TBI? Traumatic Brain Injury? Thats a pretty Huge category of insult. Blunt? Penetrating? A smack in the head can damage many things based on type of smack in the head and where the smack in the head occurred.

If received a smack in the head from the back then V1 is susceptible and cerebellum, neither of which receive hippocampal SPW (sharp Waves (aka ripples). If receive smack in the head from the front ie bouncing off a windshield from the passenger seat, then oddly enough the lower casing bone ridges of the skull can create damage to the hippocampus itself and overlying entorhinal and perirhinal cortices, as the brain slushes forward in the skull and scrapes the bottom. if the hippocampus itself is damaged then no source of SPWs so no transmission of SPWs to cortex. If only entorhinal and perirhinal then SPW return to deep layers of these same cortices maybe prevented. However, antecedents of SPWs may rely upon input from superficial layers of same cortices affecting frequency of generation of SPWs. As immediate effects of things like edema recover from TBI then those circuits supporting SPW transmission will recover to the extent that they recover. If sclerosis or scarring occurs, then those circuits exhibiting sclerosis will not recover as much.

SPW/Ripples are an entraining oscillation and meant to communicate like a carrier wave. As such, yes principal CA1 cells are entrained to the CA3 depolarization, and fire en masse, in bursts, which in turn propagates the ripple to principal cells of subiculum, where in turn the cells are entrained and propagate the ripple to deep layer enorhinal and perirhinal projections (the latter in maccaques, but not rodents).

Logothetis has done the preliminary work to correlate Local Field Potential (LFP) signals with fMRI, and a number of human and non-human primate studies show this, particularly with the visual system (as exsquisite experimental control of signals responding to stimuli is more easily obtained here), as one moves up the visual system from striate to extrastriate and other visual associative areas the signal related to stimuli degrades as other processes kick in. Logothetis' reviews of the literature also indicate the fMRI correlates better with LFP oscillations then individual units or poulations of units. Given the coarseness of LFP and fMRI (when compared to the individual firing of neurons), the match at this level of analysis should not be surprising.

Not much extracellular (extra fiber?) ephys (electrophysiology?) available that would be equivalent to LFP, and therefore no match up available to DTi as of yet.

May wish to reframe your question... essentially taking finegrained explanatory mechanism at the cellular level (ripples) and trying to match it to prevalent clinical phenomena (car accidents, blasts from IEDs), have a basic mismatch between the level of phenomena of interst and the explanatory power of the mechanism.

There are rodent models of TBI, based on concussive air blast to craniotomized brains, and similarly guided ball bearing drops. So there are ways to reframe the level of your question for better matches.

As for matching LFP and fMRI check out our latest publican in Neuron from the Suzuki lab. Hargreaves, Mattfield et al., 2012

Eric is right about all TBI not being equivalent; low-velocity trauma such as penetration with a sharp object and other relatively focal injuries tend to have a different profile. But the majority of severe injury is due to motor vehicle accident or similar magnitude of blunt forces acting on the head that include a coup-contrecoup phenomenon (often involvling both frontal and occipital/cerebellar areas), shearing and DAI, and a preponderance of laceration to the inferior frontal and temporal lobes as notes with a fairly characteristic picture of diffuse ineffeciency of learning and processing that will tend to improve over time. This would seem consistent with the ripples being at first completely then more partially blocked and/or having to find alternative paths that would be less direct. In a milder injury, where there is little permanent cell death/structural damage, but some edema and neurochemical disruption, the recovery would be quicker and more complete.