[Electrophysiological characteristics and energy provision of the brain function in traumatic shock].
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Fetal ischemia or hypoxia can lead to cerebral palsy, mental retardation and epilepsy. We propose that the production of nitric oxide and oxygen radicals by neurons when ischemic or hypoxic brain is reperfused may contribute to cerebral injury. Ischemia will depolarize neuronal membranes causing the synaptic discharge of the excitatory neurotransmitter glutamate, which in turn opens the voltage-dependent, N-methyl-D-aspartic acid-specific glutamate receptor/ionophore, allowing calcium to accumulate in the neuron. Calcium in turn activates an oxygen-dependent neuronal nitric oxide synthetase, which oxidizes arginine to produce nitric oxide (.NO) when oxygen is readmitted to brain by reperfusion. Nitric oxide reacts with the oxygen radical superoxide (O2-), also produced by reperfusion, to form peroxynitrite (ONOO-). Peroxynitrite can diffuse for several micrometers before decomposing to form the powerful and cytotoxic oxidants hydroxyl radical and nitrogen dioxide. The hypothesis is consistent with available evidence on the protective action of glutamate antagonists and of oxygen radical scavengers for limiting cerebral infarction following focal ischemia.
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We describe a method for mapping stimulation data, obtained at the time of neurosurgery for intractable epilepsy, onto a 3D MRI-based neuroanatomic model of the individual patient. The mapping is done by comparing an intraoperative photograph of the exposed cortical surface with a computer-based MR visualization of the surface, interactively indicating corresponding stimulation sites, and recording 3-D MR machine coordinates of the indicated sites. Repeatability studies were performed to validate the accuracy of the mapping technique. Six observers--a neurosurgeon, a radiologist, and four computer scientists, independently mapped 218 stimulation sites from 12 patients. The mean distance of the six locations from the mean location of each site was 2.07 mm, with a standard deviation of 1.5 mm, or within 5.07 mm with 95% confidence. Since the surgical sites are accurate within approximately 1 cm, these results show that the visualization-based approach is accurate within the limits of the stimulation maps. When incorporated within the kind of information system envisioned by the Human Brain Project, this anatomically-based method will not only provide a key link between non-invasive and invasive approaches to understanding language organization, but will also provide the basis for studying the relationship between language function and anatomical variability.
Age is a natural factor that has been found to significantly affect sensitivity to hyperbaric hyperoxia (HBO). Exposure to HBO may lead to damages in the energy metabolism of the brain cells. The aim of this study was to test the effect of HBO on the metabolic, hemodynamic and electrical activities in the newborn dog. The study was performed using one-day- to 70-day-old puppies. The puppies were placed in a pressure chamber. The pressure of pure O2 in the chamber was raised by 5 atmospheres (ATA, 75 psi = 6 ATA) within 10 min. The first biochemical change to take place during HBO was oxidation of mitochondrial NADH. The age of the puppy was found to affect the time to the initiation of seizures. In the puppies under the age of 24 days, the average time was 35.1 +/- 5.9 min. In the puppies of 24 days old and older, the average time was 5.1 +/- 0.8 min. In the younger puppies, there was a later occurrence of blood vessel contractions and a longer life span compared to the older puppies. The comparison between the puppies of different ages during exposure to HBO showed differences in the metabolic response, hemodynamic changes and electrical activity. These differences can partially explain the higher resistance in the younger puppies to HBO.
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Cerebral glucose metabolism was measured twice in a sample of 15 schizophrenics and eight controls, using positron emission tomography (PET) with 18-F-fluorodeoxyglucose. Studies were separated by three to 33 weeks. Patients were unmedicated during the first study, and the majority were receiving neuroleptics during the second study. There were no changes from study 1 to study 2 in average whole-brain metabolic rates, regional cortical activity, or the gradient of subcortical to cortical activity. The steeper subcortical to cortical gradient in schizophrenics, present in the first study, persisted in the second. Changes in this gradient were uncorrelated with changes in clinical status. Laterality (right-left) was stable across studies, and changes toward higher right relative to left hemispheric metabolism were correlated with clinical improvement. The results support the hypothesis of abnormal hemispheric activity in schizophrenia and implicate the subcortical-cortical gradient as another dimension that merits further exploration.
PURPOSE OF REVIEW: Advances have been made in identifying how areas involved in processing vestibular, ocular motor, and visual information are represented in the human cortex as well as the cortical interaction between these systems in healthy subjects. RECENT FINDINGS: While we know how some vestibular and ocular motor disorders modify visuo-vestibular interaction by changing the 'normal' cortical activation-deactivation patterns, it is still early days in functional magnetic resonance imaging studies of patients with specific disorders. Findings from current brain imaging studies of several vestibular, ocular motor, and cerebellar disorders are presented. SUMMARY: The promise of more insights into the complex neuronal networks of the human cortex is great.