Variations in cognitive profile, age of onset, and rate of decline exemplify the heterogeneity of AD [ 5].
Health workers collected information about sociodemographic profile, date of onset, and place of residence from all suspected case-patients.
Admixture analysis of age at onset (AAO) has helped delineating the clinical profile of early onset (EO) bipolar disorder (BD).
To study the depth profile of activity onset and to see whether it originates in a particular cortical layer, we detected the onsets of activity in LFP recorded simultaneously at different depth.
This observation is consistent with the depth profile of activity onset, described above.
To compare the clinical and neurocognitive profile of early-onset (EOP, <40 years), late-onset (LOP, 40 59 years) and very-late-onset (VLOP, ≥60 years) psychosis.
A series of t-tests were used to compare the continuous variables (trait EI profiles; age of onset; age of diagnosis; diagnostic delay; depression; alcohol consumption) across categorical groups (patients vs. healthy controls; RF+ patients vs. RF- patients).
We compared the clinical characteristics of observational, naturalistic, cross-sectional data from South and North American samples in order to assess the consistency in illness profile of early-onset bipolar disorder across geographic regions and to further validate onset age as a potential predictive variable of prognosis in bipolar disorder.
Our study of local mechanisms of origin of slow oscillation with multisite LFP, multiunit recordings, and simultaneous intracellular recordings from 2 to 4 neurons revealed a clear depth profile of activity onsets.
However, because of their pharmacokinetic profile, the time of onset and offset are longer (a loading dose is required) and they have the potential to accumulate in renal failure.
