Fatal insomnia and agrypnia excitata: sleep and the limbic system
by
Provini F, Cortelli P, Montagna P, Gambetti P, Lugaresi E.
Department of Neurological Sciences,
University of Bologna, Bologna, Italy.
federica.provini@unibo.it
Rev Neurol (Paris). 2008 Aug-Sep;164(8-9):692-700.

ABSTRACT

Fatal familial insomnia, a human prion disease, Morvan's chorea, an autoimmune limbic encephalopathy, and delirium tremens, the well-known alcohol (or benzodiazepine [BDZ]) withdrawal syndrome, share a clinical phenotype largely consisting in an inability to sleep associated with motor and autonomic activation. Agrypnia excitata is the term which aptly defines this clinical condition, whose pathogenetic mechanism consists in an intralimbic disconnection releasing the hypothalamus and brainstem reticular formation from corticolimbic inhibitory control. Severance of cortical-subcortical limbic structures is due to visceral thalamus degeneration in fatal familial insomnia, and may depend on autoantibodies blocking voltage-gated potassium channels within the limbic system in Morvan's chorea, and the sudden changes in gabaergic synapses down-regulated by chronic alcohol abuse within the limbic system in delirium tremens. On the basis of these findings, we suggest that a neuronal network, extending from the medulla to the limbic cortex, controls the sleep-wake cycle, operating in an integrated fashion following a caudorostral organization.

FFI
Biohappiness
Liberal Eugenics
Fatal familial insomnia
The literature of eugenics
Human self-domestication
Germline genetic engineering
Preimplantation genetic diagnosis
A life without pain? Hedonists take note'
Francis Galton and contemporary eugenics
Gene therapy and performance enhancement
5-HTT and AP-2beta gene polymorphism/spirituality

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