A reliable, noninvasive test for mild traumatic brain injury (TBI) has long proved elusive. In a recent experiment, however, we have shown that processing and identification of speech sound frequencies is measurably impaired in concussion victims and that neural responses to speech-frequency sounds can be sufficiently tracked using electrodes to warrant a clinical assessment of an injury.
Investigations into the neurological effects of closed head trauma have previously determined that the auditory system is negatively impacted by physiological changes such as demyelination, or damage to nerve coverings, and reduced levels of neurotransmitters, chemicals that transmit neural signals. However, the incidence of these impacts among patients with less severe trauma may be difficult to detect, making most auditory neurological measures unreliable as indicators of mild TBI. Our decision to test the neural response to speech-frequency sounds was based on the complexity of the brain activity involved: the demyelination, axonal injury, and tauopathy potentially resulting from brain injury would affect speech-frequency auditory responses even if they presented as very mild. Moreover, lags in speech-frequency sound processing as low as a fraction of a millisecond have been shown to be indicative of abnormality.
We measured the neural responses of a group of people diagnosed with mild TBI to speech-frequency sounds amid background noise and those of a control group of healthy people. As we expected, the injured brains exhibited both smaller and slower neural responses to speech-frequency sounds than the brains of the control group.
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The more severe a brain injury is, the more likely it is that a victim will exhibit diminished neural processing due to demyelination and diminished levels of the neurotransmitter glutamate, both of which are primary contributors to the functioning of the auditory midbrain. Thus the more severe a brain injury, the less aptly the brain can execute complex sound-processing functions.