We investigated neural mechanisms that support voice recognition in a training paradigm with fMRI. The same listeners were trained on different weeks to categorize the mid-regions of voice-morph continua as an individual's voice. Stimuli implicitly defined a voice-acoustics space, and training explicitly defined a voice-identity space. The pre-defined centre of the voice category was shifted from the acoustic centre each week in opposite directions, so the same stimuli had different training histories on different tests. Cortical sensitivity to voice similarity appeared over different time-scales and at different representational stages. First, there were short-term adaptation effects: increasing acoustic similarity to the directly preceding stimulus led to haemodynamic response reduction in the middle/posterior STS and in right ventrolateral prefrontal regions. Second, there were longer-term effects: response reduction was found in the orbital/insular cortex for stimuli that were most versus least similar to the acoustic mean of all preceding stimuli, and, in the anterior temporal pole, the deep posterior STS and the amygdala, for stimuli that were most versus least similar to the trained voice-identity category mean. These findings are interpreted as effects of neural sharpening of long-term stored typical acoustic and category-internal values. The analyses also reveal anatomically separable voice representations: one in a voice-acoustics space and one in a voice-identity space. Voice-identity representations flexibly followed the trained identity shift, and listeners with a greater identity effect were more accurate at recognizing familiar voices. Voice recognition is thus supported by neural voice spaces that are organized around flexible 'mean voice' representations.

Introduction: While amnestic mild cognitive impairment (aMCI) and non-amnestic mild cognitive impairment (naMCI) are theoretically different entities, only a few investigations studied the structural brain differences between these subtypes of mild cognitive impairment. The aim of the study was to find the structural differences between aMCI and naMCI, and to replicate previous findings on the differentiation between aMCI and healthy controls.Methods: Altogether 62 aMCI, naMCI, and healthy control subjects were included into the study based on the Petersen criteria. All patients underwent a routine brain MR examination, and a detailed neuropsychological examination.Results: The sizes of the hippocampus, the entorhinal cortex and the amygdala were decreased in aMCI relative to naMCI and to controls. Furthermore the cortical thickness of the entorhinal cortex, the fusiform gyrus, the precuneus and the isthmus of the cingulate gyrus were significantly decreased in aMCI relative to naMCI and healthy controls. The largest differences relative to controls were detected for the volume of the hippocampus (18% decrease vs. controls) and the cortical thickness (20% decrease vs. controls) of the entorhinal cortex: 1.6 and 1.4 in terms of Cohen's d. Only the volume of the precuneus were decreased in the naMCI group (5% decrease) compared to the control subjects: 0.9 in terms of Cohen's d. Significant between group differences were also found in the neuropsychological test results: a decreased anterograde, retrograde memory, and category fluency performance was detected in the aMCI group relative to controls and naMCI subjects. Subjects with naMCI showed decreased letter fluency relative to controls, while both MCI groups showed decreased executive functioning relative to controls as measured by the Trail Making test part B. Memory performance in the aMCI group and in the entire sample correlated with the thickness of the entorhinal cortex and with the volume of the amygdala.Conclusion: The amnestic mild cognitive impairment/non-amnestic mild cognitive impairment separation is not only theoretical but backed by structural imaging methods and neuropsychological tests. A better knowledge of the MCI subtypes can help to predict the direction of progression and create targeted prevention.

Aim:Hypothermia is often induced to reduce brain injury in newborns, following perinatal hypoxic–ischaemic events, and in adults following traumatic brain injury, stroke or cardiac arrest. We aimed to devise a method, based on diffusion-weighted MRI, to measure non-invasively the temperature of the cerebrospinal fluid in the lateral ventricles.Methods:The well-known temperature dependence of the water diffusion constant was used for the estimation of temperature. We carried out diffusion MRI measurements on a 3T Philips Achieva Scanner involving phantoms (filled with water or artificial cerebrospinal fluid while slowly cooling from 41 to 32°C) and healthy adult volunteers.Results:The estimated temperature of water phantoms followed that measured using a mercury thermometer, but the estimates for artificial cerebrospinal fluid were 1.04°C lower. After correcting for this systematic difference, the estimated temperature within the lateral ventricles of volunteers was 39.9°C. Using diffusion directions less sensitive to cerebrospinal fluid flow, it was 37.7°C, which was in agreement with the literature.Conclusion:Although further improvements are needed, measuring the temperature within the lateral ventricles using diffusion MRI is a viable method that may be useful for clinical applications. We introduced the method, identified sources of error and offered remedies for each.

ABSTRACT. Effects of 2 and 4 pg/kg/min dopamine infusion on cardiovascular and renal functions, cerebral blood flow (CBF) and plasma catecholamine levels were studied in sick preterm neonates during the first four days of life. Preterm infants were found to have an enhanced responsiveness to the pressor effects of dopamine during this period. Comparison of the renal effects of 2 and 4 &kg/ min dopamine in 61 preterm infants indicate that 2 pg/kg/ min dopamine induces maximum diuresis and natriuresis during the first day of life provided that systemic blood pressure is within the predicted normal range. Although administration of 4 pg/kg/min dopamine induces further increases in blood pressure and glomerular filtration rate, urine output and sodium excretion remain similar to that on 2 pg/kg/min of the drug. These findings demonstrate that the direct tubular effects of dopamine play an important role in the diuretic and natriuretic action of the drug in the one-day old preterm infant. In five preterm neonates, changes in CBF transiently paralleled the dopamine-induced alterations in systemic blood pressure indicating that autoregulation of CBF is impaired but not completely ineffective in the one-day old preterm infant. In eight term neonates, increases in blood pressure had no effect on CBF. Measurements of plasma dopamine and norepinephrine levels in 14 preterm neonates and five children suggest that decreased metabolism of dopamine may contribute to the enhanced pressor responsiveness to dopamine in sick preterm infants. Based on these findings, we propose that dopamine should be started at 2 pg/kg/min in the hypotensive and/or oliguric preterm infant, and that the dose should be increased in a stepwise manner tailored to the cardiovascular and renal response to the patient. (Pediatr Res 34: 742449,1993) Abbreviations ACA, anterior cerebral artery ANOVA, analysis of variance CBF, cerebral blood flow 6, creatinine clearance DA, dopamine (study group) DBP, diastolic blood pressure EDFV, end-diastolic flow velocity ESFV, end-systolic flow velocity CFR, glomerular filtration rate

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