**3. Anatomical and physiological consideration**

Before further consideration on injury mechanisms, it is important to appreciate the evolving anatomy and physiology in every stage of child development and its impact on injury biomechanics (**Table 1**). Note that this difference is also relevant to TBI diagnosis and management in children.

Children have a relatively higher head-body ratio and, consequently, greater relative head weight as opposed to adults. The large head size increases the possibility of experiencing head trauma, while the weight imposed results in distinct acceleration dynamics when exposed to external forces. Early-stage facial development is characterized by maximum craniofacial ratio, protruding forehead, and less developed paranasal sinuses. These unique properties subject increased likelihood of frontal trauma, especially with lesser capability of the sinuses to absorb the energy.

Younger children have thin calvarium rich in bone marrow with fontanels and sutures closing at different times. The pliable skull, along with open sutures and fontanels, allows for deformation and limited intracranial pressure (ICP) buffering. Hence, the existence of fracture should raise clinical suspicion for significant


**89**

*Traumatic Brain Injury in Children*

response to the external force.

**4. Biomechanics**

fracture initiation.

dysfunction.

reality [16, 17].

**5. Pathophysiology**

*DOI: http://dx.doi.org/10.5772/intechopen.96010*

to be maintained until proven otherwise.

volume and cerebrospinal fluid (CSF)-brain ratio [13, 15].

underlying parenchymal injury despite lacking evidence on imaging investigation. The downside of high skull plasticity with regards to cortical vessels and brain parenchyma is that it may cause stretching and shearing of these structures in

The craniocervical structures depend mainly on the ligaments and soft tissues for stabilization. Weaker neck muscles and ligaments, upper position of fulcrum of the vertebral body, and flexible articulations in younger children predispose to craniocervical instability particularly when combined with the disproportional head weight. Therefore, a high index of suspicion for concomitant spinal injury has

Cerebral white matter is less myelinated and contains more water compared to that of adults. Although the nerve fibers are pliable and less likely to rupture, their pliability increases the risk of cerebral contusion and subdural hematoma. The unmyelinated areas are significantly more prone to injury. Cerebral compliance is also affected by other age-dependent factors, such as cerebral blood flow and

The biomechanistic aspect of head trauma is composed of two forces: translation or linear (LA) and rotational (RA) accelerations. The former results from direct impact measured in gravitational force unit (g), whilst the latter results from indirect or whiplash impact and is measured as radians per second squared (rad/s2

Upon sudden impact with a surface, the head experiences deformation and deceleration in the same direction as the initial force and result in LA. The bending of the skull produces a wave-like pattern which causes tension propagating from the outer to inner skull. Tension propagation magnitude and direction determine the ensuing

Intracranial damage occurs as a consequence of either brain motion or pressure gradient established by the LA. Brain motion is proposed to potentiate focal hematoma directly. Other authors proposed that the focal site of an impact is exposed to positive gradient resulting in focal injury and the distal site is exposed to negative gradient resulting in shear stress and cavitation. Previous researches reported a strong correlation between LA and ICP, and ICP with subsequent neurologic

Holbourn was the pioneer researcher who stated that RA-mediated brain injury was caused by shear stress and strain. Impact duration should also be taken into account as different combinations of impact duration and magnitude result in different injury types. Longer duration at a lower magnitude of RA generates diffuse axonal injury, and the opposite generates subdural hematoma. Although LA and RA are often described separately, the inherent coupling of both forces is inevitable in

TBI pathogenesis involves primary and secondary injuries culminating in a temporary or permanent neurological deficit. Primary injury represents brain dysfunction as a direct result of brain deformation. Structural damage in focal, multifocal, or diffuse pattern in primary injury can only be prevented before the collision. Consequent molecular, chemical, and inflammatory cascades further extend the reversible secondary injury from minutes to days after the primary insult [18].

).
