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Alphabetical Disease Lookup





<!--<h1>Dementia </h1>--> Dementia is not a specific disease. It is a descriptive term for a collection of symptoms that can be caused by a number of disorders that affect the brain. People with dementia have significantly impaired intellectual functioning that interferes with normal activities and relationships. They also lose their ability to solve problems and maintain emotional control, and they may experience personality changes and behavioral problems such as agitation, delusions, and hallucinations. While memory loss is a common symptom of dementia, memory loss by itself does not mean that a person has dementia. Doctors diagnose dementia only if two or more brain functions - such as memory, language skills, perception, or cognitive skills including reasoning and judgment - are significantly impaired without loss of consciousness. <br><br> <strong>Different Kinds of Dementia </strong><br><br> Dementing disorders can be classified many different ways. These classification schemes attempt to group disorders that have particular features in common, such as whether they are progressive or what parts of the brain are affected. Some frequently used classifications include the following: <ul> <li> Cortical dementia - dementia where the brain damage primarily affects the brain's cortex, or outer layer. Cortical dementias tend to cause problems with memory, language, thinking, and social behavior. </li> <li> Subcortical dementia - dementia that affects parts of the brain below the cortex. Subcortical dementia tends to cause changes in emotions and movement in addition to problems with memory. </li> <li> Progressive dementia - dementia that gets worse over time, gradually interfering with more and more cognitive abilities. </li> <li>Primary dementia - dementia such as Alzheimer's disease that does not result from any other disease. </li> <li>Secondary dementia - dementia that occurs as a result of a physical disease or injury. </li> </ul> Some types of dementia fit into more than one of these classifications. For example, Alzheimer's disease is considered both a progressive and a cortical dementia. <br> Alzheimer's disease is the most common cause of dementia in people aged 65 and older. In most people, symptoms of AD appear after age 60. However, there are some early-onset forms of the disease, usually linked to a specific gene defect, which may appear as early as age 30. AD usually causes a gradual decline in cognitive abilities, usually during a span of 7 to 10 years. Nearly all brain functions, including memory, movement, language, judgment, behavior, and abstract thinking, are eventually affected. <br><br> AD is characterized by two abnormalities in the brain: amyloid plaques and neurofibrillary tangles. Amyloid plaques, which are found in the tissue between the nerve cells, are unusual clumps of a protein called beta amyloid along with degenerating bits of neurons and other cells. <br> Neurofibrillary tangles are bundles of twisted filaments found within neurons. These tangles are largely made up of a protein called tau. In healthy neurons, the tau protein helps the functioning of microtubules, which are part of the cell's structural support and deliver substances throughout the nerve cell. However, in AD, tau is changed in a way that causes it to twist into pairs of helical filaments that collect into tangles. When this happens, the microtubules cannot function correctly and they disintegrate. This collapse of the neuron's transport system may impair communication between nerve cells and cause them to die. <br><br> Researchers do not know if amyloid plaques and neurofibrillary tangles are harmful or if they are merely side effects of the disease process that damages neurons and leads to the symptoms of AD. They do know that plaques and tangles usually increase in the brain as AD progresses. <br><br> In the early stages of AD, patients may experience memory impairment, lapses of judgment, and subtle changes in personality. As the disorder progresses, memory and language problems worsen and patients begin to have difficulty performing activities of daily living, such as balancing a checkbook or remembering to take medications. They also may have visuospatial problems, such as difficulty navigating an unfamiliar route. They may become disoriented about places and times, may suffer delusions (such as the idea that someone is stealing from them or that their spouse is being unfaithful), and may become short-tempered and hostile. During the late stages of the disease, patients begin to lose the ability to control motor functions. They may have difficulty swallowing and lose bowel and bladder control. They eventually lose the ability to recognize family members and to speak. As AD progresses, it begins to affect the person's emotions and behavior. Most people with AD eventually develop symptoms such as aggression, agitation, depression, sleeplessness, or delusions. <br><br> Vascular dementia is the second most common cause of dementia, after AD. It accounts for up to 20 percent of all dementias and is caused by brain damage from cerebrovascular or cardiovascular problems - usually strokes. It also may result from genetic diseases, endocarditis (infection of a heart valve), or amyloid angiopathy (a process in which amyloid protein builds up in the brain's blood vessels, sometimes causing hemorrhagic or "bleeding" strokes). In many cases, it may coexist with AD. The incidence of vascular dementia increases with advancing age and is similar in men and women. <br><br> Symptoms of vascular dementia often begin suddenly, frequently after a stroke. Patients may have a history of high blood pressure, vascular disease, or previous strokes or heart attacks. Vascular dementia may or may not get worse with time, depending on whether the person has additional strokes. In some cases, symptoms may get better with time. When the disease does get worse, it often progresses in a stepwise manner, with sudden changes in ability. Vascular dementia with brain damage to the mid-brain regions, however, may cause a gradual, progressive cognitive impairment that may look much like AD. Unlike people with AD, people with vascular dementia often maintain their personality and normal levels of emotional responsiveness until the later stages of the disease. <br><br> People with vascular dementia frequently wander at night and often have other problems commonly found in people who have had a stroke, including depression and incontinence. <br> There are several types of vascular dementia, which vary slightly in their causes and symptoms. One type, called multi-infarct dementia (MID), is caused by numerous small strokes in the brain. MID typically includes multiple damaged areas, called infarcts, along with extensive lesions in the white matter, or nerve fibers, of the brain. <br><br> Because the infarcts in MID affect isolated areas of the brain, the symptoms are often limited to one side of the body or they may affect just one or a few specific functions, such as language. Neurologists call these "local" or "focal" symptoms, as opposed to the "global" symptoms seen in AD, which affect many functions and are not restricted to one side of the body. <br> Although not all strokes cause dementia, in some cases a single stroke can damage the brain enough to cause dementia. This condition is called single-infarct dementia. Dementia is more common when the stroke takes place on the left side (hemisphere) of the brain and/or when it involves the hippocampus, a brain structure important for memory. <br><br> Another type of vascular dementia is called Binswanger's disease. This rare form of dementia is characterized by damage to small blood vessels in the white matter of the brain (white matter is found in the inner layers of the brain and contains many nerve fibers coated with a whitish, fatty substance called myelin). Binswanger's disease leads to brain lesions, loss of memory, disordered cognition, and mood changes. Patients with this disease often show signs of abnormal blood pressure, stroke, blood abnormalities, disease of the large blood vessels in the neck, and/or disease of the heart valves. Other prominent features include urinary incontinence, difficulty walking, clumsiness, slowness, lack of facial expression, and speech difficulty. These symptoms, which usually begin after the age of 60, are not always present in all patients and may sometimes appear only temporarily. Treatment of Binswanger's disease is symptomatic, and may include the use of medications to control high blood pressure, depression, heart arrhythmias, and low blood pressure. The disorder often includes episodes of partial recovery. <br><br> Other causes of vascular dementia include vasculitis, an inflammation of the blood vessel system; profound hypotension (low blood pressure); and lesions caused by brain hemorrhage. The autoimmune disease lupus erythematosus and the inflammatory disease temporal arteritis can also damage blood vessels in a way that leads to vascular dementia. <br> Lewy body dementia (LBD) is one of the most common types of progressive dementia. LBD usually occurs sporadically, in people with no known family history of the disease. However, rare familial cases have occasionally been reported. <br><br> In LBD, cells die in the brain's cortex, or outer layer, and in a part of the mid-brain called the substantia nigra. Many of the remaining nerve cells in the substantia nigra contain abnormal structures called Lewy bodies that are the hallmark of the disease. Lewy bodies may also appear in the brain's cortex, or outer layer. Lewy bodies contain a protein called alpha-synuclein that has been linked to Parkinson's disease and several other disorders. Researchers, who sometimes refer to these disorders collectively as "synucleinopathies," do not yet know why this protein accumulates inside nerve cells in LBD. <br> The symptoms of LBD overlap with AD in many ways, and may include memory impairment, poor judgment, and confusion. However, LBD typically also includes visual hallucinations, parkinsonian symptoms such as a shuffling gait and flexed posture, and day-to-day fluctuations in the severity of symptoms. Patients with LBD live an average of 7 years after symptoms begin. <br><br> There is no cure for LBD, and treatments are aimed at controlling the parkinsonian and psychiatric symptoms of the disorder. Patients sometimes respond dramatically to treatment with antiparkinsonian drugs and/or cholinesterase inhibitors, such as those used for AD. Some studies indicate that neuroleptic drugs, such as clozapine and olanzapine, also can reduce the psychiatric symptoms of this disease. But neuroleptic drugs may cause severe adverse reactions, so other therapies should be tried first and patients using these drugs should be closely monitored. <br> Lewy bodies are often found in the brains of people with Parkinson's and AD. These findings suggest that either LBD is related to these other causes of dementia or that the diseases sometimes coexist in the same person. <br><br> Frontotemporal dementia (FTD), sometimes called frontal lobe dementia, describes a group of diseases characterized by degeneration of nerve cells - especially those in the frontal and temporal lobes of the brain. Unlike AD, FTD usually does not include formation of amyloid plaques. In many people with FTD, there is an abnormal form of tau protein in the brain, which accumulates into neurofibrillary tangles. This disrupts normal cell activities and may cause the cells to die. <br> HIV-associated dementia (HAD) results from infection with the human immunodeficiency virus (HIV) that causes AIDS. HAD can cause widespread destruction of the brain's white matter. This leads to a type of dementia that generally includes impaired memory, apathy, social withdrawal, and difficulty concentrating. People with HAD often develop movement problems as well. There is no specific treatment for HAD, but AIDS drugs can delay onset of the disease and may help to reduce symptoms. <br><br> Huntington's disease (HD) is a hereditary disorder caused by a faulty gene for a protein called huntingtin. The children of people with the disorder have a 50 percent chance of inheriting it. The disease causes degeneration in many regions of the brain and spinal cord. Symptoms of HD usually begin when patients are in their thirties or forties, and the average life expectancy after diagnosis is about 15 years. <br> Cognitive symptoms of HD typically begin with mild personality changes, such as irritability, anxiety, and depression, and progress to severe dementia. Many patients also show psychotic behavior. HD causes chorea - involuntary jerky, arrhythmic movements of the body - as well as muscle weakness, clumsiness, and gait disturbances. <br><br> Dementia pugilistica, also called chronic traumatic encephalopathy or Boxer's syndrome, is caused by head trauma, such as that experienced by people who have been punched many times in the head during boxing. The most common symptoms of the condition are dementia and parkinsonism, which can appear many years after the trauma ends. Affected individuals may also develop poor coordination and slurred speech. A single traumatic brain injury may also lead to a disorder called post-traumatic dementia (PTD). PTD is much like dementia pugilistica but usually also includes long-term memory problems. Other symptoms vary depending on which part of the brain was damaged by the injury. <br><br> Corticobasal degeneration (CBD) is a progressive disorder characterized by nerve cell loss and atrophy of multiple areas of the brain. Brain cells from people with CBD often have abnormal accumulations of the protein tau. CBD usually progresses gradually over the course of 6 to 8 years. Initial symptoms, which typically begin at or around age 60, may first appear on one side of the body but eventually will affect both sides. Some of the symptoms, such as poor coordination and rigidity, are similar to those found in Parkinson's disease. Other symptoms may include memory loss, dementia, visual-spatial problems, apraxia (loss of the ability to make familiar, purposeful movements), hesitant and halting speech, myoclonus (involuntary muscular jerks), and dysphagia (difficulty swallowing). Death is often caused by pneumonia or other secondary problems such as sepsis (severe infection of the blood) or pulmonary embolism (a blood clot in the lungs). There are no specific treatments available for CBD. The symptoms of the disease often do not respond to Parkinson's medications or other drugs. <br><br> Creutzfeldt-Jakob disease (CJD) is a rare, degenerative, fatal brain disorder that affects about one in every million people per year worldwide. Symptoms usually begin after age 60 and most patients die within 1 year. Many researchers believe CJD results from an abnormal form of a protein called a prion. Most cases of CJD occur sporadically - that is, in people who have no known risk factors for the disease. In rare cases, CJD can also be acquired through exposure to diseased brain or nervous system tissue, usually through certain medical procedures. There is no evidence that CJD is contagious through the air or through casual contact with a CJD patient. <br><br> Patients with CJD may initially experience problems with muscular coordination; personality changes, including impaired memory, judgment, and thinking; and impaired vision. Other symptoms may include insomnia and depression. As the illness progresses, mental impairment becomes severe. Patients often develop myoclonus and they may go blind. They eventually lose the ability to move and speak, and go into a coma. Pneumonia and other infections often occur in these patients and can lead to death. <br> CJD belongs to a family of human and animal diseases known as the transmissible spongiform encephalopathies (TSEs). Spongiform refers to the characteristic appearance of infected brains, which become filled with holes until they resemble sponges when viewed under a microscope. CJD is the most common of the known human TSEs. Others include fatal familial insomnia and Gerstmann-Straussler-Scheinker diseases. <br><br> <strong>Secondary Dementias</strong><br><br> Dementia may occur in patients who have other disorders that primarily affect movement or other functions. These cases are often referred to as secondary dementias. The relationship between these disorders and the primary dementias is not always clear. For instance, people with advanced Parkinson's disease, which is primarily a movement disorder, sometimes develop symptoms of dementia. Many Parkinson's patients also have amyloid plaques and neurofibrillary tangles like those found in AD. The two diseases may be linked in a yet-unknown way, or they may simply coexist in some people. People with Parkinson's and associated dementia sometimes show signs of Lewy body dementia or progressive supranuclear palsy at autopsy, suggesting that these diseases may also overlap with Parkinson's or that Parkinson's is sometimes misdiagnosed. <br><br> Other disorders that may include symptoms of dementia include multiple sclerosis; presenile dementia with motor neuron disease, also called ALS dementia; olivopontocerebellar atrophy (OPCA); Wilson's disease; and normal pressure hydrocephalus (NPH).<br><br> <strong>Dementias in Children</strong><br><br> While it is usually found in adults, dementia can also occur in children. For example, infections and poisoning can lead to dementia in people of any age. In addition, some disorders unique to children can cause dementia. <br> Niemann-Pick disease is a group of inherited disorders that affect metabolism and are caused by specific genetic mutations. Patients with Niemann-Pick disease cannot properly metabolize cholesterol and other lipids. Consequently, excessive amounts of cholesterol accumulate in the liver and spleen and excessive amounts of other lipids accumulate in the brain. Symptoms may include dementia, confusion, and problems with learning and memory. These diseases usually begin in young school-age children but may also appear during the teen years or early adulthood. <br><br> Batten disease is a fatal, hereditary disorder of the nervous system that begins in childhood. Symptoms are linked to a buildup of substances called lipopigments in the body's tissues. The early symptoms include personality and behavior changes, slow learning, clumsiness, or stumbling. Over time, affected children suffer mental impairment, seizures, and progressive loss of sight and motor skills. Eventually, children with Batten disease develop dementia and become blind and bedridden. The disease is often fatal by the late teens or twenties. <br><br> Lafora body disease is a rare genetic disease that causes seizures, rapidly progressive dementia, and movement problems. These problems usually begin in late childhood or the early teens. Children with Lafora body disease have microscopic structures called Lafora bodies in the brain, skin, liver, and muscles. Most affected children die within 2 to 10 years after the onset of symptoms. <br><br> <strong>Other Conditions that Can Cause Dementia </strong><br><br> Doctors have identified many other conditions that can cause dementia or dementia-like symptoms. Many of these conditions are reversible with appropriate treatment. <br> Reactions to medications. Medications can sometimes lead to reactions or side effects that mimic dementia. These dementia-like effects can occur in reaction to just one drug or they can result from drug interactions. They may have a rapid onset or they may develop slowly over time. <br> Metabolic problems and endocrine abnormalities. Thyroid problems can lead to apathy, depression, or dementia. Hypoglycemia, a condition in which there is not enough sugar in the bloodstream, can cause confusion or personality changes. Too little or too much sodium or calcium can also trigger mental changes. Some people have an impaired ability to absorb vitamin B12, which creates a condition called pernicious anemia that can cause personality changes, irritability, or depression. Tests can determine if any of these problems are present. <br><br> Nutritional deficiencies. Deficiencies of thiamine (vitamin B1) frequently result from chronic alcoholism and can seriously impair mental abilities, in particular memories of recent events. Severe deficiency of vitamin B6 can cause a neurological illness called pellagra that may include dementia. Deficiencies of vitamin B12 also have been linked to dementia in some cases. Dehydration can also cause mental impairment that can resemble dementia. <br><br> Infections. Many infections can cause neurological symptoms, including confusion or delirium, due to fever or other side effects of the body's fight to overcome the infection. Meningitis and encephalitis, which are infections of the brain or the membrane that covers it, can cause confusion, sudden severe dementia, withdrawal from social interaction, impaired judgment, or memory loss. Untreated syphilis also can damage the nervous system and cause dementia. In rare cases, Lyme disease can cause memory or thinking difficulties. People in the advanced stages of AIDS also may develop a form of dementia (see HIV-associated dementia, page 14). People with compromised immune systems, such as those with leukemia and AIDS, may also develop an infection called progressive multifocal leukoencephalopathy (PML). PML is caused by a common human polyomavirus, JC virus, and leads to damage or destruction of the myelin sheath that covers nerve cells. PML can lead to confusion, difficulty with thinking or speaking, and other mental problems. <br><br> Subdural hematomas. Subdural hematomas, or bleeding between the brain's surface and its outer covering (the dura), can cause dementia-like symptoms and changes in mental function. <br> Poisoning. Exposure to lead, other heavy metals, or other poisonous substances can lead to symptoms of dementia. These symptoms may or may not resolve after treatment, depending on how badly the brain is damaged. People who have abused substances such as alcohol and recreational drugs sometimes display signs of dementia even after the substance abuse has ended. This condition is known as substance-induced persisting dementia.<br><br> Brain tumors. In rare cases, people with brain tumors may develop dementia because of damage to their brains. Symptoms may include changes in personality, psychotic episodes, or problems with speech, language, thinking, and memory. <br> Anoxia. Anoxia and a related term, hypoxia, are often used interchangeably to describe a state in which there is a diminished supply of oxygen to an organ's tissues. Anoxia may be caused by many different problems, including heart attack, heart surgery, severe asthma, smoke or carbon monoxide inhalation, high-altitude exposure, strangulation, or an overdose of anesthesia. In severe cases of anoxia the patient may be in a stupor or a coma for periods ranging from hours to days, weeks, or months. Recovery depends on the severity of the oxygen deprivation. As recovery proceeds, a variety of psychological and neurological abnormalities, such as dementia or psychosis, may occur. The person also may experience confusion, personality changes, hallucinations, or memory loss. <br><br> Heart and lung problems. The brain requires a high level of oxygen in order to carry out its normal functions. Therefore, problems such as chronic lung disease or heart problems that prevent the brain from receiving adequate oxygen can starve brain cells and lead to the symptoms of dementia. <br><br> <strong>What Conditions Are Not Dementia?</strong><br><br> Age-related cognitive decline. As people age, they usually experience slower information processing and mild memory impairment. In addition, their brains frequently decrease in volume and some nerve cells, or neurons, are lost. These changes, called age-related cognitive decline, are normal and are not considered signs of dementia. <br> Mild cognitive impairment. Some people develop cognitive and memory problems that are not severe enough to be diagnosed as dementia but are more pronounced than the cognitive changes associated with normal aging. This condition is called mild cognitive impairment. Although many patients with this condition later develop dementia, some do not. Many researchers are studying mild cognitive impairment to find ways to treat it or prevent it from progressing to dementia. <br> Depression. People with depression are frequently passive or unresponsive, and they may appear slow, confused, or forgetful. Other emotional problems can also cause symptoms that sometimes mimic dementia. <br> Delirium. Delirium is characterized by confusion and rapidly altering mental states. The person may also be disoriented, drowsy, or incoherent, and may exhibit personality changes. Delirium is usually caused by a treatable physical or psychiatric illness, such as poisoning or infections. Patients with delirium often, though not always, make a full recovery after their underlying illness is treated. <br><br> <strong>Causes of Dementia </strong><br><br> All forms of dementia result from the death of nerve cells and/or the loss of communication among these cells. The human brain is a very complex and intricate machine and many factors can interfere with its functioning. Researchers have uncovered many of these factors, but they have not yet been able to fit these puzzle pieces together in order to form a complete picture of how dementias develop. <br> Many types of dementia, including AD, Lewy body dementia, Parkinson's dementia, and Pick's disease, are characterized by abnormal structures called inclusions in the brain. Because these inclusions, which contain abnormal proteins, are so common in people with dementia, researchers suspect that they play a role in the development of symptoms. However, that role is unknown, and in some cases the inclusions may simply be a side effect of the disease process that leads to the dementia. <br><br> Genes clearly play a role in the development of some kinds of dementia. However, in AD and many other disorders, the dementia usually cannot be tied to a single abnormal gene. Instead, these forms of dementia appear to result from a complex interaction of genes, lifestyle factors, and other environmental influences. <br> Variations in another gene, called apolipoprotein E (apoE), have been linked to an increased risk of late-onset AD. The apoE gene does not cause the disease by itself, but one version of the gene, called apoE epsilon4 (apoE E4), appears to increase the risk of AD. People with two copies of the apoE E4 gene have about ten times the risk of developing AD compared to people without apoE E4. This gene variant seems to encourage amyloid deposition in the brain. One study also found that this gene is associated with shorter survival in men with AD. In contrast, another version of the apoE gene, called apoE E2, appears to protect against AD. <br><br> Vascular dementia can be caused by cerebrovascular disease or any other condition that prevents normal blood flow to the brain. Without a normal supply of blood, brain cells cannot obtain the oxygen they need to work correctly, and they often become so deprived that they die. <br> The causes of other types of dementias vary. Some, such as CJD and GSS, have been tied to abnormal forms of specific proteins. Others, including Huntington's disease and FTDP-17, have been linked to defects in a single gene. Post-traumatic dementia is directly related to brain cell death after injury. HIV-associated dementia is clearly tied to infection by the HIV virus, although the exact way the virus causes damage is not yet certain. For other dementias, such as corticobasal degeneration and most types of frontotemporal dementia, the underlying causes have not yet been identified. <br><br> <strong>Risk Factors for Dementia</strong><br><br> Researchers have identified several risk factors that affect the likelihood of developing one or more kinds of dementia. Some of these factors are modifiable, while others are not. <br> Age. The risk of AD, vascular dementia, and several other dementias goes up significantly with advancing age. <br> Genetics/family history. As described in the section "What Causes Dementia?" researchers have discovered a number of genes that increase the risk of developing AD. Although people with a family history of AD are generally considered to be at heightened risk of developing the disease themselves, many people with a family history never develop the disease, and many without a family history of the disease do get it. In most cases, it is still impossible to predict a specific person's risk of the disorder based on family history alone. Some families with CJD, GSS, or fatal familial insomnia have mutations in the prion protein gene, although these disorders can also occur in people without the gene mutation. Individuals with these mutations are at significantly higher risk of developing these forms of dementia. Abnormal genes are also clearly implicated as risk factors in Huntington's disease, FTDP-17, and several other kinds of dementia. <br><br> Smoking and alcohol use. Several recent studies have found that smoking significantly increases the risk of mental decline and dementia. People who smoke have a higher risk of atherosclerosis and other types of vascular disease, which may be the underlying causes for the increased dementia risk. Studies also have found that drinking large amounts of alcohol appears to increase the risk of dementia. However, other studies have suggested that people who drink moderately have a lower risk of dementia than either those who drink heavily or those who completely abstain from drinking. <br><br> Atherosclerosis. Atherosclerosis is the buildup of plaque - deposits of fatty substances, cholesterol, and other matter - in the inner lining of an artery. Atherosclerosis is a significant risk factor for vascular dementia, because it interferes with the delivery of blood to the brain and can lead to stroke. Studies have also found a possible link between atherosclerosis and AD. <br><br> Cholesterol. High levels of low-density lipoprotein (LDL), the so-called bad form of cholesterol, appear to significantly increase a person's risk of developing vascular dementia. Some research has also linked high cholesterol to an increased risk of AD. <br><br> Plasma homocysteine. Research has shown that a higher-than-average blood level of homocysteine - a type of amino acid - is a strong risk factor for the development of AD and vascular dementia. <br> Diabetes. Diabetes is a risk factor for both AD and vascular dementia. It is also a known risk factor for atherosclerosis and stroke, both of which contribute to vascular dementia. <br><br> Mild cognitive impairment. While not all people with mild cognitive impairment develop dementia, people with this condition do have a significantly increased risk of dementia compared to the rest of the population. One study found that approximately 40 percent of people over age 65 who were diagnosed with mild cognitive impairment developed dementia within 3 years. <br><br> Down syndrome. Studies have found that most people with Down syndrome develop characteristic AD plaques and neurofibrillary tangles by the time they reach middle age. Many, but not all, of these individuals also develop symptoms of dementia. <br><br> <strong>Diagnosis </strong><br><br> Doctors employ a number of strategies to diagnose dementia. It is important that they rule out any treatable conditions, such as depression, normal pressure hydrocephalus, or vitamin B12 deficiency, which can cause similar symptoms. <br> Early, accurate diagnosis of dementia is important for patients and their families because it allows early treatment of symptoms. For people with AD or other progressive dementias, early diagnosis may allow them to plan for the future while they can still help to make decisions. These people also may benefit from drug treatment. <br> The "gold standard" for diagnosing dementia, autopsy, does not help the patient or caregivers. Therefore, doctors have devised a number of techniques to help identify dementia with reasonable accuracy while the patient is still alive. <br><br> <strong>Patient history</strong><br> Doctors often begin their examination of a patient suspected of having dementia by asking questions about the patient's history. For example, they may ask how and when symptoms developed and about the patient's overall medical condition. They also may try to evaluate the patient's emotional state, although patients with dementia often may be unaware of or in denial about how their disease is affecting them. Family members also may deny the existence of the disease because they do not want to accept the diagnosis and because, at least in the beginning, AD and other forms of dementia can resemble normal aging. Therefore additional steps are necessary to confirm or rule out a diagnosis of dementia. <br><br> <strong>Physical examination</strong><br> A physical examination can help rule out treatable causes of dementia and identify signs of stroke or other disorders that can contribute to dementia. It can also identify signs of other illnesses, such as heart disease or kidney failure, that can overlap with dementia. If a patient is taking medications that may be causing or contributing to his or her symptoms, the doctor may suggest stopping or replacing some medications to see if the symptoms go away. <br><br> <strong>Neurological evaluations </strong><br> Doctors will perform a neurological examination, looking at balance, sensory function, reflexes, and other functions, to identify signs of conditions - for example movement disorders or stroke - that may affect the patient's diagnosis or are treatable with drugs. <br><br> <strong>Cognitive and neuropsychological tests</strong><br> Doctors use tests that measure memory, language skills, math skills, and other abilities related to mental functioning to help them diagnose a patient's condition accurately. For example, people with AD often show changes in so-called executive functions (such as problem-solving), memory, and the ability to perform once-automatic tasks. <br> Doctors often use a test called the Mini-Mental State Examination (MMSE) to assess cognitive skills in people with suspected dementia. This test examines orientation, memory, and attention, as well as the ability to name objects, follow verbal and written commands, write a sentence spontaneously, and copy a complex shape. Doctors also use a variety of other tests and rating scales to identify specific types of cognitive problems and abilities. <br><br> <strong>Brain scans</strong><br> Doctors may use brain scans to identify strokes, tumors, or other problems that can cause dementia. Also, cortical atrophy -degeneration of the brain's cortex (outer layer) - is common in many forms of dementia and may be visible on a brain scan. The brain's cortex normally appears very wrinkled, with ridges of tissue (called gyri) separated by "valleys" called sulci. In individuals with cortical atrophy, the progressive loss of neurons causes the ridges to become thinner and the sulci to grow wider. As brain cells die, the ventricles (or fluid-filled cavities in the middle of the brain) expand to fill the available space, becoming much larger than normal. Brain scans also can identify changes in the brain's structure and function that suggest AD. <br><br> <strong>Laboratory tests</strong><br> Doctors may use a variety of laboratory tests to help diagnose dementia and/or rule out other conditions, such as kidney failure, that can contribute to symptoms. A partial list of these tests includes a complete blood count, blood glucose test, urinalysis, drug and alcohol tests (toxicology screen), cerebrospinal fluid analysis (to rule out specific infections that can affect the brain), and analysis of thyroid and thyroid-stimulating hormone levels. A doctor will order only the tests that he or she feels are necessary and/or likely to improve the accuracy of a diagnosis. <br><br> <strong>Psychiatric evaluation </strong><br> A psychiatric evaluation may be obtained to determine if depression or another psychiatric disorder may be causing or contributing to a person's symptoms. <br><br> <strong>Presymptomatic testing </strong><br> Testing people before symptoms begin to determine if they will develop dementia is not possible in most cases. However, in disorders such as Huntington's where a known gene defect is clearly linked to the risk of the disease, a genetic test can help identify people who are likely to develop the disease. Since this type of genetic information can be devastating, people should carefully consider whether they want to undergo such testing. <br> Researchers are examining whether a series of simple cognitive tests, such as matching words with pictures, can predict who will develop dementia. One study suggested that a combination of a verbal learning test and an odor-identification test can help identify AD before symptoms become obvious. Other studies are looking at whether memory tests and brain scans can be useful indicators of future dementia. <br><br> <strong>Is There Any Treatment? </strong><br><br> While treatments to reverse or halt disease progression are not available for most of the dementias, patients can benefit to some extent from treatment with available medications and other measures, such as cognitive training. <br> Drugs to specifically treat AD and some other progressive dementias are now available and are prescribed for many patients. Although these drugs do not halt the disease or reverse existing brain damage, they can improve symptoms and slow the progression of the disease. This may improve the patient's quality of life, ease the burden on caregivers, and/or delay admission to a nursing home. Many researchers are also examining whether these drugs may be useful for treating other types of dementia. <br> Many people with dementia, particularly those in the early stages, may benefit from practicing tasks designed to improve performance in specific aspects of cognitive functioning. For example, people can sometimes be taught to use memory aids, such as mnemonics, computerized recall devices, or note taking. <br> Behavior modification - rewarding appropriate or positive behavior and ignoring inappropriate behavior - also may help control unacceptable or dangerous behaviors. <br><br> <strong>Can Dementia be Prevented?</strong><br><br> Research has revealed a number of factors that may be able to prevent or delay the onset of dementia in some people. For example, studies have shown that people who maintain tight control over their glucose levels tend to score better on tests of cognitive function than those with poorly controlled diabetes. Several studies also have suggested that people who engage in intellectually stimulating activities, such as social interactions, chess, crossword puzzles, and playing a musical instrument, significantly lower their risk of developing AD and other forms of dementia. Scientists believe mental activities may stimulate the brain in a way that increases the person's "cognitive reserve" - the ability to cope with or compensate for the pathologic changes associated with dementia. <br><br> Researchers are studying other steps people can take that may help prevent AD in some cases. So far, none of these factors has been definitively proven to make a difference in the risk of developing the disease. Moreover, most of the studies addressed only AD, and the results may or may not apply to other forms of dementia. Nevertheless, scientists are encouraged by the results of these early studies and many believe it will eventually become possible to prevent some forms of dementia. <br><br> Possible preventive actions include: <br><br> <strong>Lowering homocysteine.</strong> In one study, elevated blood levels of the amino acid homocysteine were associated with a 2.9 times greater risk of AD and a 4.9 times greater risk of vascular dementia. A preliminary study has shown that high doses of three B vitamins that help lower homocysteine levels - folic acid, B12, and B6 - appear to slow the progression of AD. Researchers are conducting a multi-center clinical trial to test this effect in a larger group of patients. <br><br> <strong>Lowering cholesterol levels. </strong>Research has suggested that people with high cholesterol levels have an increased risk of developing AD. Cholesterol is involved in formation of amyloid plaques in the brain. Mutations in a gene called CYP46 and the apoE E4 gene variant, both of which have been linked to an increased risk of AD, are also involved in cholesterol metabolism. Several studies have also found that the use of drugs called statins, which lower cholesterol levels, is associated with a lower likelihood of cognitive impairment. <br><br> <strong>Lowering blood pressure.</strong> Several studies have shown that antihypertensive medicine reduces the odds of cognitive impairment in elderly people with high blood pressure. One large European study found a 55 percent lower risk of dementia in people over 60 who received drug treatment for hypertension. These people had a reduced risk of both AD and vascular dementia. <br><br> <strong>Exercise.</strong> Regular exercise stimulates production of chemicals called growth factors that help neurons survive and adapt to new situations. These gains may help to delay the onset of dementia symptoms. Exercise also may reduce the risk of brain damage from atherosclerosis. <br><br> <strong>Education.</strong> Researchers have found evidence that formal education may help protect people against the effects of AD. In one study, researchers found that people with more years of formal education had relatively less mental decline than people with less schooling, regardless of the number of amyloid plaques and neurofibrillary tangles each person had in his or her brain. The researchers think education may cause the brain to develop robust nerve cell networks that can help compensate for the cell damage caused by AD. <br><br> <strong>Controlling inflammation.</strong> Many studies have suggested that inflammation may contribute to AD. Moreover, autopsies of people who died with AD have shown widespread inflammation in the brain that appeared to be caused by the accumulation of beta amyloid. Another study found that men with high levels of C-reactive protein, a general marker of inflammation, had a significantly increased risk of AD and other kinds of dementia. <br><br> <strong>Nonsteroidal anti-inflammatory drugs (NSAIDs).</strong> Research indicates that long-term use of NSAIDs - ibuprofen, naproxen, and similar drugs - may prevent or delay the onset of AD. Researchers are not sure how these drugs may protect against the disease, but some or all of the effect may be due to reduced inflammation. A 2003 study showed that these drugs also bind to amyloid plaques and may help to dissolve them and prevent formation of new plaques. <br><br> The risk of vascular dementia is strongly correlated with risk factors for stroke, including high blood pressure, diabetes, elevated cholesterol levels, and smoking. This type of dementia may be prevented in many cases by changing lifestyle factors, such as excessive weight and high blood pressure, which are associated with an increased risk of cerebrovascular disease. One European study found that treating isolated systolic hypertension (high blood pressure in which only the systolic or top number is high) in people age 60 and older reduced the risk of dementia by 50 percent. These studies strongly suggest that effective use of current treatments can prevent many future cases of vascular dementia.


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