Acute and Chronic Effects of Alcohol on Preattentive Auditory Processing as Reflected by Mismatch Negativity

Abstract

Chronic alcoholism, a major worldwide health problem, is associated with a variety of neurocognitive changes in the afflicted individuals. The precise neurophysiological basis of these changes is not yet understood. Mismatch negativity (MMN) is a preattentive event-related potential component indexing cortical auditory memory traces and automatic change detection in the brain that can be used to study the neural basis of cognitive impairments in various neurodegenerative diseases. MMN studies have revealed that even a low dose of acute alcohol significantly impairs automatic change detection and involuntary attention shifting. Recent MMN results on chronic alcoholism in turn suggest that auditory sensory traces decay slightly faster and are substantially more vulnerable to the distracting effect of backward masking in alcoholics than in healthy subjects. Furthermore, chronic alcohol abuse might accelerate the age-related impairment of automatic change detection. There is also evidence that the MMN changes might predict impaired performance in behavioral memory and attention tasks in alcoholics. In MMN studies of detoxified alcoholics, however, many confounding factors have to be taken into account. For instance, postwithdrawal brain hyperexcitability might be associated with a slightly enhanced or accelerated MMN/MMNm (the magnetic equivalent of MMN). In sum, MMN and MMNm provide an objective noninvasive tool for exploring the neurophysiological functional deficits related to both acute alcohol intoxication and chronic alcoholism.

A Comparison of the mismatch negativity and a differential waveform response

“…Researchers have reported a significantly greater attenuation of the MMN response for stimuli delivered at longer ISIs in specific clinical populations including the elderly (Gaeta et al 1992;Woods 1992;Pekkonen et al 1996), children with CATCH-22 syndrome learning problems (Kraus et al 1996;Cheour et al 1997), and those suffering from Parkinson's disease (Pekkonen et al 1994), Alzheimer's disease (Kazmerski et al 1997), chronic alcoholism (Ahveninen et al 2000;Grau et al 2001), and coma (Kane et al 1993). Since certain neural refractory functions are also known to vary with different forms of CNS dysfunction (Shagrass et al 1971;Alho et al 1994;Ornitz et al 1974;Papanicolaou et al 1984;Shucard et al 1984), it is possible that in some studies, the MMN response and neural refractory effects may temporally overlap.…”

Effects of Lorazepam on the Neuromagnetic Mismatch Negativity (MMNm) and Auditory Evoked Field Component N100m

“…In neuropsychiatric research, the interest in information processes is caused by the fact that cognitive deficits are crucial in many neurologic and psychiatric diseases. As a clear, comprehensive, and differential description of MMN deficits can be very helpful for the elucidation of pathogenetic processes, MMN has been investigated in various diseases, as for example, in Alzheimer's disease (for overview Pekkonen, 2000), in dyslexia (for an overview, see Kujala and Näätänen, 2001), or in alcoholism (for an overview, see Ahveninen et al, 2000). A reduced MMN amplitude in schizophrenia seems to represent one of the most consistent findings (for an overview, see Michie et al, 2000), pointing towards the notion of a disturbed early attention process in this disease.…”

Mismatch Negativity: No Difference Between Controls and Abstinent Alcoholics

“…Research suggests the presence of information processing abnormalities in alcoholics on tasks that assess target detection (Polich et al, 1994), orienting (Fein et al, 1995), several aspects of inhibitory function (Ahveninen et al, 2000), behavioral disinhibition (LeMarquand et al, 1999), and response to reward and punishment (Bechara et al, 2001;Lejoyeux et al, 1998;Lejoyeux et al, 1999). These characteristics may be the result of chronic heavy alcohol use, or they may reflect biological vulnerabilities that predate alcohol consumption and increase risk for alcohol abuse (Begleiter et al, 1984).…”

“…While there are no doubts that acute alcohol ingestion delays MMN latency and reduces MMN amplitude, the long-term effects of chronic alcohol exposure are not as clear. One group of findings has found that abstinent alcoholics display increased MMN amplitude in comparison to control subjects (Ahveninen et al, 2000;Kathmann et al, 1995); however, these studies examined subjects with relatively shortterm (less than 2 mos) abstinence. This abstinence duration may have not been enough to get past the subtle post-withdrawal CNS hyperexcitablity associated with early cessation of alcohol, which have been shown to be detectable at 3-8 weeks after alcohol detoxification (Ahveninen et al, 2000) (Alling et al, 1982).…”