Graham K. Hubler

Blast induced mild traumatic brain injury/concussion: A physical analysis

Currently, a consensus exists that low intensity non-impact blast wave exposure leads to mild traumatic brain injury (mTBI). Considerable interest in this “invisible injury” has developed in the past few years but a disconnect remains between the biomedical outcomes and possible physical mechanisms causing mTBI. Here, we show that a shock wave travelling through the brain excites a phonon continuum that decays into specific acoustic waves with intensity exceeding brain tissue strength. Damage may occur within the period of the phonon wave, measured in tens to hundreds of nanometers, which makes the damage difficult to detect using conventional modalities.

Linking blast physics to biological outcomes in mild traumatic brain injury: Narrative review and preliminary report of an open-field blast model.

HighlightsBlast exposures are associated with traumatic brain injury (TBI); during recent conflicts most of these have been classified as mild TBI (mTBI).The role and mechanisms of primary blast wave injury remain controversial. We review blast models of TBI including shock tubes and open‐field blast.Our analyses of behavioral and pathological findings show that low level blast exposures (peak pressure < 100 kPa) induced lower mortality rates, fewer motor disabilities, and absence of lung injuries as compared to high level blast (peak pressure > 200 kPa).We present preliminary findings obtained from a reproducible open‐field blast murine model of mTBI representing a primary low level blast injury. Within scalability limits, this model closely mimics low level battlefield blast exposures and offers opportunities to advance the understanding of blast physics, resulting neuropathology, and underlying mechanisms leading to chronic effects of mTBI. ABSTRACT Blast exposures are associated with traumatic brain injury (TBI) and blast‐induced TBIs are common injuries affecting military personnel. Department of Defense and Veterans Administration (DoD/VA) reports for TBI indicated that the vast majority (82.3%) has been mild TBI (mTBI)/concussion. mTBI and associated posttraumatic stress disorders (PTSD) have been called “the invisible injury” of the current conflicts in Iraq and Afghanistan. These injuries induce varying degrees of neuropathological alterations and, in some cases, chronic cognitive, behavioral and neurological disorders. Appropriate animal models of blast‐induced TBI will not only assist the understanding of physical characteristics of the blast, but also help to address the potential mechanisms. This report provides a brief overview of physical principles of blast, injury mechanisms related to blast exposure, current blast animal models, and the neurological behavioral and neuropathological findings related to blast injury in experimental settings. We describe relationships between blast peak pressures and the observed injuries. We also report preliminary use of a highly reproducible and intensity‐graded blast murine model carried out in open‐field with explosives, and describe physical and pathological findings in this experimental model. Our results indicate close relationships between blast intensities and neuropathology and behavioral deficits, particularly at low level blast intensities relevant to mTBI.

Acoustic waves excited by phonon decay govern the fracture of brittle materials

The behavior of brittle materials under ballistic impacts is often associated with failure waves that are producing small fracture particles with a surface area requiring large energy input. Numerous attempts to explain this effect since the 1960s did not yield convincing results. Here we propose that failure waves can be interpreted as the result of the decay of the shock-excited phonon continuum into low frequency peaks in the phonon density of states. This results in a situation where pressure amplitude of the localized acoustic waves exceeds a critical fracture quantity such as the tensile strength of the material. Experimental confirmation of this model is presented by using fractured particle size analyses and comparing their results with predicted acoustic wavelengths.

Ultrastructural brain abnormalities and associated behavioral changes in mice after low-intensity blast exposure

HighlightsAnalyzed comprehensive physical data from an open‐field primary blast model in mice.Observed low intensity blast (LIB) induced nanoscale brain abnormalities in mice.The ultrastructural damages occurred in the absence of necrosis and astrogliosis.Reported associated neurobehavioral dysfunctions resulting from LIB exposure.Provide insights into the pathogenesis of primary blast injury. ABSTRACT Explosive blast‐induced mild traumatic brain injury (mTBI), a “signature wound” of recent military conflicts, commonly affects service members. While past blast injury studies have provided insights into TBI with moderate‐ to high‐intensity explosions, the impact of primary low‐intensity blast (LIB)‐mediated pathobiology on neurological deficits requires further investigation. Our prior considerations of blast physics predicted ultrastructural injuries at nanoscale levels. Here, we provide quantitative data using a primary LIB injury murine model exposed to open field detonation of 350 g of high‐energy explosive C4. We quantified ultrastructural and behavioral changes up to 30 days post blast injury (DPI). The use of an open‐field experimental blast generated a primary blast wave with a peak overpressure of 6.76 PSI (46.6 kPa) at a 3‐m distance from the center of the explosion, a positive phase duration of approximate 3.0 milliseconds (ms), a maximal impulse of 8.7 PSI × ms and a sharp rising time of 9 × 10−3 ms, with no apparent impact/acceleration in exposed animals. Neuropathologically, myelinated axonal damage was observed in blast‐exposed groups at 7 DPI. Using transmission electron microscopy, we observed and quantified myelin sheath defects and mitochondrial abnormalities at 7 and 30 DPI. Inverse correlations between blast intensities and neurobehavioral outcomes including motor activities, anxiety levels, nesting behavior, spatial learning and memory occurred. These observations uncover unique ultrastructural brain abnormalities and associated behavioral changes due to primary blast injury and provide key insights into its pathogenesis and potential treatment.