Mismatch Negativity: No Difference Between Controls and Abstinent Alcoholics

Fein, George; Whitlow, Bridget; Finn, Peter R.

doi:10.1097/01.alc.0000107199.26934.46

Cited by 19 publications

(16 citation statements)

References 39 publications

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“…The TxNA sample came from a population with a history of early abusive drinking (in the first 5 years immediately after meeting criteria for heavy alcohol consumption) that was 30 -40% less in average and peak dose than treated samples (Fein and Landman, 2005). They had an increased rate of externalizing symptoms and psychological evidence of deviance proneness compared with controls, although these rates were markedly less than those of treated samples (Fein et al, 2004). Our hypothesis is that the population studied is composed of individuals with less severe manifestations of the nexus described above who have later developed alcohol dependence but no other diagnosable psychiatric or substance abuse disorders.…”

Section: Discussionmentioning

confidence: 99%

EEG Spectral Changes in Treatment-Naive, Actively Drinking Alcoholics

Fein

Allen

2005

Alcoholism: Clinical & Experimental Research

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Increased EEG power across the theta to high beta bands distinguishes TxNAs without comorbid diagnoses from controls. These effects varied across bands in magnitude and spatial extent, suggesting different effects for the different EEG spectral generators. The authors hypothesize that the increased power in these individuals is a trait difference associated with the inherited nexus of disinhibited traits and its manifestation in alcoholism. Based on the strong negative correlations with alcohol use variables, the authors speculate that decreases in EEG power are a morbid effect of long-term alcohol abuse. They acknowledge that this hypothesized effect of alcohol abuse on EEG power is opposite to the increased EEG power that they hypothesize is associated with alcoholism and its inherited nexus of disinhibited traits. An implication of this model is that with continuing alcohol abuse, the increased EEG power in TxNAs will eventually be overpowered by the effects of long-term severe alcohol abuse. This model predicts that in very long-term alcoholics, EEG power would be equal to or lower than that of age- and sex-comparable controls.

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Section: Discussionmentioning

confidence: 99%

EEG Spectral Changes in Treatment-Naive, Actively Drinking Alcoholics

Fein

Allen

2005

Alcoholism: Clinical & Experimental Research

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“…The automatic stimulus change detector mechanism associated with MMN generation is impaired in chronic alcoholics over the age of 40, suggesting that the neurotoxic effects of chronic consumption of alcohol are more prone to appear after a critical age (Polo et al, 1999). One study showed no MMN differences between controls and alcoholics who were abstinent for an average of 6 years (Fein et al, 2004), while another (Pekkonen et al, 1998) observed that increasing durations of abstinence reduced the MMN amplitude, perhaps indicating improved efficiency of covert processes upon abstinence. Ahveninen et al (2000) found significantly enhanced MMN amplitudes to deviant sounds that correlated with reaction time lag caused by deviants, indicating pronounced distractibility and impaired reorienting to the relevant task in alcoholics.…”

Section: Chronic Alcoholism and Neuroelectrophysiologymentioning

confidence: 99%

Understanding alcohol use disorders with neuroelectrophysiology

Rangaswamy

Porjesz

2014

Handbook of Clinical Neurology

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Neurocognitive deficits associated with impairments in various brain regions and neural circuitries, particularly involving frontal lobes, have been associated with chronic alcoholism, as well as with a predisposition to develop alcohol use and related disorders (AUDs). AUD is a multifactorial disorder caused by complex interactions between behavioral, genetic, and environmental liabilities. Neuroelectrophysiological techniques are instrumental in understanding brain and behavior relationships and have also proved very useful in evaluating the genetic diathesis of alcoholism. This chapter describes findings from neuroelectrophysiological measures (electroencephalogram, event-related potentials, and event-related oscillations) related to acute and chronic effects of alcohol on the brain and those that reflect underlying deficits related to a predisposition to develop AUDs and related disorders. The utility of these measures as effective endophenotypes to identify and understand genes associated with brain electrophysiology, cognitive networks, and AUDs has also been discussed.

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“…Also, it should be noted that MMN data suggest some recovery for chronic alcoholism, as no difference in amplitude and latency between a control group and a group of alcoholics displaying a minimum of 6 months of abstinence has been evidenced. [56][57][58] The P300…”

Section: Mismatch Negativitymentioning

confidence: 99%

Event-Related Potentials in Substance Use Disorders

2013

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Mechanisms that mediate the transition from occasional, controlled, drug use to the impaired control that characterizes severe dependence are still a matter of investigation. The etiology of substance use disorders (SUDs) is complex, and in this context of complexity, the concept of "endophenotype," has gained extensive popularity in recent years. The main aim of endophenotypes is to provide a simpler, more proximal target to discover the biological underpinnings of a psychiatric syndrome. In this view, neurocognitive and neurophysiological impairments that suggest functional impairments associated with SUDs have been proposed as possible endophenotypes. Because of its large amplitude and relatively easy elicitation, the most studied of the cognitive brain event-related potentials (ERPs), the P300 component, has been proposed as one possible candidate. However, if a P300 amplitude alteration is a common finding in SUDs, it is also observable in other psychiatric afflictions, suggesting that the associations found may just reflect a common measure of brain dysfunction. On this basis, it has been proposed that a multivariate endophenotype, based on a weighted combination of electrophysiological features, may provide greater diagnostic classification power than any single endophenotype. The rationale for investigating multiple features is to show that combining them provides extra useful information that is not available in the individual features, leading ultimately to a multivariate phenotype.The aim of the present article is to outline the potential usefulness of this kind of "combined electrophysiological procedure" applied to SUDs. We present a review of ERP studies, combining data from people with SUD, family members, and normal control subjects, to verify whether the combination of 4ERPs (P50, MMN, P300, and N400) may produce profiles of cortical anomalies induced by different types of SUD (alcohol vs cocaine vs cannabis vs heroin).

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Mismatch Negativity: No Difference Between Controls and Abstinent Alcoholics

Cited by 19 publications

References 39 publications

EEG Spectral Changes in Treatment-Naive, Actively Drinking Alcoholics

EEG Spectral Changes in Treatment-Naive, Actively Drinking Alcoholics

Understanding alcohol use disorders with neuroelectrophysiology

Event-Related Potentials in Substance Use Disorders

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