I’m curious how these claims square with numerous studies showing that damage to particular cortical regions (eg the anterior cingulate cortex or the insula cortex) do impair pain behavior in mammals. For example:
LaGraize, S., Labuda, C., Rutledge, R., Jackson, R., & Fuchs, P. (2004). Differential effect of anterior cingulated cortex lesion on mechanical hypersensitivity and escape/avoidance behavior in an animal model of neuropathic pain. Experimental Neurology, 188, 139–148.
Dong, W. K., Hayashi, T., Roberts, V. J., Fusco, B. M., & Chudler, E. H. (1996). Behavioral outcome of posterior parietal cortex injury in the monkey. Pain, 64, 579–587.
The contrast between the apparent effects of partial and total damage are perplexing. The cortex surely does a lot of work in sensory processing and action selection, even if it isn’t strictly necessary for a lot of behaviors. This sort of thing makes me somewhat wary of trusting the decortication studies too much. That said, it isn’t obvious to me why they should be misleading.
The only study of nociception in decorticate rats is included here, in the learning section:
Kolb, B., & Whishaw, I. Q. (1981). Decortication of rats in infancy or adulthood produced comparable functional losses on learned and species-typical behaviors. Journal of Comparative and Physiological Psychology, 95(3), 468–483.
Decorticate rats do learn to avoid a source of shocks, apparently very quickly, but do not engage in a response common to the control rats, burying the source in sawdust. Whishaw suggests this may be the result of motor impairments.
Merker offers one way to square the difference that makes some sense to me. He points to the Sprague effect, in which some deficits caused by loss of the visual cortex of one hemisphere can to some extent be mitigated by damage to the contralateral superior colliculus. Merker suggests that what is going on is that the loss of the visual cortex in one hemisphere creates an unbalance and that balance is partially restored by the damage to the contralateral superior colliculus.
The frontal cortex takes part in action selection with input from the ACC and insular cortex. If it becomes disinhibited by the loss of the ACC / IC, then it may exert an overriding influence on midbrain faculties for action selection that could otherwise appropriately respond to noxious stimuli. Perhaps the midbrain gets a vote in what to do, but that vote is overwhelmed by the disinhibited cortex.
I’m curious how these claims square with numerous studies showing that damage to particular cortical regions (eg the anterior cingulate cortex or the insula cortex) do impair pain behavior in mammals. For example:
LaGraize, S., Labuda, C., Rutledge, R., Jackson, R., & Fuchs, P. (2004). Differential effect of anterior cingulated cortex lesion on mechanical hypersensitivity and escape/avoidance behavior in an animal model of neuropathic pain. Experimental Neurology, 188, 139–148.
Dong, W. K., Hayashi, T., Roberts, V. J., Fusco, B. M., & Chudler, E. H. (1996). Behavioral outcome of posterior parietal cortex injury in the monkey. Pain, 64, 579–587.
The contrast between the apparent effects of partial and total damage are perplexing. The cortex surely does a lot of work in sensory processing and action selection, even if it isn’t strictly necessary for a lot of behaviors. This sort of thing makes me somewhat wary of trusting the decortication studies too much. That said, it isn’t obvious to me why they should be misleading.
The only study of nociception in decorticate rats is included here, in the learning section:
Kolb, B., & Whishaw, I. Q. (1981). Decortication of rats in infancy or adulthood produced comparable functional losses on learned and species-typical behaviors. Journal of Comparative and Physiological Psychology, 95(3), 468–483.
Decorticate rats do learn to avoid a source of shocks, apparently very quickly, but do not engage in a response common to the control rats, burying the source in sawdust. Whishaw suggests this may be the result of motor impairments.
Merker offers one way to square the difference that makes some sense to me. He points to the Sprague effect, in which some deficits caused by loss of the visual cortex of one hemisphere can to some extent be mitigated by damage to the contralateral superior colliculus. Merker suggests that what is going on is that the loss of the visual cortex in one hemisphere creates an unbalance and that balance is partially restored by the damage to the contralateral superior colliculus.
The frontal cortex takes part in action selection with input from the ACC and insular cortex. If it becomes disinhibited by the loss of the ACC / IC, then it may exert an overriding influence on midbrain faculties for action selection that could otherwise appropriately respond to noxious stimuli. Perhaps the midbrain gets a vote in what to do, but that vote is overwhelmed by the disinhibited cortex.