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Journal articles on the topic 'Midline defects'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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1

Toriello, Helga V., James V. Higgins, John M. Opitz, and James F. Reynolds. "X-linked midline defects." American Journal of Medical Genetics 21, no. 1 (May 1985): 143–46. http://dx.doi.org/10.1002/ajmg.1320210121.

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2

Antonini, Sonir R. R., Alexandre S. Grecco Filho, Lucila L. K. Elias, Ayrton C. Moreira, and Margaret de Castro. "gene in midline cerebral defects." Journal of Pediatrics 139, no. 5 (November 2001): 754. http://dx.doi.org/10.1067/mpd.2001.118423.

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3

Winter, Robin M. "Diaphragmatic and multiple midline defects." American Journal of Medical Genetics 63, no. 2 (May 17, 1996): 411. http://dx.doi.org/10.1002/ajmg.1320630203.

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4

Ching, H. S., K. W. Lindsay, and B. F. O'Reilly. "Intracranial mucoceles with midline fusion defects." Journal of Neurology, Neurosurgery & Psychiatry 61, no. 4 (October 1, 1996): 428–29. http://dx.doi.org/10.1136/jnnp.61.4.428.

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5

Ruggiero, Antonio, Giuseppe Zampino, Pierpaolo Mastroiacovo, and Riccardo Riccardi. "Diamond–Blackfan Anemia and Midline Defects." Journal of Pediatric Hematology/Oncology 22, no. 5 (September 2000): 479–80. http://dx.doi.org/10.1097/00043426-200009000-00021.

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6

Parr, J. H. "Midline Cerebral Defects and Kallmann's Syndrome." Journal of the Royal Society of Medicine 81, no. 6 (June 1988): 355–56. http://dx.doi.org/10.1177/014107688808100620.

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7

Morales, J. Mark, Sanjeet G. Patel, James A. Duff, Roberto L. Villareal, and James W. Simpson. "Ectopia cordis and other midline defects." Annals of Thoracic Surgery 70, no. 1 (July 2000): 111–14. http://dx.doi.org/10.1016/s0003-4975(00)01388-6.

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8

Say, Burhan, and Donna P. Smith. "Midline field defects and Hirschsprung disease." American Journal of Medical Genetics 61, no. 3 (January 22, 1996): 293–94. http://dx.doi.org/10.1002/(sici)1096-8628(19960122)61:3<293::aid-ajmg17>3.0.co;2-o.

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9

Temple, I. K., H. Brunner, B. Jones, J. Burn, and M. Baraitser. "Midline facial defects with ocular colobomata." American Journal of Medical Genetics 37, no. 1 (September 1990): 23–27. http://dx.doi.org/10.1002/ajmg.1320370107.

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10

Zucchini, Stefano. "Pituitary abnormalities in midline brain defects." EClinicalMedicine 19 (February 2020): 100260. http://dx.doi.org/10.1016/j.eclinm.2020.100260.

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11

Wey, Philip D., Julie A. Neidich, Lloyd A. Hoffman, and Gregory S. Latrenta. "Midline Defects of the Orofaciodigital Syndrome Type VI (Váradi Syndrome)." Cleft Palate-Craniofacial Journal 31, no. 5 (September 1994): 397–400. http://dx.doi.org/10.1597/1545-1569_1994_031_0397_mdotos_2.3.co_2.

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The orofaciodigital syndromes (OFDS) represent a spectrum of anomalies of the palate, cranium, hands, and feet. Váradi syndrome, designated OFDS type VI, is a rare disorder that is additionally characterized by cerebellar anomalies. The following report is of a patient with OFDS VI and characteristic multiple midline defects: median cleft lip and palate, lingual cleft with nodules, and midline brain malformation. In addition, this case is uniquely associated with the presence of midline (metopic and sagittal) craniosynostoses as well. It is unusual that deformities which result from premature fusion of cranial vault sutures would appear synchronously in a syndrome based on the concept of failure of fusion or coalescence of facial growth centers. The midline represents an independent developmental field, whereby CNS defects and midline anomalies can present concurrently.

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12

Kim, Jin Kyu, and Sun Jun Kim. "Midline Facial Defects With Associated Brain Anomaly." Pediatric Neurology 79 (February 2018): 76–77. http://dx.doi.org/10.1016/j.pediatrneurol.2017.10.015.

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13

Czeizel, Andrew. "Periconceptional multivitamin supplementation and nonneural midline defects." American Journal of Medical Genetics 46, no. 5 (June 15, 1993): 611. http://dx.doi.org/10.1002/ajmg.1320460536.

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14

Love, Elliot W., Susan M. Sweeney, Mary E. Maloney, and Jeremy S. Bordeaux. "Columellar Advancement Flap for Midline Nasal Defects." Dermatologic Surgery 36, no. 2 (February 2010): 241–44. http://dx.doi.org/10.1111/j.1524-4725.2009.01398.x.

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15

Cowchock, Susan. "Apparently balanced chromosome translocations and midline defects." American Journal of Medical Genetics 33, no. 3 (July 1989): 424. http://dx.doi.org/10.1002/ajmg.1320330329.

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16

Cuenca, Osmar, Agustín Rodríguez, and Arturo Segovia. "ENDOSCOPIC APPROACH OF RECTUS DIASTASIS AND ABDOMINAL MIDLINE DEFECTS." CIRUGIA PARAGUAYA 41, no. 2 (August 30, 2017): 37–40. http://dx.doi.org/10.18004/sopaci.agosto.37-40.

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17

White, Yvonne A. R., Joshua T. Kyle, and Antony W. Wood. "Targeted Gene Knockdown in Zebrafish Reveals Distinct Intraembryonic Functions for Insulin-Like Growth Factor II Signaling." Endocrinology 150, no. 9 (May 14, 2009): 4366–75. http://dx.doi.org/10.1210/en.2009-0356.

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Abstract IGF-II is the predominant IGF ligand regulating prenatal growth in all vertebrates, including humans, but its central role in placental development has confounded efforts to fully elucidate its functions within the embryo. Here we use a nonplacental model vertebrate (zebrafish) to interrogate the intraembryonic functions of IGF-II signaling. The zebrafish genome contains two coorthologs of mammalian IGF2 (igf2a, igf2b), which exhibit distinct patterns of expression during embryogenesis. Expression of igf2a mRNA is restricted to the notochord, primarily during segmentation/neurulation. By contrast, igf2b mRNA is expressed in midline tissues adjacent to the notochord, with additional sites of expression in the ventral forebrain, and the pronephros. To identify their intraembryonic functions, we suppressed the expression of each gene with morpholino oligonucleotides. Knockdown of igf2a led to defects in dorsal midline development, characterized by delayed segmentation, notochord undulations, and ventral curvature. Similarly, suppression of igf2b led to defects in dorsal midline development but also induced ectopic fusion of the nephron primordia, and defects in ventral forebrain development. Subsequent onset of severe body edema in igf2b, but not igf2a morphants, further suggested a distinct role for igf2b in development of the embryonic kidney. Simultaneous knockdown of both genes increased the severity of dorsal midline defects, confirming a conserved role for both genes in dorsal midline development. Collectively, these data provide evidence that the zebrafish orthologs of IGF2 function in dorsal midline development during segmentation/neurulation, whereas one paralog, igf2b, has evolved additional, distinct functions during subsequent organogenesis.

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18

Soriano, N. S., and S. Russell. "The Drosophila SOX-domain protein Dichaete is required for the development of the central nervous system midline." Development 125, no. 20 (October 15, 1998): 3989–96. http://dx.doi.org/10.1242/dev.125.20.3989.

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SOX-domain proteins are a class of developmentally important transcriptional regulators related to the mammalian testis determining factor SRY. In common with other SOX-domain genes, the Drosophila Dichaete gene has a dynamic expression profile in the developing central nervous system, including cells of the ventral midline. We find defects in the differentiation of midline glia and concomitant axonal defects in Dichaete mutants that are rescued by driving Dichaete expression in the midline. Since Dichaete is required for the correct specification or differentiation of midline glia, we have used the ventral midline as a model system to study SOX gene function in vivo and demonstrate a genetic interaction between Dichaete and the POU domain gene ventral veinless. In mammals, a protein related to Dichaete, SOX2, also interacts with POU transcription factors. The midline phenotypes of Dichaete mutations are rescued by expression of mouse SOX2. Our data suggest that SOX gene structure, function and interactions have been conserved during evolution.

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19

Pivnick, E. K., R. A. Kaufman, G. V. N. Velagaleti, W. M. Gunther, and D. Abramovici. "Infant with midline thoracoabdominal schisis and limb defects." Teratology 58, no. 5 (November 1998): 205–8. http://dx.doi.org/10.1002/(sici)1096-9926(199811)58:5<205::aid-tera7>3.0.co;2-x.

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20

Kroll, Stephen S., Lome Rosenfield, and Stephen J. Kroll. "Perforator-Based Flaps for Low Posterior Midline Defects." Plastic and Reconstructive Surgery 81, no. 4 (April 1988): 561–66. http://dx.doi.org/10.1097/00006534-198804000-00012.

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21

Golembo, M., E. Raz, and B. Z. Shilo. "The Drosophila embryonic midline is the site of Spitz processing, and induces activation of the EGF receptor in the ventral ectoderm." Development 122, no. 11 (November 1, 1996): 3363–70. http://dx.doi.org/10.1242/dev.122.11.3363.

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The Drosophila EGF receptor (DER) is activated by secreted Spitz to induce different cell fates in the ventral ectoderm. Processing of the precursor transmembrane Spitz to generate the secreted form was shown to be the limiting event, but the cells in which processing takes place and the mechanism that may generate a gradient of secreted Spitz in the ectoderm were not known. The ectodermal defects in single minded (sim) mutant embryos, in which the midline fails to develop, suggested that the midline cells contribute to patterning of the ventral ectoderm. This work shows that the midline provides the site for Spitz expression and processing. The Rhomboid and Star proteins are also expressed and required in the midline. The ectodermal defects of spitz, rho or Star mutant embryos could be rescued by inducing the expression of the respective normal genes only in the midline cells. Rho and Star thus function non-autonomously, and may be required for the production or processing of the Spitz precursor. Secreted Spitz is the only sim-dependent contribution of the midline to patterning the ectoderm, since the ventral defects observed in sim mutant embryos can be overcome by expression of secreted Spitz in the ectoderm. While ectopic expression of secreted Spitz in the ectoderm or mesoderm gave rise to ventralization of the embryo, increased expression of secreted Spitz in the midline did not lead to alterations in ectoderm patterning. A mechanism for adjustment to variable levels of secreted Spitz emanating from the midline may be provided by Argos, which forms an inhibitory feedback loop for DER activation. The production of secreted Spitz in the midline, may provide a stable source for graded DER activation in the ventral ectoderm.

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22

Musgrove, Jamie M., and Cheryl Riley. "Septo-Optic Dysplasia: A Case Study." Neonatal Network 35, no. 1 (2016): 13–18. http://dx.doi.org/10.1891/0730-0832.35.1.13.

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AbstractSepto-optic dysplasia (SOD) is a rare congenital heterogeneous malformation. SOD was formerly known as de Morsier syndrome, which associated a midline brain defect such as an absent septum pellucidum with optic nerve hypoplasia. The diagnosis of SOD is made when there are two or more characteristics of the classic triad. The triad consists of optic nerve hypoplasia, pituitary hormone abnormalities, and midline brain defects, although it can vary in the severity of clinical presentation and phenotype. The purpose of this article is to review a case and analyze the literature regarding prevalence, etiology, clinical presentation, diagnosis, and management of SOD.

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23

Hosseinpour, Mehrdad, and Siamak Forghani. "Primary closure of large thoracolumbar myelomeningocele with bilateral latissimus dorsi flaps." Journal of Neurosurgery: Pediatrics 3, no. 4 (April 2009): 331–33. http://dx.doi.org/10.3171/2008.12.peds08226.

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Object Myelomeningocele (MMC) is the most complex congenital malformation of the CNS that is compatible with life. Different closure techniques are available for defect reconstruction, but wound healing and tension-free closure of the skin in the midline remain major considerations in large MMCs. In this study, the authors used bilateral proximally based latissimus dorsi (LD) skin island muscle pedicle flaps for closure of large thoracolumbar MMC defects. Methods Twenty infants with very large thoracolumbar MMCs were enrolled in the study. The mean of age of the patients was 4.1 ± 2.3 months. The width of the MMC was 6 ± 1.2 cm. At operation, 2 triangular V-Y flaps were designed on each side of the defect; the tip of the triangle was extended to the posterior axillary line. The LD flaps based on the thoracodorsal arteries were elevated bilaterally and advanced toward the midline with moderate tension and sutured together. Postoperatively, infants were positioned prone for 7 days and discharged on the 8th day after the operation. They were followed every 2 weeks for evaluation of wound healing. Results The wounds healed without any major complication. There was no dehiscence in the postoperative period. Conclusions The authors recommended bilateral superiorly based LD skin flaps as an effective method for closure of large thoracolumbar MMC defects. Neural tube defects are among the most common of all human birth defects.

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24

Gilbert-Barness, Enid, Diane Debich-Spicer, M. Michael Cohen, and John M. Opitz. "Evidence for the ?midline? hypothesis in associated defects of laterality formation and multiple midline anomalies." American Journal of Medical Genetics 101, no. 4 (2001): 382–87. http://dx.doi.org/10.1002/ajmg.1224.

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25

Sharrow, Mary, and Michael Tiemeyer. "Gliolectin-mediated carbohydrate binding at theDrosophilamidline ensures the fidelity of axon pathfinding." Development 128, no. 22 (November 15, 2001): 4585–95. http://dx.doi.org/10.1242/dev.128.22.4585.

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Gliolectin is a carbohydrate-binding protein (lectin) that mediates cell adhesion in vitro and is expressed by midline glial cells in the Drosophila melanogaster embryo. Gliolectin expression is maximal during early pathfinding of commissural axons across the midline (stages 12-13), a process that requires extensive signaling and cell-cell interactions between the midline glia and extending axons. Deletion of the gliolectin locus disrupts the formation of commissural pathways and also delays the completion of longitudinal pathfinding. The disruption in commissure formation is accompanied by reduced axon-glial contact, such that extending axons grow on other axons and form a tightly fasciculated bundle that arches over the midline. By contrast, pioneering commissural axons normally cross the midline as a distributed array of fibers that interdigitate among the midline glia, maximizing contact and, therefor, communication between axon and glia. Restoration of Gliolectin protein expression in the midline glia rescues the observed pathfinding defects of null mutants in a dose-dependent manner. Hypomorphic alleles generated by ethylmethanesulfonate mutagenesis exhibit a similar phenotype in combination with a deletion and these defects are also rescued by transgenic expression of Gliolectin protein. The observed phenotypes indicate that carbohydrate-lectin interactions at the Drosophila midline provide the necessary surface contact to capture extending axons, thereby ensuring that combinatorial codes of positive and negative growth signals are interpreted appropriately.

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26

Cottrill, Carol M., Janet Tamaren, and Brian Hall. "Sternal defects associated with congenital pericardial and cardiac defects." Cardiology in the Young 8, no. 1 (January 1998): 100–104. http://dx.doi.org/10.1017/s1047951100004716.

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AbstractWe describe three cases of sternal defects of varying severity associated with other congenital anomalies. In the most severe case, both anterior and posterior defects were seen, with near-absence of the sternum and pericardium continuous with a large omphalocele. This resulted in external location of organs usually confined within the thoracic and abdominal cavities. A ventricular septal defect was present, and the arterial duct was absent. The course of the ascending aorta was anomalous. The baby had anencephaly and rachischisis. In the intermediate case, a proximal sternal cleft was associated with shortening of the ster num, and absence of the manubrium. Anterior pericardial and diaphragmatic defects were seen, while a scalp defect and an encephalocele were present on the posterior aspect of the head. This baby had tricuspid atresia. The qremaining case had only an anterior defect with a shortened sternum. A supra-umbilical omphalocele contained a left ventricular diverticulum without interposing pericardium or diaphragm. Ventricular and atrial septal defects were present. The first two cases can be considered as representing fail ure of development of both an anterior and a posterior midline field. The third case, much milder than the other two, represents failure of development of an anterior field.

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27

Giffoni, Silvyo David Araújo, Vanda Maria Gimenes Gonçalves, Verônica Araújo Zanardi, and Vera Lucia Gil-da-Silva-Lopes. "Cerebellar Involvement in Midline Facial Defects with Ocular Hypertelorism." Cleft Palate-Craniofacial Journal 43, no. 4 (July 2006): 466–70. http://dx.doi.org/10.1597/04-179.1.

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Objective Twenty-four patients were evaluated to better characterize neurological and neuroradiological aspects of midline facial defects with ocular hypertelorism. Methods After a clinical genetics evaluation, the individuals were divided into two groups: 12 isolated cases (group 1) and 12 associated with multiple congenital anomalies (group 2). The investigation protocol included medical and family history, as well as dysmorphological, neurological, and neuroradiological evaluations by magnetic resonance imaging or computed tomography scan. Results Because there was no significant difference concerning the neurological aspects of groups 1 and 2, they were analyzed together. Mild hypotonia (24 of 24), abnormalities in cranial shape (24 of 24), cranial nerves (19 of 24), motor coordination (18 of 24), dynamic equilibrium (14 of 24), and language problems (8 of 24) were noted. Measurements of the posterior fossa showed hypoplastic cerebellar vermis (8 of 17), the cerebellum at lower normality limits (5 of 17), and signs of cerebellar hypoplasia (3 of 7). Conclusion This study clearly demonstrates the presence of structural and functional neurological abnormalities related to midline facial defects with ocular hypertelorism, as well as involvement of the cerebellum. It provides a basis for future investigation of midline facial defects with ocular hypertelorism and should be considered during planning of rehabilitation treatment.

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Giffoni, Silvyo David Araújo, Vanda Maria Gimenes Gonçalves, Verônica Araújo Zanardi, and Vera Lucia Gil-da-Silva-Lopes. "Cerebellar Involvement in Midline Facial Defects With Ocular Hypertelorism." Cleft Palate-Craniofacial Journal 43, no. 4 (2006): 466. http://dx.doi.org/10.1597/04-179r.1.

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29

Chua, Dennis Y., and Stephen S. Park. "Midline Forehead Flap for Reconstruction of Cutaneous Nasal Defects." JAMA Facial Plastic Surgery 16, no. 4 (July 2014): 296–97. http://dx.doi.org/10.1001/jamafacial.2014.43.

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30

Debrus, Sophie, Ursula Sauer, Simone Gilgenkrantz, Wolfgang Jost, Hans-Jürgen Jesberger, and Patrice Bouvagnet. "Autosomal recessive lateralization and midline defects: Blastogenesis recessive 1." American Journal of Medical Genetics 68, no. 4 (February 11, 1997): 401–4. http://dx.doi.org/10.1002/(sici)1096-8628(19970211)68:4<401::aid-ajmg5>3.0.co;2-o.

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31

Lambert, Rebecca W., and Leonard M. Dzubow. "A dorsal nasal advancement flap for off-midline defects." Journal of the American Academy of Dermatology 50, no. 3 (March 2004): 380–83. http://dx.doi.org/10.1016/j.jaad.2003.05.001.

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32

Martis, Gábor, Renáta Laczik, and László Damjanovich. "A komputertomográfia jelentősége az eventerált, óriás hasfali sérvek műtéteinek tervezésében." Orvosi Hetilap 158, no. 7 (February 2017): 257–63. http://dx.doi.org/10.1556/650.2017.30667.

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Abstract: Introduction: The eventrated, giant abdominal wall hernias represent a considerable challenge in our practice. Presently, preoperative evaluation of the musculo-aponeurotic elements of the abdominal wall by CT imaging is not part of routine planning of surgery. Aim: Evaluation of the abdominal wall hernia progression in time. Moreover, follow up the changes of the abdominal wall structures following series of intraabdominal surgeries. Method: Abdominal CT imaging were performed on the 1st, 3rd, 6th, 12th, 18th, and 24th postoperative months after the primary series of surgeries in the cases of 12 patients, whose reconstructive surgeries were not possible. A prospective data collection was applied. Changing of the bilateral rectus muscle morphology, the evolution in time of the midline gap, and the progressive dynamism of the midline wall defects were determined. Results: A characteristic and progressive midline defect enlargement could be settled. Data analysis yielded that the combined width of the bilateral rectus muscles is sufficient to cover the midline abdominal wall defect, although there is an “optimal” timeframe for performing the intervention. Conclusion: CT evaluation of abdominal wall prior to reconstructive surgeries of loss of abdominal wall domain has a strong significance on determining and designing the adequate surgical procedure. Orv. Hetil., 2017, 158(7), 257–263.

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33

Karlstrom, R. O., T. Trowe, S. Klostermann, H. Baier, M. Brand, A. D. Crawford, B. Grunewald, et al. "Zebrafish mutations affecting retinotectal axon pathfinding." Development 123, no. 1 (December 1, 1996): 427–38. http://dx.doi.org/10.1242/dev.123.1.427.

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We have isolated mutants in the zebrafish Danio rerio that have defects in axonal connectivity between the retina and tectum. 5-day-old fish larvae were screened by labeling retinal ganglion cells with DiI and DiO and observing their axonal projections to and on the tectum. 82 mutations, representing 13 complementation groups and 6 single allele loci, were found that have defects in retinal ganglion cell axon pathfinding to the tectum. These pathfinding genes fall into five classes, based on the location of pathfinding errors between eye and tectum. In Class I mutant larvae (belladonna, detour, you-too, iguana, umleitung, blowout) axons grow directly to the ipsilateral tectal lobe after leaving the eye. Class II mutant larvae (chameleon, bashful) have ipsilaterally projecting axons and, in addition, pathfinding mistakes are seen within the eye. In Class III mutant larvae (esrom, tilsit, tofu) fewer axons than normal cross the midline, but some axons do reach the contralateral tectal lobe. Class IV mutant larvae (boxer, dackel, pinscher) have defects in axon sorting after the midline and retinal axons occasionally make further pathfinding errors upon reaching the contralateral tectal lobe. Finally, Class V mutant larvae (bashful, grumpy, sleepy, cyclops, astray) have anterior-posterior axon trajectory defects at or after the midline. The analysis of these mutants supports several conclusions about the mechanisms of retinal axon pathfinding from eye to tectum. A series of sequential cues seems to guide retinal axons to the contralateral tectal lobe. Pre-existing axon tracts seem not to be necessary to guide axons across the midline. The midline itself seems to play a central role in guiding retinal axons. Axons in nearby regions of the brain seem to use different cues to cross the ventral midline. Mutant effects are not all-or-none, as misrouted axons may reach their target, and if they do, they project normally on the tectum. The retinotectal pathfinding mutants reveal important choice points encountered by neuronal growth cones as they navigate between eye and tectum.

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34

Edelstyn, N. M. J., F. Oyebode, M. J. Riddoch, R. Soppitt, H. Moselhy, and M. George. "A neuropsychological perspective on three schizophrenic patients with midline structural defects." British Journal of Psychiatry 170, no. 5 (May 1997): 416–21. http://dx.doi.org/10.1192/bjp.170.5.416.

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BackgroundThe relationship between midline structural defects and schizophrenia remains unclear, although a number of neuroradiological studies have reported an association between schizophrenia and a range of anomalies.MethodThree patients are reported, each diagnosed with schizophrenia and neuroradiological evidence of midline structural anomalies. MRI scans are reported in conjunction with performance over a range of neuropsychological tests designed to assess frontal and lateralised cognitive functions.ResultsEvidence of anterior dysfunction was present in all three cases, while on an individual basis patients displayed varying patterns of preserved and dysfunctional cognitive processing.ConclusionThe reported findings raise a number of interesting issues regarding the nature of hemispheric involvement in schizophrenia.

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35

Correa-Rivas, María S., Isabel Matos-Llovet, and Lourdes García-Fragoso. "Pentalogy of Cantrell: A Case Report with Pathologic Findings." Pediatric and Developmental Pathology 7, no. 6 (November 2004): 649–52. http://dx.doi.org/10.1007/s10024-004-9104-5.

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We present the case of a 28-h-old female infant born at 37 weeks of gestation with a rare congenital malformation consisting of a pentad of findings: ectopia cordis, a midline supraumbilical wall defect, a defect of the lower sternum, absent pericardium, and an anterior diaphragmatic defect. This constellation of defects is known as the pentalogy of Cantrell. Additional autopsy findings included a bilateral cleft lip and palate, bilateral pulmonary hypoplasia, an atrial septal defect, and a patent ductus arteriosus. We present this case because of its rarity and discuss the pathologic findings.

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36

Bird, Lynne M., Robert O. Newbury, Rodolfo Ruiz-Velasco, and Marilyn C. Jones. "Recurrence of diaphragmatic agenesis associated with multiple midline defects: Evidence for an autosomal gene regulating the midline." American Journal of Medical Genetics 53, no. 1 (October 15, 1994): 33–38. http://dx.doi.org/10.1002/ajmg.1320530108.

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37

Hamilton, Kimberly M., Andrea L. Wiens, and Daniel H. Fulkerson. "Lateral posterior fossa encephalocele with associated migrational disorder of the cerebellum in an infant." Journal of Neurosurgery: Pediatrics 8, no. 5 (November 2011): 479–83. http://dx.doi.org/10.3171/2011.8.peds11218.

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Encephaloceles are acquired or congenital defects in which intracranial contents protrude through a defect in the calvaria. The embryogenesis of these lesions is incompletely understood. The vast majority of lesions occur at or near the anatomical midline. The authors present an extremely rare case of a laterally oriented, pathologically proven encephalocele associated with a posterior fossa cyst and cerebellar migrational defect in an infant. The authors review past and current theories of encephalocele formation as it relates to this case.

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38

Wey, Philip D., Julie A. Neidich, Lloyd A. Hoffman, and Gregory S. LaTrenta. "Midline Defects of the Orofaciodigital Syndrome Type VI (Váradi Syndrome)." Cleft Palate-Craniofacial Journal 31, no. 5 (September 1994): 397–400. http://dx.doi.org/10.1597/1545-1569(1994)031<0397:mdotos>2.3.co;2.

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39

Morelli, Susan H., Theodore J. Pysher, Enid F. Gilbert-Barness, John M. Opitz, and David H. Viskochil. "Pathogenesis of Sirenomelia with Anencephaly and Other Midline Defects† 364." Pediatric Research 43 (April 1998): 65. http://dx.doi.org/10.1203/00006450-199804001-00385.

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40

Denny, Arlen D. "Expanded Midline Forehead Flap for Coverage of Nonnasal Facial Defects." Annals of Plastic Surgery 29, no. 6 (December 1992): 576–78. http://dx.doi.org/10.1097/00000637-199212000-00016.

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Morelli, Susan H., Luciana Young, Barbara Reid, Herbert Ruttenberg, and Michael J. Bamshad. "Clinical analysis of families with heart, midline, and laterality defects." American Journal of Medical Genetics 101, no. 4 (2001): 388–92. http://dx.doi.org/10.1002/ajmg.1221.

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Khoury, Muin J., José F. Cordero, Sonja Rasmussen, and John M. Opitz. "Ectopia cordis, midline defects and chromosome abnormalities: An epidemiologic perspective." American Journal of Medical Genetics 30, no. 3 (July 1988): 811–17. http://dx.doi.org/10.1002/ajmg.1320300314.

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Meena, Raj Kumar, and Veena Meena. "Pentalogy of cantrell with single umbilical artery: a rare fetal anomaly." International Journal of Contemporary Pediatrics 4, no. 1 (December 21, 2016): 280. http://dx.doi.org/10.18203/2349-3291.ijcp20164620.

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Pentalogy of cantrell (PC) is a rare syndrome having both specific ventral and dorsal midline defect, and rarely found to be associated with other anomalies. Most cases occur randomly for no apparent reason (sporadically). We report a 20 years old primigravida referred at 17 weeks 4 days of gestational age, for a fetal anomaly scan having an anterior abdominal wall defect in fetus. Ultrasound done, showed single live fetus gestational age of 18 weeks, with fetal heart, great vessels, stomach, and intestinal loops were found to be lying outside thoracic cavity. Fetal autopsy following termination of the pregnancy confirmed the presence of the malformations with single umbilical artery. Occurrence of both ventral and dorsal midline defects suggests that the timing of fetus insult would be between 14 to 18 days after conception when the splanchnic mesoderm (myocardium) and somatic mesoderm (sternum, abdominal wall, diaphragm and pericardium) is dividing.

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Brand, M., C. P. Heisenberg, R. M. Warga, F. Pelegri, R. O. Karlstrom, D. Beuchle, A. Picker, et al. "Mutations affecting development of the midline and general body shape during zebrafish embryogenesis." Development 123, no. 1 (December 1, 1996): 129–42. http://dx.doi.org/10.1242/dev.123.1.129.

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Tissues of the dorsal midline of vertebrate embryos, such as notochord and floor plate, have been implicated in inductive interactions that pattern the neural tube and somites. In our screen for embryonic visible mutations in the zebrafish we found 113 mutations in more than 27 genes with altered body shape, often with additional defects in CNS development. We concentrated on a subgroup of mutations in ten genes (the midline-group) that cause defective development of the floor plate. By using floor plate markers, such as the signaling molecule sonic hedgehog, we show that the schmalspur (sur) gene is needed for early floor plate development, similar to one-eyed-pinhead (oep) and the previously described cyclops (cyc) gene. In contrast to oep and cyc, sur embryos show deletions of ventral CNS tissue restricted to the mid- and hindbrain, whereas the forebrain appears largely unaffected. In the underlying mesendodermal tissue of the head, sur is needed only for development of the posterior prechordal plate, whereas oep and cyc are required for both anterior and posterior prechordal plate development. Our analysis of sur mutants suggests that defects within the posterior prechordal plate may cause aberrant development of ventral CNS structures in the mid- and hindbrain. Later development of the floor plate is affected in mutant chameleon, you-too, sonic-you, iguana, detour, schmalhans and monorail embryos; these mutants often show additional defects in tissues that are known to depend on signals from notochord and floor plate. For example, sur, con and yot mutants show reduction of motor neurons; median deletions of brain tissue are seen in sur, con and yot embryos; and cyc, con, yot, igu and dtr mutants often show no or abnormal formation of the optic chiasm. We also find fusions of the ventral neurocranium for all midline mutants tested, which may reveal a hitherto unrecognized function of the midline in influencing differentiation of neural crest cells at their destination. As a working hypothesis, we propose that midline-group genes may act to maintain proper structure and inductive function of zebrafish midline tissues.

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Singh, Ranjit, KN Abhinandan Patel, and Satyajit Dandgi. "Lip Reconstruction using Karapandzic Flap." World Journal of Dentistry 6, no. 1 (2015): 55–57. http://dx.doi.org/10.5005/jp-journals-10015-1313.

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ABSTRACT The peroral region which consists of the upper and lower lip plays a vital role functionally, esthetically as well as anatomically. The post-surgical defects of peroral structures, especially the mid line defects of the lower lip, present a considerable challenge for reconstruction. Currently, reconstruction of peroral structures are done by using local, distant and free flaps. In our case, we have reconstructed a large midline defect of more than two thirds of the lower lip by using a karapandzic flap. How to cite this article Patel KNA, Dandgi S, Singh R. Lip Reconstruction using Karapandzic Flap. World J Dent 2015; 6(1):55-57.

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Morales-Quispe, Jorge A., Cristian Aguilar, and Maria Ganiku-Furujen. "Congenital left ventricular diverticulum." Cardiology in the Young 27, no. 5 (May 2, 2017): 973–74. http://dx.doi.org/10.1017/s1047951117000245.

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Fryns, J. P., J. Delooz, and H. Berghe. "Posterior scalp defects in Opitz syndrome. Another symptom related to a defect in midline development." Clinical Genetics 42, no. 6 (June 28, 2008): 314–16. http://dx.doi.org/10.1111/j.1399-0004.1992.tb03263.x.

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Yurochko, Fedir, Vasyl Olashyn, and Dzvenyslava Kopanska. "Surgical treatment of a nasal dermoid cyst: open rhinoplasty." Polski Przegląd Otorynolaryngologiczny 8, no. 2 (April 4, 2019): 49–53. http://dx.doi.org/10.5604/01.3001.0013.1528.

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Midline nasal congenital masses are a rare congenital anomaly. Most often such defects include: vascular tumors, benign and malignant tumors and inflammatory lesions, however the most common are: gliomas, dermoid cysts and hemangiomas. Dermoid cysts (or dermoids) are a benign tumor belongs to choristom group (teratoma). Nasal dermoid cysts (NDCs) are the most common congenital defect of the nasal midline. The diagnosis is usually established at an early age - mainly by the age of 3. Due to late diagnosis and/or delay surgical treatment, facial deformities, recurrent infections (festering of cysts or subcutaneous infections), nasal blockage or intracranial complications may occur. This paper presents a clinical case of a 7-year old boy with a nasal dermoid cyst, successfully treated surgically with open rhinoplasty and follow-up period of 2 year.

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Fouedjio, Jeanne Hortence, Florent Fouelifack Ymele, Bruno Kenfack, Mandana Mehta, and Robinson Enow Mbu. "Pentalogy of Cantrell: A Report of One Case at the Yaounde Central Hospital in Cameroon." Donald School Journal of Ultrasound in Obstetrics and Gynecology 6, no. 4 (2012): 412–14. http://dx.doi.org/10.5005/jp-journals-10009-1264.

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ABSTRACT Pentalogy of Cantrell is a rare multiple congenital malformation syndrome characterized by a combination of five features: A midline supraumbilical abdominal wall defect; a defect of the lower sternum; a defect of the diaphragmatic pericardium; deficiency of the anterior diaphragm and congenital cardiac anomalies. These defects can be diagnosed as early as the first trimester of pregnancy. The complexity of these anomalies, in particular the presence of any cardiac defects, determines the management as well as the prognosis. We report a case of pentalogy of Cantrell diagnosed by ultrasound at 32 weeks of gestational age, the fetus died 3 hours after delivery. How to cite this article Ymele FF, Fouedjio JH, Kenfack B, Mehta M, Mbu RE. Pentalogy of Cantrell: A Report of One Case at the Yaounde Central Hospital in Cameroon. Donald School J Ultrasound Obstet Gynecol 2012;6(4):412-414.

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Bhatia, Snigdha, John Coon, and Monica Huff. "Case 1: Infant with Hypoglycemia and Midline Defects in Heart Failure." NeoReviews 21, no. 9 (September 2020): e616-e618. http://dx.doi.org/10.1542/neo.21-9-e616.

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