Last update:
24-Jul-2020

Traumatic brain injury (TBI) is a serious healthcare problem. The underlying pathophysiology includes diffuse axonal injury, neuronal loss, protein misfolding, persistent neuroinflammation and alterations in the neurotransmission systems. Secondary brain injury occurs as a consequence of both the primary trauma and activation of the immune system. In addition to the initially detected brain injuries, cognitive impairment constitutes a late consequence of TBI and may be a source of considerable disability. Across all levels of TBI severity, the cognitive domains most commonly affected are attention, processing speed, episodic memory and executive function. The first-line forms of treatment for post-traumatic cognitive impairment are non-pharmacological, including education, the setting of realistic expectations, lifestyle modification, and cognitive rehabilitation. Pharmacotherapy for post-traumatic cognitive impairment includes uncompetitive N-methyl-D-aspartate receptor (NMDA) antagonists, medications that directly or indirectly augment cerebral catecholaminergic or acetylcholinergic function, and agents with combinations of these properties. Better understanding of the damage mechanisms and new approaches to neuroprotection and restoration may offer a better neurocognitive outcome for the millions of survivors of TBI.

Key words: Axonal injury, Brain injury, Diffuse neuronal injury, Neurocognitive impairment.