What is a psychosis and where is it located?

摘要

Kraepelin’s dichotomy, manic-depressive insanity and dementia praecox, are contrasting and true endogenous disease entities which affect excitability, the fundamental property of the CNS. Kraepelin wanted to establish a valid classification and hit the extremes in brain structure and function at a time when we had no knowledge of brain dysfunction in “functional” psychoses. The aetiology is now known: the psychoses are part of human growth and maturation and might be classified according to their brain dysfunction, which is exactly what Kraepelin wanted. However, presumably to reduce the stigma attached to the word “psychosis”, there is currently a strong initiative to eliminate the concept. But knowledge of what is happening in the brain in a psychosis might be more helpful in reducing stigma. It is suggested that psychosis is due to an affection of the supplementary motor area (SMA), located at the centre of the Medial Frontal Lobe network. The SMA is one of the rare universally connected areas of the brain, as should be the case for such a key structure that makes decisions as to the right moment for action. This important network, which partly has continuous neurogenesis, has sufficiently widespread connections. The SMA, a premotor area located on the medial side of the frontal lobes, is one of the last regions to reach a concurrence of synaptogenesis. An affection of the SMA, a deficient or abolished Delayed Response Task, seriously disturbs our relation and adaptation to the surroundings. We usually master the Delayed Response Task around the age of 7 months, a time at which the second CNS regressive event takes place, which proceeds from the posterior to the anterior of the brain. In very late maturation, a persistent affection of the SMA might occur. We experience a chronic psychosis: infantile autism (IA), a chronic inability to act consciously, which contrasts with the episodic SMA affection post-puberty, when excitation is reduced due to excessive pruning of excitatory synapses. Silent spots are the result of insufficient fill-in mechanisms following a breakdown of circuitry. They may affect the SMA in the case of very late puberty. An acute reduction in excitation and concomitantly a marked increase in silent spots might lead to an acute psychosis. A frontal preference is likely, given that a reduction might occur anywhere in the cortex, but particularly in the areas maturing latest. The varying localisations probably explain the difficulty in accepting schizophrenia as a disease entity. The multifactorial inheritance of the dichotomy implies that the genetics are not fate, a psychotic development might be prevented given enough epigenetic factors: brain food (omega 3). Might the present dietary adversity, with its lack of brain food, be responsible for a rising incidence in psychosis? A psychosis is an understandable and preventable dysfunction of the brain, and its mechanisms are known. Primarily a disorder of reduced excitation in an attenuated CNS, this explains why all the neuroleptics are convulsants, raising excitation, in contrast to all antidepressives, which are anti-epileptic.