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Craniolacunia as the result of compression and decompression of the fetal skull.

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American Journal of Medical Genetics 27:729-730 (1987)
Letter to the Editor: Craniolacunia as the
Result of Compression and Decompression of
the Fetal Skull
To the Editor:
Craniolacunia, also known as lacunar skull defects or Lückenschadel, are
rounded or fingerlike defects in ossification in the inner table of the membranous
calvarium which are surrounded by strips of normal bone [Vogt and Wyatt, 19411.
Over 80% of newborns with spina bifida have craniolacunia apparent on skull
radiograph [Shopfner et al, 1965; Tajima et al, 19771. The radiographic abnormality
becomes less apparent during the first 6 months of life and is usually not seen in older
infants with spina bifida [McRae, 19661.
The etiology of craniolacunia in infants with spina bifida is uncertain. Several
of the hypotheses which have been suggested relate to abnormalities in intracranial
pressure. Faust [ 19311 proposed that craniolacunia result from an imbalance of
pressures on the developing cranium consisting of a relative increase in externa1
pressure from the intrauterine environment because of diminished intracranial pressure secondary to the “pressure valve” effect of the myelomeningocele sac. This
pressure imbalance would produce areas of atrophy of the developing cranium. Others
have suggested that increased intracranial pressure, perhaps causing ischemic changes
in the developing cranium, is the cause of craniolacunia [Engstler, 1905; Kerr, 1933;
Rothbart, 19361. The finding of normal head circumferences at birth in most infants
with spina bifida seems to conflict with both of these hypotheses [Tajima et al, 1977;
Stein et al, 19741. Such measurements made at birth may not reflect pressure
phenomena occurring during early fetal development or during the onset of cranial
ossification. If the fetal biparietal diameters (BPDs), measured at midtrimester, of
infants with spina bifida were significantly larger or smaller than those of unaffected
infants, this might favor either the effects of increased intracranial pressure or those
of intracranial decompression on fetal head size.
Prospective studies of BPD at midtrimester in fetuses with spina bifida ascertained through maternal semm alpha-fetoprotein screening have shown that the BPDs
in these fetuses are significantly less than those of corresponding control pregnancies,
even in those infants with evidence of early ventricular dilatation in utero Wald et al,
Received for publication Septernber 29, 1986; revision received Deccrnber 8, 1986
Address reprint requests to Dr. William G. Wilson, Department of Pediatrics, University of Virginia
Medical Center, Charlottesville, VA 22908.
O 1987 Aian R. L i s , Inc.
730
Wilson, Alford, and Schnatterly
1980; Roberts and Campbell, 19801. These findings of decreased BPDs were apparently not due to generalized growth retardation or gestational misdating, since abdominal circumferences were appropriate for the gestational ages as estimated from
menstrual dates. We propose that these observations support the hypothesis that a
condition of interna1 decompression and concomitant externa1 compression of the
calvarium exists in fetuses with spina bifida. These fetuses would have altered cranial
growth, as reflected by decreased BPDs at midtrimester and perhaps earlier. Abnormal contact between the brain and the membranous calvarium during the period of
ossification (8-12 weeks gestation) could alter the normal radial progression of
ossification, resulting in areas of poorly ossified bone bordered by bone of normal
thickness and histology [Hartley and Burnett, 1943; Shapiro, 19721. Whether the
defective ossification as is apparent radiographically at birth is due to bone atrophy,
bone resorption, or poor primary ossification remains to be determined. An imbalance
of compression and decompression during early cranial development might also help
explain the etiology of the other major cranial abnormality seen in infants with spina
bifida, the Arnold-Chiari malformation.
REFERENCES
Engstler G (1905): Ueber den Lückenschadel Neugeborener und seine Beziehung zur Spina bifida. Arch
f Kinderh 40:322-329.
Faust H (1931): Über den angeborenen Relief- und Lückenschadel und seine genetischen Beziehungen
zu Spaltbildung im Medullarrohr. Beitr z path Anat u z allg Path 86:613-632.
Hartley JB. Burnett CWF (1943): The radioiogical diagnosis of craniolacunia. Br J Radiol 16:99-108.
Kerr HD (1933): Anomalies of the skull in the new-born with special reference to “relief” or “lacuna
skuli” (“Lückenschadel”). Am J Roentgenoi 30:458-463.
McRae DL (1966): Observations on craniolacunia. Acta Radiol 5:55-64.
Roberts AB, Campbell S (1980): Small biparietal diameter of fetuses with spina bifida: Implications for
antenatal screening. Br J Obstet Gynaecol 87:927-928.
Rothbart HB (1936): Lacunar skuil of the new-born. Am J Dis Child 52: 1375-1389.
Shapiro R (1972): Anomalous parietal sutures and the bipartite parietal bone. Am J Roentgenol Radium
Ther Nucl Med 115:569-577.
Shopfner CE, Jabbour JT, Vallion RM (1965): Craniolacunia. Am J Roentgenol 93:343-349.
Stein S , Schut L, Borns P (1974): Lacunar skuil deformity (Lückenschadel) and intelligence in myelomeningocele. J Neurosurg 41: 10-13.
Tajima M. Yamada H, Kageyama N (1977): Craniolacunia in newborn with myelomeningoccle. Childs
Brain 3:297-303.
Vogt EC, Wyatt GM (1941): Craniolacunia (Lückenschadei). A report of 54 cases. Radioiogy 36: 147153.
Wald N , Cuckle H. Boreham J, Stirrat S (1980): Small biparietai diameter of fetuses with spina bifida:
Implications for antenatal screening. Br J Obstet Gynaecol 87:219-221.
William G. Wilson
Bennett A. Alford
Patricia T. Schnatterly
Department of Pediatrics
University of Virginia Medical Center
Charlottesville, Virginia (W G. W , P. T S . )
Department of Radiology
Children ’s Hospital
Birmingham, Alabama (B.A.A.)
Edited by James F. Reynolds
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skull, decompression, compression, results, craniolacunia, fetal
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