Haslach research program

Brain tissue, when exposed to external mechanical insults, such as impact and blast waves, or neurosurgery, may be subjected to internal deformation waves composed of longitudinal and shear components that induce combined translational shear and compression deformations. Such deformations of the tissue may cause traumatic brain injury (TBI).

Brain tissue is a nonlinear viscoelastic, biphasic material since it is composed of solid matter that includes neurons, glial cells and blood vessels, along with intracellular and extracellular fluid (ECF), but the role of the ECF in the mechanical response of brain tissue has been neglected in many studies. The ECF surrounds brain cells and lies in the extracellular space comprising about 20% of the brain parenchymal volume and is the medium for diffusion-based functions such as nutrient transport to, and waste removal from, the cells and non-synaptic cell-cell communication.
The configuration of brain tissue is maintained by interaction between the cellular solid matter and the brain extracellular fluid (ECF). The pattern of links between neurons, astrocytes and each other forms a mechanically weak network structure that maintains, along with the capillaries, the structural integrity of the brain by a combination of tension in axons, dendrites, and glial processes that is balanced by hydrostatic pressure in the ECF. Under mechanical deformation, disruption of the equilibrium balance of tension in the axons, dendrites and glial processes with the ECF hydrostatic pressure may lead to mechanical damage. Such an injury is a precursor of the insult induced pathological biochemical response that medical doctors study and try to ameliorate.
Trauma-induced increases in ECF hydrostatic pressure, which may induce pathological ECF flow, are one possible immediate mechanical cause of brain tissue damage. Interaction between the local ECF hydrostatic pressure and strain rate-dependent axonal stiffening is suggested as a mechanism to transmit external brain insults to the cellular level. The mechanical response is indicative of the interaction of solid elements with the ECF in the extracellular space of the tissue itself, as opposed to the motion of cerebrospinal fluid in the ventricles.
Understanding the mechanical response of the brain to impact or blast waves that cause traumatic brain injury requires high strain-rate experimental stress-strain data. Current work includes very high rate constant compressive and shear deformation as well as frequency analysis of the stress response to high frequency sinusoidal shear deformation of rat brain specimens. While some data for high strain rate unconfined compression and shear is available for the porcine brain none is published for the rat brain, a common animal model for human TBI studies.
A long-term goal is to investigate the interaction between cerebral arteries and the brain tissue under external trauma. Dangerous mechanical interaction of the cerebral vascular system with the brain parenchyma during mild traumatic brain injury may result from a combination of shear and compression deformation waves that causes non-diffusive extracellular fluid motion. This investigation would measure the mechanical response, to a combination of shear and compressive deformation, of animal model specimens containing the boundary between the cerebral vascular system and the brain parenchyma, and in particular would measure the mechanical damage that may occur to the blood-brain barrier.  Ultimately the goal is to develop a mathematical model for the mechanical interaction of the vascular system with the brain parenchyma and for flow in the glymphatic system during mild traumatic brain injury to predict forces generated in the extracellular fluid and in the walls of the cerebral arteries.