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Herbs & Plants

Brahmi (Bacopa monniera)

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Botanical Name :Bacopa monniera
Family :Scrophulariaceae/PLANTAGINACEAE Plantain Family
Genus: Bacopa
Kingdom: Plantae
Order: Lamiales
Species:
B. monnieri
Common Names :  Bacopa , Water hyssop, Brahmi, Coastal Waterhyssop, Thyme-leafed gratiola,
International Naming:
(Niirpirami) in Tamil
Phak mi, Phrommi , in Vietnamese
Lunuwila in Sinhalese (Sri Lanka)

Habitat: Native in India,Bangladesh,Burma.It commonly grows in marshy areas throughout India, Nepal, Sri Lanka, China, Taiwan, and Vietnam, and is also found in Florida and other southern states of the USA where it can be grown in damp conditions by the pond or bog garden.. Wetlands and muddy shores.

Description:
Bacopa Monniera is a genus of 70-100 aquatic plants in the family Plantaginaceae. The plants are annual or perennial, decumbent or erect stemmed plants. Crushed Bacopa leaves have the distinct scent of lemons.It is a  creeping herb with numerous branches, small oblong leaves, and light purple flowers. In India and the tropics it grows naturally in wet soil, shallow water, and marshes. The herb can be found at elevations from sea level to altitudes of 4,400 feet, and is easily cultivated if adequate water is available. Flowers and fruit appear in summer and the entire plant is used medicinally.   Brahmi is also the name given to Centella asiatica, particularly in north India, although that may be a case of mistaken identification that was introduced during the 16th century.

CLICK TO SEE THE PICTURES..>....(01).......(1).….…(2)..…....(3)..……....(4)….

Bacopa Monniera is used prominently in Ayurveda, a holistic medicine system from India, and has been used since approximately the 6th century AD.
Bacopa monnieri in Hyderabad, India.The leaves of this plant are succulent and relatively thick. Leaves are oblanceolate and are arranged oppositely on the stem. The flowers are small and white, with four or five petals. Its ability to grow in water makes it a popular aquarium plant. It can even grow in slightly brackish conditions. Propagation is often achieved through cuttings.

Edible uses:
It is used in Vietnamese cuisine, where it is called rau ??ng bi?n. It is used in cháo cá, a variety of rice congee made with fish and n?m tràm mushrooms.

Active Constituents and Pharmacokinetics:
Compounds responsible for the pharmacological effects of Bacopa include alkaloids, saponins, and sterols. Many active constituents–the alkaloids Brahmine and herpestine, saponins d-mannitol and hersaponin, acid A, and monnierin–were isolated in India over 40 years ago. Other active constituents have since been identified, including betulic acid, stigmastarol, beta-sitosterol, as well as numerous bacosides and bacopasaponins. The constituents responsible for Bacopa’s cognitive effects are bacosides A and B.5. (5-9)

Medicinal Actions & Uses:

Traditional uses: Bacopa has been used in traditional Ayurvedic treatment for epilepsy and asthma. It is also used in Ayurveda for ulcers, tumors, ascites, enlarged spleen, inflammations, leprosy, anemia, and gastroenteritis.

It has antioxidant properties, reducing oxidation of fats in the bloodstream. However, anti-epilepsy properties seem to be in very high toxic and near lethal doses, so it’s only used—at much lower non-toxic dosage—as a (cognitive) additive to regular epilepsy medication. Studies in humans show that an extract of the plant has antianxiety effects.

It is listed as a nootropic, a drug that enhances cognitive ability. In India, this plant has also been used traditionally to consecrate newborn babies in the belief that it will open the gateway of intelligence. Laboratory studies on rats indicate that extracts of the plant improve memory capacity and motor learning ability.[5] Recent studies suggest bacopa may improve intellectual activity. The sulfhydryl and polyphenol components of Bacopa monniera extract have also been shown to impact the oxidative stress cascade by scavenging reactive oxygen species, inhibiting lipoxygenase activity and reducing divalent metals. This mechanism of action may explain the effect of Bacopa monniera extract in reducing beta-amyloid deposits in mice with Alzheimer’s disease.

It is used in Rebirthing therapy to accelerate trauma release and make continuous breathing easier. Bacopa monnieri is a well known nootropic plant reported for its tranquilizing, sedative, cognitive enhancing, hepatoprotective and antioxidant action.(ref name: m mujassam)

Common uses:
Memory, attention and other cognitive functions, occasional panic and anxiety, mental/physical fatigue, immune system response

Pharmacology and Phytochemicals:
Much modern research has focused on the activity Bacopa Monniera demonstrates in the Central Nervous System. Recent studies indicate that Bacosides, B. Monniera’s primary components, enhance nerve impulse transmission, possibly helping improve concentration, learning, memory, and attention span as well as other higher order cognitive functions. Preliminary lab results also suggest it influences that production and availability of Serotonin.

Scientists state that B. Monniera likely affects multiple systems in the body in order to promote emotional well-being, mental sharpness, and physical endurance.

Mechanisms of Action:
Bacopa Monniera has been identified in clinical study as an adaptogen that increases resistance to a wide range of chemical, physical, and biological stressors.

Research:
Bacopa monnieri displays in vitro antioxidant and cell-protective effects. In animals, it also inhibits acetylcholinesterase, activates choline acetyltransferase, and increases cerebral blood flow.

Several studies have suggested that Bacopa monnieri extracts may have protective effects in animal models of neurodegeneration. Small clinical trials in humans have found limited evidence supporting improved free memory recall, with no evidence supporting other cognition-enhancing effects.


Safety

A standardized Bacopa monniera preparation was evaluated for safety and tolerability in 23 healthy adult volunteers.   Participants took 300 mg of the extract daily for 15 days, followed by 450 mg/daily for the subsequent 15 days. No adverse effects were observed in biochemical, electrocardiographic, hematological or clinical parameters in the post-treatment vs. the pre-treatment period. There were some reports of mild gastrointestinal symptoms that resolved spontaneously.

Interactions
Bacopa Monnieri might agonize (strengthen) cytochrome p450 liver isoenzymes “7-pentoxyresorufin O-dealkylase” (CYP2B1/2?) and “7-ethoxyresorufin O-deethylation” (CYP1A1), especially under stressful conditions.

Known Hazards:  Aqueous extracts of Bacopa monnieri may have reversible adverse effects on spermatogenesis, sperm count, and fertility in male mice.

The most commonly reported adverse side effects of Bacopa monnieri in humans are nausea, increased intestinal motility, and gastrointestinal upset.

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://en.wikipedia.org/wiki/Bacopa_monnieri#cite_note-11
http://www.anxiety-and-depression-solutions.com/articles/complementary_alternative_medicine/herbs_supplements/bacopa_monniera.php
http://findarticles.com/p/articles/mi_m0FDN/is_1_9/ai_114563492/
http://www.anniesremedy.com/herb_detail304.php

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News on Health & Science

Scientists in Sleeping Sickness ‘Breakthrough’

Scientists say they have identified a potential treatment for sleeping sickness, a killer disease that infects about 60,000 people in Africa a year.

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British and Canadian experts say drugs could attack an enzyme the parasite causing the illness needs to survive.

They say the orally-administered drug could be ready for human clinical trials in about 18 months.

The disease, spread by the bite of a tsetse fly,(CLICK & SEE) is caused by a parasite attacking the central nervous system.

It has similar symptoms to malaria, making it difficult to diagnose. Left untreated, it moves to the spinal column and brain, resulting in mental confusion and eventual death.

Fatal side effects
The “breakthrough” came at the University of Dundee in Scotland, where scientists were funded to research diseases neglected by major drugs companies.

Professor Paul Wyatt, director of the programme, said: “This is one of the most significant findings made in recent years in terms of drug discovery and development for neglected diseases.”

He said the research, published in the journal Nature, represented “significant strides” in the development of a full blown drug against the disease.

The World Health Organization estimates there are between 50,000 and 70,000 cases of the disease a year, with a further 60 million people at risk of infection.

The research in Dundee was backed by partners at the University of York in England and the Structural Genomics Consortium in Toronto, Canada.

The two drugs currently available to treat sleeping sickness both have associated problems.

One is arsenic-based with side effects that kill one in 20 patients and the other – eflornithine – is costly, only partially effective and requires prolonged hospital treatment, the scientists said.

You may click to see:->

Breakthrough in sleeping sickness

Sleeping sickness test ‘promising’

Source: BBC NEWS:March 31st. 2010

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Categories
Ailmemts & Remedies

Sleeping Sickness (African trypanosomiasis)

Other Names:- Human African trypanosomiasis, sleeping sickness, African lethargy, or Congo trypanosomiasis.

Defenition:
African trypanosomiasis or Sleeping sickness is infection with organisms carried by certain flies. It results in swelling of the brain. It is a parasitic disease of people and animals, caused by protozoa of the species Trypanosoma brucei and transmitted by the tsetse fly.

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The disease is endemic in some regions of Sub-Saharan Africa, covering about 36 countries and 60 million people. It is estimated that 50,000 to 70,000 people are currently infected, the number having declined somewhat in recent years.  Four major epidemics have occurred in recent history, one lasting from 1896–1906 and the other two in 1920 and 1970. In 2008 there was an epidemic in Uganda.

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History
The condition has been present in Africa since at least the 14th century, and probably for thousands of years before that. The causative agent and vector were identified in 1902–1903 by Sir David Bruce, and the differentiation between the subspecies of the protozoa made in 1910. The first effective treatment, Atoxyl, an arsenic-based drug developed by Paul Ehrlich and Kiyoshi Shiga, was introduced in 1910 but blindness was a serious side effect. Numerous drugs designed to treat the disease have been introduced since then.

Symptoms and clinical features:-
Gambienseinfections lead to drowsiness during the day, but insomnia at night. Sleep becomes uncontrollable as the disease gets worse, and eventually leads to coma.

General symptoms include:

*Anxiety
*Drowsiness
*Fever
*Headache
*Increased sleepiness
*Insomnia at night
*Mood changes
*Sweating
*Swollen lymph nodes all over the body
*Swollen, red, painful nodule at site of fly bite
*Uncontrollable urge to sleep

Symptoms begin with fever, headaches, and joint pains. As the parasites enter through both the blood and lymph systems, lymph nodes often swell up to tremendous sizes. Winterbottom’s sign, the tell-tale swollen lymph nodes along the back of the neck, may appear. If untreated, the disease slowly overcomes the defenses of the infected person, and symptoms spread to include anemia, endocrine, cardiac, and kidney diseases and disorders. The disease then enters a neurological phase when the parasite passes through the blood-brain barrier. The symptoms of the second phase give the disease its name; besides confusion and reduced coordination, the sleep cycle is disturbed with bouts of fatigue punctuated with manic periods progressing to daytime slumber and night-time insomnia. Without treatment, the disease is invariably fatal, with progressive mental deterioration leading to coma and death. Damage caused in the neurological phase can be irreversible.

In addition to the bite of the tsetse fly, the disease is contractible in the following ways:

*Mother to child infection: the trypanosome can sometimes cross the placenta and infect the fetus.
*Laboratories: accidental infections, for example, through the handling of blood of an infected person and
*organ transplantation, although this is uncommon.
*Blood transfusion
*Sexual contact (might be possible, but happens rarely)

Causes:
Sleeping sickness is caused by two organisms, Trypanosoma brucei rhodesiense and Trypanosomoa brucei gambiense. The more severe form of the illness is caused by rhodesiense.

CLICK & SEE THE PICTURES

Trypanosoma forms in a blood smear.

Tsetse flies carry the infection. When an infected fly bites you, painful, red swelling occurs at the site of the bite. The infection then spreads through your blood, causing episodes of fever, headache, sweating, and swelling of the lymph nodes.

The flagellate reproduces in the bloodstream, and the symptoms develop gradually as the burden of parasites and their harmful effects increases. It also migrates into the central nervous system, producing the characteristic symptoms.

T. brucei gambiense is the cause of a persistent infection that lasts several years until it finally develops into a coma, from which the patient cannot be woken. Hence the name ‘sleeping sickness’.

If the central nervous system is sufficiently affected, the patient can no longer be cured, and eventually dies, possibly from other infections that may be superimposed on the primary disease.

When the infection spreads to the central nervous system, it causes the symptoms typical of sleeping sickness . When it reaches the brain, behavioral changes such as fear and mood swings occur, followed by headache, fever, and weakness. Inflammation of the heart ( myocarditis) may develop.

Life cycle:-
The tsetse fly is large, brown and stealthy. While taking blood from a mammalian host, an infected tsetse fly (genus Glossina) injects metacyclic trypomastigotes into skin tissue. The parasites enter the lymphatic system and pass into the bloodstream

1.Inside the host, they transform into bloodstream trypomastigotes

2.are carried to other sites throughout the body, reach other blood fluids (e.g., lymph, spinal fluid), and continue the replication by binary fission

3.The entire life cycle of African Trypanosomes is represented by extracellular stages. A tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host

4.In the fly’s midgut, the parasites transform into procyclic trypomastigotes,

5.multiply by binary fission,

6.leave the midgut, and

7.transform into epimastigotes

8.The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission.
The cycle in the fly takes approximately 3 weeks to progress.

Diagnosis:
A physical examination may show signs of meningoencephalitis (inflammation of the brain and its covering, the meninges).

Tests include the following:

*Albumin levels
*Blood smear
*Cerebrospinal fluid tests
*Complete blood count (CBC)
*Globulin levels
*Lymph node aspiration

Most antibody and antigen test are not very helpful because they can’t distinguish between current and previous infection. Specific IgM levels in the cerebrospinal fluid may be helpful, however.

The diagnosis rests upon demonstrating trypanosomes by microscopic examination of chancre fluid, lymph node aspirates, blood, bone marrow, or, in the late stages of infection, cerebrospinal fluid. A wet preparation should be examined for the motile trypanosomes, and in addition a smear should be fixed, stained with Giemsa (or Field), and examined. Concentration techniques can be used prior to microscopic examination. For blood samples, these include centrifugation followed by examination of the buffy coat; mini anion-exchange/centrifugation; and the Quantitative Buffy Coat (QBC) technique. For other samples such as spinal fluid, concentration techniques include centrifugation followed by examination of the sediment. Isolation of the parasite by inoculation of rats or mice is a sensitive method, but its use is limited to T. b. rhodesiense. Antibody detection has sensitivity and specificity that are too variable for clinical decisions. In addition, in infections with T. b. rhodesiense, seroconversion occurs after the onset of clinical symptoms and thus is of limited use.

Three similar serological tests are available for detection of the parasite; the micro-CATT, wb-CATT, and wb-LATEX. The first uses dried blood while the other two use whole blood samples. A 2002 study found the wb-CATT to be the most efficient for diagnosis, while the wb-LATEX is a better exam for situations where greater sensitivity is required.

Possible Complications:-
Complications include injury related to falling asleep while driving or performing other activities, and progressive damage to the nervous system.

Treatment:-
First line, first stage
The current standard treatment for first stage disease is:

*Intravenous or intramuscular pentamidine (for T.b. gambiense); or
*Intravenous suramin (for T.b. rhodesiense)

The drug Eflornithine — previously used only as an alternative treatment for sleeping sickness due to its labour-intensive administration — was found to be safe and effective as a first-line treatment for the disease in 2008, according to the Science and Development Network’s Sub-Saharan Africa news updates. Researchers tracked over 1,000 adults and children at a centre in Ibba, Southern Sudan—the first use of eflornithine on a large scale— and it was highly effective in treating the issue.

According to a treatment study of Trypanosoma gambiense caused human African trypanosomiasis, use of eflornithine (DMFO) resulted in fewer adverse events than treatment with melarsoprol.

All patients should be followed up for two years with lumbar punctures every six months to look for relapse.

First line, second stage:-
The current standard treatment for second stage (later stage) disease is:

Intravenous melarsoprol 2.2 mg/kg daily for 10 consecutive days.
Alternative first line therapies include:

Intravenous melarsoprol 0.6 mg/kg on day 1, 1.2 mg/kg IV melarsoprol on day 2, and 1.2 mg/kg/day IV melarsoprol combined with oral 7.5 mg/kg nifurtimox twice a day on days 3 to 10; or
Intravenous eflornithine 50 mg/kg every six hours for 14 days.
Combination therapy with eflornithine and nifurtimox is safer and easier than treatment with eflornithine alone, and appears to be equally or more effective. It has been recommended as first-line treatment for second stage T. b. gambiensis disease.

Resistant disease:-
In areas with melarsoprol resistance or in patients who have relapsed after melarsoprol monotherapy, the treatment should be:

*melarsoprol and nifurtimox, or
*eflornithine

Outdated protocols
The following traditional regimens should no longer be used:

*(old “standard” 26-day melarsoprol therapy) Intravenous melarsoprol therapy (3 series of 3.6 mg/kg/day intravenously for 3 days, with 7-day breaks between the series) (this regimen is less convenient and patients are less likely to complete therapy);

*(incremental melarsoprol therapy) 10-day incremental-dose melarsoprol therapy (0.6 mg/kg iv on day 1, 1.2 mg/kg iv on day 2, and 1.8 mg/kg iv on days 3–10) (previously thought to reduce the risk of treatment-induced encephalopathy, but now known to be associated with an increased risk of relapse and a higher incidence of encephalopathy)

History and research:-
Suramin was introduced in 1920 to treat the first stage of the disease. By 1922, Suramin was generally combined with Tryparsamide (another pentavalent organo-arsenic drug) in the treatment of the second stage of the gambiense form. It was used during the grand epidemic in West and Central Africa in millions of people and was the mainstay of therapy until 1969.

Pentamidine, a highly effective drug for the first stage of the disease, has been used since 1939. During the fifties, it was widely used as a prophylactic agent in Western Africa, leading to a sharp decline in infection rates. At the time, it was thought that eradication of the disease was at hand.

The organo-arsenical melarsoprol (Arsobal) was developed in the 1940s, and is effective for patients with second stage sleeping sickness. However, 3 – 10% of those injected have reactive encephalopathy (convulsions, progressive coma, or psychotic reactions), and 10 – 70% of such cases result in death; it can cause brain damage in those who survive the encephalopathy. However, due to its effectiveness, melarsoprol is still used today. Resistance to melarsoprol is increasing, and combination therapy with nifurtimox is currently under research.

Eflornithine (difluoromethylornithine or DFMO), the most modern treatment, was developed in the 1970s by Albert Sjoerdsmanot and underwent clinical trials in the 1980s. The drug was approved by the United States Food and Drug Administration in 1990, but Aventis, the company responsible for its manufacture, halted production in 1999. In 2001, however, Aventis, in association with Médecins Sans Frontières and the World Health Organization, signed a long-term agreement to manufacture and donate the drug.

An international research team working in the Democratic Republic of the Congo, Southern Sudan and Angola involving Immtech International and University of North Carolina at Chapel Hill have completed a Phase IIb clinical trial and commenced a Phase III trial in 2005 testing the efficacy of the first oral treatment for Sleeping Sickness, known at this point as “DB289”.

Trypanosomiasis vaccines are undergoing research.

Drug targets and drug discovery:-
The genome of the parasite has been decoded and several proteins have been identified as potential targets for drug treatment. The decoded DNA also revealed the reason why generating a vaccine for this disease has been so difficult. T. brucei has over 800 genes that manufacture proteins that the organism mixes and matches to evade immune system detection.

Recent findings indicate that the parasite is unable to survive in the bloodstream without its flagellum. This insight gives researchers a new angle with which to attack the parasite.

A new treatment based on a truncated version of the apolipoprotein L-1 of high density lipoprotein and a single domain antibody has recently been found to work in mice, but has not been tested in humans.

The cover story of the August 25, 2006 issue of Cell journal describes an advance; Dr. Lee Soo Hee and colleagues, working at Johns Hopkins, have investigated the pathway by which the organism makes myristate, a 14-carbon length fatty acid. Myristate is a component of the variant surface glycoprotein (VSG), the molecule that makes up the trypanosome’s outer layer. This outer surface coat of VSG is vital to the trypanosome’s avoidance of immunological capture. Dr. Lee and colleagues discovered trypanosomes use a novel fatty acid synthesis pathway involving fatty acid elongases to make myristate and other fatty acids.

Prognosis:
Without treatment, death may occur within 6 months from cardiac failure or from rhodesiense infection itself. Gambiense infection causes the classic “sleeping sickness” disease and gets worse more quickly, often over a few weeks. Both diseases should be treated immediately.

Prevention and control:-
For in depth information on prevention of the disease via tsetse fly control see Tsetse fly control……...click & see

Prevention and control focus on, where it is possible, the eradication of the parasitic host, the tsetse fly. Two alternative strategies have been used in the attempts to reduce the African trypanosomiases. One tactic is primarily medical or veterinary and targets the disease directly using monitoring, prophylaxis, treatment, and surveillance to reduce the number of organisms which carry the disease. The second strategy is generally entomological and intends to disrupt the cycle of transmission by reducing the number of flies. Instances of sleeping sickness are being reduced by the use of the sterile insect technique.

Regular active surveillance, involving case detection and treatment, in addition to tsetse fly control, is the backbone of the strategy for control of sleeping sickness. Systematic screening of communities in identified foci is the best approach as case-by-case screening is not practically possible in highly endemic regions. Systematic screening may be in the form of mobile clinics or fixed screening centres where teams travel daily to the foci. The nature of gambiense disease is such that patients do not seek treatment early enough because the symptoms at that stage are not evident or serious enough to warrant seeking medical attention, considering the remoteness of some affected areas. Also, diagnosis of the disease is difficult and most health workers may not be able to detect it. Systematic screening allows early-stage disease to be detected and treated before the disease progresses, and removes the potential human reservoir. There is a single case report of sexual transmission of West African sleeping sickness, but this is not believed to be an important route of transmission.

Other animals:
Trypanosoma of both the rhodesiense and gambiense types can affect other animals such as cattle and wild animals. In animals it is known as nagana (animal African trypanosomiasis)

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


Resources:

http://en.wikipedia.org/wiki/African_trypanosomiasis
http://www.netdoctor.co.uk/travel/diseases/sleeping_sickness.htm
http://www.nlm.nih.gov/medlineplus/ency/article/001362.htm

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Ailmemts & Remedies

Ataxia

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Definition:
Ataxia (from Greek , meaning “lack of order”) is a neurological sign and symptom consisting of gross lack of coordination of muscle movements. Ataxia is a non-specific clinical manifestation implying dysfunction of parts of the nervous system that coordinate movement, such as the cerebellum. Several possible causes exist for these patterns of neurological dysfunction. The term “dystaxia” is rarely used as a synonym.

A sign of an underlying condition, ataxia can affect your movements, your speech, your eye movements and your ability to swallow.
………………….click & see
Persistent ataxia usually results from damage to your cerebellum — the part of your brain that controls muscle coordination. Many conditions may cause ataxia, including alcohol abuse, stroke, tumor, cerebral palsy and multiple sclerosis. It’s also possible to inherit a defective gene that may cause one of many ataxia variants.

Types of ataxia:-

#Cerebellar ataxia:
The term cerebellar ataxia is employed to indicate ataxia due to dysfunction of the cerebellum. This causes a variety of elementary neurological deficits, such as antagonist hypotonia, asynergy, dysmetria, dyschronometria, and dysdiadochokinesia. How and where these abnormalities manifest depend on which cerebellar structures are lesioned, and whether the lesion is bilateral or unilateral.

*Dysfunction of the vestibulocerebellum impairs balance and control of eye movements. This presents with postural instability, in which the person tends to separate the feet on standing to gain a wider base and avoid oscillations (especially posterior-anterior ones); instability is therefore worsened when standing with the feet together (irrespective of whether the eyes are open or closed: this is a negative Romberg’s test, or more accurately, denotes the inability to carry out the test as the individual is unstable even with open eyes).

*Dysfunction of the spinocerebellum presents with a wide-based “drunken sailor” gait, characterised by uncertain start and stop, lateral deviations, and unequal steps. This part of the cerebellum regulates body and limb movements.

*Dysfunction of the cerebrocerebellum presents with disturbances in carrying out voluntary, planned movements, including intention tremor (coarse trembling, accentuated over the execution of voluntary movements, possibly involving the head and eyes as well as the limbs and torso), peculiar writing abnormalities (large, unequal letters, irregular underlining), and a peculiar pattern of dysarthria (slurred speech, sometimes characterised by explosive variations in voice intensity despite a regular rhythm).

#Sensory ataxia:
The term sensory ataxia is employed to indicate ataxia due to loss of proprioception (sensitivity to joint and body part position), which generally depends on dysfunction of the dorsal columns of the spinal cord, since they carry proprioceptive information up to the brain; in some cases, the cause may instead be dysfunction of the various brain parts that receive that information, including the cerebellum, thalamus, and parietal lobes. Sensory ataxia presents with an unsteady “stomping” gait with heavy heel strikes, as well as postural instability that is characteristically worsened when the lack of proprioceptive input cannot be compensated by visual input, such as in poorly lit environments. Doctors can evidence this during physical examination by having the patient stand with his / her feet together and eyes shut, which will cause the patient’s instability to markedly worsen, producing wide oscillations and possibly a fall (this is called a positive Romberg’s test). Worsening of the finger-pointing test with the eyes closed is another feature of sensory ataxia. Also, when the patient is standing with arms and hands extended toward the examiner, if the eyes are closed, the patient’s finger will tend to “fall down” and be restored to the horizontal extended position by sudden extensor contractions (“ataxic hand”).

#Vestibular ataxia:
The term vestibular ataxia is employed to indicate ataxia due to dysfunction of the vestibular system, which in acute and unilateral cases is associated with prominent vertigo, nausea and vomiting. In slow-onset, chronic bilateral cases of vestibular dysfunction, these characteristic manifestations may be absent, and dysequilibrium may be the sole presentation.

Symptoms:-
Symptoms may vary depending on the severity and type of ataxia, of which there are many. If the ataxia is caused by an injury or another health condition, symptoms may emerge at any age, and may well improve and eventually disappear.

Initial ataxia symptoms usually include:
*Poor limb coordination.
*Dysarthria – slurred and slow speech that is difficult to produce. The patient may also have difficulties controlling volume, rhythm, and pitch.

If the ataxia advances other symptoms may also appear:

*Swallowing difficulties, which may sometimes result in choking or coughing.
*Facial expressions become less apparent.
*Tremors – parts of the body may shake or tremble unintentionally.
*Nystagmus – involuntary rapid rhythmic repetitious eye movement. Movements may be vertical, horizontal, or circular.
*Pes cavus – a foot with too high an arch.
*Cold feet – because of a lack of muscle activity.
*Problems with balance.
*Walking difficulties – in severe cases the patient may need a wheelchair.
*Vision problems.
*Hearing problems.
*Depression – as a result of having to live and cope with the symptoms.

Cerebellar ataxias:
Cerebellar ataxia early onset usually emerges between the ages of 4 and 26. Late onset ataxia generally appears after the patient is 20 years old. Late-onset ataxias usually present less severe symptoms, compared to early-onset ataxia.

Ataxia telangiectasia symptoms generally include:
*Small veins appear around the corner of the eyes, cheeks and ears.
*Physical and sexual development is usually delayed.

Friedreich’s ataxia symptoms generally include:
*The spine curves sideways (scoliosis).
*The heart muscle becomes weaker (cardiomyopathy).
*Diabetes.

For patients whose symptoms are caused by injury or illness, symptoms often improve over time, and eventually go away completely.

When to see a doctor:-
If you aren’t aware of having a condition that causes ataxia, such as multiple sclerosis, see your doctor if you:

*Lose balance
*Lose muscle coordination in a hand, arm or leg
*Have difficulty walking
*Slur your speech
*Have difficulty swallowing

Causes:-
The three types of ataxia have overlapping causes, and can therefore either coexist or occur in isolation.

Focal lesions
Any type of focal lesion of the central nervous system (such as stroke, brain tumour, multiple sclerosis) will cause the type of ataxia corresponding to the site of the lesion: cerebellar if in the cerebellum, sensory if in the dorsal spinal cord (and rarely in the thalamus or parietal lobe), vestibular if in the vestibular system (including the vestibular areas of the cerebral cortex).

Exogenous substances
Exogenous substances that cause ataxia mainly do so because they have a depressant effect on central nervous system function. The most common example is ethanol, which is capable of causing reversible cerebellar and vestibular ataxia. Other examples include various prescription drugs (e.g. most antiepileptic drugs have cerebellar ataxia as a possible adverse effect), marijuana ingestion[2] and various other recreational drugs (e.g. ketamine, PCP or dextromethorphan, all of which are NMDA receptor antagonists that produce a dissociative state at high doses).

Vitamin B12 deficiency
Vitamin B12 deficiency may cause, among several neurological abnormalities, overlapping cerebellar and sensory ataxia.

Causes of isolated sensory ataxia

Peripheral neuropathies may cause generalised or localised sensory ataxia (e.g. a limb only) depending on the extent of the neuropathic involvement. Spinal disorders of various types may cause sensory ataxia from the lesioned level below, when they involve the dorsal columns.

Non-hereditary cerebellar degeneration
Non-hereditary causes of cerebellar degeneration include chronic ethanol abuse, paraneoplastic cerebellar degeneration, high altitude cerebral oedema, coeliac disease, normal pressure hydrocephalus and cerebellitis.

Hereditary ataxias
Ataxia may depend on hereditary disorders consisting of degeneration of the cerebellum and/or of the spine; most cases feature both to some extent, and therefore present with overlapping cerebellar and sensory ataxia, even though one is often more evident than the other. Hereditary disorders causing ataxia include autosomal dominant ones such as spinocerebellar ataxia, episodic ataxia, and dentatorubropallidoluysian atrophy, as well as autosomal recessive disorders such as Friedreich’s ataxia (sensory and cerebellar, with the former predominating) and Niemann Pick disease, ataxia-telangiectasia (sensory and cerebellar, with the latter predominating), and abetalipoproteinaemia. An example of X-linked ataxic condition is the rare fragile X-associated tremor/ataxia syndrome.

GeneReview/NIH/UW entry on Hereditary Ataxia Overview

Arnold-Chiari Malformation
Arnold-Chiari malformation is a malformation of the brain. It consists of a downward displacement of the cerebellar tonsils and the medulla through the foramen magnum, sometimes causing hydrocephalus as a result of obstruction of CSF (cerebrospinal fluid) outflow.

Diagnosis:-
Besides conducting a physical exam and a neurological exam, including checking your memory and concentration, vision, hearing, balance, coordination and reflexes, your doctor may request these laboratory tests:

#Blood tests. Certain blood tests can confirm or exclude the suspected condition. A sample of your blood will be drawn from your arm through a needle. You may be required to fast from midnight the night before your appointment until after your blood is drawn. The specific tests will depend on the suspected cause, but most likely will include a complete blood count (CBC), which helps evaluate your overall health and detect a range of disorders, including infection and heavy metal poisoning.

#Urine tests. Examining a sample of your urine under a microscope (urinalysis) may suggest certain systemic abnormalities that can be related to some forms of ataxia. If your doctor suspects Wilson’s disease, you may be asked for a 24-hour urine collection to help determine the amount of copper in your system.

#Imaging studies. A computerized tomography (CT) scan or magnetic resonance imaging (MRI) of your brain may help determine potential causes.

#Genetic testing. Your doctor may recommend genetic testing to determine whether you or your child has the gene mutation that causes one of the hereditary ataxic conditions. Gene tests are available for many but not all of the hereditary ataxias.

Treatments:-
There’s no treatment specifically for ataxia and it is not curable  but a great deal can be done to ease symptoms and improve the quality of life of the patient. Treatment for coordination and balance problems usually involves the use of adaptive devices which help the patient attain as much independence as possible. These may include the use of a cane (walking stick), crutches, walker or a wheelchair. Symptoms such as tremor, stiffness, spasticity, sleep disorders, muscle weakness, depression (or frustration, sadness and anger) may be addressed with targeted physical therapy, speech therapy, medications and counseling.

Occupational therapy – the occupational therapist can help the patient manage better around the house and work. This may involve some home adaptations, wheelchair assessments, and making the kitchen more practical for the patient.

#Speech therapy – the speech therapist can help with swallowing, coughing, choking and speech problems. If speech becomes very difficult the speech therapist can help the patient learn how to use speech aids.

#Orthopedic care – this can help patients with curvature of the spine (scoliosis).

Physical therapy (physiotherapy) – a physical therapist (physiotherapist) can help maintain strength and improve mobility.

#Physical therapy to help you build strength and enhance your mobility
#Occupational therapy to help you with daily living tasks, such as feeding yourself
#Speech therapy to improve speech and aid swallowing

*Counseling – patients with ataxia commonly become frustrated and depressed; this usually results from having to cope with some symptoms which affect physical mobility and coordination. Talking to a well qualified counselor, such as a psychotherapist can help.

*Supplements and nutrition – some patients with ataxia have very low levels of vitamin E and require supplements and/or a special diet. As sensitivity to gluten is more common among ataxia patients, a gluten-free diet also helps.

*Medication – some patients with ataxia telangiectasia are prescribed gamma-globulin injections to boost their immune systems. There are also drugs for muscle spasms and uncontrollable eye movements.

Coping and support:-
The challenges you face when living with ataxia, such as loss of independence, or having a child with the condition, may make you feel alone or lead to depression and anxiety. Talking to a counselor or therapist may lessen your sense of isolation and help you cope. Or you may find encouragement and understanding in a support group, either for ataxia or for your underlying condition, such as cancer or multiple sclerosis.

Although support groups aren’t for everyone, they can be good sources of information. Group members often know about the latest treatments and tend to share their own experiences. If you’re interested, your doctor may be able to recommend a group in your area.

Other uses of the term:-
The term “ataxia” is sometimes used in a broader sense to indicate lack of coordination in some physiological process. Examples include optic ataxia (lack of coordination between visual inputs and hand movements, resulting in inability to reach and grab objects, usually part of Balint’s syndrome, but can be seen in isolation with injuries to the superior parietal lobule, as it represents a disconnection between visual-association cortex and the frontal premotor and motor cortex), and ataxic respiration (lack of coordination in respiratory movements, usually due to dysfunction of the respiratory centres in the medulla oblongata).

You may Click to see:->  Related articles from newspapers, magazines, and more

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/ataxia/DS00910
http://en.wikipedia.org/wiki/Ataxia
http://www.medicalnewstoday.com/articles/162368.php

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Healthy Tips

An Essential Mineral for Optimum Bone and Full-Body Health!

Weightloss pyramid.
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Calcium is one of the most important minerals for your body and your bones. This essential strength-building nutrient helps your body maintain proper blood vessel function… secrete hormones and enzymes… and send messages through your central nervous system.

Many people think that in order to drop a few pounds, they can simply drop many calcium-rich dairy products from their diet. Wrong! Not only will your weight loss efforts be more difficult, but you could put your heart and brain at increased risk.

So make sure you’re getting enough calcium with a balanced and nutritious diet. According to WHFoods.org, foods high in calcium include yogurt, goat’s milk, celery, broccoli, kelp, asparagus, garlic, tofu and oranges. Plus, spices such as garlic, rosemary, parsley and oregano can boost your intake of calcium.

But calcium alone can’t provide the highest protection for your bones. You need to balance your calcium intake with vitamin D, which is known as the “calcium helper” since it metabolizes the mineral for maximum health benefits. You can get vitamin D from safe sun exposure or from foods such as cod liver oil, salmon, tuna, eggs and beef liver.

So to help increase your bone mass and prevent the breakdown of bone tissue as you age, be sure to get ample amounts of calcium and vitamin D with a nutritious diet or quality supplements. These two vital nutrients are essential for a long and strong, healthy life!

Source: Better Health Research. Dec. 21st.2009

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