Fenestrae Parietales Symmetricae

Abstract

Among the many new diseases which have been described during the present century, there are a remarkable number of disea §es of the osseous system. In some instances this is due to the necessity of x-ray examination and biochemical investigation for their diagnosis, but in others, such as osteopetrosis (Albers-Schonberg disease), osteochondrodystrophy (Morquio's disease), gargoylism (dysostosis multiplex), and hypertelorism, these aids were not essential, and it is perhaps surprising that the conditions escaped recognition until relatively late. The rarity of the conditions and the reluctance of writers of textbooks to list them as distinct diseases will also have militated against their general recognition. In the case of fenestrae parietales symmetricae both causes have been operative. Probably this heredo-familial condition occurs more frequently than is generally supposed, but has received little attention. It is, however, entirely comparable to such a disease as cleidocranial dysostosis, which is widely known, not from personal experience but from its established place in textbooks. The condition of fenestrae parietales symmetricae is characterized by the presence of symmetrical defects of the parietal bones, situated close together and occurring constantly in the same position. Their site is behind the crown, near the junction of the middle and posterior thirds of the sagittal suture. The defects are of oblong shape, the long axis lying at right angles to the sagittal suture. They vary from i to 4 or 5 cm. in length and 1 to 2 cm. in width.

Enlarged parietal foramina: a review of genetics, prognosis, radiology, and treatment

“…If EPF is associated with anomalies of the cerebral vasculature, additional vascular imaging like CT, MR, or digital subtraction angiography might be warranted [21]. In young children, EPF may present as a single aperture of the parietal bone, referred to as cranium bifidum as mentioned above [7,25]. EPF is caused by a heterozygous mutation in the homeobox genes ALX4 and MSX2 located at 5q34-35 and 11p11, respectively [6].…”

“…Enlarged parietal foramina (EPF) are variable intramembranous ossification defects of the parietal bones and were first described in 1707, and received little attention until the 1940s [7,14] (Figs. 1-3, 4, and 5).…”

“…These are considered normal common variants of the parietal bones, allow for passage of emissary veins, and occur in about 60-70 % of the population [17,21] and are believed to have no correlation with instances of small parietal foramina, and in one study there has been evidence of individuals with both small parietal foramina and enlarged at the same time [4,23]. The hereditary nature of EPF and associated genes have been characterized [7]. In young children, this condition may present as a persistently enlarged posterior fontanelle caused by a single large central parietal bone defect, termed cranium bifidum [25].…”

Existence of Enlarged Parietal Foramina in Bone Collections

“…Enlarged parietal foramina (EPFs) are variable intramembranous ossification defects of the parietal bones, first described in 1707, and which have received little attention until the 1940s. 1,2 In normal fetuses, the frontal, parietal, and squamous parts of the temporal bones undergo intramembranous ossification, a direct ossification of the vascularized membrane. Broca, in 1875, 3,4 had already pointed out an unusual enlargement of the parietal foramina due to a failure in the development of the parietal bones.…”

Growing Skull Defect in an Infant with a Rare Combination of a Foramen Parietale Permagna and an Atretic Cephalocele

“…Goldsmith described 5 generations of the Catlin family with enlarged parietal foramina [7]. Transmission is autosomal dominant with incomplete penetrance; responsible genes have been identified [4,10,21].…”