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.
Anhedonia
Studies in clinical populations, healthy populations, and animal models have implicated a number of neurobiological substrates in anhedonia. Regions implicated in anhedonia include the prefrontal cortex as a whole, particularly the orbitofrontal cortex (OFC), the striatum, amygdala, anterior cingulate cortex (ACC), hypothalamus, and ventral tegmental area (VTA). Neuroimaging studies in humans have reported that deficits in consummatory aspects of reward are associated with abnormalities in the ventral striatum and medial prefrontal cortex, while deficits in anticipatory aspects of reward are related to abnormalities in hippocampal, dorsal ACC and prefrontal regions. These abnormalities are generally consistent with animal models, except for inconsistent findings with regard to the OFC. This inconsistency may be related to the difficulty in imaging the OFC due to its anatomical location, or the small number of studies performed on anhedonia; a number of studies have reported reduced activity in the OFC in schizophrenia and major depression, as well as a direct relationship between reduced activity and anhedonia.
Researchers theorize that anhedonia may result from the breakdown in the brain's reward system, involving the neurotransmitter dopamine. Anhedonia can be characterised as "impaired ability to pursue, experience and/or learn about pleasure, which is often, but not always accessible to conscious awareness".