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).
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| Neural net repair leading to seizures. |
