[Acid-base regulations in cerebrospinal fluid and brain functions].
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Placental insufficiency with fetal intrauterine growth restriction (IUGR) is an important cause of perinatal mortality and morbidity and is subsequently associated with significant neurodevelopmental impairment in cognitive function, attention capacity, and school performance. The underlying biologic cause for this association is unclear. Twenty-eight preterm infants (gestational age 32.5 +/- 1.9 wk) were studied by early and term magnetic resonance imaging (MRI). An advanced quantitative volumetric three-dimensional MRI technique was used to measure brain tissue volumes in 14 premature infants with placental insufficiency, defined by abnormal antenatal Doppler measurements and mean birth weights <10(th) percentile (1246 +/- 299 g) (IUGR) and in 14 preterm infants matched for gestational age with normal mean birth weights 1843 +/- 246 g (control). Functional outcome was measured at term in all infants by a specialized assessment scale of preterm infant behavior. Premature infants with IUGR had a significant reduction in intracranial volume (mean +/- SD: 253.7 +/- 29.9 versus 300.5 +/- 43.5 mL, p < 0.01) and in cerebral cortical gray matter (mean +/- SD: 77.2 +/- 16.3 versus 106.8 +/- 24.6 mL, p < 0.01) when measured within the first 2 wk of life compared with control premature infants. These findings persisted at term with intracranial volume (mean +/- SD: 429.3 +/- 47.9 versus 475.9 +/- 53.4 mL, p < 0.05) and cerebral cortical gray matter (mean +/- SD: 149.3 +/- 29.2 versus 189 +/- 34.2 mL, p < 0.01). Behavioral assessment at term showed a significantly less mature score in the subsystem of attention-interaction availability in IUGR infants (p < 0.01). Cerebral cortical gray matter volume at term correlated with attention-interaction capacity measured at term (r = 0.45, p < 0.05). These results suggest that placental insufficiency with IUGR have specific structural and functional consequences on cerebral cortical brain development. These findings may provide insight into the structural-functional correlate for the developmental deficits associated with IUGR.
The autoradiographic 2-deoxyglucose method for regional cerebral metabolic activity was modified for use with tritium label to determine which brain stem and spinal cord nuclei changed their functional neural activity during periaqueductal gray stimulation-produced analgesia. The greatest changes in activity during electrical stimulation of the periaqueductal gray occurred in nucleus paragigantocellularis, the ventral portion of the nucleus reticularis gigantocellularis, and the nucleus cuneiformis. Substantial increases in metabolic activity were also evident in the spinal trigeminal nucleus and the substantia gelatinosa. Many of the regions which displayed increased functional activity in the present study have been shown to possess substantial enkephalin immunoreactivity. While several of these structures have previously been implicated in modulation of nociceptive transmission, this study raises the possibility that other brain stem nuclei may also participate in analgesic mechanisms.
Positron emission tomography has enabled us to measure various fundamental parameters of human brain physiology and chemistry, such as cerebral blood flow, metabolism and synaptic function. Blood flow and oxygen metabolism is important for the understanding of cerebrovascular Disease. Glucose metabolism is useful for the determination of epileptic foci and for the evaluation of tumor malignancy. Measurement of pre- and post-synaptic function is applicable to the differential diagnosis of parkinsonism. Imaging analysis of functional neuroanatomy of these parameters are very promising for the early diagnosis of dementia, such as Alzheimer's disease. Developmennt of new radiotracers is expected for detection of early specific pathological changes and more previous changes underlying the deterioration of neurochemistry, such as genetic abnormalities.
PURPOSE: To study rehabilitation outcome in a chronic visual field defect patient using positron emission tomography (PET) imaging, clinical, and neurophysiological measures. METHODS: A patient with chronic visual field defect was rehabilitated using a computer program over a three-month period. Evaluations of rehabilitation effects were done before and after training, and after a three-month follow-up with perimetry, visual evoked potentials (VEP), subjective questionnaire, and PET activation studies of regional cerebral blood flow (rCBF). RESULTS: In perimetry, the visual field increased during the training, and the patient also experienced subjective improvement. In VEP, a previously absent P100 component was identified after the training. In PET, increases in rCBF were diffuse immediately after the training, and more occipital after the late follow-up. A significant positive correlation between the increase in rCBF and improvement in clinical measures was found in the lingual gyrus in the contralesional hemisphere. CONCLUSIONS: All clinical measures showed improvement after rehabilitation, and this was maintained during the follow-up. In PET, a more generalized effect, found at the beginning, later concentrated in the occipital cortex. The results suggest that visual training may cause plastic changes in the brain, and that these changes can be detected both with clinical measures and with functional imaging.
Despite a recent literature supporting the impact of surgery on the natural history of low-grade glioma (LGG), the indications of resection still remain a matter of debate, especially because of the frequent location of these tumors within eloquent brain areas - thus with a risk to induce a permanent postoperative deficit. Therefore, since the antagonist nature of this surgery is to perform the most extensive glioma removal possible, while preserving the function and the quality of life, new concepts were recently applied to LGG resection in order to optimize the benefit/risk ratio of the surgery.First, due to the development of functional mapping methods, namely perioperative neurofunctional imaging and intrasurgical direct electrical stimulation, the study of cortical functional organization is currently possible for each patient - in addition to an extensive neuropsychological assessment. Such knowledge is essential because of the inter-individual anatomo-functional variability, increased in tumors due to cerebral plasticity phenomena. Thus, brain mapping enables to envision and perform a resection according to individual functional boundaries.Second, since LGG invades not only cortical but also subcortical structures, and shows an infiltrative progression along the white matter tracts, new techniques of anatomical tracking and functional mapping of the subcortical white matter pathways were also used with the goal to study the individual effective connectivity - which needs imperatively to be preserved during the resection.Third, the better understanding of brain plasticity mechanisms, induced both by the slow-growing LGG and by the surgery itself, were equally studied in each patient and applied to the surgical strategy by incorporating individual dynamic potential of reorganization into the operative planning. The integration of these new concepts of individual functional mapping, connectivity and plastic potential to the surgery of LGG has allowed an extent of surgical indications, an optimization of the quality of resection (neuro-oncological benefit), and a minimization of the risk of sequelae (benefit on the quality of life). In addition, such a strategy has also fundamental applications, since it represents a new door to the connectionism and cerebral plasticity.
After each circulation block which has been successfully resuscitated comes to post-resuscitation disease the seriousness of which depends on the duration of block. It is a specific pathophysiological condition of vital organs just after the ischemic anoxia. The brain is able to tolerate only four minutes of block without its damage and represents a factor limiting the success of cardiopulmocerebral resuscitation (CPCR). The present researches in resuscitology are concentrated towards the research of the chemical nature of endotoxins created during the ischemic affection of other organs which inflicts inversely the brain. Therefore the recovering of cerebral functions from the arrest of heart activity lasting more than five minutes is always problematic because it is already under the influence of existing changes in organ systems which follow after the reperfusion.
Aquaporin-4 (AQP4) is expressed in astrocytes throughout the central nervous system, particularly at the blood-brain and brain-cerebrospinal fluid barriers. Phenotype analysis of transgenic mice lacking AQP4 has provided compelling evidence for involvement of AQP4 in cerebral water balance, astrocyte migration, and neural signal transduction. AQP4-null mice have reduced brain swelling and improved neurological outcome in models of (cellular) cytotoxic cerebral edema including water intoxication, focal cerebral ischemia, and bacterial meningitis. However, brain swelling and clinical outcome are worse in AQP4-null mice in models of vasogenic (fluid leak) edema including cortical freeze-injury, brain tumor, brain abscess and hydrocephalus, probably due to impaired AQP4-dependent brain water clearance. AQP4 deficiency or knock-down slows astrocyte migration in response to a chemotactic stimulus in vitro, and AQP4 deletion impairs glial scar progression following injury in vivo. AQP4-null mice also manifest reduced sound- and light-evoked potentials, and increased threshold and prolonged duration of induced seizures. Impaired K+ reuptake by astrocytes in AQP4 deficiency may account for the neural signal transduction phenotype. Based on these findings, we propose modulation of AQP4 expression or function as a novel therapeutic strategy for a variety of cerebral disorders including stroke, tumor, infection, hydrocephalus, epilepsy, and traumatic brain injury.
The purpose of this study was to evaluate changes in brain activity during voluntary walking in normal subjects using technetium-99m-hexamethyl-propyleneamine oxime single photon emission computed tomography. This study included 14 normal subjects. Statistical parametric mapping analysis revealed that the supplementary motor area, medial primary sensorimotor area, the striatum, the cerebellar vermis and the visual cortex were activated. These results suggested that the cerebral cortices controlling motor functions, visual cortex, basal ganglia and the cerebellum might be involved in the bipedal locomotor activities in humans.
Recent advances in our knowledge of synaptic transmission have been achieved using brain slice preparations. Since the complexes of neuronal networks often make multiple synaptic contacts to a single postsynaptic neuron, the electrical stimulation of presynaptic nerve bundle simultaneously activates not only plural presynaptic axons but also the collateral pathways. Accordingly, the mechanisms of transmitter release from a single presynaptic nerve terminal are poorly understood. Recently, a more simplified preparation of cultured neurons has been developed and the properties of transmitter release were clearly studied. However, little information exists as to whether the release properties and presynaptic modulation of single native terminals behave similarly to terminals formed in culture preparations. We have then develop a mechanical dissociation technique of single CNS neurons attaching functional native excitatory and inhibitory synaptic terminals (boutons). These dissociated neurons exhibit spontaneous synaptic activities, and their presynaptic modulation has been extensively studied. We further visualized single presynaptic boutons onto a synaptic bouton preparation and electrical stimulation was selectively given to one of the boutons. Here we show how such an electrophysiological approach allows us to understand the transmitter release in a single presynaptic element in the CNS. We discuss the pharmacological and physiological prospects.
Recent advances in magnetic resonance imaging and spectroscopy make it possible to measure localized changes in human brain activity and metabolism in single subjects during sensory stimulation and cognition. Differences between stimulated and unstimulated subjects can be visualized to a resolution of mm3 in less than 1s, a significant improvement over the more established method, positron emission tomography. Magnetic resonance spectroscopy of the human brain, measuring fluxes in several cm3, has followed changes in metabolic rates during visual stimulation.
Classification of subjects into predefined groups, such as patient vs. control, based on their functional MRI data is a potentially useful procedure for clinical diagnostic purposes. This paper presents an automated method for classifying subjects into groups based on their functional MRI data. The proposed methodology provides general framework using preprocessed time series for the whole brain volume. Using a training set of two groups of subjects, the new methodology identifies spatio-temporal features that distinguish the groups and uses these features to categorize new subjects. We demonstrate the method using simulations and a clinical application that classifies individuals into schizotypy and control groups.