Alcoholism and Human Electrophysiology : Part 2

by National Institute of Health

(Page 2 of 5)

Alpha (8.0-11.5 Hz)

The alpha rhythm is the predominant EEG rhythm in the relaxed alert person. It is obtained whether eyes are open or closed, and it is strongest over the occipital region when the person's eyes are closed. The alpha rhythm is an index of relaxation. Extensive research, dating back to the 1940s, confirms that unstable or poor alpha rhythm is found in alcoholics. Early studies determined that alcoholics manifest less prevalent and lower alpha power than nonalcoholics, but more recent studies have not been consistent with these findings.

Enoch and colleagues have reported that an alpha variant, namely low voltage alpha (LVA), is associated with a subtype of alcoholism that co-occurs with anxiety disorder. Recently, these authors found that among females, LVA is associated with a genetic variant that leads to low activity in catechol-o-methyltransferase (COMT), the enzyme that metabolizes the brain chemicals (neurotransmitters) dopamine and norepinephrine (NE). The authors hypothesize that the effect of altered NE levels on activity in the thalamus (a communication center in the brain) may partly explain the connections between LVA, anxiety, and alcoholism.

Beta (12-28 Hz)

Beta rhythm is obtained in alert subjects; it is a fast, low-voltage rhythm that is distributed over the scalp. Most studies examining resting EEG characteristics in alcoholics have reported increased beta power in alcoholics compared with nonalcoholics. Propping and colleagues reported these differences in female alcoholics compared with female nonalcoholics, but not in male alcoholics compared with male nonalcoholics. For the COGA study, researchers subdivided the beta frequency band into three bands: beta 1, beta 2, and beta 3. The alcohol-dependent group had increased power in both the beta 1 and beta 2 frequency bands at all loci over the scalp, compared with control subjects; this difference was most prominent in the central region of the brain. The alcoholic group also had increased power in the beta 3 frequency band in the frontal region. Age and clinical variables did not influence the difference.

Relapsing alcoholics have been reported to have more desynchronized, or randomly firing, beta activity over frontal areas than nonrelapsers, which suggests a functional disturbance in the prefrontal cortex (the area of the brain just behind the forehead). Bauer reported that fast beta power was superior to severity of illness, depression level, and childhood conduct problems in predicting relapse in abstinent alcoholics. Researchers have identified anterior frontal brain regions (the prefrontal cortex) as the most likely source of this fast beta activity. Because the increase in beta power in abstinent alcoholics was not related to length of abstinence and also is present in offspring of alcoholics at risk for alcohol dependence, these findings suggest that excess beta power is a "trait" rather than a "state" variable (related to underlying genetic predisposition and not to alcohol use or other factors). This is consistent with the hypothesis that an imbalance between excitatory and inhibitory neurons is involved in a predisposition to develop alcohol dependence as well as a proneness to relapse.

Beta rhythm reflects a balance between networks of nerve cells projecting from the cortex to other parts of the brain and spinal cord (pyramidal cells) (which are excitatory) and neurons that carry signals between other neurons (interneurons) (which are inhibitory). GABAA, the receptor, or binding molecule, for the neurotransmitter gamma-aminobutyric acid (GABA), is thought to regulate this rhythm.

A recent finding from the COGA project has found a genetic linkage (within families) and linkage disequilibrium (across families) between the beta frequency of the EEG and a GABAA receptor gene (they co-occur at a higher frequency than would be predicted by chance). Furthermore, several neuroimaging studies of alcoholics have shown deficits in the GABA receptors for the chemical benzodiazepine, which facilitates inhibitory GABAergic transmission. Researchers also have reported neuronal loss or shrinkage in the superior frontal and motor cortices of alcoholics. Taken together, these findings suggest that this deficit in GABA receptors in the brains of alcoholics may account for their lack of CNS inhibition (hyperexcitability). Recent findings from the COGA project indicate that the same GABAA receptor gene associated with the beta frequency of the EEG also is associated with a diagnosis of alcohol dependence, based on criteria from the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition. This suggests that variations in the GABAA receptor 2-subunit gene (GABRA2) (the gene encoding the alpha 2 subunit of the GABAA receptor) affect the level of neural excitability, which in turn affects the predisposition to develop alcohol dependence.

Event-Related Potentials (ERPs)

Unlike the resting EEG, which is a recording of ongoing brain activity, ERPs reflect brain electrical activity in response to specific sensory or cognitive events occurring at a specific time. ERPs can be used to monitor brain activity ranging from sensory reception to higher cognitive processes. ERPs are characteristic, highly reproducible waveforms that are displayed graphically as a series of peaks (designated P for positive components) and valleys (designated N for negative components). Components are described in terms of their wave height (amplitude, measured in microvolts [µV]), and the time of their occurrence following presentation of the stimulus (latency, measured in milliseconds [ms]). For example, P300 is a positive peak occurring around 300 ms after the stimulus; it also is designated as P3 (third positive peak). Early components, those with a latency of less than 100 ms, reflect responses to the physical characteristics of the stimulus, whereas later components are influenced by more cognitive factors.

About the Author

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