Alcohol Dementia - Wernicke-Korsakoff syndrome
- Jun 02, 2011
As of 2002, the United States Department of Health and Human Services reported an estimated 22 million Americans were classified as alcohol dependent, aged 12 years old and older. Its prevalence reaches across all ethnic and socioeconomic lines. Those who've indulged in excess drinking over a number of years run the risk of developing alcohol dementia
Alcohol dementia is a condition caused by excessive, long term alcohol consumption that results in problems with memory, learning and cognitive skills. Also known as Wernicke-Korsakoff Syndorme, this condition involves brain cell damage that is further exacerbated by malnutrition brought on by poor eating habits. The syndrome is actually two syndromes in one where Wernicke's disease has to do with cell damage within the brain and spinal chord, and throughout other areas of the body. Korsakoff syndrome is a psychosis in which damage to nerve cells gives rise to problems with memory, intellect and cognitive skills. Vitamin B-1 deficiencies are present as a result of the poor eating habits that normally accompany excess alcohol use.
The Diagnostic and Statistical Manual of Mental Disorders (DSM-IV-TR), the professional handbook that aids clinicians in diagnosing patients' mental disorders, refers to Korsakoff syndrome as alcohol-induced persisting amnestic disorder and includes it under the category of substance-induced persisting amnestic disorders .
The disorder was first identified in the late nineteenth century. The first phase of the condition, called Wernicke's encephalopathy, was described by German neurologist and psychiatrist Karl Wernicke in 1881. He noted three key symptoms in three patients-two-with alcoholism and one who had swallowed sulfuric acid. These patients suffered from mental confusion, eye movement disorders , and ataxia (poor motor coordination). A few years later, S. S. Korsakoff, a Russian psychiatrist, began publishing reports describing a syndrome of anterograde amnesia-an inability to form new memories-and confabulation in individuals with severe alcoholism or certain medical illnesses. (Confabulation refers to the practice of filling in gaps in memory by fabrication.) By 1900, researchers and clinicians studying alcoholism recognized a connection between the two conditions. The typical syndrome begins with acute Wernicke's encephalopathy, with Korsakoff syndrome emerging when the acute phase resolves. The symptoms of Wernicke's encephalopathy appear suddenly. The most prominent symptom initially is mental confusion including memory problems. On examination, patients have difficulty moving their eyes to follow a visual stimulus due to paralysis of the muscles controlling eye movements. For instance, a patient may have trouble looking upward or to the side with one or both eyes. Problems maintaining balance while standing or walking, a condition known as ataxia, are frequently observed as well. If left untreated, most of these symptoms may resolve spontaneously, but the severe memory disorder characteristic of Korsakoff syndrome remains.
The typical person with Korsakoff syndrome appears fairly normal on first impression. Intelligence is intact, and individuals with the syndrome can carry on a conversation quite naturally. They are usually able to recall and talk about incidents that took place before the onset of the disorder and recognize family members and old friends without much difficulty. The ability to form new memories is nearly absent, however. In the course of conversation, people with Korsakoff syndrome may repeat comments or questions several times. They will fail to recognize people they met minutes before or greet a friend with excitement and surprise after a brief trip to another room. These are the characteristics of anterograde amnesia . Research shows that anterograde amnesia results from a failure of memory formation and storage. New information is processed normally, but almost immediately forgotten, never making it into the regions of the brain where memories of the past are stored. People with Korsakoff syndrome thus have no memories of events that happened after the onset of the illness. Many previously stored memories are still available, however, explaining why individuals with Korsakoff syndrome can usually remember the distant past quite well.
The effects of alcohol dementia result from the poisonous effect that alcohol has on nerve cells within the central nervous system. Once absorbed into the bloodstream, it's effects are most prominent within the brain and the liver. As the liver is responsible metabolizing alcohol, excess consumption can lead to liver failure. Damage to the liver also contributes to the effects alcohol has in the brain. In addition to poor nutrition habits, the body's ability to absorb vitamin B1 is further hampered by excessive drinking. This vitamin is essential for nerve cell health. Neurotransmitter processes within the brain become altered as a result of excess consumption, leading to permanent damage that remains long after a person has stopped drinking.
Unlike dementia disorders caused by Alzheimer's and Parkinson's diseases, recovery from alcohol-induced dementia is possible when consumption is stopped. Abstinence prevents the condition from getting progressively worse, however damage that's already occurred may be irreversible. Signs of damage typically appear in the form of not being able to learn new things, problems with reasoning, poor judgment, and in some cases, changes in a person's overall personality can occur. Confusion, frustration and problems with remembering past events are the most prominent signs of brain damage. Symptoms of excess alcohol use can be seen in the tendency to say the same thing over and over again whether it be asking a question, telling a story, or in conversation. When this happens, the person is completely unaware that they've repeated themselves several times over.
Personality changes, communication problems, disorientation, and the inability to solve everyday problems are the most common symptoms of alcohol dementia. Personality changes may include paranoia, fear of being alone, mood swings, a lack of overall emotional response or anger. Communication problems can take the form of difficulty with using, or finding words, or not being able to follow along in a conversation. Disorientation may appear in not being able to keep track of time, not being able to recognize familiar people, or getting lost in familiar places. Difficulties with problem-solving may involve not being able to do familiar tasks, being unable to make decisions, or problems with making connections between people and events.
Causes, incidence, and risk factors
Wernicke's encephalopathy and Korsakoff syndrome are believed to be two stages of the same condition.
Wernicke's encephalopathy is caused by damaging changes in the brain, usually due to a lack of vitamin B1 (thiamine). It is most commonly observed in people with alcoholism since heavy drinkers often eat poorly, and alcoholism interferes with absorption of nutrients from the digestive system. It can also occur in people who are malnourished for other reasons. Thiamin helps produce energy needed to make neurons function properly. Insufficient thiamin can lead to damage or death of neurons.
Thiamin deficiency damages regions of the brain, particularly the thalamus and the mammillary bodies. The thalamus is a structure deep within the brain that serves many important functions. It is often called the major relay station of the brain, and many neurons make connections in the thalamus. The mammillary bodies are part of the hypothalamus, located just below the thalamus. The mammillary bodies receive many neural connections from another part of the brain called the hippocampus, which appears to be the primary part of the brain involved in the formation of memories. Neurons in the mammillary bodies make connections with the thalamus, which in turn makes connections with the cortex of the brain, where long-term memories are stored. This may explain why damage to the mammillary bodies and thalamus can lead to anterograde amnesia. Memories formed in the hippocampus are never stored since connections between hippocampus and cortex are disrupted.
A lack of vitamin B1 is common in people with alcoholism. Heavy alcohol use affects the breakdown of thiamine in the body. Even if someone who drinks alcohol heavily follows a well-balanced diet, most of the thiamine is not absorbed.
Korsakoff syndrome, or Korsakoff psychosis, tends to develop as Wernicke's symptoms go away. Korsakoff psychosis involves damage to areas of the brain involved with memory.
Eye movement disorders observed in the acute phase of the condition are probably due to damage to other nearby brain regions that make connections to the nerves controlling eye muscles. These nerves emerge from the brainstem located right below the thalamus and mammillary bodies. Nerves involved in balance also make connections with other nerves in the brainstem, but a separate part of the brain called the cerebellum may also contribute to ataxia. Reasons why some regions of the brain are selectively affected by thiamin deficiency are not yet fully understood, but selective vulnerability of certain neurotransmitters is suspected.
Alcohol Dementia Symptoms
The Korsakoff syndrome or the alcohol dementia syndrome is caused by the lack of vitamin B1 (thymine) in the body. This is due to poor nutrition and inflammation in the stomach lining. The main alcohol dementia symptoms include memory loss. The Wernicke-Korsakoff syndrome are two separate but related stages of the disorder. The Wernicke's encephalopathy precedes the Korsakoff syndrome usually. Many times Korsakoff syndrome is exhibited without an episode of Wernicke's syndrome.
The Wernicke's syndrome affects the brain and exhibits few symptoms that include:
- Involuntary, jerky eye movements
- Paralysis of muscles moving the eyes
- Poor balancing or inability to walk or staggering gait
- Confusion, drowsiness
If Wernicke's syndrome is diagnosed the person should be given immediate treatment. The treatment includes high doses of thiamine injected into the vein or muscles. Immediate treatment will help in reversal of the symptoms within a few hours. If left untreated, it may result in brain damage and even death.
- Apathy in some and talkative or repetitive behavior in others
- Double Vision
- Difficulty to learn or acquire new skills or information
- Drooping eyelids
- The person does not believe that his memory is not functioning normally
- Confabulation. This is a condition when the person invents events to fill the gaps in memory. The patient may be lying in the hospital for several weeks, but will convincingly talk about having attended a basketball game last evening.
Other Alcohol Dementia Symptoms
The other alcohol dementia symptoms one may experience include:
- Mental confusion
- Slow walking
- Language disturbances
- Poor concentration
- Lack of motivation
- Paralysis of eye muscles
- Problems with coordination
- Change in personality
When diagnosis is based on postmortem findings, the estimated prevalence of Wernicke-Korsakoff syndrome is between 1 and 2% of the population. The classic presentation with acute onset of Wernicke's encephalopathy is fairly rare, about 0.05% of all hospital admissions, although this does not account for patients who do not seek medical attention. Wernicke-Korsakoff syndrome usually follows many years of chronic alcoholism or malnutrition and is seldom seen among people under 20. Most patients are 40 years of age or older. The disorder is apparently more common in alcoholic individuals who are particularly vulnerable to malnutrition such as indigent or homeless people.
Wernicke's encephalopathy is diagnosed when patients seek medical attention and have the classic trio of signs: mental confusion, eye movement disorders, and ataxia. The diagnosis of Korsakoff syndrome is given when anterograde amnesia is present in an individual with a history of chronic, heavy drinking or malnutrition. When Korsakoff syndrome follows Wernicke's encephalopathy, the entire Wernicke-Korsakoff syndrome diagnosis is appropriate. The diagnosis is supported by neuroimaging or autopsy findings showing degeneration of the thalamus and mammillary bodies and loss of brain volume in the area surrounding the fourth ventricle-a fluid-filled cavity near the brainstem.
Although DSM-IV-TR criteria for alcohol-induced persisting amnestic disorder apply to most people with Wernicke-Korsakoff syndrome, there are some differences between the two diagnoses. Despite research findings suggesting that severe amnesia is not a necessary symptom of Wernicke-Korsakoff syndrome, the DSM-IVTR requires the presence of either anterograde or retrograde amnesia for a diagnosis of alcohol-induced persisting amnestic disorder. One additional cognitive symptom is also required. Symptoms listed in the DSM-IV-TR include language disturbance (aphasia), inability to carry out motor activities (apraxia), inability to recognize objects (agnosia), or deficits in planning, initiation, organization and abstraction (executive functions). Individuals with Wernicke-Korsakoff syndrome frequently demonstrate problems with executive functions that contribute to the symptoms of confabulation and apathy. Aphasia, apraxia, and agnosia are not common signs of Wernicke-Korsakoff syndrome.
The DSM-IV-TR also requires that memory impairment must significantly impair a person's ability to perform normal activities and functions, and it must represent a decline from a previous level of functioning. Amnesia cannot occur exclusively during states of delirium , alcohol intoxication, or withdrawal, or be exclusively associated with a dementia. Both of the these requirements are consistent with the usual presentation of Wernicke-Korsakoff syndrome.
Finally, the DSM-IV-TR requires evidence that amnesia is caused by use of alcohol. Such evidence can include an extensive history of heavy drinking; or physical examination or laboratory findings revealing other signs of heavy alcohol use, such as abnormal liver function tests. Despite this DSM-IV-TR requirement, Wernicke-Korsakoff's syndrome can occur in the absence of heavy alcohol use. Emergence of the disorder in people without alcoholism is much less common today than it was in the past, however, since vitamins are now added to many foods. In practice, most people who show the hallmark symptoms of Wernicke-Korsakoff syndrome also qualify for the DSM-IV-TR diagnosis.
The prognosis for full recovery from Wernicke-Korsakoff syndrome is poor. Once chronic Korsakoff's amnesia ensues, approximately 80% of patients will never fully recover the ability to learn and remember new information. Because they cannot learn from experience, individuals with Wernicke-Korsakoff syndrome almost always require some form of custodial care. They are usually unable to work, although some can perform simple tasks they learned prior to onset of the condition if closely supervised.
Wernicke encephalopathy is a medical emergency. Prompt recognition of the symptom complex and a high index of suspicion are crucial to ensure early treatment. Parenteral thiamine (100 mg) is the treatment of choice. Early treatment can rapidly reverse the ophthalmoplegia and improve ataxia/dysequilibrium and early mental confusion, as well as prevent development of the amnestic state. In advanced cases, where severe prolonged deficiency has led to permanent structural damage, permanent deficits are most often manifested as the amnestic state and severe ataxia.
After the initial IV dose, continue daily doses of thiamine (100 mg) as IV, IM, or oral doses depending on patient status. Supplementation of electrolytes, particularly magnesium and potassium (often low in people with alcoholism), may be required in addition to thiamine. Magnesium acts as a cofactor for many enzymes (eg, transketolase for the conversion of thiamine to thiamine pyrophosphate) and, therefore, its deficiency may lead to refractory response to thiamin supplementation. In patients who are chronically malnourished, the remainder of the B vitamins also should be supplemented. Administration of intravenous glucose to patients who are severely malnourished can exhaust their supply of thiamine and precipitate Wernicke-Korsakoff syndrome. Thus, good practice demands administration of thiamine prior to glucose infusion in patients at high risk for Wernicke-Korsakoff syndrome.
Emergency psychiatry hospitalization and evaluation is indicated when the patient is having active psychotic symptoms that pose a danger to self or others. Many such patients also meet the criteria of grave disability (ie, inability to provide basic needs such as food and shelter). In such cases, however, the patient should generally be medically and neurologically stable prior to transfer to a psychiatric facility, where acute medical work-up and monitoring may be available (eg, IV access, neuroimaging, nutritionist, neurology consultation). In most cases, patients with psychotic symptoms may require inpatient medical hospitalization and psychiatric consultation. Once medically stabilized, patients may need continued psychiatric care if severe psychotic symptoms persist.
In patients with comorbid acute alcohol withdrawal, treatment with IV/IM thiamine occurs concurrently with the indicated alcohol withdrawal procedures.
Long-term alcohol use is the most common etiology for Wernicke-Korsakoff syndrome, and abstinence provides the best chance for recovery. Referral to an alcohol recovery program should be part of the treatment regimen. Inpatient treatment versus outpatient rehabilitation depends on the needs of the individual and risks of relapse. Several other risk factors for Wernicke-Korsakoff syndrome are recognized (see Causes). Patients with these risk factors also could benefit from referral or consultation to help prevent future episodes.
A balanced diet should be resumed as early as possible. Vitamin and electrolyte supplementation should be adhered to in addition to a well-balanced diet initially, and supplementation can be tapered as the patient resumes normal intake and demonstrates symptomatic improvement.
Due to gait abnormalities, unassisted ambulation is discouraged during the initial phase of treatment. Patients may require physical therapy evaluation for gait assistance. Gait abnormalities may be permanent, depending on the severity at initial presentation and the timeliness of therapy.
Wernicke-Korsakoff syndrome is a result of thiamine deficiency. The treatment is replacement of this essential vitamin. The usual dose is 100 mg/d PO/IV/IM. However, the dosing and duration of thiamine treatment has not been sufficiency studied. In a systematic review from the Cochrane Database, Day et al only found 2 randomized studies that were of sufficient quality. There was a significant difference in favor of 200 mg/d, as compared to 5 mg/d, when the outcomes were measure after 2 days.
Overall, the current standard-of-care involves use of thiamine 100 mg/d for acute prophylaxis. Duration of treatment varies greatly and depends on the comorbid conditions and etiology. For example, thiamine would be administered indefinitely for patients with absorption problems. However, when use as prophylaxis for acute alcohol withdrawal/detoxification, thiamine could be discontinued once dietary intake is adequate. When in doubt, a serum thiamine level may be obtained to guide treatment.
For persistent cognitive impairment (eg, Korsakoff dementia), cognitive enhancers such as acetylcholinesterase inhibitors and memantine have demonstrated some benefit. However, the findings were negative in one small comparison study with rivastigmine.
Treating a person during the early stages of alcohol dementia greatly increases her chance for recovery. Abstaining from alcohol use and eating a balanced diet are necessary to rebuild the body's functioning level. Vitamin B1 supplements are also recommended to replenish the nerve cells in the brain. The treatment of any existing medical conditions, such as hypoxia (decreased oxygen circulation), infections, depression, anemia or any psychiatric conditions will further improve a person's recovery process. Ultimately, treatment approaches focus on managing the symptoms of the illness. As of yet, no specific medications or techniques exist to treat the effects of alcohol dementia. Support groups and therapy are needed to help persons readjust to everyday life.
Alcohol Dementia Recovery
The alcohol dementia prognosis shows that, it takes about two years for the person to completely recover from alcohol dementia. Studies have shown half of the people make partial alcohol dementia recovery and require support to help manage their lives. A quarter of affected people have shown total alcohol dementia recovery and the other remaining quarter do not make any kind of recovery.
Alcohol can lead to many harmful effects on your body like liver cirrhosis, damage to the nerves of legs and arms, epileptic seizures, heart disease, etc. Alcohol makes you prone to accidents that may result in severe head and body injuries. The nerve cells in the brain cells are damaged that affect your abilities to do things. There are many more ill effects of excessive use of alcohol over a long period of time. To prevent the health problems caused by alcohol and alcohol dementia syndrome, you can always approach alcohol rehabilitation centers to help you overcome alcohol addiction. I hope this article on alcohol dementia prognosis has helped clear your doubts regarding alcohol induced dementia.
Source: Mayo Foundation for Medical Education and Research
Also in this section
- The power of music to help dementia patients
- Genetic markers linking risk for type 2 diabetes and Alzheimer’s identified
- A Blood Test for Mental Illness in Women?
- Alzheimer’s disease works differently in patients with and without Down syndrome
- High blood pressure linked to reduced Alzheimer’s risk, meds may be reason
- Drug discovery for Parkinson’s disease: LCSB researchers grow neurons in 3-D
- Atlas of older brains could help diagnosis of Alzheimer’s disease
- CBT Feasible, Effective for Anxiety in Dementia
- Lack of evidence on how to care for hip fracture patients with dementia
- Molecular modeling of novel potent agents for treating Alzheimer’s disease
- Poor sleep linked to toxic buildup of Alzheimer’s protein, memory loss
- New insights could result in changes to the therapeutic strategy to combat Alzheimer’s