In this article, the authors focused on the effects of a unilateral lesion within the prefrontal cortex. Human vision works upon a rather backwards system. Information from the left side of each eye moves toward the left occipital lobe to be analyzed. The right follows an identical pattern.
So essentially, two sides of the eyeball swap information between hemispheres. From here, the information is sent forward along the current hemisphere to be analyzed by the prefrontal cortex (PFC). In a nutshell, the left and right fields of vision (of a single eye) are interpreted by different halves of the brain. This is where the problems begin to arise. If the lesion occupies the left PFC, what happens to that information? Does it simply get left unanalyzed and you lose that field in each eye?
In a static environment you could assume that the side affected by the lesion would lose greater processing for that side of the brain. However, if the brain were dynamic and could re-route the circuit, information from that field could have the potential to return. It seems that’s just what occurs but with a small cost. The information destined for the left PFC follows the tradition route back to the prefrontal cortex but stops short, makes a pass through the corpus callosum, and arrives at the contralateral prefrontal cortex (right side). The right prefrontal cortex actually picks up the slack left from the damaged area. However, as this seems almost too good to be true, this is not the case under all conditions. When an object is detected in the affected field compensation occurs. Yet, when objects are present to both fields simultaneously the right PFC solely analyzes the information from the right field. In other words, the right PFC picks up the slack so long as it has no incoming information itself.
The brain undergoes this change after repeated exposure to left field stimuli on a trial-by-trial basis. While the left PFC never fully recovers, this example shows a rather interesting compensation mechanism that can be achieved plastically. Although the paper never actually discussed this, I can’t help but wonder about the underlying cellular changes associated with this feat. Currently my assumption would just be an increase in synapses (synaptogenesis) favoring the re-wiring across the corpus callosum and to the contralateral cortex. But that’s just my guess. If anyone has any thoughts to the contrary I would certainly be willing to entertain them.
Voytek, B., Davis, M., Yago, E., Barceló, F., Vogel, E., & Knight, R. (2010). Dynamic Neuroplasticity after Human Prefrontal Cortex Damage Neuron, 68 (3), 401-408 DOI: 10.1016/j.neuron.2010.09.018
*UPDATE*: I figured using ResearchBlogger would be more efficient.