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.
Psychosis
NMDA receptor dysfunction has been proposed as a mechanism in psychosis. This theory is reinforced by the fact that dissociative NMDA receptor antagonists such as ketamine, PCP and dextromethorphan (at large overdoses) induce a psychotic state. The symptoms of dissociative intoxication are also considered to mirror the symptoms of schizophrenia, including negative psychotic symptoms. NMDA receptor antagonism, in addition to producing symptoms reminiscent of psychosis, mimics the neurophysiological aspects, such as reduction in the amplitude of P50, P300, and MMN evoked potentials. Hierarchical Bayesian neurocomputational models of sensory feedback, in agreement with neuroimaging literature, link NMDA receptor hypofunction to delusional or hallucinatory symptoms via proposing a failure of NMDA mediated top down predictions to adequately cancel out enhanced bottom up AMPA mediated predictions errors. Excessive prediction errors in response to stimuli that would normally not produce such as response is thought to confer excessive salience to otherwise mundane events. Dsyfunction higher up in the hierarchy, where representation is more abstract, could result in delusions. The common finding of reduced GAD67 expression in psychotic disorders may explain enhanced AMPA mediated signaling, caused by reduced GABAergic inhibition.