Pressure induced atrophy in the posterior cranial fossa - Suspicion of brain herniation Susan Klingner *,**,*** , Julia Gresky***, Michael Schultz*** *Institute for Prehistory and Protohistory, University of Leipzig, Germany , **Leipzig School of Human Origins – An International Max Planck Research School, Germany, ***Department of Anatomy, University of Göttingen, Germany ______________________________________________________________________________________________________________________________________________________________________________ Introduction In macerated skulls, depressions in the posterior cranial fossa are frequently observed. These lesions, which appear solitarily or in groups as roundish or oval deepenings, might be caused by various pathological processes. As a rule, they are provoked by diseases of the dural venous sinuses, the meninges and the brain which are of tumorous or inflammatory origin. An increased intracranial pressure due to bleeding, tumors or inflammations can promote the development of these depressions. Physiological depressions of occipal bone are the sulci of the superior sagittal sinus and the transverse sinuses (Fig. 1) as well as the cerebral and the cerebellar fossa (Schünke, Schulte und Schumacher 2006). Materials and Methods In the cemetery of Harting (Bavaria, southern Germany), which dates from the Early Middle Ages (6 th – 7 th century AD), 74 skulls of adult individuals were examined. In the cemetery of Wandersleben (Thuringia, central Germany), which represents a population of the first agriculturalists in Europe (linear pottery culture) and dates from the very Early Neolithic (~5600 BC), 109 skulls of adult individuals were examined. The skulls were studied using macroscopic, endoscopic, radiological, light and scanning- electron microscopic techniques. Results Seven cases from the early medieval population of Harting demonstrate vestiges caused by pressure- induced atrophy in the posterior cranial fossa (Figs. 2-4). In the Early Neolithic population of Wandersleben, 16 cases with vestiges of pressure-induced atrophy were found (Figs. 2-4). In all cases, the depressions have a roundish or oval shape and a sharp rim. They often occur in groups but also were found solitarily beneath the transverse sinus. They can extend from approximately 2 mm up to 20 mm. Their internal wall can be smooth or porous. In many cases, the impressions are subdivided into smaller compartments by thin walls (Figs. 5, 10, 13). In X-ray images the wall of the depressions is smooth and the surrounding spongy bone shows a regular trabecular structure, which indicates that it was not affected by an inflammatory process (Figs. 6, 11). In the endoscopic view (Fig. 7), the surrounding walls have smooth surfaces. No trabeculae of the diploë is visible. The presence of newly built cortical layer on the inner wall of the lesions cannot be excluded. This morphology indicates a slowly growing organization process. In the microscopic view of the thin ground sections (Figs. 8, 9), there is no hint of an inflammatory process. The spongy bone shows a regular trabecular structure. The depressions are not coated by a newly built lamina as it was expected by the endoscopic image. Furthermore, no Howship s lacunae are observable. Thus, an aggressive and quickly growing process can be excluded and there are no other vestiges of a typical inflammatory process. Therefore, pressure-induced atrophy seems to be the most likely cause of these depressions. Discussion and Perspectives In the majority of cases, the changes in the posterior cranial fossa occur together with inflammatory processes in the endocranium and here, particularly, in the internal lamina. In both populations, there was just one case in which the depressions occurred without any vestiges of inflammatory processes in close proximity. In the cases presented, the impressions show structures which developed slowly due to pressure-induced atrophy. This means that every slowly developing structure which presses against the occipital bone could produce such changes. Possible causes are tumorous events, such as meningeomas, tumors of the connective tissue, bone tumors, metastases from soft tissue tumors or brain tumors (Arntz 1932, Baló 1939) as well as brain herniations or encephaloceles (Beneke 1890, Blasius 1901, Wojno 1911, Hiller 1940, Meyer 1980). A genetic disposition must also be taken into consideration. There could be an inherited weakness of the dura mater which results in gaps of the dura. Through these gaps, the arachnoida mater could press into the diploë causing structures such as arachnoid granulations to emerge (Bauer 1930). Postmortem causes of these depressions must also be considered as a differential diagnosis. In cases with inflammatory processes of the internal lamina in the area of the cerebellar fossae, such inflammations could be of secondary origin. For future work, it would be desirable to study more endocranial lesions in macerated bones using cross-section microscopy because this technique allows significant clues to the origin and the development of pathological processes observable in ancient and recent skulls. References Arntz R (1932): Zur Pathologie der Hirnhäute. Wucherung der Endothelzellen der Arachnoidea-Zellknospen, Endotheliome der Dura mater und Hirnhernien (mit einigen Fällen). Inaugural-Dissertation. Universität Heidelberg. Bauer H (1930): Über die Entstehung der multiplen Hirnhernien zugleich ein Beitrag zu ihrer Kasuistik. Inaugural-Dissertation. Universität München. Beneke R (1890): Zwei Fälle von „multiplen Hirnhernien“. Virchows Archiv. Bd. 119. Blasius O (1901): Ein Fall von Epdermoid (Perlgeschwulst) der Balkengegend, Zugleich ein Beitrag zur Kenntnis der multiplen Hirnhernien, Ebenda Bd. 165. Hiller F (1940): Die Pathogenese der Hirnhernien. Mit 7 Textabbildungen. Eur. Arch. Psy. Neur. Sc. Bd. 112. Hft. 3. Schünke M, Schulte E und Schumacher U (2005): Prometheus Lernatlas der Anatomie. Kopf und Neuroanatomie. Thieme: Stuttgart. v Baló J (1939): Multiple Hirnhernien als Folgeerscheinungen von Hirngeschwülsten. Mit 9 Textabbildungen. Universität Szeged. v Meyer E (1890): Ueber eine basale Hirnhernie in der Gegend der Lamina cribrosa. Archiv f. pathol. Anat. Bd. 120. Hft. 2. Wojno S (1911): Über physiologische Hirnhernien. Inaugural-Dissertation. Universität Zürich. Thanks for technical support (cast and cross-sections) to I. Hettwer-Steeger and M. Brandt. Fig. 1 Occipital bone. Macroscopic view of the internal lamina (modified from Schünke, Schulte and Schumacher 2006). Contact: Susan.Klingner@paleopathology.info, juliagresky@yahoo.de 109 16 74 7 0 20 40 60 80 100 120 Adult skulls all skulls occipital bone with deepening all skulls occipital bone with deepening Wandersleben - early Neolithic Harting - early Middle Ages Fig. 2 Frequency of small depressions in the cerebellar fossa of the occipital bone. Early Neolithic and early Middle Ages. Fig. 3 Frequency of small depressions in the cerebellar fossa of the occipital bone. Additionally, vestiges of inflammatory processes. Early Neolithic and early Middle Ages. 16 15 7 6 0 2 4 6 8 10 12 14 16 occipital bone w ith deepening w ith inflammatory processes occipital bone w ith deepening w ith inf lammatory Processes Wandersleben - early Neolithic Harting - early Middle Ages Fig. 13 Occipital bone of an old mature woman from Wandersleben (W-2189). Macroscopic view of the internal lamina. One group of oval depressions and several smaller oval and roundish depressions with sharp edges in the cerebellar fossae. Fig. 10 Occipital bone of an old mature woman from Wandersleben (W-2219). Macroscopic view of the internal lamina. Two groups of oval and roundish depressions with sharp edges. Fig. 11 X-ray image (4,5 min, 45 kV) of the occipital bone presented in Figure 10. Fig. 12 Coloured cast-negative of the occipital bone presented in Figure 10. The cast simulates the soft tissue with the structures responsible for the pressure induced atrophy in the posterior cranial fossae. Fig. 5 Occipital bone of a mature male from Harting (H-13A). Macroscopic view of the internal lamina. Multiple lesions with a regular round or oval shape. Fig. 6 X-ray image of the occipital bone presented in Figure 5 (4 min, 55 kV). Fig. 7 Endoscopic image of some depressions of the left occipital bone presented in Figure 5. Fig. 8 Cross-section through the occipital bone (Fig. 5) presenting depressions (arrows) due to pressure atrophy. Overview of the thin ground section (thickness 70μm). Fig. 9 Cross-section through the bottom of one of the depressions seen in Figure 8. Microphotograph of the thin ground section (thickness 50μm) viewed in polarized light using a hilfsobjekt red 1st order (quartz) as compensator. Magnification 25x. 5 11 3 4 0 2 4 6 8 10 12 male female male female Wandersleben - early Neolithic Harting - early Middle Ages Fig. 4 Frequency of small depressions in the cerebellar fossa of the occipital bone in males and females. Early Neolithic and the early Middle Ages. Fig. 14 Cross-section through the occipital bone (Fig. 13) presenting the depressions (arrows) due to pressure atrophy. Overview of the thin ground section (thickness 50μm). The diploe is severely changed by an inflammatory process. Fig. 15 Cross-section through the bottom of one of the deepening presented in Figure 14. Microphotograph of the thin ground section (thickness 50μm) viewed in polarized light using a hilfsobjekt red 1st order (quartz) as compensator. Magnification 16x.