Wernicke-Korsakoff Research Articles

Social norms in Korsakoff's syndrome and alcohol-related dementia.

Social cognition is essential for individuals to perceive, process, and interpret social information that enables them to function effectively in society. Korsakoff's syndrome (KS) and alcohol-related dementia (ARD) are alcohol-related cognitive disorders that are likely to impair social cognition. This study aimed to investigate the ability to judge social norms in KS and ARD in comparison to healthy subjects. The study included 30 patients with KS, 10 patients with ARD, and 74 age-, sex-, and education-matched control participants. The Social Norms Questionnaire - Dutch version (SNQ-NL) was used to measure social cognition, and standardized tests were used to examine the association between social cognition and executive functioning. Both KS and ARD patients performed worse in judging social norms when compared to healthy controls, but there was no significant difference between KS and ARD. Both KS and ARD patients performed worse on the SNQ-NL, judging appropriate behavior as inappropriate (Overadhere errors), than controls. When compared to control participants, patients with KS demonstrated significantly more Break Errors, while the differences between the ARD group and the control group did not reach statistical significance. There were no significant correlations between the SNQ-NL variables and performances on standardized tests for executive functioning in both the KS and control group. This study aimed to investigate the ability to judge social norms in KS and ARD in comparison to healthy subjects. The results show that compared to a control group, both KS and ARD patients performed worse in judging social norms. KS and ARD patients scored equally low on social norms identification. Overall, these findings can further help us understand the difficulties in social behavior as experienced by patients and care staff, since problems in accurately judging social norms could possibly contribute to the severe behavioral issues as observed in alcohol-related disorders.

Thiamine Deficiency and its Implications on Microvascular Complications of Diabetes Mellitus

Thiamine is the first vitamin discovered and belongs to Vit B family. The main effect seen with thiamine deficiency is Beri-Beri, Wernicke’s encephalopathy, Wernicke-Korsak off syndrome and are considered as a serious condition but often can be reversed. The deficient status of thiamine can also cause varied affects and can overlap with other conditions to exacerbate its potent effects. It is seen that thiamine is necessary for the metabolism of glucose in the form of cofactors, deficiency of which leads to accumulation of toxic glucose metabolites leading to formation of free radicals and oxidative stress. Glucose is not only important for the formation of energy but its improper metabolism proves to have deleterious effects in the body. In this review, an attempt is made to correlate microvascular complications of diabetes with thiamine deficiency and can be discerned that oxidative stress is one of the important factors for the progress of microvascular complications, as well as diabetic ketoacidosis, atherosclerosis and cardiovascular damage in patients with diabetes mellitus and these can be prevented or maintained by optimizing thiamine levels in the body.

A - 103 Exploring the Diagnostic Criteria for Alcohol-Related Dementia: a Case Study

Abstract Objective Excessive and chronic alcohol use can cause structural/functional abnormalities in the brain, including cognitive impairment (CI) (Harper, 2009). Despite these established risks, alcohol-related dementia (ARD) has received little recognition, mainly due to lack of a distinct pathophysiological profile. Through a case differential approach (concussion vs. ARD), the authors aim to clarify diagnostic criteria for ARD. Methods A 56-year-old right-handed male presented to the emergency room after fall with head strike (no loss of consciousness) with alcohol withdrawal delirium. Symptoms of cerebellar ataxia and CI of 6-month duration were noted. Past medical history was significant for alcohol use (four standard units per day), hyperlipidemia, tobacco use, and depression/anxiety. Neuroimaging revealed cerebral atrophy and chronic small vessel ischemic disease. A neuropsychological evaluation (NPE) was conducted 18 days post-fall. Results NPE revealed relative weaknesses in working memory, complex attention, and visual abstraction. Impairments were noted in visuospatial organization/planning, processing speed, basic attention, verbal fluency, and verbal memory. Motor examination was evident for intention tremor. Conclusion Brain changes associated with ARD include volume loss, altered glucose metabolism, reduced neuronal density, changes in frontal lobe function, and white matter loss. In contrast, individuals affected by concussions may encounter challenges with attention/concentration, processing speed, and working memory. Distinguishing a clear diagnostic profile for ARD is difficult due to high rates of concomitant concussion in this population. The patient’s deficits exceed those expected due to concussion alone, with an anticipated cognitive recovery timeframe of 7–14 days (Iverson, 2006). Furthermore, neuroimaging and NPE results support the diagnostic hypothesis of ARD.

Association between alcohol consumption and incidence of dementia in current drinkers: linear and non-linear mendelian randomization analysis

Previous conventional epidemiological studies found a J-shape relationship between alcohol consumption and dementia, but this result was subject to confounding biases and reverse causation. Therefore, we aimed to investigate the potential linear or non-linear causal association between alcohol consumption and the incident risk of dementia in current drinkers. This study used data from the UK Biobank to investigate the relationship between alcohol consumption and dementia risk. 313,958 White British current drinkers, who were free of dementia during 2006-2010, were followed up until 2021. Alcohol consumption was self-reported and calculated according to the National Health Service guideline. The primary outcome was all-cause dementia identified through hospital and mortality records. We used multivariable Cox models with restricted cubic splines for conventional analysis and both non-linear and linear Mendelian Randomization (MR) analyses to assess causal relationships, employing a genetic score based on 95 SNPs identified from a meta-genome-wide association study of 941,280 people from Europe. 313,958 current drinkers consumed an average of 13.6 [IQR: 7.1-25.2] units/week alcohol (men averaged 20.2 [11.1-33.9] units/week and women 9.5 [5.3-16.7] units/week). During a mean follow-up of 13.2 years, 5394 (1.7%) developed dementia. Multivariable Cox model with restricted cubic spline functions identified a J-shaped relationship between alcohol consumption and dementia risk, with the lowest risk at 12.2 units/week. The non-linear MR failed to identify a significant non-linear causal relationship (p=0.45). Both individual-level (HR: 2.22 95%CI [1.06-4.66]) and summary-level (1.89 [1.53-2.32]) linear MR analyses indicated that higher genetically predicted alcohol consumption increased dementia risk. This study identified a positive linear causal relationship between alcohol consumption and dementia among current drinkers. The J-shaped association found in conventional epidemiological analysis was not supported by non-linear MR analyses. Our findings suggested that there was no safe level of alcohol consumption for dementia. The Shenzhen Science and Technology Program and the Strategic Priority Research Program of Chinese Academy of Sciences.

Compensation patterns and altered functional connectivity in alcohol use disorder with and without Korsakoff's syndrome.

Alcohol use disorder is a chronic disease characterized by an inappropriate pattern of drinking, resulting in negative consequences for the individual's physical, mental and social health. Korsakoff's syndrome is a complication of alcohol use disorder and is characterized by severe memory and executive deficits. The fronto-cerebellar and Papez circuits are structurally affected in patients with alcohol use disorder with and without Korsakoff's syndrome. The first objective of the present study was to measure the effect of chronic and excessive alcohol consumption on resting-state functional connectivity of these two functional brain networks. The second objective was to identify, for the first time, resting-state functional connectivity abnormalities specific to amnesic patients with Korsakoff's syndrome. In the present study, a neuropsychological assessment and a resting-state functional magnetic resonance imaging examination were conducted in 31 healthy controls (43.6 ± 6.1 years) and 46 patients (46.6 ± 9.1 years) with alcohol use disorder including 14 patients with Korsakoff's syndrome (55.5 ± 5.3 years) to examine the effect of chronic and heavy alcohol consumption on functional connectivity of the fronto-cerebellar and the Papez circuits at rest and the specificity of functional connectivity changes in Korsakoff's syndrome compared to alcohol use disorder without Korsakoff's syndrome. The resting-state functional connectivity analyses focused on the nodes of the fronto-cerebellar and Papez circuits and combined region of interest and graph theory approaches, and whether these alterations are associated with the neuropsychological profile. In patients pooled together compared to controls, lower global efficiency was observed in the fronto-cerebellar circuit. In addition, certain regions of the fronto-cerebellar and Papez circuits were functionally hyperconnected at rest, which positively correlated with executive functions. Patients with Korsakoff's syndrome showed lower resting-state functional connectivity, lower local and global efficiency within the Papez circuit compared to those without Korsakoff's syndrome. Resting-state functional connectivity positively correlated with several cognitive scores in patients with Korsakoff's syndrome. The fronto-cerebellar and Papez circuits, two normally well-segregated networks, are functionally altered by alcohol use disorder. The Papez circuit attempts to compensate for deficits in the fronto-cerebellar circuit, albeit insufficiently as evidenced by patients' overall lower cognitive performance. Korsakoff's syndrome is characterized by altered functional connectivity in the Papez circuit known to be centrally involved in memory.

Young Onset Dementia in New South Wales, Australia in 1891: What has Changed Since Then?

This study aimed to determine the prevalence and types of young onset dementia (YOD) in New South Wales (NSW), Australia, in 1891 with comparisons to 21st century estimates. Changes might inform future service planning for persons with YOD. Medical case books of two Hospitals for the Insane were examined at the State Archives and clinical and sociodemographic information extracted of persons who were under the age of 65 in April 1891, when a NSW Census occurred, and were given a dementia diagnosis or had symptoms consistent with dementia. Consensus 21st century 'probable' and 'possible' all cause dementia and major neurocognitive disorder diagnoses were determined by two psychiatrists. Prevalence estimates of moderate-severe dementia were determined and compared with 21st century estimates and dementia types. Of 161 potential dementia cases, 123 were given a consensus 'probable' dementia diagnosis, 28 a 'possible' dementia diagnosis, and ten were given a non-dementia diagnosis, with 'all cause dementia' and 'major neurocognitive disorder' diagnoses identical. Most dementia cases were male (n=119, 78.8%). 'Unspecified dementia' was the most frequent diagnosis (n=47, 31.1%), followed by dementia secondary to syphilis (n=35, 23.2%), epileptic dementia (n=30, 19.9%), alcohol-related dementia (n=17, 11.3%), and mixed dementia (n=16, 10.6%). Epileptic dementia had the youngest average age of admission (34.9years). Other than epileptic dementia, all other dementia types were more frequent in males. Prominent clinical symptoms included neurological signs (n=79, 52.3%), psychosis (n=77, 51.0%), agitation (n=75, 49.7%), and aggression (n=45, 29.8%). Most dementia cases either died in hospital (n=79, 52.3%) or were transferred to a long stay hospital (n=57, 37.7%). The estimated point prevalence of YOD in persons aged 30-59 in 1891 (86 per 100,000) was higher than current Australian and global estimates in this age group due to the high rates in males (126per 100,000), but in those aged 60-64, the prevalence in 1891 (159per 100,000) was much lower than current estimates. This first examination of YOD in the nineteenth century found high rates of dementia in those under the age of 60 compared with current estimates, particularly in men aged between 30 and 59years old, and largely due to syphilis, alcohol and epilepsy, conditions that are now treatable and thus demonstrating the potential of effective treatments for YOD.

The experiences of adult children caring for a parent with Korsakoff’s syndrome

Background: Korsakoff’s syndrome (KS) is a debilitating psychoneurological disorder that can occur in adults with alcohol use disorder (AUD). People with KS experience a sudden onset of symptoms including confabulation, anterograde and retrograde amnesias, apathy, issues with vision and gait, and lack of insight. Frequently an adult child of the parent with alcohol-induced KS becomes the caregiver, regardless of the status or quality of the relationship with their parent. While there is a rich literature base in the areas of adult children of parents with AUD and caregiving, there are no studies that have explored the experiences of adult children caring for a parent with alcohol-induced KS. This study aimed to explore the experiences of adult children who provide care for a parent or parental figure suffering from alcohol-induced Korsakoff syndrome (KS). Method: This study used a generic qualitative approach with thematic analysis using both in person and web-based video interview methods and field notes to address this gap in the literature. Eight individuals participated in the study, men (n=2) and women (n=6), with participants ranging in age from 31 to 43 years (average age 37 years). Results: Five themes emerged: addiction and the adult child, experiencing caregiver burden, experiencing a variety of emotions, professional healthcare experiences, and observations of symptoms. These themes emerged over seven anchor events in their caregiving experiences: interactions with their parent pre-diagnosis, parent’s medical emergency, hospitalization, diagnosis, housing, legal, and financial. Conclusion: The results provide a foundation for future research in the areas of KS, caregiving, and adult children of parents with AUD. They also provide a basis to inform the development of interventions with this population and demonstrate a need for more awareness of KS among healthcare professionals.

Low expression of thiamine pyrophosphokinase-1 contributes to brain susceptibility to thiamine deficiency.

Thiamine deficiency is a well-known risk factor for the development of severe encephalopathy, such as Wernicke encephalopathy and Korsakoff syndrome, but the underlying mechanism is still mysterious. This study aims to investigate the expression levels of thiamine metabolism genes in different tissues and their impact on brain susceptibility to thiamine deficiency. The mRNA and protein levels of four genes known to be associated with thiamine metabolism: thiamine pyrophosphokinase-1 (Tpk), Solute carrier family 19 member 2 (Slc19a2), Slc19a3, and Slc25a19, in the brain, kidney, and liver of mice were examined. Thiamine diphosphate (TDP) levels were measured in these tissues. Mice were subjected to dietary thiamine deprivation plus pyrithiamine (PTD), a specific TPK inhibitor, or pyrithiamine alone to observe the reduction in TDP and associated pathological changes. TPK mRNA and protein expression levels were lowest in the brain compared to the kidney and liver. Correspondingly, TDP levels were also lowest in the brain. Mice treated with PTD or pyrithiamine alone showed an initial reduction in brain TDP levels, followed by reductions in the liver and kidney. PTD treatment caused significant neuron loss, neuroinflammation, and blood-brain barrier disruption, whereas dietary thiamine deprivation alone did not. TPK expression level is the best indicator of thiamine metabolism status. Low TPK expression in the brain appears likely to contribute to brain susceptibility to thiamine deficiency, underscoring a critical role of TPK in maintaining cerebral thiamine metabolism and preventing thiamine deficiency-related brain lesions.

Нейропсихиатрия: психозы, которые не всегда следует лечить антипсихотиками

Disorders manifested by both neurological and mental disorders belong to the neuropsychiatric diseases. This category includes Alzheimer's disease, Parkinson's disease, Wernicke–Korsakoff syndrome, delirium tremens, catatonia and anti-NMDA receptor encephalitis. The etiology of psychotic disorders in neuropsychiatric diseases probably differs from that in schizophrenia and other psychoses, which causes both inefficiency and adverse events when using antipsychotics in neuropsychiatry. In the absence of a therapeutic alternative, antipsychotics can be prescribed with caution for neurodegenerative disorders, whereas catatonia is a relative, and anti-NMDA receptor encephalitis is an absolute contraindication to their use.

Protective Effects and Mechanism of Heracleum moellendorffii Hance on Alcohol-Induced Cognitive Decline in Mice.

Chronic and continuous alcohol consumption increases the risk of cognitive decline and may lead to alcohol-related dementia. We investigated the potential of Heracleum moellendorffii Hance root extract (HME) for treating alcohol-related cognitive impairment. Behavioral tests evaluated the effects of HME on cognitive function and depression. Changes in hippocampus and liver tissues were evaluated by Western blotting and H&E staining. The group treated with HME 200 mg/kg showed a significant increase in spontaneous alternation in Y-maze and a decrease in immobility in a forced swimming test (FST) compared to the vehicle-treated group. These results suggest that HME can restore memory deficits and reverse depressive symptoms caused by chronic alcohol consumption. The HME-treated group also upregulated brain-derived neurotrophic factor (BDNF), phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2), and phosphorylated cAMP response element-binding protein (CREB) in the hippocampus. Additionally, it reduced lipid vacuolation in the liver and increased the expression of aldehyde dehydrogenase 1 (ADH1). The administration of HME improves cognitive impairment and reverses depressive symptoms due to alcohol consumption, restoring neural plasticity in the hippocampus and alcohol metabolism in the liver. These findings suggest that HME is a promising treatment for alcohol-related brain disorders. Molecular mechanisms underlying the therapeutic effects of HME and its active ingredients should be investigated further.

Memantine alleviates cognitive impairment and hippocampal morphology injury in a mouse model of chronic alcohol exposure

Alcohol-related cognitive impairment (ARCI) is highly prevalent among patients with alcohol abuse and dependence. The pathophysiology of ARCI, pivotal for refined therapeutic approaches, is not fully elucidated, posing a risk of progression to severe neurological sequelae such as Korsakoff's syndrome (KS) and Alcohol-Related Dementia (ARD). This study ventures into the underlying mechanisms of chronic alcohol-induced neurotoxicity, notably glutamate excitotoxicity and cytoskeletal disruption, and explores the therapeutic potential of Memantine, a non-competitive antagonist of the N-methyl-d-aspartate (NMDA) receptor known for its neuroprotective effect against excitotoxicity. Our investigation centers on the efficacy of Memantine in mitigating chronic alcohol-induced cognitive and hippocampal damages in vivo. Male C57BL/6J mice were subjected to 30 % (v/v, 6.0 g/kg) ethanol via intragastric administration alongside Memantine co-treatment (10 mg/kg/day, intraperitoneally) for six weeks. The assessment involved Y maze, Morris water maze, and novel object recognition tests to evaluate spatial and recognition memory deficits. Histopathological evaluations of the hippocampus were conducted to examine the extent of alcohol-induced morphological changes and the potential protective effect of Memantine. The findings reveal that Memantine significantly improves chronic alcohol-compromised cognitive functions and mitigates hippocampal pathological changes, implicating a moderating effect on the disassembly of actin cytoskeleton and microtubules in the hippocampus, induced by chronic alcohol exposure. Our results underscore Memantine's capability to attenuate chronic alcohol-induced cognitive and hippocampal morphological harm may partly through regulating cytoskeleton dynamics, offering valuable insights into innovative therapeutic strategies for ARCI.

Amnesic Pathologies in Regulation of Dopamine as Supplement to Wernicke-Korsakoff Syndrome: A Limbic-Reticular Coupling View

Background: It was suggested by the limbic-reticular coupling theory that the hippocampus and amygdala regulate such descending limbic structures as the mammillary bodies, septum, hypothalamus and habenula, and in turn regulate the ascending noradrenergic, serotonergic, dopaminergic and cholinergic systems to consolidate and recall declarative memory, while the anterior and mediodorsal thalamic nuclei of Wernicke-Korsakoff syndrome beyond limbic-reticular coupling be related else to familiarity. Aim: It was aimed to highlight a portion of limbic-reticular coupling structures in alcoholic Korsakoff’s syndrome, including the dopaminergic system, habenula, mammillary bodies, etc. Methods: It was searched the papers from Pubmed and Baidu. Results and Discussions: It is highlighted that, (a) the mesolimbic dopamine, liable to be affected by alcohol, induces the hippocampal theta rhythm via septum, helping encode and consolidate new memories, such as dopaminergic enhancement of motivational declarative memory in young human adults; (b) dopamine can activate cortical gamma wave and help recall; (c) joint damage of habenula and mammillary bodies, both sending efferents to ventral tegmental area(VTA) rich in dopaminergic neurons, is sufficient to cause Korsakoff’s amnesia; (d) the loop of hippocampal CA3 to lateral septum(LS) to VTA(CA3-LS-VTA) activates dopamine for contextual memory in animals, consistent with dopaminergic antagonist impairing declarative memory recall in humans; (e) whereas thiamine deficiency, the major nutritional deficit causing Wernicke-Korsakoff syndrome, impairs noradrenergic but spares dopaminergic system. Conclusion: It is supplemented the integrative dysfunctions in regulation of such neglected dopaminergic system, including the habenula, mammillary bodies and VTA dopamine, as partial contribution to memory impairments in Korsakoff’s syndrome.

Erratum to Wernicke-Korsakoff Syndrome From Hyperemesis Gravidarum. Volume 6, Issue 1, January 2024

Erratum to Wernicke-Korsakoff Syndrome From Hyperemesis Gravidarum. Volume 6, Issue 1, January 2024

Gait ataxia in alcohol use disorder: A systematic review.

A severe and long-term alcohol use can have adverse effects on lower limb function. Over time, some individuals may develop gait ataxia, which refers to the impairment of controlled lower body movements that are important for walking and maintaining proper gait. Gait ataxia is well-documented in patients who have been diagnosed with alcohol-related Wernicke-Korsakoff syndrome (WKS); however, less is known on how common ataxia is among patients with alcohol use disorder (AUD) without WKS. To date, no study has systematically reviewed the evidence focusing on patients suffering only from AUD. Our aim was to perform a qualitative synthesis of the existing literature examining behavioral signs of gait ataxia among abstinent patients with AUD. Two facets were created encompassing keywords for "alcohol use disorder" and "measures of gait ataxia." Databases, including EMBASE, APA PsycInfo, Medline, and Cochrane Library, were searched for studies, and a quality assessment was performed. Ten studies were identified (37 ≥ ns ≤ 247), which were all rated as being of moderate (N = 7) to good quality (N = 3). The age range was 31.4-53.4 years (weighted mean age: 53.6 years), and 78.3% of the participants were male. Eight studies found that patients with AUD and without WKS exhibited behavioral signs of gait ataxia. Although there is evidence of gait ataxia among patients with AUD, heterogeneous results and methodological shortcomings such as lack of screening for neurocognitive deficits deem these findings preliminary and highlight the need for more research in the future. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Deficiency of thiamine and Wernicke-Korsakoff syndrome – review of pathophysiology, clinical presentation , diagnostics and treatment

Introduction and aim of the study: Thiamine is a water-soluble vitamine, which bioactive form is necessary for energy metabolism in all cells. Deficiency of thiamine may be caused by malnutrition, alcoholism and certain diseases and it leads to an acute neuropsychiatric disorder called Wernicke encephalopathy. Untreated patients can develop a residual syndrome called Korsakoff syndrome. The aim of our study is to present current knowledge of history, pathophysiology, causes, symptoms and treatment of vitamine B1 depletion and Wernicke-Korsakoff’s syndrome. Material and methods: Our review is based on the analysis of materials collected in „Pubmed”, „Google Scholar” and other scientific articles using keywords: „thiamine”, „thiamine deficiency”, „Wernicke encephalopathy”, „Korsakoff syndrome”. Conclusions: Despite numerous studies, Wernicke encephalopathy is still difficult to diagnose. Attention should be paid to the possibility of vitamin B1 deficiency in people who are at risk of it like alcoholics, malnourished or psychiatric patients. Wernicke encephalopathy is an acute neuropsychiatric disorder so the treatment should be started as soon as possible to reduce the risk of developing Korsakoff syndrome.

Abstract PO1-20-10: Wernicke Encephalopathy Syndrome in Metastatic Breast Cancer – A Diagnostic Dilemma or An Underdiagnosed Entity

Abstract Wernicke encephalopathy (WE) is an acute medical syndrome that manifests as a clinical triad of encephalopathy, gait ataxia, and oculomotor dysfunction, requiring urgent treatment. Early recognition and treatment can prevent severe neurological morbidity and the chronic neurological consequence of WE, known as Korsakoff syndrome. Thiamine (vitamin B1) deficiency is the root cause of WE, which can occur due to several underlying conditions, including chronic alcoholism, hyperemesis of pregnancy, malnutrition, prolonged fasting, and malignancy. In cases of malignancy, WE is often undiagnosed or misdiagnosed because the presenting symptoms can be confused with several other complications of malignancy. We present the case of a 47-year-old woman with no significant medical history who was diagnosed with triple negative metastatic breast cancer and admitted to the hospital with confusion, memory loss, and progressive lower extremity weakness. During her breast cancer treatments, she experienced significant nausea and vomiting, leading to a prolonged state of nutritional imbalance. Patient underwent extensive infectious and neurological workup for encephalopathy including lumbar puncture which was negative for leptomeningeal disease or infection. MRI brain did not show any new metastatic lesions however revealed enhancement of mammillary bodies bilaterally. Mammillary body enhancement can be seen in WE but not always present on imaging. She was treated for WE with high dose of thiamine infusion for five days, resulting in an improvement of her neurological symptoms. Diagnosing WE in cancer patients is challenging, as there are various factors to consider, such as cerebral metastasis, infection, chemotherapy treatment, and electrolyte imbalances, that can cause neurological symptoms. Cancer patients are at high risk for development of WE due to chemotherapy or whole brain radiation induced nausea and vomiting that can lead to chronic malnutrition. The typical triad of symptoms is not present in many cases and presenting symptoms can be nonspecific which makes the diagnosis challenging. As a result, WE is often underdiagnosed in such patients, making it essential to educate the physician community about this acute neurological manifestation that can be easily treated. A high index of suspicion is necessary for early recognition, and prompt treatment can prevent Korsakoff syndrome, thereby enhancing the overall quality of life of patients with malignancy. Citation Format: Archit Patel, Arya Mariam Roy, Ronald Alberico, Shipra Gandhi. Wernicke Encephalopathy Syndrome in Metastatic Breast Cancer – A Diagnostic Dilemma or An Underdiagnosed Entity [abstract]. In: Proceedings of the 2023 San Antonio Breast Cancer Symposium; 2023 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2024;84(9 Suppl):Abstract nr PO1-20-10.

A Brief Review on Korsakoff Syndrome

Korsakoff Syndrome (KS) is a residual syndrome which is characterized with neuropsychological conditions affecting the daily life of chronic drinkers of alcohol. Sergei Korsakoff is a Russian neuropsychiatrist, in the year 1887 given a note on the Korsakoff syndrome which is characterized by an extraordinary peculiar amnesia which has been associated with peripheral inflammation of the nerves. This syndrome can be chronic in onset and remains permanent. The person suffering with KS can be observed with cognitive and behavioral dysfunction. The symptoms of amnesia, executive dysfunction, confabulation, apathy and social-cognitive impairments can be observed in these affected patients. In the aspect of the pharmacological treatment of KS sufficient concentration of thiamine should be administered parenterally. In alcoholic patients, the doses of thiamine can be administered approximately 500mg or above but the evidence in this aspect is less available. Compared to the pharmacological therapy, the rehabilitation programme can be more helpful to the patients with KS. Among six studies, evidence was produced that some of the techniques which can be helpful for the compensation of memory can include use of agendas, memory cards, gadgets like mobiles and smart watches can be helpful in the patients with KS. For the better improvement of the cognition, interventions associated with errorless learning can be possible theoretically. In this learning process the patients are not permitted to make any errors. This may also support the semantic learning process.

Neurologic complications of thiamine (B1) deficiency following bariatric surgery in adolescents

BackgroundThe prevalence of obesity among children and adolescents is rising and poses a major health concern. Bariatric surgery is well established in adults and has become an option for adolescents. Thiamine (B1) deficiency is common following bariatric surgery in adults. It may present as Beri-Beri, Wernicke encephalopathy, or Korsakoff psychosis. ObjectiveOur aim was to describe the clinical features, diagnosis, and treatment of adolescents who presented with B1 deficiency after bariatric surgery at one center, and to summarize the data from the literature. PatientsThree adolescents with morbid obesity (two boys and one girl, aged 15.5 to- 17-years-old), presented at Schneider Children's Medical Center of Israel with progressive lower limb pain and weakness 2–3 month following a bariatric procedure (sleeve gastrectomy or narrowing of a bariatric band). The girl also had upper limb involvement and cerebellar signs. All three were non-compliant with micronutrient supplementation. After admission, they received intravenous B1 and oral multivitamin supplementation, and their symptoms improved considerably. ConclusionsMicronutrient supplementation following bariatric surgery is crucial to prevent deficiencies. In adolescents, compliance with micronutrient supplementation should be assessed before and after such surgery. Thiamine deficiency may cause polyneuropathy, among other symptoms. Treatment reduces the severity of neurological complications.

Transient global amnesia

Transient global amnesia

Criminal behavior in alcohol-related dementia and Wernicke-Korsakoff syndrome: a Nationwide Register Study.

Chronic heavy alcohol use may lead to permanent brain damage, cognitive impairment, and dementia. While the link between alcohol use and crime is strong, virtually no research exists on the criminal behavior of patients with the alcohol-related neurocognitive disorders of Wernicke-Korsakoff syndrome (WKS) and alcohol-related dementia (ARD). The study population included all persons diagnosed with WKS (n = 1149) or ARD (n = 2432) in Finland in 1998-2015. Data on diagnoses, mortality, and crime were obtained from Finnish nationwide registers. Crime incidences were calculated 4 years before and after diagnosis. Crime types, incidences, and mortality were compared between disorders and with the general population. Altogether 35.6% of WKS patients and 23.6% of ARD patients had committed crimes in the 4 years preceding diagnosis, most commonly property and traffic crimes, followed by violent crimes. The incidence of criminal behavior decreased significantly after diagnosis; in WKS patients, the standardized criminality ratio (SCR), the ratio of observed to expected number of crimes (95% CI), was 3.91 (3.72-4.10) in 4 years before and 2.80 (2.61-3.00) in 4 years after diagnosis. Likewise, in ARD patients, the SCRs were 2.63 (2.51-2.75) before and 0.84 (0.75-0.92) after diagnosis. No significant difference emerged in mortality between persons with and without a criminal history. Persons with alcohol-related neurocognitive disorders frequently engage in criminal behavior prior to diagnosis, especially multiple offending. In the 4 years before and after diagnosis, crime rates declined in a linear fashion, with a marked reduction after diagnosis.