Spontaneous Electrocortical Activity Research Articles

Developmental changes in spontaneous electrocortical activity and network organization from early to late childhood

We investigated the development of spontaneous (resting state) cerebral electric fields and their network organization from early to late childhood in a large community sample of children. Critically, we examined electrocortical maturation across one-year windows rather than creating aggregate averages that can miss subtle maturational trends. We implemented several novel methodological approaches including a more fine grained examination of spectral features across multiple electrodes, the use of phase-lagged functional connectivity to control for the confounding effects of volume conduction and applying topological network analyses to weighted cortical adjacency matrices. Overall, there were major decreases in absolute EEG spectral density (particularly in the slow wave range) across cortical lobes as a function of age. Moreover, the peak of the alpha frequency increased with chronological age and there was a redistribution of relative spectral density toward the higher frequency ranges, consistent with much of the previous literature. There were age differences in long range functional brain connectivity, particularly in the alpha frequency band, culminating in the most dense and spatially variable networks in the oldest children. We discovered age-related reductions in characteristic path lengths, modularity and homogeneity of alpha-band cortical networks from early to late childhood. In summary, there is evidence of large scale reorganization in endogenous brain electric fields from early to late childhood, suggesting reduced signal amplitudes in the presence of more functionally integrated and band limited coordination of neuronal activity across the cerebral cortex.

Arousal transitions in sleep, wakefulness, and anesthesia are characterized by an orderly sequence of cortical events

Many aspects of brain function are influenced by modulatory processes, including arousal. The most abrupt changes in arousal occur at the wake–sleep transition and at the induction of anesthetic conditions. They are accompanied by major electrophysiological changes, including an emergence of low-frequency (sleep-like) activity and a loss of mid-frequency (wake-like) activity that has been linked to feedback processes of the brain. Nevertheless, the causal relationship between these two types of electrophysiological changes, as well as the cortical mechanisms underlying changes in arousal and consciousness, remain poorly understood. To address this, we studied spontaneous electro-cortical activity during arousal changes in macaques. During sleep and at loss of consciousness induced by propofol anesthesia, we identified a prototypical sequence of cortical events in which the loss of mid-frequency activity preceded, by seconds, the increases in low-frequency activity. Furthermore, in visual areas, an influence of mid-frequency change onto high-frequency activity was observed across visual hierarchy. These results are consistent with the notion that drops in arousal and consciousness are facilitated by a release of feedback cortical inhibition.

The Effect of Acute Aerobic Exercise on Spontaneous Brain Activity in Children

The present study examined the immediate effect of a single session of sub maximal exercise on brain activation in children. Twelve 9- to 11-year-old boys pedaled 30 minutes on a cycle ergometer at ~65% of their maximum heart rate maximum. Electrophysiological activity was recorded before physical exercise, and10-, 20- and 30 minutes post-exercise. The results indicated that relative spectral power in the alpha1 band (8-10 Hz) decreased from 10 to 20 minutes post-exercise, and that relative spectral power in the alpha2 band (10-12 Hz) increased 20 and 30 minutes post exercise when compared to pre-exercise measurements. These concomitant changes occurring in the alpha1 and in the alpha2 bands are suggestive of an increased in attentional vigilance. The present results also suggest that a single session of sub maximal exercise produces changes in the spontaneous electro-cortical activity of the brain that last at least 30 minutes post-exercise.

Endogenous Activation of adenosine A 1 receptors promotes post-ischemic electrocortical burst suppression

Following transient global cerebral ischemia (GCI), spontaneous electrocortical activity resumes from the isoelectric line through a sequence of “bursts” of activity alternating with periods of electrical “suppression,” commonly referred to as the post-ischemic burst suppression (BS) pattern. Several lines of evidence suggest that BS reflects an impairment of neocortical connectivity. Here we tested in vivo whether synaptic depression by adenosine A 1 receptor (A 1R) activation contributes to BS patterns following GCI. Male Wistar rats were subjected to 1, 5 or 10 min of GCI using a “four-vessel occlusion” model under chloral hydrate anesthesia. Quantification of BS recovery was carried out using BS ratio. During GCI full electrocortical suppression was attained (BS ratio reached 100%). During the following reperfusion the BS ratio returned to 0. The time course of the decay was exponential after 1 and 5-min GCI and bi-exponential after 10-min GCI. The BS recovery was progressively delayed with the duration of ischemia. Administration of the A 1R antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 1.25 mg/kg i.p.) accelerated the post-ischemic BS recovery for all GCI durations. Following the 10-min GCI the effect of DPCPX was only apparent on the initial fast decay of the BS ratio. These data suggest that endogenous adenosine release promotes BS patterns during reperfusion following transient cerebral ischemia. Furthermore, the endogenous A 1R activation may be the primary underlying cause of post-ischemic BS patterns following brief ischemic episodes. It is likely that synaptic depression by post-ischemic A 1R activation functionally disrupts the connectivity within the cortical networks to an extent that promotes BS patterns.

Endogenous Activation of Adenosine A1 Receptors Accelerates Ischemic Suppression of Spontaneous Electrocortical Activity

Cerebral ischemia induces a rapid suppression of spontaneous brain rhythms prior to major alterations in ionic homeostasis. It was found in vitro during ischemia that the rapidly formed adenosine, resulting from the intracellular breakdown of ATP, may inhibit synaptic transmission via the A(1) receptor subtype. The link between endogenous A(1) receptor activation during ischemia and the suppression of spontaneous electrocortical activity has not yet been established in the intact brain. The aim of this study was to investigate in vivo the effects of A(1) receptor antagonism by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) on the time to electrocortical suppression during global cerebral ischemia. Adult male Wistar rats under chloral hydrate anesthesia were subjected to 1-min transient "four-vessel occlusion" ischemic episodes, separated by 20-min reperfusion. The rats were injected intraperitoneally with either 1.25 mg/kg DPCPX dissolved in 2 ml/kg dimethyl sulfoxide (DMSO) or the same volume of DMSO alone, 15 min before the third ischemic episode. Time to electrocortical suppression was estimated based on the decay of the root mean square of two-channel electrocorticographic recordings. During the first two ischemic episodes, electrocortical suppression appeared after approximately 12 s in both groups. After DMSO administration, ischemic suppression remained unchanged. After DPCPX administration, the time to electrocortical suppression was increased by approximately 10 s, and bursts of activity were recorded during the entire ischemia. These effects disappeared within 15 h after DPCPX administration. Our data provide evidence that during cerebral ischemia endogenous activation of A(1) receptors accelerates the electrical "shut-down" of the whole brain.

Delayed ischemic electrocortical suppression during rapid repeated cerebral ischemia and kainate‐induced seizures in rat

Global cerebral ischemia induces, within seconds, suppression of spontaneous electrocortical activity, partly due to alterations in synaptic transmission. In vitro studies have found that repeated brief hypoxic episodes prolong the persistence of synaptic transmission due to weakened adenosine release. The aim of this study was to investigate in vivo whether the time to ischemic electrocortical suppression (T(ES)) could be altered during energy stress conditions such as rapid repeated global cerebral ischemia and kainate-induced seizures. Experiments were carried out in adult rats under chloral hydrate anaesthesia. Repeated episodes of 1 min of ischemia were induced by transiently clamping the carotid arteries in a 'four-vessel occlusion' model. We devised an automatic method of T(ES) estimation based on the decay of the root mean square of two-channel electrocorticographic recordings. To distinguish the alterations in spontaneous electrocortical activity we compared T(ES) with the ischemic suppression of visual evoked potentials (VEP). During the first ischemic episode, T(ES) was approximately 15 s and remained unchanged when five ischemic episodes were separated by 10-min reperfusion intervals. When ischemia was repeated after 2 min of reperfusion T(ES) progressively increased, reaching a plateau value of approximately 24 s. A similar plateau was reached during kainate-induced seizures. The T(ES) plateau occurred prior to ischemic suppression of VEP. Our data suggest that, under conditions of acute metabolic stress in vivo, the ischemic suppression of spontaneous electrocortical activity may be delayed up to a plateau value. These findings are consistent with the hypothesis of a depletable adenosine pool; however, the restoration of synaptic transmission may be faster in vivo than in vitro.

Onset of insensibility at slaughter in calves: effects of electroplectic seizure and exsanguination on spontaneous electrocortical activity and indices of cerebral metabolism

Cerebral venous and femoral arterial blood samples were collected from 21 young calves either during electrical stunning and recovery or electrical stunning and slaughter by carotid severance or slaughter without stunning. The blood samples were analysed for P O 2 , P C0 2 , pH, glucose and lactate. The results were compared with simultaneous recordings of spontaneous electrocortical ( ECOG) activity. Calves subjected to head-only electrical stunning and slaughter became permanently insensible at the time of the stun. The six calves slaughtered without stunning lost sensibility within 10 seconds. One calf, in which a clot formed in the carotid arteries inhibiting bleeding, maintained some evidence of cortical activity beyond 52 seconds; this was high amplitude low frequency activity and analysis by Fast Fourier Transform showed sensibility was not regained. In the remaining calves the ECOG activity was lost on average within 49±3·5 ( SEM) seconds after slaughter. The cerebral extraction of metabolites increased after carotid severance, indicating inadequacy of cerebral bloodflow after slaughter. No correlations were found between indices of cerebral metabolism and the time of loss of cortical function.

The role of the vertebral arteries in maintaining spontaneous electrocortical activity after electrical stunning and slaughter in calves

This paper examines the role of the vertebral arteries of calves in determining the time to loss of spontaneous electrocortical activity after slaughter by a throat-cut severing the soft tissues of the neck ventral to the spinal column. Four calves with the vertebral arteries ligated took 43 +/- 1.3 s to lose cortical activity after the throat was cut. Four similar animals with intact vertebral arteries and the rostral end of the common carotid arteries clamped immediately after slaughter, to ensure that vertebral blood passed to the brain, took 51 +/-25 s to lose cortical activity. It was concluded that factors other than blood flow from the vertebral arteries contribute to the prolonged time to loss of electrocortical activity after slaughter that has been observed in some calves.

Differentiation between cortical and subcortical lesions following focal ischemia in cats by multimodality evoked potentials

Regional ischemia was induced in cats by occluding the middle cerebral artery. Evoked and spontaneous electrical activity as well as regional cerebral blood flow (rCBF) were recorded with platinum depth macroelectrodes in three primary cortical areas: the auditory cortex (A, middle ectosylvian gyrus) and the front and hind limb somatosensory cortex (SF and SH, lateral and medial posterior sigmoid gyrus). To distinguish among the various evoked potentials after click, median or tibial nerve stimulation, electrical field interactions had to be eliminated using a multiplex stimulation and analysis system. Spontaneous electrocortical activity was evaluated by power spectral analysis. In all areas, evoked potentials were abolished 10 min after arterial occlusion. However, rCBF behaved differently in these regions: it was severely reduced in A, decreased moderately in SF and remained unchanged in SH. The graded reduction of rCBF in the three cortical areas was related to changes in electrophysiological activity during the first minutes of ischemia. In A, auditory potentials were abolished within 3 min after occlusion, whereas in SH, the decrease of somatosensory responses started after about 5 min. In SF, two components of the EP changes were found: an early decrease immediately and a later decrease about 5 min after occlusion. The different rates of EP impairment possibly correspond to two types of ischemia. The fast EP abolishment seems to be caused by local cortical damage whereas the delayed EP decrease probably reflects impairment of subcortical white matter structures. Thus, this method may be useful for distinguishing between gray and white matter ischemia.

Experimental study of intracranial hypertension.

The present investigation was made in rabbits and cats with perfusing mock cerebrospinal fluid into fourth ventriculus to produce experimental diffusion intracranial hypertension. Under normoxia and acute hypoxia conditions, the changes in cerebral blood flow, spontaneous electrocortical activity, direct cortical response, electrocardiogram, blood pressure and cerebral perfusion pressure were measured as intracranial hypertension caused by step elevation and abrupt elevation; at the same time, the relationship mentioned above was also investigated. The experimental results are very important to clinic treatment and to the patients suffering from anoxia with intracranial hypertension.

Corticofugal influences of S1 cortex on ventrobasal thalamic neurons in the awake rat

Corticofugal influences on the responses of 39 ventrobasal (VB) thalamic neurons to repetitive stimuli were studied in awake rats by focally suppressing the evoked and spontaneous electrocortical activity of the primary (S1) somatosensory cortex with magnesium or lidocaine plus magnesium. Suppression of the S1 cortex reduced the number of spikes discharged by 19 (66%) of 29 VB units in response to each of 25 electrical stimuli delivered to the medial lemniscus; 9 units were unaffected and 1 showed an increased response to 1-10 Hz stimuli. The responses of 6 (38%) of 16 VB units to electrical somatic stimuli were also reduced following S1 cortical suppression; 9 units were unaffected and 1 showed an increased response to 20-40 Hz stimuli. A comparison of the reduced responsiveness of 5 units studied during medial lemniscal and somatic stimulation did not reveal any additional response attenuation attributable to subthalamic corticofugal influences. We conclude that, in the awake rat, somatosensory transmission to VB thalamic neurons is primarily facilitated by S1 corticothalamic neurons.

Relations between local microflow and tissue pressure in oxygen of the cerebral cortex in the awake rabbit (1 figure)

Previous experiments (Manil et al., 1983) have revealed spontaneous oscillations of the cortical tissue pressure in oxygen (CTpO2) in a frequency band going from 0.03 to 0.33 Hz. No correlation could be found with the fluctuations of the systemic blood pressure except in stress situation. These oscillations were still present even after the spontaneous electrocortical activity had completely disappeared as a result of deep barbiturate anaesthesia. It was shown that these oscillations had to be attributed to circumscribed areas of the cerebral cortex of about 2 mm. Maximal vasodilation induced by breathing 5% CO2 increased and stabilized the CTpO2. Pharmacological analysis showed that alpha-blocking agents tremendously enhanced this otherwise spontaneous phenomenon. It was thus tempting to attribute this phenomenon to some vasomotor mechanisms. However, it remained to be shown that the oscillations of the CTpO2 were linked to fluctuations of the local microflow.

Brain lactic acidosis and ischemic cell damage: 1. Biochemistry and neurophysiology.

This study explores the influence of severe lactic acidosis in the ischemic rat brain on postischemic recovery of the tissue energy state and neurophysiological parameters. Severe incomplete brain ischemia (cerebral blood flow below 5% of normal) was induced by bilateral carotid artery clamping combined with hypovolemic hypotension. We varied the production of lactate in the tissue by manipulating the blood glucose concentrations. A 30-min period of incomplete ischemia induced in food-deprived animals caused lactate to accumulate to 15-16 mumol g-1 in cortical tissue. Upon recirculation these animals showed: (1) a considerable recovery of the cortical energy state as evaluated from the tissue concentrations of phosphocreatine, ATP, ADP, and AMP; and (2) return of spontaneous electrocortical activity as well as of somatosensory evoked response (SER). In contrast, administration of glucose to food-deprived animals prior to ischemia caused an increase in tissue lactate concentration to about 35 mumol g-1. These animals did not recover energy balance in the tissue and neurophysiological functions did not return. In other experiments the production of lactate during 30 min of complete compression ischemia was increased from about 12 mumol g-1 (normoglycemic animals) to 20-30 mumol g-1 by preischemic hyperglycemia and, in separate animals, combined hypercapnia. The recovery of the cortical energy state upon recirculation was significantly poorer in hyperglycemic animals. It is concluded that a high degree of tissue lactic acidosis during brain ischemia impairs postischemic recovery and that different degrees of tissue lactic acidosis may explain why severe incomplete ischemia, in certain experimental models, is more deleterious than complete brain ischemia.

Neuroelectrical disturbance as indicator of chronic chlordane toxicity

Adult male rats equipped with chronically implanted electrodes were treated with chlordane ip to examine its influence on spontaneous electrocortical activity. Injections of 350 mg/kg resulted in characteristic signs of organochlorine poisoning, culminating in death within 1 hr. Neurotoxic effects of lethal exposure were seen as high-amplitude episodes (400–630 μV) with secondary respiratory waves leading to isoelectric tracings; respiratory depression was therefore implicated in chlordane-induced mortality. EEGs monitored from unanesthetized rats subjected to daily, low-level injections (0.15, 1.75, and 25.0 mg/kg) revealed dose-dependent alterations of brain potentials without behavioral signs of chronic toxicity. Mean spontaneous activity from all montages was significantly increased after 42 days (47–80% above predosage and control values.) Changes included a progressive shift toward fast beta rhythms (>25 Hz), reduction of delta (0.5-3 Hz) and theta (4–7 Hz) frequencies, elevation of amplitude, and replacement of sinusoidal waves by sharp, complex discharges. These changes were directly related to length of exposure, thus implying that chlordane is a cumulative neurotoxin. Starvation and concurrent chlordane treatment interacted synergistically to produce abnormal high-voltage potentials suggestive of lethal cerebral patterns. We interpreted appearance of these slow-wave spikes as evidence of chlordane mobilization from storage depots and subsequent neuroconcentration. Removal of chlordane failed to stimulate recovery of the EEG. Instead, significant deviations from controls continued after 60 days withdrawal. It may be concluded, therefore, that chlordane is a persistent neurotoxin and that electrocerebral disturbance is an early and sensitive indicator of chlordane intoxication.

Determination of the depth and reversibility of post-anoxic coma in animals.

<h2>Abstract</h2> Criteria have been formulated which make it possible to determine the depth and reversibility of post-ischaemic coma, on the basis of data about the functional recovery of the animal brain after circulatory arrest in the whole animal or in the central nervous system. These criteria include: (a) duration of complete circulatory arrest in the brain; (b) latency of recovery of spontaneous respiration and corneal reflexes after the restoration of circulation; (c) latency of recovery of spontaneous electrocortical activity; (d) latency of establishment of continuous electrocortical activity; (e) pattern of EMG recovery in respiratory muscles; (f) particular characteristics of the electrocortical potentials during the early stages of recovery. In experiments on animals these indices allow one to determine the depth and reversibility of brain injuries caused by the arrest of cerebral circulation reliably and rapidly, within 15–30 min after the beginning of resuscitation. The significance of the above experimental data for clinical situations is discussed.

Return of neuronal functions after prolonged cardiac arrest

Cardiociculatory and respiratory arrest of 30 min was produced in normothermic cats by electrical ventricular fibrillation and tracheal occlusion. Resuscitation after cardiac arrest was attempted by open-chest manual heart massage and electrical fibrillation combined with pharmacological treatment of postischemic hypotension. In 8 out of 15 animals spontaneous heart action with systolic arterial blood pressure above 80 mm Hg returned. In these 8 cats cerebral blood flow was temporarily increased and signs of neuronal functions returned: the evoked pyramidal response started to reappear after 5 min, the cortical evoked potentials after 40 min, and spontaneous electrocortical activity after 45 min. Within 6 h the pyramidal response returned to 100%, the evoked potential to 75% and the EEG to 60% of their control amplitudes. In the cats in which systolic blood pressure was below 80 mm Hg, cerebral blood flow was not increased, and signs of functional recovery did not return or returned only transitorily. It is concluded that, with the techniques used, the return of neuronal functions after cardiac arrest is limited by the vulnerability of the heart and not that of the brain.

Brain damage in the rhesus monkey resulting from profound arterial hypotension. II. Changes in the spontaneous and evoked electrical activity of the neocortex

In 15 rhesus monkeys under pentobarbital anaesthesia changes in the spontaneous electrocortical activity and in somatosensory evoked potentials have been studied during and after a period of profound arterial hypotension (whose general physiological correlates and neuropathological consequences have been described in the preceding paper). The stages in the decline and recovery of the electrocorticogram are described. A significant phase of activation was not seen; a relative increase in slow activities was more frequent than an absolute increase; silence occurred after 4–32 min. Spindles were prominent in the 15–120 min required for recovery. No features correlated specifically with the occurrence of focal cortical (arterial boundary zone) lesions. Absence of recovery was seen with diffuse cortical lesions. The decline and recovery of different components of the somatosensory evoked response is described. Study, during hypotension, of the time course of changes in the amplitude of the primary surface-positive wave of the evoked response permits the differentiation of animals that will recover with no brain damage, those that will develop discrete cortical lesions and those that will develop diffuse cortical lesions. The extent of the lesions correlates with the severity of the metabolic deficit as indicated by the evoked potential changes. Recovery of the evoked potentials occurred in about one hour in non-brain-damaged monkeys and in those with relatively small boundary zone lesions but was abnormal in animals with severe neurological disabilities. Animals with diffuse cortical lesions did not regain consciousness and showed some transient recovery of evoked responses at a thalamic level but absence of recovery at the cortical level.

The effect of (+)-tubocurarine chloride and of acute hypotension on electrocortical activity of the cat.

1. The effects of I.V. injection of tubocurarine (3 mg/kg) and of acute hypotension upon electrocortical activity of cats under sodium pentobarbitone were analysed. Technical artifacts associated with changes in brain volume were minimized.2. Initially, the superficial cortical response was reduced by tubocurarine either insignificantly or by 34% or less. Cats bled before injection of tubocurarine showed initially a similar reduction but, occasionally, a severe delayed reduction was found. Any fall in the superficial cortical response started during the secondary rise in B.P., many seconds after the B.P. had reached its lowest initial level. By contrast, spontaneous electrocortical activity was reduced approximately when the peak initial fall of B.P. occurred and it started to recover during the secondary rise in B.P. Reduction of the superficial cortical response could still be elicited after spindling had been suppressed by deep barbiturate anaesthesia. The initial thalamocortical afferent component in somatosensory area I, which was evoked by dorsal column stimulation, was less reduced by injection of tubocurarine than were the post-synaptic positive-negative components.3. The depressant effects of injected tubocurarine upon the superficial cortical response and spindle activity were approximated by rapid arterial bleeding.4. The superficial cortical response was reduced following virtual arrest of the cerebral circulation by acute exsanguination or by acute oil embolization. Such reduction most likely does not depend on systemic transport of inhibitory substances to the brain.5. After injection of tubocurarine the rate of outflow from the superior sagittal sinus was variably reduced during the initial fall in B.P., and often showed a variable, secondary increase. A net deficit in cerebral blood flow was usually present during the period of 80 sec after injection.6. The variability in the effects of injected tubocurarine upon electrocortical activity is attributed to the variability of the net deficit in cerebral blood flow.

The scalp as an electroencephalographic averager

1. 1. Studies are reported on the relative synchrony of EEG rhythms from cats, recorded unilaterally and bilaterally, using scalp-to-scalp, scalp-to-nose, pia-to-pia, and single-contact or multiple-contact pia-to-nose technics. 2. 2. High degrees of bilateral synchrony (72%) were obtained with scalp-to-scalp recording, lasser degrees (47%) with multiple-contact pia-to-nose recording, less yet (44%) with single contact pia-to-nose recording, while the degree of bilateral synchrony with pia-to-pia recording was the poorest of all (10%). 3. 3. Parallel observations were noted in the comparison of recordings obtained simultaneously from scalp and underlying cortex. The larger the number of interconnected cortical electrodes, the more nearly did the cortical trace approximate that recorded from the overlying scalp (80% vs. 52% synchrony; for six contacts and one contact respectively). 4. 4. On the basis of these observations, the scalp has been hypothesized to act as an averager of electrical activity from underlying cortical areas, averaging out the local random rhythms and transmitting the rhythms which are common to and synchronous over relatively large areas. 5. 5. The implications of these studies with respect to the presence of two types of spontaneous electrocortical activity were discussed. The findings were felt to be compatible with the simultaneous presence of ( a) random activity, intrinsic in local cortical regions and perhaps related to local cellular activity, and ( b) widely synchronized (both intra-hemispheric and bilateral) cortical activity, which is presumably under the control of a subcortical “pacemaker”.