What are the key features of Wernicke encephalopathy. How is Wernicke encephalopathy diagnosed and treated. What is the prognosis for patients with Wernicke encephalopathy. How can Wernicke encephalopathy be prevented in at-risk individuals.

Understanding Wernicke Encephalopathy: An Acute Neurological Condition

Wernicke encephalopathy (WE) is a potentially life-threatening neurological disorder caused by thiamine (vitamin B1) deficiency. It is characterized by a classic triad of symptoms: ophthalmoparesis with nystagmus, ataxia, and confusion. However, it’s important to note that not all patients present with the full triad, making diagnosis challenging in some cases.

While commonly associated with chronic alcoholism, Wernicke encephalopathy can occur in any condition that leads to thiamine deficiency. Understanding its causes, symptoms, and treatment is crucial for healthcare providers to ensure prompt diagnosis and appropriate management.

The Classic Triad of Wernicke Encephalopathy

• Ophthalmoparesis with nystagmus: Abnormal eye movements and difficulty controlling eye muscles
• Ataxia: Lack of muscle coordination affecting gait and balance
• Confusion: Altered mental status and cognitive impairment

Causes and Risk Factors for Wernicke Encephalopathy

While chronic alcoholism is the most well-known cause of Wernicke encephalopathy, several other conditions can lead to thiamine deficiency and subsequent development of WE. Understanding these risk factors is essential for early identification and prevention.

Common Causes of Thiamine Deficiency

• Chronic alcohol abuse
• Severe malnutrition
• Hyperemesis gravidarum
• Prolonged parenteral nutrition
• Malignancies
• Immunodeficiency syndromes
• Liver disease
• Hyperthyroidism
• Severe anorexia nervosa

Why does chronic alcohol consumption lead to thiamine deficiency? There are several factors at play:

1. Impaired absorption of thiamine from the intestine
2. Possible genetic predisposition
3. Inadequate diet and poor nutrition
4. Reduced storage of thiamine in the liver
5. Other concurrent nutritional deficiencies

It’s worth noting that acute infections or prolonged carbohydrate/glucose loading in thiamine-deficient individuals can precipitate Wernicke encephalopathy. This underscores the importance of administering thiamine alongside glucose in at-risk patients.

The Pathophysiology of Wernicke Encephalopathy

To truly understand Wernicke encephalopathy, it’s crucial to delve into the role of thiamine in the body and how its deficiency leads to neurological complications.

The Vital Role of Thiamine

Thiamine, also known as vitamin B1, is an essential coenzyme involved in several critical metabolic pathways. Its primary functions include:

• Acting as a cofactor for enzymes in the Krebs cycle
• Supporting the pentose phosphate pathway
• Facilitating alpha-keto-glutamic acid oxidation
• Enabling pyruvate decarboxylation

How does thiamine deficiency affect cellular metabolism? When thiamine levels are insufficient, several metabolic imbalances occur:

• Decreased levels of alpha-keto-glutarate, acetate, citrate, and acetylcholine
• Accumulation of lactate and pyruvate
• Disruption of the connection between glycolytic and citric acid cycles

These metabolic disturbances ultimately lead to neuronal cell death, particularly in the mammillary bodies and thalamus. Neuroimaging studies have revealed characteristic lesions in patients with Wernicke encephalopathy, typically symmetrical and affecting the midbrain, hypothalamus, and other specific brain regions.

Diagnosing Wernicke Encephalopathy: Challenges and Approaches

Diagnosing Wernicke encephalopathy can be challenging, as not all patients present with the classic triad of symptoms. Additionally, the prevalence of WE is likely underestimated due to missed diagnoses.

Diagnostic Challenges

Why is Wernicke encephalopathy often overlooked or misdiagnosed? Several factors contribute to this issue:

• Variable presentation of symptoms
• Lack of awareness among healthcare providers
• Absence of a definitive diagnostic test
• Overlap with other neurological conditions

Diagnostic Approaches

To improve diagnostic accuracy, healthcare providers should consider the following approaches:

1. Thorough clinical history, focusing on risk factors for thiamine deficiency
2. Careful neurological examination
3. Neuroimaging studies (CT and MRI) to identify characteristic lesions
4. Measurement of thiamine levels or erythrocyte transketolase activity (though not always reliable)
5. Low threshold for empiric thiamine treatment in suspected cases

Treatment Strategies for Wernicke Encephalopathy

Prompt recognition and treatment of Wernicke encephalopathy are crucial to prevent permanent neurological damage and potentially fatal outcomes. The cornerstone of treatment is thiamine replacement therapy.

Thiamine Replacement Protocol

What is the recommended thiamine replacement regimen for Wernicke encephalopathy? While specific protocols may vary, a general approach includes:

• Initial high-dose parenteral thiamine administration (typically 500 mg IV three times daily)
• Continuation of high-dose therapy for 3-5 days or until clinical improvement is observed
• Transition to oral thiamine supplementation for long-term maintenance

It’s important to note that glucose administration should be avoided before thiamine replacement, as it may precipitate or worsen Wernicke encephalopathy in thiamine-deficient individuals.

Supportive Care and Addressing Underlying Causes

In addition to thiamine replacement, management of Wernicke encephalopathy should include:

• Correction of other electrolyte imbalances and nutritional deficiencies
• Treatment of any underlying conditions (e.g., alcohol withdrawal)
• Supportive care for neurological symptoms (e.g., gait training, occupational therapy)
• Long-term strategies to prevent recurrence (e.g., alcohol cessation support)

Prognosis and Long-Term Outcomes of Wernicke Encephalopathy

The prognosis for patients with Wernicke encephalopathy varies depending on several factors, including the timeliness of diagnosis and treatment initiation.

Factors Influencing Prognosis

What determines the long-term outcomes for patients with Wernicke encephalopathy? Key factors include:

• Promptness of thiamine replacement therapy
• Extent of neurological damage prior to treatment
• Presence of concurrent medical conditions
• Ability to address underlying causes (e.g., alcohol cessation)
• Adherence to long-term thiamine supplementation

Potential Complications and Sequelae

Even with appropriate treatment, some patients may experience long-term consequences of Wernicke encephalopathy, such as:

• Persistent cognitive impairment
• Residual gait abnormalities
• Development of Korsakoff syndrome (a chronic neuropsychiatric condition characterized by severe memory deficits)
• Increased risk of future thiamine deficiency and WE recurrence

It’s crucial for healthcare providers to monitor patients closely and provide ongoing support to optimize long-term outcomes.

Prevention Strategies for Wernicke Encephalopathy

Given the potentially severe consequences of Wernicke encephalopathy, prevention is key, especially in high-risk populations.

Identifying At-Risk Individuals

Who should be considered at high risk for developing Wernicke encephalopathy? Key groups include:

• Individuals with chronic alcohol use disorder
• Patients with malnutrition or eating disorders
• Those undergoing bariatric surgery
• Pregnant women with hyperemesis gravidarum
• Patients receiving long-term parenteral nutrition

Preventive Measures

How can healthcare providers help prevent Wernicke encephalopathy in at-risk individuals? Strategies include:

1. Routine thiamine supplementation for high-risk patients
2. Education about the importance of a balanced diet rich in thiamine
3. Regular monitoring of nutritional status in at-risk populations
4. Prophylactic thiamine administration before glucose loading in susceptible individuals
5. Early intervention for conditions that may lead to thiamine deficiency

By implementing these preventive measures, healthcare providers can significantly reduce the incidence of Wernicke encephalopathy and its associated complications.

The Role of Interprofessional Care in Managing Wernicke Encephalopathy

Effective management of Wernicke encephalopathy requires a collaborative approach involving various healthcare disciplines. This interprofessional care model ensures comprehensive treatment and optimal patient outcomes.

Key Members of the Interprofessional Team

Who should be involved in the care of patients with Wernicke encephalopathy? An ideal team may include:

• Neurologists
• Internal medicine physicians
• Nutritionists or dietitians
• Psychiatrists (especially for patients with alcohol use disorder)
• Occupational therapists
• Physical therapists
• Nurses specialized in neurological care
• Social workers

Benefits of Interprofessional Collaboration

How does an interprofessional approach improve outcomes for patients with Wernicke encephalopathy? Key advantages include:

1. More accurate and timely diagnosis through combined expertise
2. Comprehensive treatment addressing both neurological and underlying issues
3. Improved patient education and support for long-term management
4. Better coordination of care across different healthcare settings
5. Enhanced ability to address complex psychosocial factors (e.g., in cases of alcohol use disorder)

By fostering effective communication and collaboration among team members, healthcare providers can ensure that patients with Wernicke encephalopathy receive the most comprehensive and appropriate care possible.

In conclusion, Wernicke encephalopathy remains a significant neurological condition with potentially severe consequences. Through improved understanding of its pathophysiology, risk factors, and management strategies, healthcare providers can better diagnose, treat, and prevent this disorder. By employing an interprofessional approach and focusing on both acute treatment and long-term prevention, we can significantly improve outcomes for patients at risk of or affected by Wernicke encephalopathy.

Wernicke Encephalopathy – StatPearls – NCBI Bookshelf

Continuing Education Activity

Wernicke encephalopathy is an acute neurological condition characterized by a clinical triad of ophthalmoplegia, ataxia, and confusion. This disease is caused by thiamine deficiency, which primarily affects the peripheral and central nervous systems. This should be differentiated from Korsakoff syndrome, a neuropsychiatric disorder associated with confabulation and significant deficits in anterograde and retrograde memory. This activity reviews the pathophysiology and evaluation of Wernicke encephalopathy and highlights the role of the interprofessional team in the management of patients with this illness.

Objectives:

• Describe the pathophysiology of Wernicke encephalopathy.

• Identify the causes of Wernicke encephalopathy.

• Explain the treatment for Wernicke encephalopathy.

• Explain the importance of improving care coordination among interprofessional team members to enhance outcomes for patients affected by Wernicke encephalopathy.

Access free multiple choice questions on this topic.

Introduction

Wernicke encephalopathy (WE) is an acute neurological condition characterized by a clinical triad of ophthalmoparesis with nystagmus, ataxia, and confusion. This is a life-threatening illness caused by thiamine deficiency, which primarily affects the peripheral and central nervous systems. This disorder should be differentiated from Korsakoff syndrome which is preventable and is usually suspected as a consequence of at least one episode of Wernicke’s encephalopathy. Korsakoff syndrome is a neuropsychiatric disorder associated with memory disturbances in which there are significant deficits in anterograde and retrograde memory. Immediate memory is maintained, but short-term memory is diminished with intact sensorium. The disorder is associated with patients fabricating stories in the setting of clear consciousness. Confabulations can be spontaneous or provoked with provoked confabulation commonly seen in chronic Korsakoff syndrome and spontaneous confabulation usually noted in the acute Wernicke state. [1][2]

Etiology

Thiamine deficiency is characteristically associated with severe alcohol use disorder. Although Wernicke encephalopathy mostly affects people who have a thiamine deficiency due to chronic alcoholism, various other causes include severe malnutrition, hyperemesis gravidarum, prolonged parenteral nutrition, malignancies, immunodeficiency syndromes, liver disease, hyperthyroidism, and severe anorexia nervosa. Chronic alcohol consumption may cause thiamine deficiency due to impaired absorption of thiamine from the intestine, a possible genetic predisposition, inadequate diet, reduced storage of thiamine in the liver, and other nutritional deficiencies.[3][2][4]

A common inciting event that precipitates WE is an acute infection. Other triggers include prolonged carbohydrate or glucose loading in the presence of thiamine deficiency. In general, patients who receive glucose should also be administered thiamine at the same time.

Epidemiology

Prevalence data on Wernicke encephalopathy comes mainly from autopsy studies with rates ranging between 1% and 3%. Several studies indicate that prevalence rates via analysis of clinical records are lower in comparison to necropsy studies as the diagnosis is easily overlooked or missed. The incidence of Wernicke encephalopathy is believed to be higher in developing countries due to vitamin deficiencies and malnutrition. The female to male ratio for Wernicke encephalopathy is 1:1.7, and there are no studies that show a particular race predisposed to Wernicke encephalopathy.[5]

Pathophysiology

Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied. Studies involving computed tomography (CT) and magnetic resonance imaging (MRI) of patients with Wernicke encephalopathy revealed lesions in the thalamus with dilated ventricles and volume loss in the mammillary bodies. The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum.[6][7]

History and Physical

Wernicke encephalopathy should be suspected in any patient with chronic alcohol abuse or any form of malnutrition and any of the following: acute altered mental status, ophthalmoplegia, ataxic gait, delirium, and hypotension. The classic triad of Wernicke encephalopathy is altered mental status, ataxic gait, and ophthalmoplegia. The diagnosis is made based on clinical presentation, and a definitive diagnosis is complicated as the clinical triad may not be present in up to 90% of patients.  

The hallmark sign of Wernicke encephalopathy is ocular abnormalities especially nystagmus. Other oculomotor symptoms include cranial nerve involvement of oculomotor, abducens, and vestibular nuclei causing conjugate gaze palsies. Pupillary sluggishness, ptosis, and anisocoria are also common.

Gait ataxia is also a significant finding in Wernicke encephalopathy where patients will present with a broad-based gait. Also, gait can worsen, and in many cases, patients are unable to walk. Physical examination may include a complete neurological exam with cerebellar testing. Disorientation and altered sensorium characterize encephalopathy. Some patient can present with hyperactive delirium secondary to possible alcohol withdrawal symptoms alongside Wernicke encephalopathy. Less than 5% of patients with Wernicke encephalopathy can present with the severely depressed level of consciousness that will eventually lead to coma and death. Some other warning signs could include hyperthermia and hypotension. The patient could also present with peripheral neuropathy and commonly includes the lower extremity, and an examination would reveal distal sensory loss.

WE should be a consideration in a patient with long term malnutrition and episodes of confusion and altered mental status. Over the past few decades, bariatric surgery has been associated with WE and malnutrition; the key reason is that after surgery, there is limited intake of food and the stores of thiamine are rapidly depleted.

Evaluation

Evaluation should include a thorough patient history with a focused physical exam and laboratory workup with appropriate imaging. There are no specific laboratory tests for diagnosing Wernicke encephalopathy as it is a clinical diagnosis with the above mentioned classic signs and symptoms.

The clinical diagnosis of WE is present if the patient has two of the following features:

• Eye signs

• Dietary deficiency of thiamine

• Altered mental status

• Cerebellar dysfunction

However, a complete blood count and the comprehensive metabolic panel can be completed to exclude other causes of central nervous system abnormalities. Moreover, normal brain imaging cannot rule out Wernicke encephalopathy and therefore not very beneficial either. Caine et al. criteria were established in 1997 which is now 85% sensitive if patients have two or more of the classic features that include: ataxia, confusion, and ophthalmoplegia. Also, looking for risk factors helps in evaluating the patient as Wernicke encephalopathy was classically thought of as a disease exclusively due to alcoholism. However, in recent years Wernicke encephalopathy is also seen in patients that are chronically malnourished, post-bariatric surgery, hyperemesis gravidarum, liver disease, hyperthyroidism, and severe anorexia nervosa.[1][8][9]

MRI may reveal hyperintense signaling in the periventricular thalamus, mammillary bodies and the periaqueductal gray matter.

Erythrocyte transketolase levels can detect thiamine deficiency. Levels of lactate and pyruvate are often measured since thiamine is a cofactor for pyruvate dehydrogenase enzyme.

Treatment / Management

The aim of treatment is prompt and quick correction of the thiamine deficiency in the brain. Wernicke encephalopathy is a medical emergency and considered a reversible condition, therefore, requiring immediate emergent attention although the onset of the disease may be acute or chronic. Parenteral administration of thiamine is most effective and provides for rapid administration, however, in some cases, there are persistent neurological deficits, and the acute condition can progress to chronic Korsakoff syndrome. The preferred dose of thiamine treatment for Wernicke encephalopathy may be as high as 500 mg given one to three times daily parenterally. All malnourished patient may need higher doses of thiamine. Oral dosing is not reliable and not recommended.

There is some evidence that thiamine treatment can improve the confusional state, quick resolution of ataxia, ophthalmoplegia, and nystagmus. Thiamine is generally administered before or together with glucose solutions because the glucose oxidation can decrease thiamine levels thereby exacerbating the neurological symptoms of Wernicke encephalopathy. Patients with magnesium deficiency should also be treated as this can result in reduced recovery from Wernicke encephalopathy especially in patients with alcoholism.[10][11][12]

Most patients need to be admitted to ensure that they receive IV thiamine and magnesium.

Differential Diagnosis

Differential diagnoses include:

• Hepatic encephalopathy

• Stroke

• Alcohol withdrawal syndrome

• Delirium tremens

• Chronic hypoxia

• Normal pressure hydrocephalus 

Staging

Current Guidelines on Managing WE

1. Clinical diagnosis of WE should be considered in alcoholics if the individual has a dietary deficiency, cerebellar dysfunction, eye signs, and altered mental status

2. Total thiamine levels in the blood should be measured before treatment

3. MRI can be used to support the clinical diagnosis of WE

4. Thiamine should be given IV

5. After bariatric surgery, follow thiamine levels and supplement with thiamine for at least 6 months

Prognosis

WE is a serious life-threatening disorder with enormous disability. While thiamine can induce partial improvement, the neuropsychological deficits persist in many cases. The confusional state usually improves when IV thiamine is administered by the learning and memory deficits only improve partially. A small number of patients fail to have any improvement and may develop Korsakoff psychosis, which often requires institutionalization. Very few individuals recover at this point.

Complications

• Neurological injury

• Ataxia

• Korsakoff syndrome

• Ophthalmoplegia

• Heart failure

• Lactic acidosis

Consultations

• Internist

• Endocrinologist

• Psychiatrist

• Neurologist

• Intensivist

Enhancing Healthcare Team Outcomes

The management of WE is complex and usually requires a team approach. Because the disorder can present with various manifestations, the patient is best managed by a neurologist and an intensivist. Other specialists may be required according to organ involvement. The role of the nurse, dietitian, social worker, and pharmacist cannot be overemphasized. These patients are sick, frail and malnourished. A dietary consult should be done to assess the calorie needs and determine how to provide the food as well as thiamine. Since many WE patients are managed as outpatients, the pharmacist should encourage abstinence from alcohol. Since the cornerstone of therapy is thiamine, the importance of compliance is vital. At the same time, the electrolyte deficiencies should be corrected. Finally, the family should be educated about the prognosis of these individuals and make preparations for long-term care, in case the patient develops korsakoff syndrome. Close communication between members of the team is vital to ensure that the patient is receiving the current standard of care treatment. The ultimate goal is to improve the quality of life and lessen the burden on the family.[13][14] (Level V)

Outcomes

WE is a serious medical disorder which carries enormous morbidity and mortality. Even when the condition is managed with thiamine, the global confusion usually improves rapidly, but the ataxia and ophthalmoplegia may persist for some time. Patients who minimal or neurological signs have the best outcomes with thiamine supplement. However, survivors of WE may develop korsakoff psychosis and require long-term institutionalization. Of these, less than 10% will recover to be discharged from long-term care. A significant number of patients will have long-term neurological deficits like ataxia, nystagmus and korsakoff syndrome, which seriously diminishes the quality of life. Unfortunately, there are no long-term follow-up studies and anecdotal reports indicate that many of these patients do die prematurely. [15][16][17](Level V)

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

References

1.

Karakonstantis S, Galani D, Korela D, Maragou S, Arna D, Basta M. Missing the early signs of thiamine deficiency. A case associated with a liquid-only diet. Nutr Neurosci. 2020 May;23(5):384-386. [PubMed: 30092713]

2.

Oudman E, Wijnia JW, Oey MJ, van Dam MJ, Postma A. Preventing Wernicke’s encephalopathy in anorexia nervosa: A systematic review. Psychiatry Clin Neurosci. 2018 Oct;72(10):774-779. [PubMed: 29984541]

3.

Shabbir S, Tong O, Gluck L, Robbins M. Convergence Spasm in Wernicke Encephalopathy. Neurohospitalist. 2018 Jan;8(1):NP1-NP2. [PMC free article: PMC5734497] [PubMed: 29276567]

4.

Tang L, Alsulaim HA, Canner JK, Prokopowicz GP, Steele KE. Prevalence and predictors of postoperative thiamine deficiency after vertical sleeve gastrectomy. Surg Obes Relat Dis. 2018 Jul;14(7):943-950. [PubMed: 29803410]

5.

Arts NJ, Walvoort SJ, Kessels RP. Korsakoff’s syndrome: a critical review. Neuropsychiatr Dis Treat. 2017;13:2875-2890. [PMC free article: PMC5708199] [PubMed: 29225466]

6.

Kim WJ, Kim MM. Wernicke’s Encephalopathy Presenting with Bilateral Complete Horizontal and Downward Gaze Palsy in a Malnourished Patient. Korean J Ophthalmol. 2017 Aug;31(4):372-374. [PMC free article: PMC5540996] [PubMed: 28682019]

7.

Sukop PH, Kessler FH, Valerio AG, Escobar M, Castro M, Diemen LV. Wernicke’s encephalopathy in crack-cocaine addiction. Med Hypotheses. 2016 Apr;89:68-71. [PubMed: 26968913]

8.

Jan K. Wernicke encephalopathy: (MRI) picture worth a thousand words. Oxf Med Case Reports. 2018 May;2018(5):omy013. [PMC free article: PMC5965079] [PubMed: 29868178]

9.

Diekfuss JA, De Larwelle J, McFadden SH. Diagnosis makes a difference: Perceptions of older persons with dementia symptoms. Exp Aging Res. 2018 Mar-Apr;44(2):148-161. [PubMed: 29400641]

10.

Onishi H, Ishida M, Uchida N, Shintani D, Nishikawa T, Hasegawa K, Fujiwara K, Akechi T. Subclinical thiamine deficiency identified by preoperative evaluation in an ovarian cancer patient: Diagnosis and the need for preoperative thiamine measurement. Palliat Support Care. 2019 Oct;17(5):609-610. [PubMed: 30168403]

11.

Johnson JM, Fox V. Beyond Thiamine: Treatment for Cognitive Impairment in Korsakoff’s Syndrome. Psychosomatics. 2018 Jul-Aug;59(4):311-317. [PubMed: 29751937]

12.

Oudman E, Wijnia JW, van Dam M, Biter LU, Postma A. Preventing Wernicke Encephalopathy After Bariatric Surgery. Obes Surg. 2018 Jul;28(7):2060-2068. [PMC free article: PMC6018594] [PubMed: 29693218]

13.

McKeon A, Frye MA, Delanty N. The alcohol withdrawal syndrome. J Neurol Neurosurg Psychiatry. 2008 Aug;79(8):854-62. [PubMed: 17986499]

14.

Donnelly A. Wernicke-Korsakoff syndrome: recognition and treatment. Nurs Stand. 2017 Mar 29;31(31):46-53. [PubMed: 28351256]

15.

Nakamura ZM, Tatreau JR, Rosenstein DL, Park EM. Clinical Characteristics and Outcomes Associated With High-Dose Intravenous Thiamine Administration in Patients With Encephalopathy. Psychosomatics. 2018 Jul-Aug;59(4):379-387. [PMC free article: PMC6015524] [PubMed: 29482863]

16.

Sanvisens A, Zuluaga P, Fuster D, Rivas I, Tor J, Marcos M, Chamorro AJ, Muga R. Long-Term Mortality of Patients with an Alcohol-Related Wernicke-Korsakoff Syndrome. Alcohol Alcohol. 2017 Jul 01;52(4):466-471. [PubMed: 28340112]

17.

Zahr NM, Kaufman KL, Harper CG. Clinical and pathological features of alcohol-related brain damage. Nat Rev Neurol. 2011 May;7(5):284-94. [PMC free article: PMC8121189] [PubMed: 21487421]

Disclosure: Sarayu Vasan declares no relevant financial relationships with ineligible companies.

Disclosure: Anil Kumar declares no relevant financial relationships with ineligible companies.

Wernicke Encephalopathy – StatPearls – NCBI Bookshelf

Continuing Education Activity

Wernicke encephalopathy is an acute neurological condition characterized by a clinical triad of ophthalmoplegia, ataxia, and confusion. This disease is caused by thiamine deficiency, which primarily affects the peripheral and central nervous systems. This should be differentiated from Korsakoff syndrome, a neuropsychiatric disorder associated with confabulation and significant deficits in anterograde and retrograde memory. This activity reviews the pathophysiology and evaluation of Wernicke encephalopathy and highlights the role of the interprofessional team in the management of patients with this illness.

Objectives:

• Describe the pathophysiology of Wernicke encephalopathy.

• Identify the causes of Wernicke encephalopathy.

• Explain the treatment for Wernicke encephalopathy.

• Explain the importance of improving care coordination among interprofessional team members to enhance outcomes for patients affected by Wernicke encephalopathy.

Access free multiple choice questions on this topic.

Introduction

Wernicke encephalopathy (WE) is an acute neurological condition characterized by a clinical triad of ophthalmoparesis with nystagmus, ataxia, and confusion. This is a life-threatening illness caused by thiamine deficiency, which primarily affects the peripheral and central nervous systems. This disorder should be differentiated from Korsakoff syndrome which is preventable and is usually suspected as a consequence of at least one episode of Wernicke’s encephalopathy. Korsakoff syndrome is a neuropsychiatric disorder associated with memory disturbances in which there are significant deficits in anterograde and retrograde memory. Immediate memory is maintained, but short-term memory is diminished with intact sensorium. The disorder is associated with patients fabricating stories in the setting of clear consciousness. Confabulations can be spontaneous or provoked with provoked confabulation commonly seen in chronic Korsakoff syndrome and spontaneous confabulation usually noted in the acute Wernicke state.[1][2]

Etiology

Thiamine deficiency is characteristically associated with severe alcohol use disorder. Although Wernicke encephalopathy mostly affects people who have a thiamine deficiency due to chronic alcoholism, various other causes include severe malnutrition, hyperemesis gravidarum, prolonged parenteral nutrition, malignancies, immunodeficiency syndromes, liver disease, hyperthyroidism, and severe anorexia nervosa. Chronic alcohol consumption may cause thiamine deficiency due to impaired absorption of thiamine from the intestine, a possible genetic predisposition, inadequate diet, reduced storage of thiamine in the liver, and other nutritional deficiencies.[3][2][4]

A common inciting event that precipitates WE is an acute infection. Other triggers include prolonged carbohydrate or glucose loading in the presence of thiamine deficiency. In general, patients who receive glucose should also be administered thiamine at the same time.

Epidemiology

Prevalence data on Wernicke encephalopathy comes mainly from autopsy studies with rates ranging between 1% and 3%. Several studies indicate that prevalence rates via analysis of clinical records are lower in comparison to necropsy studies as the diagnosis is easily overlooked or missed. The incidence of Wernicke encephalopathy is believed to be higher in developing countries due to vitamin deficiencies and malnutrition. The female to male ratio for Wernicke encephalopathy is 1:1. 7, and there are no studies that show a particular race predisposed to Wernicke encephalopathy.[5]

Pathophysiology

Thiamine, one of the first B vitamins to be discovered also known as Vitamin B1, is a coenzyme that is essential for intricate organic pathways and plays a central role in cerebral metabolism. This vitamin acts as a cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including alpha-keto-glutamic acid oxidation and pyruvate decarboxylation. Thiamine-dependent enzymes function as a connection between glycolytic and citric acid cycles. Therefore, deficiency of thiamine will lead to decreased levels of alpha-keto-glutarate, acetate, citrate, acetylcholine and accumulation of lactate and pyruvate. This deficiency can cause metabolic imbalances leading to neurologic complications including neuronal cell death. Neuronal death in the mammillary bodies and thalamus were implicated in multiple cases of Wernicke encephalopathy studied. Studies involving computed tomography (CT) and magnetic resonance imaging (MRI) of patients with Wernicke encephalopathy revealed lesions in the thalamus with dilated ventricles and volume loss in the mammillary bodies. The lesions are usually symmetrical in the midbrain, hypothalamus, and cerebellum.[6][7]

History and Physical

Wernicke encephalopathy should be suspected in any patient with chronic alcohol abuse or any form of malnutrition and any of the following: acute altered mental status, ophthalmoplegia, ataxic gait, delirium, and hypotension. The classic triad of Wernicke encephalopathy is altered mental status, ataxic gait, and ophthalmoplegia. The diagnosis is made based on clinical presentation, and a definitive diagnosis is complicated as the clinical triad may not be present in up to 90% of patients. 

The hallmark sign of Wernicke encephalopathy is ocular abnormalities especially nystagmus. Other oculomotor symptoms include cranial nerve involvement of oculomotor, abducens, and vestibular nuclei causing conjugate gaze palsies. Pupillary sluggishness, ptosis, and anisocoria are also common.

Gait ataxia is also a significant finding in Wernicke encephalopathy where patients will present with a broad-based gait. Also, gait can worsen, and in many cases, patients are unable to walk. Physical examination may include a complete neurological exam with cerebellar testing. Disorientation and altered sensorium characterize encephalopathy. Some patient can present with hyperactive delirium secondary to possible alcohol withdrawal symptoms alongside Wernicke encephalopathy. Less than 5% of patients with Wernicke encephalopathy can present with the severely depressed level of consciousness that will eventually lead to coma and death. Some other warning signs could include hyperthermia and hypotension. The patient could also present with peripheral neuropathy and commonly includes the lower extremity, and an examination would reveal distal sensory loss.

WE should be a consideration in a patient with long term malnutrition and episodes of confusion and altered mental status. Over the past few decades, bariatric surgery has been associated with WE and malnutrition; the key reason is that after surgery, there is limited intake of food and the stores of thiamine are rapidly depleted.

Evaluation

Evaluation should include a thorough patient history with a focused physical exam and laboratory workup with appropriate imaging. There are no specific laboratory tests for diagnosing Wernicke encephalopathy as it is a clinical diagnosis with the above mentioned classic signs and symptoms.

The clinical diagnosis of WE is present if the patient has two of the following features:

• Eye signs

• Dietary deficiency of thiamine

• Altered mental status

• Cerebellar dysfunction

However, a complete blood count and the comprehensive metabolic panel can be completed to exclude other causes of central nervous system abnormalities. Moreover, normal brain imaging cannot rule out Wernicke encephalopathy and therefore not very beneficial either. Caine et al. criteria were established in 1997 which is now 85% sensitive if patients have two or more of the classic features that include: ataxia, confusion, and ophthalmoplegia. Also, looking for risk factors helps in evaluating the patient as Wernicke encephalopathy was classically thought of as a disease exclusively due to alcoholism. However, in recent years Wernicke encephalopathy is also seen in patients that are chronically malnourished, post-bariatric surgery, hyperemesis gravidarum, liver disease, hyperthyroidism, and severe anorexia nervosa.[1][8][9]

MRI may reveal hyperintense signaling in the periventricular thalamus, mammillary bodies and the periaqueductal gray matter.

Erythrocyte transketolase levels can detect thiamine deficiency. Levels of lactate and pyruvate are often measured since thiamine is a cofactor for pyruvate dehydrogenase enzyme.

Treatment / Management

The aim of treatment is prompt and quick correction of the thiamine deficiency in the brain. Wernicke encephalopathy is a medical emergency and considered a reversible condition, therefore, requiring immediate emergent attention although the onset of the disease may be acute or chronic. Parenteral administration of thiamine is most effective and provides for rapid administration, however, in some cases, there are persistent neurological deficits, and the acute condition can progress to chronic Korsakoff syndrome. The preferred dose of thiamine treatment for Wernicke encephalopathy may be as high as 500 mg given one to three times daily parenterally. All malnourished patient may need higher doses of thiamine. Oral dosing is not reliable and not recommended.

There is some evidence that thiamine treatment can improve the confusional state, quick resolution of ataxia, ophthalmoplegia, and nystagmus. Thiamine is generally administered before or together with glucose solutions because the glucose oxidation can decrease thiamine levels thereby exacerbating the neurological symptoms of Wernicke encephalopathy. Patients with magnesium deficiency should also be treated as this can result in reduced recovery from Wernicke encephalopathy especially in patients with alcoholism. [10][11][12]

Most patients need to be admitted to ensure that they receive IV thiamine and magnesium.

Differential Diagnosis

Differential diagnoses include:

• Hepatic encephalopathy

• Stroke

• Alcohol withdrawal syndrome

• Delirium tremens

• Chronic hypoxia

• Normal pressure hydrocephalus 

Staging

Current Guidelines on Managing WE

1. Clinical diagnosis of WE should be considered in alcoholics if the individual has a dietary deficiency, cerebellar dysfunction, eye signs, and altered mental status

2. Total thiamine levels in the blood should be measured before treatment

3. MRI can be used to support the clinical diagnosis of WE

4. Thiamine should be given IV

5. After bariatric surgery, follow thiamine levels and supplement with thiamine for at least 6 months

Prognosis

WE is a serious life-threatening disorder with enormous disability. While thiamine can induce partial improvement, the neuropsychological deficits persist in many cases. The confusional state usually improves when IV thiamine is administered by the learning and memory deficits only improve partially. A small number of patients fail to have any improvement and may develop Korsakoff psychosis, which often requires institutionalization. Very few individuals recover at this point.

Complications

• Neurological injury

• Ataxia

• Korsakoff syndrome

• Ophthalmoplegia

• Heart failure

• Lactic acidosis

Consultations

• Internist

• Endocrinologist

• Psychiatrist

• Neurologist

• Intensivist

Enhancing Healthcare Team Outcomes

The management of WE is complex and usually requires a team approach. Because the disorder can present with various manifestations, the patient is best managed by a neurologist and an intensivist. Other specialists may be required according to organ involvement. The role of the nurse, dietitian, social worker, and pharmacist cannot be overemphasized. These patients are sick, frail and malnourished. A dietary consult should be done to assess the calorie needs and determine how to provide the food as well as thiamine. Since many WE patients are managed as outpatients, the pharmacist should encourage abstinence from alcohol. Since the cornerstone of therapy is thiamine, the importance of compliance is vital. At the same time, the electrolyte deficiencies should be corrected. Finally, the family should be educated about the prognosis of these individuals and make preparations for long-term care, in case the patient develops korsakoff syndrome. Close communication between members of the team is vital to ensure that the patient is receiving the current standard of care treatment. The ultimate goal is to improve the quality of life and lessen the burden on the family.[13][14] (Level V)

Outcomes

WE is a serious medical disorder which carries enormous morbidity and mortality. Even when the condition is managed with thiamine, the global confusion usually improves rapidly, but the ataxia and ophthalmoplegia may persist for some time. Patients who minimal or neurological signs have the best outcomes with thiamine supplement. However, survivors of WE may develop korsakoff psychosis and require long-term institutionalization. Of these, less than 10% will recover to be discharged from long-term care. A significant number of patients will have long-term neurological deficits like ataxia, nystagmus and korsakoff syndrome, which seriously diminishes the quality of life. Unfortunately, there are no long-term follow-up studies and anecdotal reports indicate that many of these patients do die prematurely. [15][16][17](Level V)

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References

1.

Karakonstantis S, Galani D, Korela D, Maragou S, Arna D, Basta M. Missing the early signs of thiamine deficiency. A case associated with a liquid-only diet. Nutr Neurosci. 2020 May;23(5):384-386. [PubMed: 30092713]

2.

Oudman E, Wijnia JW, Oey MJ, van Dam MJ, Postma A. Preventing Wernicke’s encephalopathy in anorexia nervosa: A systematic review. Psychiatry Clin Neurosci. 2018 Oct;72(10):774-779. [PubMed: 29984541]

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Shabbir S, Tong O, Gluck L, Robbins M. Convergence Spasm in Wernicke Encephalopathy. Neurohospitalist. 2018 Jan;8(1):NP1-NP2. [PMC free article: PMC5734497] [PubMed: 29276567]

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Tang L, Alsulaim HA, Canner JK, Prokopowicz GP, Steele KE. Prevalence and predictors of postoperative thiamine deficiency after vertical sleeve gastrectomy. Surg Obes Relat Dis. 2018 Jul;14(7):943-950. [PubMed: 29803410]

5.

Arts NJ, Walvoort SJ, Kessels RP. Korsakoff’s syndrome: a critical review. Neuropsychiatr Dis Treat. 2017;13:2875-2890. [PMC free article: PMC5708199] [PubMed: 29225466]

6.

Kim WJ, Kim MM. Wernicke’s Encephalopathy Presenting with Bilateral Complete Horizontal and Downward Gaze Palsy in a Malnourished Patient. Korean J Ophthalmol. 2017 Aug;31(4):372-374. [PMC free article: PMC5540996] [PubMed: 28682019]

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Sukop PH, Kessler FH, Valerio AG, Escobar M, Castro M, Diemen LV. Wernicke’s encephalopathy in crack-cocaine addiction. Med Hypotheses. 2016 Apr;89:68-71. [PubMed: 26968913]

8.

Jan K. Wernicke encephalopathy: (MRI) picture worth a thousand words. Oxf Med Case Reports. 2018 May;2018(5):omy013. [PMC free article: PMC5965079] [PubMed: 29868178]

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Diekfuss JA, De Larwelle J, McFadden SH. Diagnosis makes a difference: Perceptions of older persons with dementia symptoms. Exp Aging Res. 2018 Mar-Apr;44(2):148-161. [PubMed: 29400641]

10.

Onishi H, Ishida M, Uchida N, Shintani D, Nishikawa T, Hasegawa K, Fujiwara K, Akechi T. Subclinical thiamine deficiency identified by preoperative evaluation in an ovarian cancer patient: Diagnosis and the need for preoperative thiamine measurement. Palliat Support Care. 2019 Oct;17(5):609-610. [PubMed: 30168403]

11.

Johnson JM, Fox V. Beyond Thiamine: Treatment for Cognitive Impairment in Korsakoff’s Syndrome. Psychosomatics. 2018 Jul-Aug;59(4):311-317. [PubMed: 29751937]

12.

Oudman E, Wijnia JW, van Dam M, Biter LU, Postma A. Preventing Wernicke Encephalopathy After Bariatric Surgery. Obes Surg. 2018 Jul;28(7):2060-2068. [PMC free article: PMC6018594] [PubMed: 29693218]

13.

McKeon A, Frye MA, Delanty N. The alcohol withdrawal syndrome. J Neurol Neurosurg Psychiatry. 2008 Aug;79(8):854-62. [PubMed: 17986499]

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Donnelly A. Wernicke-Korsakoff syndrome: recognition and treatment. Nurs Stand. 2017 Mar 29;31(31):46-53. [PubMed: 28351256]

15.

Nakamura ZM, Tatreau JR, Rosenstein DL, Park EM. Clinical Characteristics and Outcomes Associated With High-Dose Intravenous Thiamine Administration in Patients With Encephalopathy. Psychosomatics. 2018 Jul-Aug;59(4):379-387. [PMC free article: PMC6015524] [PubMed: 29482863]

16.

Sanvisens A, Zuluaga P, Fuster D, Rivas I, Tor J, Marcos M, Chamorro AJ, Muga R. Long-Term Mortality of Patients with an Alcohol-Related Wernicke-Korsakoff Syndrome. Alcohol Alcohol. 2017 Jul 01;52(4):466-471. [PubMed: 28340112]

17.

Zahr NM, Kaufman KL, Harper CG. Clinical and pathological features of alcohol-related brain damage. Nat Rev Neurol. 2011 May;7(5):284-94. [PMC free article: PMC8121189] [PubMed: 21487421]

Disclosure: Sarayu Vasan declares no relevant financial relationships with ineligible companies.

Disclosure: Anil Kumar declares no relevant financial relationships with ineligible companies.

Alcoholic encephalopathy: causes, symptoms, signs, stages, consequences, treatment

In modern society, a severe censure of its individual representatives suffering from alcohol addiction is generally recognized. Hushing up the symptoms of a chronic disease and late seeking medical help lead to persistent changes in the psyche and the development of dangerous complications. One of them is alcoholic encephalopathy.

Without timely treatment in a specialized clinic, the disease progresses steadily, leading to permanent disability and degradation of the individual.

Alcoholic encephalopathy – what does it mean, how does it manifest itself

Alcoholic encephalopathy is a brain lesion caused by long-term abuse of alcoholic beverages. The disease causes poisoning with ethyl alcohol and its breakdown products.

Until recently, this disease was called alcoholic encephalitis, because. it was believed that the pathology is associated with inflammation of the brain tissue. Subsequently, it was established that the basis of brain disorders are gross damage to brain cells with their subsequent death. In the International Classification of Human Diseases (ICD 10), alcoholic encephalopathy is included under the code G31. 2.

Information about the frequency of occurrence of the disease is not sufficiently reliable, tk. often, the official diagnosis of patients is not made for social reasons and is generally hushed up.

Symptoms or how the disease manifests itself

The first signs of a developing gross pathology of the brain are nonspecific signs:

• sleep disorders, difficulty falling asleep;
• headache and dizziness;
• hand trembling;
• instability of blood pressure;
• decreased appetite;
• intestinal disorders, nausea and vomiting.

The psyche also changes – unmotivated fear, irritability, and sometimes aggressiveness arise. The mood is often depressed up to depression.

Acute encephalopathy

The first signs of alcoholic encephalopathy are mental disorders. Symptoms appear at night: patients are delusional, talking half asleep, jumping out of bed, making senseless movements, trying to run somewhere. During the day, symptoms lessen.

Over time, the disorders progress: patients fall into severe depression, and then in general into a stupor. They lie motionless for a long time, do not respond to addressed speech, do not react to others.

Sometimes consciousness is lost, a coma develops. Against this background, involuntary muscle movements, spasms and convulsions occur. In some patients, the body temperature rises to high numbers.

If the patient is given emergency care, there may be an improvement, but after a light period, the disease becomes chronic. Progressive memory loss, dementia are its typical manifestations.

Chronic

Acute symptoms of alcoholic encephalopathy are gradually erased. When observing a patient, they find:

• mental disorders – delusions of persecution, lack of self-criticism, false memories, poor orientation in what is happening;
• neurological disorders – trembling in the hands and body, periodic convulsive twitching of the muscles of the tongue and face, muscle pain, decreased muscle strength;
• diseases of internal organs – signs of toxic damage to the liver, icteric staining of the skin, instability of the intestines, general exhaustion.

With any variants of clinical manifestations, there are always signs of social and mental degradation of the personality.

Causes of disease

The occurrence of encephalopathy is directly related to the existing alcohol addiction. Signs of brain disorders become noticeable at stages 2-3 of chronic alcoholism. They are preceded by regular alcohol abuse for 5-20 years.

Access to alcoholic beverages is freely open in the trading network. Unlike other types of addictions, alcoholics do not experience difficulties in acquiring a psychoactive substance.

Disease pathogenesis

Many factors play a role in the mechanisms of disease development. The main ones are:

• genetic predisposition. The fact that the rate of development of pathological symptoms and complications differs markedly in different people is explained by the innate characteristics of metabolism, in particular, the deficiency or complete absence of enzymes that utilize alcohol. With their deficiency, ethanol does not break down, but accumulates in tissues and organs, has a direct damaging effect on them.
• Deficiency of B vitamins, especially vitamin B1. The lack of vitamins in alcoholism is always present, but the deficiency of thiamine is most clearly manifested. Alcohol reduces its absorption from food and accelerates excretion from the body. As a result, nerve cells begin to experience energy hunger. In them, physiological processes are inhibited and, as a result, many organs and systems suffer.
• Restructuring of biochemical processes in the body. Intermediaries in the transmission of information through nerve cells are biologically active substances (dopamine, serotonin, etc. ). Initially, alcohol stimulates their release, so after drinking small doses of alcohol, lightness and euphoria occur. In response to an excess of biostimulants, the body stops producing them. Mood swings, depression are the first signs of trouble in the biochemical processes of the body.
• Vascular damage. Alcohol overcomes the conditional barrier between the circulatory system and the brain tissue, damages the wall of the cerebral arteries. Nutrition of brain cells is disturbed. Strokes, drops in blood pressure are a direct consequence of damage to the vascular system.
• Toxic damage to the liver. Under the influence of alcohol, a “rebirth” of the liver occurs – cirrhosis, in which healthy liver cells are replaced by scar tissue. The body’s ability to neutralize alcohol continues to decrease, free ethanol poisons the internal organs and brain at an even greater rate. Added symptoms of hepatic encephalopathy.

The human body has huge hidden reserves and regenerative capabilities. For a long time, he manages to compensate for a whole cascade of pathological changes triggered by the constant presence of alcohol in the body. The appearance of pronounced signs of the disease indicates the depletion of one’s own resources and limited ability to resist the disease.

The right decision in such a situation is to contact a specialist psychotherapist or narcologist, who will help to understand the symptoms of the disease and establish their true nature.

In the arsenal of a doctor there are many opportunities to slow down pathological processes, stabilize the development of the disease and prevent its further complications.

Stages and classification of disease

The division of the disease into stages is rather conditional. In some cases, the disease develops gradually and bypasses the phase of precursors. In the classic version, the symptoms appear gradually.

period of harbingers. It lasts from 2-3 weeks with an acute form to several years with a chronic one. The patient can detect harbingers of future pathology. Complaints of headache, sleep and appetite disorders are not perceived by the patient and others as signs of a serious illness. They are often accompanied by symptoms of cardiovascular disorders (pain in the heart, shortness of breath), digestive disorders.

The stage of acute alcoholic encephalopathy begins unexpectedly and manifests with the main groups of symptoms:

• impaired consciousness – psychosis with delusions, hallucinations, etc.;
• oculomotor disorders – twitching of the eyeballs (nystagmus), intermittent strabismus, lack of movement of the eyeballs;
• gait and coordination disorders (staggering when walking, frequent falls).

Such disorders last from several weeks to 3 months, without treatment, some patients die from the developed complications.

The transition to the chronic form occurs gradually. The severity of symptoms decreases, but persistent disorders of the psyche and the nervous system as a whole, and malfunctions of the internal organs persist.

A narcologist at a specialized mental health clinic can interrupt the pathological chain. He conducts medical and, if necessary, hardware detoxification of the body, inhibits the formation of numerous complications of the disease. Self-treatment at home is ineffective.

According to the rate of development of symptoms and the predominant localization of lesions, acute alcoholic encephalopathy has:

• Acute course. It is manifested by the rapid development and increase in clinical manifestations. Cortical structures of the brain, subcortex and brain stem are affected.
• Subacute. In Gaye-Wernicke encephalopathy, disturbances in the middle parts of the brain predominate. They are associated with vitamin B1 deficiency.

Chronic forms of alcoholic encephalopathy include:

• Korsakov’s syndrome. The focus of the disease is predominantly located in the subcortical structures, spinal cord and peripheral nerves.
• Alcoholic ataxia Bekhterev. The most pronounced pathological changes in the cerebellum.
• Alcoholic encephalopathy with pellagra. With a lack of vitamin PP, the skin, cardiovascular system and gastrointestinal tract are affected.

There are other clinical variants of chronic alcoholic encephalopathy with multiple lesions and a diverse clinical picture. All of them lead to severe disruption of the work of most organs and systems with a frequent outcome in disability. With all the variety of clinical manifestations, all syndromes of alcoholic encephalopathy are united by the presence of severe damage to brain structures.

Narcologists of a specialized mental health clinic have sufficient experience and the necessary medical equipment for the full treatment of all forms of alcoholism and its complications.

Complications of the disease

Alcoholic delirium is popularly known as “delirium tremens”. It develops a few days after the interruption of the binge. Against the background of a depressive mood, inexplicable anxiety gradually increases, hallucinations appear. Most often they occur in the evening, intensify at night. Visions are frightening and threatening. Distorted perception paints real pictures with fantastic images: a hanging coat seems like a lurking killer, a piece of thread – a crawling snake, etc. Patients run away or, conversely, show aggression. They are prone to accidents, but they themselves pose a great danger to others.

Anxiety disorders and depression are frequent companions of alcoholic encephalopathy. They are almost always present in the prodrome and accompany delirium. An extremely unpleasant feature of such disorders against the background of alcoholism is their persistence, the ability to persist even after the cessation of alcohol consumption and treatment. This fact is explained by the presence of structural damage in the brain.

Suicidal tendencies. Also often accompanied by alcoholism and encephalopathy. Suicide attempts occur against the background of severe delirium and hallucinations in delirium tremens, become the result of prolonged depression.

Alcoholic epilepsy. Seizures of the epileptic type are fixed against the background of a sharp cessation of alcohol consumption. Episodes of convulsions are accompanied by loss of consciousness and a sharp increase in muscle tone. Convulsive readiness persists even against the background of the treatment of alcoholism, it requires long-term drug therapy.

“Locked Man Syndrome”. Due to damage to the nervous tissue in the region of the bridge of the brain, a person loses the ability to respond to external influences. His consciousness is completely preserved, he feels touches, pain, but he can answer them only by blinking his eyes.

Ischemic and hemorrhagic strokes are a natural consequence of alcoholism and toxic encephalopathy. Damage to the vascular wall, instability of blood pressure, impaired microcirculation in the brain lead to the formation of blood clots and blockage of the cerebral arteries. That part of the brain that stops receiving oxygen and nutrients dies. At the same time, the corresponding brain function is also lost.

Alcoholic dementia. Disorders of all forms of higher nervous activity progress. Memory, thinking, attention disappear. The disorders are irreversible, but their development can be slowed down with persistent treatment and partial social adaptation of the patient can be achieved.

infectious complications. In severe forms of alcoholic encephalopathy, patients may be in a state of coma and complete immobility. Against the background of reduced immunity, they easily develop congestive pneumonia. Human life depends on timely diagnosis of lung disease and timely treatment.

Life-threatening conditions are the end of the development of the disease. Patients die from acute or chronic insufficiency of all organs. Without emergency assistance for pulmonary and cerebral edema, coma, incessant convulsions, a person is doomed.

The prognosis of alcoholic encephalopathy is very serious. In the absence of timely treatment, acute forms become chronic or end in death. Even a single episode of the disease leaves a gross mental and neurological defect.

In the case of alcohol addiction, you should not hope for a miracle and seek help from “healers” from the people and miracle psychics. Professionals at a specialized mental health clinic can help overcome addiction and the effects of alcoholic encephalopathy.

When to see a doctor

At any stage of alcoholic encephalopathy, specialist help is needed. The doctor can correctly assess the initial symptoms of the development of brain disorders and stop their further progression. The professional has the opportunity to maximally rehabilitate the patient and adapt him to life in the family and society.

With symptoms of deterioration in the mental state, relatives need to convince the patient to seek qualified advice from a specialized clinic, not to try to treat themselves.

It is advisable to come to an appointment with a narcologist or psychotherapist with a family member of the patient who cares for him and is ready to help. Often such a person also requires treatment. For many years of communication with a dependent husband or son, a wife or mother has become accustomed to being overprotective, sacrificing her own life. They constantly experience anxiety for a loved one, they are ready to take responsibility for any actions of the patient.

Often, chronic stress makes it difficult to adequately assess the real state of affairs and insist on urgent inpatient treatment.

A psychotherapist or narcologist should conduct therapy for alcoholic encephalopathy. Subject to all medical recommendations, it is possible to achieve a noticeable improvement in the condition, to compensate for impaired body functions with medication. Psychotherapy is shown to both the patient and his family members.

Diagnostics

For the diagnosis of alcoholic encephalopathy are used:

• Questioning the patient and his relatives. In a conversation with the patient, the doctor determines the stage of alcohol dependence, learns information about the duration of the disease and the features of its course. Small details, such as indications of sleep disturbances, may indicate the risk of developing acute mental disorders.

Obtaining the necessary information may complicate the general and mental state of the patient (impaired consciousness, delusional ideas and visions, lack of self-criticism), the presence of signs of alcoholic dementia.

• Inspection. To establish the correct diagnosis helps to monitor the patient during the conversation. The person may act frightened, look around and try to hide. Pale yellow skin tone, emaciation indicate a long course of the disease and developed complications from the internal organs.
• Laboratory tests. The doctor prescribes a blood test for alcohol and its surrogates. Additionally, biochemical blood tests, tests to detect infectious lesions of the brain and liver may be required. Examination is necessary to confirm dependence and assess the possibilities of drug treatment. To distinguish between alcoholic brain damage from an infectious disease, an analysis of the cerebrospinal fluid is prescribed.
• hardware methods. The diagnosis of alcoholic encephalopathy is indirectly confirmed by changes detected by computerized brain diagnostics (CT) and magnetic resonance imaging (MRI). They make it possible to distinguish toxic lesions of the brain from acute circulatory disorders due to other causes. To determine the causes of seizures, ultrasound of the brain, encephalography and neuromyography are performed.

Treatment and prevention

In the case of an acute form of alcoholic encephalopathy, treatment is carried out in a hospital. During the period of pronounced clinical manifestations, the condition can be life-threatening, therefore, such patients are treated in the intensive care units of a specialized clinic.

To eliminate the cause of acute brain disorders, intravenous detoxification and the introduction of vitamin B1 are prescribed. The composition of the dropper includes liquids for the accelerated removal of toxins from the body, along with drugs to improve the functioning of the liver, kidneys, and heart. On the recommendation of a neurologist, medications are used to normalize blood circulation in the brain.

In case of insufficient effect from therapy, the resuscitator performs blood purification using hardware methods. To correct mental disorders, special antipsychotic drugs are prescribed.

Prevention of encephalopathy is reduced to the treatment of chronic alcoholism. Specific measures have not been developed.

Alcoholic encephalopathy is a late manifestation of alcohol dependence. In the absence of qualified assistance, severe brain damage inevitably leads to disability of the patient. Treatment in a specialized clinic can partially compensate for mental disorders and prevent their progression.

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Literature:

1. KR alcohol addiction.pdf

2. Alcoholic encephalopathy: causes, symptoms and treatment in an article by a neurologist Tolmachev A. Yu.

causes, symptoms, treatment in Moscow – Consultation and examination for encephalopathy – Neurology at Clinic No. 1

Alcoholic encephalopathy is a neurological disease caused by the negative effects of alcohol on the brain. The disease is accompanied by damage to brain cells and the resulting disruption of the nervous system and the body as a whole. In fact, alcoholic encephalopathy is not an independent disease. This is a complex of diseases occurring simultaneously within the clinical syndrome. The nervous, cardiovascular systems, and brain functions are involved.

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Causes of the disease

The cause of the development of the disease is the use of alcohol, which occurs frequently and in large doses. At first, the patient cannot ignore any symptoms, sometimes they are not noticeable even for several years of daily intake of large doses of alcohol. Particularly susceptible to the disease are persons who use alcoholic substitutes, technical liquids that are not intended for ingestion and have a devastating effect.

Symptoms

Symptoms of the disease increase as the situation worsens. At the initial stage, the so-called precursors appear. These signs include asthenia, loss of appetite, sleep disturbance. Patients tend to forego protein and fatty foods in favor of carbohydrate-rich foods. This is accompanied by metabolic disorders, the appearance of vomiting, weight loss, exhaustion of the body.

The patient can observe visual illusions, hallucinations, perform complex repetitive movements. Periods of excitement alternate with apathy. Some time after the onset of the disease, delirium develops (“white tremens”).

The main signs of alcoholic encephalopathy:

• Nausea, abdominal pain, vomiting, loss of appetite.
• Weight loss.
• Headache.
• Violation of the digestive tract.
• Weakness, chills.
• Fatigue, mood swings.
• Arrhythmia.
• Cerebral edema.
• Liver damage.
• Sweating.
• Convulsions.
• Sleep disturbance.

Types of disease

Alcoholic encephalopathy develops, as a rule, at the third stage of alcoholism. There are two main types of disease:

• Gaye-Wernicke disease. The body is depleted quickly, the face acquires an earthy or yellow tint, the skin is flabby, lethargic. A tremor appears in the arms and legs, blood pressure is lowered, digestion is disturbed. The speech is slurred, the muscles are tense, the patient observes hallucinations. If the patient is not treated, a fatal outcome is possible.
• Chronic alcoholic paralysis, or Korsakov’s syndrome. Occurs with prolonged drinking. It is characterized by disorientation in space, being in “another dimension”, hallucinations. There are neuritis of the extremities, the patient cannot move without help. Recovery is extremely rare and never complete. The most common outcome is loss of working capacity, dementia, death.

Get diagnosed with alcoholic encephalopathy at Clinic No. 1

• Functional tests
• Head MRI
• ultrasound
• Clinical tests
• EEG
• Spectroscopy

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Which doctor should I contact?

A neurologist deals with the problem of alcoholic encephalopathy. Treatment may also require the help of specialized specialists who will help in restoring other body systems.

Diagnostics

The approach to diagnosis is individual and depends on the specific clinical case. A survey of the patient and his relatives, the definition of symptoms is used. Functional tests, MRI diagnostics of the head, ultrasound, clinical tests, electroencephalography, spectroscopy are carried out.

Treatment

An integrated approach is used, including drug and non-drug methods. Therapy is carried out with vitamins, nootropics, drugs to maintain blood vessels and nerve cells. Also, patients can be prescribed hormonal drugs, life support systems, such as dialysis, hemoperfusion, parenteral nutrition. Measures to relieve intracranial pressure and cerebral edema, and eliminate intoxication of the body are also effective. Surgery with craniotomy may be indicated.

The sooner treatment is started, the greater the chance of preserving brain functions and partial return of the patient’s working capacity.

Make an appointment with a neurologist

The multidisciplinary medical center Clinic No. 1 offers a consultation with a neurologist. Patients are offered diagnostics and treatment using the latest equipment, comfortable conditions, safety, individual approach and favorable service offers. You can make an appointment by phone or through the registration form on the website.

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