Brain oscillations are still a mystery. The human dominant rhythm is in the alpha band, with a peak at 10 Hz, although each of us has an individual alpha peak frequency, usually referred to as IAF. Among the quantitative EEG parameters, IAF is regarded to be the best indicator of maturation, has the highest heritability level, and can serve as an indicator of pathology. It is further assumed that different narrow alpha band frequencies are associated with attention—suppression of irrelevant stimuli and selection of relevant information. Below alpha is theta – dominant in animals, and thought to be related to memory processes with a frontal/parietal distinction for attention and storage. Another aspect of theta and the lower delta is in cross frequency coupling, where the lower frequencies act as a gating mechanism, providing optimal neural conditions for specific processing assumed involved in binding. The association delta-beta and theta gamma, are assumed to be related to topographically more distant and/or more narrow coupling activity. The topic is extreme complex. Some up to date articles might give you a better understanding:

Arnal LH and Giraud AL (2012). Cortical oscillations and sensory predictions. Trends in Cognitive Sciences July, Vol. 16, No. 7. 390-398

Klimesch, W (2012). Alpha-band oscillations, attention, and controlled access to stored information. Trends in Cognitive Sciences December, Vol. 16, No. 12, 607-617

Sauseng et al., (2010). Control mechanisms in working memory: A possible function of EEG theta oscillations. Neuroscience and Biobehavioral Reviews 34 1015–1022

Canolty, RT and Knight RT (2010). The functional role of cross-frequency coupling. Trends in Cognitive Sciences, November, Vol. 14, No. 11, 506-515.

Hello Katrin,

As far as I remember, there are "translations" of information/experiences taking place during the resting phases, where the mainly "electronically" saved information is transcribed into a "chemical" format. Maybe this might cause the different activity waves.

A great resource on this topic is the aptly named "Rhythms of the Brain" by Gyorgy Buzsaki, though it's a bit dense. It's considered by many the definitive text on the subject (though as always with science there have been some basic errors discovered in the 7 years since publication).

Hi Katrin.

I found a helpful characterization of the different rhythms on this book:

"Quantitative EEG, Event-related Potentials and Neurotherapy" by Juri D. Kropotov.

There is a part entirely dedicated to EEG Rhythms. I hope this helps.

Brain oscillations are still a mystery. The human dominant rhythm is in the alpha band, with a peak at 10 Hz, although each of us has an individual alpha peak frequency, usually referred to as IAF. Among the quantitative EEG parameters, IAF is regarded to be the best indicator of maturation, has the highest heritability level, and can serve as an indicator of pathology. It is further assumed that different narrow alpha band frequencies are associated with attention—suppression of irrelevant stimuli and selection of relevant information. Below alpha is theta – dominant in animals, and thought to be related to memory processes with a frontal/parietal distinction for attention and storage. Another aspect of theta and the lower delta is in cross frequency coupling, where the lower frequencies act as a gating mechanism, providing optimal neural conditions for specific processing assumed involved in binding. The association delta-beta and theta gamma, are assumed to be related to topographically more distant and/or more narrow coupling activity. The topic is extreme complex. Some up to date articles might give you a better understanding:

Arnal LH and Giraud AL (2012). Cortical oscillations and sensory predictions. Trends in Cognitive Sciences July, Vol. 16, No. 7. 390-398

Klimesch, W (2012). Alpha-band oscillations, attention, and controlled access to stored information. Trends in Cognitive Sciences December, Vol. 16, No. 12, 607-617

Sauseng et al., (2010). Control mechanisms in working memory: A possible function of EEG theta oscillations. Neuroscience and Biobehavioral Reviews 34 1015–1022

Canolty, RT and Knight RT (2010). The functional role of cross-frequency coupling. Trends in Cognitive Sciences, November, Vol. 14, No. 11, 506-515.

Thanks to your suggested materials my main question is answered by now and as a by-product I have gained lots of good new information. Thank you!

There's an excellent review of brain rhythms from the physiology point of view by Wang 2010. Physiol. Rev. 90:1195-1268

My clinical laboratory has built up a long experience of EEG testing over the years. Our experience is that brain rhythms are not necessarily connected to specific functions and structures, or if they are, we haven't isolated them yet. In my opinion EEG may show the mechanism of brain excitement, but not the cause.

All rhythm types (alpha, beta, theta and delta etc.) are present in greater or lesser degree in all states of brain activity, including regulation of breathing, heartbeat and other basic physiological functions, as you indicated.

In all probability this will also be the case with higher brain functions, such as attention, as referred to by Norbert in his answer.

I have only recently joined this forum and am still finding my way around. Not long ago, I posted a link to my own article on this subject, which was originally published in 2006 in a Ukrainian medical publication. It may be interesting to you to read it.

I totally agree with Nicholas Weiler: Buzsáki's "Rhythms of the Brain" is a must in this field!!

And take care not to extrapolate the interpretation of a rhythm in a given structure of the brain to another area, or from one species to another...

In people with intellectual disability is easier to find significant correlations between intellectual tests and brain rhythms because the score´s range is much wider than in standard people. In 1999 we write “Brain rhythms and cognition in Mental Deficiency” [Ritmos cerebrales y cognición en deficientes mentales] for people working in special education. We defined the eeg bands using Principal Components Analysis on 200 subjects. Next we correlate the FFT bands with IQ and Wechsler’s scales subtest.

See for instance the correlations of frequency factors 1 and 3

Power FFT 3-6 Hz. eyes closed (N=200) correlations

Full IQ............. -.17 *

Verbal IQ ........ -.13 *

Performance IQ Ns.

Information .........-.16 *

Comprehensión..-.19 **

Arithmetic .........-.13 *

Similarities ........-.17 **

Vocabulary.........-.16 *

Power FFT 10 Hz. eyes closed correlations

Full IQ................ .25 **

Verbal IQ..............Ns.

Performance IQ... .32 **

Arithmetic................ .17 *

Picture Completion... .18 *

Picture Arrangement. .35 **

Block Design........... .20 **

Object assembly...... .24 **

Coding..................... .21 **

Mazes..................... .23 **

EEG has always much noise then you can't expect high correlations.

Now days is possible investigate the rhythms, its localization in the brain and its relations with others rhythms and areas using wavelet three-dimensional maps, the coherence, phase etc.

A very interesting forum. I would ask about an apparent contradiction I do not understand. On the one hand some papers from the animal literature talk about the increasing in the hippocampal theta rhythm (in rats) related to attention and working memory but, from human clinical literature and neurofeedback technique, it seems that children with learning disabilities found benefit on attention mainly by decreasing their theta power (specially in relation with alpha)... Does anyone have an answer to this? (I mean an explanation more far or more in deep from the obvious point that we are crossing species)

Hello Marien,

It might be you are mixing info from different brain areas, not only species... are you talking about human hippocampal theta?? or is this literature referring to scalp EEG recordings? Last time I read about it, there was controversy about the existence of hippocampal theta in primates/humans... very few studies with intrahippocampal recordings have been conducted in humans (Cantero et al, J.Neurosci. 2003), but take a look at the literature now...

@Marien: The rodent theta literature and human clinical literature regarding theta oscillations you mention are two different things; in fact, they do not have much in common except sharing the dominant frequency, hence the same name. This is because the clinical EEG studies that consider theta oscillations in humans record oscillations from the scalp; these oscillations are generated in the neocortex. As Sara rightly pointed out before, two oscillations in different areas often have independent sources.

I don't know of corresponding rodent literature of cortical theta oscillations, mainly because it does not seem to be prominently present in rodent neocortex. On the other hand, there is a small but remarkable body of human hippocampal theta literature. The difficulty is that the human hippocampus is small in proportion to the whole brain (as compared with rodents) and is folded under the temporal lobe in a way that it is not easily accessible for EEG electrodes. However, electrocorticograms and deep recordings show that it is there, having somewhat lower frequency but sharing many functional properties (see papers below).

As far as other species are concerned, hippocampal theta oscillations were initially intensely studied in rabbits; they are notoriously hard to investigate in non-human primates, for which the reason seem to be that it is reset by saccadic eye movements, resulting in very short theta bouts; and according to recent studies from Yartsev and Ulanovsky, it appears to be absent in bats.

Some good papers about human hippocampal theta:

Human theta oscillations exhibit task dependence during virtual maze navigation.

Kahana MJ, Sekuler R, Caplan JB, Kirschen M, Madsen JR.

Nature. 1999 Jun 24;399(6738):781-4.

Human memory strength is predicted by theta-frequency phase-locking of single neurons.

Rutishauser U, Ross IB, Mamelak AN, Schuman EM.

Nature. 2010 Apr 8;464(7290):903-7. doi: 10.1038/nature08860. Epub 2010 Mar 24.

Bódizs R, Kántor S, Szabó G, Szûcs A, Erõss L, Halász P (2001) Rhythmic

hippocampal slow oscillation characterizes REM sleep in humans. Hippocampus

11:747-753.

Cantero JL, Atienza M, Stickgold R, Kahana MJ, Madsen JR, Kocsis B (2003) Sleepdependent

theta oscillations in the human hippocampus and neocortex. J Neurosci

23:10897-10903.

Caplan JB, Madsen JR, Schulze-Bonhage A, Aschenbrenner-Scheibe R, Newman EL,

Kahana MJ (2003) Human theta oscillations related to sensorimotor integration and

spatial learning. J Neurosci 23:4726-4736.

Ekstrom AD, Caplan JB, Ho E, Shattuck K, Fried I, Kahana MJ (2005) Human

hippocampal theta activity during virtual navigation. Hippocampus 15:881-889.

Erratum in: Hippocampus 16:101.

Ekstrom A, Viskontas I, Kahana M, Jacobs J, Upchurch K, Bookheimer S, Fried I

(2007) Contrasting roles of neural firing rate and local field potentials in human

memory. Hippocampus 17:606-617.

I feel compelled to shamelessly plug my own review as far as alpha-band oscillations go:

Foxe, J. J., & Snyder, A. C. (2011). The role of alpha-band brain oscillations as a sensory suppression mechanism in selective attention. Frontiers in Psychology, 2:154. doi:10.3389/fpsyg.2011.00154. [Review]

It can be downloaded here:

http://www.frontiersin.org/perception_science/10.3389/fpsyg.2011.00154/full

I think it very unlikely that these rhythms (see below) were being generated in the brain, and presume that they arose in another part(s) of the body and then reenergized the brain. So where could these sources be?

*************

Surge of neurophysiological coherence and connectivity in the dying brain

Jimo Borjigina et al PNAS

Abstract The brain is assumed to be hypoactive during cardiac arrest. However, the neurophysiological state of the brain immediately following cardiac arrest has not been systematically investigated. In this study, we performed continuous electroencephalography in rats undergoing experimental cardiac arrest and analyzed changes in power density, coherence, directed connectivity, and cross-frequency coupling. We identified a transient surge of synchronous gamma oscillations that occurred within the first 30 s after cardiac arrest and preceded isoelectric electroencephalogram. Gamma oscillations during cardiac arrest were global and highly coherent; moreover, this frequency band exhibited a striking increase in anterior–posterior-directed connectivity and tight phase-coupling to both theta and alpha waves. High-frequency neurophysiological activity in the near-death state exceeded levels found during the conscious waking state. These data demonstrate that the mammalian brain can, albeit paradoxically, generate neural correlates of heightened conscious processing at near-death.

Gamma-band synchronization has been an area of interest as a psychophysical

hypothesis in perceptual binding since the late 1980’s (Fries, P. (2009). Neuronal gamma-band synchronization as a fundamental process in cortical computation.

Annual Review of Neuroscience, 32, 209–224. doi: 10.1146/annurev.neuro.051508.13560). We recently suggested an alternative hypothesis as to how this is involved in higher cortical processes with the reference below that is posted at RG. The literature we cited suggests early in development that thalamic gamma oscillations allow the formation of columns in the primary sensiory cortex. This pattern then progresses across the cortex. Our suggestion is that the column is the binary unit involved in all cortical processing and memory storage. This cell-firing frequency is involved in the dynamic formation of columns in which only the outermost neurons are synchronized. This allows column-sized (0.4 to 1.0 mm) information bits in which only a fraction of the neurons of the column are committed to that bit. Overlapping columns are believed to exist based on 3 studies we cited, and this can allow for the necessary large volume requirement to be the cortical bit.

The theorized process of new and relevant stimulus input would go something like this. Once sensory information arrives at the cortex, the primary sensory cortical columns activate. Where their efferent activity cross, new columns form, with these also reflecting the gamma activity. Each posterior sensory column has a corresponding frontal action column which forms. In new association memories this leads to activation of the medial temporal lobe columns which project to the hippocampus. The hippocampal cells are activated and serve as the pacemakers for a hippocampo-thalamo-cortico-hippocampo circuit with gamma-frequency oscillations generated on the background of theta oscillations. We reviewed one study that showed a greater area of cortical activation happens at the low frequency while the gamma frequency activity activates column sized areas. GABA was implicated as the neurotransmitter involved in limiting the column-sized spread of activity at the gamma frequency range. Anyway, the maintenance of this circuit allows the strengthening of synaptic connections among the columns involved in this new memory. Thus, instead of the current view that association memories are first "stored" in the hippocampus and later somehow transferred to other locations such as the cortex, this theory says the columns originally involved in processing are the same as those involved in the memory and hippocampal activity allows the cortical formation to occur.

I suspect that there are other frequency-to-size of cortical activation patterns as well. For example, beta activity has been shown (Wróbel, A. (2000). Beta activity: a carrier for visual attention. Acta neurobiologiae experimentalis, 60(2), 247-260) to be involved with attention. This may indicate a cortical area involving a large number of columns has increased activity such that when the expected stimulus occurs, the involved columns are already primed to respond.

Being a clinician, I always think at an application level. If what we have sugested is accurate there can be implications for a better understanding of disorders. For instance, involvement of the hippocampus is seen early in the course of Alzheimer’s disease. As mentioned, we proposed that memories are stored at the cortical level, but the hippocampus acts in the role of starter and pacemaker in a circuit that goes from the hippocampus to the thalamus to the cortex and back to the hippocampus. By maintaining the activity in the circuit, the synaptic connections among columns are strengthened which is the definition of memory formation. Hippocampal neurons set the pattern in the circuit. If disrupted or damaged, then the hippocampal neurons may lack the ability to maintain the gamma frequency firing rate which would prevent the cortical columns from forming the associated memory. Interestingly, the cholinesterase inhibitors used in the treatment of early Alzheimer’s increase the availability of acetylcholine (ACh) at the cortical level. An action of ACh is to increase the ease with which cortical neurons fire, which increases cell firing rates. By increasing the firing rates, this can feasibly allow dynamical formation of columns once again and improve memory. Please note, this is only speculation based on the theory.

In relation to schizophrenia, it has been suggested that there is a fundamental disturbance throughout the cortex in neuronal connectivity and communication (Phillips, W. A., & Silverstein, S. M. (2003). Impaired cognitive coordination in schizophrenia: Convergence of neurobiological and psychological perspectives. Behavioral and Brain Sciences, 23, 65-138.). The fact that in schizophrenia there are various forms of reduced stimulus organization (e.g., memory and thought organization) has been used to support the poor coordination view. There are multiple circuits of columns within each hemisphere and poor coordination among these circuits might be the level at which the cognitive coordination breaks down. For example, failure of frontal action columns control in coordinating other frontal and posterior columns, or the failure to form associative memory columns in the temporal cortex, may leave the circuits of columns in distal cortical areas unconnected or in conflict. This could feasibly lead to thought disorganization in which different perceptions result from simultaneous activation of separate circuits with poor coordination of which is in control.

At the receptor level, glutamatergic NMDARs are voltage dependent and it seems these are likely those involved at the gamma frequency range associated with dynamic column formation. The theory can also expalin that sleep-dependent memory consolidation happens as a function of the activation of cortical column circuits via thalamic activation which allows the strengthening of the columnnar synaptic connections and would be rflected in higher frequency EEG patterns. Hope I didn't ramble too long. The related articles I have done are:

Moss, R. A., Hunter, B. P., Shah, D., & Havens, T. (2012). A theory of hemispheric specialization based on cortical columns. Journal of Mind and Behavior, 33, 141-172

Moss, R. A. (2006). Of bits and logic: Cortical columns in learning and memory. The Journal of Mind and Behavior, 27, 215-246.

Thanks, Robert, for the background info, but this does not address the question I posed. After cardiac arrest the brain is dead, which is why neuroscientists rubbish the near death studies literature, leaving the field wide open for the life-after-death brigade.

"The literature we cited suggests early in development that thalamic gamma oscillations allow the formation of columns in the primary sensiory cortex. This pattern then progresses across the cortex."

So what is driving the thalamus in the first place? Early in development, this is likely to be sense organ(s). So, is that where the near death activity is arising in rats?

Arousal to the thalamus and then the cortex are provided via the reticular activating system and also via emotional processing (most feasible route being central amygdala to preifornical hypothalamus to intermediolateral cells in the spinal cord to the symapthetic ganglia). My best explanation of these EEG findings is that upon cardiac arrest there would be an expected attempt of survival resulting in increased arousal in both of these systems. If columnar activation synchronized by gamma frequency oscillations is actually the cortical coding system, the rise in general activity from the RAS and sympathetic ganglia should occur at that level. The bottom up activity would be via the thalamus to cortex and the top down would be a function of frontal action columns activating. Obviously, it is not possible to determine what the perceived experiences are for the rats experiencing this. Please take this as a possible physiological explanation of the EEG findings in this cited study only and not as any value judgment on near death experiences.

Article Of bits and logic: Cortical columns in learning and memory. ...