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Cecropia peltata

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Botanical Name : Cecropia peltata
Family: Urticaceae
Genus: Cecropia
Species: C. peltata
Kingdom: Plantae
Order: Rosales

Common Name :Pumpwood and Trumpet tree.,Embauba

Habitat : Cecropia peltata is native to Central America, northern South America, and the Caribbean, and it has naturalized in parts of Africa. This is an early-succession species adapted to grow rapidly in disturbed areas. It is therefore most common in secondary woods and along forest edges.

Description
Trumpet tree is an awkwardly branched, open-crowned tree with alternate leaves about a foot (30 cm) wide clustered at tips of inwardly curving stems. It can grow to 70 ft (21 m) tall, but most trees are much smaller. The leaves have 7-11 palmate lobes and are borne on long petioles which attach near the center of the leaf. Leaves are rough-textured and dark green above and felty white underneath. The smooth gray bark on young trees is ringed with leaf scars. The flowers are small inconspicuous yellow catkins. They are followed by numerous small seeds embedded in 3 in (7.5 cm) long soft-fleshed fruiting stems. Prop roots sometimes develop at the base of the tree. Cecropia peltata is often confused with C. palmata, which has leaves divided almost to the base (as opposed to a third of the way in) and longer fruits. C. peltata may also be mistaken for Didymopanax morototoni, an unrelated lookalike tree.

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Hardiness: USDA Zones 10 – 11. This is a very frost sensitive tree that throws a dramatic tantrum and flings big brown leaves all around when it gets chilled.

Cultivation;
These are fast growing, short-lived trees. Young specimens can put on 2-3 in (5-8 cm) diameter per year. They need fertile soil to grow well and dislike competition from lawn grasses.
Light: Trumpet tree does best in full sun.
Moisture: These trees grow best on well drained soils with ample moisture.

Propagation: Trumpet tree can be propagated from seed, but the seeds germinate slowly. In the wild, the seeds are dispersed by bats and birds.

Edible Uses:
The young buds may be eaten as a cooked vegetable.

Medicinal Uses:
The corrosive and astringent latex is used against warts, calluses, herpes, ulcers, dysentery, and venereal diseases. A tea made from the leaves is widely employed as a cure for asthma and thought to be useful in treating a wide variety of other ailments including liver disease, cardiovascular problems, Parkinson’s disease, and snakebite. It also is used to ease childbirth and menstrual complaints.  Various substances have been extracted from yagrumo hembra for medicinal use, including one that increases cardiac muscular contraction and acts upon the kidneys as a diuretic. A substance extracted from the roots is said to heal wounds, and the leaves are often used as a poultice to reduce swelling and as an abrasive

The leaves of both Cecropia peltata and C. palmata are used in herbal medicine under the name “embauba leaf.” A tea made from the leaves is widely employed as a cure for asthma and thought to be useful in treating a wide variety of other ailments including liver disease, cardiovascular problems, Parkinson’s disease, and snakebite.

It also is used to ease childbirth and menstrual complaints.

Other Uses;
Cecropias are widely planted for tropical landscape effects.

The trumpet tree’s main trunk is solid and composed of a soft, weak, brittle, lightweight wood. It is combined with cement to make insulation board and made into excelsior, matchsticks, crates, toys, partitions, and paper pulp. The wood ignites readily from friction and makes good tinder. A latex rubber is made from the milky sap and the inner bark yields a coarse fiber. The leaves are sometimes used as sandpaper. The hollow stems have been fashioned into musical instruments, fishing floats, life preservers, water troughs, gutters, and bottle “corks.” The dead leaves dry dark mahogany brown above and white beneath, and curl into interesting sculptural forms which can be used in dried arrangements.

In addition to providing quick (though patchy) shade and tropical atmosphere, the trumpet tree makes a fine ecological conversation piece. In the tree’s native habitat biting ants live in the hollow stems. In a mutually beneficial relationship, the small but fierce ants clean the tree of debris and protect it from leaf-cutter ants and other herbivores, while the tree provides the ants with shelter and food in the form of special food-bodies produced along the undersides of the leaf stems

WARNING
Many regions lack the ants that live in wild Latin American trumpet trees, but it is wise to be cautious around these trees until you are certain that the ones you are dealing with are ant-free.

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.herbnet.com/Herb%20Uses_DE.htm
http://www.floridata.com/ref/c/cecr_pel.cfm
http://en.wikipedia.org/wiki/Cecropia_peltata

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Ailmemts & Remedies

Restless Legs Syndrome(RLS)

Alternative Name : Wittmaack–Ekbom syndrome

Definitipon:
Restless legs syndrome (RLS)  is a neurological disorder characterized by an irresistible urge to move one’s body to stop uncomfortable or odd sensations.  It most commonly affects the legs, but can affect the arms, torso, and even phantom limbs.  Moving the affected body part modulates the sensations, providing temporary relief.
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RLS sensations can most closely be compared to an itching or tickling in the muscles, like “an itch you can’t scratch” or an unpleasant “tickle that won’t stop.” The sensations typically begin or intensify during quiet wakefulness, such as when relaxing, reading, studying, or trying to sleep.  In addition, most individuals with RLS have limb jerking during sleep, which is an objective physiologic marker of the disorder and is associated with sleep disruption. Some controversy surrounds the marketing of drug treatments for RLS. It is a “spectrum” disease with some people experiencing only a minor annoyance and others experiencing major disruption of sleep and significant impairments in quality of life

Restless legs syndrome can begin at any age and generally worsens as you get older. Women are more likely than men to develop this condition.

A number of simple self-care steps and lifestyle changes may help you. Medications also help many people with restless legs syndrome.

Symptoms:
Commonly described sensations
People typically describe restless legs syndrome (RLS) symptoms as unpleasant sensations in their calves, thighs, feet or arms, often expressed as:

*Crawling

*Tingling

*Cramping

*Creeping

*Pulling

*Painful

*Electric

*Tense

*Uncomfortable

*Itchy

*Tugging

*Gnawing

*Aching

*Burning

Sometimes the sensations seem to defy description. Affected people usually don’t describe the condition as a muscle cramp or numbness. They do, however, consistently describe the desire to move or handle their legs.

It’s common for symptoms to fluctuate in severity, and occasionally symptoms disappear for periods of time.

NIH criteria
In 2003, a National Institutes of Health (NIH) panel modified their criteria to include the following:

1.An urge to move the limbs with or without sensations.

2.Improvement with activity. Many patients find relief when moving and the relief continues while they are moving. In more severe RLS this relief of symptoms may not be complete or the symptoms may reappear when the movement ceases.

3.Worsening at rest. Patients may describe being the most affected when sitting for a long period of time, such as when traveling in a car or airplane, attending a meeting, or watching a performance. An increased level of mental awareness may help reduce these symptoms.

4.Worsening in the evening or night. Patients with mild or moderate RLS show a clear circadian rhythm to their symptoms, with an increase in sensory symptoms and restlessness in the evening and into the night.
RLS is either primary or secondary.

*Primary RLS is considered idiopathic or with no known cause. Primary RLS usually begins slowly, before approximately 40–45 years of age and may disappear for months or even years. It is often progressive and gets worse with age. RLS in children is often misdiagnosed as growing pains.

*Secondary RLS often has a sudden onset after age 40, and may be daily from the beginning. It is most associated with specific medical conditions or the use of certain drugs

Causes:
Disease mechanism
Most research on the disease mechanism of restless legs syndrome has focused on the dopamine and iron system.   These hypotheses are based on the observation that iron and levodopa, a pro-drug of dopamine that can cross the blood-brain barrier and is metabolized in the brain into dopamine (as well as other mono-amine neurotransmitters of the catecholamine class) can be used to treat RLS, levodopa being a medicine for treating hypodopaminergic (low dopamine) conditions such as Parkinson’s disease, and also on findings from functional brain imaging (such as positron emission tomography and functional magnetic resonance imaging), autopsy series and animal experiments.  Differences in dopamine- and iron-related markers have also been demonstrated in the cerebrospinal fluid of individuals with RLS.  A connection between these two systems is demonstrated by the finding of low iron levels in the substantia nigra of RLS patients, although other areas may also be involved.

Heredity
RLS runs in families in up to half the people with RLS, especially if the condition started at an early age. Researchers have identified sites on the chromosomes where genes for RLS may be present.

Pregnancy
Pregnancy or hormonal changes may temporarily worsen RLS signs and symptoms. Some women experience RLS for the first time during pregnancy, especially during their last trimester. However, for most of these women, signs and symptoms usually disappear quickly after delivery.

Related conditions
For the most part, restless legs syndrome isn’t related to a serious underlying medical problem. However, RLS sometimes accompanies other conditions, such as:

*Peripheral neuropathy. This damage to the nerves in your hands and feet is sometimes due to chronic diseases such as diabetes and alcoholism.

*Iron deficiency. Even without anemia, iron deficiency can cause or worsen RLS. If you have a history of bleeding from your stomach or bowels, experience heavy menstrual periods or repeatedly donate blood, you may have iron deficiency.

* Kidney failure. If you have kidney failure, you may also have iron deficiency, often with anemia. When kidneys fail to function properly, iron stores in your blood can decrease. This, along with other changes in body chemistry, may cause or worsen RLS.

Risk Factors:
RLS can develop at any age, even during childhood. Many adults who have RLS can recall being told as a child that they had growing pains or can remember parents rubbing their legs to help them fall asleep. The disorder is more common with increasing age.

Complications:
Although RLS doesn’t lead to other serious conditions, symptoms can range from barely bothersome to incapacitating. Many people with RLS find it difficult to get to sleep or stay asleep. Insomnia may lead to excessive daytime drowsiness, but RLS may prevent you from enjoying a daytime nap.

Diagnosis:
The diagnosis of RLS relies essentially on a good medical history and physical examination. Sleep registration in a laboratory (polysomnography) is not necessary for the diagnosis. Peripheral neuropathy, radiculopathy and leg cramps should be considered in the differential diagnosis; in these conditions, pain is often more pronounced than the urge to move. Akathisia, a side effect of several antipsychotics or antidepressants, is a more constant form of leg restlessness without discomfort. Doppler ultrasound evaluation of the vascular system is essential in all cases to rule out venous disorders which is a common etiology of RLS. A rare syndrome of painful legs and moving toes has been described, with no known cause.

Treatment:
Treatment of restless legs syndrome involves identifying the cause of symptoms when possible. The treatment process is designed to reduce symptoms, including decreasing the number of nights with RLS symptoms, the severity of RLS symptoms and nighttime awakenings. Improving the quality of life is another goal in treatment. This means improving overall quality of life, decreasing daytime somnolence, and improving the quality of sleep. All of these goals are taken care of through nonpharmacologic and pharmacologic therapies. Pharmacotherapy involves dopamine agonists as first line drugs for daily restless legs syndrome; gabapentin (Horizant™) and opioids for treatment of resistant cases.

An algorithm created by Mayo Clinic researchers and endorsed by the RLS Foundation, provides guidance to the treating physician and patient, including non pharmacological and pharmacological treatments. Treatment of primary RLS should not be considered until possible precipitating medical conditions are ruled out, especially venous disorders. RLS Drug therapy is not curative and has side effects such as nausea, dizziness, hallucinations, orthostatic hypotension and daytime sleep attacks. In addition, it can be expensive (about $100–150 per month for life), and needs to be considered with caution.

Secondary RLS may be cured if precipitating medical conditions (anemia, venous disorder) are managed effectively. Secondary conditions causing RLS include iron deficiency, varicose veins, and thyroid problems. Karl-Axel Ekbom in his 1945 doctoral thesis on RLS suspected venous disease in about 12.5% of cases. But due to the unavailability of Doppler ultrasound imaging technology (the diagnostic tool detecting abnormal blood flow in the veins, “Venous Reflux”, the pathological basis for varicose veins) at that time, Ekbom may have underestimated the role of venous disease. In uncontrolled prospective series, improvement of RLS was achieved in a high percentage of patients presenting with a combination of RLS and venous disease and had sclerotherapy or other treatment for the correction of venous insufficiency.   In Nonpharmacologic treatments there are ways patients may be able to reduce the symptoms or decrease the severity of the symptoms. One thing that may worsen the symptoms is fatigue. Therefore using relaxation techniques, soaking in a warm bath or massaging the legs can all help aid in relaxation and relief of symptoms. Another technique is avoiding caffeine, alcohol, and tobacco. Also exercising every day and maintaining a schedule of relaxation and avoiding heavy meals before bed will all help with relief of symptoms. These techniques can be used with medication or just by themselves for those who do not want medication. For symptoms that occur in the evening patients may find that activities that alert the mind like crossword puzzles, and video games may reduce symptoms. Many patients may also benefit from RLS support groups.

Stretching and shaking legs
Stretching the leg muscles can bring relief lasting from seconds to days.   Walking around brings relief also. Tiredness can be a factor and some sufferers may find going to bed usually stops the discomfort. Bouncing or shaking the legs/feet in an up and down motion, with the ball of the foot on the floor when sitting down may bring temporary relief.

Iron supplements
According to some guidelines, all people with RLS should have their serum ferritin level tested. The ferritin level, a measure of the body’s iron stores, should be at least 50 µg for those with RLS. Oral iron supplements, taken under a doctor’s care, can increase ferritin levels. For some people, increasing ferritin will eliminate or reduce RLS symptoms. A ferritin level of 50 µg is not sufficient for some sufferers and increasing the level to 80 µg may further reduce symptoms. However, at least 40% of people will not notice any improvement. Treatment with IV iron is being tested at the US Mayo Clinic and Johns Hopkins Hospital. It is dangerous to take iron supplements without first having ferritin levels tested, as many people with RLS do not have low ferritin and taking iron when it is not called for can cause iron overload disorder, potentially a very dangerous condition

Medication therapy:
Several prescription medications, most of which were developed to treat other diseases, are available to reduce the restlessness in your legs. These include:

*Medications for Parkinson’s disease. These medications reduce the amount of motion in your legs by affecting the level of the chemical messenger dopamine in your brain. Two drugs, ropinirole (Requip) and pramipexole (Mirapex), are approved by the Food and Drug Administration for the treatment of moderate to severe RLS.

Doctors commonly also use other Parkinson’s drugs to treat restless legs syndrome, such as a combination of carbidopa and levodopa (Sinemet). People with RLS are at no greater risk of developing Parkinson’s disease than are those without RLS. Side effects of Parkinson’s medications are usually mild and include nausea, lightheadedness and fatigue.

*Opioids. Narcotic medications can relieve mild to severe symptoms, but they may be addicting if used in too high doses. Some examples include codeine, oxycodone (Roxicodone), the combination medicine oxycodone and acetaminophen (Percocet, Roxicet), and the combination medicine hydrocodone and acetaminophen (Lortab, Vicodin).

*Muscle relaxants and sleep medications. This class of medications, known as benzodiazepines, helps you sleep better at night. But these medications don’t eliminate the leg sensations, and they may cause daytime drowsiness. Commonly used sedatives for RLS include clonazepam (Klonopin), triazolam (Halcion), eszopiclone (Lunesta), ramelteon (Rozerem), temazepam (Restoril), zaleplon (Sonata) and zolpidem (Ambien).

*Medications for epilepsy. Certain epilepsy medications, such as gabapentin (Neurontin), may work for some people with RLS.It may take several trials for you and your doctor to find the right medication and dosage for you. A combination of medications may work best.

Caution about medications:
One thing to remember with drugs to treat RLS is that sometimes a medication that has worked for you for a while becomes ineffective. Or you notice your symptoms returning earlier in the day. For example, if you have been taking your medication at 8 p.m., your symptoms of RLS may start at 6 p.m. This is called augmentation. Your doctor may substitute another medication to combat the problem.

Most of the drugs prescribed to treat RLS aren’t recommended for pregnant women. Instead, your doctor may recommend self-care techniques to relieve symptoms. However, if the sensations are particularly bothersome during your last trimester, your doctor may approve the use of pain relievers.

Some medications may worsen symptoms of RLS. These include most antidepressants and some anti-nausea drugs. Your doctor may recommend that you avoid these medications if possible. However, should you need to take these medications, restless legs can still be controlled by adding drugs that manage the condition.

Lifestyle and home remedies

Making simple lifestyle changes can play an important role in alleviating symptoms of RLS. These steps may help reduce the extra activity in your legs:

*Take pain relievers. For very mild symptoms, taking an over-the-counter pain reliever such as ibuprofen (Advil, Motrin, others) when symptoms begin may relieve the twitching and the sensations.

*Try baths and massages. Soaking in a warm bath and massaging your legs can relax your muscles.

*Apply warm or cool packs. You may find that the use of heat or cold, or alternating use of the two, lessens the sensations in your limbs.

*Try relaxation techniques, such as meditation or yoga. Stress can aggravate RLS. Learn to relax, especially before going to bed at night.Establish good sleep hygiene. Fatigue tends to worsen symptoms of RLS, so it’s important that you practice good sleep hygiene. Ideally, sleep hygiene involves having a cool, quiet and comfortable sleeping environment, going to bed at the same time, rising at the same time, and getting enough sleep to feel well rested. Some people with RLS find that going to bed later and rising later in the day helps in getting enough sleep.

*Exercise. Getting moderate, regular exercise may relieve symptoms of RLS, but overdoing it at the gym or working out too late in the day may intensify symptoms.

*Avoid caffeine. Sometimes cutting back on caffeine may help restless legs. It’s worth trying to avoid caffeine-containing products, including chocolate and caffeinated beverages such as coffee, tea and soft drinks, for a few weeks to see if this helps.

*Cut back on alcohol and tobacco. These substances also may aggravate or trigger symptoms of RLS. Test to see whether avoiding them helps.

*Stay mentally alert in the evening. Boredom and drowsiness before bedtime may worsen RLS. Mentally stimulating activities such as video games or crossword puzzles can help you stay alert and may reduce symptoms of RLS.

Alternative Medication:
Because restless legs syndrome is sometimes due to an underlying nutritional deficiency, taking supplements to correct the deficiency may improve your symptoms. Your doctor can order blood tests to pinpoint nutritional deficiencies and give you a good sense of which supplements may help.

Doctor may also tell you whether certain dietary supplements can interfere with the way your prescription medications work or may pose health risks for you.

If blood tests show that you are deficient in any of the following nutrients, your doctor may recommend taking dietary supplements as part of your treatment plan:

*Iron
*Folic acid
*Vitamin B
*Magnesium

More research is needed to reliably establish the safety and effectiveness of all of these supplements in the treatment of RLS.

Prognosis:
RLS is generally a lifelong condition for which there is no cure. Symptoms may gradually worsen with age, though more slowly for those with the idiopathic form of RLS than for patients who also suffer from an associated medical condition. Nevertheless, current therapies can control the disorder, minimizing symptoms and increasing periods of restful sleep. In addition, some patients have remissions, periods in which symptoms decrease or disappear for days, weeks, or months, although symptoms usually eventually reappear. Being diagnosed with RLS does not indicate or foreshadow another neurological disease.

Prevention:
Other than preventing the  causes, no method of preventing RLS has yet been established or studied.

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.mayoclinic.com/health/restless-legs-syndrome/DS00191
http://en.wikipedia.org/wiki/Restless_legs_syndrome
http://www.sleepdisordersguide.com/restless-leg-syndrome-causes.html

Homeopathy for Restless Legs Syndrome

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Progressive Supranuclear Palsy

Definition:
Progressive supranuclear palsy, also called Steele-Richardson-Olszewski syndrome,(after the Canadian physicians who described it in 1963)  is a brain disorder that causes serious problems with walking, balance and eye movements. Progressive supranuclear palsy results from deterioration of cells in areas of your brain that control movement.
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Progressive supranuclear palsy is a rare disorder that slowly worsens over time. Although it’s not life-threatening itself, progressive supranuclear palsy can lead to life-threatening complications, such as pneumonia and swallowing problems.

Because there’s no cure for progressive supranuclear palsy, treatment focuses on managing and improving the related signs and symptoms.

Males and females are affected approximately equally and there is no racial, geographical or occupational predilection. Approximately 6 people per 100,000 population have PSP.

It has been described as a tauopathy

Symptoms:
The initial symptoms in two-thirds of cases are loss of balance, lunging forward when mobilizing, fast walking, bumping into objects or people, and falls.

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Other common early symptoms are changes in personality, general slowing of movement, and visual symptoms.

Later symptoms and signs are dementia (typically including loss of inhibition and ability to organize information), slurring of speech, difficulty swallowing, and difficulty moving the eyes, particularly in the vertical direction. The latter accounts for some of the falls experienced by these patients as they are unable to look up or down.

Some of the other signs are poor eyelid function, contracture of the facial muscles, a backward tilt of the head with stiffening of the neck muscles, sleep disruption, urinary incontinence and constipation.

The visual symptoms are of particular importance in the diagnosis of this disorder. Notably, the ophthalmoparesis experienced by these patients mainly concerns voluntary eye movement. Patients tend to have difficulty looking down (a downgaze palsy) followed by the addition of an upgaze palsy. Involuntary eye movement, as elicited by Bell’s phenomenon, for instance, may be closer to normal. On close inspection, eye movements called “square-wave jerks” may be visible when the patient fixes at distance. These are fine movements, similar to nystagmus, except that they are not rhythmic in nature. Difficulties with convergence (convergence insufficiency), where the eyes come closer together while focusing on something near, like the pages of a book, is typical. Because the eyes have trouble coming together to focus at short distances, the patient may complain of diplopia (double vision) when reading.

Cardinal manifestations:

*Supranuclear ophthalmoplegia

*Neck dystonia

*Parkinsonism

*Pseudobulbar palsy

*Behavioral and Cognitive impairment

*Imbalance and Difficulties walking

*Frequent Falls

*Stiffness

*Awkward movements

*Falling

*Problems with speech and swallowing

*Dizziness

*Loss of interest in pleasurable activities (apathy)

*Depression and anxiety

*Laughing or crying for no reason

*Forgetfulness

True to its name, the signs and symptoms of progressive supranuclear palsy tend to become progressively worse as the disease advances.

Causes:
We know that the symptoms of PSP are caused by a gradual deterioration of brain cells in a few tiny but important places at the base of the brain, in the region called the brainstem. One of these areas, the substantia nigra, is also affected in Parkinson’s disease, and damage to this region of the brain accounts for the motor symptoms that PSP and Parkinson’s have in common.

Scientists do not know what causes these brain cells to degenerate. There is no evidence that PSP is contagious, and genetic factors have not been implicated. No ethnic or racial groups have been affected more often than any others, and PSP is no more likely to occur in some geographic areas than in others.

There are, however, several theories about PSP’s cause. One possibility is that an unconventional virus-like agent infects the body and takes years or decades to start producing visible effects. Creutzfeldt-Jakob disease is one disease known to be caused by such an agent. Another possibility is that random genetic mutations, of the kind that occur in all of us all the time, happen to occur in particular cells or certain genes, in just the right combination to injure these cells. A third possibility is that there is exposure to some unknown chemical in the food, air, or water which slowly damages certain vulnerable areas of the brain. This theory stems from a clue found on the Pacific island of Guam, where a common neurological disease occurring only there and on a few neighboring islands shares some of the characteristics of PSP, Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (Lou Gehrig’s disease). Its cause is thought to be a dietary factor or toxic substance found only in that area.

Another possible cause of PSP is cellular damage caused by free radicals, unstable molecules produced continuously by all cells during normal metabolism. Although the body has built-in mechanisms for clearing free radicals from the system, scientists suspect that, under certain circumstances, free radicals can react with and damage other molecules. A great deal of research is directed at understanding the role of free radical damage in human diseases.

Genetics and Causal Factors:
Fewer than 1% of those with PSP have a family member with the same disorder. A variant in the gene for tau protein called the H1 haplotype, located on chromosome 17, has been linked to PSP. Nearly all people with PSP received a copy of that variant from each parent, but this is true of about two-thirds of the general population. Therefore, the H1 haplotype appears to be necessary but not sufficient to cause PSP. Other genes, as well as environmental toxins are being investigated as other possible contributors to the cause of PSP.

Risk Factors:
Risk factors for progressive supranuclear palsy include:

*Age. Progressive supranuclear palsy typically affects people around the age of 60.
*Sex. Men are affected somewhat more often.

Complications :
Complications of progressive supranuclear palsy result primarily from hindered muscle movements. These complications may include:

*Frequent falling, which can lead to head injuries, fractures and other injuries.

*Difficulty focusing your eyes, which also can lead to injuries.

*Problems with reading, driving a car, or other tasks requiring hand-eye coordination.

*Difficulty sleeping.

*Difficulty looking at bright lights.

*Problems swallowing, which can lead to choking or inhaling food or liquid into your airway (aspiration). Aspiration can develop into pneumonia — the most common cause of death in people with progressive supranuclear palsy.

*Impulsive behaviors — for example, standing up without waiting for assistance — which can lead to falls.

Complications from progressive supranuclear palsy may eventually necessitate the use of a feeding tube due to choking hazards. To avoid injuries due to falling, a walker or a wheelchair may also be necessary.

Diagnosis:
Initial complaints in PSP are typically vague and an early diagnosis is always difficult. The primary complaints fall into these categories:

*Symptoms of dysequilibrium, such as unsteady walking or abrupt and unexplained falls without loss of consciousness.

*Visual complaints, including blurred vision, difficulties in looking up or down, double vision, light sensitivity, burning eyes, or other eye trouble.

*Slurred speech.

*Various mental complaints such as slowness of thought, impaired memory, personality changes, and changes in mood.

Progressive Supranuclear Palsy is often misdiagnosed because some of its symptoms are very much like those of Parkinson’s disease, Alzheimer’s disease, and more rare neurodegenerative disorders, such as Creutzfeldt-Jakob disease. In fact, PSP is most often misdiagnosed as Parkinson’s disease early in the course of the illness. Memory problems and personality changes may also lead a physician to mistake PSP for depression, or even attribute symptoms to some form of dementia. The key to establishing the diagnosis of PSP is the identification of early gait instability and difficulty moving the eyes, the hallmark of the disease, as well as ruling out other similar disorders, some of which are treatable.

PSP is frequently misdiagnosed as Parkinson’s disease because of the slowed movements and gait difficulty, or as Alzheimer’s disease because of the behavioral changes. It is one of a number of diseases collectively referred to as Parkinson plus syndromes. A poor response to levodopa along with symmetrial onset can help differentiate this disease from PD.

Difference between PSP &  Parkinson’s Disease:
Both PSP and Parkinson’s disease cause stiffness, movement difficulties, and clumsiness. However, patients with PSP usually stand straight or occasionally even tilt their heads backward (and tend to fall backward), while those with Parkinson’s disease usually bend forward. Problems with speech and swallowing are much more common and severe in PSP than in Parkinson’s disease, and tend to show up earlier in the course of the disease. Both diseases share other features: onset in late middle age, bradykinesia (slow movement), and rigidity of muscles. Tremor, almost universal in Parkinson’s patients, is rare in PSP. Although Parkinson’s patients markedly benefit from the drug levodopa, patients with PSP respond poorly and only transiently to this drug.

Treatment :
There is currently no effective treatment for PSP, although scientists are searching for better ways to manage the disease. In some patients the slowness, stiffness, and balance problems of PSP may respond to antiparkinsonian agents such as levodopa, but the effect is usually temporary. The speech, vision, and swallowing difficulties usually do not respond to any drug treatment.

Another group of drugs that has been of some modest success in PSP are antidepressant medications. The most commonly used of these drugs are fluoxetine (Prozac), amitriptyline (Elavil), and imipramine (Tofranil). The anti-PSP benefit of these drugs seems not to be related to their ability to relieve depression.

Non-drug treatment for PSP can take many forms. Patients frequently use weighted walking aids because of their tendency to fall backward. Bifocals or special glasses called prisms are sometimes prescribed for PSP patients to remedy the difficulty of looking down. Formal physical therapy is of no proven benefit in PSP, but certain exercises can be done to keep the joints limber.

A surgical procedure that may be necessary when there are swallowing disturbances is a gastrostomy. A gastrostomy (or a jejunostomy) is a minimally invasive procedure which is performed when the patient has difficulty swallowing or when severe choking is a definite risk. This surgery involves the placement of a tube through the skin of the abdomen into the stomach (intestine) for feeding purposes. Surgical procedures such as fetal brain cell implantation and pallidotomy, which are being tested as treatments for Parkinson’s disease, are not effective in PSP.

Life Style & Home Remedies:
To minimize the effects of progressive supranuclear palsy, you can take certain steps at home. They may include:

*Eyedrops. Eyedrops may help ease dry eyes that can occur as a result of problems blinking. They can also be helpful for persistent tearing.

*Fall-avoidance aids. Installing grab bars in hallways and bathrooms or using a walker that’s weighted can help you avoid falls. Making home modifications, such as removing scatter rugs or other items that are hard to see without looking downward, also can help with balance and vision problems. When possible, avoid climbing stairs.

Prognosis:
As there is currently no effective treatment or cure for PSP, although some of the symptoms can respond to nonspecific measures. The average age at symptoms onset is 63 and survival from onset averages 7 years with a wide variance

Researches:
Studies to improve the diagnosis of PSP have recently been conducted at the National Institute of Neurological Disorders and Stroke (NINDS). Experiments to find the cause or causes of PSP are currently under way. Therapeutic trials with free radical scavengers (agents that can get rid of potentially harmful free radicals) are being planned for the future.

In addition, there is a great deal of ongoing research on Parkinson’s and Alzheimer’s diseases at the National Institutes of Health and at university medical centers throughout the country. Better understanding of those common related disorders will go a long way toward solving the problem of PSP, just as studying PSP may help shed light on Parkinson’s and Alzheimer’s diseases.

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.healthtouch.com/bin/EContent_HT/showAllLfts.asp?lftname=NINDS156&cid=HT
http://en.wikipedia.org/wiki/Progressive_supranuclear_palsy
http://www.mayoclinic.com/health/progressive-supranuclear-palsy/DS00909
http://www.nlm.nih.gov/medlineplus/progressivesupranuclearpalsy.html

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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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Ailmemts & Remedies

Myoclonus

Definition:
Myoclonus refers to a sudden, involuntary jerking of a muscle or group of muscles. In its simplest form, myoclonus consists of a muscle twitch followed by relaxation. A hiccup is an example of this type of myoclonus. Other familiar examples of myoclonus are the jerks or “sleep starts” that some people experience while drifting off to sleep.  These simple forms of myoclonus occur in normal, healthy persons and cause no difficulties. When more widespread, myoclonus may involve persistent, shock-like contractions in a group of muscles.  Myoclonic jerking may develop in people with multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, or Creutzfeldt-Jakob disease. Myoclonic jerks commonly occur in persons with epilepsy, a disorder in which the electrical activity in the brain becomes disordered and leads to seizures.  Myoclonus may develop in response to infection, head or spinal cord injury, stroke, brain tumors, kidney or liver failure, lipid storage disease, chemical or drug poisoning, or other disorders.  It can occur by itself, but most often it is one of several symptoms  associated with a wide variety of nervous system disorders.

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Myoclonic jerks may occur alone or in sequence, in a pattern or without pattern. They may occur infrequently or many times each minute. Most often, myoclonus is one of several signs in a wide variety of nervous system disorders such as multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, subacute sclerosing panencephalitis and Creutzfeldt-Jakob disease (CJD), serotonin toxicity, and some forms of epilepsy. Some researchers indicate that jerks persistently may even cause early tremors.

In almost all instances in which myoclonus is caused by central nervous system disease it is preceded by other symptoms; for instance, in CJD it is generally a late-stage clinical feature that appears after the patient has already started to exhibit gross neurological deficits.

Anatomically, myoclonus may originate from lesions of the cortex, subcortex or spinal cord. The presence of myoclonus above the foramen magnum effectively excludes spinal myoclonus, but further localisation relies on further investigation with electromyography (EMG) and electroencephalography (EEG).

Types:
In juvenile myoclonic epilepsy, seizures usually involve the neck, shoulders, and upper arms. These seizures typically occur shortly after waking up. They normally begin between puberty and early adulthood. They can usually be controlled with medication, but it must be taken for life.

In rare cases, myoclonic seizures can be symptomatic of Lennox-Gastaut syndrome, beginning in early childhood and usually involving the face, neck, shoulders, and upper arms. In these cases, the seizures tend to be strong and difficult to control.

Progressive myoclonic epilepsy includes both myoclonic and tonic-clonic seizures. Treatment is not normally successful for any extended period of time.

Classifying the many different forms of myoclonus is difficult because the causes, effects, and responses to therapy vary widely. Listed below are the types most commonly described:

*Action myoclonus is characterized by muscular jerking triggered or intensified by voluntary movement or even the intention to move. It may be made worse by attempts at precise, coordinated movements. Action myoclonus is the most disabling form of myoclonus and can affect the arms, legs, face, and even the voice. This type of myoclonus often is caused by brain damage that results from a lack of oxygen and blood flow to the brain when breathing or heartbeat is temporarily stopped.

*Cortical reflex myoclonus is thought to be a type of epilepsy that originates in the cerebral cortex – the outer layer, or “gray matter,” of the brain, responsible for much of the information processing that takes place in the brain. In this type of myoclonus, jerks usually involve only a few muscles in one part of the body, but jerks involving many muscles also may occur. Cortical reflex myoclonus can be intensified when patients attempt to move in a certain way or perceive a particular sensation.

*Essential myoclonus occurs in the absence of epilepsy or other apparent abnormalities in the brain or nerves. It can occur randomly in people with no family history, but it also can appear among members of the same family, indicating that it sometimes may be an inherited disorder. Essential myoclonus tends to be stable without increasing in severity over time. Some scientists speculate that some forms of essential myoclonus may be a type of epilepsy with no known cause.

*Palatal myoclonus is a regular, rhythmic contraction of one or both sides of the rear of the roof of the mouth, called the soft palate. These contractions may be accompanied by myoclonus in other muscles, including those in the face, tongue, throat, and diaphragm. The contractions are very rapid, occurring as often as 150 times a minute, and may persist during sleep. The condition usually appears in adults and can last indefinitely. People with palatal myoclonus usually regard it as a minor problem, although some occasionally complain of a “clicking” sound in the ear, a noise made as the muscles in the soft palate contract.

*Progressive myoclonus epilepsy (PME) is a group of diseases characterized by myoclonus, epileptic seizures, and other serious symptoms such as trouble walking or speaking. These rare disorders often get worse over time and sometimes are fatal. Studies have identified at least three forms of PME. Lafora disease is inherited as an autosomal recessive disorder, meaning that the disease occurs only when a child inherits two copies of a defective gene, one from each parent. Lafora disease is characterized by myoclonus, epileptic seizures, and dementia (progressive loss of memory and other intellectual functions). A second group of PME diseases belonging to the class of cerebral storage diseases usually involves myoclonus, visual problems, dementia, and dystonia (sustained muscle contractions that cause twisting movements or abnormal postures). Another group of PME disorders in the class of system degenerations often is accompanied by action myoclonus, seizures, and problems with balance and walking. Many of these PME diseases begin in childhood or adolescence.

*Reticular reflex myoclonus is thought to be a type of generalized epilepsy that originates in the brainstem, the part of the brain that connects to the spinal cord and controls vital functions such as breathing and heartbeat. Myoclonic jerks usually affect the whole body, with muscles on both sides of the body affected simultaneously. In some people, myoclonic jerks occur in only a part of the body, such as the legs, with all the muscles in that part being involved in each jerk. Reticular reflex myoclonus can be triggered by either a voluntary movement or an external stimulus.

*Spinal myoclonus is myoclonus originating in the spinal cord, including segmental and propriospinal myoclonus. The latter is usually due to a thoracic generator producing truncal flexion jerk. It is often stimulus-induced with a delay due to the slow conducting propriospinal nerve fibers.

*Stimulus-sensitive myoclonus is triggered by a variety of external events, including noise, movement, and light. Surprise may increase the sensitivity of the patient.

*Sleep myoclonus occurs during the initial phases of sleep, especially at the moment of dropping off to sleep. Some forms appear to be stimulus-sensitive. Some persons with sleep myoclonus are rarely troubled by, or need treatment for, the condition. However, myoclonus may be a symptom in more complex and disturbing sleep disorders, such as restless legs syndrome, and may require treatment by a doctor.

Symptoms:
Myoclonic seizures can be described as “jumps.” They are caused by rapid contraction and relaxation of the muscles. People without epilepsy can suffer small but similar jerks in the form of hiccups or brief twitches. These are perfectly normal.

In someone with epilepsy, myoclonic seizures cause abnormal movements on both sides of the body at the same time. In reflex epilepsies, myoclonic seizures can be brought on by flashing lights or other environmental triggers (see photosensitive epilepsy).

Familiar examples of normal myoclonus include hiccups and hypnic jerks that some people experience while drifting off to sleep. Severe cases of pathologic myoclonus can distort movement and severely limit a person’s ability to sleep, eat, talk, and walk. Myoclonic jerks commonly occur in individuals with epilepsy. The most common types of myoclonus include action, cortical reflex, essential, palatal, progressive myoclonus epilepsy, reticular reflex, sleep, and stimulus-sensitive.

People with myoclonus often describe the symptoms as “jerks,” shakes” or “spasms” that are:

*Sudden
*Brief
*Involuntary
*Shock-like
*Variable in intensity and frequency
*Localized to one part of the body or all over the body
*Sometimes severe enough to interfere with eating, talking or walking

Causes:
Myoclonus may be caused by a variety of underlying problems. Doctors often separate the types of myoclonus based on their causes, which helps determine treatment. Types of myoclonus include the following categories.

Physiological myoclonus

This is the type that occurs in normal, healthy people and rarely needs treatment. Examples include:
*Hiccups
*Sleep starts
*Infant muscle twitching during sleep or after a feeding

Essential myoclonus
Essential myoclonus occurs on its own, typically without other symptoms and without being related to any underlying illness. The cause of essential myoclonus is often unexplained (idiopathic) or, in some cases, hereditary.

Epileptic myoclonus
This type of myoclonus occurs as part of an epileptic disorder. Muscle jerks may be the only symptom or one of many.

Symptomatic (secondary) myoclonus

This is a common form of myoclonus. Muscle jerks occur as a result of an underlying medical problem, such as:
*Head or spinal cord injury or infection
*Stroke
*Brain tumor
*Kidney or liver failure
*Chemical or drug poisoning
*Prolonged oxygen deprivation
*Medication reaction
*Huntington’s disease
*Alzheimer’s disease
*Parkinson’s disease
*Metabolic problems

Treatment:
Discontinuation of drugs suspected of causing myoclonus and treatment of metabolic derangements may resolve some cases of myoclonus.  When pharmacological treatment is indicated anticonvulsants are the main line of treatment. Paradoxical reactions to treatment are notable. Drugs which most people respond to may in other individuals worsen their symptoms. Sometimes this leads to the mistake of increasing the dose, rather than decreasing or stopping the drug.  Treatment of myoclonus focuses on medications that may help reduce symptoms. Drugs used include sodium valproate, clonazepam and some other anticonvulsants such as piracetam and levetiracetam.  Dosages of clonazepam usually are increased gradually until the patient improves or side effects become harmful. Drowsiness and loss of coordination are common side effects. The beneficial effects of clonazepam may diminish over time if the patient develops a tolerance to the drug.

Many of the drugs used for myoclonus, such as barbiturates, phenytoin and primidone, are also used to treat epilepsy. Barbiturates slow down the central nervous system and cause tranquilizing or antiseizure effects. Phenytoin and primidone are effective antiepileptics drugs, although phenytoin can cause liver failure or have other harmful long-term effects in patients with PME. Sodium valproate is an alternative therapy for myoclonus and can be used either alone or in combination with clonazepam. Although clonazepam and/or sodium valproate are effective in the majority of patients with myoclonus, some people have adverse reactions to these drugs.

Some studies have shown that doses of 5-hydroxytryptophan (5-HTP) leads to improvement in patients with some types of action myoclonus and PME. These differences in the effect of 5-HTP on patients with myoclonus have not yet been explained, but they may offer important clues to underlying abnormalities in serotonin receptors.

The complex origins of myoclonus may require the use of multiple drugs for effective treatment. Although some drugs have a limited effect when used individually, they may have a greater effect when used with drugs that act on different pathways or mechanisms in the brain. By combining several of these drugs, scientists hope to achieve greater control of myoclonic symptoms. Some drugs currently being studied in different combinations include clonazepam, sodium valproate, piracetam, and primidone. Hormonal therapy also may improve responses to antimyoclonic drugs in some people.
Prognosis:
Although myoclonus is not a life-threatening condition, it may result in serious, debilitating impairments. Action myoclonus, with its positive and negative myoclonus components, is generally considered the most serious. It varies from person to person as to whether it is life-long.

Research:
The National Institute of Neurological Disorders and Stroke (NINDS) conducts research relating to myoclonus in its laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major medical institutions across the country. Scientists are seeking to understand the underlying biochemical basis of involuntary movements and to find the most effective treatment for myoclonus and other movement disorders. Researchers may be able to develop drug treatments that target specific biochemical changes involved in myoclonus. By combining several of these drugs, scientists hope to achieve greater control of myoclonic symptoms.

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.ninds.nih.gov/disorders/myoclonus/myoclonus.htm
http://www.mayoclinic.com/health/myoclonus/DS00754
http://en.wikipedia.org/wiki/Myoclonus

http://insomnia.ygoy.com/2011/04/28/sleep-myoclonus/

http://www.buzzle.com/articles/palatal-myoclonus.html

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