Exploring memory impairment and post-traumatic amnesia following traumatic brain injury

Abstract

Memory disturbances are among the most common and significant consequences of traumatic brain injury (TBI). The severity of these deficits can vary widely across the trajectory of recovery from TBI and can be highly heterogenous across individuals. In the acute stages memory disturbance can occur in the form of post-traumatic amnesia (PTA), but deficits are also present into the chronic stages of recovery. I present four studies that aim to understand the characteristics and underlying mechanisms of memory impairment following TBI.

I investigated the cognitive profile of acute TBI patients with and without PTA. I found PTA patients show a transient deficit in working memory binding. I then assessed electrophysiological abnormalities to test the hypothesis that the binding deficit is underpinned by pathological low frequency slow-wave activity. PTA patients showed a significantly higher delta to alpha power ratio that correlated with binding impairment. To understand how this disruption to cortical communication impacts upon large-scale networks I performed a dynamic functional connectivity analysis on the resting state fMRI of acute TBI patients. I found four independent brain states that showed striking anti-correlation between core cognitive control networks. Patients in a more profound period of PTA spent more time in fewer states than those with less cognitive impairment. These findings suggest that PTA is likely underpinned by disruption to communication required for integration of features in working memory.

Finally, I examined enduring memory failures in chronic TBI patients and found that patients with episodic memory impairment showed differential activation of key networks required for memory and attention. Memory impairment related to the white matter integrity directly underpinning the task-derived encoding networks. These findings suggest that in chronic TBI memory impairment may be associated with failed control of attentional resources.