The pre-injury performance of rat #112 in the beam walking test was normal given that it scored 5.3 of 6. Consistent with this finding, other laboratories have reported minimal behavioral impairments in uninjured hydrocephalic Sprague-Dawley rats or golden hamsters. Tu and colleagues found no phenotypical signs of hydrocephalus in uninjured adult male and female Wistar rats, among which 43% had mild ventriculomegaly in MRI. Also, the 2-year-old R222 RNaseT2 KO hydrocephalus case reported by Ferris and colleagues appeared to have normal sensory behavior, given that it responded normally to foot shock and flashing light and startled to a loud sound.
Interestingly, a minimal cortical lesion induced by FPI resulted in severe impairment in the beam walking test within the 30-day follow-up given that the performance score dropped from 5.3 to 0, which was greater than the mean 2-points drop in the rest of the TBI cohort. Moreover, the lesion was located in the somatosensory cortex (rather than in the auditory cortex), which could explain the behavioral deficits. However, we did not notice any correlation between lesion coverage of the S1 cortices and performance in beam walking, suggesting that the motor impairment related more to hydrocephalus rather than cortical damage. Interestingly, in a model of acquired hydrocephalus induced by an intraventricular kaolin injection, slow motor and cognitive deterioration were reported over an 8-month follow-up, possibly related to stretching of the periventricular axonal pathways because of an increased ventricle volume.
Our observations in rat #112 suggest that the rapid, severe post-impact balance impairment triggered by minimal injury to the sensory cortex was augmented by pre-existing hydrocephalus.