Deviation in cerebral excitability: possible clinical implications.

Abstract

Schizophrenia, a chemical signaling disorder in the brain, is also a deteriorating neurological disorder. The deficit in cerebral excitability, and associated reduced synaptic density, imply a risk of cortical breakdown of circuitry accompanied by an insufficient fill-in mechanism, and persistent silent spots, but no total loss of function, only dysfunction. This is subjectively experienced as deficiencies of cognition, perception and sensorimotor phenomena depending upon localization and connections of the disconnected circuitry. Considering the adversity inherent in this neural network, both the fast Hebbian pre-post form of learning and the slow pre-modulatory coincidence form of learning are probably impaired. The use of Feed Back Loops which usually govern our behaviour might also be impaired. In addition, we have to consider the daily problem of insufficient drive and motivation. Manic depressive psychosis, a chemical signaling disorder in the brain, is a true functional psychosis. The raised excitatory drive and raised synaptic density imply raised risk of uncoupling of circadian rhythms via the direct glutamatergic input to the suprachiasmatic nucleus of hypothalamus (SCN). This episodic brain stem dysfunction illustrates how a deficit in inhibition renders the brain unstable. The requirements of the fast Hebbian form of learning should easily be met, and neither should the slow forms of learning present a problem in networks characterized by excessive density.(ABSTRACT TRUNCATED AT 250 WORDS)