Attention-deficit Hyperactivity Disorder (ADHD), defined as a disorder of awareness with impulsivity, has lately been characterized as a dysfunction of the striatum (neostriatum = globus pallidus + putamen). This structure is in a unique position of contextual analysis and samples information samples information from almost the entire cortex through its spiny neurons. The etiology is heterogeneous, with genetic as well as lesional factors. Among the latter, pre- and perinatal events are prominent. Advances in the understanding of the role of fetal circulatory insufficiency with loss of autoregulation and systemic hypotension have drawn attention to the vulnerability of watershed regions, including the striatum. Not only circulatory facts are important for this selectivity, however. The anatomical characteristics, with convergent glutaminergic afferent synaptic transmission from almost the entire cortex contribute to the vulnerability in ischemia-induced liberation of glutamate: The striatum becomes the victim of its virtue. Repeated hypoxic-ischemic events are particularly common in prematurity, a fact which seems to explain the high incidence of ADHD in this patient group. The magnitude, of the problem is increasing with the increased survival rate among premature infants.

Liberal acceptance, overconfidence, and increased activity of the neurotransmitter dopamine have been proposed to account for abnormal sensory experiences, for instance, hallucinations in schizophrenia. In normal subjects, increased sensory experience in Yoga Nidra meditation is linked to striatal dopamine release. We therefore hypothesize that the neurotransmitter dopamine may function as a regulator of subjective confidence of visual perception in the normal brain. Although much is known about the effect of stimulation by neurotransmitters on cognitive functions, their effect on subjective confidence of perception has never been recorded experimentally before. In a controlled study of 24 normal, healthy female university students with the dopamine agonist pergolide given orally, we show that dopaminergic activation increases confidence in seeing rapidly presented words. It also improves performance in a forced-choice word recognition task. These results demonstrate neurotransmitter regulation of subjective conscious experience of perception and provide evidence for a crucial role of dopamine.

Summary MATERIALS AND METHODSWe examined autoregulation of cerebral blood flow (CBF) over the range of oxygen tension commonly observed in the chronic fetal lamb preparation. Seventeen animals were surgically prepared under general anesthesia for chronic in utero studies. ~a s e d on measured resting arterial Po2 and calculated % saturation 24-48 h after surgery, two groups were defined: a normoxic group of eight with saturation of 57% or higher (our laboratory normal for physiologically stable preparations) and an hypoxic group of nine with saturation less than 57%. Regional CBF was measured with radiolabeled 15-pm microspheres. Autoregulation of CBF was assessed by measuring the change in CBF when fetal mean arterial blood pressure (MABP) was acutely decreased and increased by withdrawal and reinfusion of fetal blood. In normoxic animals CBF was constant over an MABP range of 42-61 torr in all four areas of the brain examined: cerebral hemispheres, basal ganglia, cerebellum, and brain stem. In hypoxic animals CBF was pressure dependent in all areas over an MABP range of 46-73 torr, i.e., autoregulation was abolished. These studies demonstrate that the mechanism of autoregulation is functionally developed in the mature fetal lamb, but operationally dependent upon arterial oxygen concentration. Below a saturation of approximately 50-60% CBF varies directly with perfusion pressure. AbbreviationsBP, blood pressure CBF, cerebral blood flow cpm, count per min i.d., internai diameter MABP, mean arterial blood pressure rCBF, regional cerebral blood flow Impairment of cerebrovascular autoregulation is now generally believed to be an important pathophysiologic mechanism in the genesis of hypoxic and hemorrhagic brain injury of the newborn (10, 20). The theoretical model states that with impairment of autoregulation the cerebral microcirculation is rendered vulnerable to changes in arterial blood pressure. Systemic hypotension results in ischemic cerebral blood flow (CBF) and cerebral infarction, whereas hypertension leads to cerebral hyperemia, rupture of poorly supported capillaries in the vulnerable subependymal germinal matrix, and cerebral hemorrhage (10, 15).Impaired autoregulation has been demonstrated in the severely asphyxiated fetal lamb (12) and in sick human newborns (1 1). The well oxygenated newborn lamp has been shown to autoregulate (16), and there is evidence that the normoxic fetal lamb has at least partial autoregulatory control of CBF (19). But the functional maturity of the autoregulatory mechanism in the fetal lamb, and its sensitivity to hypoxia, have not been clearly established.The present studies were designed to examine autoregulation in utero in the near term fetal lamb, and to determine its stability over the range of arterial oxygen tension normally encountered in chronically prepared laboratory animals.We studied 17 near term fetal lambs estimated to be 130-140 days gestation. Our methods for fetal studies in the chronically prepared sheep have been described in previous publications (12, ...

Twenty‐nine high‐risk preterm born children, from a cohort with cerebral blood flow (CBF) measurements in the first 2 d of life, were examined prospectively at the age of 5.5—7 y neurologically, neuropsychologically and by magnetic resonance imaging (MRI). They were compared to 57 control children in terms of neurology and neuropsychology. Abnormal MRI was found in 19 children. Low oxygen delivery to the brain was found in 63% of them, in contrast to 12.5% in those with normal MRI, indicating neonatal hypoxia‐ischemia as an important factor. The MRI abnormalities were mainly periventricular lesions (n = 19), especially periventricular leucomalacia (PVL, n = 17). Three of the very preterm children had severe cerebellar atrophy in addition to relatively mild periventricular abnormalities. MRI showed specific morphological correlates for the major disabilities, e.g. spastic CP (involvement of motor tracts), mental retardation (bilateral extensive white matter reduction or cerebellar atrophy) and severe visual impairment (severe optic radiation involvement). A morphological correlate for minor disabilities, i.e. functional variations in motor performance or intelligence, was not found, with the exception that symptoms of attention deficit hyperactivity disorder were related to mild MRI abnormalities. This could mean that with respect to cognitive functions, mild or unilateral periventricular MRI lesions could be compensated. However, as among preterms without mental retardation (n = 19), IQ was generally and significantly lower than in the control group; other, more chronic pathogenetic factors, not detectable by MRI alone, may play a role. □Attention deficit hyperactivity disorder, cerebral blood flow, cerebral palsy, magnetic resonance imaging, oxygen delivery, periventricular leucomalacia, prematurity

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Amplitude integrated EEG (aEEG) recordings from 32 mechanically ventilated infants, gestational age 32 weeks or less, were analysed. All recordings were started within 24 h of birth and continued for at least 50 h. Germinal layer haemorrhage (GLH) was diagnosed by repeated ultrasonography. In six infants neither GLH nor hypocalcaemia were diagnosed; aEEG in these infants rapidly became more active after birth: at 30 h of age continuous background activity was present for more than 20% of the time, and a seizure-like pattern was exceptional. In seven infants without GLH but with hypocalcaemia and other signs of metabolic derangement, continuous background activity appeared later and seizure-like activity was frequent. In the infants with GLH, depression of the background activity was apparent. This finding was particularly distinct in the presence of severe haemorrhages. Four infants developed GLH after 30 h of age. All these infants had depressed aEEG before the development of GLH, with less than 20% continuous activity at 30 h of age. In ten infants an analysis of the aEEG during the occurrence of GLH was possible. In six of these, cortical electrical activity decreased. Due to the limitation of GLH timing, it was not possible to decide whether this decrease closely preceded or followed GLH. We suggest that GLH primarily occurs in brains with a preceding metabolic and neurophysiologic abnormality, and that further functional deterioration is caused by the most severe haemorrhages.

Modifying both the top and bottom surfaces of CsPbBr3 perovskite films enhances carrier lifetime and optical gain remarkably.

Perinatal asphyxia is an important cause of neurological disability, but early prediction of outcome can be difficult. We performed proton magnetic resonance spectroscopy (MRS) and global cerebral blood flow measurements by xenon-133 clearance in 16 infants with evidence of perinatal asphyxia. Cerebral blood flow was determined daily in the first 3 days after birth in seven cases. Proton MRS was performed in 11 infants within the first week (mean 3.7 days), the rest within the first month (mean 22.2 days), and all had a scan around 3 months of age. Four infants died neonatally, three showed neurological deficits and the rest seemed to be progressing normally at neurodevelopmental follow-up at 1 year of age. A significant correlation was found between initial brain lactate levels and severe outcome (p = 0.0003) just as between cerebral hyperperfusion (mean cerebral blood flow (CBF) 86 ml(100 g)-1 min-1), (p = 0.02) and outcome. The diagnostic and prognostic implications of early MRS and CBF are predictive of poor outcome in severely asphyxiated infants.