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Parkinson’s Disease

Alternative Names : Parkinson disease, Parkinson’s, idiopathic parkinsonism, primary parkinsonism, PD, or paralysis agitans

Definition:
Parkinson’s disease is the second most common neurodegenerative disorder and the most common movement disorder. It is characterized by progressive loss of muscle control, which leads to trembling of the limbs and head while at rest, stiffness, slowness, and impaired balance. As symptoms worsen, it may become difficult to walk, talk, and complete simple tasks.
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Parkinson’s disease is a progressive disorder of the nervous system that affects movement. It develops gradually, often starting with a barely noticeable tremor in just one hand. But while tremor may be the most well-known sign of Parkinson’s disease, the disorder also commonly causes a slowing or freezing of movement. Many people with Parkinson’s disease live long productive lives, whereas others become disabled much more quickly. Premature death is usually due to complications such as falling-related injuries or pneumonia.

Friends and family may notice that your face shows little or no expression and your arms don’t swing when you walk. Speech often becomes soft and mumbling. Parkinson’s symptoms tend to worsen as the disease progresses.

While there is no cure for Parkinson’s disease, many different types of medicines can treat its symptoms. In some cases,  doctor may suggest surgery.

In the United States, about 1 million people are affected by Parkinson’s disease and worldwide about 5 million. Most individuals who develop Parkinson’s disease are 60 years of age or older. Parkinson’s disease occurs in approximately 1% of individuals aged 60 years and in about 4% of those aged 80 years. Since overall life expectancy is rising, the number of individuals with Parkinson’s disease will increase in the future. Adult-onset Parkinson’s disease is most common, but early-onset Parkinson’s disease (onset between 21-40 years), and juvenile-onset Parkinson’s disease (onset before age 21) also exist.

Descriptions of Parkinson’s disease date back as far as 5000 BC. Around that time, an ancient Indian civilization called the disorder Kampavata and treated it with the seeds of a plant containing therapeutic levels of what is today known as levodopa. Parkinson’s disease was named after the British doctor James Parkinson, who in 1817 first described the disorder in great detail as “shaking palsy.”

Symptoms:
The symptoms of Parkinson’s disease can vary from person to person. Early signs may be subtle and can go unnoticed. Symptoms typically begin on one side of the body and usually remain worse on that side even after symptoms begin to affect both sides.

Parkinson’s signs and symptoms may include:

*Tremor. The characteristic shaking associated with Parkinson’s disease often begins in a hand. A back-and-forth rubbing of your thumb and forefinger, known as pill-rolling, is common, and may occur when your hand is at rest. However, not everyone experiences tremors.

*Slowed motion (bradykinesia). Over time, Parkinson’s disease may reduce your ability to initiate voluntary movement. This may make even the simplest tasks difficult and time-consuming. When you walk, your steps may become short and shuffling. Or your feet may freeze to the floor, making it hard to take the first step.

*Rigid muscles. Muscle stiffness can occur in any part of your body. Sometimes the stiffness can be so severe that it limits the range of your movements and causes pain. People may first notice this sign when you no longer swing your arms when you’re walking.

*Impaired posture and balance. Your posture may become stooped as a result of Parkinson’s disease. Balance problems also may occur, although this is usually in the later stages of the disease.

*Loss of automatic movements. Blinking, smiling and swinging your arms when you walk are all unconscious acts that are a normal part of being human. In Parkinson’s disease, these acts tend to be diminished and even lost. Some people may develop a fixed staring expression and unblinking eyes. Others may no longer gesture or seem animated when they speak.

*Speech changes. Many people with Parkinson’s disease have problems with speech. You may speak more softly, rapidly or in a monotone, sometimes slurring or repeating words, or hesitating before speaking.

*Dementia. In the later stages of Parkinson’s disease, some people develop problems with memory and mental clarity. Alzheimer’s drugs appear to alleviate some of these symptoms to a mild degree.

Causes:
The exact cause of Parkinson’s disease is unknown, but several factors appear to play a role, including:

*Genes. Researchers have found specific genetic mutations that likely play a role in Parkinson’s disease. In addition, scientists suspect that many more changes in genes — whether inherited or caused by an environmental exposure — may be responsible for Parkinson’s disease.

*Environmental triggers. Exposure to toxins or certain viruses may trigger Parkinson’s signs and symptoms.In addition, numerous changes are found in the brains of people with Parkinson’s disease. The role of these factors in the development of the disease, if any, isn’t clear, however. These changes include:

*A lack of dopamine. A substance called dopamine acts as a messenger between two brain areas – the substantia nigra and the corpus striatum – to produce smooth, controlled movements. Most of the movement-related symptoms of Parkinson’s disease are caused by a lack of dopamine due to the loss of dopamine-producing cells in the substantia nigra. When the amount of dopamine is too low, communication between the substantia nigra and corpus striatum becomes ineffective, and movement becomes impaired; the greater the loss of dopamine, the worse the movement-related symptoms. Other cells in the brain also degenerate to some degree and may contribute to non-movement related symptoms of Parkinson’s disease.

Although it is well known that lack of dopamine causes the motor symptoms of Parkinson’s disease, it is not clear why the dopamine-producing brain cells deteriorate. Genetic and pathological studies have revealed that various dysfunctional cellular processes, inflammation, and stress can all contribute to cell damage. In addition, abnormal clumps called Lewy bodies, which contain the protein alpha-synuclein, are found in many brain cells of individuals with Parkinson’s disease. The function of these clumps in regards to Parkinson’s disease is not understood. In general, scientists suspect that dopamine loss is due to a combination of genetic and environmental factors.

*Low norepinephrine levels. People with Parkinson’s disease also have damage to the nerve endings that make another important chemical messenger called norepinephrine. Norepinephrine plays a role in regulating the autonomic nervous system, which controls automatic functions, such as blood pressure regulation.

*The presence of Lewy bodies. Unusual protein clumps called Lewy bodies are found in the brains of many people with Parkinson’s disease. How they got there and what type of damage, if any, Lewy bodies might cause is still unknown.

Risk Factors:
Risk factors for Parkinson’s disease are:

*Age : Age is the largest risk factor for the development and progression of Parkinson’s disease. Most people who develop Parkinson’s disease are older than 60 years years of age.Young adults rarely experience Parkinson’s disease. It ordinarily begins in middle or late life, and the risk continues to increase with age.

*Heredity : Having a close relative with Parkinson’s increases the chances that you’ll also develop the disease, A small number of individuals are at increased risk because of a family history of the disorder. Although your risk is still no more than about 4 to 6 percent.

*Sex: Men are more likely to develop Parkinson’s disease than women are.Men are affected about 1.5 to 2 times more often than women.

*Exposure to toxins: Ongoing exposure to herbicides and pesticides puts you at slightly increased risk of Parkinson’s.Head trauma, illness, or exposure to environmental toxins such as pesticides and herbicides may be a risk factor.
Complications:
Parkinson’s disease is often accompanied by these additional problems:

*Depression:  Depression is common in people with Parkinson’s disease. Receiving treatment for depression can make it easier to handle the other challenges of Parkinson’s disease.

*Sleep problems:  People with Parkinson’s disease often have trouble falling asleep and may wake up frequently throughout the night. They may also experience sudden sleep onset, called sleep attacks, during the day.

*Difficulty chewing and swallowing:  The muscles you use to swallow may be affected in the later stages of the disease, making eating more difficult.

*Urinary problems:  Parkinson’s disease may cause either urinary incontinence or urine retention. Certain medications used to treat Parkinson’s also can make it difficult to urinate.

*Constipation: Many people with Parkinson’s disease develop constipation because the digestive tract works more slowly. Constipation may also be a side effect of medications used to treat the disease.

*Sexual dysfunction:  Some people with Parkinson’s disease may notice a decrease in sexual desire. This may stem from a combination of psychological and physical factors, or it may be the result of physical factors alone.Medications for Parkinson’s disease also may cause a number of complications, including involuntary twitching or jerking movements of the arms or legs, hallucinations, sleepiness, and a drop in blood pressure when standing up.

Diagnosis:
A physician will diagnose Parkinson’s disease from the medical history and a neurological examination.  There is no lab test that will clearly identify the disease, but brain scans are sometimes used to rule out disorders that could give rise to similar symptoms. Patients may be given levodopa and resulting relief of motor impairment tends to confirm diagnosis. The finding of Lewy bodies in the midbrain on autopsy is usually considered proof that the patient suffered from Parkinson’s disease. The progress of the illness over time may reveal it is not Parkinson’s disease, and some authorities recommend that the diagnosis be periodically reviewed.

Other causes that can secondarily produce a parkinsonian syndrome are Alzheimer’s disease, multiple cerebral infarction and drug-induced parkinsonism.  Parkinson plus syndromes such as progressive supranuclear palsy and multiple system atrophy must be ruled out.  Anti-Parkinson’s medications are typically less effective at controlling symptoms in Parkinson plus syndromes. Faster progression rates, early cognitive dysfunction or postural instability, minimal tremor or symmetry at onset may indicate a Parkinson plus disease rather than PD itself.  Genetic forms are usually classified as PD, although the terms familial Parkinson’s disease and familial parkinsonism are used for disease entities with an autosomal dominant or recessive pattern of inheritance.

Medical organizations have created diagnostic criteria to ease and standardize the diagnostic process, especially in the early stages of the disease. The most widely known criteria come from the UK Parkinson’s Disease Society Brain Bank and the US National Institute of Neurological Disorders and Stroke. The PD Society Brain Bank criteria require slowness of movement (bradykinesia) plus either rigidity, resting tremor, or postural instability. Other possible causes for these symptoms need to be ruled out. Finally, three or more of the following features are required during onset or evolution: unilateral onset, tremor at rest, progression in time, asymmetry of motor symptoms, response to levodopa for at least five years, clinical course of at least ten years and appearance of dyskinesias induced by the intake of excessive levodopa. Accuracy of diagnostic criteria evaluated at autopsy is 75–90%, with specialists such as neurologists having the highest rates.

Computed tomography (CT) and magnetic resonance imaging (MRI) brain scans of people with PD usually appear normal.  These techniques are nevertheless useful to rule out other diseases that can be secondary causes of parkinsonism, such as basal ganglia tumors, vascular pathology and hydrocephalus.  A specific technique of MRI, diffusion MRI, has been reported to be useful at discriminating between typical and atypical parkinsonism, although its exact diagnostic value is still under investigation. Dopaminergic function in the basal ganglia can be measured with different PET and SPECT radiotracers. Examples are ioflupane (123I) (trade name DaTSCAN) and iometopane (Dopascan) for SPECT or fludeoxyglucose (18F) for PET. A pattern of reduced dopaminergic activity in the basal ganglia can aid in diagnosing PD

Treatment :
There’s no cure for Parkinson’s disease although new research is just starting to suggest that some drugs already used for the condition do have some effect in holding back progression of the disease.

A lot can be done to relieve symptoms, especially in the early stages, by replacing the missing dopamine in the brain. This can be done very effectively with a drug called levodopa – a synthetic chemical that’s converted into dopamine in the brain. However, there can be severe side-effects with prolonged usage.

Because of these problems, doctors usually try to delay using levodopa, especially in younger people. Instead, they use other drugs that boost dopamine activity or mimic its effects, known as dopamine agonists. These drugs also have side-effects and doses have to be carefully tailored to each patient’s needs.

Another option for people with more advanced Parkinson’s is injections of a drug called apomorphine which can ‘rescue’ people from sudden ‘off’ periods (episodes of greatly reduced mobility).

This drug can also be given as a continuous infusion for those with severe movement fluctuations and reduces the dose of levodopa that a person requires.

Occupational therapists and physiotherapists help people manage their condition by assisting with movement and providing advice on how to maintain independence in everyday life. Speech and language therapists help with communication or swallowing difficulties.

Deep brain stimulation is a form of surgery that can be used to treat some of the symptoms of Parkinson’s. A wire with four electrodes at its tip is implanted in one of four target sites in the brain. Then a small unit, which generates electrical signals for the stimulation, is implanted into the person’s chest. When the stimulation is switched on, electrical signals are sent to the brain to stop or reduce the symptoms of Parkinson’s. It’s not suitable for everyone with Parkinson’s, but can provide significant improvement in symptoms and quality of life.

In the future, gene therapy and stem cell therapy may hold some possibility of more effective treatment of Parkinson’s disease.

YOU MAY CLICK & SEE  : Parkinson’s disease ‘may start in gut’

Lifestyle and home remedies:
If you’ve received a diagnosis of Parkinson’s disease, you’ll need to work closely with your doctor to find a treatment plan that offers you the greatest relief from symptoms with the fewest side effects. Certain lifestyle changes also may help make living with Parkinson’s disease easier.

Healthy eating
Eat a nutritionally balanced diet that contains plenty of fruits, vegetables and whole grains. These foods are high in fiber, which is important for helping prevent the constipation that is common in Parkinson’s disease. A balanced diet also provides nutrients, such as omega-3 fatty acids, that may be beneficial for people with Parkinson’s disease.

If you take a fiber supplement, such as psyllium powder, Metamucil or Citrucel, be sure to introduce it gradually and drink plenty of fluids daily. Otherwise, your constipation may become worse. If you find that fiber helps your symptoms, use it on a regular basis for the best results.

Walking with care
Parkinson’s disease can disturb your sense of balance, making it difficult to walk with a normal gait.

These suggestions may help:

*Try not to move too quickly.
*Aim for your heel to strike the floor first when you’re walking.
*If you notice yourself shuffling, stop and check your posture. It’s best to stand up straight.

Avoiding falls
In the later stages of the disease, you may fall more easily. In fact, you may be thrown off balance by just a small push or bump.

The following suggestions may help:

*Don’t pivot your body over your feet while turning. Instead, make a U-turn.
*Don’t lean or reach. Keep your center of gravity over your feet.
*Don’t carry things while walking.
*Avoid walking backward.

Dressing
Dressing can be the most frustrating of all activities for someone with Parkinson’s disease. The loss of fine motor control makes it hard to button and zip clothes, and even to step into a pair of pants. An occupational therapist can point out techniques that make daily activities easier.

These suggestions also may help:

*Allow plenty of time so that you don’t feel rushed.
*Lay clothes nearby.
*Choose clothes that you can slip on easily, such as sweat pants, simple dresses or pants with elastic waistbands.
*Use fabric fasteners, such as Velcro, instead of buttons.

Alternative Medications:
Forms of alternative medicine that may help people with Parkinson’s include:

*Coenzyme Q10. People with Parkinson’s disease tend to have low levels of coenzyme Q10, and some research has suggested it may be beneficial. However, subsequent research hasn’t confirmed this benefit. You can buy coenzyme Q10 without a prescription in drugstores and natural food stores. Talk with your doctor before taking this supplement to ensure that it won’t interfere with any medication you may be taking.

*Massage. Massage therapy can reduce muscle tension and promote relaxation, which may be especially helpful to people experiencing muscle rigidity associated with Parkinson’s disease. These services, however, are rarely covered by health insurance.

*Tai chi. An ancient form of Chinese exercise, tai chi employs slow, flowing motions that help improve flexibility and balance. Several forms of tai chi are tailored for people of any age or physical condition.

*Yoga. Yoga is another type of exercise that increases flexibility and balance. Most poses can be modified, depending on your physical abilities.

Prognosis:
PD invariably progresses with time. Motor symptoms, if not treated, advance aggressively in the early stages of the disease and more slowly later. Untreated, individuals are expected to lose independent ambulation after an average of eight years and be bedridden after ten years.  However, it is uncommon to find untreated people nowadays. Medication has improved the prognosis of motor symptoms, while at the same time it is a new source of disability because of the undesired effects of levodopa after years of use.   In people taking levodopa, the progression time of symptoms to a stage of high dependency from caregivers may be over 15 years.  However, it is hard to predict what course the disease will take for a given individual. Age is the best predictor of disease progression. The rate of motor decline is greater in those with less impairment at the time of diagnosis, while cognitive impairment is more frequent in those who are over 70 years of age at symptom onset.

Since current therapies improve motor symptoms, disability at present is mainly related to non-motor features of the disease.Nevertheless, the relationship between disease progression and disability is not linear. Disability is initially related to motor symptoms. As the disease advances, disability is more related to motor symptoms that do not respond adequately to medication, such as swallowing/speech difficulties, and gait/balance problems; and also to motor complications, which appear in up to 50% of individuals after 5 years of levodopa usage. Finally, after ten years most people with the disease have autonomic disturbances, sleep problems, mood alterations and cognitive decline. All of these symptoms, especially cognitive decline, greatly increase disability.

The life expectancy of people with PD is reduced. Mortality ratios are around twice those of unaffected people. Cognitive decline and dementia, old age at onset, a more advanced disease state and presence of swallowing problems are all mortality risk factors. On the other hand a disease pattern mainly characterized by tremor as opposed to rigidity predicts an improved survival. Death from aspiration pneumonia is twice as common in individuals with PD as in the healthy population

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://www.bbc.co.uk/health/physical_health/conditions/parkinsons1.shtml
http://en.wikipedia.org/wiki/Parkinson’s_disease
http://www.medicinenet.com/parkinsons_disease/article.htm
http://en.wikipedia.org/wiki/Parkinson’s_disease
http://www.mayoclinic.com/health/parkinsons-disease/DS00295

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Huntington’s Disease

Definition:
Huntington’s disease (also referred to in more formal medical research as Huntington Disease) is an hereditary neurological disorder of the central nervous system that causes progressive degeneration of cells in the brain, slowly impairing a person’s ability to walk, think, talk and reason.

Most people with Huntington’s disease develop signs and symptoms in their 40s or 50s, but the onset of disease may be earlier or later in life. When disease onset begins before age 20, the condition is called juvenile Huntington’s disease. Earlier onset often results in a somewhat different presentation of symptoms and faster disease progression.

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Medications are available to help manage the symptoms of Huntington’s disease, but treatments can’t prevent the physical, mental and behavioral decline associated with the condition.

It was first described in 1872 by an American doctor, George Huntington, who studied an extended family in Long Island affected by the condition.

Symptoms:
Symptoms of Huntington’s disease commonly become noticeable between the ages of 35 and 44 years, but they can begin at any age from infancy to old age. In the early stages, there are subtle changes in personality, cognition, and physical skills. The physical symptoms are usually the first to be noticed, as cognitive and psychiatric symptoms are generally not severe enough to be recognized on their own at the earlier stages. Almost everyone with Huntington’s disease eventually exhibits similar physical symptoms, but the onset, progression and extent of cognitive and psychiatric symptoms vary significantly between individuals.

The most characteristic initial physical symptoms are jerky, random, and uncontrollable movements called chorea. Chorea may be initially exhibited as general restlessness, small unintentionally initiated or uncompleted motions, lack of coordination, or slowed saccadic eye movements. These minor motor abnormalities usually precede more obvious signs of motor dysfunction by at least three years. The clear appearance of symptoms such as rigidity, writhing motions or abnormal posturing appear as the disorder progresses. These are signs that the system in the brain that is responsible for movement is affected.[6] Psychomotor functions become increasingly impaired, such that any action that requires muscle control is affected. Common consequences are physical instability, abnormal facial expression, and difficulties chewing, swallowing and speaking. Eating difficulties commonly cause weight loss and may lead to malnutrition.  Sleep disturbances are also associated symptoms. Juvenile HD differs from these symptoms in that it generally progresses faster and chorea is exhibited briefly, if at all, with rigidity being the dominant symptom. Seizures are also a common symptom of this form of HD.

Cognitive abilities are impaired progressively. Especially affected are executive functions which include planning, cognitive flexibility, abstract thinking, rule acquisition, initiating appropriate actions and inhibiting inappropriate actions. As the disease progresses, memory deficits tend to appear. Reported impairments range from short-term memory deficits to long-term memory difficulties, including deficits in episodic (memory of one’s life), procedural (memory of the body of how to perform an activity) and working memory. Cognitive problems tend to worsen over time, ultimately leading to dementia. This pattern of deficits has been called a subcortical dementia syndrome to distinguish it from the typical effects of cortical dementias e.g. Alzheimer‘s disease.

Reported neuropsychiatric manifestations are anxiety, depression, a reduced display of emotions (blunted affect), egocentrism, aggression, and compulsive behavior, the latter of which can cause or worsen addictions, including alcoholism, gambling, and hypersexuality.  Difficulties in recognizing other people’s negative expressions have also been observed. Prevalence of these symptoms is also highly variable between studies, with estimated rates for lifetime prevalence of psychiatric disorders between 33% and 76%.  For many sufferers and their families these symptoms are among the most distressing aspects of the disease, often affecting daily functioning and constituting reason for institutionalisation. Suicidal thoughts and suicide attempts are more common than in the general population.

Mutant Huntingtin is expressed throughout the body and associated with abnormalities in peripheral tissues that are directly caused by such expression outside the brain. These abnormalities include muscle atrophy, cardiac failure, impaired glucose tolerance, weight loss, osteoporosis and testicular atrophy

Reported prevalences of behavioral and psychiatric symptoms in Huntington’s disease :
Irritability 38–73%
Apathy 34–76%
Anxiety 34–61%
Depressed mood 33–69%
Obsessive and compulsive 10–52%
Psychotic 3–11%

Causes:
Huntington’s disease is caused by a single defective gene on chromosome 4. This leads to damage of the nerve cells in areas of the brain including the basal ganglia and cerebral cortex, and to the gradual onset of physical, mental and emotional changes.

The Huntington’s Disease Association estimates between 6,500 and 8,000 people in the UK have the disease.

The tragedy is that by the time symptoms appear, the person has often had a family and may have passed on the gene to their children. Each person whose parent has Huntington’s disease has a 50 per cent chance of inheriting the gene, and everyone who inherits the gene will at some stage develop the disease.

In three per cent of cases, there’s no family history of Huntington’s disease and the genetic fault may be a new mutation.

The disease can’t be prevented from developing if someone has the faulty gene. To inherit the illness, the gene only has to come from one parent, making it autosomal dominant.

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The gene for Huntington’s disease can be detected with a blood test, which is available to those aged over 18, before symptoms begin. This can determine whether someone has the faulty gene and help them in their family planning

Risk Factors:
If one of your parents has Huntington’s disease, you have a 50 percent chance of developing the disease. In rare cases, you may develop Huntington’s disease without having a family history of the condition. Such an occurrence may be the result of a genetic mutation that happened during your father’s sperm development.

Complications:
After the onset of Huntington’s disease, a person’s functional abilities gradually worsen over time. The rate of disease progression and duration varies. The time from disease onset to death is often about 10 to 30 years. Juvenile onset usually results in death in fewer than 15 years.

The clinical depression associated with Huntington’s disease may increase the risk of suicide. Some research suggests that the greater risk of suicide occurs before a diagnosis is made and in middle stages of the disease when a person has begun to lose independence.

Eventually, a person with Huntington’s disease requires help with all activities of daily living and care. Late in the disease, he or she will likely be confined to a bed and unable to speak. However, a person’s understanding of surroundings and interactions remain intact for a long time.

Common causes of death include:

*Pneumonia or other infections
*Injuries related to falls
*Complications related to the inability to swallow

Diagnosis:
Medical diagnosis of the onset of HD can be made following the appearance of physical symptoms specific to the disease. Genetic testing can be used to confirm a physical diagnosis if there is no family history of HD. Even before the onset of symptoms, genetic testing can confirm if an individual or embryo carries an expanded copy of the trinucleotide repeat in the HTT gene that causes the disease. Genetic counseling is available to provide advice and guidance throughout the testing procedure, and on the implications of a confirmed diagnosis. These implications include the impact on an individual’s psychology, career, family planning decisions, relatives and relationships. Despite the availability of pre-symptomatic testing, only 5% of those at risk of inheriting HD choose to do so

Clinical:
A physical examination, sometimes combined with a psychological examination, can determine whether the onset of the disease has begun. Excessive unintentional movements of any part of the body are often the reason for seeking medical consultation. If these are abrupt and have random timing and distribution, they suggest a diagnosis of HD. Cognitive or psychiatric symptoms are rarely the first diagnosed; they are usually only recognized in hindsight or when they develop further. How far the disease has progressed can be measured using the unified Huntington’s disease rating scale which provides an overall rating system based on motor, behavioral, cognitive, and functional assessments. Medical imaging, such as computerized tomography (CT) and magnetic resonance imaging (MRI), only shows visible cerebral atrophy in the advanced stages of the disease. Functional neuroimaging techniques such as fMRI and PET can show changes in brain activity before the onset of physical symptoms.

Grenetic:
Because HD follows an autosomal dominant pattern of inheritance, there is a strong motivation for individuals who are at risk of inheriting it to seek a diagnosis. The genetic test for HD consists of a blood test which counts the numbers of CAG repeats in each of the HTT alleles.[38] A positive result is not considered a diagnosis, since it may be obtained decades before the symptoms begin. However, a negative test means that the individual does not carry the expanded copy of the gene and will not develop HD.

A pre-symptomatic test is a life-changing event and a very personal decision. The main reason given for choosing testing for HD is to aid in career and family decisions. Over 95% of individuals at risk of inheriting HD do not proceed with testing, mostly because there is no treatment. A key issue is the anxiety an individual experiences about not knowing whether they will eventually develop HD, compared to the impact of a positive result.  Irrespective of the result, stress levels have been found to be lower two years after being tested, but the risk of suicide is increased after a positive test result. Individuals found to have not inherited the disorder may experience survivor guilt with regard to family members who are affected. Other factors taken into account when considering testing include the possibility of discrimination and the implications of a positive result, which usually means a parent has an affected gene and that the individual’s siblings will be at risk of inheriting it. Genetic counseling in HD can provide information, advice and support for initial decision-making, and then, if chosen, throughout all stages of the testing process. Counseling and guidelines on the use of genetic testing for HD have become models for other genetic disorders, such as autosomal dominant cerebellar ataxias. Presymptomatic testing for HD has also influenced testing for other illnesses with genetic variants such as polycystic kidney disease, familial Alzheimer’s disease and breast cancer

Embryonic:
Embryos produced using in vitro fertilisation may be genetically tested for HD using preimplantation genetic diagnosis. This technique, where a single cell is extracted from a 4 to 8 cell embryo and then tested for the genetic abnormality, can then be used to ensure embryos with affected HTT genes are not implanted, and therefore any offspring will not inherit the disease. It is also possible to obtain a prenatal diagnosis for an embryo or fetus in the womb.

Differential diagnosis:
About 90% of HD diagnoses based on the typical symptoms and a family history of the disease are confirmed by genetic testing to have the expanded trinucleotide repeat that causes HD. Most of the remaining are called HD-like disorders.  Most of these other disorders are collectively labelled HD-like (HDL). The cause of most HDL diseases is unknown, but those with known causes are due to mutations in the prion protein gene (HDL1), the junctophilin 3 gene (HDL2), a recessively inherited HTT gene (HDL3—only found in one family and poorly understood), and the gene encoding the TATA box-binding protein (HDL4/SCA17). Other autosomal dominant diseases that can be misdiagnosed as HD are dentatorubral-pallidoluysian atrophy and neuroferritinopathy. There are also autosomal recessive disorders that resemble sporadic cases of HD. Main examples are chorea acanthocytosis, pantothenate kinase-associated neurodegeneration and X-linked McLeod syndrome

Treatment:
There’s no cure, but supportive care can ease many symptoms and help a person with Huntington’s disease, and their family, lead as normal a life as possible.

Drugs can relieve symptoms of involuntary movements, depression and mood swings. Speech therapy can help improve speech and swallowing problems. A high-calorie diet can help maintain weight and improve symptoms such as involuntary movement and behavioural problems.

Cognitive changes often result in loss of enthusiasm, initiative and organisational skills, which can make multi-tasking difficult. Constant nursing care is needed in the later stages of the disease and support for carers is important, too.

Secondary illnesses, such as pneumonia, are often the cause of death.

There’s extensive research into possible treatments for Huntington’s disease. One technique is the use of transplants of foetal brain cells, which appear in some cases to repair and rejuvenate the damaged area.

Meanwhile, researchers at the University of Leeds have found that one of the body’s naturally occurring proteins is causing some of the disruption that occurs in the brains of those with Huntington’s, and its effects may be modified by using drugs that are already being used to help cancer patients. But it is likely to be years, if at all, before these developments result in an effective treatment.

Prognosis:
The length of the trinucleotide repeat accounts for 60% of the variation in the age of onset and the rate of progression of symptoms. A longer repeat results in an earlier age of onset and a faster progression of symptoms. For example, individuals with a trinucleotide repeat greater than sixty repeats often develop the disease before twenty years of age, and those with less than forty repeats may not develop noticeable symptoms. The remaining variation is due to environmental factors and other genes that influence the mechanism of the disease.

Life expectancy in HD is generally around 20 years following the onset of visible symptoms.  Most of the complications that are life-threatening result from muscle coordination issues, or to a lesser extent from behavioural changes resulting from the decline in cognitive function. The largest risk is pneumonia, which is the cause of death of one-third of those with HD. As the ability to synchronise movements deteriorates, difficulty clearing the lungs and an increased risk of aspirating food or drink both increase the risk of contracting pneumonia. The second greatest risk is heart disease, which causes almost a quarter of fatalities of those with HD. Suicide is the next greatest cause of fatalities, with 7.3% of those with HD taking their own lives and up to 27% attempting to do so. It is unclear to what extent suicidal thoughts are influenced by psychiatric symptoms, as they may be considered to be a response of an individual to retain a sense of control of their life or to avoid the later stages of the disease.  Other associated risks include choking, physical injury from falls, and malnutrition.

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://www.bbc.co.uk/health/physical_health/conditions/huntingtons1.shtml
http://en.wikipedia.org/wiki/Huntington’s_disease
http://www.mayoclinic.com/health/huntingtons-disease/DS00401

http://www.healthtree.com/articles/huntingtons-disease/causes/

http://www.bothbrainsandbeauty.com/academic-discussions/huntingtons-disease-991

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Mild Memory Loss is Not a Part of Normal Aging

Getting older, in and of itself, is not the cause of so-called “senior moments”. A new study found that even these mild memory lapses are caused by the same brain lesions associated with Alzheimer’s disease and other dementias.
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Researchers found that in the last four to five years of life, people’s memory showed a very rapid decline. Pathologic lesions were found to be related to this rapid decline. The preceding years showed a much more gradual decline that was the actual result of normal aging.

According to Newswise:
“… [R]ecognizing that the earliest changes in memory are related to Alzheimer’s pathology can lead to early diagnosis and will be critical information if a treatment is developed that can alter the pathologic course of the disease.”

Resources:
Newswise September 15, 2010
Neurology September 21, 2010; 75(12):1070-8. Epub 2010 Sep 15

Posted By Dr. Mercola | October 07 2010 | 43,083 views

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Herbs & Plants

Club Moss (Lycopodium clavatum)

Botanical Name :Lycopodium clavatum
Family: Lycopodiaceae
Genus: Lycopodium

Kingdom: Plantae
Division: Lycopodiophyta
Class: Lycopodiopsida
Order: Lycopodiales
Species: L. clavatum
Synonyms: Stag’s-horn Clubmoss (English), Clubmoss
Common Names: Club Moss , Wolf’s Claw,wolf’s-foot clubmoss, stag’s-horn clubmoss or groundpine
Other common Names : Common clubmoss, Stagshorn clubmoss, Wolfpaw clubmoss, Foxtail clubmoss, Running clubmoss, Running ground-pine, Running pine[1], Running moss, Princess Pine, and others.
Deutsch: Keulen-Bärlapp, Kolben-Bärlapp · English: Ground pine, Stagshorn Clubmoos · Français : Jalousie · Italiano: Erba strega · Nederlands: Groote Wolfsklauw ·

Parts Used: spores alkaloids including lycopodine,clavatine, clavatoxine,

Habitat :Native; heaths, moors, mountains, mostly in grassy places; formerly throughout Britain and Ireland, now absent from much of lowlands.

It has a subcosmopolitan distribution, with distinct subspecies and varieties in different parts of its range:

Lycopodium clavatum subsp. clavatum
Lycopodium clavatum subsp. clavatum var. clavatum (Europe, Asia, North America)
Lycopodium clavatum subsp. clavatum var. aristatum (Mexico, Caribbean, Central America, northern South America south to northern Argentina)
Lycopodium clavatum subsp. clavatum var. asiaticum (Japan, northeast China)
Lycopodium clavatum subsp. clavatum var. borbonicum (central and southern Africa)
Lycopodium clavatum subsp. clavatum var. kiboanum (mountains of tropical Africa)
Lycopodium clavatum subsp. contiguum (southern Central America, northern South America; syn. Lycopodium contiguum)
Although globally widespread, like many clubmosses, it is confined to undisturbed sites, disappearing from farmed areas and sites with regular burning. As a result, it is endangered in many areas. In the UK it is one of 101 species named as a high priority for conservation by the wild plant charity Plantlife.

Description:
It is a spore-bearing vascular plant, growing mainly prostrate along the ground with stems up to 1 m long; the stems are much branched, and densely clothed with small spirally-arranged leaves. The leaves are 3-5 mm long and 0.7-1 mm broad, tapered to a fine hair-like white point. The branches bearing spore cones turn erect, reaching 5-15 cm above ground, and have fewer leaves than the horizontal branches. The spore cones are yellow-green, 2-3 cm long and 5 mm broad. The horizontal stems produce roots at frequent intervals along their length, allowing the stem to grow indefinitely along the ground. The stems superficially resemble small seedlings of coniferous trees, though it is not related to these.

click to see the pictures…>..(01).….(1).…...(2)..…..…(3).……..(4)....………….

Constituents: alkaloids including lycopodine,clavatine, clavatoxine, nicotine, polyphenolic acids including dihydrocaffeic,flavonoids including apigenin, triterpenes.

Medicinal Uses:
Traditionally, herbal healers employed the entire plant to relieve muscle cramping,as a diuretic in kidney and liver complaints, and may have analgesic and antiseptic properties. Nowadays, the only part of the plant used medicinally is the powdered spores by which it reproduces. It promotes healing in wounds, stops bleeding and helps drain tissues of excess fluids. The leaves and stems contain two poisons, lycopodine and clavadine, but the spores are completely non-toxic. Club moss is widely used in homeopathic medicine to treat a wide variety of ailments, but its effectiveness is not established by research. Mountain Rose Herbs (2008-06-09)

Traditional Chinese Medicine
An ingredient in the Traditional Chinese Medicine remedy Qian Ceng Ta, club moss has been used for centuries to treat fever and inflammation. More recently Qian Ceng Ta was found to contain a substance called huperzine a (HupA.) Hupezine A appears to shield brain cells from injury and it may be useful in treating strokes and epilepsy.

Many adults today wish to have better mental focus, alertness and concentration. We all suffer from memory lapses, lack of concentration and inability to focus. ADD (Attention Deficit Disorder) is a group of symptoms that can also cause mood swings, impulsiveness, behavioral and other social problems in both children and adults.

More than becoming more and more forgetful as we get older, Alzheimer’s disease leads to changes is behavior, personality and other abilities. Although Club Moss is used primarily to treat the early symptoms of Alzheimer’s, many people are taking it to improve memory and enhance mental alertness.
Click to learn more
Click to see :->

LYCOPODIUM CLAVATUM in Homeopathy medicine:

: Homeopathic Remedy

Side Effects:
Not to be used while pregnant. Not for long term use. Safe in recommended amounts.

How to Use: Club Moss
Preparation Methods :Dried spores as a powder. Most commonly found in extract and capsule form, but is suitable as a tea. Typical dosage: 50 to 100 micrograms in capsules daily.

Disclaimer:The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider.

Resources:
http://www.anniesremedy.com/herb_detail305.php
http://en.wikipedia.org/wiki/Lycopodium_clavatum
http://nlbif.eti.uva.nl/bis/flora.php?menuentry=soorten&id=1447

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Ginkgo Biloba Special Extract Protects against Alzheimer’s Disease

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For the very first time, a medicine has been shown to protect against the development of Alzheimer’s disease. French scientists were able to demonstrate that taking 240 mg of Ginkgo extract EGb 761® per day regularly over a period of at least 4 years can cut the risk of developing Alzheimer’s disease by nearly 50%.

..click to see the pictures.

“Meta-analyses of the data by independent scientists consistently substantiate the efficacy of EGb 761® at the onset of cognitive decline.”

“The results of the GuidAge study are remarkable”, according to Prof. Michael Habs. “It is the first time ever that a protective effect against Alzheimer’s disease has been demonstrated for a medicine. The multifaceted effects of the plant extract appear to positively influence the complex developmental processes of dementia.”

The GuidAge study was a large-scale study, in which 2854 elderly people with memory complaints were randomly assigned to receive either 240 mg/day of the patented Ginkgo special extract or a placebo for five years. Of those subjects taking the study medication for at least 4 years 29 out of 966 (3.0 %) taking placebo developed Alzheimer’s disease; in contrast only 15 out of 947 (1.6 %) treated with EGb 761® developed the disease (p=0.03). The result of this prospectively planned analysis shows that the Ginkgo special extract can lower the risk of dementia by 47%.

The brain pathology that leads to overt Alzheimer’s disease develops over the course of many years. It is therefore not surprising that those study participants who developed dementia early in the study gained less protective benefit from EGb 761® treatment, because they already had the disease. When these subjects as well as those who left the study prematurely, i.e. all study participants were included in the analysis, the overall treatment effect was still detectable, although not statistically significant.

The results were commented on as follows by Prof. Ralf Ihl: „There have been hints that Ginkgo biloba may exert a preventive effect. With the findings of this study we have first scientifically verifiable results suggesting that the extract may be useful for preventing the development of Alzheimer’s disease.“

The result of the GuidAge study agrees with the findings of two earlier cohort studies carried out in France, which also suggested a protective effect of EGb 761®. A study funded by the US National Institute on Aging as well found a dementia-protective effect in those subjects, who had taken their medication regularly. In another US study, a protective effect was not found, however. But towards the end of this study, the medicine was actually only taken by little more than half of the subjects. The results of the GuidAge study now again confirm the importance of a regular and long enough intake of 240 mg EGb 761® per day: A very high proportion of 93% of the participants took their medication regularly during the whole treatment period. Once again the excellent long-term safety profile of EGb 761® was confirmed.

Animal models also showed that EGb 761® intervenes in several of the processes decisive to the development of Alzheimer’s disease: the formation of harmful protein-compounds (so-called ?-amyloid) is inhibited and the nerve cell damage caused by these as well as by ageing processes reduced so that energy generation in the nerve cells can be maintained. The patented special extract EGb 761® contains a particularly high proportion of plant substances that are unique to Ginkgo, ginkgolides and bilobalide, and that are especially important for the protection of nerve cells.

The efficacy of EGb 761® in the treatment of dementia diseases has been confirmed recently in several meta-analyses of available studies. EGb 761® can also improve cognitive performance in people who do not yet show significant impairment. In summarizing the study results, Dr. Reiner Kaschel concluded: “Meta-analyses of the data by independent scientists consistently substantiate the efficacy of EGb 761® at the onset of cognitive decline.”

Tebonin® is a phytopharmaceutical for the treatment of decreasing mental capacity. It contains the patented Ginkgo special extract EGb 761®, developed and manufactured by Dr. Willmar Schwabe GmbH & Co. KG, Karlsruhe. EGb 761® is widely recognized as the best researched phytopharmaceutical world-wide and is available in more than 80 countries.

Click to see: Ginkgo Biloba Protects Your Memory
Source: Elements4Health.June 23rd.2010

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