Kraepelin's dichotomy is true: contrasting brain dysfunction at the extremes of human growth and maturation. Excitability, the fundamental property of nervous tissue, is affected.
The distribution of Kraepelin's ubiquitous dichotomy varies with standard of living and pubertal age: when one rises, the other declines. The universal similar clinical picture--mortality risk, manic depressive psychosis, episodic dysfunction of brainstem control systems (sleep-wake cycle, food, mood control mechanism)--is caused by abridged pubertal pruning of excitatory synapses, which is treated with anti-epileptics, as opposed to convulsant neuroleptics in dementia praecox, where the clinical variation reflects varying degrees of excessive pruning and deficit in excitability. Localization of cortical breakdown of circuitry, silent spots and persistent dysfunction due to insufficient fill-in mechanisms, determine the clinical picture. This ranges from dementia praecox in late puberty and poor living standards, to cognitive dysfunction (mainly with higher standards of living) with earlier puberty. This variation is the most likely explanation why the acceptance of dementia praecox as a disease entity was complicated. Kraepelin's dichotomy, episodic dysfunction against a clinical deterioration, is at the extremes of brain maturation; the fundamental property of nervous tissue, excitability, is affected. To reduce the risk of psychotic episodes, omega-3 might also be given, as it normalizes excitation at all levels. The neo-Kraepelinian atheoretical quantitative scoring systems have eliminated disease entities and neglected endogeneity in psychiatry. We are back to a pre-Kraepelinian state, without his systematic observations. What is psychiatry without Kraepelin's dichotomy? Mood stability is a fundamental personality trait with a normal distribution; what is considered within or outside normal variation is arbitrary. Given the mood-stabilizing effect of anti-epileptics and omega-3, these will increasingly dominate psychiatric treatment.
Saugstad
Letten F
LF
Institute of Neuroscience, University of Oslo, Oslo, Norway.
D001714:Bipolar Disorder / Q000175:diagnosis / Q000401:mortality / Q000523:psychology*; D006803:Human Development; D006801:Humans; D009420:Nervous System / Q000473:pathology*; D009474:Neurons / Q000502:physiology*; D011582:Psychological Theory; D011627:Puberty / Q000502:physiology*; D012043:Regression, Psychology; D043762:Reproductive Behavior / Q000502:physiology; D012559:Schizophrenia / Q000175:diagnosis / Q000401:mortality / Q000473:pathology; D012895:Sleep, REM / Q000502:physiology; D013008:Somatotypes