Fig. (1).

A cascade of the primary and secondary pathological events after traumatic brain injury (TBI). Primary injury includes structural damage that cannot be reverted by therapeutic interventions, and only sensitive to preventive measures. On the other hand, early secondary injury includes necrotic and apoptotic cell death due to the release of excitatory neurotransmitters leading to oxidative stress, mitochondrial dysfunction, damage to the structural proteins and inflammation. Although the short-term inflammatory phase is beneficial because of the activation of microglia which causes phagocytosis of debris and regeneration. But the prolonged inflammation worsens the outcome of TBI. The intermediate phase which includes the release of TNF-α and IL-β within 1 hour of injury and persists for three weeks overlaps with early features of TBI. At last, all these pathogenic events culminate into progressive tissue loss and behavioural changes like motor, sensory, cognitive deficits, post-traumatic epilepsy and electrophysiological changes. AMPA: α-amino-3-hydroxy-5-methyl-4-isooxazolepropionic acid Receptor; Cyt C: Cytochrome c; ER: Endoplasmic reticulum; ICP: Intracranial pressure; NMDA: N-methyl-D-aspartate Receptor; ROS: Reactive oxygen species. (A higher resolution/colour version of this figure is available in the electronic copy of the article).