[Peculiarities of the distribution of pulse waves in the cranial vessels in pathology of the major arteries of the brain].
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In anaesthetized dogs blood pressure (BP), carotid artery flow (CAF), oxygen tension of arterial blood (paO2) and brain surface (bs-pO2), ECG, frequency analyzed EEG were measured and/or recorded. The changes in these parameters were detected before and during ventricular fibrillation with external and direct heart massage as well as after defibrillation. Comparisons were made between the effect of oxygen and room air ventilation. The ratio of successful resuscitation was 88% with direct heart massage and O2 respiration, 76% with external thoracic massage and O2 ventilation, and 68% with external massage combined with room air respiration. The highest BP and CAF could be achieved with direct heart massage. The results suggest that the minimal requirement for success is to achieve a BP of 5 kPa (40 mmHg) and 13 ml/min CAF. In dogs with large and stiff thorax this minimal pressure and flow could not be attained. During effective massage with room air ventilation brain surface pO2 increases moderately, but with O2-respiration it returns to normal. Small or no changes in bs-pO2 indicates unfavourable prognosis. The start bs-pO2 elevation coincides with the reappearance of the first EEG waves, while pO2 increase on the brain surface precedes the normalization of EEG.
Two experiments were conducted to investigate the degree of semantic processing for unattended words. In a dichotic listening task, each participant was required to attend selectively to either a word sequence in one ear or a speech passage in the opposite ear. The selective listening was confirmed by attenuated P1-N1 and N400 waves of the event-related brain potential to unattended words. The N400 attenuation with semantic priming was observed only for attended words. In a following recognition test with a booklet and auditory presentation, the percentage of false alarms for "new" words (or lures) semantically related to "old" words was higher when the "old" words were attended in selective listening than when unattended. These findings suggest that selective attention can act before and/or at a level of semantic processing.
The aim of this project was to study respiration, circulation, and brain activity in pigs during and after a blast wave exposure. Ten anesthetized pigs were used. Seven were exposed to blast and three were controls. Physiological parameters of respiration and circulation as well as cortical activity were followed from 30 minutes before until 120 minutes after the real or simulated blast. There were no significant changes in heart rhythm, cardiac output, arterial oxygen or carbon dioxide tension, blood pH, or mixed venous saturation during the experiment. The blast exposure caused intestinal injuries but no lung damage. A transient flattening of the electroencephalogram was seen immediately after the blast in four experimental animals, in contrast to the unchanged baseline electroencephalogram of the control animals. This momentary depression of cortical activity accompanied by short-lasting apnea indicates a blast wave-induced effect on the brainstem or higher controlling center.
The correlation between brain activity and cerebral blood flow velocities during brief bursts of generalized spike and wave activity was analysed by simultaneous registration of the EEG and the intracranial flow patterns. The flow patterns of the middle cerebral artery were continuously recorded by means of transcranial Doppler ultrasonography using a specially developed monitoring system. A total of 25 bursts was investigated in 3 patients with spontaneous occurrence of generalized 3 Hz spike and wave activity and normal background EEG. Characteristic changes of the flow patterns were found in all cases: 3.41 +/- 0.98 s (n = 25) after the beginning of generalized spike and wave patterns, the flow velocity decreased by 25.84 +/- 10.45% (n = 25) below the 'preictal' flow velocity level. The period of flow velocity changes lasted several times longer than the phase of spike and wave activity.
Coordinates and moments of equivalent sources of various kinds of slow activity--local, generalized and synchronous (delta- or theta-ranges) -- were estimated on a computer on the basis of a model of single equivalent dipole, by the method of the coordinates descent. Investigation of local delta-activity caused by a volume process in the brain shows that its localization coincides with the peripheral zone of the tumour. Localization of the delta-focus enables to indicate its position not only on the surface, but in the depth of the brain as well. The dipole localization method helps to specify the concept of "secondary" slow waves and to differentiate slow activity of total brain-, brain-stem and local nature.
The peculiarities of the development of spontaneous fluctuations of the c.s.f. pressure (CSFP) (B- and plato-waves) in the early postoperative period in 169 neurosurgical patients were studied according to the location of the pathological process and the severity of the clinical condition. The dependence between the CSPF spontaneous fluctuations, the changes of intracerebral pressure, and the dynamics of bioelectrical activity of the brain was studied. The development of spontaneous wave CSFP fluctuations was found to be dependent on the location of the tumor and the severity of the clinical condition. These fluctuations occurred most frequently in patients who were in a critical state (12-8 marks on Glasgow's scale) with the process located in the diencephalo-stem brain areas. A hypothesis is suggested, according to which the cause of the wave CSFP fluctuations of the B-wave type is connected with the change of the vasomotor center to the cyclic regimen of work: the neurogenic change of the vascular tonus, causing in succession constriction and dilatation of the vessels, leads to rhythmic CSFP oscillations. CSFP plato-waves occur in cases in which the constriction phase fails to appear after the dilatation phase, i.e., the tonic pressor effect of the vasomotor center does not occur, which may be due to its exhaustion. In death of the brain and in terminal states the vasomotor center loses the ability to cause neurogenic regulation of the vascular tonus, to provide the pressor effect in particular, which leads to the disappearance of spontaneous CSFP fluctuations.
The induction of temperature elevation by focused ultrasound is a noninvasive surgical technique for destroying tissue. This technique has been used clinically in soft tissues such as liver, prostate and breast. It has long been desired to extend this technique to noninvasive treatment of brain tumors. Although the skull was once thought to be an unsurpassable barrier to focused ultrasound treatment, it has been shown that the distortion caused by the skull can be corrected to produce a useful intracranial focus. However, the attenuation experienced by the ultrasound in passing through cranial bone is large, and consequently the skull is subject to the deposition of acoustic energy as heat. The nature and extent of this heating process has been difficult to characterize empirically. It is practically difficult to implant a sufficient number of thermocouples to obtain detailed temperature data directly, and bone is an unsuitable medium in which to perform noninvasive thermometry using proton chemical shift magnetic resonance imaging. Furthermore, skull specimens used experimentally lack active blood perfusion of the skull and the overlying scalp. This paper describes the use of large-scale acoustic and thermal simulations to calculate the distribution of temperature within the skull and brain that can be expected to occur during therapeutically useful focused ultrasound sonications of the brain. The results demonstrate that standing waves may be formed within the skull during transcranial sonication leading to nonuniform skull heating. However, the results also show that these effects can be sufficiently controlled to allow therapeutic ultrasound to be focused in the cranial base region of the brain without causing thermal damage to the scalp, skull or outer surface of the brain.
Changes in auditory brain stem responses were serially investigated in a patient with downward transtentorial herniation due to acute obstructive hydrocephalus to correlate the neurological signs with the results of computerized tomography. Neurological deterioration correlated highly with disruption of auditory brain stem responses, especially with that of the components of waves V to VII. A noninvasive technique, the measurement of auditory brain stem responses is thought to be useful in detecting the severity of downward transtentorial herniation and in estimating the recovery of brain stem function after surgical treatment of intracranial hypertension.
Laser Raman spectroscopy has not been applied to brain tissue. However, this method can possibly analyze the constituent elements of living tissue of cellular and molecular level easily, and this might be essential for further brain research. I attempted to analyze the water content of brain tissues, which was measured by Raman spectrum of CH and OH groups, in normal and edematous rat brain tissues. The experimental results indicated that the peak intensity of CH group originated from protein, 2935 cm-1 in wave number, was constant in normal, dried and edematous brain tissue. Therefore it could be used as internal standard. As the peak intensity of OH group, 3390 cm-1 in wave number, was originated from water, the relative amount of water content in the brain tissues could be evaluated by OH/CH value. The OH/CH value was not significantly different between the cortex and the thalamus, but it was significantly higher in the gray matter (thalamus) than in the white matter (pons). The OH/CH value was decreased in dried specimens. In experimental edematous brain tissues, which was produced by intraperitoneal injection of organic tin, the OH/CH value was evidently increased in the thalamus but not much changed in the pons. This results were well compatible with cytotoxic edema, which was reported to be produced by organic tin. It is suggested that laser Raman spectroscopy can be used for brain edema research as one of the strong weapon, in analyzing water content of brain tissues on a cellular level.
Rats deprived of D-state sleep (and, to some extent, of slow-wave sleep) for 96 hours show a significant fall in brain acetylcholine in the telencephalon; there were no significant changes in the diencephalon and brain stem. Restraint stress and activity wheel stress produced no significant change in acetylcholine levels in any of these regions; the telencephalic response to sleep deprivation, therefore, cannot be attributed to nonspecific stress. The effects of D-state deprivation and the psychoactive anticholinergic drugs on telencephalic acetylcholine levels are similar.
Human DNA microarrays are used to study the spatiotemporal patterns of gene expression during the course of fetal monkey brain development. The 444 most dynamically expressed genes in four major brain areas are reported at five different fetal ages. The spatiotemporal profiles of gene expression show both regional specificity as well as waves of gene expression across the developing brain. These patterns of expression are used to identify statistically significant clusters of co-regulated genes. This study demonstrates for the first time in the primate the relevance, timing, and spatial locations of expression for many developmental genes identified in other animals and provides clues to the functions of many unknowns. Two different microarray platforms are used to provide high-throughput cross validation of the most important gene expression changes. These results may lead to new understanding of brain development and new strategies for treating and repairing disorders of brain function.
OBJECTIVE: To investigate the methods of evaluating brain death accurately and objectively. METHODS: Various kinds of clinical examination [including conscious state, Glasgow coma score (GCS), brain stem reflection, cranial nerve dominated actions, spinal reflection, spinal nerve dominated automatic action, respiratory and apnea testing] and laboratory methods [such as electroencephalography (EEG), brainstem auditory evoked potentral (BAEP), brainstem auditory sensery evoked potentral (SLSEP) and transeranial Doppler (TCD)] were used to evaluate 11 cases with brain death. RESULTS: Eleven cases presenting with deep coma were conssedered to have brain death. All of them had GCS score of 3 and disappearance of brain stem reflection and cranial nerve dominated automatic action. Six of them patients showed anisocoria. Nine of them pharyngeal reflex could not be detected because of tracheal cannulization, but this did not influence the evaluation of brain death. None of them showed "flat" EEG and disappearience of BAEP dominant wave. None of the SLSEP show any wave behind N13. TCD showed blood stream characteristic of brain death except in one case blood stream characteristic of increased intracraniai pressure. Apnea test and atropine test provided the final proof brain death. The former had more influence on heart rate, blood pressure and oxygen saturation while the latter were more safe and reliable. CONCLUSION: Combined and continuous observation of clinical and laboratory indices can enhance the accuracy of the evaluation of brain death.
Since the cerebral cortex is deeply infolded (to provide a large surface area) and the celerity of neuropropagation across Golgi's layer 1 (the 'molecular feltwork' of the outer brain) has the slowest rate possible in living tissue, we suggest that consciousness, sentience and cognition are wave interference phenomena related to electroencephalographic (EEG) 'rhythms' that appear and disappear for physical reasons. To investigate this proposition, we have likened the outermost layer of the cerebral cortex to the surface of a pond, on which 'brainwaves' can travel and interfere with one another in the holographic mode to convert the neuroelectric patterns on its surface into virtual images and thoughts. We are unconscious when no waves are present, and remain so when the waves are too widely spaced to produce continuous activity on the brain's outer surface. But, as that wave-spacing decreases (i.e. EEG frequency rises), we experience REM sleep and dreams, then awareness, alertness and heightened sentience and cognition until we reach an upper state of unconsciousness when there is no longer time for our brain to be renourished during the refractory period of its neurons. These physical results may be hard to accept, but they account for the limits of consciousness (discussed quantitatively later on) and show why thoughts can seem like frequency-dependent 'phantoms of the brain'. They arise, as a virtual aspect of real biologic processes, from patterns of neurodischarge on the paleo- and neo-cortices which engender (respectively) the somatic and carnal realisms of our mind and the abstract creations of our intellect.
Spike-wave seizures are often considered a relatively "pure" form of epilepsy, with a uniform defect present in all patients and involvement of the whole brain homogeneously. Here, we present evidence against these common misconceptions. Rather than a uniform disorder, spike-wave rhythms arise from the normal inherent network properties of brain excitatory and inhibitory circuits, where they can be provoked by many different insults in several different brain networks. Here we discuss several different cellular and molecular mechanisms that may contribute to the generation of spike-wave seizures, particularly in idiopathic generalized epilepsy. In addition, we discuss growing evidence that electrical, neuroimaging, and molecular changes in spike-wave seizures do not involve the entire brain homogeneously. Rather, spike-wave discharges occur selectively in some thalamocortical networks, while sparing others. It is hoped that improved understanding of the heterogeneous defects and selective brain regions involved will ultimately lead to more effective treatments for spike-wave seizures.
We have developed methodologies for identifying mRNAs with highly restricted expression within the brain. One postnatal-onset mRNA, restricted to sparse GABAergic interneurons of the cerebral cortex and hippocampus, encodes preprocortistatin, the precursor of a 14-residue peptide that shares 11 amino acids with somatostatin. Cortistatin binds to all five cloned somatostatin receptors when they are expressed in transfected cells and depresses neuronal activity, but, unlike somatostatin, it reduces locomotor activity and induces slow-wave sleep. Cortistatin, whose mRNA accumulates during sleep deprivation, apparently acts by antagonizing the effects of acetylcholine on cortical excitability, thereby causing synchronization brain slow waves. A single amino acid difference with somatostatin accounts for the dramatic differences in the effects of the two peptides on physiology and behavior. A second postnatal-onset mRNA, restricted to 1100 large neuronal cell bodies of the dorsal-lateral hypothalamus, encodes preprohypocretin, the precursor of two peptides that share homology with each other and with members of the secretin peptide family. The peptides are detected immunohistochemically in secretory vesicles at synapses of fibers that project to posterior hypothalamus and diverse targets in other brain regions. The peptides are excitatory when applied to cultured hypothalamic neurons. Recent studies by Sakurai and colleagues (1998) have identified the hypocretin peptides (called the orexins by those workers) as ligands for two orphan receptors at which they stimulate food-intake behavior. Sakurai and collaborators showed that the mRNA for these peptides accumulates during food deprivation. The hypocretin projections suggest additional homeostatic roles for the peptides. These studies suggest the common mechanism of regulation for necessary, but voluntary, behaviors (sleep and feeding) by transcription-based accumulation of peptide transmitters that create a pressure for the voluntary activities.
To determine the site of action of the sleep-promoting effect of interleukin-1 (IL-1), we continuously infused (between 11 P.M. and 5 A.M.) murine recombinant IL-1beta into seven different locations in the ventricular and subarachnoid systems of the brain in freely moving rats. When IL-1 was infused at 10 ng/6 hr into the subarachnoid space underlying the ventral surface of the rostral basal forebrain, which previously was defined as the "prostaglandin (PG) D2-sensitive sleep-promoting zone" (PGD2-SZ), the total amount of slow-wave sleep (SWS) increased by 110.7 min (IL-1 was 208.1 +/- 14.3 min vs control at 97.4 +/- 9.3 min; n = 8; p < 0.01 by paired Student's t test) from the baseline control level obtained under continuous infusion of saline vehicle. The hourly SWS during the infusion period reached the level of daytime SWS, the physiological maximum, whereas paradoxical sleep (PS) was decreased transiently. This site of action for the SWS promotion was dissociated from the site in the third ventricle sensitive to the IL-1-mediated PS suppression, fever, and anorexia. The SWS increase caused by IL-1 infusion into the PGD2-SZ was blocked completely by coadministered diclofenac, a nonselective cyclooxygenase (COX) inhibitor. Pretreatment of rats with NS-398 or piroxicam (3 mg/kg of body weight, i.p.), which are said, respectively, to possess high and relative specificity for the COX-2 enzyme, also blocked the SWS-promoting effect of IL-1. We present a hypothesis that IL-1 induces SWS, at least in part, via COX-2-mediated PG production in the PGD2-SZ.
Neurotoxicity induced by interferon (IFN) is revealed by neurobehavioral changes, such as irritability, somnolence, lack of motivation, and delayed ideation. As these side effects persist throughout IFN-alpha treatment, we studied cerebral mapped auditory evoked potentials (MAEP) in 20 hepatitis C virus antibody (HCV Ab)-positive chronic active hepatitis patients before and after administration of leukocyte IFN-alpha (i.m. 3,000,000 IU). Some of the main components of MAEP, such as morphology, latency, and power spectra, were altered before IFN injection. These parameters changed 7 h after administration as revealed by increased quality and quantity of acoustic signal reaching the brain cortex and appearance of physiologic waves in patients with mild/intermediate liver disease. These effects revealed 48 h after IFN administration.