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1
Lishman, W. A. "Alcohol and the Brain." British Journal of Psychiatry 156, no. 5 (May 1990): 635–44. http://dx.doi.org/10.1192/bjp.156.5.635.
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Some of the major effects of alcohol, and alcoholism, on the brain are reviewed, with reappraisal of evidence drawn from brain imaging, neuropathology, clinical psychology, and laboratory experimental work. A hypothesis is developed which may help to account for the wide variability encountered in individual susceptibility to alcoholic brain damage and its varied manifestations. Therapeutic implications are considered.
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Le Berre, A. P., G. Rauchs, R. La Joie, F. Mézenge, C. Boudehent, F. Vabret, S. Segobin, et al. "Impaired decision-making and brain shrinkage in alcoholism." European Psychiatry 29, no. 3 (March 2014): 125–33. http://dx.doi.org/10.1016/j.eurpsy.2012.10.002.
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AbstractAlcohol-dependent individuals usually favor instant gratification of alcohol use and ignore its long-term negative consequences, reflecting impaired decision-making. According to the somatic marker hypothesis, decision-making abilities are subtended by an extended brain network. As chronic alcohol consumption is known to be associated with brain shrinkage in this network, the present study investigated relationships between brain shrinkage and decision-making impairments in alcohol-dependent individuals early in abstinence using voxel-based morphometry. Thirty patients performed the Iowa Gambling Task and underwent a magnetic resonance imaging investigation (1.5T). Decision-making performances and brain data were compared with those of age-matched healthy controls. In the alcoholic group, a multiple regression analysis was conducted with two predictors (gray matter [GM] volume and decision-making measure) and two covariates (number of withdrawals and duration of alcoholism). Compared with controls, alcoholics had impaired decision-making and widespread reduced gray matter volume, especially in regions involved in decision-making. The regression analysis revealed links between high GM volume in the ventromedial prefrontal cortex, dorsal anterior cingulate cortex and right hippocampal formation, and high decision-making scores (P < 0.001, uncorrected). Decision-making deficits in alcoholism may result from impairment of both emotional and cognitive networks.
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Kashem, Mohammed Abul, Omar Šerý, David V. Pow, Benjamin D. Rowlands, Caroline D. Rae, and Vladimir J. Balcar. "Actions of Alcohol in Brain: Genetics, Metabolomics, GABA Receptors, Proteomics and Glutamate Transporter GLAST/EAAT1." Current Molecular Pharmacology 14, no. 2 (December 31, 2020): 138–49. http://dx.doi.org/10.2174/1874467213666200424155244.
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We present an overview of genetic, metabolomic, proteomic and neurochemical studies done mainly in our laboratories that could improve prediction, mechanistic understanding and possibly extend to diagnostics and treatment of alcoholism and alcohol addiction. Specific polymorphisms in genes encoding for interleukins 2 and 6, catechol-O-methyl transferase (COMT), monaminooxidase B (MAO B) and several other enzymes were identified as associated with altered risks of alcoholism in humans. A polymorphism in the gene for BDNF has been linked to the risk of developing deficiences in colour vision sometimes observed in alcoholics. Metabolomic studies of acute ethanol effects on guinea pig brain cortex in vitro, lead to the identification of specific subtypes of GABA(A) receptors involved in the actions of alcohol at various doses. Acute alcohol affected energy metabolism, oxidation and the production of actaldehyde and acetate; this could have specific consequences not only for the brain energy production/utilization but could influence the cytotoxicity of alcohol and impact the epigenetics (histone acetylation). It is unlikely that brain metabolism of ethanol occurs to any significant degree; the reduction in glucose metabolism following alcohol consumption is due to ethanol effects on receptors, such as α4β3δ GABA(A) receptors. Metabolomics using post-mortem human brain indicated that the catecholaminergic signalling may be preferentially affected by chronic excessive drinking. Changes in the levels of glutathione were consistent with the presence of severe oxidative stress. Proteomics of the post-mortem alcoholic brains identified a large number of proteins, the expression of which was altered by chronic alcohol, with those associated with brain energy metabolism among the most numerous. Neurochemical studies found the increased expression of glutamate transporter GLAST/EAAT1 in brain as one of the largest changes caused by alcoholism. Given that GLAST/EAAT1 is one of the most abundant proteins in the nervous tissue and is intimately associated with the function of the excitatory (glutamatergic) synapses, this may be among the most important effects of chronic alcohol on brain function. It has so far been observed mainly in the prefrontal cortex. We show several experiments suggesting that acute alcohol can translocate GLAST/EAAT1 in astrocytes towards the plasma membrane (and this effect is inhibited by the GABA(B) agonist baclofen) but neither the mechanism nor the specificity (to alcohol) of this phenomenon have been established. Furthermore, as GLAST/EAAT1 is also expressed in testes and sperm (and could also be affected there by chronic alcohol), the levels of GLAST/EAAT1 in sperm could be used as a diagnostic tool in testing the severity of alcoholism in human males. We conclude that the reviewed studies present a unique set of data which could help to predict the risk of developing alcohol dependence (genetics), to improve the understanding of the intoxicating actions of alcohol (metabolomics), to aid in assessing the extent of damage to brain cells caused by chronic excessive drinking (metabolomics and proteomics) and to point to molecular targets that could be used in the treatment and diagnosis of alcoholism and alcohol addiction.
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Ragan, Paul W., Charles K. Singleton, and Peter R. Martin. "Brain Injury Associated With Chronic Alcoholism." CNS Spectrums 4, no. 1 (January 1999): 66–68. http://dx.doi.org/10.1017/s1092852900011226.
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AbstractAlcoholism can result in a number of severe consequences to the central nervous system, including Korsakoff's psychosis, delusions, delirium, Wernicke's encephalopathy, and cerebellar degeneration. Many of these disorders have a substantially higher prevalence than had been previously believed. Neuropathologic and neuroimaging studies have been instrumental in identifying the changes undergone by the alcoholic brain and the factors that may contribute to alcohol-induced brain damage. Biologic differences appear to make women especially susceptible to central nervous system insult from alcohol abuse. The damage caused by alcohol may be associated, in part, with thiamine deficiency, neuronal excitotoxicity, and magnesium wasting.
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Hayakawa, K., H. Kumagai, Y. Suzuki, N. Furusawa, T. Haga, T. Hoshi, Y. Fujiwara, and K. Yamaguchi. "Mr Imaging of Chronic Alcoholism." Acta Radiologica 33, no. 3 (May 1992): 201–6. http://dx.doi.org/10.1177/028418519203300302.
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We evaluated the brain lesions of patients with chronic alcoholism (n = 34) in comparison with age- and sex-matched controls (n = 40) by MR imaging. T1-weighted sagittal and axial images and T2-weighted axial images were obtained with a 0.5 T superconducting MR unit. Various brain measurements were then performed, and the presence of regions of abnormal signal intensity was also compared between the two groups. The brain measurements revealed significant cerebral atrophy (characterized by lateral and 3rd ventricular dilatation, and widening of the interhemispheric fissure) as well as significant cerebellar atrophy (represented by 4th ventricular dilatation) in the alcoholic group. These changes were more prominent in patients in their fifties and sixties than in those aged in the thirties and forties. Focal hypointense lesions were observed in 20.6% of the alcoholics and in 5% of the controls (p < 0.01), while focal hyperintense lesions were observed in 61.8% of the alcoholics and in 20% of the controls (p < 0.001). The severity of these MR findings correlated well with the age of the patients. These observations suggest that alcohol is an important promotor of brain aging.
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Shri, T. K. Padma, and N. Sriraam. "EEG Based Detection of Alcoholics." International Journal of Biomedical and Clinical Engineering 1, no. 1 (January 2012): 59–76. http://dx.doi.org/10.4018/ijbce.2012010105.
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The short term and long term effects of alcohol on various organs of the body, especially on the human brain is well established by numerous studies. Invasive methods such as Transcranial Magnetic Stimulation (TMS) and non invasive imaging techniques such as Computed Tomography (CT), Magnetic Resonance Imaging (MRI), Positron Emission Tomography (PET), and functional MRI activated electro-encephalogram (EEG) have been used to study the changes in EEG activity due to alcoholism. Even with the advent of neuro imaging techniques, EEG happens to be an important tool for brain study providing a non- invasive and cost effective method to detect the effects of alcohol on the human brain. This paper discusses the harmful effects of alcohol on different organs of the body. The advances in the development of EEG signal processing algorithms over the past decade for alcoholic detection are reviewed and their limitations are reported. Further the use of EEG for mass screening of alcoholics and biometric application is discussed in detail.
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Brenner, Eric, Gayatri R. Tiwari, Manav Kapoor, Yunlong Liu, Amy Brock, and R. Dayne Mayfield. "Single cell transcriptome profiling of the human alcohol-dependent brain." Human Molecular Genetics 29, no. 7 (March 6, 2020): 1144–53. http://dx.doi.org/10.1093/hmg/ddaa038.
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Abstract Alcoholism remains a prevalent health concern throughout the world. Previous studies have identified transcriptomic patterns in the brain associated with alcohol dependence in both humans and animal models. But none of these studies have systematically investigated expression within the unique cell types present in the brain. We utilized single nucleus RNA sequencing (snRNA-seq) to examine the transcriptomes of over 16 000 nuclei isolated from the prefrontal cortex of alcoholic and control individuals. Each nucleus was assigned to one of seven major cell types by unsupervised clustering. Cell type enrichment patterns varied greatly among neuroinflammatory-related genes, which are known to play roles in alcohol dependence and neurodegeneration. Differential expression analysis identified cell type-specific genes with altered expression in alcoholics. The largest number of differentially expressed genes (DEGs), including both protein-coding and non-coding, were detected in astrocytes, oligodendrocytes and microglia. To our knowledge, this is the first single cell transcriptome analysis of alcohol-associated gene expression in any species and the first such analysis in humans for any addictive substance. These findings greatly advance the understanding of transcriptomic changes in the brain of alcohol-dependent individuals.
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Kuruoglu, Asli Çepik, Zehra Arikan, Gülin Vural, Metin Karataş, Mehmet Araç, and Erdal Işik. "Single Photon Emission Computerised Tomography in Chronic Alcoholism." British Journal of Psychiatry 169, no. 3 (September 1996): 348–54. http://dx.doi.org/10.1192/bjp.169.3.348.
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BackgroundWe examined the functional and structural cerebral changes in chronic alcoholics, analysing their association with personality features and alcohol drinking habits.MethodForty patients with alcohol dependency, including 15 with antisocial personality disorder (ASP) as defined in DSM–III–R and 10 age and sex matched healthy controls were studied after termination of withdrawal symptoms, using high resolution single photon emission tomography (SPECT), cranial computerised tomography (CT) and brainstem auditory evoked potentials (BAEP).ResultsWe found significant reductions in regional cerebral blood flow (rCBF) measurements of alcoholic patients. Low flow in frontal regions encountered in 67.5% of the patients was associated with the duration of alcohol consumption, while no such relation existed with the amount of daily intake. Patients with ASP exhibited more marked frontal hypoperfusion. Significant brain atrophy detected by CT was present in 40% of the patients and did not correlate with frontal hypoperfusion.ConclusionsPatients with ASP are more sensitive to toxic effects of alcohol. Alternatively chronic alcoholism leads to frontal lobe dysfunction recognised as ASP in the clinical setting.
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Jacobson, R. R., and W. A. Lishman. "Cortical and diencephalic lesions in Korsakoff's syndrome: a clinical and scan study." Psychological Medicine 20, no. 1 (February 1990): 63–75. http://dx.doi.org/10.1017/s0033291700013234.
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SYNOPSISTwenty-five male alcoholic Korsakoff patients were compared with age and sex-matched non-Korsakoff chronic alcoholics and healthy volunteers on clinical and CT brain scan parameters. The scans were assessed by planimetry, visual grading procedures and computerized analysis. Reliable measures of third ventricular size were developed.The Korsakoff patients had wider third ventricles, larger lateral ventricles and wider interhemispheric fissures than the comparison groups; but sulcal and Sylvian fissure widths were equivalent in Korsakoff and non-Korsakoff alcoholics.The results suggest that, in addition to their well-established diencephalic lesions, many Korsakoff patients have sustained widespread cerebral damage. Shrinkage in the frontal brain regions appears to be especially pronounced. The implications for a dual aetiology of alcoholic Korsakoff's syndrome involving thiamine deficiency and features associated with alcoholism, probably direct alcohol neurotoxicity, are discussed.
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Koob, George F., and Amanda J. Roberts. "Brain Reward Circuits in Alcoholism." CNS Spectrums 4, no. 1 (January 1999): 23–37. http://dx.doi.org/10.1017/s1092852900011196.
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AbstractThis article discusses the neurocircuitry and the neurochemical systems, as well as the molecular elements within these systems, that are believed to be important in the etiology of alcoholism. Alcoholism is a complex behavioral disorder characterized by excessive consumption of alcohol; a narrowing of the behavioral repertoire toward excessive consumption; the development of tolerance and dependence; and impairment in social and occupational functioning. Animal models of the complete syndrome of alcoholism are difficult if not impossible to achieve, but validated animal models exist for many of the different components of the syndrome.Recent work has begun to define the neurocircuits responsible for the major sources of positive and negative reinforcement that are key to animal models of excessive alcohol intake. Alcohol appears to interact with alcohol-sensitive elements within neuronal membranes that convey the specificity of neurochemical actions. Positive reinforcement appears to be mediated by an activation γ-aminobutyric acid A receptors, release of opioid peptides and dopamine, inhibition of glutamate receptors, and interaction with serotonin systems. These neurocircuits may be altered by chronic alcohol administration. This is reflected by their exhibiting opposite effects during acute alcohol withdrawal, and by the recruitment of other neurotransmitter systems, such as the stress neuropeptide corticotropin-releasing factor. These neuropharmacologic actions are believed to produce allostatic changes in set-point, which set up the vulnerability to relapse that is so characteristic of alcoholism. Future challenges include a focus on understanding exactly how these neuroadaptive changes convey vulnerability to relapse in animals with a history of alcohol dependence.
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Dujmovic, Irena, Jelena Vitas, Natasa Zlataric, and Jelena Drulovic. "Central pontine myelinolysis in a chronic alcoholic: A clinical and brain magnetic resonance imaging follow-up." Vojnosanitetski pregled 70, no. 8 (2013): 785–88. http://dx.doi.org/10.2298/vsp1308785d.
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Introduction. Central pontine myelinolysis (CPM) is a noninflammatory, demyelinating lesion usually localised in the basis pontis. Chronic alcoholism is frequently associated with this condition which may have a variable clinical outcome. Until now, brain magnetic resonance imaging (MRI) follow-up in alcoholic CPM cases after alcohol withdrawal has been rarely described. Case report. We reported a 30- year-old male with a 12-year history of alcohol abuse, who presented with inability to stand and walk, nausea, vomiting and somnolence. Neurological examination revealed: impared fixation on lateral gaze, dysarthria, mild spastic quadriparesis, truncal and extremity ataxia, sock-like hypesthesia and moderate decrease in vibration sense in legs. Brain MRI showed a trident-shaped non-enhancing pontine lesion highly suggestive of CPM. After an eight-month alcoholfree follow-up period, the patient?s clinical status significantly improved, while the extent of MRI pontine lesion was merely slightly reduced. Conclusion. The presented case demonstrates that CPM in chronic alcoholics may have a benign clinical course after alcohol withdrawal, which is not necessarily associated with the reduction of lesions on brain MRI.
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Jacobson, R. R. "Alcoholism, Korsakoff’s Syndrome and the Frontal Lobes." Behavioural Neurology 2, no. 1 (1989): 25–38. http://dx.doi.org/10.1155/1989/847937.
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A subset of the diffuse cerebral changes and psychometric deficits found in chronic alcoholics is similar to that seen in the frontal lobe syndrome. Certain features of alcoholic Korsakoff's syndrome (AKS) also point to cortical involvement, and this may have a basis in alcohol neurotoxicity. Twenty-five patients with AKS and 24 non-Korsakoff alcoholic controls were compared using an automated CT brain scan program. In addition to evidence of their diencephalic lesions (wide third ventricles), AKS patients revealed widespread cerebral damage with greater Sylvian and interhemispheric fissure (IHF) size than alcoholics. Korsakoffs were also inferior to alcoholics in performance on a category sorting test, in which non-perseverative error scores correlated significantly with IHF size. The principle of distinguishing between selective memory decline and global intellectual decline (GID) was applied to 38 patients with AKS. Indices were developed for each type of deficit and much variation found in their distributions. The degree of GID correlated significantly with IHF size, showing similar trends with other cortical measures. These results suggest a cortical substrate for the degree of GID and a frontal substrate for category sorting deficits; with a probable basis in alcohol neurotoxicity rather than thiamine deficiency, which is not known to impair cortical structure. A new model is proposed of the pathophysiology of alcoholic brain damage and AKS which includes recent work on neurotransmitter sources and thalamo-frontal connections.
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Silva, Cristiane Iozzi, Paulo Cézar Novais, Andressa Romualdo Rodrigues, Camila A. M. Carvalho, Benedicto Oscar Colli, Carlos Gilberto Carlotti Jr., Luís Fernando Tirapelli, and Daniela P. C. Tirapelli. "Expression of NMDA receptor and microRNA-219 in rats submitted to cerebral ischemia associated with alcoholism." Arquivos de Neuro-Psiquiatria 75, no. 1 (January 2017): 30–35. http://dx.doi.org/10.1590/0004-282x20160188.
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ABSTRACT Alcohol consumption aggravates injuries caused by ischemia. Many molecular mechanisms are involved in the pathophysiology of cerebral ischemia, including neurotransmitter expression, which is regulated by microRNAs. Objective: To evaluate the microRNA-219 and NMDA expression in brain tissue and blood of animals subjected to cerebral ischemia associated with alcoholism. Methods: Fifty Wistar rats were divided into groups: control, sham, ischemic, alcoholic, and ischemic plus alcoholic. The expression of microRNA-219 and NMDA were analyzed by real-time PCR. Results: When compared to the control group, the microRNA-219 in brain tissue was less expressed in the ischemic, alcoholic, and ischemic plus alcoholic groups. In the blood, this microRNA had lower expression in alcoholic and ischemic plus alcoholic groups. In the brain tissue the NMDA gene expression was greater in the ischemic, alcoholic, and ischemic plus alcoholic groups. Conclusion: A possible modulation of NMDA by microRNA-219 was observed with an inverse correlation between them.
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Victor, Maurice. "Alcoholic Dementia." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 21, no. 2 (May 1994): 88–99. http://dx.doi.org/10.1017/s031716710004899x.
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Abstract:At least four distinct cerebral diseases — Wernicke-Korsakoff, Marchiafava-Bignami, pellagrous encephalopathy, and acquired hepatocerebral degeneration — have a close association with chronic alcoholism. Each is characterized by a distinctive pathologic change and a reasonably wellestablished pathogenesis; in each the role of alcohol in the causation is secondary. The question posed in this review is whether there is, in addition to the established types of dementia associated with alcoholism, a persistent dementia attributable to the direct toxic effects of alcohol on the brain — i.e., a primary alcoholic dementia. The clinical, psychologic, radiologic, and pathologic evidence bearing on this question is critically reviewed. None of the evidence permits the clear delineation of such an entity. The most serious flaw in the argument for a primary alcoholic dementia is that it lacks a distinctive, well-defined pathology, and it must remain ambiguous until such time as its morphologic basis is established.
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Heinz, A., A. Beck, S. Q. Park, L. Deserno, and F. Schlagenhauf. "Reward-Related Learning in Alcoholism." European Psychiatry 26, S2 (March 2011): 2014. http://dx.doi.org/10.1016/s0924-9338(11)73717-8.
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The disposition and maintenance of alcohol addiction has been associated with dysfunctional learning, particularly with increased salience attribution to alcohol-associated stimuli and Pavlovian-to-instrumental transfer, which establishes an effect of alcohol-associated cues on operant alcohol seeking and consumption. Previous imaging studies showed that dopamine dysfunction in the ventral striatum is associated with increased brain activation elicited by alcohol-associated cues in brain areas associated with attention. Furthermore, brain activation elicited by non-alcohol (e.g. monetary) reward was decreased in detoxified alcohol-dependent patients. Neuroadaptation following addiction therefore seems to augment neuronal responses to well-established, drug-associated stimuli while interfering with the learning of new, reward-seeking behaviour patterns. Using functional magnetic resonance imaging (fMRI) we showed that in detoxified alcoholics, reward-dependent reversal learning is impaired compared to healthy controls, and that this impairment correlates with reduced functional connectivity between the ventral striatum and the dorsolateral prefrontal cortex. Furthermore, we will present first data from a multimodal imaging study combining fMRI and positron-emission-tomography (PET) to measure the association between dopamine synthesis reduction and impaired functional brain activation during reversal learning in detoxified alcohol-dependent patients compared with healthy controls.
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Solonsky, A., T. Shushpanova, V. Semke, and N. Bokhan. "Neuromorphologic and neurochemical regularities of prenatal exposure of developing human brain to alcohol." European Psychiatry 26, S2 (March 2011): 106. http://dx.doi.org/10.1016/s0924-9338(11)71817-x.
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ObjectiveTo identify neuromorphologic and neurochemical patterns of prenatal exposure to alcohol of developing brain of man as risk factor for development of mental pathology in offspring of mothers with alcoholism.MethodsWe studied brains of embryos and fetuses (7–12 weeks). There were obtained 53 embryos: 23 - from alcoholics and 30 - from healthy women. Age of patients was 26–39 years, disease duration - from 3 to 13 years. All cases were diagnosed with stage II alcoholism (F 10.201; F 10.202). To evaluate the properties of benzodiazepine receptors in brains of embryos sinaptoneurosomas we used method of radio receptor binding of selective ligand 3H-flyunitrazepame.ResultsDamage to cytoplasmic membrane and internal cell membrane systems, emergence and subsequent transformation of different types of spherical formations in perinuclear space, variety of options of mitochondria as a normal structure, and with signs of functional and structural pathology, increased development of Golgi complex, appearance of lipofuscin, multi-vesicular cells and myelin formation, delay of development of synaptic contacts of vesicular type, manifested in decreasing length of postsynaptic density of synaptic contacts, reducing area and perimeter of presynaptic terminals in main study group, changing nature of vascularization of brain tissue, what was expressed in reduction of average area of vessels, an increase in their number per unit of area and reducing perimeter of brain.ConclusionWe have found that alcoholism during pregnancy results in decrease of affinity of synaptosomal receptors of brains of embryos. This may affect overall neurotransmitter processes in brain.
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Harper, Clive. "The neurotoxicity of alcohol." Human & Experimental Toxicology 26, no. 3 (March 2007): 251–57. http://dx.doi.org/10.1177/0960327107070499.
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Patterns of drinking are changing throughout the world and in many countries this will be detrimental to the health and welfare of the local population. Even uncomplicated alcoholics who have no specific neurological or hepatic problems show signs of regional brain damage and cognitive dysfunction. Many of these changes are exaggerated and other brain regions damaged in patients who have additional vitamin B1 (thiamine) deficiency (Wernicke-Korsakoff syndrome). Quantitative neuropathology techniques and improvements in neuroimaging have contributed significantly to the documentation of these changes but mechanisms underlying the damage are not understood. A human brain bank targeting alcohol cases has been established in Sydney, Australia and provides fresh and frozen tissue for alcohol researchers. The tissues can be used to test hypotheses developed from structural neuropathological studies or from animal models and in vitro studies. Identification of reversible pathological changes and preventative medical approaches in alcoholism should enhance rehabilitation and treatment efforts, thereby mitigating debilitating morbidities and reducing mortality associated with this universal public health problem.
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Crabbe, J. "Alcohol and Alcoholism: Effects on Brain and Development." Journal of Studies on Alcohol 61, no. 3 (January 2000): 484–85. http://dx.doi.org/10.15288/jsa.2000.61.484.
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Lee, Moon H. "Alcohol and Alcoholism: Effects on Brain and Development." Trends in Neurosciences 23, no. 1 (January 2000): 40–41. http://dx.doi.org/10.1016/s0166-2236(99)01441-1.
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Feeney, A. "Alcohol and Alcoholism -- Effects of Brain and Development." Alcohol and Alcoholism 35, no. 2 (March 1, 2000): 216. http://dx.doi.org/10.1093/alcalc/35.2.216.
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Ceccanti, Marco, Maurizio Inghilleri, Maria Luisa Attilia, Ruggero Raccah, Marco Fiore, Abraham Zangen, and Mauro Ceccanti. "Deep TMS on alcoholics: effects on cortisolemia and dopamine pathway modulation. A pilot study." Canadian Journal of Physiology and Pharmacology 93, no. 4 (April 2015): 283–90. http://dx.doi.org/10.1139/cjpp-2014-0188.
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The hypothalamic pituitary adrenal axis and dopamine have a key role in transition from alcohol social use to addiction. The medial prefrontal cortex was shown to modulate dopaminergic activity and cortisol releasing factor (CRF) release in hypothalamic and extra-hypothalamic systems. The recent advancements in non-invasive neurostimulation technologies has enabled stimulation of deeper brain regions using H-coil transcranial magnetic stimulation (TMS) in humans. This randomized double-blind placebo-controlled pilot study aims to evaluate H-coil efficacy in stimulating the medial prefrontal cortex. Cortisolemia and prolactinemia were evaluated as effectiveness markers. Alcohol intake and craving were considered as secondary outcomes. Eighteen alcoholics were recruited and randomized into 2 homogeneous groups: 9 in the real stimulation group and 9 in the sham stimulation group. Repetitive TMS (rTMS) was administered through a magnetic stimulator over 10 sessions at 20 Hz, directed to the medial prefrontal cortex. rTMS significantly reduced blood cortisol levels and decreased prolactinemia, thus suggesting dopamine increase. Craving visual analogic scale (VAS) in treated patients decreased, as well as mean number of alcoholic drinks/day and drinks on days of maximum alcohol intake (DMAI). In the sham group there was no significant effect observed on cortisolemia, prolactinemia, mean number of alcoholic drinks/day, or drinks/DMAI. Thus, deep rTMS could be considered a potential new treatment for alcoholism.
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Wang, Shao-Cheng, Yuan-Chuan Chen, Shaw-Ji Chen, Chun-Hung Lee, and Ching-Ming Cheng. "Alcohol Addiction, Gut Microbiota, and Alcoholism Treatment: A Review." International Journal of Molecular Sciences 21, no. 17 (September 3, 2020): 6413. http://dx.doi.org/10.3390/ijms21176413.
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Alcohol addiction is a leading risk factor for personal death and disability. In 2016, alcohol use caused 2.2% of female deaths and 6.8% of male deaths, and disability-adjusted life years (DALYs) were 2.3% in female and 8.9% in male. Individuals with alcohol use disorder are at high risk of anxiety, depression, impaired cognition performance, and illicit drug use and are comorbid with liver disease, such as alcoholic hepatitis and liver cirrhosis, which is a major cause of personal death and disability worldwide. Psychological interventions, such as cognitive behavior therapy and motivational interviewing, as well as medical treatments, such as disulfiram, naltrexone, acamprosate, and nalmefene, are used for the treatment of alcohol addiction in Europe and the United States. However, the effect of current interventions is limited, and the need for additional interventions is substantial. Alcohol use impairs the intestinal barrier and causes changes to the intestinal permeability as well as the gut microbiota composition. Emerging studies have tried to reveal the role of the gut–brain axis among individuals with alcohol use disorder with or without alcohol liver disease. Bacterial products penetrate the impaired intestinal barrier and cause central inflammation; changes to the gut microbiota impair enterohepatic circulation of bile acids; alcohol abuse causes shortage of vital nutrients such as thiamine. Several studies have suggested that probiotics, through either oral administration or fecal microbiota transplantation, increased intestinal levels of potentially beneficial bacteria such as bifidobacteria and lactobacilli, improving the levels of liver-associated enzymes in patients with mild alcoholic hepatitis, and demonstrating beneficial psychotropic effects on anxiety and depression. In addition to medications for alcohol addiction, gene editing therapy such as clustered regularly interspaced short palindromic repeats (CRISPRs) may be another potential research target. Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), which are associated with ADH and ALDH genes, are major enzymes involved in alcohol metabolism, and gene editing approaches may have the potential to directly modify specific genes to treat alcoholism caused by genetic defects. Further research is needed to study the effect of the combined treatment for alcohol addiction.
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Sreemathyamma, Sunilkumar B., Prasanth Asher, Palamkunnil T. Baburaj, Raja K. Kutty, Sharmad Mohammed Haneefa Suharban Beevi, Anilkumar Peethambaran, and Sureshkumar Kunjini Leela. "Post head injury neurobehavioral sequelae: severity among alcoholics." International Surgery Journal 7, no. 10 (September 23, 2020): 3399. http://dx.doi.org/10.18203/2349-2902.isj20204143.
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Background: Alcohol use and traumatic brain injury (TBI) are closely linked public health problems. Alcohol intoxication is one of the major risk factor for TBI, and is a main determinant of prognosis in terms of mortality and functional outcome. The aim of the study is to find out the impact of alcoholism in the neurobehavioral outcome following TBI.Methods: A total of 150 head injury patients were divided into two groups: alcoholics and non-alcoholics, and evaluated between six weeks to one year after injury using the revised neurobehavioral rating scale by Levin et al (NRS-R) for the evaluation of neurobehavioral sequelae and the outcome was compared between groups.Results: The study showed significant difference between the groups indicating that the neurobehavioral sequelae were more in the chronic alcoholics group. In the comparison of individual factors, all except factors III (negative symptoms) and IV (mood and affect) were found to be significantly different. The factors I (executive), II (positive symptoms), V (oral and motor), and VI (not loading on any of the factors) were significant at 0.01 level.Conclusions: Chronic alcoholism significantly increases the risk of developing neurobehavioral sequelae after traumatic brain injury.
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Nutt, David. "Alcohol and the brain." British Journal of Psychiatry 175, no. 2 (August 1999): 114–19. http://dx.doi.org/10.1192/bjp.175.2.114.
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BackgroundAlcohol misuse, as well as being a major form of psychiatric morbidity, is also commonly associated with other psychiatric disorders. A greater understanding of the brain mechanisms underlying the adverse effects of alcohol is now possible, thanks to significant research advances made over the past decade.AimsTo elucidate for psychiatrists the growing knowledge of the importance of specific neurotransmitter interactions in the effects of alcohol.MethodA survey of the literature, extracting current knowledge of interest to psychiatrists.ResultsThere is good evidence that the acute effects of alcohol are mediated through interactions with amino acid neurotransmitters plus parallel changes in amines such as noradrenaline, dopamine and serotonin. Neuroadaptive responses at amino acid receptors probably underlie significant components of the withdrawal syndrome and probably also contribute to neuronal death found in chronic alcoholism.ConclusionsAn understanding of the pharmacology of alcohol use may lead to greater ability to treat psychiatric consequences of alcoholism, and may also prevent some of the secondary psychiatric comorbidity and later brain damage.
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Mayock, Dennis E., Dana Ness, Robin L. Mondares, and Christine A. Gleason. "Binge alcohol exposure in the second trimester attenuates fetal cerebral blood flow response to hypoxia." Journal of Applied Physiology 102, no. 3 (March 2007): 972–77. http://dx.doi.org/10.1152/japplphysiol.00956.2006.
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Alcohol is detrimental to the developing brain and remains the leading cause of mental retardation in developed countries. The mechanism of alcohol brain damage remains elusive. Studies of neurological problems in adults have focused on alcohol's cerebrovascular effects, because alcoholism is a major risk factor for stroke and cerebrovascular injuries. However, few studies have examined similar cerebrovascular effects of fetal alcohol exposure. We examined the effect of chronic binge alcohol exposure during the second trimester on fetal cerebrovascular and metabolic responses to hypoxia in near-term sheep and tested the hypothesis that fetal alcohol exposure would attenuate cerebrovascular dilation to hypoxia. Pregnant ewes were infused with alcohol (1.5 g/kg) or saline intravenously at 60–90 days of gestation (full term = 150 days). At 125 days of gestation, we measured fetal cerebral blood flow (CBF) and oxygen metabolism at baseline and during hypoxia. Maternal blood alcohol averaged 214 ± 5.9 mg/dl immediately after the 1.5-h infusion, with similar values throughout the month of infusion. Hypoxia resulted in a robust increase in CBF in saline-infused fetuses. However, the CBF response to hypoxia in fetuses chronically exposed to alcohol was significantly attenuated. Cerebral oxygen delivery decreased in both groups of fetuses during hypoxia but to a greater degree in the alcohol-exposed fetuses. Prenatal alcohol exposure during the second trimester attenuates cerebrovascular responses to hypoxia in the third trimester. Altered cerebrovascular reactivity might be one mechanism for alcohol-related brain damage and might set the stage for further brain injury if a hypoxic insult occurs.
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Peng, Hu, Xing Qin, Sainan Chen, Asli F. Ceylan, Maolong Dong, Zhaofen Lin, and Jun Ren. "Parkin deficiency accentuates chronic alcohol intake-induced tissue injury and autophagy defects in brain, liver and skeletal muscle." Acta Biochimica et Biophysica Sinica 52, no. 6 (May 19, 2020): 665–74. http://dx.doi.org/10.1093/abbs/gmaa041.
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Abstract Alcoholism leads to organ injury including mitochondrial defect and apoptosis with evidence favoring a role for autophagy dysregulation in alcoholic damage. Parkin represents an autosomal recessive inherited gene for Parkinson’s disease and an important member of selective autophagy for mitochondria. The association between Parkinson’s disease and alcoholic injury remains elusive. This study aimed to examine the effect of parkin deficiency on chronic alcohol intake-induced organ injury in brain, liver and skeletal muscle (rectus femoris muscle). Adult parkin-knockout (PRK−/−) and wild-type mice were placed on Liber-De Carli alcohol liquid diet (4%) for 12 weeks prior to assessment of liver enzymes, intraperitoneal glucose tolerance, protein carbonyl content, apoptosis, hematoxylin and eosin morphological staining, and mitochondrial respiration (cytochrome c oxidase, NADH:cytochrome c reductase and succinate:cytochrome c reductase). Autophagy protein markers were monitored by western blot analysis. Our data revealed that chronic alcohol intake imposed liver injury as evidenced by elevated aspartate aminotransferase and alanine transaminase, glucose intolerance, elevated protein carbonyl formation, apoptosis, focal inflammation, necrosis, microvesiculation, autophagy/mitophagy failure and dampened mitochondrial respiration (complex IV, complexes I and III, and complexes II and III) in the brain, liver and rectus femoris skeletal muscle. Although parkin ablation itself did not generate any notable effects on liver enzymes, insulin sensitivity, tissue carbonyl damage, apoptosis, tissue morphology, autophagy or mitochondrial respiration, it accentuated alcohol intake-induced tissue damage, apoptosis, morphological change, autophagy/mitophagy failure and mitochondrial injury without affecting insulin sensitivity. These data suggest that parkin plays an integral role in the preservation against alcohol-induced organ injury, apoptosis and mitochondrial damage.
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Pfefferbaum, Adolf. "Alcoholism damages the brain, but does moderate alcohol use?" Lancet Neurology 3, no. 3 (March 2004): 143–44. http://dx.doi.org/10.1016/s1474-4422(04)00676-3.
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Sher, Leo. "Alcohol and Suicide: Neurobiological and Clinical Aspects." Scientific World JOURNAL 6 (2006): 700–706. http://dx.doi.org/10.1100/tsw.2006.146.
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Alcohol, primarily in the form of ethyl alcohol (ethanol), has occupied an important place in the history of humankind for at least 8,000 years. In most Western societies, at least 90% of people consume alcohol at some time during their lives, and 30% or more of drinkers develop alcohol-related problems. Severe alcohol-related life impairment, alcohol dependence (alcoholism), is observed at some time during their lives in about 10% of men and 3—5% of women. An additional 5—10% of each sex develops persistent, but less intense, problems that are diagnosed as alcohol abuse. It this review, neurobiological aspects of suicidal behavior in alcoholism is discussed. In individuals with comorbid depression and alcoholism, greater serotonergic impairment may be associated with higher risk of completed suicide. Dopaminergic dysfunction may play an important role in the pathophysiology of suicidal behavior in alcoholism. Brain damage and neurobehavioral deficits are associated with alcohol use disorders and may contribute to suicidal behavior in persons with alcohol dependence or abuse. Aggression/impulsivity and alcoholism severity affect risk for suicide among individuals with alcoholism. Major depressive episodes and stressful life events particularly, partner-relationship disruptions, may precipitate suicidal behavior in individuals with alcohol use disorders. Alcohol misuse and psychosocial adversity can combine to increase stress on the person, and, thereby, potentially, increase the risk for suicidal behavior. The management of suicidal patients with alcohol use disorders is also discussed. It is to be hoped that the efforts of clinicians will reduce morbidity and mortality associated with alcohol misuse.
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Potupchik, T. V., O. F. Veselova, and I. V. Gatskikh. "Pharmacotherapeutic aspects of nootropics use in people with alcohol dependence." Medical alphabet 2, no. 19 (November 26, 2019): 37–41. http://dx.doi.org/10.33667/2078-5631-2019-2-19(394)-37-41.
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In the pharmacotherapy of chronic alcoholism a significant place is given to nootropic drugs. Currently, neurodegenerative processes are associated with the activity of various neurotrophic factors of the brain and neuropeptides. An important advantage of the use of neuropeptide drugs (cerebrolysin, semax, cortexin) in the treatment of chronic alcoholism is that they have an organ-specific multimodal effect on the brain: provide metabolic regulation, neuroprotection, functional neuromodulation and neurotrophic activity. They are recommended for relief of acute withdrawal syndrome, as well as in the post-abstinent period in asthenic syndrome and restoration of mnestic functions.
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Spanagel, Rainer. "Alcoholism: A Systems Approach From Molecular Physiology to Addictive Behavior." Physiological Reviews 89, no. 2 (April 2009): 649–705. http://dx.doi.org/10.1152/physrev.00013.2008.
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Alcohol consumption is an integral part of daily life in many societies. The benefits associated with the production, sale, and use of alcoholic beverages come at an enormous cost to these societies. The World Health Organization ranks alcohol as one of the primary causes of the global burden of disease in industrialized countries. Alcohol-related diseases, especially alcoholism, are the result of cumulative responses to alcohol exposure, the genetic make-up of an individual, and the environmental perturbations over time. This complex gene × environment interaction, which has to be seen in a life-span perspective, leads to a large heterogeneity among alcohol-dependent patients, in terms of both the symptom dimensions and the severity of this disorder. Therefore, a reductionistic approach is not very practical if a better understanding of the pathological processes leading to an addictive behavior is to be achieved. Instead, a systems-oriented perspective in which the interactions and dynamics of all endogenous and environmental factors involved are centrally integrated, will lead to further progress in alcohol research. This review adheres to a systems biology perspective such that the interaction of alcohol with primary and secondary targets within the brain is described in relation to the behavioral consequences. As a result of the interaction of alcohol with these targets, alterations in gene expression and synaptic plasticity take place that lead to long-lasting alteration in neuronal network activity. As a subsequent consequence, alcohol-seeking responses ensue that can finally lead via complex environmental interactions to an addictive behavior.
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Golovin, N. A., V. M. Sereda, E. I. Krasnoshiekova, A. D. Kharazova, and N. I. Pautova. "THE MEDICAL SOCIAL ANALYSIS OF RELATIONSHIP BETWEEN ALCOHOL DEVIATION OF WOMEN AND PSYCHIC BEHAVIORAL DISORDERS IN CHILDREN." Sociology of Medicine 16, no. 1 (June 15, 2017): 23–27. http://dx.doi.org/10.18821/1728-2810-2017-16-1-23-27.
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The social crisis of the end of XX century in Russia negatively impacted psycho-emotional condition of society and provoked increasing of drug addiction and alcoholism among population. The article applies inter-disciplinary position analyzing relationship between severe social psychological atmosphere of those years and mental, behavioral disorders in generation of children caused by alcohol abuse in generation of parents, especially mothers. The dynamics is presented concerning social mood of society, level of female alcoholism, nervous diseases morbidity of children. The mental and neurological disorders are discussed in the aspect of patterns of brain development during prenatal period. The biological sociological evaluation is given concerning impact of crisis of 1990s as a macro-social factor of mental and behavioral health of age group of persons born in 1990-2000s. The burden of crisis and negative emotional atmosphere in society, especially in the middle of 1990s, increasing of alcohol consumption and also dynamics of alcoholism and alcoholic psychosis morbidity of women during the same years, dynamics of nervous diseases morbidity of children aged 0-1 year in the Russian Federation with its surges, especially in 1994-1995, 1998 and 2009, permit to consider focused effect of social crisis on physical and mental health of newborns. During relative stabilization of 2010s, there is no such a concentration of negative factors. Also, certain positive circumstances are manifesting: learning of legal standards according which person is primarily responsible for one's own health, measures of struggle with alcoholism, development of perinatal medicine, etc.
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Akgun, Omer. "Determination of the Appropriate Kernel Structure in Electroencephalography Analysis of Alcoholic Subjects." Traitement du Signal 37, no. 4 (October 10, 2020): 571–77. http://dx.doi.org/10.18280/ts.370404.
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Alcoholism is one of the major health problems in the world. The organ most affected by alcohol is the brain. It has been shown that alcohol causes neuronal loss in the brain and reduces brain blood flow and oxygen use. Electroencephalography is a method that measures the instantaneous electrical activity of the brain. It is known that valuable information can be obtained by observing the biological effects of alcohol through EEG. As their methods of signal processing and analysis have evolved, Electroencephalography signals have attracted the attention of researchers in this field. In this study, methods of the time-frequency analysis were applied to Electroencephalography signals obtained from normal and alcoholic subjects. For this purpose, the Cohen’s class distribution was examined. Ambiguity function analysis, which was in the structure of the distribution, was applied to the signals. Then, from the kernel structure inside the distribution, the Wigner-Ville distribution, which was very common, was reached and this distribution was examined. The inadequacy of the distribution resolution was seen and analysis of the new time-frequency distributions, which were obtained by making convolution with 4 types of kernel functions (nonseparable, separable, Doppler independent, lag independent), was performed. As a result, it was shown that the resolution of time-frequency distributions could be improved with proper kernel functions. Thus, at the end of these analyses, changes that alcohol caused in brain functions were revealed.
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Ho, Allen L., Anne-Mary N. Salib, Arjun V. Pendharkar, Eric S. Sussman, William J. Giardino, and Casey H. Halpern. "The nucleus accumbens and alcoholism: a target for deep brain stimulation." Neurosurgical Focus 45, no. 2 (August 2018): E12. http://dx.doi.org/10.3171/2018.5.focus18157.
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Alcohol use disorder (AUD) is a difficult to treat condition with a significant global public health and cost burden. The nucleus accumbens (NAc) has been implicated in AUD and identified as an ideal target for deep brain stimulation (DBS). There are promising preclinical animal studies of DBS for alcohol consumption as well as some initial human clinical studies that have shown some promise at reducing alcohol-related cravings and, in some instances, achieving long-term abstinence. In this review, the authors discuss the evidence and concepts supporting the role of the NAc in AUD, summarize the findings from published NAc DBS studies in animal models and humans, and consider the challenges and propose future directions for neuromodulation of the NAc for the treatment of AUD.
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Соколик, E. Sokolik, Егоров, and A. Egorov. "Pharmacological Modulation of Compensatory Mechanisms Energy Metabolism in the Brain of Prenatal Alcoholic Animals." Journal of New Medical Technologies 21, no. 3 (September 5, 2014): 54–58. http://dx.doi.org/10.12737/5898.
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The studies have shown that drinking alcohol by woman during pregnancy can lead not only to a full fetal alcohol syndrome, but also causes less severe dysmorphic, cognitive and behavioral disordersl, i.e. fetal alcohol spectrum disorders, leads to low birth weight, fetal death, and other complications of pregnancy.
The purpose of this study was to investigate the influence of neuroprotective drugs tiocetam, cerebrocurin and piracetam on the marks of thin elements of energy metabolism and compensatory shunts in the brain of animals early age undergoing prenatal alcoholism.
In pregnant rats with alcoholism were found neuroprotective and nootropic effects of cerebrocurin and tiocetam after parenterally administered to newborn animals for a period of 25 days. The above drugs have a beneficial effect on the main elements of the energy metabolism on the neonatal brain.
On the severity of mitoprotective and energotropic mechanisms of neuroprotective action, aimed at reducing the negative impact of alcohol on the progeny, tiocetam and cerebrocurin far exceed basic nootropic drug piracetam.
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Noël, Xavier, Antoine Bechara, Damien Brevers, Paul Verbanck, and Salvatore Campanella. "Alcoholism and the Loss of Willpower." Journal of Psychophysiology 24, no. 4 (January 2010): 240–48. http://dx.doi.org/10.1027/0269-8803/a000037.
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Like other addictions, alcoholism reflects the continuation of alcohol use despite negative consequences (e.g., an ulcer or family problems made worse by alcohol consumption). Recent cognitive theories suggest that optimal information processing related to the capacity to make decisions under uncertainty conditions is impaired either prior to the initiation of alcohol use, or it is related to the consequence of its repeated utilization. In this paper, we suggest that alcoholism may be the product of an imbalance between two separate, but interacting, cognitive registers that contribute to decision making: a reactive/automatic attentional and memory system for signaling the presence of alcohol cues in the environment and for attributing to such cues pleasure and/or excitement; and a reflective/nonautomatic system for regulating the dominant reactive/automatic response. Hyperactivity within the reactive system can override the reflective system and brain/cognitive changes induced by ethanol could lead to the disruption of self-regulation. We finally develop the idea that different patterns of imbalance between reactive and reflective systems could lead to distinct patterns of clinical impulsivity involved in the vulnerability to, the development of, and the relapse into alcoholism.
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Vale, Benjamim, Juçara Castro, Marx Araújo, Herb Morais, and Lívio Macêdo. "Traumatic Brain Injury Caused by Motor Vehicle Collision and Alcoholism in Piauí." Arquivos Brasileiros de Neurocirurgia: Brazilian Neurosurgery 37, no. 03 (May 23, 2016): 174–81. http://dx.doi.org/10.1055/s-0036-1583935.
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Objectives To determine the relationship between alcohol consumption and the incidence of traumatic brain injury (TBI) with diffuse axonal injury (DAI), determining these indices, checking acquired comorbidities and characterizing the patients by gender, age and race/color, as well as describing the characteristics of the motor vehicle collision (vehicle, period of the day, day of the week and site) in people admitted to an emergency hospital in the city of Teresina, in the state of Piauí, Brazil. Methods We have analyzed the data contained in the medical records of patients admitted with a history of motor vehicle collision and severe TBI in intensive care units, based on the forms provided by the Mobile Emergency Care Service (SAMU, in the Portuguese acronym) in the period between February 28 and November 28, 2013. Results In the period covered by the present study, 200 individuals were analyzed, and 54 (27%) had consumed alcohol; of these 11 had DAI. Of the total sample, 17% (34) presented DAI, however, with unknown data regarding the consumption of alcoholic beverages. Conclusion Considering the data, we observed that the profile of the head trauma patients are brown men, mostly (53.5%) aged between 15 and 30 years. The collisions occurred mostly on weekends and at night (55%), and 89.5% of the crashes involved motorcycles.
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Ciafrè, Stefania, Valentina Carito, Giampiero Ferraguti, Antonio Greco, George N. Chaldakov, Marco Fiore, and Mauro Ceccanti. "How alcohol drinking affects our genes: an epigenetic point of view." Biochemistry and Cell Biology 97, no. 4 (August 2019): 345–56. http://dx.doi.org/10.1139/bcb-2018-0248.
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This work highlights recent studies in epigenetic mechanisms that play a role in alcoholism, which is a complex multifactorial disorder. There is a large body of evidence showing that alcohol can modify gene expression through epigenetic processes, namely DNA methylation and nucleosomal remodeling via histone modifications. In that regard, chronic exposure to ethanol modifies DNA and histone methylation, histone acetylation, and microRNA expression. The alcohol-mediated chromatin remodeling in the brain promotes the transition from use to abuse and addiction. Unravelling the multiplex pattern of molecular modifications induced by ethanol could support the development of new therapies for alcoholism and drug addiction targeting epigenetic processes.
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Carvalhão Gil, L., M. Lázaro, A. Ponte, J. Teixeira, H. Prata Ribeiro, and T. Mota. "Treatment of alcoholism – New targets?" European Psychiatry 41, S1 (April 2017): s859. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1713.
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IntroductionAlcohol use disorders (AUD) is a preventable cause of significant morbidity and mortality worldwide. AUD is a heterogeneous disorder stemming from a complex interaction of neurobiological, genetic, and environmental factors. To achieve treatment effectiveness this heterogenity should be considered, as well as safety.ObjectivesReview mechanisms underlying alcohol addiction in order to work out new, more effective treatment strategies.AimTo update on treatment for alcoholism.MethodsA literature search was performed on PubMed database.ResultsAlcohol dependence is a chronic, relapsing condition in which there is evidence of significant change in the motivation and control systems in the brain. Increasingly drug therapy is focused not just on the treatment of the acute withdrawal syndrome, but on modifying these other dysregulated brain systems. Of the numerous neurotransmitter systems that have been identified for the development of new medicines, the most promising compounds appear to be those that modulate the function of opioids, glutamate with or without gamma-aminobutyric acid, and serotonin. Other putative therapeutic medications including direct modulators of dopamine function and enzyme inhibitors also shall be discussed. At present, only four medications are approved for the treatment of alcohol dependence in Europe, that is naltrexone, acamprosate, disulfiram and the most recent nalmefene. Among other promising strategies the following drugs are mentioned: baclofen, topiramate, ondansetron, aripiprazole, rimonabant and varenicline.ConclusionsPharmacological development remains a high priority in the alcoholism field. Drugs have different safety profiles that need to be balanced with the treatment objective, individual patient preferences and comorbid conditions.Disclosure of interestThe authors have not supplied their declaration of competing interest.
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Mann, K. "Individualised Pharmacotherapy of Alcoholism." European Psychiatry 26, S2 (March 2011): 2016. http://dx.doi.org/10.1016/s0924-9338(11)73719-1.
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Treatment of alcoholism is successful but effect sizes are in the low to moderate range. Heterogeneity of patients entering treatment trials could be one potential explanation. Several attempts have been made to subgroup patient for specific treatment approaches (“matching”). A new approach includes biological data such as pharmacogenetics and neuroimaging for treatment-patient matching.In the PREDICT study (Mann et al., 2009) 426 alcohol-dependent patients were randomized either to placebo, naltrexone or acamprosate. Design and questionnaires were similar to the US COMBINE Study (Anton et al., 2006). Extending Project MATCH and the COMBINE Study we used biological and psychopathological characteristics of patients in order to test their response to naltrexone or acamprosate. In pharmacogenetics 14 SNPs from an own genome-wide association and follow-up study (Treutlein et al., 2009) were tested for differential treatment outcome. Indeed, one SNP showed a significant gene dose effect under acamprosate. Using neuroimaging we confirmed that an increase in brain activity in the ventral striatum is related to time to relapse. We also found support for our hypothesis concerning the rewarding characteristics of alcohol in a certain subgroup of patients. Here f-MRI BOLD response in the ventral striatum predicted a positive naltrexone response. Furthermore, new opioid receptors in alcoholics and normal controls were assessed using carfentanil PET.Analyses are still underway.In conclusion the treatment of alcoholism is moving towards a personalised approach. This holds the potential for a significant increase in effect sizes of our treatment trials and thus for better treatment options for our patients.
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Becker, Howard C. "Alcohol Withdrawal: Neuroadaptation and Sensitization." CNS Spectrums 4, no. 1 (January 1999): 38–40. http://dx.doi.org/10.1017/s1092852900011202.
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AbstractRepeated episodes of alcohol withdrawal may exacerbate the severity of future withdrawal occurrences. The progressive intensification of withdrawal symptoms may be manifested as a kindling-like mechanism. This sensitization process may reflect persistent perturbation in excitatory and inhibitory influences on brain function. Relapse is also thought to be affected by the kindling mechanism. Successive alcohol withdrawal experiences may also lead to neurologic damage and cognitive impairments. We review the research findings regarding the alcohol withdrawal kindling hypothesis and the implications of the kindling process on mechanisms of dependence, alcohol withdrawal treatment strategies, and the long-term repercussions of alcoholism.
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Bokhan, N. A. "Clinical prognosis of associated forms of alcoholism with co-morbid brain impairment." European Psychiatry 26, S2 (March 2011): 12. http://dx.doi.org/10.1016/s0924-9338(11)71723-0.
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ObjectiveIdentification of clinical differences of formation and prognosis of severity of associated forms of alcoholism in relevant variants of co-morbid brain impairment.Material and methodsWith clinical-psychopathological method we examined inpatient samples with stage 2 alcoholism with co-morbid traumatic (group I, n = 105); hypertensive (group II, n = 45) and vertebrogenic (spinal cord artery syndrome) (group III, n = 37) brain impairment. Control - 30 patients with alcoholism without co-morbid pathology.ResultsIn group I alcoholism is forming at early age in persons with pre-morbidly problematic social adaptation - in 62,2% conditioned by presence of excitable traits of the character. Dominance of dysphoria in intoxication and in alcohol withdrawal syndrome (AWS) predetermines formation of psychopath-like degradation with total and persistent social disadaptation. Beyond AWS, reactive lability, lingering asthenic-sub-depressive states with inclusion of dysphoric, hysteric-excitable components remain during low quality of remission. In group II later formation of alcoholism in 26,7% of cases was preceded by psychodisadaptive disturbances conditioned by pre-morbidly anxious constitution of personality. In structure of AWS anxious-phobic modality of depressive disorders against the background of cardiovascular manifestations of toxicogenic effects of ethanol determines development of torpid asthenic-depressive states (with cardiophobic and hypochondriac components). For patients from group III we have identified intermediary tempo of increasing of progression of alcoholism with obligate diencephalic psychovegetative, psychosensory and severe psychoorganic cognitive disorders against the background of asthenic, more seldom dysphoric variants of change of the personality.ConclusionPrognosis of associated forms of alcoholism is various in distinguished variants (traumatic, hypertensive, vertebrogenic) comorbid brain impairment.
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Airapetov, M. I., S. O. Eresko, A. A. Lebedev, E. R. Bychkov, and P. D. Shabanov. "Involvement of TOLL-like receptors in the neuroimmunology of alcoholism." Biomeditsinskaya Khimiya 66, no. 3 (2020): 208–15. http://dx.doi.org/10.18097/pbmc20206603208.
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Alcohol use is a global socially significant problem that remains one of the leading risk factors for disability and premature death. One of the main pathological characteristics of alcoholism is the loss of cognitive control over the amount of consumed alcohol. Growing body of evidence suggests that alterations of neuroimmune communication occurring in the brain during prolonged alcoholization are one of the main mechanisms responsible for the development of this pathology. Ethanol consumption leads to activation of neuroimmune signaling in the central nervous system through many types of Toll-like receptors (TLRs), as well as the release of their endogenous agonists (HMGB1 protein, S100 protein, heat shock proteins, extracellular matrix breakdown proteins). Activation of TLRs triggers intracellular molecular cascades leading to increased expression of the innate immune system genes, particularly proinflammatory cytokines, subsequently causing the development of a persistent neuroinflammatory process in the central nervous system, which results in massive death of neurons and glial cells in the brain structures, which are primarily associated with the development of a pathological craving for alcohol. In addition, some subtypes of TLRs are capable of forming heterodimers with neuropeptide receptors (corticoliberin, orexin, ghrelin receptors), and may also have other functional relationships.
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Liang, Xian-ting, Yan-yan Wang, Xiao-yu Hu, and Shao-bo Wang. "The Protective Effects of Water Extracts of Compound Turmeric Recipe on Acute Alcoholism: An Experimental Research Using a Mouse Model." Evidence-Based Complementary and Alternative Medicine 2021 (January 13, 2021): 1–13. http://dx.doi.org/10.1155/2021/6641919.
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Acute alcoholism (AAI) is a common emergency. Currently, there is a lack of preventive and therapeutic drugs with superior safety and efficacy. Curcuma longa, Panax ginseng, Pueraria lobata, Pueraria flower, and Hovenia dulcis Thunb., which are the components of compound turmeric recipe (CTR), are, respectively, used in China as adjuvant therapeutic agents for AAI and alcoholic liver injury, respectively. The purpose of this research was to investigate the effect of traditional compound turmeric recipe in anti-inebriation treatment and to identify its underlying mechanisms. The mice were administered with CTR mixture, and ethanol was subsequently given to mice by gavage. The effects of CTR on the righting reflex, 24-hour survival, drunken behavior, blood ethanol concentration, and pathological changes of liver are depicted. The activities of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were detected. Besides, the activities of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8), alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), cytochrome P450 (P450), superoxide dismutase (SOD), and malondialdehyde (MDA) in the liver and the levels of β-endorphin (β-EP) and leucine enkephalin (LENK) in the brain were also measured. Our results demonstrated that CTR can increase the activities of ADH, ALDH, P450, and SOD and decrease the contents of TNF-α, IL-8, and MDA in the liver. In addition, it can decrease the activities of ALT, AST, and ALP in serum and β-EP and LENK activities in the brain. CTR showed effects on prevention of acute alcoholism, promoting wakefulness, and alleviating alcoholic liver injury, which were likely mediated by the above mechanisms.
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Virkkunen, M. D. "Serotoninergic findings in habitual violence and impulsivity. A review." Acta Neuropsychiatrica 2, no. 3 (September 1990): 66–71. http://dx.doi.org/10.1017/s0924270800035110.
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SummarySeveral lines of evidence suggest that there may be abnormal brain serotonin metabolism in habitually biolent and impulsive offenders. These personality disorders are usually connected with early onset, male limited type 2 alcoholism in which one central feature is the abnormal tendency to behave aggressively and impulsively under the influence of alcohol repeatedly. Low CSF 5-HIAA has been found to correlate with familial alcoholism tendencies; paternal alcoholism. Both this and with it the tendency to abnormal oral glucose tolerance test (tendency to low blood glucose nadir) predict the new violent and impulsive crimes under the influence of alcohol. Also peripheral measures such as platelet MAO, abnormal tryptophan/LNAA ratio in plasma, whole blood serotonin, blood platelet uptake of serotonin, platelet 3H-IMI dinging (Bmax), abnormal prolactin and Cortisol secretion in fenfluramine challenge, and possibly daily urinary free Cortisol secretion correlate with impulsive aggressive behavior.
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Konar, Atheni, and NirmalChandra Sukul. "Extremely dilution of Strychnos Nux vomica mitigates alcohol-induced reduction in enthalpies associated with free water molecules in fish brain." International Journal of High Dilution Research - ISSN 1982-6206 17, no. 2 (July 16, 2021): 11. http://dx.doi.org/10.51910/ijhdr.v17i2.928.
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Background: Alcoholism is a global health problem. Extract of the seeds of Strychnos Nux vomica and its high dilution have long been used in homeopathy for alcohol induced diseases of patients. Alcoholism leads to reduced brain volume. Glial cells like astroglia contain large number of water channel proteins or aquaporin (AQP4) which mediate glial oedema resulting from ethanol intoxication. Nux vomica, a homeopathic drug of plant origin, is known to counteract alcohol effect.
Aim: The objective of this present study is to find out the level of free water molecules in the brain of a teleost fish under ethanol intoxication. The other purpose is to determine whether Nux vomica could restore the level of free water in the alcohol treated fish.
Methodology: One group of fish was exposed to 456 mM ethanol for 30 min, another exposed first to a solution of Nux vomica 200c for 20 min and then to 456 mM ethanol for 30 min. The third group served as an untreated control. The mid brain of each fish was kept in an aluminium sample pan and its free water level was assessed by differential scanning calorimetry (DSC). Data were analyzed by ANOVA.
Results and discussion: The results show that there was no significant variation in melting and freezing temperature of brain samples but the enthalpies, both freezing and melting varied significantly (P
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Gilmore, Casey S., and George Fein. "Induced Theta Activity as a Biomarker for a Morbid Effect of Alcoholism on the Brain in Long-Term Abstinent Alcoholics." Journal of Psychophysiology 27, no. 2 (January 2013): 76–83. http://dx.doi.org/10.1027/0269-8803/a000089.
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Event-related, target stimulus-phase-locked (evoked) brain activity in both the time and time-frequency (TF) domains (the P3b ERP; evoked theta oscillations) has been shown to be reduced in alcoholics. Recently, studies have suggested that there is alcohol-related information in the non-stimulus-phase-locked (induced) theta TF activity. We applied TF analysis to target stimulus event-related EEG recorded during an oddball task from 41 long-term abstinent alcoholics (LTAA) and 74 nonalcoholic controls (NAC) to investigate the relationship between P3b, evoked theta, and induced theta activity. Results showed that an event-related synchronization (ERS) of induced theta (1) was larger in LTAA compared to NAC, and (2) was sensitive to differences between LTAA and NAC groups that was independent of the differences accounted for by P3b amplitude or evoked theta. These findings suggest that increased induced theta ERS may likely be a biomarker for a morbid effect of alcohol abuse on brain function.
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Airapetov, M. I., S. O. Eresco, A. A. Lebedev, E. R. Bychkov, and P. D. Shabanov. "Ethanol induced increase of fibroblast growth factor 2 mRNA content in emotiogenic brain structures of rats." Biomeditsinskaya Khimiya 66, no. 5 (2020): 419–22. http://dx.doi.org/10.18097/pbmc20206605419.
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We studied the effects of acute, subacute, and chronic alcohol treatment of rats on the content of fibroblast growth factor 2 (FGF2) mRNA in various brain structures. Results suggest a possible role of FGF2 in the functioning of dopaminergic neurons in the midbrain. In our experiment, ethanol treatment of rats was accompanied by an increase in the FGF2 mRNA level in the emotiogenic structures of the brain. This effect was blocked by pretreatment of animals with chlorpromazine. This suggests FGF2 involvement in the mechanisms of alcohol dependence and can be considered as a possible diagnostic and therapeutic target in alcoholism.
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Solonsky, A., T. V. Shushpanova, E. G. Solonskaya, N. A. Bokhan, and S. V. Logvinov. "Effect of Prenatal Exposure to Alcohol on the Development of Brain Vessels in Human Embryos and Fetuses." European Psychiatry 41, S1 (April 2017): S639. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1052.
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IntroductionHuman embryos are most susceptible to exogenous effects during the first weeks of development.AimStudy the effects of prenatal alcohol intoxication on morphometric measures of developing vessels in the human embryonic and fetal cerebrum.MethodsEmbryos and fetuses (7–12 weeks): 23 obtained from alcoholic women with stage II alcoholism (the experimental group) and 30 from healthy women (the control group). The research involved electron microscopy, computer morphometry, parametric method of variational statistics and Scion software to determine mean vascular cross-sectional area, the relative cross-sectional area of vessels, the number of vessels per unit area, and the perimeter of vessels.ResultsFrom 10 weeks, vessels in the human brain start to differentiate into arteries and veins. At 12 weeks, capillary basal membranes were already clearly visible. We established a series of characteristics distinguishing brain tissues in the experimental group vs. that in controls: mean vessel cross-sectional areas and vessel perimeters were significantly reduced by 11 weeks vs. controls. The tendency persisted at 12 weeks. Relative vessel cross-sectional area in the experimental group was greater than in controls.ConclusionsMaternal alcoholization during pregnancy significantly influences the development of the cerebral circulatory system, manifesting mainly in changes in the vascularization of the growing brain.Disclosure of interestThe authors have not supplied their declaration of competing interest.
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Kong, Lingmei, Gengpeng Lian, Wenbin Zheng, Huimin Liu, Haidu Zhang, and Ruowei Chen. "Effect of Alcohol on Diffuse Axonal Injury in Rat Brainstem: Diffusion Tensor Imaging and Aquaporin-4 Expression Study." BioMed Research International 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/798261.
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The aim of this study is to assess the effects of alcohol on traumatic brain injury by using diffusion tensor imaging (DTI) and evaluate aquaporin-4(AQP4) expression changes in rat brainstems following acute alcohol intoxication with diffuse axonal injury (DAI). We further investigated the correlation between the AQP4 expression and DTI in the brain edema. Eighty-five rats were imaged before and after injury at various stages. DTI was used to measure brainstem apparent diffusion coefficient (ADC) and fractional anisotropy (FA), with immunostaining being used to determine AQP4 expression. After acute alcoholism with DAI, ADC values of the brainstem first decreased within 6 h and then elevated. FA values began to decline by 1 h, reaching a minimum at 24 h after trauma. There was a negative correlation between ADC values and brainstem AQP4 expression at 6 h and positive correlation at 6 h to 24 h. Changes of ADC and FA values in DAI with acute alcoholism indicate the effects of ethanol on brain edema and the severity of axonal injury. The correlations between ADC values and the brainstem AQP4 expression at different time points suggest that AQP4 expression follows an adaptative profile to the severity of brain edema.
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Mukhtar, Hamid, Saeed Mian Qaisar, and Atef Zaguia. "Deep Convolutional Neural Network Regularization for Alcoholism Detection Using EEG Signals." Sensors 21, no. 16 (August 13, 2021): 5456. http://dx.doi.org/10.3390/s21165456.
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Alcoholism is attributed to regular or excessive drinking of alcohol and leads to the disturbance of the neuronal system in the human brain. This results in certain malfunctioning of neurons that can be detected by an electroencephalogram (EEG) using several electrodes on a human skull at appropriate positions. It is of great interest to be able to classify an EEG activity as that of a normal person or an alcoholic person using data from the minimum possible electrodes (or channels). Due to the complex nature of EEG signals, accurate classification of alcoholism using only a small dataset is a challenging task. Artificial neural networks, specifically convolutional neural networks (CNNs), provide efficient and accurate results in various pattern-based classification problems. In this work, we apply CNN on raw EEG data and demonstrate how we achieved 98% average accuracy by optimizing a baseline CNN model and outperforming its results in a range of performance evaluation metrics on the University of California at Irvine Machine Learning (UCI-ML) EEG dataset. This article explains the stepwise improvement of the baseline model using the dropout, batch normalization, and kernel regularization techniques and provides a comparison of the two models that can be beneficial for aspiring practitioners who aim to develop similar classification models in CNN. A performance comparison is also provided with other approaches using the same dataset.