Identifying, Assessing, and Treating Korsakoff Syndrome Patients

2021 ◽  
Vol 209 (8) ◽  
pp. 592-599
Author(s):  
Joseph John Westermeyer ◽  
Beverly Soukup ◽  
Jessica Mayer ◽  
Kathryn Lee
Keyword(s):  
Korsakoff Syndrome

Gayet-Wernicke encephalopathy with rapid evolution toward dementia in alcoholic dependence – case report

Psihiatru ro ◽  
2019 ◽  
Vol 58 (3) (1) ◽  
pp. 18-20
Author(s):  
Cătălina Crişan ◽  
Laura Grosu ◽  
Oana Vanţa
Keyword(s):  
Case Report ◽  
Thiamine Deficiency ◽  
Withdrawal Syndrome ◽  
Rapid Evolution ◽  
Full Recovery ◽  
Wernicke Encephalopathy ◽  
Korsakoff Syndrome ◽  
Dementia Syndrome ◽  
Patients Experience

Gayet-Wernicke encephalopathy is an acute neuropsychiatric condition caused by thiamine deficiency. Only a small percentage of patients experience all three symptoms, with ophtalmoplegia, ataxia and confusion, and the full triad occurs more frequently among those who have overused alcohol. The evolution is toward full recovery, Korsakoff syndrome, dementia or death. We present the case of a 56-year-old patient, known with a diagnostic of alcoholism, who was admitted for a complicated withdrawal syndrome with delirium and who developed encephalopathy and dementia syndrome.

Aetiologies and anatomy of confabulation

2017 ◽  
Author(s):  
Armin Schnider
Keyword(s):  
Brain Damage ◽  
Limbic Encephalitis ◽  
Artery Aneurysm ◽  
Anterior Communicating Artery ◽  
Brain Areas ◽  
Anatomical Basis ◽  
Korsakoff Syndrome ◽  
Hypoxic Brain ◽  
Degenerative Dementia ◽  
The Brain

What diseases cause confabulations and which are the brain areas whose damage is responsible? This chapter reviews the causes, both historic and present, of confabulations and deduces the anatomo-clinical relationships for the four forms of confabulation in the following disorders: alcoholic Korsakoff syndrome, traumatic brain injury, rupture of an anterior communicating artery aneurysm, posterior circulation stroke, herpes and limbic encephalitis, hypoxic brain damage, degenerative dementia, tumours, schizophrenia, and syphilis. Overall, clinically relevant confabulation is rare. Some aetiologies have become more important over time, others have virtually disappeared. While confabulations seem to be more frequent after anterior brain damage, only one form has a distinct anatomical basis.

scholarly journals The Inferior Colliculus in Alcoholism and Beyond

2020 ◽  
Vol 14 ◽  
Author(s):  
Tanuja Bordia ◽  
Natalie M. Zahr
Keyword(s):  
Inferior Colliculus ◽  
Ethanol Exposure ◽  
Ethanol Withdrawal ◽  
Hypoxic Injury ◽  
Auditory Gating ◽  
Korsakoff Syndrome ◽  
Altered Metabolism ◽  
Magnetic Resonance Imaging Mri ◽  
Inferior Colliculi

Post-mortem neuropathological and in vivo neuroimaging methods have demonstrated the vulnerability of the inferior colliculus to the sequelae of thiamine deficiency as occurs in Wernicke-Korsakoff Syndrome (WKS). A rich literature in animal models ranging from mice to monkeys—including our neuroimaging studies in rats—has shown involvement of the inferior colliculi in the neural response to thiamine depletion, frequently accomplished with pyrithiamine, an inhibitor of thiamine metabolism. In uncomplicated alcoholism (i.e., absent diagnosable neurological concomitants), the literature citing involvement of the inferior colliculus is scarce, has nearly all been accomplished in preclinical models, and is predominately discussed in the context of ethanol withdrawal. Our recent work using novel, voxel-based analysis of structural Magnetic Resonance Imaging (MRI) has demonstrated significant, persistent shrinkage of the inferior colliculus using acute and chronic ethanol exposure paradigms in two strains of rats. We speculate that these consistent findings should be considered from the perspective of the inferior colliculi having a relatively high CNS metabolic rate. As such, they are especially vulnerable to hypoxic injury and may be provide a common anatomical link among a variety of disparate insults. An argument will be made that the inferior colliculi have functions, possibly related to auditory gating, necessary for awareness of the external environment. Multimodal imaging including diffusion methods to provide more accurate in vivo visualization and quantification of the inferior colliculi may clarify the roles of brain stem nuclei such as the inferior colliculi in alcoholism and other neuropathologies marked by altered metabolism.

Thiamine (Vitamin B1)

2011 ◽  
Vol 16 (1) ◽  
pp. 12-20 ◽  
Author(s):  
Aviva Fattal-Valevski
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Metabolism ◽  
Oxidant Stress ◽  
Vitamin B1 ◽  
Vitamin B ◽  
Deficient Diet ◽  
Common Cause ◽  
Korsakoff Syndrome ◽  
Reducing Substances ◽  
B Vitamin

Thiamine (vitamin B1) was the first B vitamin to have been identified. It serves as a cofactor for several enzymes involved in energy metabolism. The thiamine-dependent enzymes are important for the biosynthesis of neurotransmitters and for the production of reducing substances used in oxidant stress defenses, as well as for the synthesis of pentoses used as nucleic acid precursors. Thiamine plays a central role in cerebral metabolism. Its deficiency results in dry beriberi, a peripheral neuropathy, wet beriberi, a cardiomyopathy with edema and lactic acidosis, and Wernicke—Korsakoff syndrome, whose manifestations consist of nystagmus, ophthalmoplegia, and ataxia evolving into confusion, retrograde amnesia, cognitive impairment, and confabulation. Patients on a strict thiamine-deficient diet display a state of severe depletion within 18 days. The most common cause of thiamine deficiency in affluent countries is either alcoholism or malnutrition in nonalcoholic patients. Treatment by thiamine supplementation is beneficial for diagnostic and therapeutic purposes.

Wernicke-Korsakoff syndrome in patients with cancer: a systematic review

2016 ◽  
Vol 17 (4) ◽  
pp. e142-e148 ◽  
Author(s):  
Elie Isenberg-Grzeda ◽  
Sudhanshu Rahane ◽  
Antonio P DeRosa ◽  
Janet Ellis ◽  
Stephen E Nicolson
Keyword(s):  
Systematic Review ◽  
Patients With Cancer ◽  
Korsakoff Syndrome

scholarly journals Donepezil increases regional cerebral blood flow in a case of Korsakoff syndrome

2003 ◽  
Vol 3 (3) ◽  
pp. 119-122
Author(s):  
Atsushi OGINO ◽  
Takashi NISHIKAWA ◽  
Yoshiro SUGITA ◽  
Masatoshi TAKEDA
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Regional Cerebral Blood ◽  
Korsakoff Syndrome

Metabolic Encephalopathy - Part II

2019 ◽  
Author(s):  
Rick Gill ◽  
Matthew McCoyd ◽  
Sean Ruland ◽  
José Biller
Keyword(s):  
Nutritional Intake ◽  
Osmotic Demyelination Syndrome ◽  
Wernicke Encephalopathy ◽  
Metabolic Encephalopathy ◽  
Improve Outcome ◽  
Myxedema Coma ◽  
Hashimoto Encephalopathy ◽  
Korsakoff Syndrome ◽  
Dialysis Disequilibrium Syndrome ◽  
Neurologic Function

Normal neurologic function requires a constantly balanced environment of electrolytes.  Normal hepatic and renal function is critical in maintaining this balance while removing toxins, maintaining a physiologic pH and regulating the excretion of electrolytes.  Nutritional intake provides essential nutrients but deficiencies can lead to characteristic syndromes such as Wernicke's encephalopathy and pellagra and exposure to neurotoxic substances such as heavy metals can lead to encephalopathy.  Thyroid and adrenal dysfunction are common endocrine causes of encephalopathy and symptoms can often improve rapidly with treatment.  A subset of idiopathic encephalopathy is increasingly being recognized as having an autoimmune basis, often presenting as a paraneoplastic process, and having a constellation of symptoms which can aide in the diagnosis.  Timely recognition and treatment of the autoantibodies which target neural structures, with immunosuppressive therapy, can improve outcome in these patients.   This review contains 4 figures, 3 tables, and 42 references. Key words: osmotic demyelination syndrome,hepatic encephalopathy, renal failure, triphasic waves, dialysis disequilibrium syndrome, Wernicke encephalopathy, Korsakoff syndrome, myxedema coma, Hashimoto encephalopathy

Metabolic Encephalopathy - Part II

2019 ◽  
Author(s):  
Rick Gill ◽  
Matthew McCoyd ◽  
Sean Ruland ◽  
José Biller
Keyword(s):  
Nutritional Intake ◽  
Osmotic Demyelination Syndrome ◽  
Wernicke Encephalopathy ◽  
Metabolic Encephalopathy ◽  
Improve Outcome ◽  
Myxedema Coma ◽  
Hashimoto Encephalopathy ◽  
Korsakoff Syndrome ◽  
Dialysis Disequilibrium Syndrome ◽  
Neurologic Function

Normal neurologic function requires a constantly balanced environment of electrolytes.  Normal hepatic and renal function is critical in maintaining this balance while removing toxins, maintaining a physiologic pH and regulating the excretion of electrolytes.  Nutritional intake provides essential nutrients but deficiencies can lead to characteristic syndromes such as Wernicke's encephalopathy and pellagra and exposure to neurotoxic substances such as heavy metals can lead to encephalopathy.  Thyroid and adrenal dysfunction are common endocrine causes of encephalopathy and symptoms can often improve rapidly with treatment.  A subset of idiopathic encephalopathy is increasingly being recognized as having an autoimmune basis, often presenting as a paraneoplastic process, and having a constellation of symptoms which can aide in the diagnosis.  Timely recognition and treatment of the autoantibodies which target neural structures, with immunosuppressive therapy, can improve outcome in these patients.   This review contains 4 figures, 3 tables, and 42 references. Key words: osmotic demyelination syndrome,hepatic encephalopathy, renal failure, triphasic waves, dialysis disequilibrium syndrome, Wernicke encephalopathy, Korsakoff syndrome, myxedema coma, Hashimoto encephalopathy

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