Why is predicting consequences an important skill




















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Download references. Bianca M. You can also search for this author in PubMed Google Scholar. Correspondence to Bianca M. Reprints and Permissions. Atten Percept Psychophys 78, — Download citation. Published : 11 August Issue Date : November Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative.

Skip to main content. Search SpringerLink Search. Download PDF. Abstract Predicting the sensory consequences of our own actions contributes to efficient sensory processing and might help distinguish the consequences of self- versus externally generated actions. Experiment 1 Method Participants Twenty-four healthy, right-handed Edinburgh Handedness Inventory participants with normal or corrected-to-normal vision took part in the experiment. Stimuli and procedure The participants were tested in a quiet, dimly lit room, where they sat behind a computer screen 60 Hz at a viewing distance of 54 cm.

Full size image. Experiment 2 Method Participants A total of 24 healthy, right-handed Edinburgh Handedness Inventory with normal or corrected-to-normal vision took part in the experiment. Apparatus and procedure The stimuli, procedure, and analyses were similar to those aspects of Experiment 1 , except for the following details.

Results Unimodal versus bimodal Figure 6 depicts the mean delay detection performance as a function of delay, averaged across all participants. Table 1 Average buttonpress latencies for each condition of Experiment 2 Full size table. References Ackerley, R. Article Google Scholar Haggard, P. Literature Circles.

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Some filters moved to Formats filters, which is at the top of the page. All Resource Types. Results for predicting consequences results. Sort: Relevance. Social Skills: Predicting Consequences. This lesson package is designed to run over sessions, although the scenarios you choose can be pulled from the student's own trouble areas.

The ability to predict the. Show more details. Wish List. Glaciers have shrunk, ice on rivers and lakes is breaking up earlier, plant andanimal ranges have shifted and trees are flowering sooner. Effects that scientists had predicted in the past would result from global climate ch. Environment , General Science , Science. Show 2 included products. Zip Internet Activities. Homework , Worksheets.

Health- Consequences of Decisions- Activity for Teens. As a former Health Teacher, I used this resource for students to analyze the short and long-term effects of decisions. This is a great activity to add to a lesson you are already teaching. PDF Webquests. This web quest helps students learn and apply knowledge about plate tectonics. They are introduced to information and examples of the different types of pate interactions and the consequences of those interactions. They are also exposed to real life examples of pate interactions.

Earth Sciences , General Science , Science. Need to introduce students to the idea that our choices have consequences? Try this fun lesson!! This could be a great way to start the year and a discussion of classroom expectations! I use this product as an introduction to my 9th-grade thematic unit on Choice and Consequence. The classic text w. Handouts , Lesson Plans Individual. Predicting what will happen is a difficult skill for some of our more concrete learners.

Understanding of cause and effect even with fairly concrete examples can be a challenge for your students with language disorders. Answering What if questions can be particularly difficult; much more so than th.

Activities , Games , Lesson Plans Individual. Engage your students in learning about space debris and its consequences while practicing English language reading skills in this hybrid learning activity designed to be done independently by students whether they are in the classroom, learning online, or any combination of learning groupings.

This a. Activities , Literacy Center Ideas. Impact of the Crusades DBQ. Word Document File. The lesson begins with a map analysis students use a map to predict what they think might be an impact of the crusades and a general introduction into some of the big consequences of the conflict.

Next, students read a variety of documents to look at the positive and negative effects of the crusade. Predictive mechanisms allow us to anticipate the future state of both the environment and ourselves in order to compensate for delays in the transmission of neural signals and distinguish external events from the sensory consequences of our own actions [ 1 ]. Predictions are found at different levels of processing, from simple eye movements to complex motor acts or language processing, and they have even been identified as one of the defining functions of the human brain [ 2 ].

Efference copies [ 3 , 4 ] of motor outputs can be used to predict re-afferent sensory feedback see [ 5 ], for a review. They modulate the response properties of the corresponding sensory cortex and prepare it for re-afferent stimuli [ 5 ]. This is known as the forward model e. This process also allows sensory re-afferents from motor outputs to be recognised as the self-generated result of an action.

Since real-world actions usually stimulate several senses simultaneously e. Multisensory processing mechanisms have often been related to facilitation in a variety of tasks [ 18 ]. In these cases it has been assumed that events in a modulating modality e. However, the challenge for the brain is to connect the different kind of information in a suitable way, especially because in an early stage different unisensory brain regions, e.

The cerebellum is a good candidate brain region which might contribute to the prediction of multisensory action outcomes, since it is relevant for visual and auditory processing, timing, perceptual sequencing and predictive processing and is functional connected to visual and auditory sensory cortices see [ 23 ] for an overview.

Despite the fact that first behavioral evidence suggests the existence of multisensory predictive mechanisms for auditory-visual action consequences [ 24 ], the neural correlates of these processes remain unknown.

The principles of action prediction have been investigated with paradigms probing anticipated action effects. Behaviorally, it has been shown that self-generated stimuli are perceived as less intense compared to externally generated stimuli, a phenomenon known as sensory attenuation [ 6 ]. Sensory attenuation has been demonstrated in the somatosensory [ 25 ], auditory [ 26 ] and visual domains [ 27 , 28 ]; see [ 29 ] for a review.

These behavioral studies have been complemented by electrophysiological correlates of anticipated action effects e. Studies using fMRI suggest an involvement of the cerebellum in predicting action outcomes [ 9 , 14 , 16 , 32 ] and provide evidence for BOLD suppression for predictable compared to unpredictable e. However, up till now, sensory suppression at neural level has only been studied for individual modalities separately.

Thus, whether actions with potential consequences in multiple modalities lead to BOLD suppression in multiple sensory processing areas in the brain is unknown. Various tasks have been used to study predictive mechanisms and related sensory suppression at a neural level. These include looking at active action conditions in which the consequences are remapped to new spatial e.

Up to now, delay detection tasks have only been applied to single modalities in imaging studies. However, on behavioral level we successfully applied the delay detection task to multiple modalities and found evidence for bimodal facilitation for the detection of delays [ 24 ]. In the current study, the neural correlates of predicting multisensory action consequences were investigated using fMRI, by adopting the basic design of the behavioural study [ 24 ].

In an active condition, self-initiated hand movements button presses elicited the presentation of stimuli in the visual and auditory modality with variable short delays 0— ms between the action and its outcome. In the active condition, participants had to detect delays between action and feedback.

In the passive condition, participants only had to report whether they saw a unimodal or bimodal stimulus. Since real life actions e. Thus, compared to studies focussing on single modalities and related suppression in respective uni- sensory brain regions, we expected BOLD suppression in multiple sensory brain regions e.

Furthermore, we expected that BOLD suppression in auditory and visual sensory cortices would be independent of feedback modality, since visual, auditory and audio-visual consequences were equally predictable. One participant had to be excluded from the fMRI analysis because of excessive movement, resulting in a sample of twenty participants 8 males, age range 19—30, mean age For the subsequent analysis comparing detected vs. Written informed consent has been obtained from all participants.

During fMRI data acquisition participants wore headphones MR-Confon Optimel, Magdeburg, Germany through which auditory stimuli were delivered in the form of a pure-tone Hz beep presented for 1 second.

The visual stimulus was a black dot 1. The screen was viewed by the participants in an appropriately angled mirror. Participants placed their right hand on a button pad, with their right index finger touching the button. The button pad was fixed on their right leg. The left index and middle finger were placed on two buttons of a separate button pad located and fixed on the left leg. Stimuli were presented using Octave and the Psychtoolbox [ 43 ].

The general paradigm Fig 1 has been adapted from a previous behavioral study [ 24 ]. However, due to technical reasons an externally-controlled passive moving button could not be included in the current imaging study.

The participants had to perform button presses with their right index finger, which would elicit the appearance of either the dot on the screen, or the tone, or both.

The stimuli were presented either at the time of the button press, or with a variable delay. Thus, in bimodal trials participants only had to report whether they detected a delay between their action and the target stimulus, i. Participants were instructed at the start of each mini-block 12 trials about the target stimuli task modality via written instruction auditory task or visual task.

There were 5 mini-blocks in each run in total 60 trials per run. The task order was either visual—auditory—passive—visual—auditory, or auditory—visual—passive—auditory—visual. In active trials the delay between action and stimulus was one of the six predefined delays 0, 83, , , , or ms, presented in frames 0, 5, 10, 15, 20, or 25 frames.

In bimodal trials, the two components of the stimulus were always presented together. Unimodal and bimodal trials were randomized within each mini-block. In the active condition top participants had to wait with their button press until the cue appeared, and could take as much time as they wanted max. After a variable delay, unimodal or bimodal stimuli were presented.

Participants had to report whether they detected a delay between their button press and the stimulus of the task modality. In the passive condition bottom , an identical trial structure was used. However, no button press was performed by the participants and they had just to report whether they perceived one or two stimuli. The procedure during a trial was as follows see Fig 1. Each trial started with the presentation of a fixation cross presented for a variable intertrial interval 1, 1.

In the active condition , the cue indicated that from now on, participants could press the button with their right index finger, which triggered the unimodal or bimodal stimulus after a delay of ms. The participants were instructed to perform button presses at their own pace in a fixed time window up to four seconds after the cue onset.

The visual stimulus appeared at the location of the fixation cross, thus obscuring it. For unimodal auditory trials the fixation cross remained visible during the presentation of the tone. The cue and stimuli disappeared at the same time. In the passive condition , participants were instructed not to press the button when they saw the cue, but to just observe and listen to the presented stimuli. In these trials, the stimuli were presented automatically after a variable delay 0.

After a fixed period of six seconds after cue onset, participants had to judge whether one or two stimuli had been presented. We introduced this bimodal detection task in order to have a similar trial structure and decision processes in the active and passive conditions. Furthermore, this task was easier than the delay detection task in the active condition. Participants were instructed to be as accurate as possible, but were not required to be as fast as possible.

They were given up to 2. Then the next trial started irrespective of the answer. Missing trials were not repeated to maintain a fixed data acquisition procedure for all experimental runs and participants. Prior to the fMRI experiment, participants were familiarized with the paradigm in a behavioural training outside the scanner. First, they could press the button several times to experience delayed ms and undelayed feedback. Then, to become familiar with the paradigm, they completed one run, with the same procedure and number of trials 60 trials as the fMRI experiment in which they were given feedback about their performance correct or incorrect.

Then, they completed two more runs without feedback. All 21 of the original sample met this criterion. The fMRI experiment comprised trials in total: we presented 10 trials for each delay, thus leading to 60 unimodal visual trials VU , 60 unimodal auditory trials AU , 60 bimodal visual trials VB and 60 bimodal auditory trials AB. Furthermore, unimodal and bimodal passive control conditions were presented: 20 trials visual unimodal CV , 20 trials auditory unimodal CA and 20 trials bimodal CB.

Stimuli were presented in a rapid event-related fMRI design which was divided into five runs, each comprising 60 trials with 5 mini-blocks. Finally, the button press latencies between conditions were compared and correlated with the respective performance per condition to explore potential relationships and to rule out potential confounds due to differences in button press latencies between conditions.

In the analysis, unimodal trials were compared to all bimodal trials together. Posthoc t-tests Bonferroni corrected were conducted to verify the direction of the effects. For data preprocessing, standard realignment, coregistration between structural and functional scans, segmentation, normalisation Montreal Neurological Institute [MNI] template 2 x 2 x 2 mm and smoothing 8mm functions of SPM12 were applied.

For single subject analyses, realignment parameters were included as regressors of no interest to account for movement artifacts. Low frequencies were removed using a high-pass filter with a cut-off period of seconds. Additionally, button presses were included as single additional condition not separated for modality of no interest in the single subject models. Of note, the modulation of button presses had a significant effect on the result pattern, when comparing active vs.

Therefore, we provide additional information in the results section, when results are highly dependent on the modulation of button presses.

Parameter estimates b and t-statistic images were calculated for each subject. For anatomical localization functional data were referenced to the AAL toolbox [ 46 ] and the probabilistic cytoarchitectonic maps [ 47 ].

Exploratory connectivity analyses in the form of psychophysiological interaction PPI analyses, were conducted to better explain the condition specific association between activation change in auditory and visual cortices and the observed results in the cererebellum, motor cortex and SMA.

Interaction effects of task and feedback modality were calculated to explore specific effects for multisensory processing of action consequences. Finally, correlation analyses with behavioural data were performed to explore the relationship between BOLD suppression and behaviour.

However, there are important intra-midbrain circuits involving DRN and PAG Lovick ; Stezhka and Lovick that may mediate this midbrain contribution to predictive fear learning. The intracellular mechanisms for direct predictive learning in the midbrain have also begun to be elucidated. They also couple to an array of other second messenger systems, which include the MAP kinases. This stands in contrast to the roles of these kinases in learning about contiguous relations in the amygdala and illustrates that different mechanisms can mediate learning about predictive versus contiguous relations.

These findings support earlier suggestions for a role of opioids and their receptors in predictive learning Schull ; Bolles and Fanselow ; Fanselow The neuroanatomical overlap revealed in these experiments between the midbrain mechanisms for direct predictive learning and CR production may also be a general principle for organization of Pavlovian learning because it has been reported in other conditioning preparations Kim et al.

This overlap explains why predictive learning within one response system e. The within-subject response specificity of blocking would be otherwise impossible. The indirect actions of predictive learning on Pavlovian fear conditioning are achieved by selective attention. Predictive learning occurs by directing attention toward better predictors of danger and away from poorer predictors.

Recent evidence suggests that, during fear learning, this indirect action is achieved in the ventral striatum. Studies of reward-responsive midbrain dopamine neurons in monkeys indicate that the firing of these cells is closely linked to predictive learning Schultz These cells display high levels of firing to unexpected rewards and low levels of firing to expected rewards Waelti et al.

Conversely, these cells show high levels of firing to CSs that reliably predict rewards and low levels of firing to CSs that are not predictive of rewards Waelti et al. These changes also occur during blocking. For example, reward-responsive cells in monkey midbrain acquire stronger responses to a reward-predicting stimulus than a blocked stimulus Waelti et al.

Do these same mechanisms also contribute to predicting danger? In this experiment participants were required to predict an outcome based on visual features of a stimulus. Feedback correct or incorrect for these predictions was provided on a trial by trial basis. This suggests that the role of this structure may not be limited to learning about rewards.

Moreover, although there is evidence that dopamine and the ventral striatum make important contributions to fear learning, the nature of this contribution is only poorly understood Redgrave et al.

Studies of human conditioning have revealed activity in the ventral striatum during presentations of a CS previously paired with aversive stimulation Jensen et al. This can occur during presentations of a trained CS but prior to delivery of the US and thus, under some circumstances, does not appear directly attributable to any relief that might be occasioned by the termination of the US.

Moreover, this activity can be related to predictive error. For example, consider a recent experiment that studied predictive error during serial compound conditioning in humans participants Seymour et al. One pair of CSs was followed by a high i. There are a number of sources of predictive error, derived by TD learning rules, under these conditions.

Studies of blocking in rodent fear conditioning have provided evidence that the ventral striatum is critical for predictive fear learning. These studies have also identified some of the important neurotransmitters and neuromodulators underpinning this learning. Blocking of Pavlovian fear conditioning in rodents depends on dopamine neurotransmission in the nucleus accumbens Acb Iordanova et al. Blocking is enhanced by manipulations that increase, and is prevented by manipulations that decrease Acb dopamine neurotransmission.

Interestingly, blocking of fear conditioning depends upon the combined activity of D1 and D2 dopamine receptors because only combined microinjections of D1 and D2 selective antagonists, not microinjections of either D1 or D2 antagonists, prevented blocking Iordanova et al. Blocking and unblocking also depend on accumbal opioid receptors Iordanova et al. Examination of the associative mechanism for blocking and unblocking during rodent fear conditioning revealed that the ventral striatum determines the attention allocated to a CS and, hence, its subsequent association with shock.

A key component of theories of indirect predictive learning is that predictive learning is delayed. For example, Mackintosh et al. Iordanova et al. According to theories of direct predictive learning, infusions prior to either the first or second stage 2 trial should prevent blocking, whereas according to attentional theories, only infusions prior to the first trial should prevent blocking.

The subject also learns that CSA is a superior predictor of shock than CSB because the associative strength of CSA is higher due to it being paired with shock in stage 1 i. The data showed that only infusions prior to the first trial prevented blocking. These findings provide compelling evidence that an important role of the ventral striatum during fear learning is the attentional selection between competing predictors of danger.

This selection results in the allocation of attention to, and therefore learning about, the best predictor of danger events at the expense of worse predictors. Understanding these brain mechanisms for attentional regulation during fear may have important clinical implications. Many instances of pathological fear and anxiety, including generalized anxiety Mathews and MacLeod ; Mogg et al.

Anxiety patients selectively attend to danger and threat-related cues at the expense of other stimuli. This attentional bias may emerge from alterations in ventral striatal mechanisms for predicting danger. The ability to predict sources of danger in the environment is essential for adaptive behavior and survival.

Learning about predictive relations is distinct, at both the behavioral and neural levels, from learning about contiguous relations. Learning about contiguous relations requires activation of amygdala NMDA receptors and recruitment of the signal transduction cascades subsequent to this activation. Despite their distinct neural and behavioral bases, learning about predictive relations and learning about contiguous relations cannot occur independently.

The mechanisms for predicting danger are complementary to the mechanisms for fear memory formation. Predicting danger depends upon retrieving a fear memory, but it also regulates new fear memory formation by regulating attention to the CS and by regulating what is learned about the shock US.

Within these models, learning depends critically upon the activation of simultaneous mental representations of the CS and the US into the focus working memory. Contiguous relations are important because only closely spaced presentations of the CS and US allow for their mental representations to be simultaneously active in the focus of working memory and learned about.

If a long trace interval is introduced, then the CS representation will have decayed from the focus working memory by the time the US is presented and thus the CS will not be learned about. Predictive relationships are important because knowledge of the CS—US causal relationship gates the ability of the CS and US representations to be activated to the focus of working memory.

The amygdala synaptic mechanisms for fear memory formation are sensitive to predictive relations Bauer et al. The question is how this sensitivity is achieved. Following the general architecture of SOP, the mechanisms of indirect and direct predictive fear learning reviewed here might be understood as regulating the access of the CS and shock US, respectively, to amygdala-based mechanisms for fear memory formation Fig.

Studies of the neural mechanisms that allow organisms to predict sources of danger in their environment are beginning to reveal greater complexity and subtlety in the brain mechanisms for fear learning than was previously realized. These studies show that structures not typically viewed as important for fear learning are important for predictive learning.

This complexity is perhaps somewhat unsurprising given the key role that predictive learning plays in enabling adaptive responses to threat. What is surprising is that understanding of the brain mechanisms for predicting danger, as opposed to those important for storage of fear memories, is so incomplete. Likewise, knowledge of the brain mechanisms for predicting danger is remarkably limited when compared to knowledge of the brain mechanisms for predicting rewards Schultz and Dickinson ; Schultz A more complete understanding of these mechanisms is needed.

The behavioral approaches reviewed in the first part of this article can be used to dissociate learning about contiguous versus predictive relations during fear conditioning. The empirical studies, described in the latter parts of this article, which have adopted these approaches, provide important insights into the neural substrates for predicting danger. However these studies also leave unanswered many important questions, for example, about the circuit level and molecular mechanisms that allow the ventral striatum and midbrain to regulate fear learning.

The exact relationship between the neural mechanisms for predicting danger and predicting rewards is also unclear. Certain theoretical traditions place emphasis on opponent interactions between aversive fear and appetitive reward motivational systems in regulating associative learning Konorski ; Dickinson and Dearing Other theoretical approaches suppose commonalities between the brain mechanisms for predictive danger and for predicting rewards Redgrave et al.

The data reviewed here indicate some overlap between these processes, at least at the level of the ventral striatum. Finally, an increased understanding of the neural mechanisms for predicting danger should shed light on the brain mechanisms for pathological anxiety because many instances of pathological anxiety are characterized by excessive and biased attention toward danger. Predicting danger: The nature, consequences, and neural mechanisms of predictive fear learning Gavan P.

McNally 1 and R. Previous Section Next Section. View this table: In this window In a new window. Table 1 Some possible behavioral designs for studying predictive fear learning. Figure 1. Figure 2. Figure 3. Roles of the ventral striatum and midbrain in predicting danger. Previous Section. Bakal C. Medline Google Scholar. Bauer E. Betts S.

Web of Science Google Scholar. Biegler R. Process 25 : — Bolles R. Brain Sci. Carrive P. Brain Res. Davis M. Delamater A. Dickinson A. Google Scholar. Exp Psychol.



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