How cognitive assessment through clinical neurophysiology may help optimize chronic alcoholism treatment
Alcohol dependence constitutes a serious worldwide public health problem. The last few decades have seen many pharmacological studies devoted to the improvement of alcoholism treatment. Although psychosocial treatments (e.g. individual or group therapy) have historically been the mainstay of alcoholism treatment, a successful approach for alcohol dependence consists in associating pharmacologic medications with therapy, as 40-70% of patients following only psychosocial therapy typically resume alcohol use within a year of post-detoxification treatment. Nowadays, two main pharmacological options, naltrexone and acomprosate, both approved by the US Food and Drug Administration, are available and seemingly improve on the results yielded by standard techniques employed in the management of alcoholism. However, insufficient data exist to confirm the superiority of one drug over the other, and research is ongoing to determine what type of alcohol-dependent individual benefits the most from using either medication. Available data on the application of both drugs clearly suggest different practical applications. Thus, a fundamental question remains as to how we can identify which alcoholic patients are likely to benefit from the use of naltrexone, acamprosate or both, and which are not. The aim of the present manuscript is to suggest the use of cognitive event-related potentials as an interesting way to identify subgroups of alcoholic patients displaying specific clinical symptoms and cognitive disturbances. We propose that this may help clinicians improve their treatment of alcoholic patients by focusing therapy on individual cognitive disturbances, and by adapting the pharmaceutical approach to the specific needs of the patient.
Available from: Salvatore Campanella
- "Moreover , analyses were systematically redone to control for a possible influence of demographic variables that differed between groups and that are known to either influence cue reactivity and/or P3 component parameters i.e., family history of alcoholism  , anti-craving medication (e.g.  ), tobacco smoking (e.g. ) and education level. "
[Show abstract] [Hide abstract]
ABSTRACT: One of the major challenges in alcohol dependence is relapse prevention, as rates of relapse following detoxification are high. Drug-related motivational processes may represent key mechanisms in alcoholic relapse. In the present study, event-related potentials (ERPs) were recorded during a visual oddball task administered to 29 controls (11 females) and 39 patients (9 females). Deviant stimuli were related or unrelated to alcohol. For patients, the task was administered following a 3-week detoxification course. Of these, 19 relapsed during the three months follow-up period. The P3, an ERP component associated with activation of arousal systems in the brain and motivational engagement, was examined with the aim to link the fluctuation of its amplitude in response to alcohol versus non-alcohol cues to the observed relapse rate. Results showed that compared to relapsers, abstainers presented with a decreased P3 amplitude for alcohol related compared to non-alcohol related pictures (p=.009). Microstate analysis and sLORETA topography showed that activation for both types of deviant cues in abstainers originated from the inferior and medial temporal gyrus and the uncus, regions implicated in detection of target stimuli in oddball tasks and of biologically relevant stimuli. Through hierarchical regression, it was found that the P3 amplitude difference between alcohol and non-alcohol related cues was the best predictor of relapse vulnerability (p=.013). Therefore, it seems that a devaluation of the motivational significance of stimuli related to alcohol, measurable through electrophysiology, could protect from a relapse within three months following detoxification in alcohol-dependent patients.
Copyright © 2015 Elsevier B.V. All rights reserved.
Behavioural Brain Research 01/2015; 282. DOI:10.1016/j.bbr.2014.12.057 · 3.03 Impact Factor
Available from: Ashwini K Pandey
[Show abstract] [Hide abstract]
ABSTRACT: Alcohol dependence is characterized as a multi-factorial disorder caused by a complex interaction between genetic and environmental liabilities across development. A variety of neurocognitive deficits/dysfunctions involving impairments in different brain regions and/or neural circuitries have been associated with chronic alcoholism, as well as with a predisposition to develop alcoholism. Several neurobiological and neurobehavioral approaches and methods of analyses have been used to understand the nature of these neurocognitive impairments/deficits in alcoholism. In the present review, we have examined relatively novel methods of analyses of the brain signals that are collectively referred to as event-related oscillations (EROs) and show promise to further our understanding of human brain dynamics while performing various tasks. These new measures of dynamic brain processes have exquisite temporal resolution and allow the study of neural networks underlying responses to sensory and cognitive events, thus providing a closer link to the physiology underlying them. Here, we have reviewed EROs in the study of alcoholism, their usefulness in understanding dynamical brain functions/dysfunctions associated with alcoholism as well as their utility as effective endophenotypes to identify and understand genes associated with both brain oscillations and alcoholism.
Journal of Addiction Research & Therapy 01/2012; Suppl 7(1). DOI:10.4172/2155-6105.S7-001 · 1.77 Impact Factor
Available from: Marcelo Lopez
[Show abstract] [Hide abstract]
ABSTRACT: Dopamine (DA) receptors in the medial prefrontal cortex (mPFC) exert powerful effects on cognition by modulating the balance between excitatory and inhibitory neurotransmission. The present study examined the impact of chronic intermittent ethanol (CIE) exposure on cognitive function and DA receptor-mediated neurotransmission in the rat mPFC. Consistent with alterations in executive function in alcoholics, CIE-exposed rats exhibited deficits in behavioral flexibility in an operant set-shifting task. Since alterations in dopaminergic neurotransmission in the mPFC have been implicated in a number of behavioral disorders including addiction, studies were then performed in the adult acute slice preparation to examine changes in DA receptor function in the mPFC following CIE exposure. In slices obtained from control rats, DA receptor stimulation was observed to exert complex actions on neuronal firing and synaptic neurotransmission that were not only dependent upon the particular receptor subtype but also whether it was a pyramidal cell or a fast-spiking interneuron. In contrast to slices from control rats, there was a near complete loss of the modulatory actions of D2/D4 receptors on cell firing and neurotransmission in slices obtained immediately, 1 and 4 weeks after the last day of CIE exposure. This loss did not appear to be associated with changes in receptor expression. In contrast, CIE exposure did not alter D1 receptor function or mGluR1 modulation of firing. These studies are consistent with the suggestion that chronic alcohol exposure disrupts cognitive function at least in part through disruption of D2 and D4 receptor signaling in mPFC.
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience 03/2014; 34(10):3706-18. DOI:10.1523/JNEUROSCI.0623-13.2014 · 6.34 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.