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.
Short-term effects of alcohol consumption
Alcohol has a powerful effect on glutamate as well. Alcohol decreases glutamate's ability to bind with NMDA and acts as an antagonist of the NMDA receptor, which plays a critical role in LTP by allowing Ca2+ to enter the cell. These inhibitory effects are thought to be responsible for the "memory blanks" that can occur at levels as low as 0.03% blood level. In addition, reduced glutamate release in the dorsal hippocampus has been linked to spatial memory loss. Chronic alcohol users experience an upregulation of NMDA receptors because the brain is attempting to reestablish homeostasis. When a chronic alcohol user stops drinking for more than 10 hours, apoptosis can occur due to excitotoxicity. The seizures experienced during alcohol abstinence are thought to be a result of this NMDA upregulation. Alteration of NMDA receptor numbers in chronic alcoholics is likely to be responsible for some of the symptoms seen in delirium tremens during severe alcohol withdrawal, such as delirium and hallucinations. Other targets such as sodium channels can also be affected by high doses of alcohol, and alteration in the numbers of these channels in chronic alcoholics is likely to be responsible for as well as other effects such as cardiac arrhythmia. Other targets that are affected by alcohol include cannabinoid, opioid and dopamine receptors, although it is unclear whether alcohol affects these directly or if they are affected by downstream consequences of the GABA/NMDA effects. People with a family history of alcoholism may exhibit genetic differences in the response of their NMDA glutamate receptors as well as the ratios of GABA subtypes in their brain. Alcohol inhibits sodium-potassium pumps in the cerebellum and this is likely how it corrupts cerebellar computation and body co-ordination.