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Mechanical properties were determined in living adult rat brain. Reconstructed magnetic resonance images of the rat brain before and after 2 mm compression with a 4.06 mm diameter vinyl screw showed the total volumetric strain was maximal at the site of indentation. The pressure response to stepwise brain compression showed a linear relationship to the point of respiratory compromise. Instrumented indentation was performed on live brain with intact dura using a 4-mm-diameter flat punch indenter to a maximum depth 1.2 mm at loading-unloading rates not exceeding 0.34 N/min and 1.2 mm/min. The calculated elastic modulus showed no consistent change after death. Creep deformation over 15 s was 7.86+/-1.6% in live brain and 27.0+/-0.24% after death. In constant multicycle indentation, displacement from 1st to 10th cycle increased 8.0+/-1.7% in life and 12.9+/-2.8% after death. The results suggest that elastic properties of rat intracranial contents do not change immediately after death, while changes in the viscous properties are substantial. The process of measuring these properties can alter physiological parameters.

BACKGROUND: The mechanisms of hydrocephalus formation remain unclear. OBJECTIVE: To measure intracranial biomechanical changes in rats with hydrocephalus. METHODS: Stress-strain relationships were determined by using force-controlled indentation through a craniotomy. Cortical blood flow and intracerebral pressures were monitored. In normal rats, deformability of intracranial contents was examined by applying 100 (20-100 mN) indentation cycles and during a 2-hour stress (100 mN) holding test. Hydrocephalus was induced in 56-day rats by cisternal kaolin injection. Magnetic resonance imaging was used to measure ventricle size and cortical blood flow. RESULTS: Application of a constant small force for 2 hours or 100 cycles of a small indentation caused progressive intracranial deformation. Following kaolin injection, the ventricles of 3-to 4-day, 7-to 9-day, and 12-to 15-day hydrocephalic rats progressively enlarged, the dorsal cerebrum thickness decreased by .40%, and cortical blood flow decreased by 20%. After 3 to 4 days, intracranial pressure and intraparenchymal pulse pressure increased significantly by 85%, and diminished thereafter. After 7 to 9 days, there was a transient significant increase of the intracranial stiffness (indentation modulus). Viscoelastic strain during application of a constant force significantly increased by .50% at 7 to 9 and 12 to 15 days. CONCLUSION: The observation that very small forces applied exogenously or endogenously (through pulsatile brain micromotions) cause progressive intracranial deformation suggests that the brain behaves in a poroviscoelastic manner. Intracranial pulsatility is increased during the early phases of ventriculomegaly. Small viscoelastic property changes of the intracranial contents accompany the ventriculomegaly. Consolidation of brain tissue by the pulsatile forces likely occurs through displacement of intraparenchymal fluids.

Object. The goal of this study was to examine the mechanical properties of living rat intracranial contents and corresponding brain structural alterations following parietal cerebral cortex contusion.Methods. After being anesthetized, young adult rats were subjected to parietal craniotomy followed by cortical contusion using a calibrated weight-drop method. Magnetic resonance imaging was used to visualize the contusion. At the site of contusion, instrumented force-controlled indentation was performed 2 hours to 21 days later on the intact dural surface. The force-deformation (stress-strain) relationship was used to calculate elastic (indentation modulus) and strain changes over time, and constant hold or cyclic stress was used to evaluate viscoelastic deformation. These measurements were followed by histological studies.Results. At contusion sites, the indentation modulus was significantly decreased at 1-3 days and tended to be above control values at 21 days. Multicycle indentation showed that the brain tended to accumulate more strain (an indicator of viscosity) by 1 day after the contusion. Imaging and histological studies showed local edema and hemorrhage at 6 hours to 3 days and accumulation of reactive astrocytes, which began at 3 days and was pronounced by 21 days.Conclusions. The viscoelastic properties of living rat brain change following contusion. Initially, edema and tissue necrosis occur, and the brain becomes less elastic and less viscous. Later, along with undergoing reactive astroglial changes, the brain tends to become stiffer than normal. These quantitative data, which are related to the physical changes in the brain following trauma and which reflect subjective impressions upon palpation, will be useful for understanding emerging diagnostic tools such as magnetic resonance elastography.

Surface dialysis of cryogenically injured rat brain controls CSF pressure and reduces intraparenchymal spread of edema fluid in the acute period after injury. The authors postulate that edema fluid moves into the osmotic cell rather than spreading through the uninjured brain. Long-term experiments will be needed to prove that this combination therapy is effective.

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