Mania as a dysfunction of reentry: application of Edelman's and Tononi's hypothesis for consciousness in relation to a psychiatric disorder.
The concept of reentry as the most important element in a hypothesis for consciousness proposed by Edelman and Tononi is reviewed. Reentry, is a process of ongoing parallel and recursive signalling between separate neuronal groups along parallel reciprocally fibers that link these groups anatomically. Reentry alters the activity of the target areas it interconnects until a synchronous activity across these areas is created, this may be the direct biological mechanism of consciousness. The repetitive process of reentry may explain how the millisecond time scale of neural signalling is turned into the time scale of seconds characterizing our impression of the duration of a given content of consciousness. It is suggested that reentry may be faster in mania, and specifically that the repetitive recursive signalling is faster in mania, hereby allowing reentry to produce a conscious state, faster than usual. Faster reentry may on a molecular level be caused by faster propagation of nerve impulses, which may be in accordance with a number of hypotheses where mania is seen as a disorder of ionic conductance, nerve cell excitability, action potential firing, membrane abnormalities, and cortical instability. Also the antiepileptic drugs used to treat mania may point to reentry as a factor in this disorder. On a more integrated level faster reentry processes may explain several of the core symptoms of the manic state. Also the drug induced switch from depression to mania in bipolar patients may be explained by the concept of reentry.
Laboratory of Neuropsychiatry, Rigshospitalet--6102, DK-2100 Copenhagen, Denmark. mellerup@rh.dk
Erling
E
Mellerup
Flemming
F
Kristensen
D001714:Bipolar Disorder / Q000209:etiology / Q000503:physiopathology*; D001927:Brain Diseases / Q000150:complications / Q000503:physiopathology*; D003243:Consciousness; D003244:Consciousness Disorders / Q000209:etiology / Q000503:physiopathology; D006801:Humans; D001523:Mental Disorders / Q000209:etiology / Q000503:physiopathology; D008959:Models, Neurological; D009415:Nerve Net / Q000503:physiopathology*; D009435:Synaptic Transmission