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Alcoholism
Published in Mark S. Gold, R. Bruce Lydiard, John S. Carman, Advances in Psychopharmacology: Predicting and Improving Treatment Response, 2018
Charles A. Dackis, Mark S. Gold
The acutely psychotic, alcoholic patient is very likely not to have schizophrenia. Therefore, a careful diagnostic evaluation of such patients is critical for their proper management. Psychotic symptomatology can be associated with alcohol intoxication, alcohol withdrawal, delerium tremens, and post-intoxication states. These psychotic states tend to be less persistent than schizophrenia, and usually clear within a few days of sobriety. Antipsychotic medications are indicated once medical stabilization has been attained. Psychotic patients should also be suspected to have abused other substances, and antibody-based urine and blood screening for substances of abuse are indicated. Another common cause of psychosis in the alcoholic population is organic brain syndrome. Alcohol-related dementia is often associated with hallucinations and paranoia, and should be managed with antipsychotic medications when present. Psychotic, alcoholic patients require a complete medical and neurological evaluation before an accurate psychiatric diagnosis can be made. Often the diagnosis of schizophrenia can only be definitively made at a future time after a long period of sobriety.
Wernicke-Korsakoff Syndrome
Published in Jenny Svanberg, Adrienne Withall, Brian Draper, Stephen Bowden, Alcohol and the Adult Brain, 2014
Scalzo Simon, Bowden Stephen, Hillbom Matti
The symptomatic presentation of WKS as alcohol-related dementia and potential for long-term recovery with improved health and nutrition has been reviewed in detail elsewhere but is still not well appreciated (Bowden, 1990, 2010; Victor, 1994; Zahr et al., 2011). In an autopsy study of 8,735 cases, Torvik and colleagues (1982) examined the brains of 713 cases with a known alcohol-use disorder. Despite the large sample, Torvik and colleagues failed to detect a single instance of a patient labeled “alcohol-related dementia” in life, which could not be accounted for by WKS pathology or less commonly another dementia not due to alcohol, such as Alzheimer's or vascular dementia. Further, upon retrospective analysis of the clinical records of 20 cases with inactive (chronic) pathology of WE, only five cases were reported to have a clinical amnesia, the others were reported to have exhibited more generalized cognitive impairment. Torvik and colleagues concluded that WE was the primary pathology underlying all reported cases of alcohol-related dementia.
Cognitive Disorders
Published in David F. O'Connell, Dual Disorders, 2014
Patients may present for treatment in chemical dependency facilities during the middle phase of dementia. Patients with alcohol-related dementia usually show a marked increase in functioning following detoxification and a few weeks of abstinence. The disorientation and cognitive dysfunction gradually clear, and studies have shown that the cognitive impairment due to chronic alcoholism gradually improves for several months following cessation of alcohol use. Dementia due to Wernicke-Korsakoff Syndrome, in contrast, may show little or no improvement or a gradual decline.
Professional Perspectives on Supporting Those with Alcohol-Related Neurocognitive Disorders: Challenges & Effective Treatment
Published in Alcoholism Treatment Quarterly, 2021
Robert M. Heirene, Bev John, Marie O’Hanrahan, Ioannis Angelakis, Gareth Roderique-Davies
Alcohol-related neurocognitive disorders (ARNDs) result from excessive and chronic alcohol consumption combined with dietary deficiencies and/or liver dysfunction (Fama et al., 2017; Ritz et al., 2016). Seven ARND syndromes1 are recognized (Zahr & Pfefferbaum, 2017), including Wernicke-Korsakoff’s syndrome (WKS) and Hepatic Encephalopathy (see Table 1). Although, it is important to note that the Alcohol-Related Dementia (ARD) diagnosis remains contentious (see Heirene, John, & Roderique-Davies, 2018). Moreover, in addition to the seven syndromes, the Diagnostic Statistical Manual (DSM-5; American Psychiatric Association, 2013) refers to “Alcohol-related neurocognitive disorders”, including mild and major forms, the latter of which is further divided into amnestic-confabulatory (i.e., WKS) and non-amnestic forms (potentially reflecting ARD). The umbrella term “Alcohol-Related Brain Damage” (ARBD) has also been used to encompass the spectrum of brain damage and functional consequences occurring in those with Alcohol Use Disorders (AUDs), subsuming WKS, ARD, and others under one diagnostic rubric (Heirene et al., 2018).
Preserved intellectual functioning in Korsakoff’s syndrome? Actual and premorbid intelligence in patients with major or mild alcohol-related cognitive disorder
Published in Journal of Substance Use, 2019
Rhody Haalboom, Loes van Aken, Serge J. W. Walvoort, Jos I. M. Egger, Roy P. C. Kessels
In addition to KS, a subgroup of patients with Alcohol Use Disorder (AUD) presents with cognitive impairment in a milder form, not fulfilling the criteria for KS (Green et al., 2010; Oscar-Berman, Kirkley, Gansler, & Couture, 2004). These patients can be classified as having alcohol-related cognitive impairment with an etiology that is qualitatively distinct from the thiamine depletion that causes (Wernicke-)Korsakoff Syndrome (Arts et al., 2017), but that is related to their chronic alcohol use (Hayes, Demirkol, Ridley, Withall, & Draper, 2016). These AUD patients meet the DSM-5 criteria for Alcohol-Induced Mild Neurocognitive Disorder (APA, 2013), with minimal functional decline in daily life due to the cognitive deficits (i.e., not fulfilling the criteria for Alcohol-Related Dementia), without a disproportionate amnesia or confabulations.
Lifetime marijuana and alcohol use, and cognitive dysfunction in people with human immunodeficiency virus infection
Published in Substance Abuse, 2018
Sara A. Lorkiewicz, Alicia S. Ventura, Timothy C. Heeren, Michael R. Winter, Alexander Y. Walley, Meg Sullivan, Jeffrey H. Samet, Richard Saitz
Marijuana use and heavy alcohol use can negatively alter brain activity and cognitive function. Acute and long-term effects of delta-9-tetrahydrocannabinol (Δ9-THC) include altered brain metabolism and changes in neuronal networks, respectively, and proinflammatory states as well as frontal cortical atrophy are often seen in individuals with alcohol use disorders.14–17,21,22 Deficits in memory, specifically delayed recall, are most often observed due to acute and chronic marijuana use, but these deficits are often absent after several weeks of abstinence.14–16,18,19 In people with symptomatic HIV infection, marijuana use is associated with greater cognitive dysfunction compared with asymptomatic or uninfected individuals, indicating a potential negative, synergistic effect of comorbid marijuana use and HIV infection.20 Alcohol affects cognition on a continuum, ranging from mild cognitive impairment to more severe conditions such as Wernike-Korsakoff's syndrome and alcohol-related dementia.23,24 In the presence of HIV infection, alcohol increases the risk of cognitive dysfunction across all ages. Minor or subclinical cognitive deficits caused by marijuana use or heavy alcohol use may be exacerbated and manifest in the presence of HIV infection.20,25,26