About Us Downloads Contact
Diffuse Slow Activity
Beta Spindles
EEG vs. Perfusion
Neurological EEG

Low voltage EEG

Low voltage EEG can be considered a normal variant and occurs in as many as 7-14% of the population (Enoch et al., 2002). This usually appears as a very low amplitude EEG (see example below). In the QEEG this is often seen as a decrease in virtually all frequency bands. When this EEG Phenotype is observed, coherence, phase and assymetry data should be ignored due to the low signal-to-noise ratio of the signal.

'Normal' EEG

'Low Voltage fast EEG'

Example of normal EEG        Example of typical Low voltage fast EEG

Example of 'normal EEG'

 Example of Low Voltage EEG

The Low voltage fast pattern has been linked to alcoholism and GABA-A receptor genes (Porjesz et al., 2002) more specifically to gene number 4's regulation over GABA receptors (Bierut et al., 2002). Other research has demonstrated a relation between low voltage EEG and low voltage ERP amplitudes, which are both more prevalent in alcoholism (Enoch et al., 2002).

To further test the hypothesis that low voltage EEG is related to decreased GABA-ergic function, we conducted a small experiment. This was inspired by Jay Gunkelman and a replication from a similar experiment conducted earlier in Juri Kropotov's lab on a subject who displayed a low-voltage EEG without any presence of alpha. After Cognac intake a clear increase in posterior alpha activity was observed (Juri Kropotov: unpublished, personal communication).

According to the literature, alcohol intake should lead to increased beta and increased theta based on averaged group data (Stenberg et al., 1994). Alcohol exerts most of it's effects through the GABA-ergic system. However, based on the above literature and the EEG Phenotype paper we hypothesized that alcohol - by it's GABA-ergic function - should specifically lead to increased alpha in healthy subjects with a low-voltage fast EEG . The increased GABA-ergic activity should reinstantiate the alpha rhythm again in these subjects by hyperpolarization of thalamic neurons.

Below see the data from 1 healthy subject after increasing doses of Vodka. These are the Z-score maps for the alpha band during Eyes Closed. It can be clearly seen that this can be considered a low voltage EEG, with hardly any alpha. T=0 is the pre-assessment without alcohol intake. T=1; T=2 and T=3 represent increasing doses' of vodka, where T=3 is after 0.4 litre of pure Vodka. In this figure it can be clearly seen that when the dose of ethanol increases alpha starts re-appearing. In the highest dose one also sees a slowing of the alpha into the 8-9 Hz. No consistent dose-response effects were seen for the other frequency bands.
QEEG: spectral content in alpha band after increasing dosis of alcohol
QEEG: Single Hertz Bins for the alpha band. Note the increase in spectral content at 9 Hz with increasing doses of alcohol and the further slowing of alpha at T=3.

This example clearly demonstrates the need for Personalized Medicine, as the effect of ethanol on individuals with specific EEG phenotypes is clearly different as based on published group studies (the same as with ADHD). Also, given the literature behind the low voltage EEG phenotype and it's linkage to alcoholism makes the disorder more understandable, especially from a self-medication point of view. The neurofeedback treatment recommendation for this EEG phenotype consists of Alpha uptraining and SMR training.

The low voltage fast van be considered a normal variant, however a low voltage slow EEG is usually considered a diffuse and non-specific abnormality (make sure it is not due to drowsiness). For a more detailed description and more background info related to this subtype also see Johnstone, Gunkelman & Lunt (2005).

Porjesz, B., Almasy, L., Edenberg, H.J., Wang, K., Chorlian, D.B., Foroud, T., Goata, A., Rice, J.P., O'Connor, S.J., Rohrbaugh, J., Kupermans, S., Bauer, L.O., Reich, T. & Begleiter, H. (2002). Linkage disequilibrium between the beta frequency of the human EEG and a GABAA receptro gene locus. Proc Natl Acad Sci USA, 99 (6): 3729-3733.

Enoch, M.A., White, K.V., Harris, C.R., Rohrbaugh, J.W. & Goldman, D. (2002) The relationship between two intermediate phenotypes for alcoholism: low voltage alpha EEG and low P300 ERP amplitude. J Stud Alcohol, 63 (5): 509-517.

Bierut, L.J., Saccone, N.L., Rice, J.P., Goate, A., Foroud, T., Edenberg, H., Almasy, L., Conneally, P.M., Crowe, R., Hesselbrock, V., Li, T.K., Nurnberger, J. Jr., Porjesz, B., Schuckit, M.A., Tischfield, J., Begleiter, H. & Reich, T. (2002) Defining alcohol-related phenotypes in humans. The Collaborative Study on the Genetics of Alcoholism, 26 (3), 208-213.

Stenber, G., Sano, M., Rosen, I. & Ingvar, D.H. (1994) EEG Topography of acute ethanol effects in resting and activated normals. J. Stud Alcohol 55 (6): 645-56

Johnstone, J., Gunkelman, & J.  Lunt, J. (2005) Clinical database development: Characterization of EEG Phenotypes. Clinical EEG and Neuroscience, 36(2); 99-107