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A Case of Extensive Hyperostosis Frontalis Interna in an 87‐year‐old, Female Human Cadaver
Author(s) -
Prather Andrew D.,
Talarico Ernest F.,
Hardt Kevin D.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a971-a
Subject(s) - calvaria , frontal bone , anatomy , hyperostosis , parietal bone , medicine , skull , pathology , biology , biochemistry , in vitro
Hyperostosis frontalis interna ( HFI ) is a condition that involves thickening of the inner surface of the frontal bones with sparing of the midline. Little is known about the etiology and clinical presentation of HFI . We report unusual findings in the case of a woman with extensive hyperostosis of the frontal bones and a large hyperostotic nodule in the parietal bone with impingement on the precentral gyrus; separating it from the common form of HFI . The calvaria and brain were photographed, specimens of bone were paraffin embedded, and sections stained using the Von Kossa Method with MacNeal’s tetrachrome. Medical records were reviewed, and additional history obtained through interviews with the donor’s family. The calvaria showed extensive, bilateral thickening of frontal bones with irregular topography. A 3.5 cm bony nodule was visible on the inner table of the left parietal bone. The dura and cerebrum showed compression in this region. The dura was strongly adherent to hyperostotic areas. Microscopic analysis revealed that hyperostotic bone contained extensive remodeling of the compact bone of the endocranial plate to a spongy phenotype. Quantitative analysis of sections showed a lower proportion of lamellar bone (37.6–38.4%, frontal) than in the control (60.1%, unaffected parietal). This is an extensive case of Type D HFI with both frontal and parietal involvement, and a significantly larger proportion of spongy bone in affected regions. The patient exhibited several symptoms that have been previously correlated to HFI; we suggest that the HFI disease process was responsible for the manifestation of these symptoms.