AMERICAN JOURNAL OF PHYSICAL ANTHROPOLOGY 88:111-112 (1992)

Notes and Comments

Cranial Thickening: A Reply to Dr. Stuart-Macadam

Stephen Webb Department of Prehistory, Research School of Pacific Studies, Australian National University, Canberra, Australia

The main point of my article (Cranial Thickening in an Australian hominid as a possible paleoepidemiological indicator) was to highlight the extraordinary thickening in the vault of the WLH 50 hominid from the Willandra region of western New South Wales. The view I expressed in the paper was that such thickening was not normal and could only be attributed to some kind of pathology. I “tentatively” (not immutably or emphatically) attributed this morphology to changes brought about by some kind of ane- mia. Because of the extensive and massive thickening of the diploeic structures, I sug- gested that it may have been caused by a genetically determined anemia. I have al- ready stated my reasons for suggesting why the extensive and very thick diploeic expan- sion in WLH 50 was less likely to have been caused by an acquired anemia and do not want to repeat them here. My conclusion suggested that this individual may have been a heterozygotic sufferer of a genetic anemia-hence the ability to reach adult- hood.

In my article I went on to propose, first, that such an anemia may have been a pre- cursor to one (or all) of the balanced adap- tive polymorphisms we are familiar with to- day, and, second, that we should be aware of expecting to see the same diagnostic fea- tures for a given pathology in ancient homi- nids as we might among modern popula- tions. My conclusions were reached after I undertook what I regarded as a reasonable differential diagnosis, given the limited amount of remains, and I stand by the “ten- tative” conclusion at which I arrived.

I agree with Dr. Stuart-Macadam that the

“hair-on-end” morphology in the published radiograph is not as obvious as it might be. It is obvious, however, on the original radio- graphs, and I would be only too glad to sup- ply a copy of one of these to her if she so wishes. Although a “hair-on-end’’ artifact can occur in 4% of individuals, WLH 50 was radiographed several times with the same result.

Although normal skulls may display “diploeic” or “compact” vault morphology, WLH 50 cannot conform to the diploeic type as Stuart-Macadam suggests. There are two reasons for this. The first is that the cranial tables of this individual are very thin, no more than 1 mm thick. The diploeic compo- nent on the other hand measures in the range of 14-17 mm. In other words, the ratio of compact to diploeic bone is nowhere near the same. Second, when dealing with the sort of thickness found in this individual, which has a maximum of 19 mm, it seems to me quite inappropriate to refer to the vaults in modern populations in which these sort of measurements are never encountered un- less overtly pathological individuals are un- der discussion.

In pointing out paleopathological criteria for diagnosing anemia in dry bone, Stuart- Macadam lists specifically “features such as outer bone table thinning, diploeic thicken- ing, and ‘hair-on-end’ trabeculation.” WLH 50 has all these. Overt porotic hyperostosis or symmetrical osteoporosis cannot be de- tected, but superficial erosion to many parts of the outer surfaces of this calvarium and the filling of cracks and crevices with cal- cium carbonate make these features diffi- cult to detect.

In my article, I tried to adhere to a rigor- ous differential diagnosis based on known diseases that cause expansion of the diploeic tissues. On occasion, however, a rare and more exotic malformation exposes only too

Received September 25,1991; accepted November 8,1991

0 1992 WILEY-LISS, INC.

112 s. WEBB

well the weaknesses in paleopathological di- agnosis. At these times it is justified and perhaps necessary to make a cautionary suggestion for the likely origin of the lesion or condition. Stuart-Macadam’s reply to my article is important because it highlights the professional dialectic that is so essential in paleopathological research. This is particu- larly so when dealing with peculiar or rare pathologies and disease states among hu- mans living in the distant past. I welcome this but believe, however, that there is a cer- tain danger in being too inflexible or specific when using modern pathological criteria to deal with diseases that existed tens of thou- sands of years ago. Certainly there is no rea- son to expect ancient lesions to match per- fectly those with which we are familiar among contemporary human populations.

An example of such inflexibility is shown when Dr. Stuart-Macadam discusses the “probability” of the existence of genetic ane- mias in the late Pleistocene and the survival of evidence for them. None of her three points is substantial. The frequency of changes such as that seen in WLH 50 is, indeed, extremely low: WLH 50 is the only example in this region. Although only “very few examples” of “suspected genetic ane- mias” have been recorded, is it not possible that WLH 50 is another? The fact that they are rare is not firm grounds for dismissing the possibility.

Stuart-Macadam’s point brings me back to an issue I discussed in my original article. That issue was the possibility that WLH 50 was a heterozygous sufferer, which would confer survivability as this particular adap- tive mechanism should. The exaggerated diploeic thickening, which may not occur among heterozygous sufferers in modern populations, may have indeed occurred among people living over 25,000 years ago.

Again, there is no reason to expect that the criteria for pathological conditions among those living so long ago should match ex- actly those we find in more recent popula- tions. Disease has its own evolutionary his- tory, and we know even less about that than we do about our own evolutionary history.

The fact that WLH 50 survived the vagar- ies of nature (point 3) is not unusual. The robust construction and fossilised condition of WLH 50 did allow it to survive together with the morphological features incorpo- rated within it. I agree that the probabilities of this happening are extremely low, as they are with all human remains that come down to us from the Pleistocene, but they do hap- pen, and where would human evolutionary studies be without them?

In the end, Dr. Stuart-Macadam dis- misses the evidence for genetic anemia in WLH 50 because in her opinion the probabil- ity of such an individual existing in the late Pleistocene is “extremely low.” I am disap- pointed that her criticism is not more solid and that it is based on a limited view of past epidemiology. I am further disappointed that she merely argues that there is insuffi- cient evidence for attributing these changes to anemia, without offering another possible conclusion. Indeed, the paleopathologist al- most never has enough evidence, and, to many medical practitioners, paleopathologi- cal “evidence” is never sufficient to warrant our conclusions. It is clear that Stuart-Mac- adam and I differ in our conclusions also, as our colleagues in other branches of biologi- cal anthropology do over other problematic areas of research. I would, however, wel- come further discussions with her after she personally views the cranium of WLH 50. Unfortunately, if the reburial issue in Aus- tralia continues on its present course that may not be possible.