Neuropsychological and Neuropsychiatric Deficits Following Traumatic Brain Injury: Common Patterns and Neuropathological Mechanisms

Traumatic Brain Injury (TBI) in all degrees of injury severity mainly induces deviant cognitive, emotional and behavioral alterations that lead to their respective disorders. This brief overview strives to define the variables that determine the risk of occurrence of these disorders and to describe the common patterns of these disorders and their relevant neuropathogenetic mechanism(s). In addition, post-traumatic deficits can interact and exacerbate the probability, persistence and severity of each variable relative to one another. Since, neural substrates and pathways further complicate these TBI sequels, identifying the neuropathogenetic basis of these deficits using human brain mapping techniques has been a milestone in the investigations of the TBI field. It has been found that TBI-induced functional disturbance of one or more specific neural networks may cause a distinct disorder. However, this matter is a topic of discussion in TBI research. Evidently, prevalent, unpleasant TBI consequences such as motivational deficits, antisocial behaviors, aggression, disability of inhibitory control and executive function are mostly associated with the disruption of neural circuits originated from separate parts of the prefrontal cortex connected to thalamic nuclei and basal ganglia. Evidence strictly emphasizes the abnormality of the Default Mode Network (DMN) either within the network or between it and other neural networks for a majority of cognitive, emotional and sleep disorders after TBI. Therefore, imbalanced neural circuits due to TBI may serve as diagnostic and prognostic biomarkers for post-traumatic neuropsychological and neuropsychiatric disorders as well as a guide for circuitbased neurotherapy.