Ask the expert

It is difficult to say exactly why. There are certainly several possible causes, ranging from genetic factors to age at onset and the person’s state of health at the time of onset. Parkinson’s is not just a single, uniform disease, but can be seen as an umbrella term for several different disease processes.

Dose gaps depend on several factors – partly how long a particular medicine remains active in the body and brain, and partly how much the disease has affected the nerve cells in the brain. Dopamine is stored in the nerve endings in the brain and L-dopa medication replenishes these stores, but this capacity decreases as a result of the disease process. By combining different types of medication, increasing the number of doses and the strength of each dose, it is possible to compensate for and counteract the gradual worsening of symptoms. The dosage of medication is not the same in the early years as it is after around 5–10 years, or after 25 years; it usually increases over time.

If, despite adjustments to medication and various combinations of medicines, it is not possible to achieve good function, it may be appropriate to consider so-called advanced treatments.

One way of assessing whether the time is right and appropriate for potential advanced treatment is to apply the 5–2–1 method. This involves taking anti-Parkinson’s medication on at least 5 occasions, and despite this, experiencing at least 2 hours of ‘off’ symptoms (symptoms between doses), as well as further signs of disease progression, such as hyperkinesia, for at least 1 hour per day.

It is then recommended that the patient be referred to the regional centres for advanced treatments for an assessment of whether they meet the criteria for potential advanced treatment.

Over time, the numbers are almost equal for men and women. Women live longer, which means a slightly higher proportion of women are affected. However, there are about 1.5 times as many men in the younger age groups (from 50 onwards), and women usually develop the condition later in life. The disease can begin as early as the age of 20 and becomes more common with age.

Around 2,000–2,500 people are diagnosed with Parkinson’s disease every year.

You have the right to seek care wherever you wish in Sweden and can do so using a self-referral, or ‘own care request’. This applies to outpatient care, i.e. clinic appointments, but for inpatient care – such as admission to start advanced treatment – a specialist referral is required. The most convenient option is, of course, to be in contact with a neurologist as close to home as possible. If you cannot get help at your nearest county hospital, there are, of course, the seven university hospitals (in Gothenburg, Linköping, Lund, Stockholm, Umeå, Uppsala and Örebro). However, there are often long waiting times.

Dag Nyholm

The figure varies and is difficult to state precisely, but up to 50% may have been lost by the time the first symptoms appear, and this loss is usually confined to a small area, causing symptoms in, for example, one arm or one leg.

Question: I’ve had the diagnosis for 12 years. My new neurologist has reduced my Sifrolen from 2 tablets to 1. I’m on 7.5 mg of Madopark a day. 1.5 x 5. I was prescribed Entacapone 5. I became so incredibly tired that I had to stop taking Entacapone. Things improved. Now, however, I have such severe pain in my back and knees that I am completely incapacitated. Another new symptom is that food gets stuck in my throat. It hurts when that happens and I have to drink water to get it down. Is this Parkinson’s or just ‘normal’ symptoms of other illnesses? I’ve had X-rays of my knees and there’s no sign of osteoarthritis. I have ‘OFF’ periods for much of the day. Life feels as though it’s over

. Answer: Back and knee pain can, of course, be caused by many things, such as lumbago, osteoarthritis and much more. But it can also be a symptom of Parkinson’s, especially if it’s linked to ‘OFF’ periods characterised by stiffness and slowness. In that case, increasing the dose might help – which you seem to have tried – but there are many different ways to do this. Food getting stuck in your throat can also be due to Parkinson’s, as the swallowing muscles become sluggish. This may also improve to some extent if your treatment is optimised, though that can be difficult. In that case, it’s important not to swallow large, dry pieces of food, but to break the food down into smaller pieces and drink something alongside it. A speech and language therapist can examine your swallowing in more detail and offer further advice.

Dag Nyholm

Parkinson’s disease is a degenerative condition (characterised by a gradual deterioration) caused by the loss of function in some of the dopamine-producing cells in the brain. Most people are diagnosed in their 60s, but the condition is most common in older people.

There are around 50 neurological disorders that share similar symptoms at some stage of their progression, which complicates diagnosis. Parkinson’s disease is a diagnosis of a disease process, and requires that the course of the disease, characterised by a slow progression of symptoms, can be monitored. It takes time to establish the pattern of the disease. There are several mechanisms that contribute to the symptoms, and several processes that interact to influence the manifestations of the disease.

It is also easy to confuse Parkinson’s disease with a common cause of tremors, Essential Tremor, which begins with tremors, not at rest but in the posture or position of the arms in particular, and often during movement – something that most people with Parkinson’s disease do not experience (at the onset of the disease).

Dizziness is a sensation that can have many different causes and can be described in many different ways. The most common types of dizziness associated with Parkinson’s disease are dizziness caused by loss of balance and dizziness caused by a drop in blood pressure. Balance can be improved through physiotherapy. It is important to monitor drops in blood pressure, i.e. if your blood pressure drops significantly within 2 minutes of standing up from a lying position. If you feel faint in such situations, you may need medication to raise your blood pressure.

Shortness of breath, however, is not typical of Parkinson’s, and you should have your heart and lung function checked before concluding that it is due to Parkinson’s. Shortness of breath associated with missed doses has, however, been reported, and in such cases it improves when the medication is working at its best.

Dag Nyholm

This is partly an outdated concept from a time when only L-dopa was available. The aim now is that, through combination therapy using different types of anti-Parkinson’s medication, it should be possible to achieve a consistent and stable therapeutic effect for a considerably longer period than if only one type of medication were used.

The disease process leads to a gradual reduction in the production and storage of dopamine in the nerve cells, which can manifest as ‘dose gaps’. Dopamine acts like lubricating oil in a servo motor, but it leaks, so it needs to be replenished with increasingly frequent doses. By taking different classes of anti-Parkinson’s medication— L-dopa, enzyme inhibitors and long-acting dopamine agonists respectively, this can be partially counteracted. The period leading up to the onset of clear dose-related fluctuations is sometimes referred to as the ‘honeymoon phase’, but is now more commonly termed the ‘early phase of Parkinson’s disease’. ‘Wearing-off’ is the term used to describe this phenomenon, and the term ‘off’ period is often used to describe the symptoms experienced during a wearing-off episode. The opposite is the ‘on’ state, i.e. when a beneficial effect of the medication is present.

A five-year ‘honeymoon’ period of beneficial effects from Parkinson’s medication is not an absolute limit, and with modern treatment it should be possible to achieve a 7- or 10-year complication-free treatment phase. Parkinson’s disease is a degenerative condition, which means that the condition worsens over time. However, it is not correct to set absolute timeframes, as this varies from person to person and also depends on the stage of the disease and how the medication is administered.

The most common symptoms are stiffness, tremors at rest, slow movements and difficulties with fine motor skills, such as fastening buttons. Non-motor symptoms, to name a few, can include fatigue, a reduced sense of smell, poor sleep and low mood, which may occur before the motor symptoms appear.

No, it is not common to become very sensitive to the cold (or heat) with Parkinson’s disease. In your case, Sjögren’s syndrome is probably a more likely cause, particularly as you describe having polyneuropathy – both circulation and the sensory nerves may be affected in that case. Nevertheless, we do know that Parkinson’s can also affect the autonomic nervous system, which, amongst other things, regulates body temperature. However, it is more common to experience sweating during ‘off’ periods. Another factor is that muscles that get cold are more likely to become stiff and tense, which could explain why you’re experiencing dystonia in your legs. However, it doesn’t sound like a typical dose gap, unless it’s clear that this only happens a long time after your last dose of levodopa.

Dag Nyholm

Yes, it may be the case that people are born with a tendency to develop Parkinson’s; this is known as a ‘genetic predisposition’, and the disease develops in conjunction with certain environmental factors. There is strong evidence to suggest that the disease process begins at least many years before a diagnosis can be made.

Dag Nyholm

Freezing of gait (i.e. becoming ‘frozen’ whilst walking) can manifest in various ways. Some people have difficulty getting started, i.e. finding it hard to begin walking, whilst others freeze in their tracks when they reach a doorway or other narrow passage. There are many different ways to break out of such ‘freezes’. First and foremost, it is important to be on the right medication, as Parkinson’s medication often helps. If it is still difficult, you can try out different strategies involving so-called ‘cueing’ – a term derived from the word ‘cue’, as in a billiards cue. Examples of this include counting to three and then starting, patting your legs as a starting signal, or singing a song or chant. Kicking something, such as a walking stick you’re holding, can help get the movement going, or stepping over a line or other object. Nordic walking can work well for getting into a rhythm. A physiotherapist can help with further tips.

Dag Nyholm

No, probably not. Hyperkinesia occurs as a side effect once the disease has reached that stage (usually after a few years, but not in everyone). If you are undermedicated all the time, you will certainly not develop hyperkinesia, but on the other hand, you won’t feel very well either. The vast majority of people do not find hyperkinesia a cause for concern; in fact, they feel at their best when experiencing hyperkinesia, as that is when the medication is working most effectively. And if hyperkinesia does become troublesome, there are several effective treatments available to manage it. Opinions may differ on this subject, but I think you should take enough medication to feel well for the time being. There’s no need to ‘put up with it’, but of course you shouldn’t overdose either.

Dag Nyholm

The risks of not seeing a doctor are, firstly, that you may have a condition other than Parkinson’s, and secondly, that you may feel unwell ‘unnecessarily’ if you do have Parkinson’s and would feel better with medication. You do not ‘automatically’ lose your driving licence simply because you are diagnosed with Parkinson’s. And your driving ability may actually improve with Parkinson’s medication, at least in terms of improved mobility in terms of speed and agility. In the longer term (over several years), driving ability can sometimes deteriorate; in such cases, the most common effect is that reaction times become slightly slower.

Dag Nyholm

That’s a short question, and one that’s difficult to answer as there are many possible causes.

The brief advice is to contact your doctor, who can assess what has happened; after that, it’s likely advisable to be referred to a speech and language therapist.

Background: Aphasia (the inability to either understand or produce speech) involves a loss of speech function, meaning, for example, that a person cannot understand speech or formulate language. In the early stages and for most of the course of Parkinson’s disease, aphasia does not occur at all. These language functions are part of the cerebral cortex, which is not affected by the disease process that causes Parkinson’s disease. The most common cause of aphasia is a stroke, in which case aphasia occurs very suddenly. Symptoms of aphasia may develop gradually over several years and are usually limited to certain functions or aspects of language, such as no longer being able to use a second language that one was previously able to speak. If it occurs early, either before or after the onset of motor symptoms typical of parkinsonism (stiffness, slow movements and tremors), this presentation may be consistent with Lewy body dementia. In very advanced Parkinson’s disease, after many years of having the condition, partial aphasia may develop, but it is quite rare for this to lead to significant communication problems.

It is considerably more common for other speech difficulties to occur in Parkinson’s disease. The most common is a low volume of speech – hypophonia – which makes it difficult to understand what the person is trying to communicate. Awareness of this is the most important thing, and it is worth bearing in mind that it is one’s own perception of one’s voice that is distorted – a person with Parkinson’s disease perceives the volume of their own voice as normal, but in reality it is low. It is possible to train this, and a specific method, Lee Silverman Voice Therapy, has a proven therapeutic effect that can be sustained over the long term if the technique is applied.

Other causes of speech difficulties include unclear speech, which is due to difficulties with articulation, known as dysarthria. It is sometimes possible to adjust treatment to improve articulation, but this can be difficult as it involves the coordination of around 20 (small) muscles that affects how speech is formed, and the need for medication for this function differs from that for, for example, walking, which depends on much larger muscle groups that are coordinated in a different way. Treatment with DBS (deep brain stimulation) can sometimes affect speech – both improving and impairing it – but it is usually possible to adjust the DBS settings to achieve clear speech.

There are also stammer-like symptoms – with difficulty getting past the first syllables of a word. This can be likened to ‘freezing of gait’ – ‘festination’, or the ‘freezing’ of one’s steps when about to start walking. This can often be improved through medication adjustments and speech and language therapy.

In extreme cases, where the disease is very advanced, or if there is a sudden interruption in regular medication, anarthria may occur (i.e. a complete inability to articulate). In such cases, it is also impossible to swallow, and medication must therefore be administered by means other than orally.

Håkan Widner

Parkinson’s disease does not show up on an MRI (magnetic resonance imaging), but the scan can be carried out to rule out other causes of the symptoms. The symptoms you describe could be due to causes other than Parkinson’s disease. Lack of motivation can be a symptom of Parkinson’s that may need to be treated with, for example, antidepressant medication.

Dag Nyholm

The description of the period following a diagnosis of Parkinson’s disease arose when L-dopa was first introduced in the late 1960s and early 1970s. It was the therapeutic effect of L-dopa that was experienced as a relief from many symptoms, but many people developed a range of complications shortly after starting L-dopa, hallucinations, violent involuntary movements, rapid, sudden dose-related fluctuations with freezing episodes, etc., which we no longer see to anywhere near the same extent today. The period before these complications arose was described by doctors as a ‘honeymoon’ phase, which quickly gave way to more severe conditions.

Great progress has been made in modifying the effects of L-dopa using various combinations of medicines, and we no longer see these conditions; although fluctuations involving dose gaps and hyperkinetic episodes do develop over time, the aim is that, for the majority of patients, these should not occur within 5, or rather 7–10, years, by which time a stable, non-fluctuating therapeutic effect is intended.

The ‘honeymoon period’ thus referred to a period during which the therapeutic effect of (a type of) medication was effective and free from complications. Unfortunately, this persists in the seriously mistaken belief that L-dopa only works for a limited period (5 years!) and that one should not start treatment with L-dopa too early, as it only lasts for a short time. This is incorrect, and the professional recommendation is to start treatment upon diagnosis, as the disease has already been present for several years. However, it is necessary to combine different types of medication to avoid dose gaps and other complications, and the doses should be ‘optimal’ and ‘individualised’, i.e. tailored to symptoms and effects.

A very readable medical article in English has recently been published on the concept of the ‘honeymoon’ (honeymoon phase), which also quotes patients who, like the enquirer, find no connection whatsoever between a ‘honeymoon’ phase and being diagnosed with Parkinson’s disease.

It is therefore an outdated concept that now only leads to misunderstandings and paints a picture of drug treatment that is no longer accurate, but was very much the case around 50 years ago.

Håkan Widner

It is not correct to say that patients with Parkinson’s disease are entitled to a ‘special dental care allowance’.

It is not the diagnosis of Parkinson’s disease that is the deciding factor, but rather the degree of difficulty in maintaining oral hygiene and any dry mouth.

It is therefore not correct to say that a certificate should be issued automatically once the diagnosis has been made; rather, it is the degree of difficulty and need that forms the basis for most financial support schemes in Sweden.

There are also two different types of support that are often confused:

The special dental care allowance is paid by the Swedish Social Insurance Agency (Försäkringskassan), and information is available at 1177.se:

“How do I go about getting the special dental care allowance?”

A medical certificate is usually required to show which condition or symptoms you have. The certificate must generally not be more than three months old. Therefore, please remember to book your first appointment with the dentist or dental hygienist within three months of receiving your medical certificate.

What does the special dental care allowance cover?

The special dental care allowance is 600 kronor per half-year. The money is deducted when you pay for your dental appointment.

The allowance must be used by 30 June and 31 December each year.

You can claim the allowance for dental check-ups and preventive dental care. This could include, for example, teeth cleaning and fluoride treatment to prevent dental diseases and problems.

Preventative dental care may also involve receiving information on how to keep your teeth clean and what constitutes a healthy diet for your teeth.

For other dental treatments, you pay as usual.

Dental staff decide whether you are eligible for the allowance

It is the dentist or dental hygienist who decides whether you are eligible for the special dental care allowance. How the assessment is carried out depends on the diagnosis for which you are applying for the allowance. Dental staff may, for example, use medical certificates and information about your medication and prescriptions when making their assessment.

Dry mouth, which is a common side effect of these medicines, puts you at risk of developing cavities. You can experience dry mouth even if you find it difficult to swallow saliva. In other words, your mouth may feel dry even if your condition causes you to drool.

You can apply for a special dental care allowance if you have dry mouth as a side effect of medication.

The allowance is valid at all dental practices affiliated with the Swedish Social Insurance Agency. You are entitled to the allowance even if you change your dentist or dental hygienist.

Further information is available on the Swedish Social Insurance Agency’s website.”

There is also a dental care subsidy paid by the region in which you live; this is granted if a doctor (a neurologist or other doctor – not a dentist) writes a medical certificate confirming that, due to Parkinson’s disease, you have difficulty maintaining your oral hygiene or undergoing dental treatment. In that case, you can receive dental care at the same rate as other healthcare.

Dental care

The condition increases the risk of tooth decay and tooth loss. You therefore need to brush your teeth thoroughly and clean between your teeth every day. It is a good idea to visit a dental hygienist regularly. The dental hygienist can advise you on self-care, treatments and aids to help prevent dental problems. You will also receive help with removing tartar if you have any.

You can apply for dental care support if, due to Parkinson’s disease, you find it difficult to maintain your oral hygiene or undergo dental treatment. In that case, you can receive dental care at the same rate as other healthcare.

Each region has detailed information on how the rules for dental care support are organised locally, and these vary across the country.

Håkan Widner

There is a study from Taiwan showing that people with diverticula (pouch-like outpouchings) in the bowel are at a slightly higher risk of developing Parkinson’s. You have probably had diverticula for a long time, which have now become inflamed (diverticulitis). It’s not common for Parkinson’s to cause this, but your Parkinson’s does affect, for example, bowel motility. So there is a certain link, but diverticulitis is an acute condition from which you will be ‘cured’ by the operation.

Dag Nyholm

An established method means that it can be applied outside of clinical trials, i.e. that it is possible to carry out in the same way that DBS (Deep Brain Stimulation) surgery is possible today. This presupposes that the various clinical trial phases – Phases 1 to 3 – all demonstrate that it is a safe method, and that the benefits are sufficient to make it reasonable to recommend such a surgical procedure. Further studies and research are required to meet these requirements. If everything goes according to plan and no unexpected obstacles arise to throw a spanner in the works, it might possibly be used as a routine method for some patients in 5–6 years’ time at the earliest.

No one knows, but there are many studies underway at various stages – in laboratories using cells, various animal models of the disease, computer and AI simulations of effects, as well as in clinical trials and studies. There are normally 1 million dopamine-producing nerve cells, each with 20,000 nerve endings that are influenced by at least 5 other neural signalling systems, each with at least a few billion nerve endings; in addition, the effects of many thousands of different genes and regulatory factors are also at play, influencing the course of events. This results in immense complexity within the brain’s various signalling systems. When you lift a stone, a host of further questions arise that need to be resolved. Having said that, we naturally hope that a solution will come as soon as possible, but realistically it will take many years – unless, of course, someone suddenly manages to solve it. Such things have happened before.

‘Disease-modifying medication’ refers to treatment that reduces or otherwise prevents the progression of the disease. There are currently many studies underway, some involving drugs that are already authorised, whilst others are entirely new. However, it is difficult to prove a potential disease-modifying effect that is distinct from the symptom-relieving effect of increased dopamine in the brain, as it is a deficiency that causes the symptoms.

According to the regulations governing the development of a completely new drug, it takes at least 3–5 years to demonstrate safety, tolerability and proven efficacy, but it may take longer if it is difficult to distinguish between symptom relief and disease-slowing effects.

Around 5–10 per cent of all people with Parkinson’s disease in the advanced stage are assessed as likely to benefit from the more advanced treatments. These differ in many ways, and it is highly individual as to which symptoms the various treatments work best for.

There are a number of criteria for determining when and for which symptoms benefits can be achieved, and it is important to both assess and investigate suitability, taking into account personal circumstances and preferences regarding the type of advanced treatment one might prefer. This usually takes place in conjunction with testing different symptoms and treatment effects.

It is a common misconception that L-dopa only works for a limited period. This is completely incorrect in the case of Parkinson’s disease, as L-dopa tablets never stop working. It is in conditions other than Parkinson’s disease that the effect wears off, which is what has led to this confusion.

The effect of L-dopa changes over time, and symptom relief usually becomes shorter (dose gaps), meaning that more tablets are required per day, and the beneficial effects last for a shorter period.

To achieve a longer-lasting effect, L-dopa tablets can also be supplemented with various other types of tablets or other treatments to ensure a more consistent effect.

The main principle is to use medication to replace the deficiency of neurotransmitters in the brain. Parkinson’s disease can be regarded as a deficiency disorder, and by replacing neurotransmitters, the deficiency can be corrected over the long term. The most widespread and usually earliest deficiency to occur is that of dopamine. Dopamine can be replaced in three ways.

Levodopa (also known as L-dopa) treatment is by far the most important cornerstone of treatment for Parkinson’s disease. L-dopa is taken up by nerve cells, where it is converted and stored as dopamine. In the early stages of the disease, it is released in the same way as normal/natural dopamine. As the disease progresses, other cells are able to convert L-dopa into dopamine, and it then acts in a different way; however, throughout the course of the disease, L-dopa will be able to alleviate symptoms.

L-dopa can be combined with other medicines designed to prolong the effect of dopamine. There are several types of adjunctive medicines that work primarily by improving the function of the dopamine that has been produced. They may be available in combination tablets with L-dopa (e.g. carbidopa and benserazide, and entacapone), or as separate tablets (e.g. rasagiline and safinamide). There are also several types of dopamine agonists that mimic the body’s own dopamine and prolong or enhance the effect of L-dopa tablets.

There are a range of additional medicines for various symptoms that are independent of dopamine, and some treatments can be administered using pumps to maintain steady drug levels. An effective method of influencing the brain’s electrical signals is by modulating this mechanism using electrodes implanted in the brain, known as deep brain stimulation (DBS).

The treatment of Parkinson’s disease aims to optimise symptom relief so that the patient can feel as well as possible and enjoy a good quality of life.

There is as yet no established treatment that slows the progression of the disease or cures it, but several strategies and medicines are being investigated with the aim of influencing the disease process.

It is difficult to answer this question. It is sometimes difficult to make a diagnosis, and it is not possible to determine, based on the information provided, whether this is a case of Parkinson’s disease at all or whether it is some other condition that fully explains the symptoms. It’s also possible that something else is occurring alongside Parkinson’s disease, which could then interfere with the effectiveness of treatments that previously worked but no longer do so to the same extent. So-called normal pressure hydrocephalus (NPH) is a fairly common condition that can resemble, at least in part, Parkinson’s disease, but where medication (anti-Parkinson’s medication) usually has only a minor or more temporary effect. It is common for shunt surgery to be effective, and if it does not function optimally, the symptoms may recur. In such cases, the shunt’s function should be assessed and, if possible, its settings adjusted. Dizziness may be due to shunt dysfunction, but it can also be caused by, for example, low blood pressure and many other conditions not directly related to either Parkinson’s disease or NPH. You should contact your doctor about this if you have not already been examined.

Håkan Widner

A brief overview of physiology (body functions): When you eat, the food is chewed and enters the stomach – the lower oesophageal sphincter closes after a mouthful, hydrochloric acid is secreted, and the stomach churns the chewed food into a paste which is then emptied in small portions into the small intestine. Nothing is absorbed in the stomach – neither nutrients nor medicines.

It is therefore advantageous to take the medicine before eating – it does not have to be a specific time beforehand – but the tablet is more likely to reach the small intestine more quickly if taken with a little liquid.

A brief note on pharmacology: L-dopa dissolves and is absorbed slightly better/faster with a slightly acidic drink, but the difference is minor. The type of tablet taken is more important – tablets labelled ‘Quick’ are absorbed most rapidly, whilst sustained-release tablets are designed to remain in the small intestine for longer. Combination tablets containing entacapone act as sustained-release tablets.

Håkan Widner

The pumps (there are several different types) have the advantage of delivering a steady level of medication, so that symptoms are managed continuously, thereby reducing fluctuations in symptoms. The downside is that the treatments are ‘invasive’ (via a plastic cannula under the skin or a tube to the stomach) and that you need to carry the pump with you. Yes, you can switch between the Duodopa and Lecigon levodopa pumps whilst keeping the same PEG tube system. You just need to make a few minor adjustments to the connection. There is a website where the company that manufactures Duodopa provides information: https://duodopapatient.se/leva-med-duodopa/ and an American version here: https://www.duopa.com/  Previously (before the COVID-19 pandemic), ‘pump meetings’ were organised in Sweden to provide information about the treatments and give people the chance to meet up. There are plans (now for 2023) to organise new ones.

Dag Nyholm

No, Parkinson’s disease is not a barrier to having a massage. It can be a way of loosening up stiff muscles and joints, but the effect is short-lived and does not replace Parkinson’s medication.

Håkan Widner

Alcohol does not actually affect the efficacy of Parkinson’s medicines, but many people with Parkinson’s choose to avoid alcohol, probably because they feel that alcohol impairs their motor control. From a purely chemical perspective, L-dopa is compatible with small amounts of alcohol, whilst drinking alcohol is generally discouraged during treatment with dopamine agonists and amantadine. This is because alcohol affects the brain and can exacerbate side effects from the medicines, such as tiredness and confusion.

Dag Nyholm

This type of treatment is not specifically focused on Parkinson’s. For specific treatment of Parkinson’s disease, you need to contact the ‘mainstream’ healthcare system. It is entirely possible to learn to manage your condition using many different methods, but there is a risk that so-called complementary treatments may be expensive and do not always have strong scientific backing.

There are several aspects to what is meant by DBS working and helping. A power source is required, and it remains effective as long as there is sufficient power in the batteries. Some equipment manufacturers offer rechargeable units, which can withstand a large number of recharge cycles, and a general lifespan of more than 15 years is stated. For battery-powered devices, the lifespan depends on how much power is required – and can typically vary between 1½ and 4/5 between battery replacements.

There are now more than 100,000 patients with Parkinson’s disease who have undergone DBS surgery at one of the three possible target sites, which can alleviate the symptoms of Parkinson’s disease. The experience from all these patients is that there is no evidence to suggest that the effect of deep brain stimulation diminishes as a result of the stimulation itself; in other words, the electrical blockade does not become less effective beyond the adjustments that are often required as the brain adapts slightly.

The beneficial effect lasts for a very long time, but the disease is progressive and continues to advance, meaning that some symptoms develop and worsen, and it is not always possible to adjust the current or medication to counteract them.

Before DBS surgery, attempts are made to identify what can be improved and alleviated, such as tremors. If one monitors the effect of DBS treatment on a patient’s tremors over time, it is highly likely that this effect will persist for a long time. We recently had a patient who received DBS for a specific symptom; the treatment has been effective for over 30 years, and the battery has been replaced approximately every five years. There are also many patients with Parkinson’s disease who have electrodes implanted in the subthalamic nucleus (STN) and who continue to experience significant beneficial treatment effects more than 20 years after surgery. This becomes clear, for example, when the stimulation is switched off, partly to determine whether there is a therapeutic benefit.

It is also recognised that there is a therapeutic benefit in being able to take a lower dose of anti-Parkinson’s medication following DBS surgery. This effect persists over time, although medication doses may need to be adjusted more or less regularly even after DBS surgery. If one is unsure about the benefits of DBS treatment, the device can be switched off under controlled conditions to observe the symptoms afterwards; this sometimes occurs when it is time to replace the battery, and the question arises as to whether it is worthwhile undergoing surgery and a battery replacement. If the stimulation is switched off for a period, it is easy to determine whether it provides sufficient symptom relief. Experience shows that a very high proportion of patients and their families agree to continue the treatment.

Which patients are suitable for DBS treatment varies depending on their symptoms and the target site.

This requires tests and examinations, which are carried out at the regional motor disorders units specialising in advanced treatments for conditions such as Parkinson’s disease. Doctors can refer patients for an assessment.

A general rule of thumb is the same as for potential pump therapy, i.e. that the symptoms are severe enough to justify the medical risks associated with medication pumps or DBS treatment, and that treatment attempts with available medicines or combinations of medicines have not been sufficiently successful. If a patient is taking at least five doses of anti-Parkinson’s medication, and yet still experiences two hours of so-called ‘off’ time and one hour of involuntary movements such as fluctuations, these are some of the factors that are relevant for an assessment. There are also other factors; for example, one of the target sites for DBS treatment, the VIM nucleus (which refers to a specific target site in the thalamus – the ventral intermediate nucleus), is suitable for tremors that are very difficult to treat, and the procedure is usually performed on one side. It is primarily older people and those who require high doses of medication to control tremors who are suitable candidates, as well as those whose tremors affect their ability to, for example, eat or drink. There is virtually no age limit for undergoing this type of surgery, but there are several factors that may make it unsuitable to undergo surgery at any of the other target sites, the globus pallidus (GPi), which is particularly well-suited for treating so-called fluctuations and painful dystonia/muscle contractions. The STN target is the most common, and if a patient is suitable for this, there are several factors suggesting that good treatment outcomes can be achieved following surgery; however, this must be assessed on a case-by-case basis.

Yes, this sounds like typical dystonia (involuntary muscle contractions) associated with Parkinson’s disease. This symptom is usually improved by increasing the medication. If it persists, however, botulinum toxin injections can be used to relax the dystonic muscles. This treatment is available at many, though not all, major hospitals in Sweden and is repeated approximately every three months.

Dag Nyholm

Question: It can be difficult to confirm a diagnosis of Parkinson’s disease, and one sometimes hears of people who have undergone extensive treatment before it became apparent that the diagnosis was incorrect. I wonder what results can be expected from treatment with Parkinson’s medication in patients who do not have the disease? How, for example, are the key symptoms – bradykinesia (reduced amplitude and/or frequency of repetitive movements), rigidity (muscle stiffness) and tremor (shaking) – affected?

Answer: In principle, nothing happens if you take Parkinson’s medication when you do not have Parkinson’s disease. You may, of course, experience side effects, such as nausea, but you will not become hyperkinetic if you do not have a disorder of the dopamine system. So it is not dangerous to try the treatment. Sometimes there is some effect on the motor symptoms if you have atypical parkinsonism, particularly MSA-P (Multiple System Atrophy).

Dag Nyholm

Joint pain and other aches and pains could be caused by factors other than Parkinson’s. Pain caused by Parkinson’s is often relieved, as you mention, by L-dopa if it is linked to muscle stiffness. However, there are also several other types of pain that can occur with Parkinson’s and which may require different kinds of treatment. Parkinson’s is not solely caused by a dopamine deficiency. Consulting a physiotherapist may be helpful in analysing the type of pain.

Dag Nyholm

Yes, you can. Benserazide and carbidopa do not interfere with each other but have the same effect (they inhibit the decarboxylase enzyme, which would otherwise convert L-dopa). Both of these substances inhibit the enzyme in the gut and the blood. The brain is not affected by them at all, but absorbs levodopa to a much greater extent than it would without enzyme inhibitors. There are no major advantages or disadvantages to taking both on the same day, apart from the fact that they come in different types of tablet formulations.

Dag Nyholm

Yes, in principle, but nothing is 100 per cent certain. A response to L-dopa for symptoms such as slowness of movement or tremors provides strong evidence that it is ‘typical’ Parkinson’s disease. However, sometimes L-dopa is quite effective even in cases of other diagnoses. In such cases, it is necessary to look more closely at the specific symptoms and how the response develops over the long term. And then, of course, there is the placebo effect – that is, feeling better as a result of a new treatment even though it is not actually effective.

Dag Nyholm

It’s difficult to say why – it’s best to ask your doctor.

One of the differences is that Ropinirole has a so-called long half-life (how long a single tablet remains active in the body and brain), and there is less risk of developing ‘fluctuations’ such as dose gaps and other effects associated with a short half-life, which Madopark has (around 90 minutes), whilst Ropinirole has a half-life of between 6 and 7 hours and can be formulated as a sustained-release tablet with an effect lasting over 24 hours.

Often, a combination of different classes of medication is most effective – several classes are available: L-dopa, which can be enhanced by the enzyme inhibitor COMT, and MAO-B, dopamine agonists such as Ropinorol, Pramipexole, rotigotine, apomorphine, as well as other agents such as amantadine, memantine and others.

Håkan Widner

There is as yet no evidence that the anti-inflammatory asthma medicine Montelukast slows the progression of Parkinson’s disease, but there are studies in both animals and humans that appear promising. This needs to be investigated in more and larger research studies, which are currently underway. The treatment cannot be recommended for people who do not have asthma.

Dag Nyholm

This is a common phenomenon associated with fluctuations in the effectiveness of treatment. There are two biological explanations; one is that there is, for example, a narrowing in or around a joint or nerve root in the spine, and when the medication is less effective, this leads to the muscles tensing (becoming shorter) and the narrowing becoming even more constricted, resulting in pain, for example. In this case, the constriction is the root cause, but it is the varying effect of Parkinson’s on muscle tension that gives rise to the varied symptoms. It may also be the muscle tension itself that causes the pain – this is common in the early symptoms of Parkinson’s disease, often before diagnosis, and may be mistaken for chronic tennis elbow, shoulder pain, etc.  The pain may also vary in these cases, but is then not related to medication but to normal activity.

Another, probably less common cause of pain or aches – though it may manifest as various sensory symptoms – is that the dopamine deficiency can give rise to symptoms in the thalamus, which plays a key role in the interaction between muscle control and sensory functions (the thalamus integrates information about, for example, the position of an arm and coordinates movement by, for example, reading the arm’s position relative to the body so that the muscles can be controlled. The thalamus may therefore, due to a dopamine deficiency, misinterpret sensory signals so that they are perceived as pain during an ‘off’ phase.

It need not be actual damage to a joint or muscle that gives rise to varying symptoms, but stiff muscles during ‘off’ periods place greater strain on (tender) muscle attachments, and make narrow passages for nerve fibres even narrower, which gives rise to pain.

Håkan Widner

Yes, antidepressants are often very effective against anxiety – so you don’t have to be depressed to take them. There are many different types that work, such as venlafaxine, mirtazapine, sertraline and others.

Dag Nyholm

There are a few studies on this, which show cautiously positive results, but not enough to provide scientific support. Dopamine agonists are quite similar to one another in their ‘receptor profiles’, i.e. which dopamine receptors they bind to. Consequently, there is no significant difference between taking two different agonists at a low dose compared with taking one of them at a higher dose. The effects and side effects are likely to be quite similar. It is an advantage to take just one type, in case the dose needs to be adjusted.

Dag Nyholm

This probably suggests that the dose needs to be increased, perhaps by adding an adjunct to L-dopa (Madopar), such as a COMT inhibitor (Entacapon/Comtess), or the MAO-B inhibitor rasagiline/safinamide, or possibly a dopamine agonist. Alternatively, I could increase the Madopark dose or take it more frequently.

Håkan Widner

Physical exercise at a level you can manage is one of the most important activities you can do for yourself. Strength training, swimming, aqua aerobics, yoga, table tennis and boxing, to name but a few. There are several scientific reports showing very positive results from physical exercise, best described as physical activity that raises the heart rate.

There is experimental evidence that neural connections are strengthened by physical exercise and that more dopamine becomes available over time. A good workout is estimated to have an effect equivalent to a 100 mg tablet of L-dopa over the course of a day, provided it is done regularly. Furthermore, one should not underestimate the social aspect of exercise, which has also been shown to have beneficial effects.

Oat porridge is excellent, if you like it. There are no specific dietary recommendations regarding breakfast. There are a few things that may be worth knowing about diet and Parkinson’s. The best-known is the issue of protein. As levodopa is an amino acid (a component of protein), it can be displaced by the amino acids in food when it is being absorbed from the gut. This mainly applies to amino acids in meat and dairy products. That is why the patient information leaflet states that you should not take levodopa with food. In practice, however, only a small number of people with Parkinson’s notice such an effect, and if it does happen, it is only a temporary deterioration – it has no long-term impact. So my advice is to ignore that rule. In other words: feel free to take the medicine with food if it’s convenient for you. If you notice that the effect is reduced after a meal containing meat and dairy products, it may be a good idea to take the medicine on an empty stomach.

Another aspect of your diet is that living with Parkinson’s takes up energy. If you start to lose weight, it may be a good idea to consume extra calories (butter, cream, etc.).

Many people start the day with a high-fibre meal to stimulate bowel movements, as the bowels tend to be sluggish. High-fibre porridge is one example. Remember that fibre needs fluid to be effective, so aim to drink 2 litres of fluid a day.

Finally: Some people experience a drop in blood pressure, manifesting as dizziness or a feeling of faintness when they stand up from a lying position, or feel extremely tired after breakfast. The first step to counter this is to drink plenty of fluids to keep your blood pressure up.

Dag Nyholm

Yes, to some extent – caffeine can temporarily increase tremors, but it also (temporarily) increases dopamine levels, so it can alleviate the symptoms for a short time. There is a medicine that is not authorised in Sweden but is authorised in Japan, which is based on the effects via chemical pathways in nerve cells – adenosine – through which caffeine partly acts. This is probably why caffeine has (likely incorrectly) been cited as having a protective effect, i.e. that coffee drinkers are thought to have a lower risk and fewer coffee drinkers develop Parkinson’s disease. Quite simply, caffeine affects the nerve cells in such a way that symptoms are reduced for a (short) period, but it has no decisive effect on the progression of the disease.

Håkan Widner

It will take many years of research before we know whether this particular bacterium can be treated and whether such treatment is effective and safe. Antibiotic treatments are complex matters and should not be used unless there is strong scientific evidence to support their use.

Dag Nyholm

At present, it is reasonable to hope that this ‘piece of the jigsaw’ in the progression of the disease will be investigated in more and larger research studies. Whether the discovery will have any practical significance cannot be answered at this stage. We can always hope. There is a strong focus on gut bacteria in research at the moment.

Dag Nyholm