Diseases of the Nervous System
George Feuer, Felix A. de la Iglesia in Molecular Biochemistry of Human Disease, 2020
Direct effects of acute alcohol intoxication or drunkeness include euphoria, an apparent decrease of the anxiety levels, nausea, dizziness, unsteady gait, and slurred speech287 (Table 4). The initial state can further progress to stupor and coma with respiratory depression. The degree of intoxication is largely dependent on the amount of alcohol consumed and the rate of alcohol metabolism. The metabolism is relatively constant, but modified by previous alcohol consumption and actual dietary intake. Interactions occur between alcohol and barbiturate or diazepam on the hypothalamus-pituitary-adrenal function in chronic alcoholics.405 The consumption of large amounts of alcohol during pregnancy may cause damage to the embryo and abnormal fetal development.463 Chronic alcoholic mothers may give birth to children with dysmorphic features and mentally deficient children.274,550
The Neuropsychological Consequences of Alcohol and Drug Abuse
John Brick in Handbook of the Medical Consequences of Alcohol and Drug Abuse, 2012
Alcohol ranks as one of the most serious substances of abuse due to the prevalence of alcohol abuse in the general population and the severity of its toxic effects. It has been estimated that between 5 and 12 million individuals abuse alcohol, with a significantly greater proportion being male (Hartman, 1995; Thompson, 2000). The acute effects of alcohol intoxication are well known and include changes in psychomotor and cognitive functioning, as well as changes in affect. Some of the effects of chronic alcohol abuse are also well known and have been extensively reviewed, particularly the dramatic effect of alcohol on memory in the case of Korsakoff’s syndrome (Butters, 1984; Butters and Miliotis, 1985). Less clear and still somewhat controversial are answers to the following questions:What are the cognitive effects of chronic alcohol abuse in the absence of Korsakoff’s syndrome?What, if any, are the direct toxic effects of alcohol on brain tissue?Are there cognitive predictive factors for individuals at high risk for alcohol abuse?What is known about the recovery of cognitive functions after abstinence from chronic alcohol abuse?
Addictions and dependencies: their association with offending
John C. Gunn, Pamela J. Taylor in Forensic Psychiatry, 2014
The immediately observable effects of alcohol intoxication are impairments such as slurred speech, slowed mental and physical reaction times, and difficulty walking. They may be apparent even at small doses, are dose-dependent and are due to the depressant effects of alcohol caused by reduced excitatory actions of the neurotransmitter glutamate and increased inhibitory actions of gamma-aminobutyric acid (GABA) (National Institute on Alcohol Abuse and Alcoholism, 2000). In most cases, the impairments caused by intoxication are temporary, but intoxication can lead to death from respiratory failure, accidents associated with loss of consciousness (e.g. hypothermia; choking on vomit) or accidents associated with cognitive or motor impairment (e.g. road or machinery accidents).
GINS complex subunit 2 (GINS2) plays a protective role in alcohol-induced brain injury
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Chunhua Liu, Renfu Wang, Yu Zhang
Despite its presence in almost all societies, alcohol consumption continues to contribute greatly to the global burden of disease, accounting for around 3.8% of global deaths and 4.6% of global disability-adjusted-life-years [35]. Acute alcohol intoxication occurs following ingestion of significant amounts of alcohol over a short period of time. Symptoms of acute alcohol intoxication vary with severity and can include impaired judgement, memory deficits, inappropriate aggressive behaviour, coma, and other harmful cognitive-behavioural conditions [36]. While alcohol has been extensively studied, especially for its social and economic consequences, the genetic and molecular mechanisms of alcohol’s effects on the CNS have not been fully elucidated. In the present study, using patient serum, an experimental mouse model of acute alcohol intoxication, and primary mouse microglia, we carried out extensive analyses of the effects of GINS2 knockdown on alcohol-induced neuroinflammation and neurotoxicity. Ultimately, our study has established a crucial, protective role for GINS2 in acute alcohol intoxication, thus providing the basis for further research into clinical biomarkers of acute alcohol intoxication and effective clinical treatments.
Drinking until Intoxication: A Qualitative Study among Underage Adolescents Admitted to the Emergency Room
Published in Alcoholism Treatment Quarterly, 2020
Nienke de Wit, Gera E. Nagelhout, Gert-Jan Meerkerk, Johanna Ooms, Annelieke P. Le Net-van Bruggen, Mariken Gruppen, Carole Lasham, Merel van Loon, Dike van de Mheen
Several risk factors that may have contributed to an alcohol intoxication were found in this study. First, the assumption of having your own limit instead of a standardized limit of drinks seemed to contribute to excessive drinking resulting in an intoxication among adolescents without them being aware of it. Thereby, binge drinking was unknowingly normalized or even romanticized, where some adolescents experienced being tipsy before in an enjoyable way. However, an alcohol intoxication caused by binge drinking was not something they imagined would happen to them. This might call for a focus on normsetting among adolescents (Lemmers, Mulder, Onrust, Verdurmen, & Van Hasselt, 2016) and for re-framing “binge drinking”, since this term may not reflect the reality of young people’s experiences involving alcohol use (Szmigin et al., 2008).
Description of the predictors of persistent post-concussion symptoms and disability after mild traumatic brain injury: the SHEFBIT cohort
Published in British Journal of Neurosurgery, 2019
James Booker, Saurabh Sinha, Kishor Choudhari, Jeremy Dawson, Rajiv Singh
The results show a worse outcome with alcohol intoxication is present, in both the RPQ and RHFUQ measures. Graphical interpretation of this interaction shows that when patients have few PPCS, alcohol intoxication leads to worse long-term disability. However, when patients suffer many PPCS, alcohol intoxication appears to have a protective affect against long-term disability (see Figure 3). This reflects the conflicting evidence in the literature with regards to the effect of alcohol on recovery after mTBI.30, 34 It is known that alcohol intoxication lowers the apparent GCS score and hence, an exaggerated perception of TBI severity.35 As a result, patients with alcohol intoxication have been shown to have better recovery trajectories compared to non-intoxicated patients.36 Anecdotally, in this study alcohol intoxication often seemed to reflect patients with chaotic-lifestyles and social problems. This is likely to have negatively impacted patient’s coping strategy and recovery. Further research is needed to elaborate on this finding.