Cognitive neuroscience of visual object recognition
Agnosia is a rare occurrence and can be the result of a stroke, dementia, head injury, brain infection, or hereditary.
Apperceptive agnosia is a deficit in object perception creating an inability to understand the significance of objects.
Similarly, associative visual agnosia is the inability to understand the significance of objects; however, this time the deficit is in semantic memory. Both of these agnosias can affect the pathway to object recognition, like Marr's Theory of Vision. More specifically unlike apperceptive agnosia, associative agnosic patients are more successful at drawing, copying, and matching tasks; however, these patients demonstrate that they can perceive but not recognize.
Integrative agnosia(a subtype of associative agnosia) is the inability to integrate separate parts to form a whole image. With these types of agnosias there is damage to the ventral (what) stream of the visual processing pathway.
Object orientation agnosia is the inability to extract the orientation of an object despite adequate object recognition. With this type of agnosia there is damage to the dorsal (where) stream of the visual processing pathway.
This can affect object recognition in terms of familiarity and even more so in unfamiliar objects and viewpoints.
A difficulty in recognizing faces can be explained by prosopagnosia. Someone with prosopagnosia cannot identify the face but is still able to perceive age, gender, and emotional expression. The brain region that specifies in facial recognition is the fusiform face area. Prosopagnosia can also be divided into apperceptive and associative subtypes. Recognition of individual chairs, cars, animals can also be impaired; therefore, these object share similar perceptual features with the face that are recognized in the fusiform face area.
Neurotoxin
Ammonia toxicity is often seen through two routes of administration, either through consumption or through endogenous ailments such as liver failure. One notable case in which ammonia toxicity is common is in response to cirrhosis of the liver which results in hepatic encephalopathy, and can result in cerebral edema (Haussinger 2006). This cerebral edema can be the result of nervous cell remodeling. As a consequence of increased concentrations, ammonia activity in-vivo has been shown to induce swelling of astrocytes in the brain through increased production of cGMP (Cyclic Guanosine Monophosphate) within the cells which leads to Protein Kinase G-mediated (PKG) cytoskeletal modifications. The resultant effect of this toxicity can be reduced brain energy metabolism and function. Importantly, the toxic effects of ammonia on astrocyte remodling can be reduced through administration of L-carnitine. This astrocyte remodeling appears to be mediated through ammonia-induced mitochondrial permeability transition. This mitochondrial transition is a direct result of glutamine activity a compound which forms from ammonia in-vivo. Administration of antioxidants or glutaminase inhibitor can reduce this mitochondrial transition, and potentially also astrocyte remodeling.