Effects Of Acute Intoxication Research Articles

Acute Ammonia Intoxication-Induced Seizures but not Ammonia Per Se Contribute to the Electrophysiological Changes in Rat Brain

Background and Aim: Hepatic encephalopathy (HE) is a major complication in patients with mild to severe liver disease. HE is characterized by confusion, inverted sleep-wake cycles, disorientation, behavioral changes, impaired cognition, and motor disturbances, as well as increased brain edema and intracranial pressure. The molecular basis for these changes in HE remains unclear. Elevated blood and brain ammonia levels have been strongly implicated in its pathogenesis. Whether ammonia play any role in electrophysiological changes in HE that may be involved in neurobehavioral, biochemical and molecular changes observed in HE was examined. Methods: Male Wister albino rats were injected (i.p) with ammonium acetate (500 and 800 mg/kg) and liver toxin acetaminophen (AMPN, 500 mg/kg). Results: The AACE-treated group developed seizures within 10 min and survived post-treatment without any additional seizure incident. However, more than 70% of AMPN treated animals died after 56 hours. Hippocampal slices were prepared from these animals (1 hr after AACE and 40 h after AMPN, pre-coma stage) and electrophysiological changes were measured. A paired-pulse facilitation (PPF) sequence in which stimulation pulse pairs were delivered at intervals of 20-480 ms and the filed excitatory postsynaptic potential (EPSP) slope were calculated. A depressed PPF was observed in slices from both AACE and AMPN treated animals. Further, inhibition of seizures in AACE group showed reversal of these electrophysiological changes, while these inhibitors failed to prevent electrophysiological changes induced by AMPN. Additionally, seizure inducing agent's picrotoxin (PCT) and pentylenetetrazol (PTZ) showed electrophysiological changes similar to AACE, and that inhibition of PCT and PTZ induced seizures reversed electrophysiological changes. Conclusion: These findings suggest that the effect of acute ammonia intoxication on electrophysiological changes may be due to the effect of ammonia-induced seizures, but not due to ammonia per se. The author have none to declare.

Lectin histochemistry for detecting cadmium-induced changes in the glycosylation pattern of rat placenta

Cadmium (Cd) is an industrial and environmental pollutant that produces toxic effects on gametogenesis, pre- and post-implantation embryos, and the placenta. Because the effects of acute Cd intoxication on the placenta are not well understood, we investigated changes in its glycosylated components in Cd treated dams at days 4, 7, 10 and 15 of gestation using lectin histochemistry. CdCl2 was administered to pregnant rats; control animals received sterile normal saline. Placentas were processed for DBA, Con A, SBA, PNA, UEA-I, RCA-I and WGA lectin histochemistry to evaluate changes in the carbohydrate pattern of the placenta that might modify cell interactions and contribute to embryonic alterations. Lectin binding was analyzed in the yolk sac; trophoblast giant cells; trophoblast I, II and III; spongiotrophoblast cells and endovascular trophoblast cells in the chorioallantoic placenta. Our lectin binding patterns showed that Cd caused alteration of SBA and DBA labeling of trophoblast-derived cells, which suggested increased expressions of α and β GalNAc. Cd also caused decreased UEA-1 binding affinity, which indicated fewer α-L-Fuc residues in placentas of Cd treated dams. The nonreactivity in trophoblast I of the control placentas incubated with Con-A contrasted with the labeling in placentas of experimental dams, which indicated increased expression of terminal α-D-Man, and α-D-Glc residues. We found that Cd altered the reactivity of placenta to several lectins, which indicated modification of the glycotype presented by the fetal component of the placenta. We report that Cd exerts a deleterious effect on the glycosylation pattern of the placenta.

Acute Alcohol Intoxication Exacerbates Rhabdomyolysis-Induced Acute Renal Failure in Rats.

Traumatic and nontraumatic rhabdomyolysis can lead to acute renal failure (ARF), and acute alcohol intoxication can lead to multiple abnormalities of the renal tubules. We examined the effect of acute alcohol intoxication in a rat model of rhabdomyolysis and ARF. Intravenous injections of 5 g/kg ethanol were given to rats over 3 h, followed by glycerol-induced rhabdomyolysis. Biochemical parameters, including blood urea nitrogen (BUN), creatinine (Cre), glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and creatine phosphokinase (CPK), were measured before and after induction of rhabdomyolysis. Renal tissue injury score, renal tubular cell expression of E-cadherin, nuclear factor-κB (NF-κB), and inducible nitric oxide synthase (iNOS) were determined. Relative to rats in the vehicle group, rats in the glycerol-induced rhabdomyolysis group had significantly increased serum levels of BUN, Cre, GOT, GPT, and CPK, elevated renal tissue injury scores, increased expression of NF-κB and iNOS, and decreased expression of E-cadherin. Ethanol exacerbated all of these pathological responses. Our results suggest that acute alcohol intoxication exacerbates rhabdomyolysis-induced ARF through its pro-oxidant and inflammatory effects.

Reversal of Ethanol-induced Intoxication by a Novel Modulator of Gβγ Protein Potentiation of the Glycine Receptor

The acute intoxicating effects of ethanol in the central nervous system result from the modulation of several molecular targets. It is widely accepted that ethanol enhances the activity of the glycine receptor (GlyR), thus enhancing inhibitory neurotransmission, leading to motor effects, sedation, and respiratory depression. We previously reported that small peptides interfered with the binding of Gβγ to the GlyR and consequently inhibited the ethanol-induced potentiation of the receptor. Now, using virtual screening, we identified a subset of small molecules capable of interacting with the binding site of Gβγ. One of these compounds, M554, inhibited the ethanol potentiation of the GlyR in both evoked currents and synaptic transmission in vitro When this compound was tested in vivo in mice treated with ethanol (1-3.5 g/kg), it was found to induce a faster recovery of motor incoordination in rotarod experiments and a shorter sedative effect in loss of righting reflex assays. This study describes a novel molecule that might be relevant for the design of useful therapeutic compounds in the treatment of acute alcohol intoxication.

The effects of acute alcohol intoxication on the cognitive mechanisms underlying false facial recognition.

RationaleFalse face recognition rates are sometimes higher when faces are learned while under the influence of alcohol. Alcohol myopia theory (AMT) proposes that acute alcohol intoxication during face learning causes people to attend to only the most salient features of a face, impairing the encoding of less salient facial features. Yet, there is currently no direct evidence to support this claim.ObjectivesOur objective was to test whether acute alcohol intoxication impairs face learning by causing subjects to attend to a salient (i.e., distinctive) facial feature over other facial features, as per AMT.MethodsWe employed a balanced placebo design (N = 100). Subjects in the alcohol group were dosed to achieve a blood alcohol concentration (BAC) of 0.06 %, whereas the no alcohol group consumed tonic water. Alcohol expectancy was controlled. Subjects studied faces with or without a distinctive feature (e.g., scar, piercing). An old-new recognition test followed. Some of the test faces were “old” (i.e., previously studied), and some were “new” (i.e., not previously studied). We varied whether the new test faces had a previously studied distinctive feature versus other familiar characteristics.ResultsIntoxicated and sober recognition accuracy was comparable, but subjects in the alcohol group made more positive identifications overall compared to the no alcohol group.ConclusionsThe results are not in keeping with AMT. Rather, a more general cognitive mechanism appears to underlie false face recognition in intoxicated subjects. Specifically, acute alcohol intoxication during face learning results in more liberal choosing, perhaps because of an increased reliance on familiarity.

Alcohol and substances acute intoxication in a population of suicide attempters

IntroductionThe effects of psychotropic drugs and alcohol acute intoxication are important risk factors for attempted suicide among individuals with and without substance use disorder (SUD).AimsThe first aim of this study is describing the socio-demographic features and clinical history of subjects who were acutely intoxicated when attempting suicide. The second aim is to compare their features with those of subjects without acute alcohol and substances intoxication at suicide attempt time.MethodsDeterminants of ER psychiatric consultations were studied prospectively during the period 2008–2014 at the “Maggiore della Carità” Hospital in Novara, Italy. For each patient, a data sheet was filled in by experienced psychiatrists, in order to gather demographic features, psychiatric history and present clinical issues like blood and urine dosage of amphetamine and methamphetamine, cannabinoid, cocaine and alcohol. Comparison of qualitative data was performed by means of the Chi2 test. Statistical significance was set at P ≤ 0.05.ResultsWe collected a sample of 495 suicide attempters who referred to our ER. Statistical analysis of demographic and clinical data is still ongoing.ConclusionsPreliminary results point out that acute alcohol and drugs intoxication at suicide attempt time is much more frequent in subjects without a SUD. Implications will be discussed.Disclosure of interestThe authors have not supplied their declaration of competing interest.

In vivo quantification of demyelination and recovery using compartment-specific diffusion MRI metrics validated by electron microscopy

There is a need for accurate quantitative non-invasive biomarkers to monitor myelin pathology in vivo and distinguish myelin changes from other pathological features including inflammation and axonal loss. Conventional MRI metrics such as T2, magnetization transfer ratio and radial diffusivity have proven sensitivity but not specificity. In highly coherent white matter bundles, compartment-specific white matter tract integrity (WMTI) metrics can be directly derived from the diffusion and kurtosis tensors: axonal water fraction, intra-axonal diffusivity, and extra-axonal radial and axial diffusivities. We evaluate the potential of WMTI to quantify demyelination by monitoring the effects of both acute (6weeks) and chronic (12weeks) cuprizone intoxication and subsequent recovery in the mouse corpus callosum, and compare its performance with that of conventional metrics (T2, magnetization transfer, and DTI parameters). The changes observed in vivo correlated with those obtained from quantitative electron microscopy image analysis. A 6-week intoxication produced a significant decrease in axonal water fraction (p<0.001), with only mild changes in extra-axonal radial diffusivity, consistent with patchy demyelination, while a 12-week intoxication caused a more marked decrease in extra-axonal radial diffusivity (p=0.0135), consistent with more severe demyelination and clearance of the extra-axonal space. Results thus revealed increased specificity of the axonal water fraction and extra-axonal radial diffusivity parameters to different degrees and patterns of demyelination. The specificities of these parameters were corroborated by their respective correlations with microstructural features: the axonal water fraction correlated significantly with the electron microscopy derived total axonal water fraction (ρ=0.66; p=0.0014) but not with the g-ratio, while the extra-axonal radial diffusivity correlated with the g-ratio (ρ=0.48; p=0.0342) but not with the electron microscopy derived axonal water fraction. These parameters represent promising candidates as clinically feasible biomarkers of demyelination and remyelination in the white matter.

Does acute alcohol intoxication cause transaminase elevations in children and adolescents?

Several long-term effects of alcohol abuse in children and adolescents are well described. Alcohol abuse has severe effects on neurodevelopmental outcome, such as learning disabilities, memory deficits, and decreased cognitive performance. Additionally, chronic alcohol intake is associated with chronic liver disease. However, the effects of acute alcohol intoxication on liver function in children and adolescents are not well characterized. The aim of this study was to determine if a single event of acute alcohol intoxication has short-term effects on liver function and metabolism. All children and adolescents admitted to the Department of Pediatrics and Adolescent Medicine between 2004 and 2011 with the diagnosis "acute alcohol intoxication" were included in this retrospective analysis. Clinical records were evaluated for age, gender, alcohol consumption, blood alcohol concentration, symptoms, and therapy. Blood values of the liver parameters, CK, creatinine, LDH, AP, and the values of the blood gas analysis were analyzed. During the 8-year study period, 249 children and adolescents with the diagnosis "acute alcohol intoxication" were admitted, 132 (53%) girls and 117 (47%) boys. The mean age was 15.3 ± 1.2 years and the mean blood alcohol concentration was 0.201 ± 0.049%. Girls consumed significantly less alcohol than boys (64 g vs. 90 g), but reached the same blood alcohol concentration (girls: 0.199 ± 0.049%; boys: 0.204 ± 0.049%). The mean values of liver parameters were in normal ranges, but AST was increased in 9.1%, ALT in 3.9%, and γGT in 1.4%. In contrast, the mean value of AST/ALT ratio was increased and the ratio was elevated in 92.6% of all patients. Data of the present study showed significant differences in the AST/ALT ratio (p < 0.01) in comparison to a control group. Data of the present study indicate that there might be an effect of acute alcohol intoxication on transaminase levels. The AST/ALT ratio seems to reflect the damage in hepatocytes after intensive alcohol consumption. The present study indicates a sex-specific difference in alcohol metabolism and effects between girls and boys: girls need less alcohol than boys to achieve the same blood alcohol levels than boys, and are more prone to loss of consciousness.

Marijuana Legalization: Impact on Physicians and Public Health.

Marijuana is becoming legal in an increasing number of states for both medical and recreational use. Considerable controversy exists regarding the public health impact of these changes. The evidence for the legitimate medical use of marijuana or cannabinoids is limited to a few indications, notably HIV/AIDS cachexia, nausea/vomiting related to chemotherapy, neuropathic pain, and spasticity in multiple sclerosis. Although cannabinoids show therapeutic promise in other areas, robust clinical evidence is still lacking. The relationship between legalization and prevalence is still unknown. Although states where marijuana use is legal have higher rates of use than nonlegal states, these higher rates were generally found even prior to legalization. As states continue to proceed with legalization for both medical and recreational use, certain public health issues have become increasingly relevant, including the effects of acute marijuana intoxication on driving abilities, unintentional ingestion of marijuana products by children, the relationship between marijuana and opioid use, and whether there will be an increase in health problems related to marijuana use, such as dependence/addiction, psychosis, and pulmonary disorders. In light of this rapidly shifting legal landscape, more research is urgently needed to better understand the impact of legalization on public health.

Research on the Effects of Alcohol and Sexual Arousal on Sexual Risk in Men who have Sex with Men: Implications for HIV Prevention Interventions.

The purpose of this paper was to describe and appraise the research evidence on the effects of acute alcohol intoxication and sexual arousal on sexual risk behaviors in men who have sex with men (MSM) and to examine its implications for design of HIV prevention interventions that target MSM. Toward that end, the paper begins with a discussion of research on sexual arousal in men and alcohol and their acute effects on sexual behaviors. This is followed by a review of empirical evidence on the combined acute effects of alcohol and sexual arousal in heterosexual men (the large majority of studies) and then in MSM. The empirical evidence and related theoretical developments then are integrated to derive implications for developing effective HIV prevention interventions that target MSM.

Hallucinogen Persisting Perception Disorder (HPPD) and Flashback Phenomena – Differential Diagnosis and Explanation Models

The purpose of this article is to provide an overview of the current research on "Hallucinogen Persisting Perception Disorder" (HPPD) and "Flashback" phenomena. The definition and diagnostic features of "Flashback" and HPPD remained often unclear and since the 1960 s interchangeable. Relevant literature was identified by means of a computerized MEDLINE search including the years 1994-2014. Finally 75 journal articles out were included in the review. Consistent with the ICD-10 (F16.70) definition "Flashback" is often used to describe brief visual perceptual, mood, and altered states of consciousness effects reminiscent of acute hallucinogen intoxication effects. Many users regard flashback phenomena as benign and even pleasant. HPPD is described in DSM-5 as a visual perceptual disorder, sometimes persisting for months or years causing severe individual distress. The prevalence of flashback and HPPD is unknown. It is considered to be remarkable in view of the relatively few case reports published out of millions of hallucinogen users since the 1960 s and 1970 s. Despite a multitude of etiological and therapeutic approaches the exact pathophysiological mechanisms underlying HPPD remain elusive. At present HPPD appears to be further a DSM-5-genuine but still puzzling disorder. The different consequences including new therapeutic approaches are discussed in clinical context.

Bacterial Genotoxins: Merging the DNA Damage Response into Infection Biology.

Bacterial genotoxins are unique among bacterial toxins as their molecular target is DNA. The consequence of intoxication or infection is induction of DNA breaks that, if not properly repaired, results in irreversible cell cycle arrest (senescence) or death of the target cells. At present, only three bacterial genotoxins have been identified. Two are protein toxins: the cytolethal distending toxin (CDT) family produced by a number of Gram-negative bacteria and the typhoid toxin produced by Salmonella enterica serovar Typhi. The third member, colibactin, is a peptide-polyketide genotoxin, produced by strains belonging to the phylogenetic group B2 of Escherichia coli. This review will present the cellular effects of acute and chronic intoxication or infection with the genotoxins-producing bacteria. The carcinogenic properties and the role of these effectors in the context of the host-microbe interaction will be discussed. We will further highlight the open questions that remain to be solved regarding the biology of this unusual family of bacterial toxins.

Effects of Alcohol and Sexual Prejudice on Aggression Toward Sexual Minorities.

This study was the first to test the moderating effect of acute alcohol intoxication on the relation between heterosexual men's sexual prejudice and perpetration of aggression toward gay men and lesbians. Participants were 320 heterosexual men aged 21-30 recruited from a large southeastern United States city. Participants completed a measure of prejudice toward sexual minorities and were randomly assigned to one of eight experimental groups within a 2 (Beverage: Alcohol, No-Alcohol Control) × 2 (Opponent Gender: Male, Female) × 2 (Opponent Sexual Orientation: Homosexual, Heterosexual) design. Following beverage consumption, participants were provoked via reception of electric shocks from a fictitious opponent. Participants' physical aggression was measured using a shock-based aggression task. The association between sexual prejudice and aggression toward the gay male opponent was stronger among intoxicated, relative to sober, participants. This pattern of association was not observed among participants who competed against the heterosexual male, heterosexual female, or lesbian opponent. Findings provide the first experimental evidence that alcohol intoxication moderates sexually-prejudiced aggression toward gay men. These data offer a first step toward understanding how alcohol facilitates bias-motivated aggression. Such knowledge contributes to the empirical foundation needed to guide the development of interventions for alcohol-related aggression toward sexual minorities.

Executive Functioning in Alcohol Use Studies: A Brief Review of Findings and Challenges in Assessment.

There is a wealth of research about the links between executive functioning (EF) and alcohol use. However, difficulty may arise in interpreting findings because of the variability between studies regarding the specific components of EF measured, as well as the variability of tasks used to examine each EF construct. The current article considers each of these problems within the context of a literature review that focuses on two topics: (1) the efficacy of EF in predicting alcohol use and alcohol-related consequences, and (2) the effect of acute alcohol intoxication on EF task performance. An additional goal was to identify and describe commonly used EF measures with the intention of providing alcohol researchers information on the assessment of different EF domains. Our findings indicate that there is strong evidence supporting a relation between EF difficulties (particularly response inhibition and information updating) and alcohol use, with additional evidence of a significant interaction between EF and implicit associations on alcohol use. In contrast, research supporting a link between set shifting abilities and later alcohol use is scarce. Additionally, this review found evidence of alcohol acutely affecting many EF processes (particularly response inhibition). Overall, there is a need to replicate these findings with commonly used EF tasks (versus developing numerous tasks within individual laboratories) to better advance our understanding of the relation between EF and alcohol use.

Dormant Masculinity: Moderating Effects of Acute Alcohol Intoxication on the Relation Between Male Role Norms and Antigay Aggression.

Acute alcohol intoxication was examined as a moderator of the association between men's adherence to traditional gender norms and aggression towards a gay male. Participants were 164 heterosexual drinking men between the ages of 21-30. Participants completed a battery of questionnaires that included a measure of adherence to male role norms (i.e., status, toughness, antifemininity), were randomly assigned to consume an alcohol or no-alcohol control beverage, and completed the Taylor Aggression Paradigm in which electric shocks were administered to, and received from, a fictitious gay or heterosexual male opponent. Results indicated a greater adherence to both the toughness (β = .50, p = .002) and antifeminine (β = .37, p = .023) norms predicted high levels of aggression towards a gay man only among participants who were intoxicated. This interaction effect was not detected for the status norm. Consistent with previous research, findings suggest that adherence to the toughness norm does not increase sober men's risk of aggression toward gay men. However, this is the first study to demonstrate that alcohol intoxication may activate concepts of toughness, and thus influence men to act in line with this facet of the masculine concept. Importantly, these data support the view that men's adherence to various dimensions of masculinity may be dormant in some contexts, only to be activated, and subsequently demonstrated, in other contexts.

The effect of acute alcohol intoxication on gut wall integrity in healthy male volunteers; a randomized controlled trial

The aim of the study is to determine the effect of acute alcohol consumption on enterocytes. Chronic alcohol consumption has been known to induce a decrease in gut wall integrity in actively drinking alcoholics and patients with alcohol-induced liver disease. Data on the extent of the damage induced by acute alcohol consumption in healthy human beings is scarce. Studies show that heavy incidental alcohol consumption is a growing problem in modern society. Data on this matter may provide insights into the consequences of this behavior for healthy individuals. In a randomized clinical trial in crossover design, 15 healthy volunteers consumed water one day and alcohol the other. One blood sample was collected pre-consumption, five every hour post-consumption, and one after 24 h. Intestinal fatty acid binding protein (I-FABP) was used as a marker for enterocyte damage. Liver fatty acid binding protein (L-FABP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyl transferase (GGT) were used as markers for hepatocyte damage. Lipopolysaccharide binding protein (LBP) and soluble CD14 (sCD14) were used as a measure of translocation. Interleukin-6 (IL-6) was used to assess the acute inflammatory response to endotoxemia. Alcohol consumption caused a significant increase in serum I- and L-FABP levels, compared to water consumption. Levels increased directly post-consumption and decreased to normal levels within 4 h. LBP, sCD14, and IL-6 levels were not significantly higher in the alcohol group. Moderate acute alcohol consumption immediately damages the enterocyte but does not seem to cause endotoxemia.

Elevation of BDNF exon I-specific transcripts in the frontal cortex and midbrain of rat during spontaneous morphine withdrawal is accompanied by enhanced pCreb1 occupancy at the corresponding promoter.

Brain-derived neurotrophic factor (BDNF) is believed to play a crucial role in the mechanisms underlying opiate dependence; however, little is known about specific features and mechanisms regulating its expression in the brain under these conditions. The aim of this study was to investigate the effects of acute morphine intoxication and withdrawal from chronic intoxication on expression of BDNF exon I-, II-, IV-, VI- and IX-containing transcripts in the rat frontal cortex and midbrain. We also have studied whether alterations of BDNF exon-specific transcripts are accompanied by changes in association of well-known transcriptional regulators of BDNF gene-phosphorylated (active form) cAMP response element binding protein (pCreb1) and methyl-CpG binding protein 2 (MeCP2) with corresponding regulatory regions of the BDNF gene. Acute morphine intoxication did not affect levels of BDNF exons in brain regions, while spontaneous morphine withdrawal in dependent rats was accompanied by an elevation of the BDNF exon I-containing mRNAs both in the frontal cortex and midbrain. During spontaneous morphine withdrawal, increased associations of pCreb1 were found with promoter of exon I in the frontal cortex and promoters of exon I, IV and VI in the midbrain. The association of MeCP2 with BDNF promoters during spontaneous morphine withdrawal did not change. Thus, BDNF exon-specific transcripts are differentially expressed in brain regions during spontaneous morphine withdrawal in dependent rats and pCreb1 may be at least partially responsible for these alterations.

Effects of alcohol intoxication and autonomic arousal on delay discounting and risky sex in young adult heterosexual men

ObjectivesThe relationship between alcohol use and risky sexual behavior is complex and depends on psychological and environmental factors. The alcohol myopia model predicts that, due to alcohol's impact on attention, the behavior of intoxicated individuals will become increasingly directed by salient cues. Autonomic arousal (AA) may have a similar effect on attention. Experiential delay discounting (DD) may be increased by both alcohol consumption and AA due to their common effects and may mediate the relationship between these conditions and risky sex. MethodsThis study employed a 3 (alcohol, placebo, control)×2 (high, low arousal) experimental design to examine the effects of acute alcohol intoxication and AA on experiential delay discounting, subjective sexual arousal, and risky sex. ResultsPath models revealed complex results that only partially supported study hypotheses. Ratings of subjective sexual arousal did not differ across either beverage or arousal conditions. DD was also unrelated to any study variable. However, subjective sexual arousal was positively related to risky sexual intentions. Alcohol intoxication was also positively associated with increased unprotected sex intentions, consistent with past studies. ConclusionsThese results affirm the role of subjective sexual arousal and alcohol intoxication in risky sexual decision-making, yielding effect sizes similar to comparable past studies. The lack of differences across autonomic arousal groups also suggests that effects of attentional myopia may be behavior-specific. Failure to replicate effects of alcohol intoxication on DD also suggests reservation regarding its involvement in alcohol-involved risky sex.

Ethanol, Trauma, and the Brain

Alcohol intoxication plays a significant and causal role in various fatal injuries. In comparison to sober individuals, intoxicated people have a greater generic risk for being involved in hazardous activities that may result in fatal injuries. However, it is not clear whether the biological effects of acute alcohol intoxication result in worse injuries than those sustained by sober individuals who are injured by identical mechanisms. Alcohol intoxication has a neuroprotective effect in experimental animal models of traumatic brain injury (TBI) but the evidence for a similar effect in humans is controversial. Earlier studies found such a protective effect, but more recent large epidemiological studies have not confirmed this finding; some studies also suggest a dose-related protective or exacerbating effect of alcohol intoxication on TBI. There are two apparent alcohol-associated syndromes in which an otherwise survivable blunt force impact to the head of an intoxicated individual is fatal at the scene. The first is a fatal cardiorespiratory arrest (the so-called alcohol concussion syndrome or “commotio medullaris”); the second is “traumatic basilar subarachnoid hemorrhage” (secondary to tears in the cerebral arteries, particularly the intracranial and extracranial vertebral arteries).

Interactive effects of contextual cues and acute alcohol intoxication on the associations between alcohol expectancy activation and urge to drink.

This study examined the joint effects of contextual cues and alcohol intoxication on the associations between activation of positive and negative alcohol expectancies in memory and self-reported urges to drink alcohol after a laboratory alcohol administration. Young adult heavy drinkers were randomly assigned to drink a moderate dose of alcohol or a placebo (alcohol manipulation), and then listened to positive or negative drinking scenarios (cue manipulation). Before and after these manipulations, participants completed an alcohol expectancy Stroop task assessing positive and negative expectancy activation, as well as self-report measures of urges to drink. Regression analyses revealed that the alcohol and cue manipulations had a joint, moderating impact on the associations between expectancy activation and postcue changes in urge to drink. Specifically, both increased activation of negative expectancies and decreased activation of positive expectancies predicted decreases in urges to drink, but only for intoxicated participants in the negative cue condition. There were no associations between expectancy activation and urges to drink for those in the positive cue condition regardless of beverage condition. Results suggest that whether memory activation of alcohol expectancies has an impact on urge to drink after alcohol is on board may depend on the relevance of the activated expectancies to the current drinking context. This process appears to be influenced by a complex interaction between contextual cues in the environment and the pharmacological effects of alcohol.