Age-related changes to electroencephalographic markers of visuomotor error processing and learning in prism adaptation.

Aging is associated with changes in cognitive function, including declines in learning, memory, and executive function. Prism adaptation (PA) is a useful paradigm to measure changes in explicit and implicit mechanisms of visuo-motor learning with age, but the neural correlates are not well understood. In the present study, we used PA to investigate visuo-motor learning and error processing in older adults. Twenty older adults (56-85 yrs) and 20 younger adults (18-33 yrs) underwent a goal-oriented reaching task while wearing prism goggles as continuous EEG was recorded to examine neural correlates of error detection. We examined behavioural measures of PA, as well as ERP components previously found associated with the early and late phases of adaptation to visual distortion caused by the prism goggles. Our results indicate important age-related behavioural and neurophysiological differences. Older adults reached more slowly than younger adults but showed the same accuracy throughout the prism exposure. Older adults also displayed larger aftereffects, indicating preserved visuomotor adaptation. EEG results indicated similar initial error processing in older and younger adults, as measured by the feedback error related negativity (FRN). As seen previously in young adults, the P3a and P3b declined over the prism exposure phase in both groups. Older adults displayed reduced P3a amplitude compared to the younger group in the early phase of adaptation, however, suggesting reduced attentional orienting. Finally, the older group exhibited a greater P3b amplitude compared to the younger group in the later phases of adaptation, potentially a marker of enhanced context updating underlying spatial realignment, leading to their larger aftereffect. Implications for age-related learning differences and clinical applications are discussed.

EEG Microstates in Early Phase Psychosis: The Effects of Acute Caffeine Consumption.

Individuals with schizophrenia use on average twice as much caffeine than the healthy population, but the underlying cortical effects of caffeine in this population are still not well understood. Using resting electroencephalography (EEG) data, we can determine recurrent configurations of the electric field potential over the cortex. These configurations, referred to as microstates, are reported to be altered in schizophrenia and can give us insight into the functional dynamics of large-scale brain networks. In the current study, we use a placebo-controlled, randomized, double-blind, repeated-measures design to examine the effects of a moderate dose of caffeine (200mg) on microstate classes A, B, C, and D in a sample of individuals within the first five years of psychosis onset compared to healthy controls. The results support the reduction of microstate class C and D, as well as the increase of microstate class A and B in schizophrenia. Further, acute caffeine administration appears to exacerbate these group differences by reducing class D, and increasing occurrences of class A and B states in the patient group only. The current results support the hypothesis of a microstate class D reduction as an endophenotypic marker for psychosis and provide the first descriptive account of how caffeine is affecting these microstate classes in an early phase psychosis sample.

Alteration of Resting Electroencephalography by Acute Caffeine Consumption in Early Phase Psychosis.

Individuals with schizophrenia use twice as much caffeine on average when compared to healthy controls. Knowing the high rates of consumption, and the potential negative effects of such, it is important we understand the cortical mechanisms that underlie caffeine use, and the consequences of caffeine use on neural circuits in this population. Using a randomized, placebo controlled, double-blind, repeated measures design, the current study examines caffeine's effects on resting electroencephalography (EEG) power in those who have been recently diagnosed with schizophrenia (SZ) compared to regular-using healthy controls (HC). Correlations between average caffeine consumption, withdrawal symptoms, drug related symptoms and clinical psychosis symptoms were measured and significant correlations with neurophysiological data were examined. Results showed caffeine had no effect on alpha asymmetry in the SZ group, although caffeine produced a more global effect on the reduction of alpha2 power in the SZ group. Further, those with more positive symptoms were found to have a greater reduction in alpha2 power following caffeine administration. Caffeine also reduced beta power during eyes closed and eyes open resting in HC, but only during eyes closed resting conditions in the SZ group. These findings provide a descriptive profile of the resting EEG state following caffeine administration in individuals with schizophrenia. The findings ultimately suggest caffeine does not affect alpha or beta power as readily in this population and a higher dose may be needed to achieve the desired effects, which may elucidate motivational factors for high caffeine use.