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Artículos de revistas sobre el tema "Alcohol-related brain damage"

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Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 20 de febrero de 2023

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1

Erdozain, Amaia M., Benito Morentin, Lynn Bedford, Emma King, David Tooth, Charlotte Brewer, Declan Wayne et al. "Alcohol-Related Brain Damage in Humans". PLoS ONE 9, n.º 4 (3 de abril de 2014): e93586. http://dx.doi.org/10.1371/journal.pone.0093586.

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Lovinger, David M. "Excitotoxicity and Alcohol-Related Brain Damage". Alcoholism: Clinical and Experimental Research 17, n.º 1 (febrero de 1993): 19–27. http://dx.doi.org/10.1111/j.1530-0277.1993.tb00720.x.

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3

Halliday, Glenda, Kerry Baker y Clive Harper. "Serotonin and alcohol-related brain damage". Metabolic Brain Disease 10, n.º 1 (marzo de 1995): 25–30. http://dx.doi.org/10.1007/bf01991780.

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4

Smith, Caine C., Donna L. Sheedy, Holly P. McEwen, Anthony S. Don, Jillian J. Kril y Greg T. Sutherland. "Lipidome changes in alcohol‐related brain damage". Journal of Neurochemistry 160, n.º 2 (11 de noviembre de 2021): 271–82. http://dx.doi.org/10.1111/jnc.15530.

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5

Rao, Rahul y Brian Draper. "Alcohol-related brain damage in older people". Lancet Psychiatry 2, n.º 8 (agosto de 2015): 674–75. http://dx.doi.org/10.1016/s2215-0366(15)00215-1.

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6

Guerrini, I., A. D. Thomson y H. M. Gurling. "Molecular Genetics of Alcohol-Related Brain Damage". Alcohol and Alcoholism 44, n.º 2 (16 de enero de 2009): 166–70. http://dx.doi.org/10.1093/alcalc/agn101.

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7

Harper, C. "The Neuropathology of Alcohol-Related Brain Damage". Alcohol and Alcoholism 44, n.º 2 (16 de enero de 2009): 136–40. http://dx.doi.org/10.1093/alcalc/agn102.

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8

Aziz, Victor M. "Alcohol-related brain damage (ARBD): a service need". International Psychogeriatrics 26, n.º 10 (3 de julio de 2014): 1747–49. http://dx.doi.org/10.1017/s1041610214001252.

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Alcohol-related dementia (ARD) is a controversial concept. Alcohol-related brain damage (ARBD) is a term used to cover a spectrum of conditions and disorders: this includes alcohol-related dementia, Korsakoff's syndrome, Wernicke's encephalopathy, alcohol-related brain injury, and alcohol amnesic syndrome. In other words, these are the conditions that have been induced by chronic alcohol consumption, resulting in some degree of brain damage. The prevalence data are varied.

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9

Place, Charlie. "Alcohol related brain damage – a case of neglect?" Advances in Dual Diagnosis 7, n.º 3 (12 de agosto de 2014): 129–36. http://dx.doi.org/10.1108/add-02-2014-0008.

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Purpose – The purpose of this paper is to argue that alcohol-related brain damage (ARBD) is a neglected problem. ARBD is a term that has begun to be used over the past decade to describe prolonged cognitive impairment caused by alcohol use, including Wernicke's encephalopathy and Korsakoff syndrome, alcohol dementia and alcohol-related brain injury. Design/methodology/approach – The paper provides an overview of ARBD describing the research around its prevalence and prognosis. There is a consensus in the literature that there is little research and a lack of awareness of this condition. The author uses case studies from his own experience working with people with ARBD to describe the difficulties in accessing appropriate assessment and care for this group, and suggests that they are often excluded in a way that is familiar from the experience of the person with “dual diagnosis”. Findings – Recommendations are made including raising awareness, improving screening for cognitive impairment and developing specialist services. Originality/value – ARBD appears to have been neglected in the “dual diagnosis” world and this paper attempts to address this, and so should be of interest to a wide range of professionals working with substance use, mental health, homelessness and social work.

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10

Jauhar, Sameer y Iain D. Smith. "Alcohol-related brain damage: not a silent epidemic". British Journal of Psychiatry 194, n.º 3 (marzo de 2009): 287–88. http://dx.doi.org/10.1192/bjp.194.3.287b.

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Alexander-Kaufman, Kimberley y Clive Harper. "Transketolase: Observations in alcohol-related brain damage research". International Journal of Biochemistry & Cell Biology 41, n.º 4 (abril de 2009): 717–20. http://dx.doi.org/10.1016/j.biocel.2008.04.005.

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12

Nazarko, Linda. "Alcohol-related brain damage: diagnosis, treatment and medical management". British Journal of Neuroscience Nursing 16, n.º 1 (2 de febrero de 2020): 36–43. http://dx.doi.org/10.12968/bjnn.2020.16.1.36.

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Alcohol misuse is often a hidden problem and alcohol-related brain damage is thought to account for around 10% of cases of dementia ( Gupta and Warner, 2008 ; Brust, 2010 ). In England, an estimated 589 101 adults are alcohol-dependent and 24% of adults in England and Scotland regularly drink more than Department of Health and Social Care (DHSC) guidelines ( Burton et al, 2016 ). Alcohol misuse can affect many aspects of health and can lead to alcohol-related brain damage (ARBD). This article explains about the pathophysiology and clinical features of ARBD, and how it is diagnosed, treated and managed.

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13

Lázaro, M., L. Carvalhão Gil, A. Ponte y T. Mota. "Do not forget alcohol damage – Cognitive impairments related to alcohol". European Psychiatry 41, S1 (abril de 2017): s868. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1740.

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IntroductionChronic excessive alcohol consumption may lead to structural and functional damage of the brain. Alcohol-related cognitive impairments are well-established and confirmed by neuropsychological and neuroimaging studies. However, the influence of each neuropathological mechanisms is still under discussion. This topic is increasingly becoming focus of attention in psychiatry.ObjectivesReview the neuropathology, clinical features, neuropsychology and management of alcohol-related cognitive impairments.AimsEvaluate clinical impact, management and prognosis of alcohol-related cognitive impairments.MethodsA literature search was performed on PubMed and Medscape database.ResultsAccording to our literature research, there is a debate concerning the relative contributions of the direct toxic effect of alcohol and the impact of thiamine deficiency on the alcohol-related cognitive impairments. Research about this issue is challenging, considering the multiple patterns of alcohol abuse, the personal and lifestyle factors, and the vulnerability of specific brain regions. The cognitive decline is linked to neuroanatomical alterations and primarily affects executive functions, episodic memory, and visuospatial capacities. These deficits may range from mild to severe but usually remain undiagnosed, unless they are specifically investigated. Maintenance of lasting abstinence is associated with cognitive recovery, but some impairments may persist and interfere with the prognosis.ConclusionRecognizing and screening for alcohol-related cognitive impairments is crucial to offer significant benefits to patients by optimising management strategies.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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14

Wilson, Kenneth. "Alcohol-related brain damage: a 21st-century management conundrum". British Journal of Psychiatry 199, n.º 3 (septiembre de 2011): 176–77. http://dx.doi.org/10.1192/bjp.bp.111.092569.

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SummaryAlcohol-related brain damage has a growing impact on service provision. Despite the benefit of therapeutic interventions and a relatively good prognosis in the context of service provision, few services exist. Both national and local initiatives are required in order to provide psychosocial rehabilitation for this marginalised group of patients.

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15

Harper, Clive. "The Pathology of Alcohol-Related Brain Damage: An Overview". Australian Drug and Alcohol Review 7, n.º 1 (enero de 1988): 51–55. http://dx.doi.org/10.1080/09595238880000121.

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16

Lennane, K. Jean. "Patients with Alcohol-Related Brain Damage: Therapy and Outcome". Australian Drug and Alcohol Review 7, n.º 1 (enero de 1988): 89–92. http://dx.doi.org/10.1080/09595238880000201.

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17

Zahr, Natalie M., Kimberley L. Kaufman y Clive G. Harper. "Clinical and pathological features of alcohol-related brain damage". Nature Reviews Neurology 7, n.º 5 (12 de abril de 2011): 284–94. http://dx.doi.org/10.1038/nrneurol.2011.42.

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18

Wise, J. "Alcohol related brain damage often goes undiagnosed, says report". BMJ 348, may20 6 (20 de mayo de 2014): g3409. http://dx.doi.org/10.1136/bmj.g3409.

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19

Keady, John, Charlotte L. Clarke, Heather Wilkinson, Catherine E. Gibb, Linda Williams, Anna Luce y Ailsa Cook. "Alcohol-related brain damage: Narrative storylines and risk constructions". Health, Risk & Society 11, n.º 4 (agosto de 2009): 321–40. http://dx.doi.org/10.1080/13698570903015743.

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20

Jauhar, Sameer, E. Jane Marshall y Iain D. Smith. "Alcohol and cognitive impairment". Advances in Psychiatric Treatment 20, n.º 5 (septiembre de 2014): 304–13. http://dx.doi.org/10.1192/apt.bp.113.011981.

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SummaryThe relationship between alcohol use and cognitive impairment has been notoriously difficult to disentangle. We present what is known about cognitive impairment associated with alcohol use/misuse, covering the spectrum from mild and subtle cognitive change through to severe alcohol-related brain damage, including Wernicke-Korsakoff syndrome. We highlight aids to the diagnosis and management of these conditions, and emphasise the benefits of prompt treatment on outcome. We also review progress in understanding their neurobiology. Suggestions for possible service configuration based on both our clinical practice and national guidelines are given.Learning Objectives•Gain an understanding of the spectrum of clinical presentations found in alcohol-related brain damage.•Understand that the aetiology of these conditions is complex and not solely due to the neurotoxic effects of alcohol.•Be better able to plan for the rehabilitation of individuals with established alcohol-related brain damage in your local service area.

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21

Amanullah, Talha Muneer, David Henstock y Bushra Azam. "Alcohol Related Brain Damage Presentations in an Acute General Hospital". BJPsych Open 8, S1 (junio de 2022): S81—S82. http://dx.doi.org/10.1192/bjo.2022.266.

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AimsAlcohol-related brain damage (ARBD) is used to describe a variety of clinical syndromes associated with excessive intake of alcohol. It can present with cognitive and neurological syndromes, including Wernicke's encephalopathy, Korsakoff's syndrome, alcohol dementia, cerebellar atrophy and frontal lobe dysfunction, Central pontine myelinolysis and Marchiafava Bignami disease. In up to 25% of cases ARBD can be complicated by traumatic head injury and brain blood supply disturbances. In the absence of clear national guidelines, standards or established pathways of care across most of the UK, most patients are unable to access appropriate service provision. The North Derbyshire mental health liaison team (MHLT) provides assessment and diagnosis of acute alcohol related brain injury, assess severity (based on clinical presentation, investigation findings, cognitive assessment) and provide a care plan with follow-up to various community services. Aim and objectives: To find out the discharge outcome for patients with ARBD diagnosis by the north MHLT, help us identify service gaps and look at ways to improve patient's care in this group.MethodsWe retrospectively analysed 300 patients who were referred to liaison team for drug and alcohol problems and were seen by the drug and alcohol lead nurse within the liaison team. Patients who were given a diagnosis of ARBD by the liaison team were included in the study.We looked at 1.Age and gender distribution2.Team who gave the initial diagnosis3.Discharge destination4.Community follow-up and engagementResultsWe identified 17 patients who were given diagnosis of ARBD. There was relatively equal distribution of male to female patients. Majority of diagnosis’ were given by liaison team. The discharge destination was variable with around half referred to ARBD rehabilitation unit and Derbyshire recovery partnership. Engagement was poor with only 20% of patients engaging with services.ConclusionRecommendations: 1.Detailed cognitive tests need doing for screening and to establish severity2. Consideration for which neuroimaging modalities can help aid diagnosis, if any, should be made. 3.ARBD leaflets to be given4.ARBD diagnosed patients who do not need rehabilitation unit, should be referred for social care assessment as an inpatient and / or be followed up in the community under Care Act5. Considerations with the Multi Disciplinary Team for ways to improve engagement in the community, perhaps with more frequent and robust follow-ups.

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22

Svanberg, Jenny y Jonathan J. Evans. "Neuropsychological Rehabilitation in Alcohol-Related Brain Damage: A Systematic Review". Alcohol and Alcoholism 48, n.º 6 (16 de agosto de 2013): 704–11. http://dx.doi.org/10.1093/alcalc/agt131.

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23

Carlen, Peter L. y D. Adrian Wilkinson. "Reversibility of alcohol-related brain damage: Clinical and experimental observations". Acta Medica Scandinavica 221, S717 (24 de abril de 2009): 19–26. http://dx.doi.org/10.1111/j.0954-6820.1987.tb13038.x.

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24

Nazarko, Linda. "Dementia 5. Alcohol-related brain damage (ARBD): diagnosis, treatment and medical management". British Journal of Healthcare Assistants 13, n.º 12 (2 de diciembre de 2019): 600–607. http://dx.doi.org/10.12968/bjha.2019.13.12.600.

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Alcohol misuse is often a hidden problem and alcohol-related brain damage is thought to account for around 10% of cases of dementia ( Brust, 2010 ; Gupta and Warner, 2008 ). In England, an estimated 589 101 adults are alcohol-dependent and 24% of adults in England and Scotland regularly drink more than Department of Health and Social Care (DHSC) guidelines ( Burton et al, 2016 ). Alcohol misuse can affect many aspects of health and can lead to alcohol-related brain damage (ARBD). This article, the fifth in a series on dementia, explains about the pathophysiology and clinical features of ARBD, and how it is diagnosed, treated and managed.

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25

Wurm, Christopher S. E. "How much does alcohol-related brain damage extend length of stay in alcohol-related liver disease?" Internal Medicine Journal 47, n.º 7 (julio de 2017): 834–35. http://dx.doi.org/10.1111/imj.13469.

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26

Nogueira, V., M. Mendes, I. Pereira y J. Teixeira. "Alcohol-related dementia – an overlooked entity?" European Psychiatry 64, S1 (abril de 2021): S419—S420. http://dx.doi.org/10.1192/j.eurpsy.2021.1120.

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IntroductionThe relationship between alcohol use and dementia is complex. There is a J-shaped relationship between alcohol use and cognitive impairment and evidence shows that one-quarter of the dementia population have alcohol related problems. It is estimated that alcohol-related dementia (ARD) contributes for about 10% of all cases of dementia, especially early-onset dementia, but is largely overlooked or seen as a comorbid factor.ObjectivesTo clarify the relationship between alcohol use, alcohol-related brain damage and dementia; to review the clinical features, neuropathology, nosology and neuropsychology of ARD and alcohol-induced persisting amnestic syndrome (Wernicke-Korsakoff syndrome- WKS).MethodsWe performed a review of systematic reviews from the last 10 years. A total of 28 systematic reviews were identified.ResultsHeavy alcohol use has been shown to be a contributory factor and necessary factor in the development of multiple brain diseases. It may cause brain damage in multiple ways: direct neurotoxic effect of acetaldehyde; thiamine deficiency. It is also a risk factor for other conditions, such as hepatic encephalopathy, epilepsy and head injury.ConclusionsClinical observation favors the diagnosis of ADR as a distinct entity, but broader evidence reflects significant commonality between ARD and WKS, tough neuropsychological studies have largely attempted to differentiate these syndromes. Repeated episodes of WKS may cause cognitive deterioration. In contrast to other common causes of dementia, the decline in cognitive functioning in ARD is relatively non-progressive if abstinence is maintained, or even partially reversible, as supported by neuroimaging evidence. Given the increase in per capita consumption, it is expected a disproportionate increase in ARD.

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Stacey, Phillip S. y Karen A. Sullivan. "Preliminary Investigation of Thiamine and Alcohol Intake in Clinical and Healthy Samples". Psychological Reports 94, n.º 3 (junio de 2004): 845–48. http://dx.doi.org/10.2466/pr0.94.3.845-848.

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Insufficient thiamine intake during heavy alcohol dependence has been well established as a precursor to alcohol-related brain damage, including Wernicke-Korsakoff syndrome. This study compared the alcohol and thiamine intakes of 35 alcohol-dependent patients upon admission for detoxification with 49 healthy young undergraduates. Subjects were interviewed using a retrospective diary that recorded alcohol and food and vitamin consumption for the previous seven days. As predicted, the clinical group consumed significantly less thiamine than the healthy group, and well below the minimum safe daily intakes. Findings have implications for the prevention of alcohol-related brain damage and public health policy.

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28

Thomson, A. D., I. Guerrini, D. Bell, C. Drummond, T. Duka, M. Field, M. Kopelman et al. "Alcohol-Related Brain Damage: Report from a Medical Council on Alcohol Symposium, June 2010". Alcohol and Alcoholism 47, n.º 2 (1 de marzo de 2012): 84–91. http://dx.doi.org/10.1093/alcalc/ags009.

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29

Lennane, K. Jean. "Management of moderate to severe alcohol‐related brain damage (Korsakoff's syndrome)". Medical Journal of Australia 145, n.º 3-4 (agosto de 1986): 136–43. http://dx.doi.org/10.5694/j.1326-5377.1986.tb113772.x.

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Jacques, Alan. "Alcohol-Related Brain Damage – The Concerns of the Mental Welfare Commission". Alcohol and Alcoholism 35, Supplement_1 (1 de mayo de 2000): 11–15. http://dx.doi.org/10.1093/alcalc/35.supplement_1.11.

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31

Leong, KK, M. Paramlall, H. Swanepoel y J. Herrod. "35 Processing speed (PS) improvement in alcohol related brain damage (ARBD)". Journal of Neurology, Neurosurgery & Psychiatry 93, n.º 12 (14 de noviembre de 2022): e3.29. http://dx.doi.org/10.1136/jnnp-2022-bnpa.35.

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IntroductionARBD is characterised by cognitive impairment, a causative link to excessive alcohol ingestion and thiamine deficiency. It is complex; with deficits in anterograde memory, executive function, attention, PS, visuospatial skills and IQ and approximately 25% have ischaemic or traumatic head injury events.1Oslin’s Alcohol Dementia Criteria2recommends assessment after three months for evaluation of long standing cognitive deficits due to abstinence related improvement; not observed in patients with concomitant vascular lesions. Domains studied include verbal fluency (VF), memory, abstraction and perceptual motor skills. There are no treatment guidelines for ARBD cognitive deficits. Various cognitive domains showed some improvement with Donepezil, Rivastigmine and Memantine; but not in PS. Our patient, showed such an improvement with Memantine.Case summaryWe present a case of a 68-year-old man with a 30 year history of alcohol dependence of 9 units per day (substantially increased in the 7 years pre-admission), resulting in self-neglect, impulsivity, aggression, hallucinations, and chronic neuropsychiatric sequelae and cognitive impairments. He met the criteria for ARBD1with prolonged cognitive impairment, causative association with alcohol use requiring thiamine replacement3; CT abdomen showed hepatic atrophy and MRI head demonstrated moderate small vessel disease. Self-neglect, impulsivity, aggression, and hallucinations improved with three month’s alcohol abstinence, however, neuropsychiatric complications persisted. Ten months abstinence- self report mood disorder screening and typical dementia blood screen were unremarkable. A Wechsler Adult Intelligence Scale (WAIS-IV UK) was performed and Memantine commenced (uptitrated to BNF maximum.)ResultsThe WAIS-IV 3 month follow up showed statistical improvement in Perceptual reasoning, PS and General Ability index.DiscussionPrevious ARBD studies indicate abstinence related improvements in delayed recall, VF and general intellectual functioning, but, not in memory and inhibition4. Memantine (non-competitive NMDA antagonist) is associated with improved VF, confrontational naming, word list memory, constructional praxis recall and trail making A; no studies have measured PS using specific neuropsychological tests. PS is associated with the superior longditudinal fasiculus and white matter tracts within parietal and temporal cortices and left middle frontal gyrus5. Functional neuroimaging has shown white matter loss in the prefrontal cortex, superior prefrontal association cortex, cerebellum, hypothalmus and corpus callosum6. Alcohol possibly upregulates NMDA receptors and glutamate excitotoxicity with impaired oligodendrocyte function and white matter lesions7. Memantine, possibly prevents glutamate toxicity and may improve oligodendrocyte function myelination restoration. Therefore, PS improvements may be related to lesion repair secondary to Memantine effect on Oligodendrocyte function.

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32

Sutherland, Greg T., Donna Sheedy y Jillian J. Kril. "Using Autopsy Brain Tissue to Study Alcohol-Related Brain Damage in the Genomic Age". Alcoholism: Clinical and Experimental Research 38, n.º 1 (27 de agosto de 2013): 1–8. http://dx.doi.org/10.1111/acer.12243.

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33

Lange, E. H., S. Nerland, K. N. Jørgensen, L. Mørch-Johnsen, R. Nesvåg, C. B. Hartberg, U. K. Haukvik et al. "Alcohol use is associated with thinner cerebral cortex and larger ventricles in schizophrenia, bipolar disorder and healthy controls". Psychological Medicine 47, n.º 4 (10 de noviembre de 2016): 655–68. http://dx.doi.org/10.1017/s0033291716002920.

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BackgroundExcessive alcohol use is associated with brain damage but less is known about brain effects from moderate alcohol use. Previous findings indicate that patients with severe mental illness, particularly schizophrenia, are vulnerable to alcohol-related brain damage. We investigated the association between levels of alcohol consumption and cortical and subcortical brain structures in schizophrenia and bipolar disorder patients and healthy controls, and investigated for group differences for this association.Method1.5 T structural magnetic resonance images were acquired of 609 alcohol-using participants (165 schizophrenia patients, 172 bipolar disorder patients, 272 healthy controls), mean (s.d.) age 34.2 (9.9) years, 52% men. Past year alcohol use was assessed with the Alcohol Use Disorder Identification Test – Consumption part (AUDIT-C). General linear models were used to investigate associations between AUDIT-C score and cortical thickness, surface area, and total brain and subcortical volumes.ResultsIncreasing AUDIT-C score was linearly associated with thinner cortex in medial and dorsolateral frontal and parieto-occipital regions, and with larger left lateral ventricle volume. There was no significant interaction between AUDIT-C score and diagnostic group. The findings remained significant after controlling for substance use disorders, antipsychotic medication and illness severity.ConclusionThe results show a dose-dependent relationship between alcohol use and thinner cortex and ventricular expansion. The findings are present also at lower levels of alcohol consumption and do not differ between schizophrenia or bipolar disorder patients compared to healthy controls. Our results do not support previous findings of increased vulnerability for alcohol-related brain damage in severe mental illness.

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Clergue-Duval, Virgile, Laurent Coulbault, Frank Questel, Nicolas Cabé, Alice Laniepce, Clément Delage, Céline Boudehent et al. "Alcohol Withdrawal Is an Oxidative Stress Challenge for the Brain: Does It Pave the Way toward Severe Alcohol-Related Cognitive Impairment?" Antioxidants 11, n.º 10 (21 de octubre de 2022): 2078. http://dx.doi.org/10.3390/antiox11102078.

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Alcohol use is a leading cause of mortality, brain morbidity, neurological complications and minor to major neurocognitive disorders. Alcohol-related neurocognitive disorders are consecutive to the direct effect of chronic and excessive alcohol use, but not only. Indeed, patients with severe alcohol use disorders (AUD) associated with pharmacological dependence suffer from repetitive events of alcohol withdrawal (AW). If those AW are not managed by adequate medical and pharmacological treatment, they may evolve into severe AW, or be complicated by epileptic seizure or delirium tremens (DT). In addition, we suggest that AW favors the occurrence of Wernicke’s encephalopathy (WE) in patients with known or unknown thiamine depletion. We reviewed the literature on oxidative stress as a core mechanism in brain suffering linked with those conditions: AW, epileptic seizure, DT and WE. Thus, we propose perspectives to further develop research projects aiming at better identifying oxidative stress brain damage related to AW, assessing the effect of repetitive episodes of AW, and their long-term cognitive consequences. This research field should develop neuroprotective strategies during AW itself or during the periwithdrawal period. This could contribute to the prevention of severe alcohol-related brain damage and cognitive impairments.

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Gilchrist, Gail y David S. Morrison. "Prevalence of alcohol related brain damage among homeless hostel dwellers in Glasgow". European Journal of Public Health 15, n.º 6 (14 de septiembre de 2005): 587–88. http://dx.doi.org/10.1093/eurpub/cki036.

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Fox, Geoffrey A. y Allison M. Fox. "The Effects of Brain Damage on the Performance of Hand Movement Sequences". Brain Impairment 2, n.º 2 (1 de diciembre de 2001): 140–44. http://dx.doi.org/10.1375/brim.2.2.140.

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AbstractThe frontal lobes, if damaged, may lead to a host of divergent abnormalities, depending on the extent, site, depth, and laterality of the damage. Because of the extensive connections which exist between the frontal lobes and the other systems of the brain, damage to a more remote system may cause frontal system disorder through disconnection. The Hand Movement Test (HMT, Kaufman & Kaufman, 1983) is thought to be sensitive to damage affecting these systems, although the test was developed for use with children rather than adults. This paper examines the effects of three diverse neuropsychological disorders, where damage to the frontal lobes or to their interconnections has been implicated, on hand movement sequencing performance in adults. The three groups studied included patients diagnosed with alcohol-related brain damage (n = 57), patients diagnosed with mild traumatic brain injury (n = 21), and patients diagnosed with age-related dementia (n = 30). HMT performance was significantly poorer in all three clinical groups relative to controls, supporting the addition of this brief, paediatric test in neuropsychological evaluations assessing these disorders.

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37

Hu, Jian, Yan Xia, Zheng Wu, Lei Liu y Chunling Tang. "Fluoxetine Might Alleviate Brain Damage and Hypercortisolemia Related to Chronic Alcohol in Rats*". Journal of Studies on Alcohol and Drugs 71, n.º 2 (marzo de 2010): 290–94. http://dx.doi.org/10.15288/jsad.2010.71.290.

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38

Horton, Lindsay, Tim Duffy y Colin R. Martin. "Assessing outcomes of alcohol-related brain damage (ARBD): What should we be measuring?" Drugs: Education, Prevention and Policy 22, n.º 2 (5 de enero de 2015): 151–59. http://dx.doi.org/10.3109/09687637.2014.991278.

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39

Clifford, Christine A. y David Maddocks. "Alcohol-Related Brain Damage: the Neuropsychological Deficits and their Implication for Independent Living". Australian Drug and Alcohol Review 7, n.º 1 (enero de 1988): 79–81. http://dx.doi.org/10.1080/09595238880000181.

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40

Matsumoto, I. "Proteomics Approach in the Study of the Pathophysiology of Alcohol-Related Brain Damage". Alcohol and Alcoholism 44, n.º 2 (16 de enero de 2009): 171–76. http://dx.doi.org/10.1093/alcalc/agn104.

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41

McCorkindale, A. N., D. Sheedy, J. J. Kril y G. T. Sutherland. "The effects of chronic smoking on the pathology of alcohol-related brain damage". Alcohol 53 (junio de 2016): 35–44. http://dx.doi.org/10.1016/j.alcohol.2016.04.002.

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42

Rao, Rahul y Ilana Crome. "Alcohol misuse in older people". BJPsych Advances 22, n.º 2 (marzo de 2016): 118–26. http://dx.doi.org/10.1192/apt.bp.115.014480.

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SummaryThe clinical and public mental health aspects of alcohol misuse in older people (both men and women) have increasing relevance for both old age and addiction psychiatrists. Clinical presentations are often complex and involve a number of different psychiatric, physical and psychosocial factors. The assessment, treatment and aftercare of alcohol-related and comorbid other mental disorders will also involve a broad range of interventions from a wide range of practitioners. Given its growing clinical relevance, there are particular areas, such as alcohol-related brain damage and drug interactions with alcohol, that deserve special attention.

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43

Morrison, Fraser y Simon Pestell. "The application of cognitive behaviour therapy to individuals with co-morbid depression and alcohol-related brain damage". Clinical Psychology Forum 1, n.º 206 (febrero de 2010): 13–18. http://dx.doi.org/10.53841/bpscpf.2010.1.206.13.

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Price, John, Sheila Mitchell, Bevan Wiltshire, Joan Graham y Gail Williams. "A Follow-Up Study of Patients with Alcohol-Related Brain Damage in the Community". Australian Drug and Alcohol Review 7, n.º 1 (enero de 1988): 83–87. http://dx.doi.org/10.1080/09595238880000191.

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Horton, L., T. Duffy, C. Hollins Martin y C. R. Martin. "Comprehensive assessment of alcohol-related brain damage (ARBD): gap or chasm in the evidence?" Journal of Psychiatric and Mental Health Nursing 22, n.º 1 (21 de mayo de 2014): 3–14. http://dx.doi.org/10.1111/jpm.12156.

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46

Wilson, Kenneth, Angela Halsey, Helen Macpherson, Jane Billington, Sharon Hill, Gavin Johnson, Keerthy Raju y Pat Abbott. "The Psycho-Social Rehabilitation of Patients with Alcohol-Related Brain Damage in the Community†". Alcohol and Alcoholism 47, n.º 3 (25 de enero de 2012): 304–11. http://dx.doi.org/10.1093/alcalc/agr167.

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Hernández, José A., Rosa C. López-Sánchez y Adela Rendón-Ramírez. "Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage". Oxidative Medicine and Cellular Longevity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/1543809.

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The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells. This metabolism of ethanol can induce the oxidation of the fatty acids in phospholipids, and the bioactive aldehydes produced are known to be associated with neurotoxicity and neurodegeneration. As such, here we will review the role of lipids in the neuronal damage induced by ethanol-related oxidative stress and the role that lipids play in the related compensatory or defense mechanisms.

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48

Connor, Paul D. "Synthesizing Animal and Human Studies of Prenatal Alcohol Exposure". Journal of the International Neuropsychological Society 7, n.º 5 (julio de 2001): 648–49. http://dx.doi.org/10.1017/s1355617701225120.

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The primary focus of this volume is on the impact of alcohol on brain development. It is a perfect example of how research on both animals and humans can interact to produce very important findings. In the case of prenatal alcohol exposure, dialogue between animal and human researchers has proved to be very profitable for both lines of research. Initial observations by human researchers identified a syndrome of facial stigmata, physical malformations, and early behavioral disturbances that was related to maternal alcohol abuse during pregnancy. They gave this syndrome the name Fetal Alcohol Syndrome. However, human researchers were unable to state unequivocally that prenatal alcohol exposure was teratogenic to the fetus. Thus, they turned to animal researchers who were able to model Fetal Alcohol Syndrome in a variety of animals and to confirm the teratogenicity of alcohol on the developing fetus. The quarter century of studies of the damage caused by prenatal alcohol exposure is replete with such interactions between these two groups of researchers. Without the input and pioneering studies of animal researchers on the effects of prenatal alcohol exposure, human researchers would have much less understanding of the damage caused by alcohol exposure in utero or insights into possible treatment or remediation strategies for those damaged by alcohol exposure.

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Mayock, Dennis E., Dana Ness, Robin L. Mondares y Christine A. Gleason. "Binge alcohol exposure in the second trimester attenuates fetal cerebral blood flow response to hypoxia". Journal of Applied Physiology 102, n.º 3 (marzo de 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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Erdozain, A., B. Morentin, N. Osna, D. Tuma, K. Kharbanda, L. Collado y W. G. Carter. "FOC7PATHOLOGYFOC7-1DAMAGE TO THE CYTOSKELETAL ARCHITECTURE IS A PATHOLOGICAL HALLMARK OF ALCOHOL-RELATED BRAIN DAMAGE". Alcohol and Alcoholism 50, suppl 1 (septiembre de 2015): i42.4—i43. http://dx.doi.org/10.1093/alcalc/agv079.28.

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