I really love walking into the morgue (I know it does not sound right), learning something new, and interacting with all these wonderful minds.
One of the autopsies I observed this time was about a woman found dead in her cabin on a cruise ship. She got her knee surgery before she boarded, and was prescribed antibiotics. When the Medical Examiner opened her up, she immediately found pulmonary fluid in her chest cavity (which could indicate infection). Later, she opened up her skull, and learned that her skull has a feature, Hyperostosis frontalis interna (HFI), which usually sees that on middle-aged women, sometimes men. The individuals with this feature are having a thicker frontal and occipital bone when compares with the parietal and temple bones. She also found a piece of little bone that is ossifying when she was removing her brain. Afterwards, she decided to dissect her knee too. When she opened the knee, it was totally infected. And the surgery apparently has removed her knee cap and replaced with an artificial one.
The bone from the surgery however never healed. Superficially, other than her surgical wound, she got few circular 3mm wide wounds (probably got from the infections).
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More on Hyperostosis frontalis interna (HFI) (may choose to skip this and read on about the next case 🙂 )
Hyperostosis frontalis interna (HFI) (Source: radiopedia.org)
Hyperostosis frontalis interna (HFI) is an independent yet pathological condition with an unknown etiology thus far. It refers to the manifestation of accretion of bone on the inner table of the frontal bone. Yet, this phenomenon of bone thickening on endocranial surface usually not extending beyond the coronal suture (Ruhli and Henneberg 2001). HFI was first described by Morgagni in 1769 and even with the great jump in medicine and pathology in almost three centuries, the origin and the detailed etiology are still unknown. Yet, with all the studies have done, HFI is most likely presence in post-menopausal women, which may link its presence to the hormone level disturbance in human body (Hajdu et al. 2009; Hershkovitz et al. 1999; Ruhli and Henneberg, 2001, May et al. 2010).
The origin of HFI still remains as a mystery till today. Hajdu et al. (2009) suggested that HFI could possibly link with unknown genetic predisposition, environment, hormones allocation and metabolic diseases. Specifically, HFI is clinically associated with Morgagni’s syndrome, or MSM—Morgagni-Stewart-Morel syndrome, which is a hormonal disorder that demonstrates symptoms like obesity, hirsutism and metal retardation (Barber et al., 1997; May et al., 2010).
Hershkovitz et al. (1999), May et al. (2010), and Ruhli and Henneberg (2001) purport that hormonal influences are key to understand the etiology of this phenomenon, especially about the hormonal regulation in females. Hershkovitz et al. (1999) quoted Ritcher (1939) that HFI under his study will disappear after passing of the endocrine imbalance of menopause. Ruhli and Henneberg (2001) hypothesized that because of the decrease of selective pressure has increased the metabolic rate due to the higher level of leptin (a 167 amino acid peptide coded by ob gene), which in turns may cause an increase of localized bone overgrowth (Rhuli and Henneberg, 2001). Given that leptin is strongly correlated to body mass index. Obesity, according to Haffner and Bauer (1993), is widely recognized as a major effect on bone density. This study suggests that however the adjustment for glucose and insulin concentrations does not explain the exact association between bone density and obesity, rather the bone density increased may be due to stress on the skeleton early in life, which lead to increase of bone formation, or to increase estrogen or androgen concentrations (Haffner and Bauer, 1993). Ruhli et al. (2004) particularly quoted Rudali (1968) changes of metabolism of female hormones in fat cells could link up HFI and adiposity. Other than leptin, Ruhli et al. (2004) suggested a possible microevolution of human sex steroids as the etiology of HFI.
The overgrowth bony tissue of HFI grows specifically on the inner plate of the frontal bone of the skull. It usually comes in the form of bilateral nodular, and only restricted to the area between the superior sagittal sinus medially and middle meningeal artery posteriorly (May et al., 2010). Yet, it is still unknown for frontal bone as the spot for this hormone target. Hershkovitz et al. (1999) suggested that one of clues might be the fact that HFI process “almost always begins in the middle one third of the frontal squama,” given that Morel (1930) considered that spot would be the original centers of ossification of the bone. Hormones such as estrogen may have trigger the primary center of ossification of the frontal bone to grow extra bones (Hershkovitz et al., 1999). HFI can be traced via dried skulls with naked eye inspection, radiographic studies and computerized tomography (CT) scan images. Yet, plain radiographies could be ineffective for detecting the early stages of HFI as opposed to naked eyes inspection as lesions in gauge can be distinguished) (Hajdu et al., 2010).
Various neurophysiologic, metabolic, radiologic studies performed and failed to suggest a direct linkage between HFI and behavioral disorders, rather suggesting the bone nodular lesions shown on x-ray are coincidence (Smith and Hemphill, 1956) Most of the cases of HFI are asymptomatic.
HFI are ethnicity-related and chronologically affected. Scholars like Hajdu and many others agreed that it seems that it is impossible to compare different populations and different centuries in order to get a general possible trend for now. Also, Raikos et al. (2011) pointed out that it is a rare case to find female with HFI in antiquity but males. Ruhli et al. (2004) compared the data collected before industrial revolution and those after and found resemble results as Raikos et al. (2011) but a big change for the data after industrial revolution. Ruhli et al. (2004) suggested the change of female life cycle through social developments and the longevity of modern population initiate the change. It is important to remember however, lower life span in historical times do not mean a lower prevalence of HFI (Ruhli and Henneberg, 2001).
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Back to the case…
The other male deceased was a 45-year man that survived from a four car accident April after he had a head surgery. The surgery, according to the Medical Examiner has taken out almost his right hemisphere of the skull to release pressure (which is called Trephination). He suspected that the accident caused a lot of internal bleeding, and the blood rushed all into the skull. The blood not only had increased the pressure inside the skull but also changed the shape of the brain—it presses the brain towards the left hemisphere of the brain.
The deceased has been in coma since, and stayed in the hospital. The coma did age him pretty fast (he looked like an old man by the time he was on the autopsy table) and took away lots of his nutrients.
Hajdu, T., Fóthi, E., Bernert, Z., Molnár, E., Lovász, G., Ko˝vári, I., Köhler, K., & Marcsik, A. (2009). Appearance of hyperostosis frontalis interna in some osteoarcheological series from Hungary HOMO – Journal of Comparative Human Biology, 60 (3), 185-205 DOI: 10.1016/j.jchb.2008.07.004
Hershkovitz I, Greenwald C, Rothschild BM, Latimer B, Dutour O, Jellema LM, & Wish-Baratz S (1999). Hyperostosis frontalis interna: an anthropological perspective. American journal of physical anthropology, 109 (3), 303-25 PMID: 10407462
Raikos, A., Paraskevas, G., Yusuf, F., Kordali, P., Meditskou, S., Al-Haj, A., & Brand-Saberi, B. (2011). Etiopathogenesis of hyperostosis frontalis interna: A mystery still Annals of Anatomy – Anatomischer Anzeiger, 193 (5), 453-458 DOI: 10.1016/j.aanat.2011.05.004
Rühli, F., & Henneberg, M. (2002). Are hyperostosis frontalis interna and leptin linked? A hypothetical approach about hormonal influence on human microevolution Medical Hypotheses, 58 (5), 378-381 DOI: 10.1054/mehy.2001.1481