Apperceptive agnosia
Each patient that suffers from apperceptive agnosia does not have brain damage in exactly the same area. However, brain damage in proximity to the occipital lobe is largely correlated with the patterns of deficit seen in apperceptive agnosics. For example, patient JB suffered extensive damage to the parietal-occipital areas to the left cerebral hemisphere leading to his deficit in the ability to name distinguish between structurally similar object.
Mechanism of anoxic depolarization in the brain
During brain ischemia, glutamate is released in excess from the presynaptic terminal, leading to the uncontrollable opening of the glutamate receptors, including the NMDA and AMPA receptors, which allows for an excessive influx of Ca into the intracellular environment. Purinergic and NMDA receptors activate the pannexin-1 channels, which become hyperactive and allow the release of ATP from the intracellular environment. As the extracellular glutamate and ATP increase, several complexes are activated and converge into apoptotic and necrotic cascade pathways, which cause neuronal damage and death.