Head Injury Mechanisms and the Concept of Preventive Management: A Review and Critical Synthesis

Abstract

Recent advances in head injury research have produced a plethora of useful data coupled with a paucity of conceptual integration across the four ways in which this research is pursued. These research orientations are the epidemiological, biomechanical, basic neuroscientific, and clinicopathologic/therapeutic (including rehabilitation). This overview of the history and current state of the art assumes that biomechanics is the basic science of causation in head injury research and when fully integrated with its counterparts, physiology and pathology, it can serve to overcome our conceptual handicaps. A paradigm integrating biomechanics; into the sequence of preventive, protective, acute therapeutic, and rehabilitative interventions will be described as the concept of preventive management. From this we derive the hypothesized claim that the exact biomechanics and the physiopathologic response at the time of injury (at the macroscopic and microscopic levels) determine the sequence of so-called secondary effects that are conceived as the inexorable delayed manifestations of the primary events and concomitant boundary conditions. Knowledge of these events will enable accurate predictions of the natural history and outcome of head injuries from observations carried out in the early acute phase. Examples to test this claim will be given with particular reference to the two types of traumatic brain injury (TBI) phenomenologically associated with disturbances of consciousness, the onset of which can be either immediate or delayed. The current economics and availability of computational power provide a significant opportunity for the development of selected experimental, physical, and simulated models of head injury on the basis of which the complex neurovascular and nonneural cellular and fluid elements of the nervous system may be accurately modeled. This approach will significantly improve the efficiency and quality of the essential biological and clinical observations and model experiments required to validate the theoretical methods and their predictions.

Biophysical Linkage between MRI and EEG Amplitude in Closed Head Injury

“…Biomechanical studies of closed head injury have shown that fluid dynamic tissue boundaries determine the physical consequences of forces imparted to the human skull (Ommaya, 1968(Ommaya, , 1995Holbourn, 1943). …”

“…The majority of biomechanical studies over the past 30 years support a ''centripetal'' force vector which is maximum at the outer cortex with a gradient to the subcortex and brain stem (Ommaya, 1995), a rotational vector (Holbourn, 1943(Holbourn, , 1945Lee and Advani, 1970), and a shear vector (Advani et al, 1982;Ommaya et al, 1994). The geometrical summation of these forces results in maximum injury in that part of cortex that is in contact with the skull, e.g., the gray matter of the frontal and temporal lobes, which largely occurs independent of the direction of impact to the skull (Ommaya, 1995;Sano et al, 1967).…”

“…The geometrical summation of these forces results in maximum injury in that part of cortex that is in contact with the skull, e.g., the gray matter of the frontal and temporal lobes, which largely occurs independent of the direction of impact to the skull (Ommaya, 1995;Sano et al, 1967). Two other invariant consequences of blunt force injuries to the skull are: (1) shear forces which are maximal at the boundaries between different densities of tissue (e.g., gray vs white matter) and (2) a percussion shock wave that travels from the point of impact, making contact with the opposite side of the skull in Ͻ200 ms, resulting in a ''coup countre-coup'' injury (Ommaya, 1995;Sano et al, 1967). All of these forces are capable of seriously disrupting the molecular integrity and function of cortical neurons and glia (Povlishock and Coburn, 1989).…”

“…9D. With increased biomechanical force, a ''centripetal'' vector invades the white matter and subcortical structures (Ommaya, 1995) as reflected by increased ␦ EEG waves. This suggests that lengthened T2 and/or reduced relaxation contrast (Thatcher et al, 1997) is due to injury to the gray and white matter with the distinction between hypotheses 1 and 2 being that of the extent of neuronal destruction.…”

Rare retinal haemorrhages in translational accidental head trauma in children

“…8,20 The factors determining the severity of injuries in falls are the height of the fall, the landing surface, and the position on falling. Falls are considered to cause predominantly translational acceleration, which produces mainly focal brain damage.…”