Экомузей «Салгирка» – проект или реальность?!

В статье обосновывается создание в г. Симферополе "Экомузея Салгирка",посвященного человеку, его природному и культурному окружению. В проекте предлагается создание музея на базе Таврического национального университета им В.И. Вернадского и принадлежащей ему территории парка Салгирка, приводится вариант классификации ресурсов экомузея, намечаются первые шаги в его организаци, описавается структура технологической карты по территории парка, разработанная автором.У статті улаштовується створення в м.Сімферополі "Экомузея Салгирка", присвяченого людині, його природному і культурному оточенню. У проекті пропонується створення музею на базі Таврического національного університету ім В.І Вернадського і приналежної йому території парку Салгирка, приводиться варіант класифікації ресурсів экомузея, намічаються перші кроки в його организаци, описуеться структура технологічної карти по території парку, розроблена автором

Wernicke's Encephalopathy in Acute and Chronic Kidney Disease:A Systematic Review

Thiamine (vitamin B1) deficiency is relatively common in patients with kidney disease. Wernicke's encephalopathy (WE) is caused by vitamin B1 deficiency. Our aim was to systematically review the signs and symptoms of WE in patients with kidney disease. We conducted a systematic literature review on WE in kidney disease and recorded clinical and radiographic characteristics, treatment and outcome. In total 323 manuscripts were reviewed, which yielded 46 cases diagnosed with acute and chronic kidney disease and WE published in 37 reports. Prodromal characteristics of WE were loss of appetite, vomiting, weight loss, abdominal pain, and diarrhea. Parenteral thiamine 500 mg 3 times per day often led to full recovery, while Korsakoff's syndrome was found in those receiving low doses. To prevent WE in kidney failure, we suggest administering high doses of parenteral thiamine in patients with kidney disease who present with severe malnutrition and (prodromal) signs of thiamine deficiency.</p

A Clinician&rsquo;s View of Wernicke-Korsakoff Syndrome

The purpose of this article is to improve recognition and treatment of Wernicke-Korsakoff syndrome. It is well known that Korsakoff syndrome is a chronic amnesia resulting from unrecognized or undertreated Wernicke encephalopathy and is caused by thiamine (vitamin B1) deficiency. The clinical presentation of thiamine deficiency includes loss of appetite, dizziness, tachycardia, and urinary bladder retention. These symptoms can be attributed to anticholinergic autonomic dysfunction, as well as confusion or delirium, which is part of the classic triad of Wernicke encephalopathy. Severe concomitant infections including sepsis of unknown origin are common during the Wernicke phase. These infections can be prodromal signs of severe thiamine deficiency, as has been shown in select case descriptions which present infections and lactic acidosis. The clinical symptoms of Wernicke delirium commonly arise within a few days before or during hospitalization and may occur as part of a refeeding syndrome. Wernicke encephalopathy is mostly related to alcohol addiction, but can also occur in other conditions, such as bariatric surgery, hyperemesis gravidarum, and anorexia nervosa. Alcohol related Wernicke encephalopathy may be identified by the presence of a delirium in malnourished alcoholic patients who have trouble walking. The onset of non-alcohol-related Wernicke encephalopathy is often characterized by vomiting, weight loss, and symptoms such as visual complaints due to optic neuropathy in thiamine deficiency. Regarding thiamine therapy, patients with hypomagnesemia may fail to respond to thiamine. This may especially be the case in the context of alcohol withdrawal or in adverse side effects of proton pump inhibitors combined with diuretics. Clinician awareness of the clinical significance of Wernicke delirium, urinary bladder retention, comorbid infections, refeeding syndrome, and hypomagnesemia may contribute to the recognition and treatment of the Wernicke-Korsakoff syndrome

BNF Recommendations for the treatment of Wernicke's encephalopathy : Lost in translation?

We agree with Thomson and Marshall (2013) that the current prescribing of thiamine replacement therapy for Wernicke's Encephalopathy (WE) is ambiguous. In response to their article, we also advocate that any consensus on accurate thiamine treatment for WE should receive sufficient international attention, since too many patients with WE are currently inaccurately treated leading to unnecessary cases of Korsakoff's syndrome. WE is a neurologic disease caused by thiamine (vitamin B1) deficiency. Most patients with WE have a background of chronic alcoholism and self-neglect (Sechi and Serra, 2007). Importantly, WE is also a life-threatening condition associated with a classic triad of acute neurological symptoms resembling delirium: confusion, ataxia and eye-movement disorders (McCormick et al., 2011; Wijnia and Oudman, 2013). Usually, but not necessarily, patients will develop Korsakoff's syndrome characterized by chronic amnesia (Kopelman, 2002). Slingedael offers a long-stay facility for patients with Korsakoff's syndrome in Rotterdam, The Netherlands. For triage purposes, confused alcoholic patients with probable Wernicke–Korsakoff's syndrome related cognitive disorders are visited by our physicians and psychologists, usually when they are inpatients of general or psychiatric hospitals in the Rotterdam region (∼1.2 million inhabitants). In daily practice, we see very disappointing results with respect to the quantity of patients that have been appropriately treated with parenteral thiamine after admission to general or psychiatric hospitals. In fact, up to 90% of the confused alcoholics that have been visited by members of our team did not receive parenteral thiamine or received parenteral thiamine just once. This while current Dutch recommendations state that confused inpatients at risk of developing WE should receive 250 mg i.m. or i.v. for at least 3 to 5 days; up to 500 mg i.v. for patients that have presumed WE (Van den Brink and Jansen, 2009). Implementations of the guidelines have been documented (Laurent and van der Schrieck - de Loos, 2009). Therefore, we suggest that besides the clarity of the guidelines for treatment of WE also successful propagation for treatment guidelines is necessary to prevent the detrimental effects of unsuccessfully treated WE, namely Korsakoff's syndrome

Korsakoff's syndrome is preventable

Wernicke-Korsakoff syndrome (WKS) is a life-threatening neuropsychiatric disorder caused by thiamine (vitamin B1) deficiency. Wernicke-Korsakoff syndrome is associated with mammillary body edema and small vessel ischemia. Many patients who develop WKS have a history of serious alcoholism and self-neglect. It is a common condition as around 15% of the alcoholics show specific WKS neuropathology. Originally, the syndrome was described as a triad of ataxia, eye movement disorders, and mental status change, but recent studies have suggested that patients frequently only show the mental status change [1]. Although it has been known for over 60 years that treatment with high doses of parenteral (intravenous or intramuscular) thiamine replacement therapy has the potency to improve the neuropsychiatric syndrome in the early stage of WKS [2], this is still uncommon medical practice. Recently published studies on treatment perspectives of WKS in general and psychiatric hospitals are alarming: European as well as American studies demonstrated that most patients did not receive thiamine at all or only received it orally in low doses [3] and [4]. Both types of treatment lead to unnecessary cases of chronic WKS (also Korsakoff's syndrome) characterized by severe amnesia and lifelong impaired autonomy [4]. Based on the currently available literature, we suggest that any sign of mental confusion, cognitive defect, or change in mobility in an admitted alcoholic should alarm a clinician for treatable WKS. Parenteral thiamine replacement therapy is well tolerated and regularly ameliorates neuropathology in WKS. According to the European Federation of Neurological Societies and the Royal College of Physicians, parenteral thiamine should be given 200 mg up to 500 mg 3 times daily until symptoms of acute WKS resolute [5]. Importantly, in many cases, the benefit of treating WKS outweighs the risks of treating unnecessarily. The treatment is lifesaving and has the potential to reverse this acute neuropsychiatric syndrome. It is recommended to have a high suspicion of WKS in alcoholic patients and preventively treat them as such

Korsakoff's syndrome is preventable

Wernicke-Korsakoff syndrome (WKS) is a life-threatening neuropsychiatric disorder caused by thiamine (vitamin B1) deficiency. Wernicke-Korsakoff syndrome is associated with mammillary body edema and small vessel ischemia. Many patients who develop WKS have a history of serious alcoholism and self-neglect. It is a common condition as around 15% of the alcoholics show specific WKS neuropathology. Originally, the syndrome was described as a triad of ataxia, eye movement disorders, and mental status change, but recent studies have suggested that patients frequently only show the mental status change [1]. Although it has been known for over 60 years that treatment with high doses of parenteral (intravenous or intramuscular) thiamine replacement therapy has the potency to improve the neuropsychiatric syndrome in the early stage of WKS [2], this is still uncommon medical practice. Recently published studies on treatment perspectives of WKS in general and psychiatric hospitals are alarming: European as well as American studies demonstrated that most patients did not receive thiamine at all or only received it orally in low doses [3] and [4]. Both types of treatment lead to unnecessary cases of chronic WKS (also Korsakoff's syndrome) characterized by severe amnesia and lifelong impaired autonomy [4]. Based on the currently available literature, we suggest that any sign of mental confusion, cognitive defect, or change in mobility in an admitted alcoholic should alarm a clinician for treatable WKS. Parenteral thiamine replacement therapy is well tolerated and regularly ameliorates neuropathology in WKS. According to the European Federation of Neurological Societies and the Royal College of Physicians, parenteral thiamine should be given 200 mg up to 500 mg 3 times daily until symptoms of acute WKS resolute [5]. Importantly, in many cases, the benefit of treating WKS outweighs the risks of treating unnecessarily. The treatment is lifesaving and has the potential to reverse this acute neuropsychiatric syndrome. It is recommended to have a high suspicion of WKS in alcoholic patients and preventively treat them as such

Subtle object location perception deficits in Korsakoff’s syndrome

(Wernicke-)Korsakoff’s syndrome (KS) is a neuropsychiatric syndrome, caused by vitamin B1 (thiamine) deficiency often resulting from chronic alcohol consumption. KS is characterized by severe cognitive problems, such as impaired explicit memory and executive functions. Visuospatial perception (VSP) refers to the identification of objects (object perception), and the localization of objects (space perception). Object perception can be described as the cooperation between visual representation and semantic information on the objects’ functional properties. Space perception is the mental representation of visual space and objects within it from a more or less fixed view point. Although VSP is fundamental to everyday functioning and higher order cognitive functions, little knowledge is available on VSP in KS. The aim of the present study was therefore to investigate VSP in KS. Fifteen KS patients and 15 healthy controls performed the Visual Object and Space Perception battery (VOSP) for visuospatial functioning. Results show a selectively reduced performance of KS patients on object perception, but not on space perception tasks. Specifically, subclinical problems in the identification of degraded and atypical positioned objects were present in KS, and not related to general cognitive functioning. These results suggest that the thalamic nucleus, a brain circuit most typically damaged in KS, is critically involved in object integration. Moreover, this relative new perspective on VSP related to KS warrants further research on the neuropsychological evaluation of KS to index possible mild deficits in this domain, possibly negatively affecting everyday functioning in KS

Visuospatial declarative learning despite profound verbal declarative amnesia in Korsakoff's syndrome

Korsakoff's syndrome (KS) is a neuropsychiatric disorder characterised by severe amnesia. Although the presence of impairments in memory has long been acknowledged, there is a lack of knowledge about the precise characteristics of declarative memory capacities in order to implement memory rehabilitation. In this study, we investigated the extent to which patients diagnosed with KS have preserved declarative memory capacities in working memory, long-term memory encoding or long-term memory recall operations, and whether these capacities are most preserved for verbal or visuospatial content. The results of this study demonstrate that patients with KS have compromised declarative memory functioning on all memory indices. Performance was lowest for the encoding operation compared to the working memory and delayed recall operation. With respect to the content, visuospatial memory was relatively better preserved than verbal memory. All memory operations functioned suboptimally, although the most pronounced disturbance was found in verbal memory encoding. Based on the preserved declarative memory capacities in patients, visuospatial memory can form a more promising target for compensatory memory rehabilitation than verbal memory. It is therefore relevant to increase the number of spatial cues in memory rehabilitation for KS patients

Procedural Learning and Memory Rehabilitation in Korsakoff’s Syndrome - a Review of the Literature

Korsakoff’s syndrome (KS) is a chronic neuropsychiatric disorder caused by alcohol abuse and thiamine deficiency. Patients with KS show restricted autonomy due to their severe declarative amnesia and executive disorders. Recently, it has been suggested that procedural learning and memory are relatively preserved in KS and can effectively support autonomy in KS. In the present review we describe the available evidence on procedural learning and memory in KS and highlight advances in memory rehabilitation that have been demonstrated to support procedural memory. The specific purpose of this review was to increase insights in the available tools for successful memory rehabilitation and give suggestions how to apply these tools in clinical practice to increase procedural learning in KS. Current evidence suggests that when memory rehabilitation is adjusted to the specific needs of KS patients, this will increase their ability to learn procedures and their typically compromised autonomy gets enhanced