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New Drugs to Battle Multiple Sclerosis

Several new drugs that treat inflammation caused by the disease are showing promise, although serious side effects are still an issue.

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Multiple sclerosis remains a cruel medical mystery. It strikes in the prime of life and runs an unpredictable course that can end in total disability. Scientists are a long way from halting the disease entirely, but several promising drugs are in late-phase clinical trials and experts anticipate better lives for patients in the near future.

“We will see many new drugs on the market and many new options for patients,” says Dr. Diego Centonze, a neurologist at Tor Vergata University in Rome, who is running clinical trials for three new experimental compounds, including one called fingolimod that is the first oral MS drug to move to Phase 3 clinical trials.

In the early 1990s, there were no Food and Drug Administration-approved therapies for MS on the market. Today, there are at least half a dozen, and Centonze expects as many as eight or nine by 2010.

But there are still many challenges, says Dr. Ari Green, assistant director of the multiple sclerosis center at UC San Francisco, which also is running drug company-sponsored trials. None of the approved drugs is ideal, and each of the new experimental drugs has significant adverse side effects.

MS is an autoimmune disease: The body’s immune system attacks some of its own tissues. The common form, known as relapsing-remitting, begins when disease-fighting lymphocytes launch an attack on the brain and spinal cord. These relapses cause short-term inflammation and symptoms such as numbness, but eventually lead to a progressive decline of the nervous system.

The less common form of MS — primary progressive — doesn’t manifest itself with acute attacks, although patients still exhibit neurodegeneration, leading to fatigue, pain, problems with walking and balance, dizziness and bladder and bowel dysfunction.

Currently approved drugs primarily work by reducing the activity of lymphocytes or reducing their ability to travel from the blood into the nervous system. Some of the new ones do that too — while others function in different ways.

The first drugs to gain approval in the mid-1990s were interferon beta-1b (Betaseron), interferon beta-1a (Avonex or Rebif) and glatiramer acetate (Copaxone). Because they have minimal side effects (such as flu-like symptoms) they are used as a first line of defense. But they are only moderately effective, says Dr. Rhonda Voskuhl, director of the UCLA multiple sclerosis program. Patients “fail them, and then move on” to more powerful drugs such as natalizumab (Tysabri) and mitroxantrone.

Mitroxantrone, approved in 2000, is a chemotherapeutic drug that suppresses the immune system and can lead to leukemia or heart damage.

Natalizumab (Tysabri), which received accelerated FDA approval in 2004 and is considered the most effective drug available today, was taken off the market in February 2005 after three patients in clinical trials developed progressive multifocal leukoencephalopathy, a fatal viral disease. After an FDA review, it has been available under a special program in which patients are closely monitored for opportunistic infections.

On the horizon
There’s clearly a lot of room for improvement, which is one reason why doctors are excited about options on the horizon.

Fingolimod, originally developed to prevent organ rejection in transplant patients, blocks a signal that allows T-cell lymphocytes to cross into the brain. At the American Academy of Neurology meeting this year, researchers reported that 173 patients with a relapsing form of MS showed a decline in the relapse rate over 36 months from 0.31 relapses per year to 0.20, a 30% decrease in their relapse rate when they took fingolimod. In just six months, the number of patients with brain lesions decreased from an average of 2.2 per patient when taking the placebo down to 1.29. In addition, after 36 months, brain scans revealed that 89% of patients had no evidence of inflammation.

Fingolimod is promising not only for effectiveness but because it comes in pill form, Centonze says. “For patients that must receive injections every other day or every single day, the quality of life is really affected. Taking pills can change this.”

Another compound on the horizon is alemtuzumab (Campath), a monoclonal antibody designed and FDA-approved for fighting leukemia. In a trial of 334 patients published in October in the New England Journal of Medicine, researchers reported that the drug could reduce the relapse rate in early-stage MS patients by two-thirds relative to the standard MS drug interferon beta-1a.

UCSF’s Green says the findings are impressive because this is the first MS trial to compare a new drug to an approved compound rather than a placebo and yet “it still had a remarkable effect on reducing disease activity.”

Rituximab, an antibody that was designed for treating rheumatoid arthritis, is also being studied, in a clinical trial headquartered at UCSF. Rituximab is directed at the immune system’s B cells, rather than T cells that have been targeted by MS researchers since the 1970s.

Biology of MS
In February, a team led by Dr. Stephen Hauser of UCSF reported in the New England Journal of Medicine that in a 48-week trial of 104 patients, rituximab halved the number of patients experiencing relapses relative to a placebo. “It’s led to a whole new understanding of the biology of MS,” Green says. “There are now a ton of potential therapies that are going to be B-cell directed.”

But the downside of taking powerful modulators of the immune system are their serious side effects, including making patients more susceptible to infections and other chronic diseases. Two patients died after taking fingolimod, one with a brain infection and the other with shingles.

And in the alemtuzumab trial published in October, researchers reported that one-quarter of the patients developed an autoimmune disease attacking the thyroid and three developed an autoimmune disease of the blood platelets.

“Drugs like this are toxic,” Voskuhl says. “It’s a hard sell to people who are very young to expose them to drugs that have dramatic side effects.”

A larger problem with the current slate of therapeutics is that they address only the inflammation side of the disease. “But we now know for sure that neurodegeneration is not just caused by inflammation,” Centonze says.

As excited as he is about the burgeoning treatment options, he says, “Before judging the real quality of these drugs, you must treat many, many patients for several years.”
Sources:Los Angles Times

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Featured

Parkinson’s Linked to Vitamin D

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Scientists are testing whether vitamin D supplements can ease symptoms of Parkinson’s disease. Parkinson’s gets progressively worse

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A US team found 55% of Parkinson’s patients had insufficient levels of vitamin D, compared to 36% of healthy elderly people. However, the Emory University researchers do not yet know if the vitamin deficiency is a cause or the result of having Parkinson’s.

The study appears in the journal Archives of Neurology.

Parkinson’s disease affects nerve cells in several parts of the brain, particularly those that use the chemical messenger dopamine to control movement.

The most common symptoms are tremor, stiffness and slowness of movement. These can be treated with oral replacement of dopamine.

Previous studies have shown that the part of the brain affected most by Parkinson’s, the substantia nigra, has high levels of the vitamin D receptor, which suggests vitamin D may be important for normal functions of these cells.

Sunlight :

Vitamin D is found in the diet, but is primarily formed in the skin by exposure to sunlight.

However, the body’s ability to produce the vitamin decreases with age, making older people more prone to deficiency.

One theory is that people with Parkinson’s may be particularly vulnerable because their condition limits the amount of time they spend out of doors.

However, scientists say it may also be possible that low vitamin D levels are in some way related to the genesis and origin of the disease.

The researchers examined vitamin D levels in 100 people with Parkinson’s, 100 with Alzheimer’s disease and 100 who were healthy. The groups were matched for age, and economic circumstance.

Among the Parkinson’s group 23% of patients had vitamin D levels so low that they could be described as deficient. In the Alzheimer’s group the figure was 16%, and in the healthy group 10%.

The researchers said the findings were striking because the study group came from the South West of the US, where sunny weather is the norm.

‘Intriguing finding’

Researcher Dr Marian Evatt said: “We found that vitamin D insufficiency may have a unique association with Parkinson’s, which is intriguing and warrants further investigation.”

Dr Kieran Breen, director of research, Parkinson’s Disease Society said: “Further research is required to determine at what stage the deficiency in vitamin levels occur in the brains of people with Parkinson’s and whether the provision of a dietary supplement, or increased exposure to sunlight may help alleviate symptoms or have an effect on the rate of the condition’s progression.

“This would help us answer the question as to whether the decrease in vitamin D levels in Parkinson’s is a cause or effect of the condition.”

Doctors have known for decades that vitamin D plays a role in bone formation.

More recently, scientists have been uncovering its effects elsewhere, including producing peptides that fight microbes in the skin, regulating blood pressure and insulin levels, and maintaining the nervous system.

Low vitamin D levels also appear to increase the risk of several cancers and auto-immune diseases such as multiple sclerosis and diabetes.

Click to see SEE ALSO ->
Vitamin E cuts Parkinson’s risk
Drug ‘may slow down Parkinson’s’
Parkinson’s Disease

Sources: BBC NEWS:13Th. Oct.’08

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Why Migraines Strike

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A migraine is more than just a headache; it is intensely painful and has distinct phases. The disorder used to be considered vascular, but recent research has revealed it to be neurological in origin, related to a wave of nerve cell activity that sweeps across the brain.

The root of migraine may reside in brain stem malfunctioning. Debate still swirls about the precise cause of migraines, but new discoveries are already permitting the development of new treatments.

At the moment, only a few drugs can prevent migraines, all of them developed for other diseases such as hypertension, depression and epilepsy. But they work in only 50 percent of patients, and even then, only 50 percent of the time, and can also induce a range of potentially serious side effects.

New techniques are now being tested, such as drugs that work by preventing gap junctions, a form of ion channel, from opening, thereby halting the flow of calcium between brain cells.

Sources:
Scientific American July 2008

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WHY CORNER

Why Do Parts of Our Body ‘Fall Asleep’?

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The weird “separate” sensations we experience when a particular limb “falls asleep” are the result of nerves under pressure.

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For example, if an arm has fallen asleep, it is most likely that the person had slept on the arm. The sleeping position squeezed and exerted pressure on the nerves, which were as a result unable to carry messages to the brain as well as other parts of the body. And if the position also squeezed the blood vessels, it would mean that oxygen carried by them did not reach the nerves.

When one removes the pressure on the nerves and on the blood vessels, in this case by a change in the position, the nerve fibres awaken in order of their thickness and of the thickness of their myelin sheaths (protective covering). Hence, the thickest and most protected ones awaken last. This gradual awakening process causes the different sensations we experience as the affected body part returns to normalcy.

The first sensation we experience is a tingling sensation, followed by a burning sensation, as the fibres that control pain and temperature now function and are again able to transmit these messages to the brain. Not until later, does the numbness we feel disappear, simply because the fibres that control touch and position are thicker fibres with thicker myelin sheaths.

Similar fibres, known as motor neurons, travel in the same nerves, but take direct orders from the brain to the spinal cord to the muscles, and awaken shortly after those controlling touch and position. For this reason, after the numbness disappears, we regain our ability to move the affected body part, and life is finally back to normal.

Sources: The Telegraph (Kolkata, India)

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Ailmemts & Remedies

Multiple Sclerosis (MS)

Definition:-
Multiple sclerosis(MS) is an autoimmune disease that affects the central nervous system (the brain and spinal cord).Multiple sclerosis (abbreviated MS, formerly known as disseminated sclerosis or encephalomyelitis disseminata) is a chronic, inflammatory, demyelinating disease that affects the central nervous system (CNS)]. Disease onset usually occurs in young adults, is more common in women, and has a prevalence that ranges between 2 and 150 per 100,000 depending on the country or specific population.MS was first described in 1868 by Jean-Martin Charcot…….….CLICK & SEE

It damages the myelin sheath, the material that surrounds and protects your nerve cells. This damage slows down or blocks messages between your brain and your body, leading to the different symptoms.

Multiple sclerosis...MRI of the brain..Nerve supply to the pelvis..Central nervous system
Myelin and nerve structure

Causes:-
No one knows what causes MS. It may be an autoimmune disease, which happens when your body attacks itself. Multiple sclerosis affects woman more than men. Usually, the disease is mild, but some people lose the ability to write, speak or walk. There is no cure for MS, but medicines may slow it down and help control symptoms. Physical and occupational therapy may also help.

The disorder most commonly begins between ages 20 and 40, but can be seen at any age.

Though the exact cause is not known, but MS is believed to result from damage to the myelin sheath, the protective material which surrounds nerve cells. It is a progressive disease, meaning the nerve damage (neurodegeneration) gets worse over time.

In addition to nerve damage, another part of MS is inflammation. Inflammation occurs when the body’s own immune cells attack the nervous system. The inflammation destroys the myelin, leaving multiple areas of scar tissue (sclerosis). It also causes nerve impulses to slow down or become blocked, leading to the symptoms of MS. Repeated episodes, or flare ups, of inflammation can occur along any area of the brain and spinal cord.

Symptoms vary because the location and extent of each attack varies. Usually episodes that last days, weeks, or months alternate with times of reduced or no symptoms (remission).

Recurrence (relapse) is common although non-stop progression without periods of remission may also occur.

Researchers are not sure what triggers an attack. Patients with MS typically have a higher number of immune cells than a healthy person, which suggests that an immune response might play a role. The most common theories point to a virus or genetic defect, or a combination of both. There also appears to be a genetic link to the disease.

MS is more likely to occur in northern Europe, the northern United States, southern Australia, and New Zealand than in other areas. Geographic studies indicate there may be an environmental factor involved.

People with a family history of MS and those who live in a geographical area with a higher incidence rate for MS have a higher risk of the disease.

Symptoms:-
*Decreased ability to control small movements
*Decreased attention span
*Decreased coordination
*Decreased judgment
*Decreased memory
*Depression
*Difficulty speaking or understanding speech
*Dizziness
*Double vision
*Eye discomfort
*Facial pain
*Fatigue
*Loss of balance
*Movement problems – slowly progressive; beginning in the legs
*Muscle atrophy
*Muscle spasms (especially in the legs)
*Muscle spasticity (uncontrollable spasm of muscle groups)
*Numbness or abnormal sensation in any area
*Pain in the arms or legs
*Paralysis in one or more arms or legs
*Slurred speech
*Tingling
*Tremor in one or more arms or legs
*Uncontrollable rapid eye movements
*Urinary frequency (frequent need to urinate)
*Urinary hesitancy (difficult to begin urinating)
*Urinary urgency (strong urge to urinate)
*Urine leakage (incontinence)
*Vertigo
*Vision loss — usually affects one eye at a time
*Walking/gait abnormalities
*Weakness in one or more arms or legs

Additional symptoms that may be associated with this disease:

*Constipation
*Hearing loss

Note: Symptoms may vary with each attack. They may last days to months, then reduce or disappear, then recur periodically. With each recurrence, the symptoms are different as new areas are affected. Fever can trigger or worsen attacks, as can hot baths, sun exposure, and stress.

Diagnosis:-
Multiple sclerosis is difficult to diagnose in its early stages. In fact, a definite diagnosis cannot be made until other disease processes (differential diagnoses) have been ruled out and, in the case of relapsing-remitting MS, there is evidence of at least two anatomically separate demyelinating events separated by at least thirty days. In the case of primary progressive, a slow progression of signs and symptoms over at least 6 months is required.

Exams and Tests:-

Symptoms of MS may mimic many other neurologic disorders. Diagnosis is made by ruling out other conditions.

A history of at least two attacks separated by a period of reduced or no symptoms may be a sign of relapsing-remitting MS.

If the health care provider can see decreases in any functions of the central nervous system (such as abnormal reflexes), a diagnosis of MS may be suspected.

A neurological exam may show localized decreases in nerve function. This may include decreased or abnormal sensation, decreased ability to move a part of the body, speech or vision changes, or other loss of neurologic functions. The type of neurologic deficit usually indicates the location of the damage to the nerves.

There may be a positive Babinski’s reflex.

Eye examination may show abnormal pupil responses, changes in the visual fields or eye movements, rapid eye movements triggered by movement of the eye, decreased visual acuity, or problems with the internal structures of the eye.

Tests that indicate or confirm multiple sclerosis include:-

*Head MRI scan
*Spine MRI
*Lumbar puncture (spinal tap)
*Cerebrospinal fluid tests, includingCSF oligoclonal banding

Treatment:-

There is no known cure for multiple sclerosis at this time. However, there are promising therapies that may slow the disease. The goal of treatment is to control symptoms and maintain a normal quality of life.

Medications used may include:

*Immune modulators to help control the immune system, including interferons (Avonex, Betaseron, or Rebif), monoclonal

*antibodies (Tysabri), and glatiramer acetate (Copaxone)

*Steroids to decrease the severity of attacks when they occur

*Medicines to reduce muscle spasms such as Lioresal (Baclofen), tizanidine (Zanaflex), or a benzodiazepine

*Cholinergic medications to reduce urinary problems

*Antidepressants for mood or behavior symptoms

*Amantadine for fatigue

Physical therapy, speech therapy, occupational therapy, and support groups can help improve the person’s outlook, reduce depression, maximize function, and improve coping skills.

A planned exercise program early in the course of the disorder can help maintain muscle tone.

A healthy lifestyle is encouraged, including good general nutrition. Adequate rest and relaxation can help maintain energy levels. Attempts should be made to avoid fatigue, stress, temperature extremes, and illness to reduce factors that may trigger an MS attack.

More Support Groups:
For additional information, Click to see multiple sclerosis resources.

Prognosis:-

The outcome is variable and unpredictable. Although the disorder is chronic and incurable, life expectancy can be normal or nearly so. Most people with MS continue to walk and function at work with minimal disability for 20 or more years.

The factors felt to best predict a relatively benign course are female gender, young age at onset (less than 30 years), infrequent attacks, a relapsing-remitting pattern, and low burden of disease on imaging studies.

The amount of disability and discomfort varies with the severity and frequency of attacks and the part of the central nervous system affected by each attack. Commonly, there is initially a return to normal or near-normal function between attacks. As the disorder progresses, there is progressive loss of function with less improvement between attacks.

Possible Complications :

*Progressive disability

*Urinary tract infections

*Side effects of medications used to treat the disorder.

When to Contact a Medical Professional:-

Call your health care provider if you develop any symptoms of MS, as he or she is the only one who can distinguish multiple sclerosis from other serious disorders such as stroke or infection.

Call your health care provider if symptoms progressively worsen despite treatment.

Call your health care provider if the condition deteriorates to the point where home care is no longer possible.

Click to See:

Multiple Sclerosis (MS) and Ayurveda

Understanding the Root Causes of Multiple Sclerosis on Ayurvedic view

Ayurvedic Treatment For Multiple Sclerosis

Homeopathic Treatment, Cure & Medicines for Multiple Sclerosis

Does homeopathy really help cure MS.(Multiple Sclerosis )

Esperanza – Treatment Program for Multiple Sclerosis

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.nlm.nih.gov/medlineplus/ency/article/000737.htm
National Institute of Neurological Disorders and Stroke
http://en.wikipedia.org/wiki/Multiple_sclerosis

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