Contrecoup injury of the prefronto-thalamic tract in a patient with mild traumatic brain injury: A case report.

RATIONALE: We report on a patient with mild traumatic brain injury (TBI) with contrecoup injury of the prefronto-thalamic tract (PTT), as demonstrated by diffusion tensor tractography (DTT). PATIENT CONCERNS: A 62-year-old female patient suffered a head trauma after falling backward. While working at a height of 85cm above the floor, she fell backward and struck the occipital area of her head on the ground. The patient experienced cognitive dysfunction and depressive mood after the head trauma. DIAGNOSES: The patient was diagnosed as mild TBI due to falling backward. INTERVENTIONS: Clinical evaluation of her brain was performed at 2 months after onset. OUTCOMES: DTT at 2 months after onset revealed narrowings in the right ventrolateral and both orbitofrontal PTTs, whereas both the dorsolateral and left ventrolateral PTTs were not reconstructed. LESSONS: Injuries of the PTTs associated with a contrecoup brain injury were demonstrated in a patient with mild TBI.

Investigation of cavitation as a possible damage mechanism in blast-induced traumatic brain injury.

Cavitation was investigated as a possible damage mechanism for war-related traumatic brain injury (TBI) due to an improvised explosive device (IED) blast. When a frontal blast wave encounters the head, a shock wave is transmitted through the skull, cerebrospinal fluid (CSF), and tissue, causing negative pressure at the contrecoup that may result in cavitation. Numerical simulations and shock tube experiments were conducted to determine the possibility of cranial cavitation from realistic IED non-impact blast loading. Simplified surrogate models of the head consisted of a transparent polycarbonate ellipsoid. The first series of tests in the 18-inch-diameter shock tube were conducted on an ellipsoid filled with degassed water to simulate CSF and tissue. In the second series, Sylgard gel, surrounded by a layer of degassed water, was used to represent the tissue and CSF, respectively. Simulated blast overpressure in the shock tube tests ranged from a nominal 10-25 pounds per square inch gauge (psig; 69-170 kPa). Pressure in the simulated CSF was determined by Kulite thin line pressure sensors at the coup, center, and contrecoup positions. Using video taken at 10,000 frames/sec, we verified the presence of cavitation bubbles at the contrecoup in both ellipsoid models. In all tests, cavitation at the contrecoup was observed to coincide temporally with periods of negative pressure. Collapse of the cavitation bubbles caused by the surrounding pressure and elastic rebound of the skull resulted in significant pressure spikes in the simulated CSF. Numerical simulations using the DYSMAS hydrocode to predict onset of cavitation and pressure spikes during cavity collapse were in good agreement with the tests. The numerical simulations and experiments indicate that skull deformation is a significant factor causing cavitation. These results suggest that cavitation may be a damage mechanism contributing to TBI that requires future study.