Thousands of people in France are living with a largely unrecognized and preventable form of dementia known as Korsakoff’s syndrome, often misdiagnosed as simple “alcoholic dementia” or other cognitive impairments. This condition, resulting from a vitamin deficiency, could be avoided with proper diagnosis and treatment, experts say.
When considering early-onset dementia – memory problems before the age of 65 – Alzheimer’s disease is often the first condition that comes to mind. However, alcohol misuse is actually the leading cause of dementia before 65 in Western countries, a fact often overlooked by both the public and healthcare professionals.
Korsakoff’s syndrome is among the cognitive disorders linked to alcohol consumption. The severe, chronic, and irreversible condition develops from a combination of alcohol’s direct toxicity to neurons and, crucially, a deficiency in thiamine (vitamin B1). While thiamine deficiencies are easily diagnosed and prevented, they are frequently missed, leading to devastating consequences for patients.
Research indicates a strong link between excessive alcohol consumption and the risk of dementia. A French study examining a large national cohort of over 57,000 cases of early-onset dementia revealed that approximately 60% of cases occurring before age 65 were related to alcohol.
Alcohol and Dementia
The connection between alcohol and dementia is well-established. Studies show that excessive alcohol intake significantly increases dementia risk. For example, a Finnish study found that alcohol use disorder multiplies the risk of early-onset dementia by approximately 5.7 times in men and 6.1 times in women. A recent literature review similarly indicates that excessive alcohol consumption is responsible for 8% of new dementia cases in men aged 45 to 64.
Alzheimer’s Society in the UK estimates that approximately one in eight people with early-onset dementia suffers from alcohol-related cognitive impairment, frequently diagnosed between the ages of 40 and 50.
Cognitive deficits related to alcohol exist on a spectrum, ranging from those associated with “binge drinking” to alcohol use disorder, culminating in the devastating Korsakoff’s syndrome, which irreversibly destroys memory.
Memory Loss and Confusion
Patients with Korsakoff’s syndrome experience severe memory impairments. Memories from before the onset of the illness disappear (known as “retrograde amnesia”), and they are also unable to form new memories (“anterograde amnesia”). Often, these gaps are filled with false memories, fabrications that allow patients to maintain a semblance of normalcy, and false recognitions.
The syndrome also manifests as a loss of temporal and spatial awareness – patients struggle to situate themselves in time and space. They become unable to recall familiar routes, such as the path to their weekly grocery store.
They also suffer from problems with balance and difficulty walking, due to impaired coordination (“ataxia”) and eye movement problems. Individuals with Korsakoff’s syndrome also experience “anosognosia” – an inability to recognize their own deficits. Behavioral disturbances can also occur.
Korsakoff’s syndrome typically develops following another condition, Wernicke’s encephalopathy. If this acute phase is treated promptly, the progression can be favorable. Unfortunately, up to 80% of people with Wernicke’s encephalopathy are not diagnosed and do not receive appropriate treatment, which consists of simple vitamin supplementation.
Korsakoff’s syndrome, the chronic and irreversible form of Wernicke’s encephalopathy, develops.
A Vitamin B1 Deficiency
The symptoms of Wernicke’s encephalopathy and Korsakoff’s syndrome are due to lesions in various areas of the brain. These damages are a consequence of a deficiency in vitamin B1. Also known as thiamine, this vitamin plays a vital role in maintaining the nervous system. It is an “essential” vitamin, meaning the human body cannot produce it and it must be obtained through diet – an intake of 1 mg to 2 mg per day is sufficient to meet the needs of a healthy person.
Naturally present in certain foods, thiamine is also added to others and can be consumed as a dietary supplement. Sources of thiamine include brown rice, whole grains, pork, poultry, soybeans, nuts, peas, dried beans, and enriched or fortified cereal products.
While Wernicke’s encephalopathy can result from nutritional problems due to a diet poor in thiamine (in various regions of the world, thiamine deficiency causes beriberi), in nearly 90% of cases, the condition affects patients with alcohol use disorder. These individuals often eat too little, with alcoholic beverages providing a portion of their energy intake.
alcohol consumption decreases gastrointestinal absorption and hepatic storage of thiamine, while increasing its use by cells. Diarrhea and vomiting can also worsen absorption problems.
This means that Korsakoff’s syndrome could largely be prevented by early thiamine administration, particularly in individuals with alcohol use disorder, even without clear neurological symptoms. However, this inexpensive and generally safe vitamin is rarely prescribed in emergency departments, addiction treatment centers, or general practice.
A lack of awareness that only a minority of patients present with the classic complete clinical picture contributes to this issue. This has prompted patient and family associations to raise awareness about the lack of recognition, diagnosis, and management of these conditions.
A Silent Health Scandal
Wernicke’s encephalopathy is often misdiagnosed because the classic triad of symptoms – “confusion, oculomotor disturbances, ataxia” – is complete in only 16% of patients.
The classic criteria should be abandoned in favor of the Caine criteria, established by neuropsychologist Diana Caine and colleagues. Validated by clinical and neuropathological studies and recommended by professional societies, these criteria are now considered the most reliable, increasing the sensitivity of Wernicke’s encephalopathy diagnosis by a factor of four.
Caine’s Clinical Criteria (1997) for Diagnosing Wernicke’s Encephalopathy
- Documented nutritional deficits: very low BMI, weight loss, severe malnutrition, malabsorption, very restrictive diet, frequent vomiting;
- Oculomotor disturbances: nystagmus, ophthalmoplegia, paralysis of gaze, diplopia;
- Cerebellar syndrome: ataxia, unsteady gait, dysmetria, balance disorders;
- Confusional state or memory disorders: disorientation, fluctuating attention, moderate to severe memory impairment.
In patients with alcohol use disorder, the presence of even one criterion should raise a high suspicion of Wernicke’s encephalopathy, justifying immediate thiamine administration, even without clear neurological symptoms.
irreversible brain lesions occur rapidly, and once Korsakoff’s syndrome is established, there is no cure. Only cognitive remediation or social support approaches can then limit the damage.
This situation has led several patient and family associations to raise awareness about the lack of recognition, diagnosis, and management of these pathologies, potentially affecting 60,000 to 100,000 people in France.
Primarily Affecting Men
Each year in France, between 600 and 900 people develop Korsakoff’s syndrome. Currently, little data exists regarding its epidemiology. However, it is known to primarily affect individuals with severe alcohol use disorder and prolonged thiamine deficiency.
The risk of developing the syndrome increases significantly with high alcohol consumption (6 to 8 glasses of alcohol per day for men and women, respectively) maintained over a prolonged period (several years, often more than ten). It is also aggravated by malnutrition, repeated withdrawal episodes without care, or illnesses that increase needs or reduce absorption.
A recent Finnish study reported an incidence of 3.7 (for men) and 1.2 (for women) per 100,000 person-years. These studies also reveal that 56 to 84% of patients surviving untreated Wernicke’s encephalopathy develop Korsakoff’s syndrome.
A retrospective observational study, published in 2025 and conducted on 1,320 patients treated at the Public Assistance–Hospitals of Paris (AP–HP) between 2017 and 2022, revealed that the majority of patients were male (72.9%). Their average age was 62.9 years, and they were primarily treated in internal medicine departments (22.1%).
The main pathologies associated with Korsakoff’s syndrome were hypertension (frequency of 34%) and a depressive episode (frequency of 23.7%). The median three-year follow-up of these patients showed a poor prognosis, resulting in severe cognitive impairment, low recovery rates, and a high mortality rate (30.2%).
Finally, the study conducted on patients at the AP-HP estimated the average annual hospital costs for patients with Korsakoff’s syndrome: 15,346 euros per patient, representing an annual deficit of 8,507 euros per case and per hospital. The authors emphasize the need for a specific care pathway to improve the survival of these individuals.
An Intolerable Medical Odyssey
Many patients with Korsakoff’s syndrome experience a difficult medical odyssey. They are often considered too young for geriatrics, too disoriented for traditional social care facilities, too stable for acute psychiatry, and too complex for addiction centers.
Korsakoff’s syndrome concentrates several blind spots in our healthcare system: the stigmatization of alcohol use disorders, the marginalization of people in precarious situations, and the underinvestment in nutritional prevention. These patients, often young, are perceived as responsible for their condition, which hinders access to care. Reading the numerous existing testimonials is revealing.
Unlike other countries, such as the Netherlands or Belgium, France does not have a specialized care pathway. The lack of a structured response exacerbates loss of autonomy, burdens families, and makes reintegration almost impossible. However, a care home in Roubaix has been specifically created to accommodate women with the syndrome.
A National Plan to End Denial
Korsakoff’s syndrome is not the result of simple excess, but rather an avoidable cascade of medical (particularly the failure to early identify alcohol misuse), nutritional, and social negligence.
It is possible to combat this scourge by implementing four types of actions:
- Systematic prescription of thiamine intravenously or intramuscularly for any patient suspected of alcohol use disorder or in withdrawal.
- Organization of training campaigns for healthcare professionals to identify early Wernicke’s encephalopathy and avoid diagnostic errors.
- Creation, at the regional level, of specialized structures to accommodate patients with Korsakoff’s syndrome to provide care, cognitive rehabilitation, and social support.
- Integration of the risk of alcohol-related dementia into public health prevention policies and addiction care pathways.
Korsakoff’s syndrome is not inevitable. It is the product of collective denial of a preventable form of dementia, often developing at age 40 or 50, in indifference. If nothing is done, these patients will continue to disappear slowly, in an unjustifiable medical and political silence.
In at-risk patients, beware of glucose!
- Administering glucose to a patient at risk during their care can precipitate the onset of acute encephalopathy. Giving sugar to someone lacking vitamin B1 risks “burning” their last reserves and damaging their brain within hours. It is recommended to administer thiamine before or at the same time as glucose.
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