Frequently Asked Questions

What is Dementia?
What is Alzheimer's disease?
What is Vascular Dementia?
What is Dementia with Lewy Bodies?
What is Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)?
What is Parkinson's Disease?
What is Normal Pressure Hydrocephalus (NPH)?
What is Frontotemporal Dementia?
What is Wernicke-Korsakoff Syndrome (Alcohol-Related Dementia)?
What is Progressive Supranuclear Palsy (PSP)?

What is Dementia?

Many different conditions and diseases cause dementia. The term "dementia" is used loosely to describe severe memory loss and impairment in other thinking (or "cognitive") abilities that interfere with the individual's daily life and social interactions.

Dementia refers to global impairment in cognitive and functional abilities. The word "cognitive" refers to thinking abilities and the word "functional" refers to one's ability to do things. People with dementia often have serious problems with memory. In particular, they have trouble forming new memories. Other aspects of thinking are also frequently impaired. For example, persons with dementia may have trouble with language, such as having difficulty comprehending what others say, or they may have trouble with names of peoples and things or their sentences may not always make good sense. They may have trouble with calculations, with attention, and with planning and organizing their behavior. These memory and other thinking problems affect the person's ability to perform everyday activities.

What is Alzheimer's disease?

Alzheimer's disease (AD) is a specific type of dementia. It is a progressive, degenerative disease that causes slow decline of nerve cells in the brain. Individuals with Alzheimer's disease experience progressive and irreversible loss in thinking abilities, including language and memory. Changes are also witnessed in mood, personality, sleepo-wake cycles, and behavior. In AD nerve cells involved in learning and short-term memory are affected early which is the reason memory loss is an early symptoms of Alzheimer's disease. More info on Alzheimer's Disease .

What is Vascular Dementia?

While Alzheimer’s disease is the most common type of dementia, the second most common type of dementia is vascular dementia. Vascular dementia is associated with problems in the circulation of blood to the brain (cerebrovascular disease). Risk factors for this type of dementia include: high blood pressure, diabetes mellitus, high cholesterol, history of transient ischemic attacks (TIA), heart rhythm abnormalities, and evidence of disease in arteries elsewhere in the body.

Vascular dementia is a disease that occurs when cells in the brain are deprived of oxygen. The brain is supplied with oxygen by a network of blood vessels called the vascular system. If there is a blockage in the vascular system, or if it is diseased, blood, and consequently, oxygen is prevented from reaching the brain. As a result, cells in the brain die, leading to the symptoms of dementia. Vascular disease is associated with many risk factors, including lifestyle, diet, consumption of alcohol and tobacco, and heredity. Individuals with high blood pressure, a high level of fats in their blood, and diabetes are at particular risk for developing vascular disease. Vascular dementia may be caused by stroke, by multiple small strokes, or Binswanger's disease (characterized by damage to small blood vessels in white matter of the brain). Symptoms of vascular dementia may include memory loss, difficulties in communicating, and eventually a loss of physical abilities as the disease progresses. Currently there is no way to reverse damage to the brain caused by vascular dementia. Depending on the severity of damage, however, it is possible to limit or delay the severity of decline. People who have been diagnosed with vascular dementia will be treated for the specific disease that has caused the condition. For instance, medications to control blood pressure and prevent blood clotting may be prescribed to individuals who have vascular dementia due to stroke. However, only symptomatic treatment is available for patients with vascular dementia due to diseases such as Binswanger's disease, which is slowly progressive and has no cure. For such individuals, life expectancy is typically no more than 5 years aft er onset.

As in Alzheimer s disease, research efforts in vascular dementia are currently being conducted at a wide array of institutions, including national research facilities and universities. The NINDS, National Institute on Aging, and the National Institute of Mental Health are among the national organizations that support research on vascular dementia.

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What is Dementia with Lewy Bodies?

Dementia with Lewy bodies (DLB) is the second most frequent cause of dementia in elderly adults and is associated with the presence of abnormal structures (Lewy bodies) in nerve cells in certain brain regions. Because these structures and many of the symptoms of dementia with Lewy bodies are associated with both Parkinson's and Alzheimer's diseases, researchers do not yet understand whether dementia with Lewy bodies is a distinct clinical entity or perhaps a variant of Alzheimer's or Parkinson's disease. Symptoms of DLB may include typical features of Parkinson s disease such as loss of spontaneous movement (bradykinesia), rigidity (muscles feel stiff and resist movement), tremor, and shuffling gait. Other symptoms may resemble those of Alzheimer's disease, such as acute confusion, loss of memory, and impaired cognition. New onset of visual hallucinations may be an early sign of DBL, and patients may suffer from other psychiatric disturbances such as delusions and depression. Onset of the disorder usually occurs in older adults, although younger people can be affected as well, and there is a progressive deterioration over time.

Currently there is no cure for DLB. Treatments are aimed at controlling symptoms, often involving the use of medication to control behaviors associated with Parkinson's and psychiatric disorders. Patients should be aware that medication designed to control Parkinson's symptoms may help to reduce tremor and loss of muscle movement but at the same time can potentially worsen such symptoms as hallucinations and delusions. Conversely, neuroleptic drugs prescribed for psychiatric symptoms may in fact markedly worsen tremor or other movement symptoms.

Research efforts related to dementia with Lewy bodies are underway at several locations, including the NINDS. These efforts include basic investigations of Lewy bodies aimed at understanding the biological consequences of Lewy body formation and the mechanisms of disease progression. Knowledge gained by such basic research provides the necessary foundation for future clinical research.

What is Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL)?

CADASIL is a genetic form of subcortical vascular dementia. [Visit our CADASIL Section for more information]

What is Parkinson's Disease?

Parkinson's disease (PD) is a progressive, neurological disease that mainly affects movement. Parkinson's disease results from the destruction of nerve cells in a part of the brain called the basal ganglia. Different parts of the brain work together by sending signals to each other to coordinate all of our thoughts, movements, emotions, and senses. When we want to move, a signal is relayed between different parts of the brain using chemicals.

A chemical (neurotransmitter) called dopamine is produced in a group of cells called the substantia nigra and is essential for normal movement. When the cells die they can no longer produce and send dopamine so the signal to move doesn't get communicated. Another chemical in the brain, acetylcholine, is balanced by dopamine. When there is not enough dopamine, there is too much acetylcholine, causing the tremors and muscle stiffness that many people with PD experience.

It is estimated that 500,000 to 1,500,000 people in the US have Parkinson s with 50,000 new cases reported annually. Parkinson's is more common in people 60 years old and older. However, some people begin to show symptoms before they are 40 years old.

The primary symptoms of Parkinson's disease are: rigidity or stiffness, tremor, slow movement (bradykinesia), loss of movement (akinesia), balance and walking problems ( shuffling gait), and stooped posture. People with Parkinson's may also develop some of the following symptoms: Depression, memory problems, mental confusion, and/or dementia. Speech problems, swallowing problems, restlessness, eyelid closure, difficulty writing, skin problems, anxiety, urinary tract infections, excessive sweating, lack of facial expression, sexual problems, and sleep disorders are other symptoms that could manifest from Parkinson s disease. All persons with PD do not develop the same symptoms. These symptoms change over time as the disease progresses. About 25% of all patients with PD develop dementia.

Although there are no specific tests for PD, there are several ways to make a diagnosis. Usually a diagnosis is based on a neurological exam that covers the evaluation of symptoms and their severity. If symptoms are severe enough, a trial test of anti-Parkinson's drugs such as levod combined with anticholinergic agents may be used. Brain scans (MRI or CT) may be made to rule out other disease whose symptoms resemble PD. Symptoms usually affect one side of the body more than the other. Diagnosis of Parkinson s disease requires the presence of at least two of the primary symptoms listed above.

Parkinson's disease has the following five stages:

Stage I: Symptoms are only on one side of the body
Stage II: Symptoms are on both sides of the body
Stage III: Balance is impaired
Stage IV: Assistance is required to walk and other symptoms are severe
Stage V: Wheelchair bound

What is Normal Pressure Hydrocephalus (NPH)?

NPH is a type of hydrocephalus that occurs mostly in older adults. Hydrocephalus is an abnormal (excessive) accumulation of fluid in the head. The fluid is called cerebrospinal fluid, commonly referred to as CSF. The CSF is located and produced within cavities of the brain called ventricles. The function of CSF is to cushion the delicate brain and spinal cord tissue from injuries and maintain proper balance of nutrients around the central nervous system. Normally, the bloodstream absorbs most of the CSF produced on a daily basis. Every day your body produces a certain amount of CSF and that same amount of CSF is absorbed in the brain. When an imbalance occurs, an excess of CSF fluid builds up resulting in the condition known as hydrocephalus. The excess fluid buildup causes the ventricles to expand. Left untreated, hydrocephalus will create increased intracranial pressure (increased pressure in the head) and may result in increased symptoms or brain damage.

A major difference between most types of hydrocephalus and NPH is that in NPH the excess CSF buildup might not be associated with a large increase in intracranial pressure. In NPH, the abnormal accumulation of CSF, causing enlarged ventricles, is thought to stretch the nerve tissue of the brain causing a triad of symptoms including dementia, gait instability (difficulty walking, possibly with falls), and urinary incontinence. NPH normally occurs in adults 60-years-old and older, and in as many as 10% of all patients with symptoms of dementia.

For most patients the cause of NPH cannot be determined. In some cases, history of previous brain injury or surgery can result in hydrocephalus. Examples are brain hemorrhage, aneurysm, trauma, tumors or cysts, infections or subdural hematomas. In other cases, the imbalance in the production or absorption of CSF causes the hydrocephalus.

Diagnosis of NPH is often difficult due to the symptoms being similar to other disorders. In many cases the NPH is thought to be mild dementia, Alzheimer's, Parkinson's or simply old age factors. Many cases go completely unrecognized and are never treated. Diagnostic procedures for normal pressure hydrocephalus may include one or more of these tests: ultrasound, computerized tomography (CT), magnetic resonance imaging (MRI), lumbar puncture or tap, continuous lumbar CSF drainage, intracranial pressure monitoring, measurement of cerebrospinal fluid outflow resistance or isotopic cisternography, and neuropsychological testing.

The treatment of choice for patients who show a positive response to a lumbar tap is surgical placement of a shunt. A shunt is an implantable device designed to drain CSF fluid away from the brain thereby allowing the enlarged ventricles to return to a normal state. As CSF fluid builds and the pressure in the ventricle increases, a one-way valve in the shunt opens, and the excess CSF fluid drains into the abdomen where it is easily absorbed. This technique is very effective in improving the troubling symptoms of NPH. Once the diagnosis of NPH is suspected there is no single perfect test to determine if a patient will respond to the shunt.

Visit All About NPH and the Hydrocephalus Association for more information.

What is Frontotemporal Dementia?

Frontotemporal Dementia (FTD) is a form of dementia characterized by a slowly progressive deterioration of social skills and changes in personality, along with impairment of intellect, memory, and language. Pick's disease is a form of FTD in which abnormal structures called Pick bodies are found in the nerve cells in the brain's frontal and temporal lobes. Although FTD varies greatly in the way it affects individuals, there is a common core of symptoms that may be present at different stages of the disease. These symptoms include loss of memory, lack of spontaneity, difficulty in thinking or concentrating, and disturbances of speech. Other symptoms include gradual emotional dullness, loss of moral judgment, and progressive dementia. Some individuals become disinhibited. Although the disease usually affects individuals between the ages of 40 and 60, the age of onset may range from 20 to 80.

Patients with FTD typically have atrophy of the frontal and temporal lobes of the brain. Some nerve cells have characteristic abnormalities (i.e, Pick bodies) when viewed under a microscope. The cause of the disease is unknown. Currently, there is no cure or specific treatment for FTD. Its progression cannot be slowed and there is an inevitable progressive deterioration. However, some of the symptoms of the disease may be treated effectively. The length of progression varies, ranging from less than 2 years in some to more than 10 years in others. Death is usually caused by infection.

Research on the causes, prevention, and treatment of FTD is currently underway at several facilities. The National Institute of Neurological Disorders and Stroke is conducting a pathogenetic study of patients with Pick's Disease. The study involves functional brain imaging with positron emission tomography (PET) and experimental interventions. The National Institute on Aging also conducts research relevant to Pick's disease.

What is Wernicke-Korsakoff Syndrome (Alcohol-Related Dementia)?

Wernicke-Korsakoff Syndrome (WKS) is a neurological disorder. WKS is caused by a deficiency in the B vitamin, thiamine. Thiamine plays a role in metabolizing glucose to produce energy for the brain. An absence of thiamine therefore results in an inadequate supply of energy to the brain, particularly the hypothalamus (which regulates body temperature, growth and appetite and has a role in emotional response. It also controls pituitary functions that affect metabolism and hormones) and mammillary bodies (where neural pathways connect various parts of the brain involved in memory functions). The disease is typically associated with chronic alcoholism, but may be associated with malnutrition or other conditions which cause nutritional deficiencies.

WKS symptoms may be long lasting or permanent and should be distinguished from the acute affects of alcohol consumption or from a period of alcohol "withdrawal." The disease is characterized by mental confusion, amnesia (a permanent gap in memory) and impaired short-term memory. An estimated 80% of persons with WKS continue to have a chronic memory disorder. Individuals often appear apathetic and inattentive and some may experience agitation. In addition, WKS tends to impair the person's ability to learn new information or tasks. Individuals with WKS are known to "confabulate" (make up or invent information to compensate for, or fill in the gaps of a poor memory). Other symptoms include ataxia (weakness in limbs or lack of muscle coordination, unsteady gait), slow walking, rapid, tremor-like eye movements or paralysis of eye muscles. Fine motor function (e.g., hand or finger movements) may be diminished and sense of smell also may be affected. In the advanced stages, coma can occur. Although treatable if caught early enough, the death rate from WKS is relatively high, about 10% to 20%.

Recent medical research suggests that the genetic marker APOE4 is a significant predictor of global intellectual deficits in people with WKS. Individuals with the ApoE genotype may experience a certain interaction with heavy alcohol use which could predispose them to WKS. Concerns about an inherited susceptibility to WKS should be discussed with a genetic counselor.

If caught early enough, WKS is a preventable, treatable disease. Treatment consists of thiamine replacement therapy, sometimes along with other vitamins. Dosages may vary and should be monitored closely by a physician. If alcoholic consumption stops and treatment is properly administered, individuals with early-stage WKS can expect a marked recovery and may be capable of learning simple, repetitive tasks.

However, the person's confusion may take some time to subside and even incomplete recovery of memory can take up to a year. In the later stages, if damage to the brain is irreversible, individuals are likely to have lasting problems with memory and gait (for example, lack of muscle coordination and numbness or weakness in limbs).

What is Progressive Supranuclear Palsy (PSP)?

Progressive supranuclear palsy (PSP) is a rare brain disorder that causes serious and permanent problems with control of gait (walking), balance, and eye movements. The most obvious sign of the disease is an inability to aim the eyes properly, which occurs because of lesions in the area of the brain that coordinates eye movements. Some patients describe this effect as a blurring. PSP patients often show alterations of mood and behavior, including depression and apathy as well as progressive mild dementia. It must be emphasized that the pattern of signs and symptoms can be quite different from person to person. The symptoms of PSP are caused by a gradual deterioration of brain cells in a few tiny but important places at the base of the brain, in the region called the brainstem. PSP is often misdiagnosed because some of its symptoms are very much like those of Parkinson's disease, Alzheimer's disease, and more rare neurodegenerative disorders, such as Creutzfeldt-Jakob disease. The key to establishing the diagnosis of PSP is the identification of early gait instability and difficulty moving the eyes, the hallmark of the disease, as well as ruling out other similar disorders, some of which are treatable.

There is currently no effective treatment for PSP, although scientists are searching for better ways to manage the disease. In some patients the slowness, stiffness, and balance problems of PSP may respond to antiparkinsonian agents such as levodopa combined with anticholinergic agents, but the effect is usually temporary. The speech, vision, and swallowing difficulties usually do not respond to any drug treatment. Another group of drugs that has been of some modest success in PSP are antidepressant medications. The most commonly used of these drugs are Prozac, Elavil, and Tofranil. The anti-PSP benefit of these drugs does not seem related to their ability to relieve depression. Non-drug treatment for PSP can take many forms. Patients frequently use weighted walking aids because of their tendency to fall backward. Bifocals or special glasses called prisms are sometimes prescribed for PSP patients to remedy the difficulty of looking down. Formal physical therapy is of no proven benefit in PSP, but certain exercises can be done to keep the joints limber. A surgical procedure, a gastrostomy, may be necessary when there are swallowing disturbances. This surgery involves the placement of a tube through the skin of the abdomen into the stomach (intestine) for feeding purposes.

PSP gets progressively worse but is not itself directly life-threatening. It does, however, predispose patients to serious complications such as pneumonia secondary to difficulty in swallowing (dysphagia). The most common complications are choking and pneumonia, head injury, and fractures caused by falls. The most common cause of death is pneumonia. With good attention to medical and nutritional needs, however, most PSP patients live well into their 70s and beyond.

Visit The Society of Progressive Supranuclear Palsy and the National Institute of Neurological Disorders and Stroke