Effects of birth advancement in Chiari malformation in a surgical myelomeningocele model in rabbits

Fontecha, César G.; Aguire, Marius; Soldado, Francisco; Peiró, José L.; Torán, Núria; Vidal, Núria; Martínez, Vicente

doi:10.1016/j.jpedsurg.2009.08.003

Cited by 6 publications

(8 citation statements)

References 32 publications

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“…The degree of hindbrain herniation was 80% in the not treated group, 36.8% in birth advancement plus steroid treatment, 41.8% in birth advancement, and 44.4% in steroid treatment. Treated groups showed less severe hindbrain herniation than non-treated animals, although no significant differences between treated animals were noted [83].…”

Section: Authorsmentioning

confidence: 79%

“…Year Contribution Brunelli and Brunelli [76] 1984 First published attempt of surgical creation of spinal defect Calvano et al [77] 1998 Creation of spinal defect with holmium laser Housley et al [78] 2000 First successful surgical creation of MMC Grande et al [79] 2002 Absent evoked potential responses in hindlimbs of MMC fetuses Pedreira et al [80] 2003 Repair attempt with cellulose graft Juliá et al [81] 2006 Reduced neurologic sequelae with covering of the defect Fontecha et al [82] 2007 Impact of preterm delivery and steroid treatment, defect healing and hindbrain herniation Fontecha et al [83] 2010 Impact of preterm delivery and steroid treatment on severity of Chiari malformation Shieh et al [84] 2019 Use of TRASCET in the rabbit model of spina bifida to induce defect coverage with neoskin physical examination [81]. Evoked potential amplitudes of hindlimbs were flat on M animals and significantly reduced on T animals, when compared to controls, which were considered normal.…”

Section: Authorsmentioning

confidence: 99%

“…Fontecha et al [83] studied once again the effect of preterm delivery and steroid (betamethasone) treatment; this time regarding alterations associated with the Chiari II malformation. After creation of a myelomeningocele defect and consecutive histological analysis, the degree of hindbrain herniation was determined by the percentage of descent of the cerebellar vermis using the distance between the end of the occipital bone and the beginning of the first vertebral arch.…”

Section: Authorsmentioning

confidence: 99%

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State of the art in translating experimental myelomeningocele research to the bedside

et al. 2021

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Myelomeningocele (MMC), the commonest type of spina bifida (SB), occurs due to abnormal development of the neural tube and manifest as failure of the complete fusion of posterior arches of the spinal column, leading to dysplastic growth of the spinal cord and meninges. It is associated with several degrees of motor and sensory deficits below the level of the lesion, as well as skeletal deformities, bladder and bowel incontinence, and sexual dysfunction. These children might develop varying degrees of neuropsychomotor delay, partly due to the severity of the injuries that affect the nervous system before birth, partly due to the related cerebral malformations (notably hydrocephalus-which may also lead to an increase in intracranial pressure-and Chiari II deformity). Traditionally, MMC was repaired surgically just after birth; however, intrauterine correction of MMC has been shown to have several potential benefits, including better sensorimotor outcomes (since exposure to amniotic fluid and its consequent deleterious effects is shortened) and reduced rates of hydrocephalus, among others. Fetal surgery for myelomeningocele, nevertheless, would not have been made possible without the development of experimental models of this pathological condition. Hence, the aim of the current article is to provide an overview of the animal models of MMC that were used over the years and describe how this knowledge has been translated into the fetal treatment of MMC in humans.

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Section: Authorsmentioning

confidence: 79%

Section: Authorsmentioning

confidence: 99%

Section: Authorsmentioning

confidence: 99%

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State of the art in translating experimental myelomeningocele research to the bedside

et al. 2021

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“…HH was classified if the position of cerebellar tonsil descended below the reference line. 26 The lumbar spine tissue was dehydrated in gradient ethanol solutions (70.0%-99.9%) ended with 100% technical toluene (VWR Chemicals) before embedding in paraffin blocks. For each pup, the central level of the defect was serially sectioned at 4 μm with an interval of 100 μm (4 cross-sections/sample) on an automated microtome (Epredia TM HM 355S, Fisher Scientific).…”

Section: Pathologymentioning

confidence: 99%

Local host response of commercially available dural patches for fetal repair of spina bifida aperta in rabbit model

et al. 2023

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Objective Fetal surgery for spina bifida aperta (SBA) by open hysterotomy typically repairs anatomical native tissue in layers. Increasingly, fetoscopic repair is performed using a dural patch followed by skin closure. We studied the host response to selected commercially available patches currently being used in a fetal rabbit model for spina bifida repair. Methods SBA was surgically induced at 23–24 days of gestation (term = 31 days). Fetal rabbits were assigned to unrepaired (SBA group), or immediate repair with Duragen™ or Durepair™. Non‐operated littermates served as normal controls. At term, spinal cords underwent immunohistochemical staining including Nissl and glial fibrillary acidic protein. We hypothesized that spinal cord coverage with a dural patch and skin closure would preserve motor neuron density within the non‐inferiority limit of 201.65 cells/mm2 and reduce inflammation compared to unrepaired SBA fetuses. Results Motor neuron density assessed by Nissl staining was conserved both by Duragen (n = 6, 89.5; 95% CI −158.3 to −20.6) and Durepair (n = 6, 37.0; 95% CI −132.6 to −58.5), whereas density of GFAP‐positive cells to quantify inflammation was lower than in unrepaired SBA‐fetuses (SBA 2366.0 ± 669.7 cells/mm2 vs. Duragen 1274.0 ± 157.2 cells/mm2; p = 0.0002, Durepair 1069.0 ± 270.7 cells/mm2; p < 0.0001). Conclusions Covering the rabbit spinal cord with either Duragen or Durepair followed by skin closure preserves motor neuron density and reduces the inflammatory response.

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“…Studies in other laboratory animals, such as guinea pigs and rabbits, were first primarily focused on environmental factors such as maternal hyperthermia, nutrition or the effects of chemicals or drugs on development (Edwards, Saunders, & Shiota, 2003; Sim et al, 2012; Smith, Upfold, Edwards, Shiota, & Cawdell‐Smith, 1992). More recently, rabbit models using surgically generated meningomyelocele‐like defects have been utilized to study NTD repair methods (Fontecha et al, 2010; George & Fuh, 2003; Housley et al, 2000). There are some suggestions that neural tube closure in human embryos resembles that of rabbit embryos more strongly than those from mice, as the sites of closure being more similar in location (Juriloff & Harris, 2018; Nakatsu et al, 2000).…”

Section: Use Of Underutilized Animal Models May Better Inform Human Ntdsmentioning

confidence: 99%

Comparison of inherited neural tube defects in companion animals and livestock

Zarzycki

Thomas

Mazrier

2020

Birth Defects Research

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Neural tube defects (NTDs) are congenital malformations resulting from the improper or incomplete closure of the neural tube during embryonic development. A number of similar malformations of the protective coverings surrounding the central nervous system are also often included under this umbrella term, which may not strictly fit this definition. A range of NTD phenotypes exist and have been reported in humans and a wide range of domestic and livestock species. In the veterinary literature, these include cases of anencephaly, encephalocele, dermoid sinus, spina bifida, and craniorachischisis. While environmental factors have a role, genetic predisposition may account for a significant part of the risk of NTDs in these animal cases. Studies of laboratory model species (fish, birds, amphibians, and rodents) have been instrumental in improving our understanding of the neurulation process. In mice, over 200 genes that may be involved in this process have been identified and variant phenotypes investigated. Like laboratory mouse models, domestic animals and livestock species display a wide range of NTD phenotypes. They remain, however, a largely underutilized population and could complement already established laboratory models. Here we review reports of NTDs in companion animals and livestock, and compare these to other animal species and human cases. We aim to highlight the potential of nonlaboratory animal models for mutation discovery as well as general insights into the mechanisms of neurulation and the development of NTDs.

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Effects of birth advancement in Chiari malformation in a surgical myelomeningocele model in rabbits

Cited by 6 publications

References 32 publications

State of the art in translating experimental myelomeningocele research to the bedside

State of the art in translating experimental myelomeningocele research to the bedside

Local host response of commercially available dural patches for fetal repair of spina bifida aperta in rabbit model

Comparison of inherited neural tube defects in companion animals and livestock

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