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[Clinical application of magnetoencephalography for brain infarction].

Magnetoencephalography (MEG) is a noninvasive functional imaging technique that provides information regarding neuronal activity with high spatial resolution. Analyses of spikes and slow waves in various brain disorder have performed using spontaneous magnetic field, and functional mapping studies have performed using evoked magnetic field. The goal of this study was to determine the characteristics of MEG findings in these two magnetic fields for ischemic stroke patients. In the first examination, we recorded the spontaneous magnetic activity with a 37-channel neuromagnetometer and counted the number of equivalent current dipoles (neuromagnetic sources) which were divided into 6 groups with different frequencies of every 4 Hz. There were much more dipoles below 8 Hz in stroke patients than in normal controls, which tended to distribute in the hypoperfusion area near the infarct. In the second examination, we recorded auditory evoked responses for tone burst stimuli and analyzed the localization of dipoles for the 100-m.sec. component after the onset of the stimuli. The dipoles lay near the Heschl gyrus in most of control group. On the contrary, they often distributed apart from the Heschl gyrus in stroke patients with severely damaged regional oxygen metabolism measured by positron emission tomography, indicating an inappropriate response for auditory stimuli. In conclusion, MEG brought interesting informations for the brain function of stroke patients.

Brain↗

Mechanisms of central conduction time prolongation in brain-stem auditory evoked potentials.

The wave I-wave V delay in the auditory brain-stem response is commonly used as a diagnostic tool in otoneurology. Normative values have been established for different populations and different types of stimuli. This I-V delay has been known for some time as "central conduction time" or "central transmission time." This implies that the measure reflects in normal and in pathologic cases delays due to nerve conduction, synaptic transmission, and neural integration and is not caused by cochlear processes. By virtue of the traveling wave delay in the cochlea, amounting to some 4 ms from the base to the "500-Hz place," it is conceivable that this delay contributes to the I-V delay. From a series of 69 pontine angle tumors in which the auditory brain-stem response was recorded, we selected cases with an apparent peripheral origin of a prolonged I-V delay by comparing the whole-click response to responses derived from high-pass noise masking. It seems that cases with an increased I-V delay in the whole-click response but (almost) normal I-V delays in the narrow-band response are indicative of small intracanalicular acoustic neuroma.

Brain Stem↗

Improved wave V resolution by dual-channel brain stem auditory evoked potential recording.

Brain stem auditory evoked potentials were recorded simultaneously from the vertex and ear contralateral to stimulation (Ac-Cz) and from the vertex and ear ipsilateral to stimulation (A1-Cz). There was clearer definition of wave V and less latency variability between trials in Ac-Cz channel recordings, resulting in enhanced wave form stability and greater reproducibility of wave I-V interpeak latencies. The clinical interpretation of dual-channel recordings is currently limited by the complexity of the auditory pathways, but the technique itself shows promise as a routine clinical procedure.

Adolescent↗

The electromicrophysiology of delta waves induced by systemic atropine.

Delta waves in the EEG can be induced by the intravenous administration of atropine. In cats we have investigated with several computer averaging programs the relationship of extracellular unit discharge to the EEG on the surface and within the cortex. We have also studied the laminar profiles and the vertical current density profiles of these slow waves. Our results indicate that surface-positive delta waves are related to events associated with excitation of cortical neurons, while surface-negative delta waves are related to a decreased probability of unit firing suggesting the possibility of inhibition. Laminar analysis of atropine-induced slow waves indicated that these were probably generated by pyramidal cells in a similar way to delta waves induced by brain lesions. These results suggest that a disturbance in cholinergic input to the cortex might be responsible for delta waves in the EEG.

Animals↗

Adaptations and pathologies linked to dynamic stabilization of neural circuitry.

Brain circuits for infrequently employed memories are reinforced largely during sleep by self-induced, electrical slow-waves, a process referred to as "dynamic stabilization" (DS). The essence of waking brain function in the absence of volitional activity is sensory input processing, an enormous amount of which is visual. These two functions: circuit reinforcement by DS and sensory information processing come into conflict when both occur at a high level, a conflict that may have been the selective pressure for sleep's origin. As brain waves are absent at the low temperatures of deep torpor, essential circuitry of hibernating small mammals would lose its competence if the animals did not warm up periodically to temperatures allowing sleep and circuit reinforcement. Blind, cave-dwelling vertebrates require no sleep because their sensory processing does not interfere with DS. Nor does such interference arise in continuously-swimming fishes, whose need to process visual information is reduced greatly by life in visually relatively featureless, pelagic habitats, and by schooling. Dreams are believed to have their origin in DS of memory circuits. They are thought to have illusory content when the circuits are partially degraded (incompetent), with synaptic efficacies weakened through infrequent use. Partially degraded circuits arise normally in the course of synaptic efficacy decay, or pathologically through abnormal regimens of DS. Organic delirium may result from breakdown of normal regimens of DS of circuitry during sleep, leaving many circuits incompetent. Activation of incompetent circuits during wakefulness apparently produces delirium and hallucinations. Some epileptic seizures may be induced by abnormal regimens of DS of motor circuitry. Regimens of remedial DS during seizures induced by electroconvulsive therapy (ECT) apparently produce temporary remission of delirium by restoring functional or 'dedicated' synaptic efficacies in incompetent circuitry. Sparing of sensory circuitry in fatal familial insomnia seemingly owes to supernormal circuit use in the virtual absence of sleep. ECT shocks and cardioverter defibrillation may have analogous remedial influences.

Adaptation, Psychological↗

[The effect of volatile anesthetics on EEG, auditory evoked potentials and somatosensory evoked potentials in dogs].

We compared the changes in EEG and evoked potentials among dogs anesthetized with halothane (H), isoflurane (I) or enflurane (E). The mean frequency of EEG with H was higher than that with I and E at 1 and 2 MAC. The amplitude of the 5th wave of auditory brain stem response with H was larger than that with I and E at 2 MAC. In terms of the Pa wave of auditory middle latency response, the amplitude with H was larger than that with E at 1 MAC, and the incidence of the wave with H was higher than that with I and E at 2 MAC. The amplitudes of N2 and N3 waves of somatosensory evoked potentials with H and I tended to decrease with increasing MAC, whereas those with E increased temporarily at 1 MAC. The inhibitory effects on EEG and evoked potentials were different among three volatile anesthetics.

Anesthetics, Inhalation↗

The effect of broadband noise on the human brain-stem auditory evoked response. IV. Additivity of forward-masking and rate-induced wave V latency shifts.

The additivity of forward masking and repetitive stimulation effects on wave V of the brain-stem auditory evoked response (BAER) was investigated. The effects of repetitive stimulation were evaluated for a stimulus train (called the adaptation series), with a 12.5-ms within-train interclick interval. The forward masker was a 100-ms, 80-dB SPL broadband noise with forward-masker intervals ranging from 12.5-87.5 ms. Forward masking and repetitive stimulation increased the latency of wave V of the BAER. The combined forward masking/adaptation series produced less wave V latency shift than the summed individual effects. Forward masking reduced wave V amplitude at brief forward masker intervals, while repetitive stimulation did not affect wave V amplitude. Wave V amplitude was decreased for the combined forward masking/adaptation series, and the time course of amplitude recovery of the combination was prolonged compared to the forward masking alone condition. The nonadditivity of forward masking and rate effects on wave V latency is similar to that found for repetitive stimulation and simultaneous masking [Burkard and Hecox, J. Acoust. Soc. Am. 74, 1204-1213 (1983)]. These findings are consistent with the position that forward masking and rate effects on wave V latency are produced by overlapping mechanisms.

Adult↗

Effects of pulsed and continuous wave 902 MHz mobile phone exposure on brain oscillatory activity during cognitive processing.

The aim of the current double-blind studies was to partially replicate the studies by Krause et al. [2000ab, 2004] and to further investigate the possible effects of electromagnetic fields (EMF) emitted by mobile phones (MP) on the event-related desynchronisation/synchronisation (ERD/ERS) EEG (electroencephalogram) responses during cognitive processing. Two groups, both consisting of 36 male participants, were recruited. One group performed an auditory memory task and the other performed a visual working memory task in six exposure conditions: SHAM (no EMF), CW (continuous wave EMF) and PM (pulse modulated EMF) during both left- and right-side exposure, while the EEG was recorded. In line with our previous studies, we observed that the exposure to EMF had modest effects on brain oscillatory responses in the alpha frequency range ( approximately 8-12 Hz) and had no effects on the behavioural measures. The effects on the EEG were, however, varying, unsystematic and inconsistent with previous reports. We conclude that the effects of EMF on brain oscillatory responses may be subtle, variable and difficult to replicate for unknown reasons.

Acoustic Stimulation↗

Brain perfusion monitoring with frequency-domain and continuous-wave near-infrared spectroscopy: a cross-correlation study in newborn piglets.

The newborn piglet brain model was used to correlate continuous-wave (CW) and frequency-domain (FD) near-infrared spectroscopy. Six ventilated and instrumented newborn piglets were subjected to a series of manipulations in blood oxygenation with the effects on brain perfusion known to be associated with brain hypoxia-ischaemia. An excellent agreement between the CW and FD was demonstrated. This agreement improved when the scattering properties (determined by the FD device) were employed to calculate the differential pathlength factor, an important step in CW data processing.

Animals↗

Operant controlled neural event: formal and systematic approach to electrical coding of behavior in brain.

Traditional studies of electrophysiological correlates of behavior contain inherent high variability resulting from the arbitrary choice of behaviors, brain locations, and wave parameters. The operant control of neural events is a formal and systematic approach to the study of prespecified parameters and components of brain activity as they encode behaviors. Two studies in which the electrical activity of brain was the criterion for reinforcement demonstrate the acquisition, under such operant control, of two mutually exclusive behaviors or states which selectively alter evoked potential components.

Animals↗

[Variability of V waves of auditory evoked potentials in patients with supratentorial transverse displacement of the brain caused by intracranial hematoma].

The authors present a comparative analysis of the characteristics of the V wave of the brain stem auditory evoked potentials in relation to the degree of transverse shifting of the third ventricle. The investigations were carried out in 48 patients with non-traumatic intracerebral haematoma. A high correlation was found between the size of the amplitude and ventricle shift. No such correlation was observed with the interpeak time of the I--V waves.

Adult↗

Effect of aminophylline and relief from hypoxia on central sleep apnoea due to medullary damage.

A 17-year old boy presented with severe, predominantly central sleep apnoeas secondary to structural damage in the medulla. At low O2 saturation, the electroencephalogram showed the sudden onset of slow waves. Hypercapnic ventilatory response was low and hypoxic ventilatory response was absent. Low flow oxygen therapy dramatically improved the apnoea score, probably by relieving hypoxic brain depression. Slow waves also disappeared with oxygen therapy. Aminophylline was effective on apnoea score and duration (p less than 0.001). This beneficial effect could be explained by an improvement of the normal oscillations of respiration at the onset of sleep, a change in arousability or a stimulation of the ascending reticular system. These findings suggest a possible role of hypoxic depression in the manifestations of central sleep apnoeas and demonstrate the beneficial effect of low flow oxygen and aminophylline in treating certain central sleep apnoeas.

Adolescent↗

[Brain contusion: morphology, pathogenesis and treatment].

Focal cerebral contusions can be dynamic and expansive, leading to a delayed neurological deterioration. In head--injured patients, the rise in intracranial pressure (ICP), subsequent to uncontrollable swelling, is the only and the most frequent cause of death. Studies show that brain swelling, after traumatic brain injury (TBI), is caused by brain edema rather than cerebral blood volume (CBV). CBV is reduced in proportion to cerebral blood flow (CBF) reduction, following a severe TBI. Cerebrovascular damages, leading to subsequent reductions in regional CBF, may play an important role in secondary cell damages following TBI. The histological examination revealed the formation of microthrombosis in the contused area, extending from the center to the peripheral areas within 6 hours after injury. In the pericontusional zone and surrounding parenchyma, vasoresponsivity may be nearly three times normal, which suggests hypersensitivity to hyperventilation and other phenomena. Glutamate is the most widely distributed excitatory neurotransmitter in the mammalian brain. However, when glutamate is present in excessive quantities, it may overactivate specific ion channels, especially the N-methyl-D-aspartate channel. A shift of potassium into the extracellular space will result in rapid swelling of astrocytes, which absorb quantities of potassium to preserve ionic homeostasis. This process may cause rapid cytotoxic edema, which is probably, a major factor in causation of posttraumatic raised ICP. The presence of a focal contusion and primary or secondary ischemic events were the clinical features most strongly correlated with high dialysate of glutamate. Raised ICP was significantly more common, and outcome was worse in patients with high levels of glutamate. Contusion is a key factor in the development of blood brain barrier (BBB) permeability. BBB endures at least 7 days post TBI. Biphasing opening of the BBB, following head trauma and a possible second wave of secondary brain damage, was confirmed. Brain tissue pO2 monitoring might become an important tool in the treatment regime for TBI patients. Histologically the loss of CA3 pyramidal cells in the hippocampus was observed ipsilaterally in the cortical contusion and bilaterally in diffuse axonal injury. Aggressive, early hyperventilation after TBI augments neuronal death in CA3 hippocampus. Due to high mortality associated with such cerebral contusions, a standard practice has evolved into evacuating contusions in patients who had deterioration in the level of consciousness, lesions more than 30 sec and CT suggestion of raised ICP.

Blood-Brain Barrier↗

Oscillations in the insect brain: do they correspond to the cortical gamma-waves of vertebrates?

gamma-waves, relatively high-frequency oscillations (30-80 Hz) that can be recorded in the olfactory system and the visual cortex of vertebrates, have recently attracted much attention. A role as an information carrier is under discussion, a possible involvement in "feature linking" has been suggested, and they have also been implicated functionally in phenomena such as mind consciousness or awareness. It has long been known that stimulus-dependent high-frequency oscillations (hf waves) can also be recorded from the optic lobes of arthropods. These oscillations in flies have been examined and found to be analogous to the gamma-waves in many respects. Based on knowledge of the anatomy and physiology of the visual system in flies, the most plausible interpretation of the function of these oscillations differs from the interpretations of the vertebrate gamma-waves currently under consideration.

Animals↗

Brain-stem monitoring. II. Preterminal BAEP changes observed until brain death in deeply comatose patients.

Preterminal BAEP changes were studied until brain death in 8 head-injured patients out of a series of 38 comas monitored by means of a system allowing high-rate sequential recording. Two different modalities of BAEP degradation were disclosed: (1) simultaneous latency increase of all components associated with a decrease of cerebral perfusion pressure (CPP), consistent with ongoing ischaemia of the posterior fossa; (2) deterioration of brain-stem components (waves III-V) with preserved or even enhanced wave I. The latter pattern was not consistently associated with any haemodynamic change and might be related to mechanical factors causing rostro-caudal deterioration of brain-stem function. The time course of BAEP degradation ranged from a few minutes to more than 10 h. In the case of slow preterminal evolution definitely pathological trends were identified even when individual BAEPs were still within normal limits. Such trends would have remained unnoticed in single BAEP records. Hypothermia and anaesthetic drugs were found to induce falsely alarming BAEP changes very similar to those seen during preterminal evolution. Our results suggest that continuous brain-stem monitoring could be helpful for management of comatose head-injured patients.

Blood Pressure↗

Relationship between brain glucose metabolism positron emission tomography (PET) and electroencephalography (EEG) in children with continuous spike-and-wave activity during slow-wave sleep.

We studied the relationship between brain glucose metabolism patterns and objectively measured interictal epileptiform abnormalities in six children with intractable epilepsy and continuous spike-and-wave activity during slow-wave sleep. Five of the six patients showed lateralized positron emission tomographic (PET) findings, with the hemisphere showing a relative increase in glucose metabolism concordant with the presumed origin of the generalized interictal spike activity delineated by quantitative electroencephalographic (EEG) analysis. One of these five patients achieved seizure freedom following cortical resection involving the areas of unilateral multifocal hypermetabolism, and another patient has been approved for cortical resection. The results in the present study add further support to the hypothesis that the generalized spike-waves in most cases of continuous spike-and-wave activity during slow-wave sleep are the result of secondary bilateral synchrony. Resective surgery can be effective in selected patients with uncontrolled seizures associated with continuous spike-and-wave activity during slow-wave sleep provided that there is concordance between focal abnormalities on PET and EEG.

Brain Chemistry↗

Alzheimer's disease Braak Stage progressions: reexamined and redefined as Borrelia infection transmission through neural circuits.

Brain structure in health is a dynamic energized equation incorporating chemistry, neuronal structure, and circuitry components. The chemistry "piece" is represented by multiple neurotransmitters such as Acetylcholine, Serotonin, and Dopamine. The neuronal structure "piece" incorporates synapses and their connections. And finally circuits of neurons establish "architectural blueprints" of anatomic wiring diagrams of the higher order of brain neuron organizations. In Alzheimer's disease, there are progressive losses in all of these components. Brain structure crumbles. The deterioration in Alzheimer's is ordered, reproducible, and stepwise. Drs. Braak and Braak have described stages in the Alzheimer disease continuum. "Progressions" through Braak Stages benchmark "Regressions" in Cognitive function. Under the microscope, the Stages of Braak commence in brain regions near to the hippocampus, and over time, like a tsunami wave of destruction, overturn healthy brain regions, with neurofibrillary tangle damaged neurons "marching" through the temporal lobe, neocortex and occipital cortex. In effect the destruction ascends from the limbic regions to progressively destroy the higher brain centers. Rabies infection also "begins low and finishes high" in its wave of destruction of brain tissue. Herpes Zoster infections offer the paradigm of clinical latency of infection inside of nerves before the "marching commences". Varicella Zoster virus enters neurons in the pediatric years. Dormant virus remains inside the neurons for 50-80 years, tissue damage late in life (shingles) demonstrates the "march of the infection" down neural pathways (dermatomes) as linear areas of painful blisters loaded with virus from a childhood infection. Amalgamation of Zoster with Rabies models produces a hybrid model to explain all of the Braak Stages of Alzheimer's disease under a new paradigm, namely "Alzheimer's neuroborreliosis" in which latent Borrelia infections ascend neural circuits through the hippocampus to the higher brain centers, creating a trail of neurofibrillary tangle injured neurons in neural circuits of cholinergic neurons by transsynaptic transmission of infection from nerve to nerve.

Alzheimer Disease↗

From periodic travelling waves to travelling fronts in the spike-diffuse-spike model of dendritic waves.

In the vertebrate brain excitatory synaptic contacts typically occur on the tiny evaginations of neuron dendritic surface known as dendritic spines. There is clear evidence that spine heads are endowed with voltage-dependent excitable channels and that action potentials invade spines. Computational models are being increasingly used to gain insight into the functional significance of a spine with an excitable membrane. The spike-diffuse-spike (SDS) model is one such model that admits to a relatively straightforward mathematical analysis. In this paper we demonstrate that not only can the SDS model support solitary travelling pulses, already observed numerically in more detailed biophysical models, but that it has periodic travelling wave solutions. The exact mathematical treatment of periodic travelling waves in the SDS model is used, within a kinematic framework, to predict the existence of connections between two periodic spike trains of different interspike interval. The associated wave front in the sequence of interspike intervals travels with a constant velocity without degradation of shape, and might therefore be used for the robust encoding of information.

Action Potentials↗