Alzheimer's Disease Research0

People with Alzheimer's disease and those with mild cognitive impairment, or even healthy people who want to help scientists test new treatments may be able to take part in clinical trials. Clinical trials are studies done with people to find out if a new drug or treatment is both safe and effective.
New therapies are tested on people only after laboratory and animal studies show that the therapy is safe and has promising results. The Food and Drug Administration sets strict rules to make sure that people who agree to be in the studies are treated as safely as possible.

People who take part in clinical trials say that the biggest benefit is having regular contact with experts who have lots of practical experience and a broad understanding about the disease. They also feel they are making a valuable contribution to knowledge that will help people who develop Alzheimer's in the future.

Scientists are testing a number of drugs in clinical trials to see if they prevent Alzheimer's disease, slow the disease, or help reduce behavioral symptoms. Many drugs and therapies are tested in clinical trials. Some ideas that seem promising turn out to have little or no benefit when they are carefully studied in a clinical trial.

There is evidence that inflammation in the brain may contribute to the damage caused by Alzheimer's disease. Some studies have suggested that drugs such as nonsteroidal anti-inflammatory drugs, or NSAIDs, might help slow the progression of Alzheimer's. So far, however, clinical trials have not shown a benefit from these drugs.

Research has suggested a link between Alzheimer's disease and factors that increase the risk for heart disease. Medicines already used to help reduce the risk of heart disease may help lower the chances of developing Alzheimer's disease or may slow its progression. Clinical trials of drugs known as statins, commonly used to lower cholesterol, have begun to see if they might help slow down the progression of Alzheimer's disease.

Studies have shown that people with Alzheimer's often have higher levels of an amino acid called homocysteine in their blood. High levels of homocysteine are known to increase the risk of heart disease. Folic acid and vitamins B6 and B12 can reduce levels of homocysteine in the blood, and scientists are conducting clinical trials to see whether these substances can also slow rates of mental decline.

Recently, scientists have focused on a type of memory change called mild cognitive impairment, or MCI. MCI is different from both Alzheimer's disease and age-related memory change. People with MCI have ongoing memory problems but do not have noticeable problems in other areas like confusion, attention problems, and difficulty with language.

Several years ago, a clinical trial showed that vitamin E slowed the progress of some consequences of Alzheimer's disease by about seven months. Other studies are considering whether antioxidants -- such as vitamin E and C -- can slow Alzheimer's. One clinical trial is examining whether vitamin E and/or selenium supplements can prevent Alzheimer's or stop mental decline. More studies on other antioxidants are ongoing or being planned.

Studies have linked keeping the brain active with a reduced risk of Alzheimer's disease. In a study of healthy older people and people with possible or probable Alzheimer's, scientists found that the healthy people had taken part in more mentally stimulating activities in their early and middle adulthood years than those who later developed Alzheimer's. The healthy group also spent more hours in these types of activities.

A growing body of research suggests that the more formal education a person has, the better his or her memory and learning ability will be, even if the brain turns out to have the type of plaques associated with Alzheimer's disease.

Some studies have suggested that estrogen used by women to treat the symptoms of menopause also protects the brain. Experts also wondered whether using estrogen could reduce the risk of Alzheimer's or slow the disease. However, clinical trials to test estrogen have not shown that it can slow the progression of Alzheimer's in women who have already been diagnosed with the disease. And one study found that women over the age of 65 who used estrogen with a progestin were at greater risk for dementia, including Alzheimer's. The study also showed that older women who used only estrogen could increase their risk of developing dementia. Scientists believe that more research is needed to find out if estrogen may play some role in Alzheimer's. They would like to know whether starting estrogen therapy around the time of menopause, rather than at age 65 or older, will protect memory or prevent Alzheimer's disease, and an NIH clinical trial is testing this possibility.

Early studies suggested that extracts from the leaves of the ginkgo biloba tree might be of some help in treating symptoms of Alzheimer's disease. There is no evidence yet that gingko biloba will cure or prevent Alzheimer's. Scientists are now trying to find out in a clinical trial whether ginkgo biloba can delay mental decline or prevent Alzheimer's disease or other types of dementia in older people.

Will a vaccine someday prevent Alzheimer's disease? Early vaccine studies in mice successfully reduced beta-amyloid plaques in the brain and improved the way mice performed on memory tests. But when the studies were conducted in humans, they had to be stopped because some participants experienced side effects. However, scientists are continuing to study variations of the vaccine approach in the hope that they will reduce beta-amyloid in the brain while minimizing harmful side effects.

Scientists have come a long way in their understanding of Alzheimer's disease. Findings from years of research have begun to clarify differences among age-related memory changes, mild cognitive impairment, and Alzheimer's disease. Scientists also have made great progress in defining the changes that take place in the Alzheimer's disease brain. This allows them to pinpoint possible targets for treatment.

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Alzheimer's Disease Treatments0

There is no known cure for Alzheimer's, but there are treatments that can prevent some symptoms from getting worse for a limited time. Ongoing research offers clues to the way Alzheimer's develops and the reasons it starts. It also offers hope that some day it may be possible to delay the onset of Alzheimer's, slow its progress, or even prevent it altogether. Alzheimer's disease develops slowly, starting with mild memory problems and ending in death. The course the disease takes and how fast changes occur vary from person to person. The time from diagnosis to end of life varies. It can be as little as 3 years if the person is over 80 when diagnosed. Or it may be as long as 10 years or more if the person is younger.

A person with Alzheimer's should be under a doctor's care and may see a neurologist, psychiatrist, family doctor, internist, or geriatrician -- a specialist who treats older adults. The doctor can treat the person's physical and behavioral problems and answer the many questions that the person or the family may have.

No treatment can stop Alzheimer's disease. However, for some people in the early and middle stages of the disease, the drugs Aricept®, Exelon® or Razadyne® -- previously known as Reminyl® -- may help prevent some symptoms from becoming worse for a limited time. Aricept® is also approved for severe symptoms of Alzheimer's. Another drug, Namenda®, is approved for use in moderate to severe forms of the disease, although it is also limited in its effects.

Also, some medicines may help control behavioral symptoms of Alzheimer's disease such as sleeplessness, agitation, wandering, anxiety, and depression. Treating these symptoms often makes patients more comfortable and makes their care easier for caregivers.

Family members and friends can assist people in the early stages of Alzheimer's in continuing their daily routines, physical activities, and social contacts. People with Alzheimer's should be kept up-to-date about the details of their lives, such as the time of day, where they live, and what is happening at home or in the world.

Memory aids may help in the day-to-day living of patients in the earlier stages of Alzheimer's. Some families find that a big calendar, a list of daily plans, notes about simple safety measures, and written directions describing how to use common household items are very useful aids.

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Alzheimer's Disease Diagnosis0

An early, accurate diagnosis of Alzheimer's disease helps patients and their families plan for the future. It gives them time to discuss care options while the patient can still take part in making decisions. And even though no drug can slow the onset or the progression of Alzheimer's, early diagnosis offers the best chance to treat the symptoms of the disease.
Today, the only definite way to diagnose Alzheimer's disease is to find out whether there are plaques and tangles in brain tissue. To look at brain tissue, doctors must wait until they do an autopsy, which is an examination of the body done after a person dies. Therefore, doctors can only make a diagnosis of "possible" or "probable" Alzheimer's disease while the person is still alive. At specialized centers, doctors can diagnose Alzheimer's disease correctly up to 90 percent of the time.

Doctors use several tools to diagnose "probable" Alzheimer's disease:

1. A complete medical history with questions about the person's general health, past medical problems, and any difficulties carrying out daily activities.
2. Medical tests, such as tests of blood, urine or spinal fluid.
3. Tests to measure memory, problem solving, attention, counting, and language.
4. Brain scans that allow the doctor to look at a picture of the brain to see if anything does not look normal.

Sometimes, these test results help the doctor find other possible causes of the person's symptoms. For example, thyroid problems, drug reactions, depression, brain tumors, and blood vessel disease in the brain can cause symptoms similar to those of Alzheimer's. Some of these other conditions can be treated successfully.

Recently, scientists have focused on a type of memory change called mild cognitive impairment, or MCI. MCI is different from both Alzheimer's disease and age-related memory change. People with MCI have ongoing memory problems but do not have noticeable problems in other areas like confusion, attention problems, and difficulty with language.

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Alzheimer's Disease Symptoms0

Alzheimer's disease begins slowly. At first, the only symptom may be mild forgetfulness. People in the early stage of Alzheimer's disease may have trouble remembering recent events, activities, or the names of familiar people or things. Simple math problems may become hard to solve. Such difficulties may be a bother, but usually they are not serious enough to cause alarm. However, as the disease goes on, forgetfulness begins to interfere with daily activities. People may forget the way home or find it hard to cope with daily life. Such symptoms are more easily noticed and become serious enough to cause people with Alzheimer's disease or their family members to seek medical help.

People in the middle stages of Alzheimer's disease may forget how to do basic tasks, like brushing their teeth or combing their hair. They can no longer think clearly. They begin to have problems speaking, understanding, reading, or writing. Later on, people with Alzheimer's disease may become anxious, agitated or aggressive, or wander away from home. Eventually, patients need total care.

Signs of mild Alzheimer's can include:

1.     memory loss
2.     confusion about the location of familiar places
3.     taking longer to accomplish normal daily tasks
4.     trouble handling money and paying bills
5.     poor judgment leading to bad decisions
6.     loss of spontaneity and sense of initiative
7.     mood and personality changes
8.     increased anxiety
9.     increasing memory loss and confusion
10.     shortened attention span
11.     problems recognizing friends and family members
12.     difficulty with language, including problems with reading and writing
13.     difficulty working with numbers
14.     difficulty organizing thoughts and thinking logically
15.     inability to learn new things or cope with new or unexpected situations
16.     restlessness, agitation, anxiety, tearfulness
17.     wandering -- especially in the late afternoon or at night
18.     repetitive statements or movement, occasional muscle twitches
19.     hallucinations and delusions, suspiciousness or paranoia, irritability
20.     loss of impulse control
21.     perceptual-motor problems

Symptoms of severe Alzheimer's include

1.     Inability to recognize family or loved ones
2.     Inability to communicate
3.     loss of sense of self
4.     weight loss
5.     seizures, skin infections, difficulty swallowing
6.     groaning, moaning, or grunting
7.     increased sleeping
8.     lack of bladder and bowel control
9.     total dependence on the caregive

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Alzheimer's Disease Causes0

Scientists do not yet fully understand what causes Alzheimer's disease. There probably is not one single cause, but several factors that affect each person differently. Age is the most important known risk factor for Alzheimer's disease. The number of people with the disease doubles every 5 years beyond age 65.
Family history is another risk factor. Scientists believe that genetics may play a role in the causes of Alzheimer's disease. For example, early-onset familial Alzheimer's disease, a rare form of Alzheimer's disease that occurs between the ages of 30 and 60, is inherited.

The more common form of Alzheimer's disease is known as late-onset. It occurs later in life, and no obvious family pattern is seen in most cases. One risk factor for this type of Alzheimer's disease is a gene that makes one form of a protein called apolipoprotein E, or apoE.

Everyone has apoE, which helps carry cholesterol in the blood. Only about 15 percent of people have the form that increases the risk of Alzheimer's. It is likely that other genes may also increase the risk of Alzheimer's or protect against it, but they remain to be discovered.

Scientists still need to learn a lot more about causes and risk factors. In addition to genetics and apoE, they are studying education, diet, environment, and molecular changes in the brain to learn what role they might play in the development of this disease.

Scientists are finding more clues that some of the risk factors for heart disease and stroke -- like high blood pressure, high cholesterol, and low levels of the vitamin folate -- may also increase the risk of Alzheimer's. Researchers are also investigating the possibility that physical, mental, and social activities may protect against Alzheimer's.

Studies have shown that keeping the brain active may be associated with a reduced risk of Alzheimer's. In a study with nuns, priests, and brothers known as the Religious Orders study, researchers asked more than 700 participants to describe the amount of time they spent in mentally stimulating activities.

These activities included listening to the radio, reading newspapers, playing puzzle games, and going to museums. After following the participants for four years, researchers found that the risk of developing Alzheimer's was 47 percent lower on average for those who did these mentally stimulating activities most frequently than for those who did them least frequently.

There are no treatments, drugs, or pills that can prevent Alzheimer's, but people can take some steps that may reduce their risk. These include:

1.     lowering cholesterol and homocysteine levels
2.     lowering high blood pressure levels
3.     controlling diabetes
4.     exercising regularly
5.     engaging in activities that stimulate the mind
6.     A healthy diet is important. Although no special diets or nutritional supplements have been found to prevent or reverse Alzheimer's disease, a balanced diet helps maintain overall good health.

Research has not shown that these steps will lower your risk for Alzheimer's, and studies designed to directly test their ability to do so are currently in progress. However, all of these things are good to do anyway because they lower the risk for other diseases and help maintain and improve your overall health and well-being.

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Alzheimer's Disease0

Dementia is a brain disorder that seriously affects a person's memory, thinking, and reasoning skills. People with dementia often have trouble thinking and speaking clearly, remembering recent events, and learning new things. Over time, it becomes hard for them to handle everyday activities and take care of themselves. There are many causes of dementia, but Alzheimer's disease is the most common cause of dementia in older persons. Scientists think that up to 4.5 million people in the United States suffer from Alzheimer's disease. The disease usually begins after age 65 and risk goes up with age. While younger people also may get Alzheimer's disease, it is much less common.

About 5 percent of men and women ages 65 to 74 have Alzheimer's disease, and nearly half of those age 85 and older may have the disease. It is important to note, however, that Alzheimer's disease is not a normal part of aging.

Alzheimer's disease is named after Dr. Alois Alzheimer, a German doctor. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. He found abnormal clumps and tangled bundles of fibers. The clumps are now called amyloid plaques and the tangles are called neurofibrillary tangles. Today, these plaques and tangles in the brain are considered signs of Alzheimer's disease.

Scientists also have found other brain changes in people with Alzheimer's disease. There is a loss of nerve cells and pathways in areas of the brain that are vital to memory and other mental abilities. There also are lower levels of some of the chemicals in the brain that carry complex messages back and forth between nerve cells.

Alzheimer's disease is characterized by the general atrophy (dying back) of the cerebral cortex with accumulation of proteins into neuritic (senile) plaques in the cortex and neurofibrillary tangles in the brain. The initial symptom of the disease is usually memory loss. Impairments in behavior and decline in daily living activities become more apparent as the neurodegeneration progresses. The most important risk factor for the disease is advancing age, but heredity also plays a significant role. Several different classes of medications are available to treat multiple aspects of mental impairment. These treatments do not slow the progression of the disease. Once dementia has set in, patients are usually in need of assistance with daily living or may be candidates for a skilled nursing facility. Although exercise, a healthy diet, and mentally stimulating activities are helpful to the patient, studies have shown they are not preventative. Research into the mechanisms of the disease has guided the search for new treatment. Some medications under investigation include anti-inflammatories, stem cells, and vaccines.

Alzheimer's disease may disrupt normal thinking and memory by blocking these messages between nerve cells.

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Autism Management0

The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. No single treatment is best and treatment is typically tailored to the child's needs. Although many psychosocial interventions have some positive evidence, suggesting that some form of treatment is preferable to no treatment, the methodological quality of systematic reviews of these studies has generally been poor, their clinical results are mostly tentative, and there is little evidence for the relative effectiveness of treatment options. Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills, and often improve functioning and decrease symptom severity and maladaptive behaviors; claims that intervention by around age three years is crucial are not substantiated. Available approaches include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy. and is well-established for improving intellectual performance of young children.

Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails. More than half of U.S. children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics. Aside from antipsychotics, there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD. A person with ASD may respond atypically to medications, the medications can have adverse effects, Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function after birth, Though most alternative treatments, such as melatonin, have only mild adverse effects some may place the child at risk. A 2008 study found that compared to their peers, autistic boys have significantly thinner bones if on casein-free diets; in 2005, botched chelation therapy killed a five-year-old child with autism.

Treatment is expensive; indirect costs are more so. For someone born in 2000, a U.S. study estimated an average lifetime cost of $ (net present value in dollars, inflation-adjusted from 2003 estimate), with about 10% medical care, 30% extra education and other care, and 60% lost economic productivity. Publicly supported programs are often inadequate or inappropriate for a given child, and unreimbursed out-of-pocket medical or therapy expenses are associated with likelihood of family financial problems; one 2008 U.S. study found a 14% average loss of annual income in families of children with ASD, and a related study found that ASD is associated with higher probability that child care problems will greatly affect parental employment. U.S. states increasingly require private health insurance to cover autism services, shifting costs from publicly funded education programs to privately funded health insurance. After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.

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Autism Classification0

Autism is one of the five pervasive developmental disorders (PDD), which are characterized by widespread abnormalities of social interactions and communication, and severely restricted interests and highly repetitive behavior. Unlike with autism, people with Asperger syndrome have no substantial delay in language development. whereas autism itself is often called ''autistic disorder'', ''childhood autism'', or ''infantile autism''. In this article, ''autism'' refers to the classic autistic disorder; in clinical practice, though, ''autism'', ''ASD'', and ''PDD'' are often used interchangeably.

The manifestations of autism cover a wide spectrum, ranging from individuals with severe impairments—who may be silent, mentally disabled, and locked into hand flapping and rocking—to high functioning individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication. Because the behavior spectrum is continuous, boundaries between diagnostic categories are necessarily somewhat arbitrary. or on how much support the individual requires in daily life; these subdivisions are not standardized and are controversial. Autism can also be divided into syndromal and non-syndromal autism; the syndromal autism is associated with severe or profound mental retardation or a congenital syndrome with physical symptoms, such as tuberous sclerosis. Although individuals with Asperger syndrome tend to perform better cognitively than those with autism, the extent of the overlap between Asperger syndrome, HFA, and non-syndromal autism is unclear.

Some studies have reported diagnoses of autism in children due to a loss of language or social skills, as opposed to a failure to make progress, typically from 15 to 30 months of age. The validity of this distinction remains controversial; it is possible that regressive autism is a specific subtype,

Research into causes has been hampered by the inability to identify biologically meaningful subpopulations and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics. Newer technologies such as fMRI can help identify biologically relevant phenotypes (observable traits) that can be viewed on brain scans, to help further neurogenetic studies of autism. It has been proposed to classify autism using genetics as well as behavior, with the name ''Type 1 autism'' denoting rare autism cases that test positive for a mutation in the CNTNAP2 gene.

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Autism Mechanism0

Autism's symptoms result from maturation-related changes in various systems of the brain. The behaviors appear to have multiple pathophysiologies. Autism appears to result from developmental factors that affect many or all functional brain systems, and to disturb the timing of brain development more than the final product. Neuroanatomical studies and the associations with teratogens strongly suggest that autism's mechanism includes alteration of brain development soon after conception. Just after birth, the brain of an autistic child grows faster than usual, followed by normal or relatively slower growth in childhood. The early overgrowth seems to be most prominent in areas underlying the development of higher cognitive specialization.

1.  Disturbed neuronal migration during early gestation.
2.  Unbalanced excitatory–inhibitory networks. or by poorly regulated synthesis of synaptic protein. Disrupted synaptic development may also contribute to epilepsy, which may explain why the two conditions are associated.

Interactions between the immune system and the nervous system begin early during the embryonic stage of life, and successful neurodevelopment depends on a balanced immune response. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD. Although some abnormalities in the immune system have been found in specific subgroups of autistic individuals, it is not known whether these abnormalities are relevant to or secondary to autism's disease processes. As autoantibodies are found in conditions other than ASD, and are not always present in ASD, the relationship between immune disturbances and autism remains unclear and controversial.

Several neurotransmitter abnormalities have been detected in autism, notably increased blood levels of serotonin. Whether these cause structural or behavioral abnormalities is unclear. Also, some inborn errors of metabolism are associated with autism but probably account for less than 5% of cases. Several studies have tested this hypothesis by demonstrating structural abnormalities in MNS regions of individuals with ASD, delay in the activation in the core circuit for imitation in individuals with Asperger syndrome, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD. However, individuals with autism also have abnormal brain activation in many circuits outside the MNS and the MNS theory does not explain the normal performance of autistic children on imitation tasks that involve a goal or object.

ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks.

In autism there is evidence for reduced functional connectivity of the default network, a large-scale brain network involved in social and emotional processing, with intact connectivity of the task-positive network, used in sustained attention and goal-directed thinking. In people with autism the two networks are not negatively correlated in time, suggesting an imbalance in toggling between the two networks, possibly reflecting a disturbance of self-referential thought. A 2008 brain-imaging study found a specific pattern of signals in the cingulate cortex which differs in individuals with ASD.

The underconnectivity theory of autism hypothesizes that autism is marked by underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes. Evidence for this theory has been found in functional neuroimaging studies on autistic individuals and by a brain wave study that suggested that adults with ASD have local overconnectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex. Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.

From studies based on event-related potentials, transient changes to the brain's electrical activity in response to stimuli, there is considerable evidence for differences in autistic individuals with respect to attention, orientiation to auditory and visual stimuli, novelty detection, language and face processing, and information storage; several studies have found a preference for non-social stimuli. For example, magnetoencephalography studies have found evidence in autistic children of delayed responses in the brain's processing of auditory signals.

Neuropsychology
Two major categories of cognitive theories have been proposed about the links between autistic brains and behavior.

The first category focuses on deficits in social cognition. The empathizing–systemizing theory postulates that autistic individuals can systemize—that is, they can develop internal rules of operation to handle events inside the brain—but are less effective at empathizing by handling events generated by other agents. An extension, the extreme male brain theory, hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing;

These theories are somewhat related to the earlier theory of mind approach, which hypothesizes that autistic behavior arises from an inability to ascribe mental states to oneself and others. The theory of mind hypothesis is supported by autistic children's atypical responses to the Sally–Anne test for reasoning about others' motivations, and the mirror neuron system theory of autism described in ''Pathophysiology'' maps well to the hypothesis.

The second category focuses on nonsocial or general processing. Executive dysfunction hypothesizes that autistic behavior results in part from deficits in working memory, planning, inhibition, and other forms of executive function. A strength of the theory is predicting stereotyped behavior and narrow interests; two weaknesses are that executive function is hard to measure and that executive function deficits have not been found in young autistic children. A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals. These theories map well from the underconnectivity theory of autism.

Neither category is satisfactory on its own; social cognition theories poorly address autism's rigid and repetitive behaviors, while the nonsocial theories have difficulty explaining social impairment and communication difficulties. A combined theory based on multiple deficits may prove to be more useful.

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Autism Screening0

About half of parents of children with ASD notice their child's unusual behaviors by age 18 months, and about four-fifths notice by age 24 months. In contrast, the UK National Screening Committee recommends against screening for ASD in the general population, because screening tools have not been fully validated and interventions lack sufficient evidence for effectiveness.

Screening tools include the Modified Checklist for Autism in Toddlers (M-CHAT), the Early Screening of Autistic Traits Questionnaire, and the First Year Inventory; initial data on M-CHAT and its predecessor CHAT on children aged 18–30 months suggests that it is best used in a clinical setting and that it has low sensitivity (many false-negatives) but good specificity (few false-positives). Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture.

Genetic screening for autism is generally still impractical. Autism is defined in the DSM-IV-TR as exhibiting at least six symptoms total, including at least two symptoms of qualitative impairment in social interaction, at least one symptom of qualitative impairment in communication, and at least one symptom of restricted and repetitive behavior.

Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with parts of objects. Onset must be prior to age three years, with delays or abnormal functioning in either social interaction, language as used in social communication, or symbolic or imaginative play. The disturbance must not be better accounted for by Rett syndrome or childhood disintegrative disorder. ICD-10 uses essentially the same definition.

Several diagnostic instruments are available. Two are commonly used in autism research: the Autism Diagnostic Interview-Revised (ADI-R) is a semistructured parent interview, and the Autism Diagnostic Observation Schedule (ADOS) uses observation and interaction with the child. The Childhood Autism Rating Scale (CARS) is used widely in clinical environments to assess severity of autism based on observation of children. A differential diagnosis for ASD at this stage might also consider mental retardation, hearing impairment, and a specific language impairment The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as depression.

Clinical genetics evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause. consensus guidelines in the U.S. and UK are limited to high-resolution chromosome and fragile X testing. As new genetic tests are developed several ethical, legal, and social issues will emerge. Commercial availability of tests may precede adequate understanding of how to use test results, given the complexity of autism's genetics. Metabolic and neuroimaging tests are sometimes helpful, but are not routine. In the UK the National Autism Plan for Children recommends at most 30 weeks from first concern to completed diagnosis and assessment, though few cases are handled that quickly in practice. A 2009 U.S. study found the average age of formal ASD diagnosis was 5.7 years, far above recommendations, and that 27% of children remained undiagnosed at age 8 years. Although the symptoms of autism and ASD begin early in childhood, they are sometimes missed; years later, adults may seek diagnoses to help them or their friends and family understand themselves, to help their employers make adjustments, or in some locations to claim disability living allowances or other benefits.

Underdiagnosis and overdiagnosis are problems in marginal cases, and much of the recent increase in the number of reported ASD cases is likely due to changes in diagnostic practices. The increasing popularity of drug treatment options and the expansion of benefits has given providers incentives to diagnose ASD, resulting in some overdiagnosis of children with uncertain symptoms. Conversely, the cost of screening and diagnosis and the challenge of obtaining payment can inhibit or delay diagnosis. It is particularly hard to diagnose autism among the visually impaired, partly because some of its diagnostic criteria depend on vision, and partly because autistic symptoms overlap with those of common blindness syndromes.

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Autism Prognosis0

There is no known cure. A few autistic children have acquired speech at age 5 or older. Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination. Although core difficulties tend to persist, symptoms often become less severe with age. Acquiring language before age six, having an IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely with severe autism.

A 2004 British study of 68 adults who were diagnosed before 1980 as autistic children with IQ above 50 found that 12% achieved a high level of independence as adults, 10% had some friends and were generally in work but required some support, 19% had some independence but were generally living at home and needed considerable support and supervision in daily living, 46% needed specialist residential provision from facilities specializing in ASD with a high level of support and very limited autonomy, and 12% needed high-level hospital care.

A 2005 Swedish study of 78 adults that did not exclude low IQ found worse prognosis; for example, only 4% achieved independence. A 2008 Canadian study of 48 young adults diagnosed with ASD as preschoolers found outcomes ranging through poor (46%), fair (32%), good (17%), and very good (4%); 56% of these young adults had been employed at some point during their lives, mostly in volunteer, sheltered or part-time work.

 Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children. because of inadequate data, these numbers may underestimate ASD's true prevalence. PDD-NOS's prevalence has been estimated at 3.7 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, and childhood disintegrative disorder at 0.02 per 1,000.

The number of reported cases of autism increased dramatically in the 1990s and early 2000s. This increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness, though unidentified environmental risk factors cannot be ruled out. The available evidence does not rule out the possibility that autism's true prevalence has increased; The risk is greater with older fathers than with older mothers; two potential explanations are the known increase in mutation burden in older sperm, and the hypothesis that men marry later if they carry genetic liability and show some signs of autism.

Autism is associated with several other conditions:

• Genetic disorders. About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome, and ASD is associated with several genetic disorders.
• Mental retardation. The fraction of autistic individuals who also meet criteria for mental retardation has been reported as anywhere from 25% to 70%, a wide variation illustrating the difficulty of assessing autistic intelligence. For ASD other than autism, the association with mental retardation is much weaker.
• Anxiety disorders are common among children with ASD; there are no firm data, but studies have reported prevalences ranging from 11% to 84%. Many anxiety disorders have symptoms that are better explained by ASD itself, or are hard to distinguish from ASD's symptoms.
• Epilepsy, with variations in risk of epilepsy due to age, cognitive level, and type of language disorder.
• Several metabolic defects, such as phenylketonuria, are associated with autistic symptoms.
• Minor physical anomalies are significantly increased in the autistic population.
• Preempted diagnoses. Although the DSM-IV rules out concurrent diagnosis of many other conditions along with autism, the full criteria for ADHD, Tourette syndrome, and other of these conditions are often present and these comorbid diagnoses are increasingly accepted.

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Autism Causes0

It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for autism's characteristic triad of symptoms. Complexity arises due to interactions among multiple genes, the environment, and epigenetic factors which do not change DNA but are heritable and influence gene expression. Studies of twins suggest that heritability is 0.7 for autism and 0.9 for the broader autism phenotype, and siblings of those with autism are about 25 times more likely to be autistic than the general population. Hence, a substantial fraction of autism cases may be traceable to genetic causes that are highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome.

Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion. Gene replacement studies in mice suggest that autistic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes. All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, it is strong evidence that autism arises very early in development. Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies, Environmental factors that have been claimed to contribute to or exacerbate autism, or may be important in future research, include certain foods, infectious disease, heavy metals, solvents, diesel exhaust, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines, Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination, and this has given rise to theories that vaccines or their preservatives cause autism. Although these theories lack convincing scientific evidence and are biologically implausible, parental concern about autism has led to lower rates of childhood immunizations and higher likelihood of measles outbreaks.

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Autism History0

A few examples of autistic symptoms and treatments were described long before autism was named. The ''Table Talk'' of Martin Luther contains the story of a 12-year-old boy who may have been severely autistic. According to Luther's notetaker Mathesius, Luther thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated. The earliest well-documented case of autism is that of Hugh Blair of Borgue, as detailed in a 1747 court case in which his brother successfully petitioned to annul Blair's marriage to gain Blair's inheritance. The Wild Boy of Aveyron, a feral child caught in 1798, showed several signs of autism; the medical student Jean Itard treated him with a behavioral program designed to help him form social attachments and to induce speech via imitation.

The New Latin word ''autismus'' (English translation ''autism'') was coined by the Swiss psychiatrist Eugen Bleuler in 1910 as he was defining symptoms of schizophrenia. He derived it from the Greek word ''autós'' (a?t??, meaning ''self''), and used it to mean morbid self-admiration, referring to "autistic withdrawal of the patient to his fantasies, against which any influence from outside becomes an intolerable disturbance".

The word ''autism'' first took its modern sense in 1938 when Hans Asperger of the Vienna University Hospital adopted Bleuler's terminology ''autistic psychopaths'' in a lecture in German about child psychology. Asperger was investigating an ASD now known as Asperger syndrome, though for various reasons it was not widely recognized as a separate diagnosis until 1981. Almost all the characteristics described in Kanner's first paper on the subject, notably "autistic aloneness" and "insistence on sameness", are still regarded as typical of the autistic spectrum of disorders.

Kanner's reuse of ''autism'' led to decades of confused terminology like ''infantile schizophrenia'', and child psychiatry's focus on maternal deprivation led to misconceptions of autism as an infant's response to "refrigerator mothers". Starting in the late 1960s autism was established as a separate syndrome by demonstrating that it is lifelong, distinguishing it from mental retardation and schizophrenia and from other developmental disorders, and demonstrating the benefits of involving parents in active programs of therapy. As late as the mid-1970s there was little evidence of a genetic role in autism; now it is thought to be one of the most heritable of all psychiatric conditions. Although the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD, and many primary care physicians and medical specialists still express some beliefs consistent with outdated autism research. The Internet has helped autistic individuals bypass nonverbal cues and emotional sharing that they find so hard to deal with, and has given them a way to form online communities and work remotely. Sociological and cultural aspects of autism have developed: some in the community seek a cure, while others believe that autism is simply another way of being.

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What is Autism?0

Autism is a disorder of neural development that is characterized by impaired social interaction and communication, and by restricted and repetitive behavior. These signs all begin before a child is three years old. and tend to continue through adulthood, although often in more muted form.

Unusual social development becomes apparent early in childhood. Autistic infants show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Autistic toddlers differ more strikingly from social norms; for example, they have less eye contact and turn taking, and are more likely to communicate by manipulating another person's hand. Most autistic children display moderately less attachment security than non-autistic children, although this difference disappears in children with higher mental development or less severe ASD. Older children and adults with ASD perform worse on tests of face and emotion recognition.

Contrary to common beliefs, autistic children do not prefer being alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they feel. Functional friendships, such as those resulting in invitations to parties, may affect their quality of life more deeply.

Communication
About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs. Differences in communication may be present from the first year of life, and may include delayed onset of babbling, unusual gestures, diminished responsiveness, and vocal patterns that are not synchronized with the caregiver. In the second and third years, autistic children have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Autistic children are less likely to make requests or share experiences, and are more likely to simply repeat others' words (echolalia)

In a pair of studies, high-functioning autistic children aged 8–15 performed equally well, and adults better than individually matched controls at basic language tasks involving vocabulary and spelling. Both autistic groups performed worse than controls at complex language tasks such as figurative language, comprehension and inference. As people are often sized up initially from their basic language skills, these studies suggest that people speaking to autistic individuals are more likely to overestimate what their audience comprehends.

• Restricted behavior is limited in focus, interest, or activity, such as preoccupation with a single television program, toy, or game.
• Self-injury includes movements that injure or can injure the person, such as eye poking, skin picking, hand biting, and head banging.

Other Symptoms
Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family.

An estimated 0.5% to 10% of individuals with ASD show unusual abilities, ranging from splinter skills such as the memorization of trivia to the extraordinarily rare talents of prodigious autistic savants. Many individuals with ASD show superior skills in perception and attention, relative to the general population.

Sensory abnormalities are found in over 90% of those with autism, and are considered core features by some, although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders. Differences are greater for under-responsivity (for example, walking into things) than for over-responsivity (for example, distress from loud noises) or for sensation seeking (for example, rhythmic movements).

An estimated 60%–80% of autistic people have motor signs that include poor muscle tone, poor motor planning, and toe walking.

Unusual eating behavior occurs in about three-quarters of children with ASD, to the extent that it was formerly a diagnostic indicator. Selectivity is the most common problem, although eating rituals and food refusal also occur; this does not appear to result in malnutrition. Although some children with autism also have gastrointestinal (GI) symptoms, there is a lack of published rigorous data to support the theory that autistic children have more or different GI symptoms than usual; studies report conflicting results, and the relationship between GI problems and ASD is unclear.

Parents of children with ASD have higher levels of stress. Siblings of children with ASD report greater admiration of and less conflict with the affected sibling than siblings of unaffected children or those with Down syndrome; siblings of individuals with ASD have greater risk of negative well-being and poorer sibling relationships as adults.

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Parkinson's Disease Support0

In 1957, William Black, President of Chock full o'Nuts coffee company, founded the Parkinson's Disease Foundation (PDF) after one of his company's employees was diagnosed with Parkinson's. Black launched the organization with a $250,000 grant to support Parkinson's Research. While at first a regional organization, PDF expanded the scope of its activities throughout the U.S., and merged with the United Parkinson Foundation in 1999. Today, PDF focuses on funding research to learn the causes of and find a cure for Parkinson's, as well providing education and support for people with Parkinson's in the U.S. Since it was founded in 1957, PDF has provided more than $80 million to research.

PDF also leads PDtrials, a collaborative initiative of Parkinson’s organizations dedicated to increasing education and awareness about clinical research. Central to this initiative is the www.pdtrials.org website that provides information and education about Parkinson's clinical research, and provides a portal for people with Parkinson's to search for specific clinical trials using criteria such as location, trial type, and symptom.

Another famous sufferer of young-onset Parkinson's is Michael J. Fox, whose book, ''Lucky Man'' (2000), focused on his experiences with the disease and his career and family travails in the midst of it. Fox established ''The Michael J. Fox Foundation for Parkinson's Research'' to develop a cure for Parkinson's disease within this decade.

Another foundation that supports Parkinson's research was established by Davis Phinney, a notable figure in the cycling world. Phinney has competed in the Olympics, Pan-Am Games and has competed as a pro-cyclist for nearly twenty years. The Davis Phinney Foundation strives to improve the lives of those living with Parkinson's disease.

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Parkinson's Disease Treatment0

Parkinson's disease is a chronic disorder that requires broad-based management including patient and family education, support group services, general wellness maintenance, physiotherapy, exercise, and nutrition.
Dopamine agonists

The dopamine agonists bromocriptine, pergolide, pramipexole, ropinirole , piribedil, cabergoline, apomorphine, and lisuride are moderately effective. These have their own side effects including those listed above in addition to somnolence, hallucinations and/or insomnia. Several forms of dopamine agonism have been linked with a markedly increased risk of problem gambling. Dopamine agonists initially act by stimulating some of the dopamine receptors. However, they cause the dopamine receptors to become progressively less sensitive, thereby eventually increasing the symptoms.

Dopamine agonists can be useful for patients experiencing on-off fluctuations and dyskinesias as a result of high doses of L-dopa. Apomorphine can be administered via subcutaneous injection using a small pump which is carried by the patient. A low dose is automatically administered throughout the day, reducing the fluctuations of motor symptoms by providing a steady dose of dopaminergic stimulation. After an initial "apomorphine challenge" in hospital to test its effectiveness and brief patient and primary caregiver (often a spouse or partner), the latter of whom takes over maintenance of the pump. The injection site must be changed daily and rotated around the body to avoid the formation of nodules. Apomorphine is also available in a more acute dose as an autoinjector pen for emergency doses such as after a fall or first thing in the morning. Nausea and vomiting are common, and may require domperidone (an antiemetic).

MAO-B Inhibitors
Selegiline and rasagiline reduce the symptoms by inhibiting monoamine oxidase-B (MAO-B). MAO-B breaks down dopamine secreted by the dopaminergic neurons, so inhibitting it will result in inhibition of the breakdown of dopamine. Metabolites of selegiline include L-amphetamine and L-methamphetamine (not to be confused with the more notorious and potent dextrorotary isomers). This might result in side effects such as insomnia. Use of L-dopa in conjunction with selegiline has increased mortality rates that have not been effectively explained. Another side effect of the combination can be stomatitis. One report raised concern about increased mortality when MAO-B inhibitors were combined with L-dopa; however subsequent studies have not confirmed this finding. Unlike other non selective monoamine oxidase inhibitors, tyramine-containing foods do not cause a hypertensive crisis.

Surgery and Deep Brain Stimulation
Treating Parkinson's disease with surgery was once a common practice, but after the discovery of levodopa, surgery was restricted to only a few cases. Studies in the past few decades have led to great improvements in surgical techniques, and surgery is again being used in people with advanced PD for whom drug therapy is no longer sufficient.

Deep brain stimulation is presently the most used surgical means of treatment, but other surgical therapies that have shown promise include surgical lesion of the subthalamic nucleus and of the internal segment of the globus pallidus, a procedure known as pallidotomy.

Neurorehabilitation
There is partial evidence that speech or mobility problems can improve with rehabilitation although studies are still scarce and of low quality. Regular physical exercise and/or therapy can be beneficial to the patient for maintaining and improving mobility, flexibility, strength, gait speed, and quality of life.

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Parkinson's Disease Research0

Gene Therapy

Currently under investigation is gene therapy. This involves using a non-infectious virus to shuttle a gene into a part of the brain called the subthalamic nucleus (STN). The gene used leads to the production of an enzyme called glutamic acid decarboxylase (GAD), which catalyses the production of a neurotransmitter called GABA. GABA acts as a direct inhibitor on the overactive cells in the STN.

GDNF infusion involves the infusion of GDNF (glial-derived neurotrophic factor) into the basal ganglia using surgically implanted catheters. Via a series of biochemical reactions, GDNF stimulates the formation of L-dopa. GDNF therapy is still in development.

Neuroprotective Treatments
Neuroprotective treatments are at the forefront of PD research, but are still under clinical scrutiny. These agents could protect neurons from cell death induced by disease presence resulting in a slower progression of disease. Agents currently under investigation as neuroprotective agents include anti-apoptotic drugs (CEP 1347 and CTCT346), lazaroids, bioenergetics, antiglutamatergic agents and dopamine receptors. Clinically evaluated neuroprotective agents are the monoamine oxidase inhibitors selegiline and rasagiline, dopamine agonists, and the complex I mitochondrial fortifier coenzyme Q10.
Neural transplantation

The first prospective randomised double-blind sham-placebo controlled trial of dopamine-producing cell transplants failed to show an improvement in quality of life although some significant clinical improvements were seen in patients below the age of 60. A significant problem was the excess release of dopamine by the transplanted tissue, leading to dystonias. Research in African green monkeys suggests that the use of stem cells might in future provide a similar benefit without inducing dystonias.
Alternative Treatments

Nutrients have been used in clinical studies and are used by people with PD in order to partially treat PD or slow down its deterioration. The L-dopa precursor L-tyrosine was shown to relieve an average of 70% of symptoms. Ferrous iron, the essential cofactor for L-dopa biosynthesis was shown to relieve between 10% and 60% of symptoms in 110 out of 110 patients.

More limited efficacy has been obtained with the use of THFA, NADH, and pyridoxine—coenzymes and coenzyme precursors involved in dopamine biosynthesis. Vitamin C and vitamin E in large doses are commonly used by patients in order to theoretically lessen the cell damage that occurs in PD. This is because the enzymes superoxide dismutase and catalase require these vitamins in order to nullify the superoxide anion, a toxin commonly produced in damaged cells. However, in the randomized controlled trial, DATATOP of patients with early PD, no beneficial effect for vitamin E compared to placebo was seen.

''Mucuna pruriens'', is a natural source of therapeutic quantities of L-dopa, and has been under some investigation.

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Parkinson's Disease Pathophysiology0

The symptoms of Parkinson's disease result from the greatly reduced activity of pigmented dopamine-secreting (dopaminergic) cells in the pars compacta region of the substantia nigra (literally "black substance"). These neurons project to the striatum and their loss leads to alterations in the activity of the neural circuits within the basal ganglia that regulate movement, in essence an inhibition of the direct pathway and excitation of the indirect pathway.

The direct pathway facilitates movement and the indirect pathway inhibits movement, thus the loss of these cells leads to a hypokinetic movement disorder. The lack of dopamine results in increased inhibition of the ventral anterior nucleus of the thalamus, which sends excitatory projections to the motor cortex, thus leading to hypokinesia.

There are four major dopamine pathways in the brain; the nigrostriatal pathway, referred to above, mediates movement and is the most conspicuously affected in early Parkinson's disease. The other pathways are the mesocortical, the mesolimbic, and the tuberoinfundibular. Disruption of dopamine along the non-striatal pathways likely explains much of the neuropsychiatric pathology associated with Parkinson's disease.

The mechanism by which the brain cells in Parkinson's are lost may consist of an abnormal accumulation of the protein alpha-synuclein bound to ubiquitin in the damaged cells. The alpha-synuclein-ubiquitin complex cannot be directed to the proteosome. This protein accumulation forms proteinaceous cytoplasmic inclusions called Lewy bodies. The latest research on pathogenesis of disease has shown that the death of dopaminergic neurons by alpha-synuclein is due to a defect in the machinery that transports proteins between two major cellular organelles — the endoplasmic reticulum (ER) and the Golgi apparatus. Certain proteins like Rab1 may reverse this defect caused by alpha-synuclein in animal models.

Excessive accumulations of iron, which are toxic to nerve cells, are also typically observed in conjunction with the protein inclusions. Iron and other transition metals such as copper bind to neuromelanin in the affected neurons of the substantia nigra. Neuromelanin may be acting as a protective agent. The most likely mechanism is generation of reactive oxygen species. Iron also induces aggregation of synuclein by oxidative mechanisms. Similarly, dopamine and the byproducts of dopamine production enhance alpha-synuclein aggregation. The precise mechanism whereby such aggregates of alpha-synuclein damage the cells is not known. The aggregates may be merely a normal reaction by the cells as part of their effort to correct a different, as-yet unknown, insult. Based on this mechanistic hypothesis, a transgenic mouse model of Parkinson's has been generated by introduction of human wild-type alpha-synuclein into the mouse genome under control of the platelet-derived-growth factor-ß promoter.

A recent view of Parkinson's disease implicates specialized calcium channels that allow substantia nigra neurons, but not most neurons, to repetitively fire in a "pacemaker" like pattern. The consequent flooding of calcium into these neurons may aggravate damage to mitochondria and may cause cell death. One study has found that, in experimental animals, treatment with a calcium channel blocker isradapine had a substantial protective effect against the development of Parkinson's disease.

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Parkinson's Disease Prognosis0

PD is not considered to be a fatal disease by itself, but it progresses with time. The average life expectancy of a PD patient is generally lower than for people who do not have the disease. In the late stages of the disease, PD may cause complications such as choking, pneumonia, and falls that can lead to death.

The progression of symptoms in PD may take 20 years or more. In some people, however, the disease progresses more quickly. There is no way to predict what course the disease will take for an individual person. With appropriate treatment, most people with PD can live productive lives for many years after diagnosis. There are some indications that Parkinson's disease acquires resistance to drug treatment by evolving into a Parkinson-plus disorder, usually Lewy Body Dementia, although transitions to Progressive Supranuclear Palsy or Multiple System Atrophy are not unknown.

In at least some studies, it has been observed that mortality was significantly increased, and longevity decreased among nursing home patients as compared to community dwelling patients.

One commonly used system for describing how the symptoms of PD progress is called the Hoehn and Yahr scale. Another commonly used scale is the Unified Parkinson's Disease Rating Scale (UPDRS). This much more complicated scale has multiple ratings that measure motor function, and also mental functioning, behavior, mood, and activities of daily living. Both the Hoehn and Yahr scale and the UPDRS are used to measure how individuals are faring and how much treatments are helping them. It should be noted that neither scale is specific to Parkinson's disease; that patients with other illnesses can score in the Parkinson's range.

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Parkinson's Disease Diagnosis0

Typically, the diagnosis is based on medical history and neurological examination conducted by interviewing and observing the patient in person using the Unified Parkinson's Disease Rating Scale. A radiotracer for SPECT scanning machines called DaTSCAN and made by General Electric is specialized for diagnosing Parkinson's Disease, but it is only marketed in Europe. Due to this, the disease can be difficult to diagnose accurately, especially in its early stages.

Due to symptom overlap with other diseases, only 75% of clinical diagnoses of PD are confirmed to be idiopathic PD at autopsy.

Early signs and symptoms of PD may sometimes be dismissed as the effects of normal aging. The physician may need to observe the person for some time until it is apparent that the symptoms are consistently present. Usually doctors look for shuffling of feet and lack of swing in the arms.

Doctors may sometimes request brain scans or laboratory tests in order to rule out other diseases. However, CT and MRI brain scans of people with PD usually appear normal.

Clinical practice guidelines introduced in the UK in 2006 state that the diagnosis and follow-up of Parkinson's disease should be done by a specialist in the disease, usually a neurologist or geriatrician with an interest in movement disorders.

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