10 Most Common Types of Dementia
- Alzheimer’s Disease (AD)
- CTE: Chronic Traumatic Encephalopathy, Boxer’s Syndrome, Dementia Pugilistica
- Corticobasal Degeneration (CBD)
- Creutzfeld-Jakob Disease (CJD)
- Frontotemporal Dementia (FTD)
- Gerstmann-Straussler-Scheinker (GSS) Disease, Familial British Dementia, Familial Danish Dementia, & Fatal Familial Insomnia
- HIV-Associated Dementia (HAD)
- Huntington’s Disease (HD)
- Lewy Body Dementia (LBD)
- Vascular Dementia
- Secondary Dementias (Parkinson’s, NPH…)
- Childhood Dementias
- Other Causes of Dementia
- Conditions That Are NOT Dementia
What Is Dementia?
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.
The 10 Most Common Types of Dementia
Alzheimer’s disease (AD) is the most common cause of dementia in people aged 65 and older. Experts believe that up to 4 million people in the United States are currently living with the disease: one in ten people over the age of 65 and nearly half of those over 85 have AD. At least 360,000 Americans are diagnosed with AD each year and about 50,000 are reported to die from it.
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.
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.
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.
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.
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.
On average, patients with AD live for 8 to 10 years after they are diagnosed. However, some people live as long as 20 years. Patients with AD often die of aspiration pneumonia because they lose the ability to swallow late in the course of the disease.
CTE: Chronic Traumatic Encephalopathy, Boxer’s Syndrome, Dementia Pugilistica
Chronic Traumatic Encephalopathy (CTE) is a progressive degenerative disease of the brain
CTE has been most commonly found in professional athletes participating in American football, ice hockey, professional wrestling and other contact sports who have experienced repetitive brain trauma. It has also been found in soldiers exposed to a blast or a concussive injury, in both cases resulting in characteristic degeneration of brain tissue and the build-up of an abnormal protein called tau.
Repeated concussions and injuries less serious than concussions (“sub-concussions”) incurred during the play of contact sports over a long period have not yet been found to result in CTE. In the case of blast injury, a single exposure to a blast and the subsequent violent movement of the head in the blast wind can cause the condition.
Symptoms of the neurodegeneration can develop months, years, or even decades after the last brain trauma or end of active athletic involvement. The brain degeneration is associated with memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, and, eventually, progressive dementia.
CTE has a variant called Dementia pugilistica (pugil means boxer in latin) or Boxer’s syndrome, since head trauma is commonly 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.
Corticobasal Degeneration (CBD)
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. Drugs such as clonazepam may help with myoclonus, however, and occupational, physical, and speech therapy can help in managing the disabilities associated with this disease. The symptoms of the disease often do not respond to Parkinson’s medications or other drugs.
Creutzfeldt-Jakob Disease (CJD)
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. However, about 5 to 10 percent of cases of CJD in the United States are hereditary, caused by a mutation in the gene for the prion protein. 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.
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.
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 disease (see below).
In recent years, a new type of CJD, called variant CJD (vCJD), has been found in Great Britain and several other European countries. The initial symptoms of vCJD are different from those of classic CJD and the disorder typically occurs in younger patients. Research suggests that vCJD may have resulted from human consumption of beef from cattle with a TSE disease called bovine spongiform encephalopathy (BSE), also known as “mad cow disease.”
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.
Experts believe FTD accounts for 2 to 10 percent of all cases of dementia. Symptoms of FTD usually appear between the ages of 40 and 65. In many cases, people with FTD have a family history of dementia, suggesting that there is a strong genetic factor in the disease. The duration of FTD varies, with some patients declining rapidly over 2 to 3 years and others showing only minimal changes for many years. People with FTD live with the disease for an average of 5 to 10 years after diagnosis.
Because structures found in the frontal and temporal lobes of the brain control judgment and social behavior, people with FTD often have problems maintaining normal interactions and following social conventions. They may steal or exhibit impolite and socially inappropriate behavior, and they may neglect their normal responsibilities. Other common symptoms include loss of speech and language, compulsive or repetitive behavior, increased appetite, and motor problems such as stiffness and balance problems. Memory loss also may occur, although it typically appears late in the disease.
Pick’s Disease (A Type of FTD)
In one type of FTD called Pick’s disease, certain nerve cells become abnormal and swollen before they die. These swollen, or ballooned, neurons are one hallmark of the disease. The brains of people with Pick’s disease also have abnormal structures called Pick bodies, composed largely of the protein tau, inside the neurons. The cause of Pick’s disease is unknown, but it runs in some families and thus it is probably due at least in part to a faulty gene or genes. The disease usually begins after age 50 and causes changes in personality and behavior that gradually worsen over time. The symptoms of Pick’s disease are very similar to those of AD, and may include inappropriate social behavior, loss of mental flexibility, language problems, and difficulty with thinking and concentration. There is currently no way to slow the progressive degeneration found in Pick’s disease. However, medication may be helpful in reducing aggression and other behavioral problems, and in treating depression.
In some cases, familial FTD is linked to a mutation in the tau gene. This disorder, called frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), is much like other types of FTD but often includes psychiatric symptoms such as delusions and hallucinations.
Primary Progressive Aphasia (PPA) (Overlaps FTD)
According to the Mayo Clinic, “Primary progressive aphasia (uh-FAY-zhuh) impairs language capabilities. People with primary progressive aphasia may have trouble expressing their thoughts and comprehending or finding words.
PPA may begin in people as early as their forties. “Aphasia” is a general term used to refer to deficits in language functions, such as speaking, understanding what others are saying, and naming common objects.
Symptoms often begin gradually and progress slowly over a period of years. As the disease progresses, memory and attention may also be impaired and patients may show personality and behavior changes. Many, but not all, people with PPA eventually develop symptoms of dementia.
Primary progressive aphasia has three types, which cause different symptoms.
- Semantic Dementia (SD)
- Difficulty comprehending spoken or written language, particularly single words
- Difficulty comprehending word meanings
- Difficulty naming objects
Lopogenic Progressive Aphasia (LPA)
- Difficulty retrieving correct words in speech
- Frequent pauses in your speech while searching for words
- Slow speech
- Difficulty repeating phrases or sentences
- Progressive Nonfluent-agrammatic Aphasia (PNFA)
- Difficulty speaking
- Hesitant, halting speech
- Making errors in speech sounds
- Difficulty understanding sentences
- Using grammar incorrectly
Symptoms may vary depending on the speaking situation and the type of primary progressive aphasia. For example, a person may need to pause frequently to find words during a conversation requiring a high level of precision but then have no pauses when exchanging small talk. Reading and writing also are usually affected.
- Semantic Dementia (SD)
Gerstmann-Straussler-Scheinker (GSS) Disease, Familial British Dementia, Familial Danish Dementia, Fatal Familial Insomnia
Familial British dementia, familial Danish dementia, fatal familial insomnia and Gerstmann-Straussler-Scheinker (GSS) disease are rare hereditary dementias. Symptoms of GSS typically include ataxia and progressive dementia that begins when people are between 50 and 60 years old. The disease may last for several years before patients eventually die. Fatal familial insomnia causes degeneration of a brain region called the thalamus, which is partially responsible for controlling sleep. It causes a progressive insomnia that eventually leads to a complete inability to sleep. Other symptoms may include poor reflexes, dementia, hallucinations, and eventually coma. It can be fatal within 7 to 13 months after symptoms begin but may last longer. Familial British dementia and familial Danish dementia have been linked to two different defects in a gene found on chromosome 13. The symptoms of both diseases include progressive dementia, paralysis, and loss of balance.
HIV-Associated Dementia (HAD)
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.
Huntington’s Disease (HD)
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.
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.
Lewy Body Dementia
Lewy body dementia (LBD) is one of the most common types of progressive dementia. Symptoms of Lewy body dementia overlap with those of other diseases, making it hard to diagnose.
LBD usually occurs sporadically, in people with no known family history of the disease. However, rare familial cases have occasionally been reported.
Lewy body dementia, involves protein aggregates called Lewy bodies, balloon-like structures that form inside of nerve cells. The initial symptoms may vary, but over time, people with these disorders develop very similar cognitive, behavioral, physical, and sleep-related symptoms. Lewy body dementia is one of the most common causes of dementia, after Alzheimer’s disease and vascular disease. Types of Lewy body dementia include:
Dementia with Lewy bodies (DLB), one of the more common forms of progressive dementia. Symptoms such as difficulty sleeping, loss of smell, and visual hallucinations often precede movement and other problems by as long as 10 years, which consequently results in DLB going unrecognized or misdiagnosed as a psychiatric disorder until its later stages. Neurons in the substantia nigra that produce dopamine die or become impaired, and the brain’s outer layer (cortex) degenerates. Many neurons that remain contain Lewy bodies.
Later in the course of DLB, some signs and symptoms are similar to AD and may include memory loss, poor judgment, and confusion. Other signs and symptoms of DLB are similar to those of Parkinson’s disease, including difficulty with movement and posture, a shuffling walk, and changes in alertness and attention. Given these similarities, DLB can be very difficult to diagnose. There is no cure for DLB, but there are drugs that control some symptoms. The medications used to control DLB symptoms can make motor function worse or exacerbate hallucinations.
Parkinson’s disease dementia (PDD), a clinical diagnosis related to DLB that can occur in people with Parkinson’s disease. PDD may affect memory, social judgment, language, or reasoning. Autopsy studies show that people with PDD often have amyloid plaques and tau tangles similar to those found in people with AD, though it is not understood what these similarities mean. A majority of people with Parkinson’s disease develop dementia, but the time from the onset of movement symptoms to the onset of dementia symptoms varies greatly from person to person. Risk factors for developing PDD include the onset of Parkison’s-related movement symptoms followed by mild cognitive impairment and REM sleep behavior disorder, which involves having frequent nightmares and visual hallucinations.
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.
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.
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.
There are several types of vascular dementia, which vary slightly in their causes and symptoms.
Multi-Infarct Dementia (MID), a Type of Vascular Dementia
One type of vascular dementia is called multi-infarct dementia (MID). It 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.
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.
Single-Infarct Dementia, a Type of Vascular Dementia
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.
Binswanger’s Disease, a Type of Vascular Dementia
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.
CADASIL, a Type of Vascular Dementia
Another type of vascular dementia is linked to a rare hereditary disorder called CADASIL, which stands for cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy. CADASIL is linked to abnormalities of a specific gene, Notch3, which is located on chromosome 19. This condition causes multi-infarct dementia as well as stroke, migraine with aura, and mood disorders. The first symptoms usually appear in people who are in their twenties, thirties, or forties and affected individuals often die by age 65. Researchers believe most people with CADASIL go undiagnosed, and the actual prevalence of the disease is not yet known.
Other Causes of Vascular Dementia
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.
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.
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). (For more on NPH, watch the video or read the article on this site called, .)
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.
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.
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.
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.
A number of other childhood-onset disorders can include symptoms of dementia. Among these are mitochondrial myopathies, Rasmussen’s encephalitis, mucopolysaccharidosis III (Sanfilippo syndrome), neurodegeneration with brain iron accumulation, and leukodystrophies such as Alexander disease, Schilder’s disease, and metachromatic leukodystrophy.
What Other Conditions Can Cause Dementia?
Doctors have identified many other conditions that can cause dementia or dementia-like symptoms. Many of these conditions are reversible with appropriate treatment.
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.
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.
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.
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.
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.
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.
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.
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.
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.
What Conditions Are NOT Dementia?
Mild Cognitive Impairment (MCI)
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.
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.
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.
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.
- NIH (U.S. National Institutes of Health)
- Aethlon Medical and Exosome Sciences
- Mesulam M (1982). “Slowly progressive aphasia without generalized dementia“. Annals of Neurology 11 (6): 592–8. doi:10.1002/ana.410110607. PMID 7114808.
- The Mayo Clinic