Meuli M, et al. The spinal cord lesion in human fetuses with myelomeningocele: Implications for fetal surgery. J Pediatr Surg. The first report to describe the detailed structure of myelomeningocele lesions in human fetuses and to provide evidence of progressive damage to the exposed open spinal cord; the prenatal approach to repair of myelomeningocele has been based on this evidence. Open spina bifida: birth findings predict long-term outcome. Arch Dis Child. This 40 -year follow -up of people whose myelomeningocele lesions were repaired soon after birth shows that higher spinal cord lesions have a worse prognosis than lower lesions, encompassing continence, ability to walk, and capacity to live and work independently.
Economic burden of neural tube defects and impact of prevention with folic acid: a literature review. Eur J Pediatr. Oxford Univ. Press; Epidemiology and Control of Neural Tube Defects. International Center on Birth Defects. International Center on Birth Defects; Li Z, et al. Extremely high prevalence of neural tube defects in a 4 county area in Shanxi Province, China. Moore CA, et al. Elevated rates of severe neural tube defects in a high-prevalence area in northern China.
Am J Med Genet. Canfield MA, et al. Anencephaly and spina bifida among Hispanics: maternal, sociodemographic, and acculturation factors in the National Birth Defects Prevention Study. Cragan JD, et al.
Surveillance for anencephaly and spina bifida and the impact of prenatal diagnosis — United States, — Impact of prenatal diagnosis and elective termination on prevalence and risk estimates of neural tube defects in California, — Am J Epidemiol. The prevalence of congenital anomalies in Europe. Adv Exp Med Biol. Spina bifida and anencephalus in Greater London. J Med Genet. Wyszynski DF, editor. Hypothesis: the female excess in cranial neural tube defects reflects an epigenetic drag of the inactivating X chromosome on the molecular mechanisms of neural fold elevation.
Leck I. Causation of neural tube defects: clues from epidemiology. Br Med Bull. Maternal overweight and obesity and the risk of congenital anomalies: a systematic review and metaanalysis. Waller DK, et al. Prepregnancy obesity as a risk factor for structural birth defects. Arch Pediatr Adolesc Med. Prepregnancy obesity: a complex risk factor for selected birth defects.
This paper provides a critical synoptic view of the importance and complexity of obesity as a risk factor for human birth defects. The impact of folic acid intake on the association among diabetes mellitus, obesity, and spina bifida. Am J Obstet Gynecol. Proportion of neural tube defects attributable to known risk factors. Fetal spina bifida: loss of neural function in utero. J Neurosurg. An update to the list of mouse mutants with neural tube closure defects and advances toward a complete genetic perspective of neural tube closure.
Genetics and development of neural tube defects. J Pathol. Mouse mutants with neural tube closure defects and their role in understanding human neural tube defects. A consideration of the evidence that genetic defects in planar cell polarity contribute to the etiology of human neural tube defects. Murdoch JN, et al. Interactions between planar cell polarity genes cause diverse neural tube defects.
Dis Model Mech. Pickell L, et al. Methylenetetrahydrofolate reductase deficiency and low dietary folate increase embryonic delay and placental abnormalities in mice. Narisawa A, et al. Mutations in genes encoding the glycine cleavage system predispose to neural tube defects in mice and humans.
Hum Mol Genet. Pai YJ, et al. Glycine decarboxylase deficiency causes neural tube defects and features of nonketotic hyperglycinemia in mice. Nat Commun. Robert E, Guidbaud P. Maternal valproic acid and congenital neural tube defects.
Phiel CJ, et al. Histone deacetylase is a direct target of valproic acid, a potent anticonvulsant, mood stabilizer, and teratogen. J Biol Chem. Neural tube defects along the Texas-Mexico border, — Marasas WFO, et al. Fumonisins disrupt sphingolipid metabolism, folate transport, and neural tube development in embryo culture and in vivo: a potential risk factor for human neural tube defects among populations consuming fumonisincontaminated maize.
J Nutr. Neural tube defects in embryos of diabetic mice: role of the Pax-3 gene and apoptosis. The development of the human brain, the closure of the caudal neuropore, and the beginning of secondary neurulation at stage Anat Embryol.
Ybot-Gonzalez P, et al. Convergent extension, planarcell- polarity signalling and initiation of mouse neural tube closure. Neural plate morphogenesis during mouse neurulation is regulated by antagonism of BMP signalling. Curly tail: a year history of the mouse spina bifida model. Schoenwolf GC. Histological and ultrastructural studies of secondary neurulation of mouse embryos. Am J Anat. Stem cells, signals and vertebrate body axis extension.
This paper reviews the important studies that have shown the existence of multipotent progenitor cells at the caudal extremity of the embryo, and that have determined the signalling pathways involved in secondary neurulation and formation of the lower body axis.
Spinal lipomas: clinical spectrum, embryology, and treatment. Neurosurg Focus. Barkovich AJ, Raybaud C. Pediatric Neuroimaging.
The cause of Chiari II malformation: a unified theory. Pediatr Neurosci. The cerebellum in children with spina bifida and Chiari II malformation: quantitative volumetrics by region. Fletcher JM, et al. Spinal lesion level in spina bifida: a source of neural and cognitive heterogeneity.
Ware AL, et al. Anatomical and diffusion MRI of deep gray matter in pediatric spina bifida. Neuroimage Clin. Treble-Barna A, et al. Prospective and episodic memory in relation to hippocampal volume in adults with spina bifida myelomeningocele. Barkovich AJ, Norman D. Anomalies of the corpus callosum: correlation with further anomalies of the brain.
Am J Roentgenol. Crawley JT, et al. Structure, integrity, and function of the hypoplastic corpus callosum in spina bifida myelomeningocele. Brain Connect. Herweh C, et al.
How innocent is corpus callosum dysgenesis? Pediatr Neurosurg. Juranek J, et al. Neocortical reorganization in spina bifida. Del Bigio MR. Neuropathology and structural changes in hydrocephalus. Dev Disabil Res Rev. This report integrates the results of animal and human studies to further our understanding of the effects of hydrocephalus on the brain. Hasan KM, et al.
White matter microstructural abnormalities in children with spina bifida myelomeningocele and hydrocephalus: a diffusion tensor tractography study of the association pathways.
J Magn Reson Imaging. Diffusion tensor imaging evaluation of white matter in adolescents with myelomeningocele and Chiari II malformation. Pediatr Radiol. Williams VJ, et al. Examination of frontal and parietal tectocortical attention pathways in spina bifida meningomyelocele using probabilistic diffusion tractography. Hampton LE, et al. Hydrocephalus status in spina bifida: an evaluation of variations in neuropsychological outcomes. J Neurosurg Pediatr.
Functional significance of atypical cortical organization in spina bifida myelomeningocele: relations of cortical thickness and gyrification with IQ and fine motor dexterity. Cereb Cortex. Cerebellar motor function in spina bifida meningomyelocele. Covert orienting in three etiologies of congenital hydrocephalus: the effect of midbrain and posterior fossa dysmorphology.
J Int Neuropsychol Soc. Hannay HJ, et al. Auditory interhemispheric transfer in relation to patterns of partial agenesis and hypoplasia of the corpus callosum in spina bifida meningomyelocele.
Taylor HB, et al. Motor contingency learning and infants with spina bifida. A model of neurocognitive function in spina bifida over the life span. This work provides a framework for understanding the variability in cognitive and motor outcomes for people with myelomeningocele, based on genetic, neurological and environmental factors.
Early prenatal diagnosis of anencephaly. Early termination of anencephalic pregnancy after detection by raised alpha-fetoprotein levels. Amniotic fluid acetylcholinesterase electrophoresis as a secondary test in the diagnosis of anencephaly and open spina bifida in early pregnancy Report of the Collaborative Acetylcholinesterase Study.
Wald NJ, et al. Maternal serum-alpha-fetoprotein measurement in antenatal screening for anencephaly and spina bifida in early pregnancy. Report of UK collaborative study on alpha-fetoprotein in relation to neural-tube defects.
Wald NJ. Prenatal screening for open neural tube defects and Down syndrome: three decades of progress. Prenat Diag. Ultrasound in the diagnosis of spina bifida. Small biparietal diameter of fetuses with spina bifida: implications for antenatal screening. Br J Obstet Gynaecol. Can prenatal ultrasound findings predict ambulatory status in fetuses with open spina bifida? Ultrasound screening for spina bifida: cranial and cerebellar signs.
A sonographic sign which predicts which fetuses with hydrocephalus have an associated neural tube defect. J Ultrasound Med. Thiagarajah S, et al. Early diagnosis of spina bifida: the value of cranial ultrasound markers. Obstet Gynecol. Bahlmann F, et al. Cranial and cerebral signs in the diagnosis of spina bifida between 18 and 22 weeks of gestation: a German multicenter study.
The early diagnosis of neural tube defects. Evaluation of the lemon and banana signs in one hundred thirty fetuses with open spina bifida. This investigation demonstrates the importance of the cranial signs in prenatal ultrasonography screening for spina bifida. Chitty LS. Ultrasound screening for fetal abnormalities.
The changing prevalence of neural tube defects: a population-based study in the north of England, — Paediatr Perinat Epidemiol.
Prenatally diagnosed neural tube defects: ultrasound, chromosome, and autopsy or postnatal findings in cases. This work studies the underlying aetiology of NTDs and demonstrates the benefit of autopsy and other investigations in determining aetiology.
Buyukkurt S, et al. Prenatal determination of the upper lesion level of spina bifida with threedimensional ultrasound.
Fetal Diagn Ther. Van Der Vossen S, et al. Role of prenatal ultrasound in predicting survival and mental and motor functioning in children with spina bifida. Ultrasound Obstet Gynecol. Folic acid in early pregnancy: a public health success story.
This paper nicely summarizes the very extensive literature on folic acid and NTDs, including data obtained from human genetic studies and from animal experiments. Vitamin deficiencies and neural tube defects.
Smithells RW, et al. Apparent prevention of neural tube defects by periconceptional vitamin supplementation. This is the randomized clinical trial on which primary prevention of spina bifida by folic acid is based. Prevention of the first occurrence of neural-tube defects by periconceptional vitamin supplementation.
N Engl J Med. Changes in the birth prevalence of selected birth defects after grain fortification with folic acid in the United States: findings from a multistate population-based study.
Wheat flour fortification with folic acid: changes in neural tube defects rates in Chile. The Costa Rican experience: reduction of neural tube defects following food fortification programs. Nutr Rev. De Wals P, et al. Reduction in neural-tube defects after folic acid fortification in Canada.
Decline in the prevalence of neural tube defects following folic acid fortification and its cost-benefit in South Africa. Decline in the incidence of neural tube defects after the national fortification of flour — Saudi Med J.
Effects of folic acid fortification on the prevalence of neural tube defects. Rev Saude Publica. Ricks DJ, et al. Rev Panam Salud Pubica. Neural tube defects in Australia: trends in encephaloceles and other neural tube defects before and after promotion of folic acid supplementation and voluntary food fortification. Oakley GP Jr. Folic acid-preventable spina bifida: a good start but much to be done.
Am J Prev Med. Not all cases of neural-tube defect can be prevented by increasing the intake of folic acid. Br J Nutr. The role of folic acid fortification in neural tube defects: a review. Crit Rev Food Sci Nutr. Rintoul NE, et al. A new look at myelomeningoceles: functional level, vertebral level, shunting, and the implications for fetal intervention. Kulkarni AV, et al. Endoscopic third ventriculostomy and choroid plexus cauterization in infants with hydrocephalus: a retrospective Hydrocephalus Clinical Research Network study.
McComb JG. Spinal and cranial neural tube defects. Semin Pediatr Neurol. Bauer SB. The management of the myelodysplastic child: a paradigm shift.
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Minus Related Pages. On This Page. Links with this icon indicate that you are leaving the CDC website. An incision is made at the side of the apex of adhesion between the dura mater and the spinal cord or the cyst containing protruded spinal cord, the nerve within the cauda equina. Corresponding tethering should be the cyst is carefully protected, and annular resection released. The redundant cyst wall should be trimmed of the remaining parts is done under direct vision.
The par spinal Complete dissection is performed to release the spinal muscle and fascia should be dissected around the laminar cord and neural fibers adhered to the cyst wall.
Because defect and the spinal defect covered using the reinforced a subcutaneous lipoma invades the spinal cord in cases suture technique. The aim of or an ultrasonic aspirator as much as possible to expose surgery is to dissect adhesion between the lipoma and the layer of neural placode. Finally, interrupted suturing the dura mater, reduce the volume of the lipoma, and is performed for the split spinal cord, which is placed into release spinal cord tethering and compression to allow the spinal canal.
The redundant bulging dura mater is the reconstructed spinal cord to be suspended in the trimmed, and expanded suturing to the dural sac is done subarachnoid space satisfactorily. The surgical technique for a spinal cord lipoma involves Surgical procedures for the two subtypes of cutting open the dura mater from the cephalic normal myelomeningocele or lipomyelomeningocele are similar.
The tumor For type I, the only requirement is to dissect and cut membrane should be cut open and the lipoma should be off the herniated distal end of the spinal cord from gradually removed outside the spinal cord with a micro the bulging dura mater [Figure 17].
After most lipoma lesions outside the spinal spinal cord herniation in type II, the herniated spinal cord are removed and the spinal cord is decompressed, cord cannot be cut off as is done in type I because it the spinal cord should be slowly lifted from the ventral may break the spinal cord into two parts and result in side of the spinal canal. At this point, the boundary of irreversible neurological damage.
The spinal cord should spinal cord is not yet isolated and the lipoma close to be separated from the bulging dural sac along the course the spinal cord surface should not be removed in a hurry of the spinal cord and placed back into the spinal to avoid damaging the spinal cord below it. The spinal canal [Figure 18]. The spinal cord should be gently pulled aside at this point to further should be dissected and cut off from both sides of the identify the distal end of the dural sac inside the sacral dura mater using a micro scissor in a cephalic to caudal canal because the course of the dural sac end slants direction to release the tethering and expose the spinal upward within the sacral canal.
After the sacral sac end cord boundary. Then the fat and fibrous tissue should is reached, dissection should be carried out from both be further removed from the spinal cord surface safely, sides to the midline to completely isolate the conus effectively, and maximally using the ultrasonic aspirator medullaris from the end of the dural sac and entirely or CO2 laser knife until the layer of the neural plate release the tethered spinal cord.
After the boundary of is exposed. The small amount of fat tissue within the the conus medullaris is totally exposed, the fibrous fat spinal cord should not be forcefully removed in order to tissue on the surface of the conus medullaris should protect spinal cord function.
Surgery for sacrococcygeal spinal cord lipoma is more difficult than surgery for lumbosacral spinal Finally, the opened spinal cord should be repaired with cord lipoma. In patients with lumbosacral spinal interrupted suture to reduce the risk of postoperative cord lipoma, the conus medullaris is located in the adhesion between the dorsal side of the spinal cord and middle segment of the lumbosacral dura mater and the suture site in the dura mater, and minimize the the boundary is easily observed.
As long as the normal possibility of secondary tethering. The bony septum However, in patients with sacrococcygeal spinal cord outside the dura mater should be removed as much as lipoma, the conus medullaris is located in the distal possible using a ranger or small awl. In most cases, there end of the dural sac. The lipoma on the surface of are many blood vessels around the septum, which may the conus medullaris not only grows together with the cause massive bleeding if injured. The dura of the two conus medullaris, but also grows outside the sacral spinal cords should be cut open.
Often there are fibrous canal and connects with the normal fat tissue in the adhesions between the spinal cord and the dura mater at sacrococcygeal area without boundaries. Because the the site of the septum, and any such adhesions should be lipoma completely covers the conus medullaris and completely separated.
Our method is to diminish the fat from and S1 spinouts processes. The dura mater and arachnoid the cephalic end, lift the spinal cord from the ventral mater should be cut open and the filum terminale side after the fat becomes thinned, and then cut off identified according to midline location, yellow or silver the spinal cord from the dura mater. The filum terminale should be cord should be further removed in a cephalic to caudal separated from the peripheral nerve and slightly rotated direction, and the lipoma of the conus medullaris to identify the presence of nerve adhesion on the ventral and tethering should then be treated.
The key point side. After electrocoagulation, 5 mm of filum terminale is to accurately identify the boundary between the should be cut off as a specimen for pathological distal end of the dural sac and the conus medullaris evaluation. If dissection toward the midline cord.
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