The mismatch negativity (MMN) is an EEG-derived event-related potential (ERP) elicited by any violation of a predicted auditory ‘rule’, regardless of whether one is attending to the stimuli, and is thought to reflect updating of the stimulus context. Chronic schizophrenia patients exhibit robust MMN deficits, while MMN reduction in first-episode and early phase psychosis is significantly less consistent. Traditional two-tone “oddball” MMN measures of sensory information processing may be considered too simple for use in early phase psychosis in which pathology has not progressed fully, and a paradigm that probes higher order processes may be more appropriate for elucidating auditory change detection deficits. This study investigated whether MMN deficits could be detected in early phase psychosis (EP) patients using an abstract ‘missing stimulus’ pattern paradigm (Salisbury, 2012). The stimuli were 400 groups of six tones (1000 Hz, 50 ms duration, 330 ms stimulus onset asynchrony), which was presented with an inter-trial interval of 750 ms. Occasionally a group contained a deviant, meaning that it was missing either the 4th or 6th tone (50 trials each). EEG recordings of 13 EP patients (≤5 year duration of illness) and 15 healthy controls (HC) were collected. Patients and controls did not significantly differ on age or years of education.
Analyses of MMN amplitudes elicited by missing stimuli revealed amplitude reductions in EP patients, suggesting that these deficits are present very early in the progression of the illness. While there were no correlations between MMN measures and measures such as duration of illness, medication dosage or age, MMN amplitude reductions were correlated with positive symptomatology (i.e. auditory hallucinations).
These findings suggest that MMNs elicited by the ‘missing stimulus’ paradigm are impaired in psychosis patients early in the progression of illness and that previously reported MMN-indexed deficits related to auditory hallucinations in chronic patients may also be present in EP patients. As such, this paradigm may have promise in identifying early processing deficits in this population.
The highest potential for the reduction in caffeine intake is by reducing coffee consumption; the elimination of any other caffeine source would not result in substantial decreases in caffeine intake.
The caffeine content of 124 products, including coffee, coffee-based beverages, energy drinks, tea, colas, yoghurt and chocolate, were determined using RP-HPLC with UV detection after solid-phase extraction. Highest concentrations of caffeine were found for coffee prepared from pads (755 mg l⁻¹) and regular filtered coffee (659 mg l⁻¹). The total caffeine content of coffee and chocolate-based beverages was between 15 mg l⁻¹ in chocolate milk and 448 mg l⁻¹ in canned ice coffee. For energy drinks the caffeine content varied in a range from 266 to 340 mg l⁻¹. Caffeine concentrations in tea and ice teas were between 13 and 183 mg l⁻¹. Coffee-flavoured yoghurts ranged from 33 to 48 mg kg⁻¹. The caffeine concentration in chocolate and chocolate bars was between 17 mg kg⁻¹ in whole milk chocolate and 551 mg kg⁻¹ in a chocolate with coffee filling. A caffeine assessment tool was developed and validated by a 3-day dietary record (r²= 0.817, p < 0.01) using these analytical data and caffeine saliva concentrations (r²= 0.427, p < 0.01).
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