What Is Sleep Apnea? Causes, Risk Factors, and Effects

Sleep apnea is a fairly common sleep disorder that can affect both adults and children. It causes you to stop breathing or experience low breathing at certain points during sleep. Each period of not breathing is known as an apnea and can last anywhere from a few seconds to minutes. This can occur any number of times from 5 to 30 or more every hour. The condition can be diagnosed by spending a night in a sleep lab and suffers have problems with daytime fatigue, slowed reactions and vision problems. There are three different types of this condition which we will detail below.

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What is Low Latent Inhibition? Find out its Pros, Cons and diagnosis

Michael Scofield is the main protagonist in the American television series Prison Break. In this series, Michael was diagnosed to be suffering from LOW LATENT INHIBITION. It is here, i got an idea to right a post about LLI.

The brains of creative people appear to be more open to incoming stimuli from the surrounding environment. Other people's brains might shut out this same information through a process called "latent inhibition" - defined as an animal's unconscious capacity to ignore stimuli that experience has shown are irrelevant to its needs. Through psychological testing, the researchers showed that creative individuals are much more likely to have low levels of latent inhibition.

This means that creative individuals remain in contact with the extra information constantly streaming in from the environment. The normal person classifies an object, and then forgets about it, even though that object is much more complex and interesting than he or she thinks. The creative person, by contrast, is always open to new possibilities.

As you grow, the mind learns to label objects and filter out extraneous information.This filtering process is called 'latent inhibition' - and it means that the conscious mind is only aware of a fraction of the data being processed by the brain. In some rare cases, the ability to filter incoming data is decreased. People with LLI (low latent inhibition) are incapable of seeing things in terms of labels. They notice an awful lot more. Reality becomes more vivid and alive. Everyone has different levels of latent inhibition. It can become a problem if the inhibition process is radically decreased. LLI is not a disease. You do not suffer from it. It is a dysfunction that has both positive and negative sides.

For most people, reality is experienced piecemeal. They concentrate on one task at the exclusion of other things. Whilst typing on the computer, hearing diminishes, smell diminishes - the awareness is narrowed. With LLI this is not the case at all. The input is constant. Your awareness does not fluctuate. It only oscillates between hyper-awareness and extreme-awareness - with the latter being something to be concerned about. LLI puts you in touch with the raw immediacy of reality. The overwhelming sensory input means that you experience everything simultaneously: the humming of the computer, the flickering of the monitor, the feel of the clothing you wear, your emotions, the bird in your garden, the smell of coffee... Every miniscule detail happening around you is felt in its entirety. This does not mean that you read every word, remember every facet, but you do see it, smell it, hear it, taste it and feel it. The information is absorbed. Your mind is sponge-like in its capacity to pick things up. You learn from them, and demonstrate new insights and understanding.

Pros-

• You notice more, hear more, smell more and feel more through tactile contact. Without any conscious effort, your mind is in possession of a broader intake of information.
• Upon encountering any form of stimulus (that interests you), your mind automatically dismantles and explores its components.
• You usually see through the lies and the deceptions that people use in everyday life.
• When learning, you can often make instantaneous changes.
• Self-correction is easy because the underlying principle is more evident. Clearer.
• You make connections and associations between seemingly unrelated material.
• Comprehension is typically easy. You notice the non-verbal background information and this often provides a more comprehensive picture than what is being spoken.
• There are exponential leaps of insight taking place all the time, with the background reasoning intact. Wave-upon-wave of permutations, options, variables and choices.
• Creativity is a given. You see alternatives.
• You notice things that other people miss.
• There is no talking voice in your head. No 'chattering monkey'. The volume and complexity of the information drowns out conscious thought entirely.
• Verbalising what takes place in your mind is impossible. Words render only a fraction of the entirety.
• You see the world more thoroughly.
• Listening to other people talking/thinking aloud can be infuriating. They are at point A when you have reached point N already.
• Learning is not limited to defined periods of academic study. The assimilation of information is constant, ongoing and never static. There are no lulls or pauses. Everything offers a lesson.
• Within the maelstrom of information there exists a place of calm and quietude. The eye of the storm. No verbalisation exists. No internal narrative. Just presence. No sense of self to intrude of interrupt.
  

Cons-

• Education is awkward. Schools are not set-up to cater with this disorder. The way in which things are approached by schools seems piecemeal and incomplete.
• It is difficult to write/type/speak quickly enough to articulate ideas and the breadth of the permutations involved.
• Tact is necessary. People lie constantly.
• LLI makes driving a car difficult. Your brain notices countless dangers and variables, and you become overwhelmed and nervous.
• Hypervigilance can lead to anxiety.
• Illusions are not very effective. You see through things without wanting to. Conventions and traditions have no significance.
• You do not value what other people value.
• Filtering out the variables and honing your options to something workable can be very difficult. Every solution potentially harbours new problems, new variables and new concerns.
• People may find you to be a little odd, unorthodox or a little intense.
• You have a habit of saying things that do not fit the accepted norm of behaviour. You often choose to disregard conventions because they serve no constructive purpose.
• Background noise is a major problem. Noisy neighbours can cause serious stress.
• Noticing things does not mean that you understand them. If anything, the abundance of what might be known lessens the desire to accumulate widespread knowledge.
  

AWARENESS:
A person experiencing LLI is not initially aware that they have the condition. To them, how they regard the world seems perfectly normal. Nothing unusual is apparent - they do not know anything else. The condition may become apparent through the differences in what you say and see, relative to other people. In many cases the condition remains undiagnosed.

DO YOU HAVE LLI?
If you believe you have LLI, you probably don't. It is hard to self-diagnose yourself because individuals with LLI don't know any different than what they see every day. They believe everyone sees what they see.

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Tourette Syndrome, Its causes, Symptoms and Possible treatment

What is Tourette Syndrome?

Often mistakenly referred to as Turrets Sundrome, it is a neurological disease that impacts the central nervous system of a person. It normally affects young people and often goes away in later years. About one out of every 100 people is said to be affected with this disorder. Teenagers are often found to develop this disorder. The condition is more common in boys than girls.

The disease often occurs with other psychological conditions like Obsessive Compulsive Disorder (OCD), Attention Deficit Hyperactivity Disorder (ADHD) and Depression.

History of Tourette Syndrome:

This medical condition was first diagnosed in 1825 by Dr Georges Gilles de la Tourette, a French neurologist. In 1885, he published an account of the syndrome in nine of his patients. As he was the pioneer in describing the disorder, it has been named after him.

Tourettes Syndrome Symptoms:

This complex neurological disorder is characterized by some peculiar symptoms. The oddity of these symptoms made many people look upon the disease as a bizarre condition.

Motor tics:

This condition is mainly characterized by involuntary muscular movements. The movements are most prominently visible in the face even though other parts of the body are also affected. A Tourettes sufferer constantly grimaces, jerks his shoulders, clicks his tooth or moves his limbs.

The patient can stop it only for a while but not for extended periods. These tics or twitches are called motor tics. These are often misinterpreted by other people who think that the person is making faces at them. Sometimes the patient may even touch other people. In rare cases, the tics may evolve into self-injurious actions like lip-biting or excessive scratching.

Vocal tics:

Vocal tics or making sounds is another of the notable Tourette Syndrome symptoms. In the early stages of the disorder, the vocal tics include making sounds like grunting, barking, throat clearing, sighing, sniffing or clicking the tongue. In the later stages, these may develop into complicated and annoying symptoms like uttering words and phrases out of context. Many sufferers of this syndrome repeat words spoken by themselves or others. In certain cases, the patient may even utter swear words loudly and repeatedly. These are involuntary actions which the sufferer cannot stop at his or her will.

Associated symptoms:

There are often other problems related to the condition. These associated symptoms of Tourette Syndrome include

• Obsessive actions

• Autism

• Sleep irregularities

• Depression

• Anxiety

• Compulsive disorders

• Learning problems

• Restless leg syndrome

• Hyperactivity

Tourett Syndrome sufferers, however, have normal intelligence. The disorder does not affect their IQ.

Tourette Syndrome Causes:

It is not clear exactly what causes Tourette Syndrome. However, researchers have found that heredity is mainly responsible for this disorder. It has been established that most people with the Tourette disorder have inherited it from their parents. But it is unclear how the disease passes on from parents to offsprings. The disease is not contagious. It is believed that a person with a parent suffering from the syndrome has 50% of chance of developing the disorder in his or her adolescent years.

The disorder affects the neurotransmitter chemicals in the brain, especially the dopamine. Dopamine is necessary for the normal functioning of the central nervous system. An imbalance in dopamine immediately affects the motor functions in the body. It impacts the voluntary movements in the system. A severe reduction in dopamine can also lead to Parkinson’s disease.

Other factors like infections and social environment can also play a role in making the disorder more severe. Psychological factors like stress and anxiety can also aggravate the condition. It is not known, however, if these cause Tourettes Syndrome as well.

Diagnosis of Tourette Syndrome:

Tourette Syndrome Treatment is done after a proper diagnosis of the disorder. The condition is often mistaken with other diseases like asthma, autism and Lesch-Nyhan Syndrome that involve certain symptoms similar to the disease. The disorder is usually treated after careful observation of the patients’ symptoms. Physical examinations like urine test are done to check the presence of drugs in the system. The medical history of the patient as well as that of his family members is also analyzed.

Treatment for Tourette Syndrome:

The disorder is not usually treated unless they interfere with everyday activities. Medication, psychological counseling and therapies are generally used to cure this neurological ailment.

Medications:

• Medicines are used to reduce the frequency of tics in the sufferer. The drugs include

• Tranquilizers – Clonidine, Mellaril and Navane are some of the drugs used to reduce stress in the patient.

• Antidepressants – Drugs like Lithobid, Sertraline and Paxil increases the serotonin level and boosts nerve impulses

• Stimulants – Medicines like Pemoline, Dexedrine and Ritalin are used to control hyperactivity in Tourette patients.

Psychological counseling:

Stress and anxiety is found to aggravate tics. If needed, the patient is counseled by an experienced psychiatrist to reduce psychological stress. Tourette Syndrome in children is often cured by counseling.

Therapies:

Patients are taught to control their tics and monitor situations where they are aggravated. They are imparted training on how to reduce their movements and check their use of profane words. They are also taught to self-monitor their progress. In some cases, calm activities are advised that can soothe the mind and cure the symptoms.

Famous people with Tourette Syndrome:

There have been quite a few celebrities with Tourette Syndrome. The US National Team goalkeeper Tim Howard and ex-Major League baseball player Jim Eisenreich were victims of this disorder. But they defied this condition to climb high in their careers. Eisenrich once famously said that the ambition of his life was to become a quality player and a source of inspiration for children suffering from Tourettes condition. Author Samuel Johnson and composer Mozart were also suspected to be the Tourettes sufferers.

Tourette Syndrome Statistics:

• About 272,000 people are supposed to be affected with Tourettes disorder in the USA.

• A recent study shows that only 13.6% of Tourettes Syndrome patients keep suffering from the disease for lifetime.

• 75% of Tourettes sufferers develop this disorder after 11 years of age.

• A 2000 study showed that about 10 in every 1000 US children suffered from this condition.

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Poor Plaque protein Elimination is Linked to Alzheimer’s disease

Alzheimer’s disease appears to be caused by the brain’s poor elimination of a plaque component, beta-amyloid protein, rather than simply the accumulation of it, researchers from Washington University School of Medicine, St. Louis revealed in the journal Science. We already knew that beta-amyloid protein accumulation occurs in Alzheimer’s patients; this study reveals something nobody knew – that it is the poor clearance of the protein rather than its accumulation that is at the heart of the problem.

The authors say the brain’s failure to clear away a waste product (beta-amyloid) of normal metabolism fast enough results in a build-up of it, leading to the growth of plaques that can corrupt brain cells and cause Alzheimer’s disease.

Randall Bateman, MD, said:

“Clearance is impaired in Alzheimer’s disease. We compared a group of 12 patients with early Alzheimer’s disease to 12 age-matched and cognitively normal subjects. Both groups produced amyloid-beta (a-beta) at the same average rate, but there’s an average drop of about 30 percent in the clearance rates of the group with Alzheimer’s.”

The researchers have worked out that a decade of poor beta-amyloid clearance would be enough for an accumulation equal to that seen in Alzheimer patients’ brains.

The authors say their findings will have major implications for Alzheimer treatment and diagnosis.

Scientists will now want to find out how beta-amyloid, also known as a-beta, a byproduct of normal metabolism, is expelled from the brain, broken down, and got rid of by the body. The more they find out about this, the better doctors will become at diagnosing Alzheimer’s before symptoms appear. Pharmaceutical companies might also be able to develop medications one day that restore effective a-beta clearance from the brain before Alzheimer’s symptoms appear, hopefully preventing the disease.

We have long known that a-beta plays a vital role in the formation of brain plaques that are found during autopsies of people with Alzheimer’s disease.
Experts say that the brain expels a-beta, which is produced by brain cell activity, by moving it to the spinal fluid, from where it is disposed. Some previous studies had suggested that low a-beta levels in the spinal fluid might possibly be an indicator of Alzheimer’s disease before symptoms appear, perhaps because a-beta is still stuck in the brain and building up there.

The results of this study will lay to rest some experts’ doubts about whether a-beta might not be causatively linked to Alzheimer’s.

Bateman said:

“These findings support the idea that impaired a-beta clearance is fundamentally linked to Alzheimer’s disease.”

In this study, the researchers used SILK (stable isotope-linked kinetics), a process they developed themselves. SILK allows them to measure a-beta clearance rates, as well as production rates. The patients were given an intravenous drip the amino acid leucine that had been very slightly altered to label it.

The labeled leucine is picked up by the brain and incorporated into the new copies of a-beta proteins, as well as some others. Over a period of a few hours, periodic samples of the patients’ cerebrospinal fluid were taken through a lumbar catheter. They purified the a-beta from the samples and could determine how much of it included labeled leucine. The scientists were eventually able to measure the individual’s a-beta production rate.

As soon as the percentage of a-beta containing labeled leucine peaked, the scientists stopped introducing the labeled laucine and took periodic samples of the participants cerebrospinal fluid. This way they could measure how quickly their nervous systems eliminated the labeled a-beta. In other words, they could work out the how good the brain was at clearing out a-beta.

The study involved 24 subjects; 12 healthy individuals and 12 with early Alzheimer’s.

There was a considerable difference between the a-beta clearance rates of the Early Alzheimer’s Group and the Healthy Group. However, some participants in the Healthy Group had clearance rates very close to those in the Alzheimer’s Group. The question now is – are these seemingly healthy patients developing Alzheimer’s before symptoms begin to appear...?

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Alzheimer's Disease Animation, Causes, Sign symptoms And Treatment

Introduction:

Alzheimer's disease (AD) is a degenerative disease of the brain from which there is no recovery. The disease slowly attacks nerve cells in all parts of the cortex of the brain and some surrounding structures, thereby impairing a person's abilities to govern emotions, recognize errors and patterns, coordinate movement, and remember.

Causes:

Researchers are finding specific biologic factors involved with Alzheimer's disease. Various environmental and genetic players appear to contribute to or trigger the process by which these factors destroy nerve cells leading to this disease.

Biologic Factors in the Brain:

Imaging techniques in patients with Alzheimer's disease have found significant loss of cells and volume in the regions of the brain devoted to memory and higher mental functioning. Important abnormalities have specifically been observed during biopsies:

• Twisted nerve cell fibers, known as neurofibrillary tangles
• A sticky protein called beta amyloid

The Effects of Neurofibrillary Tangles and Beta Amyloid in Alzheimer's Disease. These biologic factors appear to be involved in the development Alzheimer's disease in the following ways:

• Neurofibrillary tangles are the damaged remains of microtubules, the support structure that allows the flow of nutrients through the neurons (nerve cells). A key component in these tangled fibers is an abnormal form of the tau protein, which in its healthy version helps in the assembly of the microtubule structure. The defective tau, however, appears to block the actions of the normal version.
• Beta Amyloid (also called A beta) is the second significant finding. This insoluble protein accumulates and forms sticky patches called neuritic plaque, which are found surrounded by the debris of dying nerve cells in the brains of Alzheimer's victims.
• Amyloid precursor protein (APP) is a large nerve-protecting protein that is the source of beta amyloid. In Alzheimer's certain enzymes, particularly those called gamma-secretases, snip APP into beta amyloid pieces. This process is controlled by factors called presenilin proteins. (Genetic abnormalities that affect either APP or presenilin proteins occur in some inherited cases of early-onset Alzheimer's.)
• High levels of beta amyloid are associated with reduced levels of the neurotransmitter acetylcholine. (Neurotransmitters are chemical messengers in the brain.) Acetylcholine is part of the cholinergic system, which is essential for memory and learning and is progressively destroyed in Alzheimer's disease.
• Beta amyloid may also disrupt channels that carry sodium, potassium, and calcium. These elements serve the brain as ions, producing electric charges that must fire regularly in order for signals to pass from one nerve cell to another. If the channels that carry ions are damaged, an imbalance can interfere with nerve function and signal transmission.

Other Proteins. Researchers have now identified other important proteins in the areas of the brain affected by Alzheimer's disease.

• ERAB (endoplasmic-reticulum associated binding protein) appears to combine with beta amyloid, which in turn attracts new beta amyloid from outside the cells. High amounts of ERAB may also enhance the nerve-destructive power of beta amyloid.
• AMY plaques resemble beta amyloid so closely that researchers were able to detect them only with the use of highly sophisticated techniques.
• Elevated levels of a protein called prostate apoptosis response-4 (Par-4) may cause nerve cells to self-destruct.

Oxidation and the Inflammatory Response:

Researchers are also attempting to discover why beta amyloid is so toxic to nerve cells. Some researchers are focusing on two processes in the body that may be involved with Alzheimer's disease: oxidation and the inflammatory process. There is some evidence that such events can begin decades before Alzheimer's disease actually develops. One scenario for their role in Alzheimer's is as follows:
The Role of Oxidation.

• As beta amyloid breaks down it releases unstable chemicals called oxygen-free radicals. Once released, oxygen-free radicals bind to other molecules through a process called oxidation.
• Oxidation is the result of many common chemical processes in the body, but when oxidants are overproduced, they can cause severe damage in cells and tissue, including even affecting genetic material in cells (its DNA). Oxidation is known to play a role in many serious diseases, including coronary artery disease and cancers, and experts believe it may also contribute to Alzheimer's.

The Inflammatory Response.

• One result of oxidation is the marshaling of immune factors to repair the cellular injuries it produces. Overproduction of some of these factors, however, produces the so-called inflammatory response, in which the immune process itself can actually damage the body's own cells themselves.
• Principle immune cells in the brain are called macrophage/microglia (M phi). In the healthy brain, they play an important protective role against invading organisms. However, when they are activated by beta amyloid oxidation, they release toxic molecules called cytokines, which are known to cause harm. For example, significantly high levels of interleukin-6, a specific cytokine, have been detected in people with Alzheimer's.
• Other inflammatory factors of specific interest in Alzheimer's research are the enzyme cyclooxygenase (COX) and its products called prostaglandins. Excess amounts of these factors may increase levels of glutamate. Glutamate is an amino acid that excites nerves and, when overproduced, is a powerful nerve-cell killer.
• The inflammatory process has also been associated with the release of soluble toxins called amyloid beta derived diffusible ligands, which some investigators believe may prove to key players in the destructive process.

Genetic Factors:

Major research targets in Alzheimer's disease are the factors responsible for beta amyloid build-up and concentration in certain people and not in others. Genetic factors are believed to play a role in many cases. In 2003, the National Institute on Aging (NIA) launched the ambitious AD Genetics Initiative, a 3-year national project to bank genetic material from families who have at least two members with late-onset Alzheimer's.
The ApoE Gene and Late-Onset Alzheimer's. The major target in genetic research on late-onset Alzheimer's disease (called LOAD) has been apolipoprotein E (ApoE), which plays a role in the movement and distribution of cholesterol for repairing nerve cells during development and after injury.

The gene for ApoE comes in three major types:

• ApoE4. Studies have reported the greatest deposits of beta amyloid in people with ApoE4, which is now believed to be a major risk factor for late-onset Alzheimer's. Some evidence suggests that the ApoE protein removes beta amyloid but the ApoE4 variant does so less efficiently than other ApoE types. (ApoE4 has also been studied for years as a risk factor for heart disease.)
• ApoE3 and ApoE2. Fewer beta amyloid deposits have been observed in people with the ApoE3, and the fewest deposits have been observed in people with ApoE2, which may actually be protective.

People inherit a copy of one type from each parent, but Alzheimer's disease is not inevitable even in people with two copies of the ApoE4 gene. Reports vary widely in estimating the extent of risk:

• People without ApoE4 have an estimated risk of between 9 - 20% for developing Alzheimer's by age 85.
• In people with one copy of the gene, the risk is between 25 - 60%.
• In people with two copies, the risk ranges from 50 - 90%. (Only 2% of the population carries two copies of the ApoE4 gene.)

Some researchers suspect that some specific variation of the ApoE4 gene or combinations with other genes are critical for the disease, since many people who carry the ApoE4 exhibit no signs of Alzheimer's. For example, evidence suggests that genetic factors play a role in a common subtype of late-onset Alzheimer's disease that also includes psychosis. An important 2002 genetic study has identified certain genetic linkages associated with ApoE4 that appear to play a strong role in this subtype.

Genetic Factors for Early-Onset Alzheimer's. Scientists are coming closer to identifying defective genes responsible for early-onset Alzheimer's, an uncommon, but extremely aggressive form of the disease.

• Mutations in genes known as presenilin-1 (PS1) and presenilin-2 (PS2) account for most cases of early-onset inherited Alzheimer's disease. The defective genes appear to accelerate beta amyloid plaque formation and apoptosis, a natural process by which cells self-destruct.
• Genetic mutations in the genes that control amyloid precursor protein (APP) are also being targeted as causes of early-onset Alzheimer's. The genetic disease Down syndrome, for example, overproduces beta-amyloid precursor protein (APP), the source of beta amyloid, and almost always leads to early Alzheimer's. Other APP mutations are being identified.

Environmental Factors:

Researchers are also investigating environmental factors (infections, metals, industrial and other toxins) that may trigger oxidation, inflammation, and the disease process, particularly in people with a genetic susceptibility to Alzheimer's.
Infectious Organisms. Slow, infectious viruses cause a number of other degenerative neurologic diseases, such as kuru and Creutzfeldt-Jakob disease.

Risk Factors:

Alzheimer's disease is the seventh leading cause of death in Americans adults. It affects an estimated 4.5 million Americans and 8 million more people worldwide. Age is the greatest risk factor for Alzheimer's disease. The number of cases of Alzheimer's disease doubles every 5 years in people over 65. By age 85, almost half of all people are afflicted. People with the disease survive, on average, half as long as similarly aged adults without the disease.
With the increasing numbers of aging adults, unless effective methods for prevention and treatment are developed, Alzheimer's disease will reach epidemic proportions, afflicting an estimated 14 million Americans within 50 years. Evidence points to older age, high blood pressure, cholesterol levels, and a family history of the disease as the most important risk factors for Alzheimer's disease.

Gender and Estrogen Loss:

Several studies have reported that women have a much higher risk for Alzheimer's disease than men. If there is a gender difference, it is likely to be due estrogen, the primary female hormone, which appears to have properties that protect against the memory loss and lower mental functioning associated with normal aging. Such actions include blocking production of beta amyloid, offering antioxidant protection, and regulating blood sugar (glucose) levels in the brain. The drop in estrogen levels after menopause may explain a higher risk for Alzheimer's disease in older women than in men. (Testosterone, the male hormone, converts to estrogen, which may help protect men.) Studies have been mixed, however, on the association between the decline in natural estrogen levels and mental functioning in older women.

Family History and Populations Differences;

People with a family history of the disease are at higher than average risk for Alzheimer's disease. Researchers are identifying important genetic factors, notably the ApoE4 gene, that may be responsible for late- and early-onset cases.
Dietary and other cultural factors that increase the risk for hypertension and unhealthy cholesterol levels may also play a role. For example, a study of Japanese men showed that their risk increased if they emigrated to America. And the disease is much less common in West Africa than in African Americans, who share the same or higher risk with Caucasians Americans.

Symptoms;

The early symptoms of Alzheimer's disease (AD) may be overlooked because they resemble signs of natural aging. Older adults who begin to notice a persistent mild memory loss of recent events may have a condition called mild cognitive impairment (MCI). MCI is now believed to be a significant sign of early-stage Alzheimer's in older people. Studies now suggest that older individuals who experience such mild memory abnormalities can later develop Alzheimer's disease.
Early symptoms of Alzheimer's disease may include:

• Forgetfulness (particularly of recent events or information)
• Loss of concentration (having trouble planning or completing familiar tasks, difficulty with abstract thinking such as simple arithmetic problems)
• Language problems (forgetting the names of objects, mixing up words, difficulty completing sentences)
• Confusion about time and place (difficulty recognizing familiar neighborhoods or remembering how arrived at a location, confusion about months or seasons )
• Impaired judgement (dressing inappropriately or making poor financial decisions)
• Impaired movement and coordination (slowing of movements, halting gait, reduced sense of balance)
• Mood and behavior changes (rapid mood swings, emotional outbursts, personality changes, increased fear or suspicion)
• Apathy and depression (loss of interest in activities, increased sleeping, sitting in front of the television for long periods of time)

Diagnosis:

A definitive test to diagnose Alzheimer's disease, even in patients showing signs of dementia, has not yet been developed. A number of expert groups have developed criteria to help diagnose Alzheimer's disease and rule out other disorders. A diagnosis often involves answering questions about the patient:

• Do psychologic tests indicate dementia?
• Does the patient have deficits in two or more areas of mental functioning (such as language, motor skills, and perceptions)?
• Has memory and mental functions gotten progressively worse?
• Is consciousness disturbed? (It is not in Alzheimer's disease.)
• Is the patient over age 40?
• Are other medical or physical conditions present that could account for the same symptoms?
• Are daily activity impaired or has the behavior changed?
• Is there a family history of Alzheimer's disease?
• Are there other symptoms, such as depression, insomnia, incontinence, delusions, hallucinations, dramatic verbal, emotional or physical outbursts, sexual disorders, and weight loss?

Other steps involved in making a decision include laboratory tests (EEG and possibly tests to rule out other diseases) and psychological testing to determine the presence of dementia.

Ruling out Conditions of Normal Aging that Can Cause Alzheimer's-like Symptoms;

Although some memory impairment occurs in many people as they age, only some of these people develop Alzheimer's disease. Many similar symptoms can occur in healthy older individuals from other conditions associated with aging:

• Fatigue
• Grief or depression
• Illness
• Vision or hearing loss
• The use of alcohol or certain medications
• Simply the burden of too many details to remember at once

Ruling Out Other Causes Memory Loss or Dementia;

The first step in diagnosing Alzheimer's disease is to rule out other conditions that might cause memory loss or dementia. There are a number of causes for dementia in the elderly besides Alzheimer's disease:

• Vascular dementia (abnormalities in the vessels that carry blood to the brain)
• Lewy bodies variant (LBV), also called dementia with Lewy bodies
• Parkinson's disease
• Frontotemporal dementia

Experts believe that 60% of cases of dementia are due to Alzheimer's, 15% to vascular injuries, and the rest are a mixture of the two or caused by other factors.
Vascular Dementia. Vascular dementia is primarily caused by either multi-infarct dementia (multiple small strokes) or Binswanger's disease (which affects tiny arteries in the midbrain). One major analysis suggested that patients with vascular dementia have better long term verbal memory than patients with Alzheimer's disease, but poorer executive function (less ability to integrate and organize).

Lewy Bodies Variant. Lewy bodies are abnormalities found in the brains of patients with both Parkinson's disease and Alzheimer's. They can also be present in the absence of either disease; in such cases, the condition is called Lewy bodies variant (LBV). In all cases, the presence of Lewy bodies is highly associated with dementia. LBV was defined in 1997 and some experts believe it may be responsible for about 20% of people who have been diagnosed with Alzheimer's. They can be difficult to distinguish. Compared to Alzheimer's disease patients, those with LBV may be more likely to have hallucinations and delusions early on, to walk with a stoop (similar to Parkinson's disease), to have more fluctuating attention problems, and to perform better than Alzheimer's disease patients on verbal recall but less well with organizing objects.
Parkinson's Disease. Dementia is about six times more common in the elderly Parkinson patient than in the average older adult. It is most likely to occur in older patients who have had major depression. Unlike in Alzheimer's, language is not usually affected in Parkinson's related dementia. Visual hallucinations occur in about a third of people on long-term medications.

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