Toward a biaxial model of "bipolar" affective disorders: spectrum phenotypes as the products of neuroelectrical and neurochemical alterations.

摘要: Abstract Based upon a synthesis of findings related to affective illness, pathophysiologic hypothesis and possible nosology are proposed. The authors reviewed recent (2001–2004) phenomenologic, diagnostic treatment literature for implications selectively genetic, neuroimaging, neurochemical neuropathological studies (1966–2004) that might inform the hypothesized model. Modern DSM illness is based accumulation observations in purely descriptive tradition has little basis. A new perspective, bipolar spectrum, deriving from clinical, theoretical epidemiologic considerations, appears more promising building bridges with emerging neurobiology disorder. Research seeking associations between structural alterations (molecular, cellular system-level) behavioral-level processes provided many clues, but no population-wide, major genetic loci have been identified. Three general hypotheses emerged implicating: 1) presynaptic electrical signaling, an early suggestion which received less consideration, 2) neurotransmitter–receptor systems (first messenger) 3) post-receptor signaling (second- third messenger). current ‘biaxial’ proposes: regulation may be understood terms two primary functional spectra: mood range tonicity, these spectra, turn, determined by capacity neuroelectrical modulation–and their interaction, proposed pathophysiology suggests molecular loci, predict phenomenologic patterns responsiveness.