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Alzheimer’s disease

Other Names: Alzheimer’s disease (AD), also known as Alzheimer disease, or just Alzheimer’s

Definition:
Alzheimer’s is a chronic neurodegenerative disease that usually starts slowly and gets worse over time. It destroys memory and other important mental functions.
It’s the most common cause of dementia — a group of brain disorders that results in the loss of intellectual and social skills. These changes are severe enough to interfere with day-to-day life.
In this disease, the brain cells themselves degenerate and die, causing a steady decline in memory and mental function….CLICK  & SEE

Alzheimer’s is a type of dementia that is more common with increasing age. People with a family history of the condition are also at increased risk of developing it.

At present Alzheimer’s disease medications and management strategies may temporarily improve symptoms. This can sometimes help people with Alzheimer’s disease maximize function and maintain independence.But because there’s no cure for this disease, it’s important to seek supportive services and tap into one’s support network as early as possible.

Symptoms:
At first, increasing forgetfulness or mild confusion may be the only symptoms of Alzheimer’s disease that one notices. But over time, the disease robs one of more of one’s memory, especially recent memories. The rate at which symptoms worsen varies from one person to other person.

If some one has Alzheimer’s, he or she may be the first to notice that the person are having unusual difficulty remembering things and organizing different thoughts. Or may not be recognizing that anything is wrong, even when changes are noticeable by the family members, close friends or co-workers.

Brain changes associated with Alzheimer’s disease lead to growing trouble with:
Alzimer’s is a slowly progressive chronic disease. It progresses in different stages:
Stages of Alzheimer’s disease:

*Effects of ageing on memory but not AD
*Forgetting things occasionally
*Misplacing items sometimes
*Minor short-term memory loss
*Not remembering exact details

Early stage Alzheimer’s:

*Not remembering episodes of forgetfulness
*Forgets names of family or friends
*Changes may only be noticed by close friends or relatives
*Some confusion in situations outside the familiar

Middle stage Alzheimer’s:

*Greater difficulty remembering recently learned information
*Deepening confusion in many circumstances
*Problems with sleep
*Trouble knowing where they are

Late stage Alzheimer’s:

*Poor ability to think
*Problems speaking
*Repeats same conversations
*More abusive, anxious, or paranoid

Causes:
Scientists believe that for most people, Alzheimer’s disease results from a combination of genetic, lifestyle and environmental factors that affect the brain over time.

Less than 5 percent of the time, Alzheimer’s is caused by specific genetic changes that virtually guarantee a person will develop the disease.

Although the causes of Alzheimer’s are not yet fully understood, its effect on the brain is clear. Alzheimer’s disease damages and kills brain cells. A brain affected by Alzheimer’s disease has many fewer cells and many fewer connections among surviving cells than does a healthy brain.

As more and more brain cells die, Alzheimer’s leads to significant brain shrinkage. When doctors examine Alzheimer’s brain tissue under the microscope, they see two types of abnormalities that are considered hallmarks of the disease:

*Plaques. These clumps of a protein called beta-amyloid may damage and destroy brain cells in several ways, including interfering with cell-to-cell communication. Although the ultimate cause of brain-cell death in Alzheimer’s isn’t known, the collection of beta-amyloid on the outside of brain cells is a prime suspect.

*Tangles. Brain cells depend on an internal support and transport system to carry nutrients and other essential materials throughout their long extensions. This system requires the normal structure and functioning of a protein called tau.

In Alzheimer’s, threads of tau protein twist into abnormal tangles inside brain cells, leading to failure of the transport system. This failure is also strongly implicated in the decline and death of brain cells.

Click & see: Transmittable Alzheimer’s’ concept raised :

Risk Factors:
Age:
Increasing age is the greatest known risk factor for Alzheimer’s. Alzheimer’s is not a part of normal aging, but your risk increases greatly after 65 years of age. Nearly half of those older than age 85 have Alzheimer’s.

People with rare genetic changes that virtually guarantee they’ll develop Alzheimer’s begin experiencing symptoms as early as their 30s.

Family history and genetics:

The risk of developing Alzheimer’s appears to be somewhat higher if a first-degree relative — parent or sibling — has the disease. Scientists have identified rare changes (mutations) in three genes that virtually guarantee a person who inherits them will develop Alzheimer’s. But these mutations account for less than 5 percent of Alzheimer’s disease.

Most genetic mechanisms of Alzheimer’s among families remain largely unexplained. The strongest risk gene researchers have found so far is apolipoprotein e4 (APOE e4). Other risk genes have been identified but not conclusively confirmed.

Sex: Women may be more likely than are men to develop Alzheimer’s disease, in part because they live longer.

Mild cognitive impairment:

People with mild cognitive impairment (MCI) have memory problems or other symptoms of cognitive decline that are worse than might be expected for their age, but not severe enough to be diagnosed as dementia.

Those with MCI have an increased risk — but not a certainty — of later developing dementia. Taking action to develop a healthy lifestyle and strategies to compensate for memory loss at this stage may help delay or prevent the progression to dementia.

Past head trauma: People who’ve had a severe head trauma or repeated head trauma appear to have a greater risk of Alzheimer’s disease.

Lifestyle and heart health:

There’s no lifestyle factor that’s been conclusively shown to reduce your risk of Alzheimer’s disease.

However, some evidence suggests that the same factors that put you at risk of heart disease also may increase the chance that you’ll develop Alzheimer’s. Examples include:

*Lack of exercise (a sedentry life style)
*Smoking
*High blood pressure
*High blood cholesterol
*Elevated homocysteine levels
*Poorly controlled diabetes
*A diet lacking in fruits and vegetables

These risk factors are also linked to vascular dementia, a type of dementia caused by damaged blood vessels in the brain. Working with your health care team on a plan to control these factors will help protect your heart — and may also help reduce your risk of Alzheimer’s disease and vascular dementia

Diagnosis:
There is no specific test today that can confirms the Alzheimer’s disease. The doctor will make a judgment about whether Alzheimer’s is the most likely cause of the symptoms based on the information that the patient provides and results of various tests that can help clarify the diagnosis.

The doctor will Physical and neurological exam:

The doctor will perform a physical exam, and is likely to check the overall neurological health by testing the patient following:

*Reflexes
*Muscle tone and strength
*Ability to get up from a chair and walk across the room
*Sense of sight and hearing
*Coordination
*Balance

The doctor may ask the patient to under take the following tests:

1. Blood test: The tests may help the doctor to rule out other potential causes of memory loss and confusion, such as thyroid disorders or vitamin deficiencies

2. Mental status testing: The doctor may conduct a brief mental status test to assess the patient’s memory and other thinking skills. Short forms of mental status testing can be done in about 10 minutes.

3. Neuropsychological testing : The doctor may recommend a more extensive assessment of the patient’s thinking and memory. Longer forms of neuropsychological testing, which can take several hours to complete, may provide additional details about the mental function compared with others’ of a similar age and education level.

4. Brain imaging: Images of the brain are now used chiefly to pinpoint visible abnormalities related to conditions other than Alzheimer’s disease — such as strokes, trauma or tumors — that may cause cognitive change. New imaging applications — currently used primarily in major medical centers or in clinical trials — may enable doctors to detect specific brain changes caused by Alzheimer’s.

Brain-imaging technologies include:

i) Magnetic resonance imaging (MRI). An MRI uses radio waves and a strong magnetic field to produce detailed images of your brain. You lie on a narrow table that slides into a tube-shaped MRI machine, which makes loud banging noises while it produces images. MRIs are painless, but some people feel claustrophobic inside the machine and are disturbed by the noise.

MRIs are used to rule out other conditions that may account for or be adding to cognitive symptoms. In addition, they may be used to assess whether shrinkage in brain regions implicated in Alzheimer’s disease has occurred.

ii) Computerized tomography (CT). For a CT scan, you’ll lie on a narrow table that slides into a small chamber. X-rays pass through your body from various angles, and a computer uses this information to create cross-sectional images (slices) of your brain. It’s currently used chiefly to rule out tumors, strokes and head injuries.

Positron emission tomography (PET). During a PET scan, you’ll be injected in a vein with a low-level radioactive tracer. You’ll lie on a table while an overhead scanner tracks the tracer’s flow through your brain.

The tracer may be a special form of glucose (sugar) that shows overall activity in various brain regions. This can show which parts of your brain aren’t functioning well. New PET techniques may be able to detect your brain level of plaques and tangles, the two hallmark abnormalities linked to Alzheimer’s.

Future diagnostic tests:

Researchers are working with doctors to develop new diagnostic tools to help definitively diagnose Alzheimer’s. Another important goal is to detect the disease before it causes the symptoms targeted by current diagnostic techniques — at the stage when Alzheimer’s may be most treatable as new drugs are discovered. This stage is called preclinical Alzheimer’s disease.

New tools under investigation include:

* Additional approaches to brain imaging
* More-sensitive tests of mental abilities
* Measurement of key proteins or protein patterns in blood or spinal fluid (biomarkers)

Treatment:
Current Alzheimer’s medications can help for a time with memory symptoms and other cognitive changes. Two types of drugs are currently used to treat cognitive symptoms:

Cholinesterase inhibitors. These drugs work by boosting levels of a cell-to-cell communication chemical depleted in the brain by Alzheimer’s disease. Most people can expect to keep their current symptoms at bay for a time.

Less than half of those taking these drugs can expect to have any improvement. Commonly prescribed cholinesterase inhibitors include donepezil (Aricept), galantamine (Razadyne) and rivastigmine (Exelon). The main side effects of these drugs include diarrhea, nausea and sleep disturbances.

Memantine (Namenda). This drug works in another brain cell communication network and slows the progression of symptoms with moderate to severe Alzheimer’s disease. It’s sometimes used in combination with a cholinesterase inhibitor.

Creating a safe and supportive environment:

Adapting the living situation to the needs of a person with Alzheimer’s is an important part of any treatment plan. For someone with Alzheimer’s, establishing and strengthening routine habits and minimizing memory-demanding tasks can make life much easier.

One can take these steps to support a person’s sense of well-being and continued ability to function:

*Always keep keys, wallets, mobile phones and other valuables in the same place at home, so they don’t become lost.
*See if the doctor can simplify the medication regimen to once-daily dosing, and arrange for the finances to be on automatic payment and automatic deposit.
*Develop the habit of carrying a mobile phone with location capability so that one can call in case the person is lost or confused and people can track the location via the phone. Also, program important phone numbers into the person’s phone, so that he or she does not have to try to recall them.
*Make sure regular appointments are on the same day at the same time as much as possible.
*Use a calendar or white board in the home to track daily schedules. Build the habit of checking off completed items so that you can be sure they were completed.
*Remove excess furniture, clutter and throw rugs.
*Install sturdy handrails on stairways and in bathrooms.
*Ensure that shoes and slippers are comfortable and provide good traction.
*Reduce the number of mirrors. People with Alzheimer’s may find images in mirrors confusing or frightening.

Exercise:

Regular exercise is an important part of everybody’s wellness plan — and those with Alzheimer’s are no exception. Activities such as a daily 30-minute walk can help improve mood and maintain the health of your joints, muscles and heart.

Exercise can also promote restful sleep and prevent constipation. Make sure that the person with Alzheimer’s carries identification if she or he walks unaccompanied.

People with Alzheimer’s who develop trouble walking may still be able to use a stationary bike or participate in chair exercises. You may be able to find exercise programs geared to older adults on TV or on DVDs.

Yoga & Meditation : It is proved that even an acute Alzheimer’s patient can improve a lot if he or she does Yoga & meditation regularly under the guidance of an expart teacher.

Alzheimer’s patients should be careful of taking daily nutritional food in time.

Study results have been mixed about whether diet, exercise or other healthy lifestyle choices can prevent or reverse cognitive decline. But these healthy choices promote good overall health and may play a role in maintaining cognitive health, so there’s no harm in including the above good and healthy lifestyle.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
Resources:
https://en.wikipedia.org/wiki/Alzheimer%27s_disease
http://www.mayoclinic.org/diseases-conditions/alzheimers-disease/basics/definition/con-20023871

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Aphasia

Description:
Aphasia is the name given to a collection of language disorders caused by damage to the brain.  The word aphasia comes from the wordn aphasia, in Ancient Greek, which means A requirement for a diagnosis of aphasia is that, prior to the illness or injury, the person’s language skills were normal . The difficulties of people with aphasia can range from occasional trouble finding words to losing the ability to speak, read, or write, but does not affect intelligence. This also affects visual language such as sign language. The term “aphasia” implies a problem with one or more functions that are essential and specific to language function. It is not usually used when the language problem is a result of a more peripheral motor or sensory difficulty, such as paralysis affecting the speech muscles or a general hearing impairment.
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Stroke is the most common cause of aphasia in the United States. Approximately 500,000 individuals suffer strokes each year, and 20% of these individuals develop some type of aphasia. Other causes of brain damage include head injuries, brain tumors, and infection. About half of the people who show signs of aphasia have what is called temporary or transient aphasia and recover completely within a few days. An estimated one million Americans suffer from some form of permanent aphasia. As yet, no connection between aphasia and age, gender, or race has been found.
Aphasia is sometimes confused with other conditions that affect speech, such as dysarthria and apraxia. These condition affect the muscles used in speaking rather than language function itself. Dysarthria is a speech disturbance caused by lack of control over the muscles used in speaking, perhaps due to nerve damage. Speech apraxia is a speech disturbance in which language comprehension and muscle control are retained, but the memory of how to use the muscles to form words is not.

Symptoms:
Aphasia is condition characterized by either partial or total loss of the ability to communicate verbally or using written words. A person with aphasia may have difficulty speaking, reading, writing, recognizing the names of objects, or understanding what other people have said. Aphasia is caused by a brain injury, as may occur during a traumatic accident or when the brain is deprived of oxygen during a stroke. It may also be caused by a brain tumor, a disease such as Alzheimer’s, or an infection, like encephalitis. Aphasia may be temporary or permanent. Aphasia does not include speech impediments caused by loss of muscle control.
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To understand and use language effectively, an individual draws upon word memory-stored information on what certain words mean, how to put them together, and how and when to use them properly. For a majority of people, these and other language functions are located in the left side (hemisphere) of the brain. Damage to this side of the brain is most commonly linked to the development of aphasia. Interestingly, however, left-handed people appear to have language areas in both the left and right hemispheres of the brain and, as a result, may develop aphasia from damage to either side of the brain.

People with aphasia may experience any of the following behaviors due to an acquired brain injury, although some of these symptoms may be due to related or concomitant problems such as dysarthria or apraxia and not primarily due to aphasia. Aphasia symptoms can vary based on the location of damage in the brain. Signs and symptoms may or may not be present in individuals with aphasia and may vary in severity and level of disruption to communication. Often those with aphasia will try to hide their inability to name objects by using words like thing. So when asked to name a pencil they may say it is a thing used to write.

*inability to comprehend language
*inability to pronounce, not due to muscle paralysis or weakness
*inability to speak spontaneously
*inability to form words
*inability to name objects (anomia)
*poor enunciation
*excessive creation and use of personal neologisms
*inability to repeat a phrase
*persistent repetition of one syllable, word, or phrase (stereotypies)
*paraphasia (substituting letters, syllables or words)
*agrammatism (inability to speak in a grammatically correct fashion)
*dysprosody (alterations in inflexion, stress, and rhythm)
*incomplete sentences
*inability to read
*inability to write
*limited verbal output
*difficulty in naming
*speech disorder
*Speaking gibberish
*inability to follow or understand simple requests

Causes:
Aphasia is most commonly caused by stroke. It can also be caused by other brain diseases, including cancer (brain tumor), epilepsy, and Alzheimer’s disease, or by a head injury. In rare cases, aphasia may also result from herpesviral encephalitis. The herpes simplex virus affects the frontal and temporal lobes, subcortical structures, and the hippocampal tissue, which can trigger aphasia. In acute disorders, such as head injury or stroke, aphasia usually develops quickly. Aphasia usually develops more slowly from a brain tumor, infection, or dementia.

Although all of the disease listed above are potential causes, aphasia will generally only result when there is substantial damage to the left hemisphere of the brain, either the cortex (outer layer) and/or the underlying white matter. Substantial damage to tissue anywhere within the region shown in blue on the figure below can potentially result in aphasia.  Aphasia can also sometimes be caused by damage to subcortical structures deep within the left hemisphere, including the thalamus, the internal and external capsules, and the caudate nucleus of the basal ganglia.  The area and extent of brain damage or atrophy will determine the type of aphasia and its symptoms.  A very small number of people can experience aphasia after damage to the right hemisphere only. It has been suggested that these individuals may have had an unusual brain organization prior to their illness or injury, with perhaps greater overall reliance on the right hemisphere for language skills than in the general population.

Finally, certain chronic neurological disorders, such as epilepsy or migraine, can also include transient aphasia as a prodromal or episodic symptom.  Aphasia is also listed as a rare side-effect of the fentanyl patch, an opioid used to control chronic pain.

Classification:
Aphasia is best thought of as a collection of different disorders, rather than a single problem. Each individual with aphasia will present with their own particular combination of language strengths and weaknesses. Consequently, it is a major challenge just to document the various difficulties that can occur in different people, let alone decide how they might best be treated. Most classifications of the aphasias tend to divide the various symptoms into broad classes. A common approach is to distinguish between the fluent aphasias (where speech remains fluent, but content may be lacking, and the person may have difficulties understanding others), and the nonfluent aphasias ( where speech is very halting and effortful, and may consist of just one or two words at a time).

However, no such broad-based grouping has proven fully adequate. There is a huge variation among patients within the same broad grouping, and aphasias can be highly selective. For instance, patients with naming deficits (anomic aphasia) might show an inability only for naming buildings, or people, or colors.

Classical-Localizationist approaches:
Localizationist approaches aim to classify the aphasias according to their major presenting characteristics and the regions of the brain that most probably gave rise to them. Inspired by the early work of nineteenth century neurologists Paul Broca and Carl Wernicke, these approaches identify two major subtypes of aphasia and several more minor subtypes:

*Broca’s aphasia (also known as Motor aphasia or Expressive aphasia), which is characterized by halted, fragmented, effortful speech, but relatively well-preserved comprehension. It has been associated with damage to the posterior left prefrontal cortex, most notably Broca’s area. Individuals with Broca’s aphasia often have right-sided weakness or paralysis of the arm and leg, because the left frontal lobe is also important for body movement, particularly on the right side.

*Wernicke’s aphasia (also known as Sensory aphasia or Receptive aphasia), which is characterized by fluent speech, but marked difficulties understanding words and sentences. Although fluent, the speech may lack in key substantive words (nouns, verbs adjectives), and may contain incorrect words or even nonsense words. This subtype has been associated with damage to the posterior left temporal cortex, most notably Wernicke’s area. These individuals usually have no body weakness, because their brain injury is not near the parts of the brain that control movement.

*Other, more minor subtypes include Conduction aphasia, a disorder where speech remains fluent, and comprehension is preserved, but the person may have disproportionate difficulty where repeating words or sentences. Other include Transcortical motor aphasia and Transcortical sensory aphasia which are similar to Broca’s and Wernicke’s aphasia respectively, but the ability to repeat words and sentences is disroportionately preserved.

Recent classification schemes adopting this approach, such as the “Boston-Neoclassical Model”  also group these classical aphasia subtypes into two larger classes: the nonfluent aphasias (which encompasses Broca’s aphasia and transcortical motor aphasia) and the fluent aphasias (which encompasses Wernicke’s aphasia, conduction aphasia and transcortical sensory aphasia). These schemes also identify several further aphasia subtypes, including: Anomic aphasia, which is characterized by a selective difficulty finding the names for things; and Global aphasia where both expression and comprehension of speech are severely compromised.

Many localizationist approaches also recognize the existence of additional, more “pure” forms of language disorder that may affect only a single language skill.  For example, in Pure alexia, a person may be able to write but not read, and in Pure word deafness, they may be able to produce speech and to read, but not understand speech when it is spoken to them.

Cognitive neuropsychological approaches:
Although localizationist approaches provide a useful way of classifying the different patterns of language difficulty into broad groups, one problem is that a sizeable number of individuals do not fit neatly into one category or another. Another problem is that the categories, particularly the major ones such as Broca’s and Wernicke’s aphasia, still remain quite broad. Consequently, even amongst individuals who meet the criteria for classification into a subtype, there can be enormous variability in the types of difficulties they experience.

Instead of categorizing every individual into a specific subtype, cognitive neuropsychological approaches aim to identify the key language skills or “modules” that are not functioning properly in each individual. A person could potentially have difficulty with just one module, or with a number of modules. This type of approach requires a framework or theory as to what skills/modules are needed to perform different kinds of language tasks. For example, the model of Max Coltheart identifies a module that recognizes phonemes as they are spoken, which is essential for any task involving recognition of words. Similarly, there is a module that stores phonemes that the person is planning to produce in speech, and this module is critical for any task involving the production of long words or long strings of speech. One a theoretical framework has been established, the functioning of each module can then be assessed using a specific test or set of tests. In the clinical setting, use of this model usually involves conducting a battery of assessments, each of which tests one or a number of these modules. Once a diagnosis is reached as to the skills/modules where the most significant impairment lies, therapy can proceed to treat these skills.

In practice, the cognitive neuropsychological approach can be unwieldy due to the wide variety of skills that can potentially be tested. Also, it is perhaps best suited to milder cases of aphasia: If the person has little expressive or receptive language ability, sometimes test performance can be difficult to interpret. In practice, clinicians will often use a blend of assessment approaches, which include broad subtyping based on a localizationist framework, and some finer exploration of specific language skills based on the cognitive neuropsychological framework.
Other forms of aphasia:

Progressive aphasias:
Primary progressive aphasia (PPA) is associated with progressive illnesses or dementia, such as frontotemporal dementia / Pick Complex Motor neuron disease, Progressive supranuclear palsy, and Alzheimer’s disease, which is the gradual process of progressively losing the ability to think. It is characterized by the gradual loss of the ability to name objects. People suffering from PPA may have difficulties comprehending what others are saying. They can also have difficulty trying to find the right words to make a sentence. There are three classifications of Primary Progressive Aphasia : Progressive nonfluent aphasia (PNFA), Semantic Dementia (SD), and Logopenic progressive aphasia (LPA)

Progressive Jargon Aphasia is a fluent or receptive aphasia in which the patient’s speech is incomprehensible, but appears to make sense to them. Speech is fluent and effortless with intact syntax and grammar, but the patient has problems with the selection of nouns. Either they will replace the desired word with another that sounds or looks like the original one or has some other connection or they will replace it with sounds. As such, patients with jargon aphasia often use neologisms, and may perseverate if they try to replace the words they cannot find with sounds. Substitutions commonly involve picking another (actual) word starting with the same sound (e.g., clocktower – colander), picking another semantically related to the first (e.g., letter – scroll), or picking one phonetically similar to the intended one (e.g., lane – late).

Deaf aphasia:
There have been many instances showing that there is a form of aphasia among deaf individuals. Sign language is, after all, a form of communication that has been shown to use the same areas of the brain as verbal forms of communication. Mirror neurons become activated when an animal is acting in a particular way or watching another individual act in the same manner. These mirror neurons are important in giving an individual the ability to mimic movements of hands. Broca’s area of speech production has been shown to contain several of these mirror neurons resulting in significant similarities of brain activity between sign language and vocal speech communication. Facial communication is a significant portion of how animals interact with each other. Humans use facial movements to create, what other humans perceive, to be faces of emotions. While combining these facials movements with speech, a more full form of language is created which enables the species to interact with a much more complex and detailed form of communication. Sign language also uses these facial movements and emotions along with the primary hand movement way of communicating. These facial movement forms of communication come from the same areas of the brain. When dealing with damages to certain areas of the brain, vocal forms of communication are in jeopardy of severe forms of aphasia. Since these same areas of the brain are being used for sign language, these same, at least very similar, forms of aphasia can show in the Deaf community. Individuals can show a form of Wernicke’s aphasia with sign language and they show deficits in their abilities in being able to produce any form of expressions. Broca’s aphasia shows up in some patients, as well. These individuals find tremendous difficulty in being able to actually sign the linguistic concepts they are trying to express

Diagnosis:
Following brain injury, an initial bedside assessment is made to determine whether language function has been affected. If the individual experiences difficulty communicating, attempts are made to determine whether this difficulty arises from impaired language comprehension or an impaired ability to speak. A typical examination involves listening to spontaneous speech and evaluating the individual’s ability to recognize and name objects, comprehend what is heard, and repeat sample words and phrases. The individual may also be asked to read text aloud and explain what the passage means. In addition, writing ability is evaluated by having the individual copy text, transcribe dictated text, and write something without prompting.
A speech pathologist or neuropsychologist may be asked to conduct more extensive examinations using in-depth, standardized tests. Commonly used tests include the Boston Diagnostic Aphasia Examination, the Western Aphasia Battery, and possibly, the Porch Index of Speech Ability.

The results of these tests indicate the severity of the aphasia and may also provide information regarding the exact location of the brain damage. This more extensive testing is also designed to provide the information necessary to design an individualized speech therapy program. Further information about the location of the damage is gained through the use of imaging technology, such as magnetic resonance imaging (MRI) and computed tomography scans.
Treatment:
Initially, the underlying cause of aphasia must be treated or stabilized. To regain language function, therapy must begin as soon as possible following the injury. Although there are no medical or surgical procedures currently available to treat this condition, aphasia resulting from stroke or head injury may improve through the use of speech therapy. For most individuals, however, the primary emphasis is placed on making the most of retained language abilities and learning to use other means of communication to compensate for lost language abilities.
Speech therapy is tailored to meet individual needs, but activities and tools that are frequently used include the following:

Exercise and practice. Weakened muscles are exercised by repetitively speaking certain words or making facial expressions, such as smiling.
Picture cards. Pictures of everyday objects are used to improve word recall and increase vocabulary. The names of the objects may also be repetitively spoken aloud as part of an exercise and practice routine.

Picture boards. Pictures of everyday objects and activities are placed together, and the individual points to certain pictures to convey ideas and communicate with others.
Workbooks. Reading and writing exercises are used to sharpen word recall and regain reading and writing abilities. Hearing comprehension is also redeveloped using these exercises.
Computers. Computer software can be used to improve speech, reading, recall, and hearing comprehension by, for example, displaying pictures and having the individual find the right word.

Prognosis:
The degree to which an individual can recover language abilities is highly dependent on how much brain damage occurred and the location and cause of the original brain injury. Other factors include the individual’s age, general health, motivation and willingness to participate in speech therapy, and whether the individual is left or right handed. Language areas may be located in both the left and right hemispheres in left-handed individuals. Left-handed individuals are, therefore, more likely to develop aphasia following brain injury, but because they have two language centers, may recover more fully because language abilities can be recovered from either side of the brain. The intensity of therapy and the time between diagnosis and the start of therapy may also affect the eventual outcome.

Prevention:
Because there is no way of knowing when a stroke, traumatic head injury, or disease will occur, very little can be done to prevent aphasia. However  it can be adviced to be careful in movement of aged person specially for those having high bloodpressure, diabetis and other form of diseases.

Following are some precautions that should be taken to avoid aphasia, by decreasing the risk of stroke, the main cause of aphasia:

*Exercising regularly
*Eating a healthy diet
*Keeping alcohol consumption low and avoiding tobacco use
*Controlling blood pressure

History:
The first recorded case of aphasia is from an Egyptian papyrus, the Edwin Smith Papyrus, which details speech problems in a person with a traumatic brain injury to the temporal lobe.During the second half of the 19th century, Aphasia was a major focus for scientists and philosophers who were working in the beginning stages in the field of psychology.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:
http://en.wikipedia.org/wiki/Aphasia
http://medical-dictionary.thefreedictionary.com/aphasia

Foe Turns Friend

A-beta, a protein implicated in Alzheimer’s, may be the brain’s shield against germs.
………………...CLICK & SEE THE PICTURES
For years, a prevailing theory has been that one of the chief villains in Alzheimer’s disease has no real function other than as a waste product that the brain never properly disposed of.

The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognising friends and family.

But now researchers at Harvard suggest that the protein has a real and unexpected function — it may be part of the brain’s normal defences against invading bacteria and other microbes.

Other Alzheimer’s researchers say the findings, reported in the current issue of the journal PLoS One, are intriguing.

The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimer’s disease.

To his surprise, many looked just like genes associated with the so-called innate immune system, a set of proteins the body uses to fight infections. The system is particularly important in the brain, because antibodies cannot get through the blood-brain barrier, the membrane that protects the brain. When the brain is infected, it relies on the innate immune system to protect it.

That evening, Tanzi wandered into the office of a junior faculty member, Robert Moir, and mentioned what he had seen. As Tanzi recalled, Moir turned to him and said, “Yeah, well, look at this.”

He handed Tanzi a spreadsheet. It was a comparison of A-beta and a well-known protein of the innate immune system, LL-37. The likenesses were uncanny. Among other things, the two proteins had similar structures. And like A-beta, LL-37 tends to clump into hard little balls.

In rodents, the protein that corresponds to LL-37 protects against brain infections. People who make low levels of LL-37 are at increased risk of serious infections and have higher levels of atherosclerotic plaques, arterial growths that impede blood flow.

The scientists could hardly wait to see if A-beta, like LL-37, killed microbes. They mixed A-beta with microbes that LL-37 is known to kill — listeria, staphylococcus, pseudomonas. It killed eight out of 12. “We did the assays exactly as they have been done for years,” Tanzi said. “And A-beta was as potent or, in some cases, more potent than LL-37.”

Then the investigators exposed the yeast Candida albicans, a major cause of meningitis, to tissue from the hippocampal regions of brains from people who had died of Alzheimer’s and from people of the same age who did not have dementia when they died.

Brain samples from Alzheimer’s patients were 24 per cent more active in killing the bacteria. But if the samples were first treated with an antibody that blocked A-beta, they were no better than brain tissue from non-demented people in killing the yeast.

The innate immune system is also set in motion by traumatic brain injuries and strokes and by atherosclerosis that causes reduced blood flow to the brain, Tanzi noted.

And the system is spurred by inflammation. It’s known that patients with Alzheimer’s have inflamed brains, but it hasn’t been clear whether A-beta accumulation was a cause or an effect of the inflammation. Perhaps, Tanzi said, A-beta levels rise as a result of the innate immune system’s response to inflammation; it may be a way the brain responds to a perceived infection. But does that mean Alzheimer’s disease is caused by an overly exuberant brain response to an infection?

That’s one possible reason, along with responses to injuries and inflammation and the effects of genes that cause A-beta levels to be higher than normal, Tanzi said. However, some researchers say that all the pieces of the A-beta innate immune systems hypothesis are not in place.

Dr Norman Relkin, director of the memory disorders programme at New York-Presbyterian / Weill Cornell hospital, said that although the idea was “unquestionably fascinating”, the evidence for it was “a bit tenuous”.

As for the link with infections, Dr Steven DeKosky, an Alzheimer’s researcher at the Virginia School of Medicine, noted that scientists have long looked for evidence linking infections to Alzheimer’s and have come up mostly empty handed.

But if Tanzi is correct about A-beta being part of the innate immune system, that would raise questions about the search for treatments to eliminate the protein from the brain.

“It means you don’t want to hit A-beta with a sledgehammer,” Tanzi said.

But other scientists not connected with the discovery said they were impressed by the new findings. “It changes our thinking about Alzheimer’s disease,” said Dr Eliezer Masliah, who heads the experimental neuropathology laboratory at the University of California, San Diego.

Source : New York Times News Service

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Stress a Trigger for Skin Disease

Researchers from University of Medicine Berlin and McMaster University in Canada have found that stress may activate immune cells in the skin, leading to inflammatory skin disease.

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This cross talk between stress perception, which involves the brain, and the skin is mediated through the “brain-skin connection”.

The immune cells in skin can over-react, resulting in inflammatory skin diseases like atopic dermatitis and psoriasis.

Study leader Petra Arck hypothesized that stress could exacerbate skin disease by increasing the number of immune cells in the skin.

The researcher said that the team exposed mice to sound stress, and found that the stress challenge resulted in higher numbers of mature white blood cells in the skin.

Moreover, blocking the function of two proteins that attract immune cells to the skin, LFA-1 and ICAM-1, prevented the stress-induced increase in white blood cells in the skin.

Based on their observations, the researchers came to the conclusion that stress activates immune cells, which in turn are central in initiating and perpetuating skin diseases. The study by Arck appears in the November issue of The American Journal of Pathology.

Sources: The Times Of India

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Women’s Health

What are some of the main health issues of concern to women?
Women have most of the same health concerns that men have. But women face many health problems unique to them or that more often or more seriously affect women than men. Doctors of chiropractic have always recognized this and have developed and provided a wide variety of treatment options specifically suited to women’s health needs. Because of this (and because most women tend to have a heightened awareness of their physical condition and are accustomed to seeking help from health professionals), more women than men regularly rely on chiropractic care.…click & see

Women must contend with specific health concerns raised by their female physiology, by the fact that the female body is designed to be able to bear children.
Issues involving pregnancy and the menstrual cycle are centrally important health matters for women. Being pregnant, preparing for pregnancy, and recovering from childbirth are female indispositions. Pain during the menstrual period (dysmenorrhea), premenstrual syndrome (PMS), and chronic pelvic pain are among the distressing conditions which disturb the otherwise healthy lives of many women.

Older women are much more likely than men to develop such serious ailments as Alzheimer’s disease (which burdens the afflicted with near-total memory loss and reduced mental functioning) and osteoporosis (in which the bones become weak, brittle, and porous; the posture stooped with the shoulders rounded). These are just two of the problems of aging that women must be aware of and can take steps to prevent.

Less ominous, but more pervasive, are headaches. Women may get headaches during menstrual periods and pregnancy, as well as under ordinary circumstances. They are more likely to be troubled enough by headache pain to find a way to overcome it. Similarly, women are often victims of osteoarthritis (degenerative joint disease) and have a 200 to 300 percent greater chance than men of suffering rheumatoid arthritis.

What can chiropractic do?

Chiropractic offers demonstrated relief for many of women’s health problems. Chiropractic adjustments have been shown to lessen the discomfort of dysmenorrhea and chronic pelvic pain. Numerous back disorders that strike women are addressed and remedied daily, all over the world, by chiropractors skilled in treating those problems and in improving their patients’ capacity to cope and to improve.

More and more women have become interested in diet, nutrition, weight loss, exercise, sports and physical activity, and methods for maintaining wellness and general fitness  about which chiropractors have considerable knowledge that they are eager to share with their patients. Chiropractic wellness programs are particularly well-suited to the special needs of pregnant women, new mothers, women who are overweight, who are in stressful situations, and others who need to protect and strengthen their bones, nerves, joints, muscles and overall health.

Great numbers of women rely on chiropractors because of the caring interaction that develops between patient and doctor and because of chiropractic’s effective combination of expert diagnosis, effective spinal adjustments and soft tissue therapy, exercise and nutritional guidance, and lifestyle counseling.

Source:ChiroFind.com