Pathogenesis of developmental defects induced in the rat by amniotic sac puncture

Kennedy, Laura; Persaud, T. V. N.

doi:10.1159/000144714

Cited by 85 publications

(28 citation statements)

References 6 publications

(8 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Unusual locations and extents of meningomyeloceles and craniofacial defects in patients 1 4 and the presence of aberrant tissue bands in patients 1-5 provide evidence in favor of Torpin's conception. Analogous defects have been produced experimentally by early rupture of the amnion [Kennedy and Persaud, 1977;Kino, 1975;Poswillo, 1966;Trasler et al, 19561.…”

Section: Discussionmentioning

confidence: 77%

Amniotic band sequence and its neurocutaneous manifestations

Chen

González

1987

Am. J. Med. Genet.

View full text Add to dashboard Cite

Six new cases of the amniotic band sequence with a wide spectrum of defects were studied with respect to neurocutaneous manifestations, including histopathologic characteristics. Fetuses 1 and 2 were stillborn. Despite severe craniofacial involvement, infants 3 and 4 survived 1 yr and 22 months, respectively. Patients 5 and 6 had only limb defects. Craniofacial and neurologic manifestations of our longer-survival patients with severe craniofacial anomalies were microcephaly, encephalocele, micro- or anophthalmia, mental retardation, hydrocephaly, seizures, EEG abnormalities, impaired body temperature control, impaired vision, hypertonia, and other psychomotor deficits. Characteristic cutaneous manifestations seen in our patients were clefting, schisis, fibrous strings, ring constriction, lymphedema. pseudosyndactyly, and intrauterine amputation. Histologic examination of the amniotic bands attaching to the skin showed autolyzed amnion in patient 2, erosion of the band into upper dermis in patient 1, and fibrosis underlying the constricted areas in patient 5. Prenatal diagnosis by ultrasonography is possible in patients with severe craniofacial defects (patient 2). A brief review of the literature is offered.

show abstract

Section: Discussionmentioning

confidence: 77%

Amniotic band sequence and its neurocutaneous manifestations

Chen

González

1987

Am. J. Med. Genet.

View full text Add to dashboard Cite

show abstract

“…Nonetheless, common anomalies that were variably observed included evidence of compression and reduced growth, Robin type cleft palate, and limb anomalies compatible with those seen in the ABDC (Table I). Several of the experimental studies demonstrated that the initiating event in development of the limb and other malformations was an area of hemorrhage [Poswillo and Sopher, 1971;Poswillo, 1975;Kennedy and Persaud, 1977]. There followed a series of articles in the 1980s attributing a variety of birth defects, in addition to limb defects, to a presumptive vascular cause [Hoyme et al, 1981;Van Allen et al, 1982;Stevenson et al, 1986;Bavinck and Weaver, 1986].…”

Section: Review Of Prior Hypothesesmentioning

confidence: 99%

“…One of these is illustrated and simply shows a bulge at the intact vertex; no further detail is given. Kennedy and Persaud [1977] noted some abnormal cranial protrusion which was interpreted as being schisis. No rate or illustration was provided.…”

Section: Relevance Of Animal Data To Lbwd/bwcmentioning

confidence: 99%

Limb–body wall defect. Is there a defensible hypothesis and can it explain all the associated anomalies?

Hunter

Seaver

Stevenson

2011

American J of Med Genetics Pt A

View full text Add to dashboard Cite

Aside from gastroschisis and omphalocele, major defects of the ventral body (thoracoabdominal) wall are relatively uncommon and almost universally lethal. They are most often associated with other anomalies including those of the limbs that may range from amelia to mild positional deformations, unusual craniofacial malformations, and a variety of visceral abnormalities that include the heart, lungs, genitourinary system, and gut. This complex of ventral wall anomalies has been discussed under a broad and changing nomenclature that has included amniotic band disruption complex, amnion rupture sequence, limb-body wall defect (or complex), and simply body wall complex. Three major theories have been suggested to explain this complex: early amnion rupture (operating through uterine pressure and/or disruption by amniotic bands), vascular compromise (primarily hypoperfusion), and an early intrinsic defect of the developing embryo. We present four patients that illustrate the spectrum of ventral body wall defects, and from there critique the current hypotheses of pathogenesis. We conclude that this association of malformations originates as early as the embryonic disc stage, and that some of the observed associated anomalies are secondary complications of the primary disturbance in embryogenesis. We propose a new explanation for the atypical facial clefts and cranial malformations that are often observed.

show abstract

“…Others have performed amniotic sac puncture in rats and found that this caused hemorrhagic lesions, tissue necrosis, limb reduction, and cephalic changes 43 . They attributed these findings to intrauterine compression related to lost amniotic fluid and uterine pressure and subsequent obstruction of circulation.…”

mentioning

confidence: 99%