#49. The Reentrant-pathway Theory of Mental Illness [Neuroscience]

NE

Red, theory; black, fact.

This theory is a further development of post #45, “The Denervation supersensitivity Theory of Mental Illness.”

The basic idea here is that if a region of cerebral cortex is overgrown relative to a major synaptic partner, not only will it be starved of synaptic input from the partner, but it will also produce excess axons going to that partner that will have difficulty finding enough dendritic territories on which to synapse. Both difficulties can be solved at one stroke, however, if the overgrown area synapses on itself. The logic is similar to the application of valence rules in chemistry.

This mode of repair will produce cyclic signaling pathways (called “reentrant” in Neurospeak) that could support endlessly circulating neural activity. This is therefore an alternative way of getting what I have called “autonomous activity” from disregulated cortical growth, with no need to invoke the phenomenon of denervation supersensitivity. The loop circumnavigation time would have to be long enough to allow for the recovery of any refractory periods that may follow nerve-impulse firing.

The autonomous activity will give rise to hallucinations (called psychotic symptoms) if the re entrant pathway is in sensory cortex, and to manic behavior if in cortex with decidedly motoric functions, which would include planning. Since I have conjectured in these pages that an emotion is a high-level motor command, a re entrant pathway in frontal limbic cortex would produce an apparent emotion disconnected from conscious experience and if in posterior limbic cortex, a hallucinated emotion trigger.

The situation is very similar if a cortical area is normal in size but one of its main synaptic partners is reduced in size by disease. In epileptogenesis, the post-damage remodelling of the local neural networks is known to be associated with new-synapse formation and the sprouting of axon collaterals. The hyperexcitable brain tissue responsible for triggering seizures is known to lie just outside the dead core zone of the damaged region, and can therefore be called “overgrown” relative to the dead zone, which has zero functioning neurons.

All this is compatible with the formation, during the epileptogenesis latent period, of a pair of counter circulating, polysynaptic “ring roads” around the perimeter of the damaged area. This process would be determined by simple rules of valency satisfaction. Both ring roads would be capable of carrying autonomous activity that progresses to a seizure. This might only happen if inhibitory tone is also compromised. Hallucinations and seizures seem to be different grades of the same phenomenon.  Indeed, auditory hallucinations commonly occur in association with temporal-lobe seizures. The temporal lobe is the location of the auditory cortex (Brodmann areas 41 and 42).