Wernicke’s encephalopathy (WE) is an acute neurological disorder caused by thiamine deficiency.¹ WE falls under the umbrella of alcohol related brain damage (ARBD) conditions and includes weakness of the eye muscles, problemed balance, coordination, speech and confusion.²

Wernicke’s encephalopathy (WE) can be successfully treated before the onset of irreversible brain damage.³ However, if inadequately treated, 17-20% can die and of those who survive, 84% will develop Korsakoff’s psychosis with 25% requiring long-term institutional care.⁴

Korsakoff’s psychosis can be defined as: “An abnormal mental state in which memory and learning are affected out of all proportion to other cognitive functions in an otherwise alert and responsive patient”¹

Korsakoff’s psychosis typically follows or accompanies WE, however symptoms of Korsakoff’s psychosis may not become apparent until the confusional state associated with WE resolves⁵

Using Caine’s criteria, a patient is diagnosed with WE when they demonstrate two of the four signs above.⁷ Of those people who misuse alcohol, post mortem studies have shown that Wernicke’s encephalopathy may occur in as many as 12.5%.⁸

Symptoms can include:^6,7,24

90–95% of Wernicke’s encephalopathy cases in developed countries are due to chronic alcohol misuse.^9,10

However, Wernicke’s encephalopathy can develop in patients who have severe thiamine deficiency but not a history of chronic alcohol misuse such as the following: ^5,11-13

• Cancer patients^5,11,13
• Type of malignancy
• Side effects of treatment
• Thyrotoxicosis⁵
• Genetic enzyme abnormality¹²
• Parenteral nutrition⁵
• Protracted vomiting and/or diarrhoea^5,12,13 
• Including morning sickness
• Chronic renal failure¹²
• Magnesium depletion⁵
• Chronic diuretic therapy
• Intestinal tract surgery
• Crohn’s disease
• Gastrointestinal surgery^5,13
• Acquired immunodeficiency syndrome (AIDS)¹²
• Infectious febrile diseases⁵
• Unbalanced nutrition (for any reason)^5,12,13

Postmortem studies reported incidence of Wernicke’s encephalopathy:

• 0.8–2.1% of the general population^14-17
  • Men account for more than 75% of all cases
  • Age span of 30–90 years
  • Mean age around 60 years
• Incidence in people with known alcohol misuse: 12.5%¹³

Clinical studies (during lifetime):

• In patients diagnosed with WE during their lifetime:¹⁸
  • 78% were men
  • Age at diagnosis was 49–66 years
• Of patients aged 50 years and over who were hospitalised with a dementia diagnosis, the incidence of WE was 0.5%¹⁹

Signs of Wernicke’s encephalopathy (WE) include:⁶

• Dietary deficiencies – significant weight loss over a short period of time, poor diet, or evidence of malnourishment
• Eye signs – ophthalmoplegia, nystagmus, or gaze palsy
• Cerebellar dysfunction – ataxia, abnormal past pointing, or dysdiadochokinesia
• Altered mental state or mild memory impairment – disorientation, confusion

Using Caine’s criteria, a patient is diagnosed with WE when they demonstrate two of the four signs above. The diagnosis of WE alone, or with Wernicke-Korsakoff's, or with hepatic encephalopathy, increased from 22% to 85%.⁷

Assessing a patient’s cognition allows for identification of neurological impairment. Evidence of cognitive damage can be recorded using a variety of simple tests like the 6-Item Cognitive Impairment Test (6CIT). 

The 6CIT is a brief and simple test of cognition designed to identify general confusion (not specifically ARBD) so it is important to try and establish for how long and how much the person has been drinking and a history may be required from someone who knows the person well. 

When a person is presenting with cognitive impairment a full range of blood tests, a comprehensive neurological examination and scans should also be undertaken.²⁰

Wernicke’s encephalopathy (WE) confirmed at post-mortem is missed by routine clinical examination during lifetime in 65–95% of cases.^5,16,17,21 A number of other illnesses or diseases can present in a similar manner to WE and must be excluded.⁵

Incorrect diagnosis can lead to significant delays in initiation of correct treatment and worse outcomes.⁵

There can be a multiple of reasons for this including:^22,23

• The patient is misdiagnosed with another condition affecting the brain.
• As diagnosis does not include any one assessment tool or laboratory result, it can be difficult to detect, so may be missed or misdiagnosed.
• Due to the symptoms of WE, an accurate medical history from the patient may be difficult to obtain.
• As patients with WE may have little contact from friends and family, inadequate knowledge may be known about their history and lifestyle habits.

Differential diagnoses can include:^22-24

• Hepatic encephalopathy
• Stroke
• Alcohol withdrawal syndrome
• Intoxication
• Delirium tremens
• Chronic hypoxia
• Normal pressure hydrocephalus
• Dementia e.g., Alzheimer’s Disease or mental illness

Wernicke’s encephalopathy can be successfully treated before the onset of irreversible brain damage.³

Treatment should start immediately, even while the patient is drunk.⁵ However if the metabolic requirements of the brain cannot be met:¹²

12.5% of people misusing alcohol develop Wernicke’s encephalopathy⁸

If Wernicke’s encephalopathy is not treated and the metabolic requirements of the brain are not met:¹²

• Up to 20% will die
• Of those who survive, 84% will develop Korsakoff's psychosis