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Background and ObjectivesThe study examined the effects of an alcohol challenge on naturalistic drinking among alcohol‐dependent individuals and explored brief motivational interviewing (MI) as a potential intervention for these participants.MethodAlcohol‐dependent individuals (n = 32, eight females) completed the intake assessment, alcohol challenge, one MI session, and 1‐month follow‐up (87.5% retention) where they completed measures of drinking and motivation for change.ResultsAs expected, multilevel mixed models revealed that drinking did not increase post‐alcohol challenge. Participants reported a reduction in ambivalence, drinking days, and a trend towards fewer total drinks between the MI and 1‐month follow‐up.ConclusionsConsistent with other studies, the alcohol challenge did not worsen alcohol use. Results support further investigation of brief MI for alcohol‐dependent participants in alcohol challenges.Scientific SignificanceAlcohol administration to alcohol‐dependent participants appears to not exacerbate naturalistic drinking. MI may be a feasible intervention for non‐treatment seeking alcohol‐dependent participants in alcohol challenge studies. (Am J Addict 2014;23:96–101)

Pages vi-xi are misnumbered as pages iv-ix. ; Alcohol is one of the most widely used psychoactive substance in the world, yet there are conflicting findings related to its long-term effect on cognition. Some research has identified a U-shaped relationship between alcohol consumption and cognition, while negative relationships have been identified in other studies. Methodological issues, particularly the time at which alcohol consumption was measured relative to when cognition was measured, wide variability in definitions of "moderate" alcohol consumption, and selecting appropriate comparison groups, have made exploring the effects of alcohol on cognition during aging difficult. The current study examined the relationship between drinking at three separate time points (between the ages of 50 and 74) and cognition in older adulthood. Results revealed that the quantity of self-reported drinks over the three time points was a significant predictor of cognition in older adulthood (b=0.001; p0.05). Overall, the results suggest no that there is not a meaningful relationship between alcohol consumption and cognitive functioning in older adulthood in this sample. There were few consistent heavy drinkers (n=71), but a large number of consistent moderate drinkers (n=1,847), although even the moderate drinkers did not consume much alcohol (mean alcohol consumption = 15.3 drinks/month; median alcohol consumption = 5.0 drinks/month). This may have limited the ability to detect clinically meaningful differences. Future studies should rely on more standardized alcohol measures, large, diverse samples, and inclusion of cognitive measures assessing visuospatial abilities and executive functioning, in order to better ...

Recent theories of the effects of ethanol on the brain have focused on its direct actions on neuronal membrane proteins. However, neuromolecular mechanisms whereby ethanol produces its CNS effects in low doses typically used by social drinkers (e.g., 2–3 drinks, 10–25 mm, 0.05–0.125 gm/dl) remain less well understood. We propose the hypothesis that ethanol may act by introducing a level of randomness or “noise” in brain electrical activity. We investigated the hypothesis by applying a battery of tests originally developed for nonlinear time series analysis and chaos theory to EEG data collected from 32 men who had participated in an ethanol/placebo challenge protocol. Because nonlinearity is a prerequisite for chaos and because we can detect nonlinearity more reliably than chaos, we concentrated on a series of measures that quantitated different aspects of nonlinearity. For each of these measures the method of surrogate data was used to assess the significance of evidence for nonlinear structure. Significant nonlinear structure was found in the EEG as evidenced by the measures of time asymmetry, determinism, and redundancy. In addition, the evidence for nonlinear structure in the placebo condition was found to be significantly greater than that for ethanol. Nonlinear measures, but not spectral measures, were found to correlate with a subject’s overall feeling of intoxication. These findings are consistent with the notion that ethanol may act by introducing a level of randomness in neuronal processing as assessed by EEG nonlinear structure.

Prenatal alcohol exposure is known to cause damage to the central nervous system. This study sought to further elucidate the structural brain damage that occurs following prenatal alcohol exposure in both children and rats. Two children with histories of maternal alcohol abuse but who did not qualify for a diagnosis of Fetal Alcohol Syndrome (FAS), based on established criteria, underwent magnetic resonance imaging. Reduced volumes were found for the cerebrum and cerebellum. In addition, the proportional volume of the basal ganglia was reduced, although the proportional volumes of cortical and subcortical fluid, cortical gray matter, limbic and nonlimbic cortex, and diencephalic structures were unaffected. These findings are compared with our recent MRI findings in two cases of FAS. In addition, the caudate-putamen and ventricular areas were assessed in rats exposed to alcohol prenatally. Whereas the overall brain section area was not reduced in size, the area of the caudate-putamen was reduced and that of the ventricles was enlarged.

BACKGROUND: On the subject of cerebral infarction, it is a common saying that “time is brain”. The prognosis of a patient who has received thrombolysis after such an infarction becomes significantly better as the time from symptom debut until the thrombolytic bolus lessens. Identifying the factors that contribute to longer times before thrombolysis for patients could thus be meaningful, and this is exactly what the aim of this assignment is. METHODS: Data was collected from the digital documents of patients who had received thrombolytic treatment from Akershus University Hospital. Both linear and categorical variables were registered from fields such as the patients’ background, vitals and disease severity. Time from onset to arrival at the hospital and time from arrival to the start of the infusion were registered in detail, and potentially delaying factors such as uncertain time of symptom debut and suspected contraindications were explored. The official Norwegian limit for delayed thrombolysis is 40 minutes, and thus this was chosen as the limit in this assignment as well. RESULTS: A total of 100 patients were registered, having received thrombolysis in 2015 and 2016. 50 men and 50 women were registered, with a mean age of 67.6. The mean NIHSS on arrival was 7.63 (standard variance 6.06). The mean time from symptom debut until arrival was 90.09 min (standard variance 48.91) and the mean time from arrival until the thrombolysis was given was 46.24 min (standard variance 33.40). 48.0% of the patients received thrombolysis more than 40 min after arrival, thus defining it as delayed treatment. The factors which showed a significant association with delayed treatment, using a confidence interval of 95%, were smoking (p=0.028), necessary prethrombolytic reduction in blood pressure (p=0.002), suspected contraindication (p=0.023) and uncertain severity of disease (p=0.001). Factors that unexpectedly showed no significant association with delayed treatment were uncertain time of symptom debut and high NIHSS on arrival. CONCLUSION: Factors that may have contributed to delayed thrombolysis were smoking, prethrombolytic reduction of blood pressure, suspected contraindications and uncertain severity of disease. In order to shorten the time from arrival to treatment, the effects of these factors on the efficiency of the thrombolytic procedure must be minimized. This could be attempted by using tools such as stricter, clearer guidelines and hospital campaigns targeting the attitudes of the personnel. All this being said, this assignment has made it clear that the treatment of cerebral infarctions is largely successful.

Background and PurposeVarenicline, a neuronal nicotinic acetylcholine receptor (nAChR) modulator, decreases ethanol consumption in rodents and humans. The proposed mechanism of action for varenicline to reduce ethanol consumption has been through modulation of dopamine (DA) release in the nucleus accumbens (NAc) via α4*‐containingnAChRsin the ventral tegmental area (VTA). However, presynapticnAChRson dopaminergic terminals in theNAchave been shown to directly modulate dopaminergic signalling independently of neuronal activity from theVTA. In this study, we determined whethernAChRsin theNAcplay a role in varenicline's effects on ethanol consumption.Experimental ApproachRats were trained to consume ethanol using the intermittent‐access two‐bottle choice protocol for 10 weeks. Ethanol intake was measured after varenicline or vehicle was microinfused into theNAc(core, shell or core‐shell border) or theVTA(anterior or posterior). The effect of varenicline treatment onDArelease in theNAcwas measured using bothin vivomicrodialysis andin vitrofast‐scan cyclic voltammetry (FSCV).Key ResultsMicroinfusion of varenicline into theNAccore and core‐shell border, but not into theNAcshell orVTA, reduced ethanol intake following long‐term ethanol consumption. During microdialysis, a significant enhancement in accumbalDArelease occurred following systemic administration of varenicline andFSCVshowed that varenicline also altered the evoked release ofDAin theNAc.Conclusion and ImplicationsFollowing long‐term ethanol consumption, varenicline in theNAcreduces ethanol intake, suggesting that presynapticnAChRsin theNAcare important for mediating varenicline's effects on ethanol consumption.

Brain circuits that include the cortex and basal ganglia make up the bulk of the forebrain, and influence behaviors related to almost all aspects of affective, cognitive and sensorimotor functions. The learning of new actions as well as association of existing action repertoires with environmental events are key functions of this circuitry. Unfortunately, the cortico-basal ganglia circuitry is also the target for all drugs of abuse, including alcohol. This makes the circuitry susceptible to the actions of chronic alcohol exposure that impairs circuit function in ways that contribute to cognitive dysfunction and drug use disorders. In the present review, we describe the connectivity and functions of the associative, limbic and sensorimotor cortico-basal ganglia circuits. We then review the effects of acute and chronic alcohol exposure on circuit function. Finally, we review studies examining the roles of the different circuits and circuit elements in alcohol use and abuse. We attempt to synthesize information from a variety of studies in laboratory animals and humans to generate hypotheses about how the three circuits interact with each other and with the other brain circuits during exposure to alcohol and during the development of alcohol use disorders. This article is part of the Special Issue entitled "Alcoholism".

Patients with pure autonomic failure (PAF) and multiple system atrophy (MSA) may complain of feeling light-headed after alcohol ingestion particularly on assumption of the upright posture. The reasons for this have not been investigated. We therefore studied the effects of oral alcohol (40% vodka in sugar-free orange juice) and placebo (juice only) on the systemic and regional (including superior mesenteric artery, SMA) blood flow in nine patients with PAF and six patients with MSA. After alcohol, there was a fall in supine blood pressure (BP) and vasodilatation in the SMA but no change in cardiac output, or forearm muscle and cutaneous blood flow in either PAF or MSA; BP fell further during head-up tilt with no changes in levels of plasma catecholamines. After placebo, there were no changes while supine. We conclude that alcohol lowers supine BP and dilates the SMA with no change in muscle or cutaneous blood flow. Alcohol also enhances the fall in BP during head-up tilt. This may explain the symptoms experienced by PAF and MSA patients after alcohol.

AbstractParavertebral block is commonly used in the treatment for acute and chronic pain. The duration of paravertebral block could theoretically be prolonged with neurolytic agents. We report two cases of ultrasound‐guided neurolytic paravertebral blocks in patients suffering from intense cancer‐related thoracic pain. Ultrasound was used to identify the space and plane of injection at the mid‐thoracic level. Absolute alcohol was used to block the nerves at different segments. The two patients had great pain relief. Neurolytic paravertebral block can be a useful technique in patients with intractable cancer pain. Because of the risk of complication, it is recommended that this technique should be limited to relief of intractable pain in cancer patients with a poor prognosis.