Mild traumatic brain injury and delayed alteration of memory processing

Citation: Foster PP (2015) Mild traumatic brain injury and delayed alteration of memory processing. A commentary on History of mild traumatic brain injury is associated with deficits in relational memory, reduced hippocampal volume, and less neural activity later in life A brain traumatism may result from focal impact upon the head and/or sudden acceleration/deceleration kinetic forces applied to the brain within the rigid skull, or by a complex association of both. Approximately 500,000 to 3 million US cases occur per year. A major problem is that traumatic brain injury (TBI) classified as " mild " may not be reflected by lesions on conventional neuroimaging scans which appear " normal " albeit some mild TBI patients with " normal scans " may express long-term cognitive deficits (Irimia et al., 2012b). This raises overarching questions: would mild TBI result in cognitive deficits years later? How would memory consolidation and long-term potentiation then be affected? Monti et al. attempt to answer some of these questions in the article which appeared in Vol. 5 of Frontiers in Aging Neuroscience (Monti et al., 2013) by studying the relational memory, i.e., the performance of acquiring and retaining memory to construct association of elements of a scene or events in patients having experienced TBI early in their lives. Relational memory impairment is one of the behavioral phenotypes of mild TBI following the selective damage of specific intrinsic connectivity networks, ICNs (Barbey et al., 2015). The interest of Monti's study is the determination of post-TBI disrupted networks by visualization of their connectivity which will ultimately serve as patient-personalized diagnostic tools (Irimia et al., 2012a). The salience (SN) and the default mode networks (DMN) underlie some mechanisms of memory performance tested in their article using encoding trials via the presentation of visual scenes to memorize (Monti et al., 2013) and entails the appropriate functioning of those networks. An injury to a single white matter tract can lead to an alteration of the encoding and recognition processes. A key player in memory processing is the hippocampus which is also the center of white matter efferent or afferent projections. In humans, neurons in the hippocampus are more sensitive to post-traumatic degeneration and prone to apoptotic decay (Beauchamp et al., 2011). Even after a single TBI event, hippocampal atrophy may arise within months (Fotuhi et al., 2012). The remarkable cross-sectional study by Monti et al. was designed to correlate the history of …