Parkinson’s disease, treatable with early diagnosis

By Carol Aloysius

Parkinson’s disease (PD) is on the increase. Many factors have contributed to this mostly due to increased awareness of its symptoms and patients presenting themselves to their medical officer for early diagnosis.

Although the bulk of the population who suffer from the disease are elderly persons, there are a few exceptions. There are also several myths surrounding this debilitating disease of the nervous system.

Consultant Neurologist of Anuradhapura Teaching Hospital Dr Darshana Sirisena explains to the Sunday Observer what this disease is and how it can be controlled.

Excerpts…

Question: Parkinson’s disease now appears to be on the increase. Your comments?

Answer: Prevalence and incidence of Parkinson's disease (PD) has not changed overall. However the fact is that the number of patients being diagnosed with PD is increasing. So we can assume that these numbers may reflect a rise in the disease incidence.

This may be due to many reasons, such as patients now being more aware of the symptoms so that seek medical advice leading to early diagnosis. In addition at present neurological services are available throughout the country which also contributes heavily to early and correct diagnosis.

Q. Have you any official statistics on the number of Lankan patients with the disease?

A. Unfortunately we have no such data with us. However, in my experience our figures are on par with world a figure which is about 187 per 100,000 populations.

But when it applies to those above 39 years it almost doubles. Life time risk of developing PD is about two percent and this too doubles when a close relative is affected.

Q. Who are the people most at risk age wise and gender wise?

A. Any person can get PD but people above 60 years and males are more at risk. (Male to female ratio is 3:2)

Q. What are the causes?

A. The vast majority of patients do not have a cause for getting the disease. Therefore it is called as “Idiopathic Parkinson Disease”. But in a minority of patients, genes and environmental factors are shown to cause Parkinson's Disease.

Q. The genetic factor is still being debated on. What is your opinion? Is the disease inherited, or only in a small proportion of families?

A. Currently about 10 percent of newly diagnosed patients report that someone in their family has PD which favours that genetics play a role. At the same time twin studies have shown negative results. So in conclusion genes do not play a major role in causing PD.

Q. Does a toxic environment contribute to the disease? If so, what kind of toxic substances?

A. Yes, environmental interactions have contributed to the aetiology of PD, but only in the case of a minority. MPTP (a neurotoxin) had resulted in PD like symptoms. In addition a substance found in pesticides (ziram) has also been implicated as an aetiological factor for PD. Anyway, compared to the overall disease burden these factors are negligible.

Q. Oxidative stress is said to damage the nerves. What is it?

A. Antioxidant defends and protects cells. Post-mortem studies has shown that certain important antioxidants are lacking in PD brains implicating oxidative stress as a pathological phenomenon in causing PD. Simply oxidative stress, results in accumulation of certain neurotoxins which in turn damage nerve cells ultimately causing PD. This hypothesis needs further research.

Q. Do certain medications also trigger symptoms? Like anti-psychotics given for treating patients with severe paranoia and schizophrenia?

A. Yes .Certain anti-psychotic medications given for schizophrenia and psychiatric conditions can result in Parkinsonism. This is known as drug induced Parkinsonism. This is a common cause for Parkinsonism and usually develops within 3 months of initiating such medications. In addition to anti psychotics some other medications such as certain anti-epileptic and cardiac drugs could also cause similar symptoms.

Q. Do blood vessel disorders also lead to PD?

A. Yes. Strokes or other vascular (blood vessel disorders) causes can mimic Parkinson like symptoms which are called as vascular Parkinsonism. This could usually differentiate from PD clinically as well with certain investigations such as brain imaging.

Q. What are the symptoms?

A. Classical symptoms of Parkinsonism are shaking of body (tremor) which initially involves hands, rigidity (stiffness of the muscles), bradykinesia (slowness of movements), and tendency to fall due to impaired postural reflexes.

Q. How early can one detect them?

A. It is important to detect PD early as there are medications which can control the symptoms effectively. If someone has doubts about whether he/she or a close relative has the above symptoms, they need to seek medical advice preferably a neurologist so can easily diagnose PD. Parkinson's disease is entirely a clinical diagnosis as there is no definite investigation that can diagnose PD. Investigations only help to rule out other conditions which mimics PD.

Q. It is preventable?

A. No. It is not preventable simply because it does not have any modifiable risk factors as Diabetes and other non communicable diseases. But early diagnosis could lead to good quality of life.

Q. Can PD be cured? Or only controlled?

A. Parkinson's Disease could not be cured and only the symptoms can be controlled with medications as in diabetes, hypertension.

Q. How can it be controlled, by surgery, drugs?

A. It can be controlled largely by medications. There are many drugs which are effective. Levodopa is the most effective out of the lot and available freely. Important thing is how and when to initiate these medications which is usually decided by the treating neurologist after discussing with the patient and relatives. As the disease progresses these medications become less effective and result in disabling complications.

Surgical options are available but they are expensive and currently not available in our country. In other countries surgery is usually indicated for advanced disease patients where medications can offer only a little.

Q. Are there new breakthroughs today like stem cell surgery to delay the disease?

A. Though there are lots of researches currently being carried out to find whether any process or medication could halt the disease progression, there are no major breakthroughs so far including stem cell surgery.

Q. What kind of care does a patient require once you get the disease - at home?

A. In the initial stages of the disease where the symptoms are mild and well controlled with medications patients are encouraged to be active and mobile as much as possible and also to be function independently as long as possible. When the disease progresses and becomes advanced, patients are more prone to falls.

So they should work closely with the treating physician to prevent such falls. It is also important that the patient gets a good understanding about the disease,medications,complications and this is mainly be possible by discussing everything with the treating physician.

Q. Are there diet restrictions?

A. No there are no special dietary restrictions but it is important to time the medications (mainly levodopa) as the absorption is affected by meals. Mostly patients are advised to take medications 20-30minutes before meals.

Q. How does the disease progress?

A. In most Parkinson's disease patients, the symptoms get worse gradually over years. As the disease progresses complications will develop which could be due to disease itself or to medications which are disabling in most instances.

Q. What are the complications of the disease? Can it lead to other diseases?

A. Complications are many and could be either due to disease itself or due to medications. Commonest is that drugs become less effective (wearing off) so that patient has to take them more often. In addition they could develop dance like involuntary movements (dyskinesias) which are disabling and mostly due to medications itself. There are lots of other complications which are called non-motor complications and they include depression, anxiety, fatigue, psychosis, sleep disturbances, constipation, urinary retention and sensory symptoms such as pain, numbness, restless legs etc.

Q. Can having non communicable diseases like diabetes and cardiac problems complicate the symptoms?

A. No they are not.

Q. Any Foundation or special services available to Parkinson's victims in Sri Lanka? If so where?

A: Unfortunately we do not have such organised, dedicated services such as “Parkinson Support Groups” as in other countries. But at present all major hospitals in the country have neurological services provided by a consultant Neurologist and his team.

They can provide all the advice and services a Parkinson's patient and his relatives need.

Q. Any other comments you wish to add?

A. Most important thing is early diagnosis and initiating rational management depending on stage of the illness. This is only possible by consulting a qualified physician especially a neurologist.

So if someone is doubtful of having Parkinson’s disease or already diagnosed as having PD, the most important thing is to consult a neurologist and clarify your doubts and learn about the illness.

Decoding the secrets of the gut

A new technique based on atomic force microscopy was developed at the Institute of Food Research to help ‘read’ information encoded in the gut lining.

The lining of our gut is an important barrier between the outside world and our bodies. Laid out, the gut lining would cover the area of a football pitch.

It must let nutrients from our foods through, but prevent invasion by disease-causing bacteria, at the same time hosting the trillions of beneficial bacteria needed for proper digestion and immune function.

At the forefront of the defensive system is a layer of mucus that lines the entire gut surface. In the large bowel, the mucus layer is an organised structure, with an inner layer that blocks bacteria, and an outer layer where beneficial bacteria (commensals) can flourish. The mucus layer is made up of large proteins called mucins with characteristic sugary, or glycosylated, chains.

Dr Nathalie Juge and colleagues from the Institute of Food Research, is leading studies aiming to understand the role of mucus in maintaining a healthy gut and how mucins interact with bacteria in our guts.

At the molecular level, mucins exhibit clusters of glycosylation that give the proteins a ‘bottle-brush’ appearance. The size of these molecular sugar chains varies with location and age of the tissue, and abnormalities in mucins are seen in inflammatory bowel diseases such as ulcerative colitis, Crohn's disease and colon cancer.

A myriad of different conformations that the sugar chains can take up means that mucins are incredibly diverse. The differences are believed to help commensal bacteria by providing specific binding sites, as well as necessary nourishment.

Pathogenic bacteria have also evolved mechanisms to bind to mucins, as part of their arsenal to overcome our defences. We, however, are a long way behind these bacteria in understanding the coded information contained in these complex sugar chains.

Understanding this ‘glycocode’ would give us a new way to look at the crucial interactions between good and bad micro-organisms in our guts, and may also provide new insights into gut diseases.

These interactions happen at the molecular level, so for us to understand them we need tools that work at this level. IFR has a history of pioneering use of one such tool, atomic force microscopy (AFM). The tip of an atomic force microscope AFM combines very high-resolution imaging with an ability to probe the forces between molecules. AFM works by running a very fine stylus (tip) mounted on the end of a flexible cantilever over the surface of a molecule, much like a blind person reading Braille.

A laser is bounced off the cantilever, amplifying the signal so that AFM can detect distances down to a millionth the width of a sheet of paper.

Patrick Gunning and Andrew Kirby, from IFR's AFM group, adapted this technique by attaching sugar-binding molecules called lectins to the AFM cantilever, via a flexible linker. They used this to probe mucins bound to a surface. The findings of this collaborative work were published in The FASEB Journal.

“It's a bit like fishing” said Dr Gunning. “The mucin molecules are immersed in saline, and float like a sea of kelp. We use lectins as the bait. We drop the line down until we hit the bottom, and then lift it back up. If the lectin finds a target sugar molecule on the mucin, it snags.”

Measuring the distance between the snags gives a picture of what the overall mucin molecule looks like. By repeating this thousands of times, and then working with IFR's biomathematicians, it was possible to produce a ‘fingerprint’ that characterise different mucins, which means that we could differentiate between mucins derived from different parts of the gut.

The researchers now want to look at the mucins derived from diseased tissues, to further investigate differences in the glycocode. They would also like to understand how bacteria read and possibly manipulate the glycocode. In the lab, the researchers used specific enzymes targeting certain sugars on the mucin molecules.

This affected the mucin's molecular structure, which in turn altered its spatial distribution. Certain bacteria in our guts also secrete these enzymes, as a means of rewriting the glycocode for their own benefit. With this new technique in hand, the researchers will continue their efforts to unravel the secrets inside our own bodies.

MNT

New training package could prevent sudden cardiac death in athletes

Progress on curbing the leading killer of athletes - sudden cardiac death - by spotting heart problems early, has been slow. But the development of a series of online tutorials for sports and cardiology doctors looks set to reverse this trend.

The tutorials, which are free to any doctor around the globe, thanks to the backing of the American Medical Society for Sports Medicine (AMSSM) and FIFA, aim to teach physicians how to read heart monitor tracings (ECGs) and spot abnormalities linked to potentially fatal disorders.

Some inborn heart conditions are difficult to detect, because they progress silently, and are only diagnosed when intense exercise triggers a lethal heart rhythm - sudden cardiac arrest.

According to the American Heart Association, over 7000 people under the age of 18 die every year in the US of a sudden cardiac arrest.

Studies suggest the risk is three times higher in competitive athletes. Last year in the UK, footballer Fabrice Muamba collapsed on the pitch following a sudden cardiac arrest at the age of 24. He received prompt expert medical attention which helped him make a remarkable recovery.

But many athletes are not as lucky, and trying to pick up those most at risk is the only way of warding off sudden cardiac arrest, which could be - and often is - deadly.

And interpreting ECGs in athletes can be difficult, because their hearts have adapted to the stress of extensive training and top level performance.

Initiated by Professor Jonathan Drezner, AMSSM President, in association with BMJ Learning and the British Journal of Sports Medicine, and developed and written by international experts in sports medicine and sports cardiology, the online tutorials guide doctors on how to recognise ECG changes that indicate problems rather than healthy cardiac adaptation.

“Whether used for diagnostic or screening purposes, ECG interpretation is a fundamental skill for doctors involved in the cardiovascular care of athletes,” said Prof Drezner.

He said, “These online learning modules provide doctors with a common basis for interpreting an athlete's ECG, improving their chances of making an accurate diagnosis, and of picking up potentially life-threatening problems earlier.”

The modules draw on a series of papers presenting new consensus standards on ECG interpretation in athletes, published in the British Journal of Sports Medicine.

 - MNT

High heart rate at rest signals higher risk of death

A high heart rate (pulse) at rest is linked to a higher risk of death even in physically fit, healthy people, suggests research published in the journal Heart.

A resting heart rate - the number of heart beats per minute - is determined by an individual's level of physical fitness, circulating hormones, and the autonomic nervous system. A rate at rest of between 60 and 100 beats per minute is considered normal.

People who are very physically active tend to have a low heart rate at rest, but the authors wanted to find out if heart rate had any bearing on an individual's risk of death, irrespective of their level of cardiorespiratory fitness.

They therefore tracked the health of just under 3,000 men for 16 years, all of whom were part of the Copenhagen Male Study.

This was set up in 1970-71 to monitor the cardiovascular health of middle aged men at 14 large companies in Copenhagen.

In 1971 all participants were interviewed by a doctor about their health and lifestyle, including smoking and exercise, and given a check-up.

Their cardiorespiratory fitness was assessed using a cycling test, set at three different levels of exertion.

In 1985-6, just under 3,000 of these original participants were given a further check-up, to include measurements of height, weight, blood pressure, blood fats and blood glucose. Their resting heart rate was also recorded (ECG and VO2Max). Sixteen years later in 2001, the researchers checked national Danish registers to find out which of these men had survived. Almost four out of 10 (39 percent; 1,082) of the men had died by 2001.

Unsurprisingly, a high resting heart rate was associated with lower levels of physical fitness, higher blood pressure and weight, and higher levels of circulating blood fats. Similarly, men who were physically active tended to have lower resting heart rates.

- Medicalxpress