Visual Extinction - Physiological Basis

Physiological Basis

Visual extinction arises from damage to the parietal lobe of the brain. This damage most frequently arises following a stroke or other infarction in that area – however, any traumatic event sufficient to cause widespread tissue damage in the area may cause sufficient harm. Although both sides of the brain are vulnerable to such damage, it is more unusual for extinction to occur when the left hemisphere is damaged than the right.

When presented with simultaneous stimuli, the patient will ignore the contralesional stimuli, and only report the ipsilesional. Their ability to report the stimuli correctly when presented singly indicates that this is not a problem with vision per se. This bias against contralesional stimuli is evident even when patients are presented with two signals within the ipsilesional visual field, whose processing remains intact following the damage, since it is done in the opposite brain hemisphere. This implies that extinction can be somewhat controlled by biasing the point of visual fixation contralesionally, such that all relevant stimuli are contained within the functioning side of the visual field, findings supported in experiment

Fatigue and habituation effects have previously been connected to visual extinction; experiments such as those done by Vuilleumier and Rafal eliminate the connection of these effects with visual extinction.

Historically, it was believed that the parietal damage weakened afferent neuron input to the visual cortex, and so the extinction event was caused by the signals originating in the contralesional field being lost during transmission. However, this does not account for the ability of extinction patients being able to correctly identify contralesional stimuli in isolation. A more current theory is called the "race theory."

Race theory holds that stimuli are competing for processing power within the brain. Following parietal damage, all contralesional messages are lowered in priority for the brain’s processing in some way – potentially by signal transmission delay – such that when presented with alternative stimuli, the contralesional stimulus doesn’t arrive at the decision center simultaneously with the ipsilesional stimulus, and thus is denied conscious processing.

The race theory sees some support in findings by Marzi et al., where patients who show extinction also display aggravated delays in their reaction time to stimuli, both when compared to patients who have other forms of right-brain damage and undamaged patients. In the study, patients were shown to be able to focus their attention and improve reaction time, but still have subnormal performance. This theory is given further support by Gorea and Sagi’s inducing of extinction-like events in undamaged patients when presented with simultaneous stimuli of different intensities, with the lower intensity stimulus being extinguished by the mere presence of the high intensity stimulus.

Extinction frequency may also be affected by reporting method, due to how visual processing interacts with the rest of the brain. Reported extinctions drop when the patient is told to relay the extinction news by a method other than speaking – particularly, the use of the eyes in a feedback loop (looking to the side if there is a single stimuli, and up if there are two). This may work by eliminating the need for hemispheric transfer of information – routing the response to the motor cortex instead of the visual cortex – and so shortening the path and response time, a conclusion supported by increased detection of isolated contralesional stimuli under such circumstances.

Although extinction is compared with hemispatial neglect, the two are different disorders. It is possible to exhibit one without the other, and the neural basis for each appears to be different, hemispatial neglect arising from tempo-parietal junction damage. Although patients may exhibit these disorders simultaneously, this occurs in less than half of the afflicted population.