Posted 31 July 2001

By Catalin Obreja
N.T.C.P. - not-for-profit research association
ntcp@neurostaff.org
http://ntcp.neurostaff.org

Different epidemiological studies showed that the traumatic brain injuries (TBI) are correlated with higher incidence (1, 2, 3, 4) and earlier onset (3) of Alzheimer's disease (AD), particularly when associated with APOE epsilon 4 allele (2, 4) and when the loss of consiousness exceeds five minutes (3). Thus, the TBI is probably one of the main environmental factors in the AD pathogenesis.

In AD, the earliest loss of neurons occurs in the nucleus basalis and the entorhinal cortex (5). Post traumatic diffuse axonal injury (DAI) is concentrated in the deep cerebral regions (6), near the entorhinal cortex and including the nucleus basalis.

TBI biomechanics explores the mechanical phenomenon that causes the initial cranio-cerebral lesions and thus represents the starting point for the overall understanding of the TBI pathophysiology.

TBI is the consequence of the spatio-temporal pressure variations occurring inside the brain during head traumas. The spatial distribution of the pressure gradient (PG) is responsible for the tissue strains (compression, tensile, shear), the cerebral lesions' localization and the consequent neurological signs (7). Beside the skull's deformation -- caused by the contact loading and determining skull vibrations and/or fractures -- classical biomechanical theories concern two inertial phenomena: the linear acceleration and the rotational head movements (8, 9). The first theory explains the superficial brain lesions. The second theory seems to better explain the deep cerebral lesions and the concussion mechanism but is still a controversial topic (10).

The stereotactical theory presented here mainly considers the approximately spherical shape of the interface skull-brain. The skull-brain relative movements, caused by the acceleration phenomena - linear or rotational - and by the skull vibrations, generate secondary pressure waves with approximately spherical wave fronts that concentrically propagate toward the deep cerebral structures. The wave front's spoke and its surface progressively decreases. According to the energy conservation law, the amplitude of the pressure waves progressively increases. Thus, the PG will be maximal in areas close from the geometrical center of the implied skull vault segment (11, 12, 13).

The stereotactical phenomenon can explain many common post-traumatic neurological signs (the initial loss of consciousness, the post-traumatic amnesia) and is compatible with previously reported experimental results (11, 12, 13). Its complementarity with the classical biomechanical theories could allow us to integrate the TBI biomechanics in a common concept in order to better understand the TBI pathophysiology and its relationship with Alzheimer's disease.

References

1. Plassman BL et al. Documented head injury in early adulthood and risk of Alzheimer's disease and other dementias. Neurology 2000 Oct 24;55(8):1158-66. Abstract

2.Mayeux R, et al. Synergistic effects of traumatic head injury and apolipoprotein-epsilon 4 in patients with Alzheimer's disease. Neurology 1995 Mar;45(3 Pt 1):555-7. Abstract

3.Schofield PW, et al.. Alzheimer's disease after remote head injury: an incidence study. J Neurol Neurosurg Psychiatry 1997 Feb;62(2):119-24.Abstract

4.Tang MX, et al. Effect of age, ethnicity, and head injury on the association between APOE genotypes and Alzheimer's disease. Ann N Y Acad Sci 1996 Dec 16;802:6-15. Abstract

5.Perry EK, et al. Correlation of cholinergic abnormalities with senile plaques and mental scores in senile dementia. Br J Med 1978;2:1457-1459. Abstract

6. Blumbergs, PC, Scott, G, Manavis, J, Wainwright, H, Simpson, DA, McLean, AJ. Staining of amyloid precursor to study axonal damage in mild head injury. Lancet 1994;344:1055-6. Abstract

7. Teasdale, G, Mathew, P. Mechanisms of cerebral concussion, contusion and other effects of head injury. In: Julian R. Youmans editor, Neurological surgery. 4th ed. New York: W B Saunders Co, p 1533-46, 1996.

8. Holbourn, AS. Mechanics of head injuries. Lancet 1943;2:438-41.

9. Thibault, LE, Gennarelli, TA. Brain injury: an analysis of neural and neurovascular trauma in the nonhuman primate. 34th Annual proceedings of the Association for the Advancement of Automotive Medicine, Des Plaines, IL, 1990, p 337-51.

10. McLean, AJ. Brain injury without head impact? J Neurotrauma 1995 Aug;12(4):621-5 Abstract

11. Obreja, C. The Stereotactical Phenomena in Brain Injury Biomechanics - what long-term consequences? Neurobiology of Aging 2000; 21(1S):S148.

12. Obreja, C. Stereotactical Phenomena in Brain Injury Biomechanics Restorative Neurology and Neuroscience 2000; 16(3-4):310-1.

13. Obreja, C. Stereotactical Phenomena in Traumatic Brain Injury Biomechanics: Diffuse Axonal Injury and Brain Concussion. Neuroskills – January 2001. Link to NeuroSkills