Blakemore et al. Article Summary

Posted by on July 9, 2011

In the article “Why Can’t You Tickle Yourself,” the authors review several studies which seek to explain why we cannot tickle ourselves in comparison to their hypothesis.  Through their research the authors also make inferences about patients with auditory hallucinations and/or passivity experiences.  The proposal set forth by them is that there is a decrease in feeling sensory effects by self produced physical sensation due to sensory predictions that are made by an internal forward model of the motor system.  Through this article summary, I will explore and discuss the studies presented by the authors of the article while attempting to explain what the authors believe they’ve discovered in response to their proposal.

There is a system in our brains which makes predictions about the sensory consequences of movements made by our body based on the motor commands.  When the prediction and actual sensation are much the same, we feel no tickliness, but when they are not, we feel it.  The motor commands caused by the self make it easier for the system to make a prediction, causing the actual sensation to be close enough to the predicted sensation; therefore, the prediction causes a decrease in the feeling of a sensory effect.  On the other hand, when the movement is not self-produced the prediction becomes much harder for the system to accurately predict and therefore the person experiences tickliness.  The authors believe this is the system, an internal forward model, by which the brain works on sensory and motor commands.  Moreover, the authors believe that defects in such systems cause the hallucinations and/or passivity experiences of patients.

The authors compare their claim to Frith’s, in his study of schizophrenic patients.  Frith shares the similar claim that he believes a defect in such a self-monitoring mechanism could be the reason for auditory hallucinations and passivity experiences in some individuals.  Frith suggests that these unusual experiences come from a lack of awareness by the patients of their intended actions.  The authors further expand this theory by stating that this phenomenon is due to a lack of awareness of predicted limb movement in reference to the forward model.

Furthermore, the authors compare their research, hypothesis, and results to that of Weiskrantz and his colleagues.  Weiskrantz’s research supports the evidence that sensory consequences of actions that are self-produced differ from those externally produced when the sensory input is the same in both cases;  also, that externally produced sensory consequences are much more tickly than those self-produced.  The difference is that his research’s conclusions lead to the idea that the necessary factor for attenuation is a self-produced motor command and not necessarily the same stimulus as the motor command; that the stimulus and motor command may differ so long as there is movement that is self-produced and simultaneously occurring.  This is contrary to the hypothesis posited by the authors who support the internal forward model.

To test their hypothesis with that of Weiskrantz and his colleagues, the authors created an experiment based on Weiskrantz and his colleagues’ study.  The experiment though proved to show that it was not important just for movement to occur, but for the sensory stimulus to match the prediction of the movement.  As the differentiation between the two increased, there was a resulting increase in tickliness.  Therefore, through the experiment’s conclusions it became apparent that the sensory feedback must correspond to the sensory prediction made by the internal forward model.

Physiological evidence is also presented by the authors of such attenuating activity belonging to the cerebellum through the support of computational, neurophysiologic, and functional neuroimaging data.  Mainly, the areas of the brain concerned were the SII and ACG in comparison to the right anterior cerebellar cortex.  While in SII and ACG activity was attenuated by all movement and not just that which resulted in tactile stimulation, the right anterior cerebellar cortex was selectively deactivated by the self-produced movements resulting in tactile stimulation and was greatly activated by external movement causing tactile stimulation.  This evidence suggests that the cerebellum differentiates between movements according to their sensory consequences, and the authors believe this further suggests “that the cerebellum is involved in predicting the specific sensory consequences of movements and in providing the signal that is used to attenuate the somatosensory response to self-produced tactile stimulation.” (Blakemore 4)

Finally, to test Frith’s proposal about abnormality in the functioning of the internal forward model in patients with schizophrenia, the authors setup another experiment.  Ultimately their research proved that those who do not experience any auditory hallucinations or passivity, experience less tickliness by self-produced stimuli than externally produced; those with the symptoms, though, experienced no decrease in sensory perception of tactile stimuli.  The research conclusions are therefore in support of Frith’s proposal that the system operates abnormally for those with the symptoms.

The research presented by the authors does seem credible towards the conclusion of an existing internal forward model in our minds.  Their experiments are clearly defined and described, and the evidence presented seems to be logically consistent with the research, so I see no reason to doubt the authors’ claims.

Through this paper I have discussed the several studies the authors present in comparison to their idea of an internal forward model, while also presenting the physiological evidence the authors believe may locate the region where this model is located.  Also, it has been described how the internal forward model is consistent with those with schizophrenic symptoms.

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