaine for cesarean section

Background： Spinal hyperbaric ropivacaine may produce more predictable and reliable anesthesia than plain ropivacaine for cesarean section. The dose-response relation for spinal hyperbaric ropivacaine is undetermined. This double-blind, randomized, dose-response study determined the ED50 （50% effective dose） and ED95 （95% effective dose） of spinal hyperbaric ropivacaine for cesarean section anesthesia. Methods： Sixty parturients undergoing elective cesarean section delivery with use of combined spinal-epidural anesthesia were enrolled in this study. An epidural catheter was placed at the L1-L2 vertebral interspace then lumbar puncture was performed at the L3-L4 vertebral interspace, and parturients were randomized to receive spinal hyperbaric ropivacaine in doses of 10.5 mg, 12 mg, 13.5 mg, or 15 mg in equal volumes of 3 ml. Sensory levels （pinprick） were assessed every 2.5 min until a T7 level was achieved and motor changes were assessed by modified Bromage Score. A dose was considered effective if an upper sensory level to pin prick of T7 or above was achieved and no intraoperative epidural supplement was required. ED50 and ED95 were determined with use of a logistic regression model. Results： ED50 （95% confidence interval） of spinal hyperbaric ropivacaine was determined to be 10.37 （5.23-11.59） mg and ED95 （95% confidence interval） to be 15.39 （13.81-23.59） mg. The maximum sensory block levels and the duration of motor block and the rate of hypotension, but not onset of anesthesia, were significantly related to the ropivacaine dose. Conclusion： The ED50 and ED95 of spinal hyperbaric ropivacaine for cesarean delivery under the conditions of this study were 10.37 mg and 15.39 mg, respectively. Ropivacaine is suitable for spinal anesthesia in cesarean delivery.     

Congenital spinal intradural arachnoid cyst associated with intrathoracic meningocele in a child

Congenital spinal intradural arachnoid cyst associated with intrathoracic meningocele is very rare. We report a case in a 9-year-old Chinese boy who presented with a two-week history of progressive paraparesis and gait ataxia. Magnetic resonance imaging revealed that a dorsal intradural extramedullary cystic lesion extended from T1 to T5 and compressed the spinal cord. A left lateral intrathoracic meningocele pouch was found incidentally at the level of T1. The arachnoid cyst as well as meningocele was removed and the spinal cord compression was relieved. Arachnoid cyst was confirmed by histological examination. The patient recovered well postoperatively. This is the second report of such a case in the world according to the available literature. The take-home message for our case is that the surgical approach should be individualized, depending on the size and location.     

Spinal cord decompression reduces rat neural cell apoptosis secondary to spinal cord injury

Objective: To determine whether spinal cord decompression plays a role in neural cell apoptosis after spinal cord injury. Study design: We used an animal model of compressive spinal cord injury with incomplete paraparesis to evaluate neural cell apoptosis after decompression. Apoptosis and cellular damage were assessed by staining with terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate nick-end labelling (TUNEL) and immunostaining for caspase-3, Bcl-2 and Bax. Methods: Experiments were conducted in male Spragne-Dawley rats (n=78) weighing 300-400 g. The spinal cord was compressed posteriorly at T10 level using a custom-made screw for 6 h, 24 h or continuously, followed by decompression by removal of the screw. The rats were sacrificed on Day 1 or 3 or in Week 1 or 4 post-decompression. The spinal cord was removed en bloc and examined at lesion site, rostral site and caudal site (7.5 mm away from the lesion). Results: The numbers of TUNEL-positive cells were significantly lower at the site of decompression on Day l, and also at the rostral and caudal sites between Day 3 and Week 4 post-decompression, compared with the persistently compressed group. The numbers of cells between Day 1 and Week 4 were immunoreactive to caspase-3 and B-cell lymphoma-2 (Bcl-2)-associated X-protein (Bax), but not to Bcl-2, correlated with those of TUNEL-positive cells. Conclusion: Our results suggest that decompression reduces neural cell apoptosis following spinal cord injury.     

CX3CR1 contributes to streptozotocin-induced mechanical allodynia in the mouse spinal cord

Journal of Zhejiang University-SCIENCE B - 趋化因子 (CX3CL1)...     

Case Report:Congenital spinal intradural arachnoid cyst associated with intrathoracic meningocele in a child

Congenital spinal intradural arachnoid cyst associated with intrathoracic meningocele is very rare.We report a case in a 9-year-old Chinese boy who presented with a two-week history of progressive paraparesis and gait ataxia.Magnetic resonance imaging revealed that a dorsal intradural extramedullary cystic lesion extended from T1 to T5 and compressed the spinal cord.A left lateral intrathoracic meningocele pouch was found incidentally at the level of T1.The arachnoid cyst as well as meningocele was removed and the spinal cord compression was relieved.Arachnoid cyst was confirmed by histological examination.The patient recovered well postoperatively.This is the second report of such a case in the world according to the available literature.The take-home message for our case is that the surgical approach should be individualized,depending on the size and location.     

Deletion analysis of SMN1 and NAIP genes in southern Chinese children with spinal muscular atrophy

Spinal muscular atrophy (SMA) is a disorder characterized by degeneration of lower motor neurons and occasionally bulbar motor neurons leading to progressive limb and trunk paralysis as well as muscular atrophy. Three types of SMA are recognized depending on the age of onset, the maximum muscular activity achieved, and survivorship: SMA1, SMA2, and SMA3. The survival of motor neuron (SMN) gene has been identified as an SMA determining gene, whereas the neuronal apoptosis inhibitory protein (NAIP) gene is considered to be a modifying factor of the severity of SMA. The main objective of this study was to analyze the deletion of SMN1 and NAIP genes in southern Chinese children with SMA. Here, polymerase chain reaction (PCR) combined with restriction fragment length polymorphism (RFLP) was performed to detect the deletion of both exon 7 and exon 8 of SMN1 and exon 5 of NAIP in 62 southern Chinese children with strongly suspected clinical symptoms of SMA. All the 32 SMA1 patients and 76% (13/17) of SMA2 patients showed homozygous deletions for exon 7 and exon 8, and all the 13 SMA3 patients showed single deletion of SMN1 exon 7 along with 24% (4/17) of SMA2 patients. Eleven out of 32 (34%) SMA1 patients showed NAIP deletion, and none of SMA2 and SMA3 patients was found to have NAIP deletion. The findings of homozygous deletions of exon 7 and/or exon 8 of SMN1 gene confirmed the diagnosis of SMA, and suggested that the deletion of SMN1 exon 7 is a major cause of SMA in southern Chinese children, and that the NAIP gene may be a modifying factor for disease severity of SMA1. The molecular diagnosis system based on PCR-RFLP analysis can conveniently be applied in the clinical testing, genetic counseling, prenatal diagnosis and preimplantation genetic diagnosis of SMA. Project supported by the National Natural Science Foundation of China (No. J0710043), and the Natural Science Foundation of Zhejiang Province (No. 2007C33049), China     

Deletion analysis of SMN1 and NAIP genes in southern Chinese children with spinal muscular atrophy

Spinal muscular atrophy (SMA) is a disorder characterized by degeneration of lower motor neurons and occasionally bulbar motor neurons leading to progressive limb and trunk paralysis as well as muscular atrophy. Three types of SMA are rec-ognized depending on the age of onset, the maximum muscular activity achieved, and survivorship: SMA1, SMA2, and SMA3. The survival of motor neuron (SMN) gene has been identified as an SMA determining gene, whereas the neuronal apoptosis inhibitory protein (NAIP) gene is considered to be a modifying factor of the severity of SMA. The main objective of this study was to analyze the deletion of SMN1 and NAIP genes in southern Chinese children with SMA. Here, polymerase chain reaction (PCR) combined with restriction fragment length polymorphism (RFLP) was performed to detect the deletion of both exon 7 and exon 8 of SMNI and exon 5 of NAIP in 62 southern Chinese children with strongly suspected clinical symptoms of SMA. All the 32 SMAI patients and 76% (13/17) of SMA2 patients showed homozygous deletions for exon 7 and exon 8, and all the 13 SMA3 patients showed single deletion of SMN1 exon 7 along with 24% (4/17) of SMA2 patients. Eleven out of 32 (34%) SMA1 patients showed NAIP deletion, and none of SMA2 and SMA3 patients was found to have NAIP deletion. The findings of homozygous deletions of exon 7 and/or exon 8 of SMN1 gene confirmed the diagnosis of SMA, and suggested that the deletion of SMN1 exon 7 is a major cause of SMA in southern Chinese children, and that the NA1P gene may be a modifying factor for disease severity of SMA 1. The molecular diagnosis system based on PCR-RFLP analysis can conveniently be applied in the clinical testing, genetic counseling, prenatal diagnosis and preimplantation genetic diagnosis of SMA.