Conditions that require Frail care

Dementia is not a specific disease. It's an overall term that describes a wide range of symptoms associated with a decline in memory or other thinking skills severe enough to reduce a person's ability to perform everyday activities.
Alzheimer's disease accounts for 60 - 80 percent of cases. Vascular dementia, which occurs after a stroke, is the second most common dementia type. But there many other conditions that can cause symptoms of dementia, including some that are reversible , such as thyroid problems and vitamin deficiencies.
Dementia is often incorrectly referred to as 'senility' or 'senile dementia', which reflects the formerly widespread but incorrect belief that serious mental decline is a normal part of aging. Frail care assistance is important for people who suffer from dementia.

While symptoms of dementia can vary greatly, at least two of the following core mental functions must be signigicantly impaired to be considered dementia:

People with dementia may have problems with short-term memory, keeping track of a purse or wallet, paying bills, planning and preparing meals, remembering appointments or traveling out of the neighborhood.
Many dementias are progressive, meaning symptoms start out slowly and gradually get worse. If you or a loved one is experiencing memory difficulties or other changes in thinking skills, don't ignore them. See a doctor soon to determine the cause. Professional evaluation may detect a treatable condition.

Dementia is caused by damage to brain cells. This damage interferes with the ability of brain cells to communicate with each other. When brain cells cannot communicate normally, thinking, behavior and feelings can be affected.
The brain has many distinct regions, each of which is responsible for different functions (for example, memory, judgment and movement). When cells in a particular region are damaged, that region cannot carry out its functions normally.
Different types of dementia are associated with particular types of brain cell damage in particular regions of the brain. For example, in Alzheimer's disease, high levels of certain proteins inside and outside brain cells make it hard for brain cells to stay healthy and to communicate with each other. The brain region called the hippocampus is the center of learning and memory in the brain, and the brain cells in this region are often the first to be damaged. That's why memory loss is often one of the earliest symptoms of Alzheimer's.
While most changes in the brain that cause dementia are permanent and worsen over time, thinking and memory problems caused by the following conditions may improve when the condition is treated or addressed:

There is no one test to determine if someone has dementia. Doctors diagnose Alzheimer's and other types of dementia based on a careful medical history, a physical examination, laboratory tests, and the characteristic changes in thinking, day-to-day function and behavior associated with each type. Doctors can determine that a person has dementia with a high level of certainty. But it's harder to determine the exact type of dementia because the symptoms and brain changes of different dementias can overlap. In some cases, a doctor may diagnose ``dementia`` and not specify a type. If this occurs it may be necessary to see a specialist such as a neurologist or gero-psychologist.

The most common early symptom of Alzheimer's is difficulty remembering newly learned information. Just like the rest of our bodies, our brains change as we age. Most of us eventually notice some slowed thinking and occasional problems with remembering certain things. However, serious memory loss, confusion and other major changes in the way our minds work may be a sign that brain cells are failing.
The most common early symptom of Alzheimer's is difficulty remembering newly learned information because Alzheimer's changes typically begin in the part of the brain that affects learning. As Alzheimer's advances through the brain it leads to increasingly severe symptoms, including disorientation, mood and behavior changes; deepening confusion about events, time and place; unfounded suspicions about family, friends and professional caregivers; more serious memory loss and behavior changes; and difficulty speaking, swallowing and walking.
People with memory loss or other possible signs of Alzheimer's may find it hard to recognize they have a problem. Signs of dementia may be more obvious to family members or friends.

Microscopic changes in the brain begin long before the first signs of memory loss.
The brain has 100 billion nerve cells (neurons). Each nerve cell connects with many others to form communication networks. Groups of nerve cells have special jobs. Some are involved in thinking, learning and remembering. Others help us see, hear and smell.
To do their work, brain cells operate like tiny factories. They receive supplies, generate energy, construct equipment and get rid of waste. Cells also process and store information and communicate with other cells. Keeping everything running requires coordination as well as large amounts of fuel and oxygen.
Scientists believe Alzheimer's disease prevents parts of a cell's factory from running well. They are not sure where the trouble starts. But just like a real factory, backups and breakdowns in one system cause problems in other areas. As damage spreads, cells lose their ability to do their jobs and, eventually die, causing irreversible changes in the brain.

Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells.
Plaques are deposits of a protein fragment called beta-amyloid (BAY-tuh AM-uh-loyd) that build up in the spaces between nerve cells.
Tangles are twisted fibers of another protein called tau (rhymes with “wow”) that build up inside cells.
Though autopsy studies show that most people develop some plaques and tangles as they age, those with Alzheimer’s tend to develop far more and in a predictable pattern, beginning in the areas important for memory before spreading to other regions.
Scientists do not know exactly what role plaques and tangles play in Alzheimer's disease. Most experts believe they somehow play a critical role in blocking communication among nerve cells and disrupting processes that cells need to survive.
It's the destruction and death of nerve cells that causes memory failure, personality changes, problems carrying out daily activities and other symptoms of Alzheimer's disease.

Today, Alzheimer's is at the forefront of biomedical research.
Researchers are working to uncover as many aspects of Alzheimer's disease and related dementias as possible. Ninety percent of what we know about Alzheimer's has been discovered in the last 20 years. Some of the most remarkable progress has shed light on how Alzheimer's affects the brain. The hope is this better understanding will lead to new treatments. Many potential approaches are currently under investigation worldwide.

Inadequate blood flow can damage and eventually kill cells anywhere in the body. The brain has one of the body's richest networks of blood vessels and is especially vulnerable.
In vascular dementia, changes in thinking skills sometimes occur suddenly following strokes that block major brain blood vessels. Thinking problems also may begin as mild changes that worsen gradually as a result of multiple minor strokes or other conditions that affect smaller blood vessels, leading to cumulative damage. A growing number of experts prefer the term ``vascular cognitive impairment (VCI)`` to ``vascular dementia`` because they feel it better expresses the concept that vascular thinking changes can range from mild to severe.
Vascular brain changes often coexist with changes linked to other types of dementia, including Alzheimer's disease and dementia with Lewy bodies. Several studies have found that vascular changes and other brain abnormalities may interact in ways that increase the likelihood of dementia diagnosis.
Vascular dementia is widely considered the second most common cause of dementia after Alzheimer's disease, accounting for 10 percent of cases. Many experts believe that vascular dementia remains underdiagnosed — like Alzheimer's disease — even though it's recognized as common.

Symptoms can vary widely, depending on the severity of the blood vessel damage and the part of the brain affected. Memory loss may or may not be a significant symptom depending on the specific brain areas where blood flow is reduced.
Vascular dementia symptoms may be most obvious when they happen soon after a major stroke. Sudden post-stroke changes in thinking and perception may include:

These changes may happen at the same time as more familiar physical stroke symptoms, such as a sudden headache, difficulty walking, or numbness or paralysis on one side of the face or the body.
Multiple small strokes or other conditions that affect blood vessels and nerve fibers deep inside the brain may cause more gradual thinking changes as damage accumulates. Common early signs of widespread small vessel disease include impaired planning and judgment; uncontrolled laughing and crying; declining ability to pay attention; impaired function in social situations; and difficulty finding the right words.

Because vascular cognitive impairment may often go unrecognized, many experts recommend professional screening with brief tests to assess memory, thinking and reasoning for everyone considered to be at high risk for this disorder. Individuals at highest risk include those who have had a stroke or a transient ischemic attack (TIA, also known as a ``ministroke``). Additional high-risk groups include those with high blood pressure, high cholesterol, or other risk factors for heart or blood vessel disease.
Professional screening for depression is also recommended for high-risk groups. Depression commonly coexists with brain vascular disease and can contribute to cognitive symptoms.
If brief screening tests suggest changes in thinking or reasoning, a more detailed assessment is needed. Core elements of a workup for vascular dementia typically include:

According to a 2011 scientific statement issued by the American Heart Association (AHA) and the American Stroke Association (ASA), and endorsed by the Alzheimer's Association and the American Academy of Neurology (AAN), the following three criteria suggest the greatest likelihood that mild cognitive impairement (MCI) or dementia is caused by vascular changes:

As with Alzheimer's disease, advancing age is a major risk factor for vascular cognitive impairment or dementia.
Additional risk factors are the same ones that raise risk for heart problems, stroke and other diseases that affect blood vessels. Many of these vascular factors also raise risk for Alzheimer's. The following strategies may reduce your risk of diseases that affect your heart and blood vessels — and also may help protect your brain:

Most experts estimate that dementia with Lewy bodies is the third most common cause of dementia after Alzheimer's disease and vascular dementia, accounting for 10 to 25 percent of cases.
The hallmark brain abnormalities linked to DLB are named after Frederich H. Lewy, M.D., the neurologist who discovered them while working in Dr. Alois Alzheimer's laboratory during the early 1900s. Alpha-synuclein protein, the chief component of Lewy bodies, is found widely in the brain, but its normal function isn't yet known.
Lewy bodies are also found in other brain disorders, including Alzheimer's disease and Parkinson's disease dementia. Many people with Parkinson's eventually develop problems with thinking and reasoning, and many people with DLB experience movement symptoms, such as hunched posture, rigid muscles, a shuffling walk and trouble initiating movement.
This overlap in symptoms and other evidence suggest that DLB, Parkinson's disease and Parkinson's disease dementia may be linked to the same underlying abnormalities in how the brain processes the protein alpha-synuclein. Many people with both DLB and Parkinson's dementia also have plaques and tangles — hallmark brain changes linked to Alzheimer's disease.

Symptoms of dementia with Lewy bodies include:

As with other types of dementia there is no single test that can conclusively diagnose dementia with Lewy bodies. Today, DLB is a ``clinical`` diagnosis, which means it represents a doctor's best professional judgment about the reason for a person's symptoms. The only way to conclusively diagnose DLB is through a postmortem autopsy.
Many experts now believe that DLB and Parkinson's disease dementia are two different expressions of the same underlying problems with brain processing of the protein alpha-synuclein. But most experts recommend continuing to diagnose DLB and Parkinson's dementia as separate disorders.
The diagnosis is DLB when:

There are no treatments that can slow or stop the brain cell damage caused by dementia with Lewy bodies. Current strategies focus on helping symptoms.
If your treatment plan includes medications, it's important to work closely with your physician to identify the drugs that work best for you and the most effective doses. Treatment considerations involving medications include the following issues:

The brain changes caused by Parkinson's disease begin in a region that plays a key role in movement. As Parkinson's brain changes gradually spread, they often begin to affect mental functions, including memory and the ability to pay attention, make sound judgments and plan the steps needed to complete a task.
The key brain changes linked to Parkinson's disease and Parkinson's disease dementia are abnormal microscopic deposits composed chiefly of alpha-synuclein, a protein that's found widely in the brain but whose normal function isn't yet known. The deposits are called ``Lewy bodies``.
Lewy bodies are also found in several other brain disorders, including dementia with Lewy bodies (DLB). Evidence suggests that dementia with Lewy bodies, Parkinson's disease and Parkinson's disease dementia may be linked to the same underlying abnormalities in brain processing of alpha-synuclein.
Another complicating factor is that many people with both dementia with Lewy bodies and Parkinson's disease dementia also have plaques and tangles — hallmark brain changes linked to Alzheimer's disease.
Parkinson's disease is a fairly common neurological disorder in older adults, estimated to affect nearly 2 percent of those older than age 65. The National Parkinson Foundation estimates that 1 million Americans have Parkinson's disease. It is estimated that 50 to 80 percent of those with Parkinson's disease eventually experience Parkinson's disease dementia.

Symptoms of dementia with Lewy bodies include:

As with other types of dementia there is no single test that can conclusively diagnose dementia with Lewy bodies. Today, DLB is a ``clinical`` diagnosis, which means it represents a doctor's best professional judgment about the reason for a person's symptoms. The only way to conclusively diagnose DLB is through a postmortem autopsy.
Many experts now believe that DLB and Parkinson's disease dementia are two different expressions of the same underlying problems with brain processing of the protein alpha-synuclein. But most experts recommend continuing to diagnose DLB and Parkinson's dementia as separate disorders.
The diagnosis is DLB when:

The nerve cell damage caused by frontotemporal dementia leads to loss of function in these brain regions, which variably cause deterioration in behavior and personality, language disturbances, or alterations in muscle or motor functions.
There are a number of different diseases that cause frontotemporal degenerations. The two most prominent are 1) a group of brain disorders involving the protein tau and 2) a group of brain disorders involving the protein called TDP43. For reasons that are not yet known, these two groups have a preference for the frontal and temporal lobes that cause dementia.
The disorders grouped under FTD fall into three subtypes.
FTD used to be called Pick's disease after Arnold Pick, a physician who in 1892 first described a patient with distinct symptoms affecting language. Some doctors still use the term ``Pick's disease.`` Other terms you may see used to describe FTD include frontotemporal disorders, frontotemporal degenerations and frontal lobe disorders.

Behavior variant frontotemporal dementia (bvFTD). This condition is characterized by prominent changes in personality, interpersonal relationships and conduct that often occur in people in their 50s and 60s, but can develop as early as their 20s or as late as their 80s. In bvFTD, the nerve cell loss is most prominent in areas that control conduct, judgment, empathy and foresight, among other abilities.Primary progressive aphasia (PPA). This is the second major form of frontotemporal degeneration that affects language skills, speaking, writing and comprehension. PPA normally comes on in midlife, before age 65, but can occur in late life also. The two most distinctive forms of PPA have somewhat different symptoms:

Disturbances of motor (movement or muscle) function. There are three disorders that are a part of the frontotemporal degeneration spectrum that produce changes in muscle or motor functions with or without behavior (bvFTD) or language (PPA) problems.

Both bvFTD and PPA are far less common than Alzheimer’s disease in those over age 65 years. However, in the 45 to 65 age range, bvFTD and PPA are nearly as common as younger-onset Alzheimer’s. Only rough estimates are available, but there may be 50,000 to 60,000 people with bvFTD and PPA in the United States, the majority of whom are between 45 and 65 years of age.

The diagnosis of bvFTD and PPA are based on expert evaluation by a doctor who is familiar with these disorders. The type of problems experienced by the patient and the results of neurological exams are the core of the diagnosis. Brain scans such as magnetic resonance imaging (MRI) and glucose positron emission scans are very helpful additional tests, but they must be interpreted in the context of the patient’s history and neurological exam.

Prion diseases, such as Creutzfeldt-Jakob disease (CJD), occur when prion protein, which is found throughout the body but whose normal function isn't yet known, begins folding into an abnormal three-dimensional shape. This shape change gradually triggers prion protein in the brain to fold into the same abnormal shape.
Through a process scientists don't yet understand, misfolded prion protein destroys brain cells. Resulting damage leads to rapid decline in thinking and reasoning as well as involuntary muscle movements, confusion, difficulty walking and mood changes.
CJD is rare, occurring in about one in 1 million people annually worldwide.

Specific Creutzfeldt-Jakob disease symptoms experienced by an individual and the order in which they appear can differ significantly. Some common symptoms include:

Rapid symptom progression is one of the most important clues that a person may have Creutzfeldt-Jakob disease.
There is no single test — or any combination of tests — that can conclusively diagnose sporadic CJD in a living person, but the following tests may help determine whether an individual has CJD:

Sporadic Creutzfeldt-Jakob disease has no known cause. Most scientists believe the disease begins when prion protein somewhere in the brain spontaneously misfolds, triggering a ``domino effect`` that misfolds prion protein throughout the brain. Genetic variation in the prion protein gene may affect risk of this spontaneous misfolding.Mutations in the prion protein gene also may play a yet-to-be-determined role in making people susceptible to acquired CJD from external sources. Scientists don't yet know the why acquired CJD seems to be transmitted through such a limited number of external sources. Researchers have found no evidence that the abnormal protein is commonly transmitted through sexual activity or blood transfusions.
Familial CJD is caused by variations in the prion protein gene that increases the risk of an individual developing CJD. Researchers have identified more than 50 prion protein mutations in those with inherited CJD. Genetic testing can determine whether family members at risk have inherited a CJD-causing mutation. Experts strongly recommend professional genetic counseling both before and after genetic testing for hereditary CJD.

Normal pressure hydrocephalus occurs when excess cerebrospinal fluid accumulates in the brain's ventricles, which are hollow fluid-filled chambers. NPH is called ``normal pressure`` because despite the excess fluid, cerebrospinal fluid pressure as measured during a spinal tap is often normal. As brain ventricles enlarge with the excess cerebrospinal fluid, they can disrupt and damage nearby brain tissue, causing symptoms of NPH.
NPH primarily affects people in their 60s and 70s. Scientists aren't certain how many older adults have this disorder because common symptoms of NPH are also common in other brain disorders.

There is no single test to determine if someone has normal pressure hydrocephalus. And even though the three hallmark symptoms listed above are considered the ``classic`` signs of this disorder, not everyone with NPH has all of these symptoms.
Brain imaging to detect enlargement of the ventricles, often with magnetic resonance imaging (MRI), plays a key role in diagnosing NPH. Several brain disorders, including Alzheimer's disease, can cause overall brain tissue shrinkage that makes the ventricles look larger than normal. In NPH, although the ventricles are enlarged, brain tissue may not appear shrunken.
Because the symptoms of NPH may overlap with those of Alzheimer's and other dementias, experts recommend that a person with suspected NPH undergo examination by a neurologist with extensive experience evaluating brain disorders that affect movement, thinking skills and physical functions.
If symptoms and an MRI strongly suggest NPH, a large-volume spinal tap may be used to identify those who may benefit from a shunt. In this procedure, doctors remove a larger-than-usual amount of spinal fluid, and then observe the person for 30 to 60 minutes to note any improvements in walking or thinking and reasoning. Most people originally suspected of having NPH do not improve following a CSF removal test.

In some cases, normal pressure hydrocephalus is caused by other brain disorders such as hemorrhages, infections or inflammation. But in most cases, the fluid buildup happens for unknown reasons.

Researchers have not found effective nonsurgical treatments for normal pressure hydrocephalus. Drugs that remove excess fluid throughout the body, such as diuretics, haven't been shown to help. Sign up for our enews to receive updates about Alzheimer’s and dementia care and research.
NPH can sometimes be treated with surgical insertion of a shunt, a long, thin tube that drains excess CSF from the brain to the abdomen. Difficulty walking is the symptom most likely to improve after surgery. Thinking changes and bladder control are less likely to get better. Shunting doesn't help everyone with NPH, and there's uncertainty about how best to identify those most likely to benefit.
More research is needed to:

The effectiveness of shunting in NPH has never been demonstrated in a randomized clinical trial. Most of these studies were small and followed people for a limited time. Available data suggest that difficulty walking is the symptom most likely to improve. Several studies found a significant rate of postsurgical complications. Findings also showed that short-term benefits of shunt insertion tended to decline over time.

Huntington's disease is a progressive brain disorder caused by a single defective gene on chromosome 4 — one of the 23 human chromosomes that carry a person’s entire genetic code.
This defect is ``dominant,`` meaning that anyone who inherits it from a parent with Huntington's will eventually develop the disease. The disorder is named for George Huntington, the physician who first described it in the late 1800s.
The defective gene codes the blueprint for a protein called huntingtin. This protein's normal function isn't yet known, but it's called ``huntingtin`` because scientists identified its defective form as the cause of Huntington's disease. Defective huntingtin protein leads to brain changes that cause abnormal involuntary movements, a severe decline in thinking and reasoning skills, and irritability, depression and other mood changes.

Symptoms of Huntington's disease usually develop between ages 30 and 50, but they can appear as early as age 2 or as late as 80. The hallmark symptom of Huntington's disease is uncontrolled movement of the arms, legs, head, face and upper body. Huntington's disease also causes a decline in thinking and reasoning skills, including memory, concentration, judgment and ability to plan and organize.
Huntington's disease brain changes lead to alterations in mood, especially depression, anxiety, and uncharacteristic anger and irritability. Another common symptom is obsessive-compulsive behavior, leading a person to repeat the same question or activity over and over.

Scientists identified the defective gene that causes Huntington's disease in 1993. A diagnostic genetic test is now available.The test can confirm that the defective gene for huntingtin protein is the cause of symptoms in people with suspected Huntington's disease and can detect the defective gene in people who don't yet have symptoms but are at risk because a parent has Huntington's.

The defective gene identified in 1993 causes virtually all Huntington’s disease.
The huntingtin gene defect involves extra repeats of one specific chemical code in one small section of chromosome 4. The normal huntingtin gene includes 17 to 20 repetitions of this code among its total of more than 3,100 codes. The defect that causes Huntington's disease includes 40 or more repeats. Genetic tests for Huntington's disease measure the number of repeats present in an individual's huntington protein gene.
Scientists don't yet understand the normal function of huntingtin protein or how a few dozen extra repeats in its genetic blueprint lead to the devastating symptoms of Huntington's disease. Researchers are eager to solve these mysteries to find the answer to Huntington's. These solutions also may offer important insights into a wide range of other brain disorders, including Alzheimer's, Parkinson'sdisease and amyotrophic lateral sclerosis (ALS).

There is currently no cure for Huntington's disease and no way to slow or stop the brain changes it causes. Treatments focus on managing symptoms. A group of international experts recommended the following treatments as first-line strategies for three of the disease's most troubling symptoms:

Other Huntington's symptoms, such as anxiety, depression and insomnia, also should be treated according to generally accepted guidelines and benefit greatly from frail care assistance. Experts encourage people with Huntington's to keep all their medical appointments and not to get discouraged if it takes their health care team some time to find the best drugs and the most effective doses.

Thiamine (vitamin B-1) helps brain cells produce energy from sugar. When levels fall too low, brain cells cannot generate enough energy to function properly. As a result, Korsakoff syndrome may develop.
Korsakoff syndrome is most commonly caused by alcohol misuse, but can also be associated with AIDS, chronic infections, poor nutrition and certain other conditions. See causes and risks below.
Korsakoff syndrome is often, but not always, preceded by an episode of Wernicke encephalopathy, which is an acute brain reaction to severe lack of thiamine. Wernicke encephalopathy is a medical emergency that causes life-threatening brain disruption, confusion, staggering and stumbling, lack of coordination, and abnormal involuntary eye movements.
Because the chronic memory loss of Korsakoff syndrome often follows an episode of Wernicke encephalopathy, the chronic disorder is sometimes known as Wernicke-Korsakoff syndrome. But Korsakoff syndrome can also develop in individuals who have not had a prior episode of Wernicke encephalopathy. We recommend frail care assistance to people who suffer from this ailment.

Korsakoff syndrome causes problems learning new information, inability to remember recent events and long-term memory gaps. Memory problems may be strikingly severe while other thinking and social skills are relatively unaffected. For example, individuals may seem able to carry on a coherent conversation, but moments later be unable to recall that the conversation took place or to whom they spoke.Those with Korsakoff syndrome may ``confabulate,`` or make up, information they can't remember. They are not ``lying`` but may actually believe their invented explanations. Scientists don't yet understand why Korsakoff syndrome may cause confabulation.

Korsakoff syndrome is a clinical diagnosis representing a physician's best judgment about the cause of a person's symptoms. There are no specific lab tests or brain scan procedures to confirm that a person has this disorder. The syndrome may sometimes be hard to identify because it may be masked by symptoms of other conditions common among those who misuse alcohol, including intoxication or withdrawal, infection or head injury.
Experts recommend that a medical workup for memory loss or other cognitive changes always include questions about an individual's alcohol use. Anyone admitted to the hospital for an alcohol-related condition should be professionally screened for memory loss and cognitive change.

Scientists don't yet know exactly how Korsakoff syndrome damages the brain. Research has shown that severe thiamine deficiency disrupts several biochemicals that play key roles in carrying signals among brain cells and in storing and retrieving memories. These disruptions destroy brain cells and cause widespread microscopic bleeding and scar tissue.
Most cases of Korsakoff syndrome result from alcohol misuse. Scientists don't yet know why heavy drinking causes severe thiamine deficiency in some alcoholics, while others may be affected primarily by alcohol's effects on the liver, stomach, heart, intestines or other body systems.
Researchers have identified several genetic variations that may increase susceptibility to Korsakoff syndrome. Poor nutrition also may raise risk. Sign up for our enews to receive updates about Alzheimer’s and dementia care and research.
Korsakoff syndrome also can be caused by anorexia, overly-stringent dieting, fasting, starvation or weight-loss surgery; uncontrolled vomiting; AIDS; kidney dialysis; chronic infection; or cancer that has spread throughout the body.

Some experts recommend that heavy drinkers and others at risk of thiamine deficiency take oral supplements of thiamine and other vitamins under their doctor's supervision.
Many experts also recommend that anyone with a history of heavy alcohol use who experiences symptoms associated with Wernicke encephalopathy be given injectable thiamine until the clinical picture grows clearer.
Once acute symptoms improve, individuals should be carefully evaluated to determine if their medical history, alcohol use and pattern of memory problems may be consistent with Korsakoff syndrome. For those who develop Korsakoff syndrome, extended treatment with oral thiamine, other vitamins and magnesium may increase chances of symptom improvement. Giving up alcohol is also an effective treatment.
In those who develop Korsakoff syndrome, with or without a preceding episode of Wernicke encephalopathy, there are few studies on long-term outcomes. Available data suggest that about 25 percent of those who develop Korsakoff syndrome eventually recover, about half improve but don't recover completely, and about 25 percent remain unchanged. Some research suggests that those who recover from an episode may have a normal life expectancy if they abstain from alcohol.