An Experimental Animal Model that Parallels Neurosensory Assessments of Concussion

ABSTRACT Introduction Tactile-based quantitative sensory assessments have proven successful in differentiating concussed vs. non-concussed individuals. One potential advantage of this methodology is that an experimental animal model can be used to obtain neurophysiological recordings of the neural activity in the somatosensory cortex evoked in response to the same tactile stimuli that are used in human sensory assessments and establish parallels between various metrics of stimulus-evoked cortical activity and perception of the stimulus attributes. Materials and Methods Stimulus-evoked neural activity was recorded via extracellular microelectrodes in rat primary somatosensory cortex (S1) in response to vibrotactile stimuli that are used in two particular human sensory assessments (reaction time (RT) and amplitude discrimination). Experiments were conducted on healthy control and brain-injured (BI) rats. Results Similar to the effects of mild traumatic brain injuries (mTBI) on human neurosensory assessments, comparable experimentally induced brain injuries in rats resulted in the following: (1) elevation of S1 responsivity to vibrotactile stimulation that depended nonlinearly on stimulus amplitude, significantly reducing its capacity to discriminate between stimuli of different amplitudes; (2) 50% reduction in S1 signal-to-noise ratios, which can be expected to contribute to elevation of RT in BI rats; and (3) 60% increase in intertrial variability of S1 responses to vibrotactile stimulation, which can be expected to contribute to elevation of RT variability in BI rats. Conclusions The results demonstrate suggestive similarities between neurophysiological observations made in the experimental rat mTBI model and observations made in post-concussion individuals with regard to three sensory assessment metrics (amplitude discrimination, RT, and RT variability). This is the first successful model that demonstrates that perceptual metrics obtained from human individuals are impacted by mTBI in a manner consistent with neurophysiological observations obtained from rat S1.