Journal of Clinical EEG & Neuroscience, October 2005
|Ultrafast EEG Activities and Their Significance
E. Niedermeyer, Guest Editor
|Paper Recordings of Ultrafast Frequencies in Experimental Epilepsy
|Neural Mechanisms of the Ultrafast Activities
Isamu Ozaki and Isao Hashimoto
|High-Frequency Oscillations in Somatosensory System
Hitoshi Mochizuki and Yoshikazu Ugawa
|High-Frequency Signals (>400 Hz): A New Window in Electrophysiological Analysis of the Somatosensory System
Y. Okada, I. Ikeda, T. Zhang and Y. Wang
|500-1000 Hz Responses in the Somatosensory System: Approaching Generators and Function
|Phase Clustering of High Frequency EEG: MEG Components
Fernando H. Lopes da Silva, Jaime Parra Gomez, Dimitri N. Velis and Stiliyan Kalitzin
|Full-Band EEG (FbEEG): A New Standard For Clinical Electroencephalography
Sampsa Vanhatalo, Juha Voipio and Kai Kaila
|2005 Author and Subject Index||318|
The true frequency range of the EEG is much broader than it has been assumed and taught for decades. The EEG apparatuses with inkwriting pens recording on paper are incapable of giving us trustworthy tracings beyond 80/sec. With the introduction of digital EEG machines, the exploration of the 60 to 1000 Hz range has already begun in the past few years (but, strangely enough, had been in use during the pioneer age when short photographic EEG recordings were made).
The new wave of ultrafast recording began in the domain of somatosensory evoked potentials (SSEP). In the field of EEG (strictly speaking), research work started very recently.
Ultrafast EEG activity promises new insights into the electrophysiological basis of epileptic phenomena. Activities from 150- to 500/sec have been noted in recent studies (including personal work). Faster frequencies (500-1000/sec) are likely to play a major role in the electrophysiology of neurocognition and motor initiation. Such EEG-based neurocognitive studies will provide us with in-real-time data and thus outperform PET scanning and functional MRI.
Even ultrafast EEG activity has its limitation, which appears to lie around 1000/sec. Faster frequencies (1000-3000 Hz) — recorded mainly with cathode ray oscillography — are probably incompatible with the shortest duration of true field potentials and might be nothing but “neuronal chatter.”
Digital EEG technology has facilitated the recording of fast activity above 50 Hz, but previous work carried out in this field is, commonly, no longer referred to in the literature. This paper presents a summary of our experience in experimental epilepsy when frequencies above 100 Hz were recorded. It was shown that conventional recordings (1-70 Hz) do not correlate with the onset of clinical seizures and can actually lead to misleading neurophysiologic conclusions. Ultrafast activity (100-1500 Hz), on the other hand, showed excellent correlation with clinical behavior and pointed to the low brainstem for the origin of nonfocal tonic-clonic seizures. In the animal analogue of absence seizures the cortex, including cingulate gyrus, thalamus, and cerebellum, showed greater involvement than other brain structures.
Ultrafast activity has a very limited electrical field, and evoked responses remain restricted to the corresponding sensory pathways. Focal penicillin administration led not only to spike generation but also to associated ultrafast frequency bursts in that area. It appears likely that ultrafast burst activity may be a better marker for focal cortical epileptogenesis than spikes or sharp waves, which can be transmitted from a distance.
A brief review of previous studies is presented on ultrafast activities > 300 Hz (high frequency oscillations, HFOs) overlying the cortical response in the somatosensory evoked potential (SEP) or magnetic field (SEF). The characteristics of somatosensory HFOs are described in terms of reproducibility and origin (area 3b and 1) of the HFOs, changes during a wake-sleep cycle, effects of higher stimulus rate or tactile interference, etc. Also, several hypotheses on the neural mechanisms of the HFOs are introduced; the early HFO burst is probably generated from action potentials of thalamocortical fibers at the time when they arrive at the area 3b (and 1), since this component is resistant to higher stimulus rate > 10Hz or general anesthesia: by contrast, the late HFO burst is sensitive to higher stimulus rate, reflecting activities of a postsynaptic neural network in the somatosensory cortices, area 3b and 1. As to possible mechanisms of the late HFO burst genesis, an interneuron hypothesis, a fast inhibitory postsynaptic potential (IPSP) hypothesis of the pyramidal cell and a chattering cell hypothesis will be discussed on the basis of physiological and pathological features of the somatosensory HFOs.
The recent revival of interest in high-frequency oscillation (HFO) is triggered by getting an opportunity to noninvasively monitor the timing of highly synchronized and rapidly repeating population spikes generated in the human somatosensory system. HFOs could be recorded from brainstem, cuneothalamic relay neurons, thalamus, thalamocortical radiation, thalamocortical terminals and cortex with deep brain or surface electrodes, or with magnetoencephalography. Here we briefly review the HFOs at each level of somatosensory pathways. HFOs recorded at brainstem might be produced by volume conduction from oscillations of the medial lemniscus. Thalamic HFOs at around 1000 Hz frequency would be generated within the somatosensory thalamus. Cortical HFOs would be generated by at least a few different mechanisms, thalamo-cortical projection terminals, interneurons and pyramidal cells of the primary sensory cortex. HFOs have been studied in several ways: their modulation by arousal changes, movements or drugs, their recovery function, effects of transcranial magnetic stimulation on them and also their changes in patients with various neurological diseases.
High-frequency signals (HFSs) between 400-1500 Hz in Magnetoencephalography (MEG) and Electroencephalography (EEG) provide a new window in electrophysiological analysis of the somatosensory system in humans and in other animals. The HFS in the primary somatosensory (SI) cortex precedes the conventional N20. In the swine model, they appear to be due to spiking in thalamocortical axonal terminals and in the soma and dendrites of cortical neurons. These spiking activities seem to activate slower conductances in the pyramidal cells in layers II-III and V, which give rise to N20. The HFS monitoring may be useful for separately evaluating the electrophysiology of the subcortical and cortical components of the somatosensory pathway.
Spontaneous and stimulus-induced oscillatory EEG activities range over a wide scope of frequencies from 1 Hz to 1 kHz. In the ultrafast domain, trains of 5-10 micro-potentials are superimposed to primary thalamic and cortical components in somtosensory evoked potentials (SEP) as brief bursts of 1000 Hz and 600 Hz, respectively. Over the last years, hypotheses on generators and functions of this frequency-edge of population activity have been elaborated in numerous studies. Here, the relevant findings and ideas were surveyed from the body of literature. Special emphasis was paid to the anatomical and cellular origin of burst SEP, their assumed impact on somatosensory coding and perspectives for scientific as well as clinical applications.
The study of phase consistency of high frequency EEG/MEG components can reveal properties of neuronal networks that are informative about their excitability state. The clue is that these properties are easier to put in evidence when the response of the neuronal networks is evoked by an adequate stimulation paradigm. The latter may be considered a probe of neuronal excitability state capable of revealing hidden information contained in the phase structure of neuronal activities. In this context the high frequency band components appear to be the most reactive signals.
A variety of neuroimaging techniques, such as functional magnetic resonance imaging (fMRI), positron emission tomography (PET) and magnetoencephalography (MEG), have been established during the last few decades, with progressive improvements continuously taking place in the underlying technologies. In contrast to this, the recording bandwidth of the routine clinical EEG (typically around 0.5-50 Hz) that was originally set by trivial technical limitations has remained practically unaltered for over half a decade. An increasing amount of evidence shows that salient EEG signals take place and can be recorded beyond the conventional clinical EEG bandwidth. These physiological and pathological EEG activities range from 0.01 Hz to several hundred Hz, and they have been demonstrated in recordings of spontaneous activity in the preterm human brain, and during epileptic seizures, sleep, as well as in various kinds of cognitive tasks and states in the adult brain. In the present paper, we will describe the practical aspects of recording the full physiological frequency band of the EEG (Full-band EEG; FbEEG), and we review the currently available data on the clinical applications of FbEEG.
Recording the FbEEG is readily attained with commercially available direct-current (DC) coupled amplifiers if the recording setup includes electrodes providing a DC-stable electrode-skin interface. FbEEG does not have trade-offs that would favor any frequency band at the expense of another. We present several arguments showing that elimination of the lower (infraslow) or higher (ultrafast) bands of the EEG frequency spectrum in routine EEG has led, and will lead, to situations where salient and physiologically meaningful features of brain activity remain undetected or become seriously attenuated and distorted. With the currently available electrode, amplifier and data acquisition technology, it is to be expected that FbEEG will become the standard approach in both clinical and basic science.