Presentation on theme: "Modelling the classic Attentional Blink and its emotional variant Nikos Fragopanagos* & John Taylor** *Sponsored by the BBSRC **Sponsored by the BBSRC."— Presentation transcript:
Modelling the classic Attentional Blink and its emotional variant Nikos Fragopanagos* & John Taylor** *Sponsored by the BBSRC **Sponsored by the BBSRC and the EU under the GNOSYS project Cognitive Robotics, Intelligence and Control (COGRIC 2006)
Outline Introduction Looking at the evidence Building blocks of the model Masking in the AB & the need for a monitor Results Extending attention model with amygdala Conclusions
Introduction (1/3) Moving the focus of attention from one target to another when these targets are embedded in a rapid stream of stimuli is hard. It becomes even harder when the temporal distance between the two targets is ms. This gives rise to the phenomenon called Attentional Blink (hereforth the AB). Understanding the AB can shed some light to the mechanism of attention and the limits of its capacity
Introduction (3/3) Two main models have been proposed for the AB: –The two-stage model suggests that all items presented in the rapid visual stream are processed to the point of conceptual representations without awareness (stage 1). The transfer of T2 representations into working memory is assumed to be impaired, as long as working memory (stage 2) is still engaged with T1. –The interference model suggests that not the impaired transfer of T2 to working memory, but the interference of the representations of T1 and T2 within working memory causes the AB.
Looking at the evidence (1/4) There are two types of evidence for the AB: –Behavioural data & brain imaging data The behavioural data indicate that in the dual- target condition the target 2 detection accuracy curve is U-shaped around a minimum of ~300ms.
Looking at the evidence (2/4) The AB is a high temporal resolution demanding task for brain imaging. So focus on EEG (in the form of ERPs) that can capture the temporal dynamics of brain activation. According to Vogel et al. (1998): –P1, N1 & N400 are preserved. –P2 & P3 are diminished. What are the implications of these results?
Looking at the evidence (3/4) The N1/P1 are early ERPs that could correspond to initial processing in the visual cortex and also early prefrontal activation by incoming stimuli. The N400 is related to semantic processing indicating perceptual awareness. The P3 has been suggested to arise from access to working memory by the input signal. The P2 signal at 200 ms was proposed (JGT) as an indication of the corollary discharge of attention movement, being crucial for the related input stimulus activity to access its sensory buffer.
Looking at the evidence (4/4) Based on the chronometrical characterisics of the AB ERPs we hypothesise that T1s P3 has suitable timing for attacking T2s P2 and thus causing the AB. But how is the P2 of T2 responsible for the AB?
Building blocks of the model (1/6) The Input module codes for the various visual stimuli using one node for each item.
Building blocks of the model (2/6) The Input feeds forward to an Object Map (eg in temporal cortex). Early visual cortex processing is not included in the model.
Building blocks of the model (3/6) Input also activates Goals in PFC (exogenously) that bias the IMC which in turn gain-modulates the input to the Object Map accordingly.
Building blocks of the model (4/6) The IMC gives rise to a Corollary Discharge signal which is used to preactivate the Working Memory thus facilitating target processing.
Building blocks of the model (5/6) Then (after the Corollary Discharge signal) the Object Map activates the appropriate site in the Working Memory.
Building blocks of the model (6/6) Finally, the Working Memory having built up sufficient activation turns off all the Corollary Discharge nodes to prevent other stimuli entering.
Masking in the AB & the need for a monitor (1/3) In the AB both targets are masked. If T1s mask is replaced by a blank then the AB is significantly reduced. How do we tackle this?
Masking in the AB & the need for a monitor (2/3) We suggest that the mask of T1 causes a deterioration to T1 in the IMC thus rendering it weaker to reach awareness in the Working Memory. To capture this deficit we introduce an endogenous section of the Goals that retains the desired state of the system. The predicted state of the system is given by the Corollary Discharge which holds a copy of the IMC-controlled attention movement.
Masking in the AB & the need for a monitor (3/3) Comparison of the desired state with the predicted state yields the deficit caused to T1 by its mask. This comparison is run in the Monitor module.
Results (1/6) ERPs-equivalent for first item (T1) in RSVP:
Results (2/6) The main mechanism that causes the AB is the turning off of all the Corollary Discharge nodes by the Working Memory node for T1 in order to prevent other stimuli getting through and interfering with it. This renders T2s Corollary Discharge node ineffective; thus with no Working Memory preactivation T2 cannot reach awareness. This manifests as T2s P2 (Corollary Discharge) and P3 (Working Memory) being diminished.
Results (3/6) ERPs-equivalent for T2 in Lag3:
Results (4/6) Additionally when the Monitor detects an error in the activation of the T1 Corollary Discharge due to interference by its mask in the IMC, it tries to compensate by boosting the T1 node in the IMC and also by inhibiting all the other nodes until such time as T1s Working Memory has reached a sufficient level of activation. This causes an increase of the AB effect manifested as a steepening of the T2 detection curve dip (as shown in the following figures).
Results (5/6) T1&T2 Working Memory potentials (T1 unmasked) :
Results (6/6) T1&T2 Working Memory potentials (T1 masked) :
Extending attention model with amygdala (1/4) Anderson and Phelps, 2001 (Emotional Attentional Blink): Variation of the classic AB using emotional words as second targets. Red: control Blue: amygdala patient Triangles: neutral Circles: emotional
Extending attention model with amygdala (2/4) Simulate by extending attention model with amygdala:
Extending attention model with amygdala (3/4) ERPs for T2 in Lag3 when no amygdala
Extending attention model with amygdala (4/4) ERPs for T2 in Lag3: amygdala input from T2s object rep, & fed back to same site => Breakthrough Attentional Blink
Conclusions (1/2) Our model is able to fit the overall temporal flow of activity in the brain as observed by ERP results. It gives an explanation of the AB effect compatible with the general features of a two- stage process. The main feature of the model which helps explain the nature of the AB is the inhibitory destruction of the corollary discharge signal associated with the second target by the working memory buffer activity of the first target.
Conclusions (2/2) Additionally when T1 processing is not reaching the expected goal level, a monitor detects this and sends a boosting signal back to T1 and an inhibitory signal back to the other stimuli to protect T1 from them. This mechanism helps explain the alleviating effect of removing T1s mask to the AB dip. It also provides a novel point of view of the scarce nature of attention.