Parkinson: short overview
- Typical symptoms: slowed movements, lack of movement, stiff muscles, trembling at rest, lack of stability in upright posture, rigid facial expression
- Causes: In Parkinson’s disease: death of dopamine-producing cells in the brain; in secondary Parkinson’s syndrome: other diseases, drugs or poisoning; in genetically determined Parkinson’s syndrome: genetic changes
- Important research: Physical and neurological examination, L-dopa test, computer tomography (CT), magnetic resonance imaging (MRI)
- Treatment options: Medication (such as Levo-Dopa), physiotherapy, speech therapy, ergotherapy, deep brain stimulation (THS)
Stiff muscles, slowed movements and trembling hands are typical features of PD.
Early symptoms of Parkinson’s
Signs of progressive brain disease can appear years before the main symptoms. Such early symptoms of Parkinson’s are:
- REM sleep behavioral disorder: Normally a person is “paralyzed” in dream sleep. In REM sleep behavioral disorder, the dreamed movements are partly executed (speaking, laughing, gesticulating, etc.) This can be dangerous for the person concerned and the sleeping partner.
- The sense of smell is reduced or completely absent (hyposmia/anosmia).
- Pain in muscles and joints (dysesthesia), often in the shoulder and arm area
- The arms swing along with the body in a reduced way when walking.
- Getting up, washing, dressing, eating etc. takes longer than before.
- Visual disorders (such as impaired colour vision)
- The handwriting appears cramped and becomes smaller, especially at the end of a line or page.
- Fatigue, exhaustion
- stiff, uncertain feeling, shakiness
- The patient withdraws and neglects his hobbies.
Many of these early symptoms of Parkinson’s are very unspecific. They can therefore have many other causes (such as advanced age). Therefore, they are often not recognized as early signs of Parkinson’s disease.
REM sleep behavioral disorder
The most important early sign is the REM sleep behavioral disorder: Those who show this form of sleep disorder generally have an increased risk of so-called neurodegenerative diseases. These are progressive diseases that are associated with the loss of nerve cells. Most people with REM sleep behavior disorder develop Parkinson’s disease later. Others suffer from a certain form of dementia (Lewy Body Dementia).
Parkinson: Main symptoms
The symptoms of Parkinson’s disease usually develop gradually. Relatives and friends often notice them earlier than the patient himself.
In most cases, the Parkinson’s signs begin on one side of the body. Later they also spread to the other side. In the course of the disease they also become more and more pronounced.
The typical Parkinson symptoms are:
- slowed movements (bradykinesis) up to a lack of movement (hypokinesia) or motionlessness (akinesia)
- stiff muscles (rigor)
- Muscle tremor at rest (Parkinson tremor)
- lack of stability of the upright posture (postural instability)
Slowed movements (bradykinesis): All body movements are unnaturally slow. This means, for example, that people with Parkinson’s disease walk remarkably slowly and in small steps. Over time, the gait becomes shuffling and the patients bend forward. This is one of the most striking symptoms. Parkinson’s patients can also sit down and get up again only slowly and with difficulty. Sometimes the affected persons are suddenly blocked in their movements – they seem to freeze. This is what physicians call “freezing” .
The symptoms of Parkinson’s disease also affect gestures and facial expressions: the face increasingly looks like a rigid mask. Those affected usually speak softly and monotonously, making it harder to understand them. Swallowing also often causes them problems, for example when drinking or eating. Another sign of Parkinson’s disease is impaired fine motor skills: those affected find it difficult to write, button their coat or brush their teeth, for example.
If the body movements are particularly slowed down or the patient is sometimes completely motionless, doctors speak of akinesia (akinesia).
Stiff muscles (rigor): In Parkinson’s disease there is no paralysis, but muscle strength is largely retained. However, the muscles are permanently tense, even at rest. This is painful for those affected. Especially the shoulder and neck area can be painful.
Muscle stiffness can be detected by the so-called cogwheel phenomenon: when the doctor tries to move the patient’s arm, the stiff muscles prevent this. Therefore the arm can only be moved a little bit at a time and jerkily. It almost feels as if there is a cogwheel in the joint, which allows movement only until the next notch and then engages. The cogwheel phenomenon is usually tested on the elbow or wrist. It is a typical sign of Parkinson’s disease, but it can also occur with other diseases.
Muscle tremor at rest (rest tremor): In Parkinson’s disease, arms and legs typically begin to tremble at rest. This is why the disease is also called “shaking palsy”. One side of the body is usually more affected than the other. Also, the arm usually shakes more than the leg.
Parkinson’s tremor typically occurs at rest. In this way Parkinson’s disease can be distinguished from other diseases with tremor. If, for example, the hand does not shake at rest, but as soon as you want to make a targeted movement, doctors speak of so-called intention tremor. Its cause is damage or disorder in the cerebellum.
By the way, most people who tremble have neither Parkinson’s nor any other identifiable neurological disease. The cause of this “essential tremor” is unknown.
Lack of stability of the upright posture: Unconsciously every person corrects his posture at any time when walking and standing upright. The whole thing is controlled by so-called positioning and holding reflexes. Reflexes are automatic movements that are triggered by certain stimuli. These are unconscious, involuntary movements or muscle tensions. The holding and standing reflexes of the human being are responsible for the fact that even in movement the body can be automatically balanced and does not fall.
In Parkinson’s disease, the positioning and holding reflexes are typically impaired. Those affected therefore have difficulty in maintaining a stable upright position. It’s called postural instability. It is the reason why Parkinson’s patients can no longer easily “catch” sudden, unforeseen movements, for example when they stumble or when a sudden gust of wind blows. Therefore they are insecure when walking and fall easily.
Parkinson: accompanying symptoms
The main symptoms of Parkinson’s disease are sometimes accompanied by other symptoms:
Parkinson’s patients are more likely to suffer from depression than healthy people and than people with other chronic diseases. Sometimes the depression only develops during the course of Parkinson’s disease. In other patients it precedes the motor symptoms (slowing down of movement etc.).
In addition, Parkinson’s disease can lead to a decline in intellectual performance and dementia (see below). Those affected have increasing difficulty in thinking. However, it should not be forgotten that even most healthy people think more slowly in old age and find it harder to remember things. So this does not necessarily indicate Parkinson’s.
In many Parkinson’s patients, the facial skin produces excessive amounts of sebum. This makes it greasy and shiny. Doctors speak of the so-called “ointment face”: the patient’s face looks as if the person concerned had applied a thick layer of ointment or face cream.
Possible Parkinson’s symptoms also include bladder dysfunction: many patients can no longer control their bladder properly. It can happen that urine is involuntarily passed (incontinence) and patients wet themselves at night (enuresis). But the opposite is also possible: some patients have problems passing water (urinary retention).
In Parkinson’s disease, the bowel is often sluggish, so that constipation develops. Such constipation can also occur as an early sign of Parkinson’s disease.
Men sometimes show potency problems (erectile dysfunction). This impotence can result from the disease itself as well as from the Parkinson’s drugs.
All the accompanying symptoms mentioned can also be triggered by other diseases, not only Parkinson’s.
Parkinson’s patients are more susceptible to dementia than the general population: about one third of patients develop dementia in addition to the disease. According to some studies, the risk of dementia in Parkinson’s is even higher (up to 80 percent).
The symptoms of Parkinson’s dementia are primarily disturbed attention and slowed thinking. This is an important difference to Alzheimer’s – the most common form of dementia. Alzheimer’s patients mainly suffer from memory disorders. In Parkinson’s dementia, on the other hand, such symptoms only occur in later stages of the disease.
You can read more about this topic in the article Dementia in Parkinson’s disease.
Physicians also call Parkinson’s disease primary or idiopathic Parkinson’s syndrome (IPS). “Idiopathic” means that no tangible cause for the disease can be found. This “real” Parkinson’s accounts for about 75 percent of all Parkinson’s syndromes. It is the focus of this text. The rare genetic forms of Parkinson’s disease, the “secondary Parkinson’s syndrome” and the “atypical Parkinson’s syndrome” must be distinguished from this. They are briefly described below.
Idiopathic Parkinson: Dopamine deficiency
Parkinson’s disease originates in a specific region of the brain, the so-called “black substance” (substantia nigra) in the midbrain. This region of the brain contains a lot of iron and the pigment melanin. Both color the “Substantia nigra” strikingly dark (compared to the otherwise light brain tissue).
In the “substantia nigra” there are special nerve cells that produce the nerve messenger substance (neurotransmitter) dopamine. Dopamine is very important for controlling movement. In idiopathic Parkinson’s disease, more and more dopamine-producing nerve cells die off. Why, we don’t know.
This progressive cell death causes the dopamine level in the brain to drop further and further – a dopamine deficiency develops. The body can compensate for it for a long time: Only when about 60 percent of the dopamine-producing nerve cells have died, does the dopamine deficiency become noticeable: The patient moves more and more slowly (bradykinesis) or sometimes not at all (akinesia).
However, the dopamine deficiency is not the sole cause of Parkinson’s disease: it also upsets the delicate balance of nerve messengers: because less and less dopamine is available, the amount of the messenger acetylcholine, for example, increases in relative terms. Experts suspect that this is the cause of tremor and muscle stiffness (rigor) in Parkinson’s disease.
What happens in Parkinson’s? The messenger substance dopamine in the brain is crucial for movement coordination in humans. There is too little dopamine in idiopathic Parkinson’s disease. Therefore, there is not sufficient signal transmission to perform movements normally.
The imbalance of neurotransmitters in Parkinson’s could also be responsible for the fact that many patients become additionally depressed. Because it is known that the balance of nerve messengers is generally disturbed in depression. However, the connection between Parkinson’s disease and depression has not yet been conclusively clarified.
Causes of Parkinson’s: Many assumptions, little evidence
It is still unclear why nerve cells in the substantia nigra die in Parkinson’s disease. Research results suggest that several factors are involved in the development of Parkinson’s disease.
For example, scientists have discovered that the nerve cells of Parkinson’s patients are only insufficiently able to eliminate harmful substances. Cell-damaging substances are for example the so-called “free radicals”. These are aggressive oxygen compounds that are produced during various metabolic processes in the cell.
It is possible that the nerve cells of Parkinson’s patients are not able to break down these dangerous substances before they cause damage. Or the detoxification capacity of the cells is normal, but excessive amounts of “free radicals” are produced in Parkinson’s disease. In both cases, the cell-damaging substances could accumulate in the nerve cells and cause them to die.
There are also other possible causes of Parkinson’s disease that are currently being discussed and researched.
Genetic forms of Parkinson’s disease
When a family member has Parkinson’s disease, many relatives feel insecure. They wonder if Parkinson’s is hereditary. In the vast majority of cases, however, Parkinson’s disease is the idiopathic Parkinson’s disease described above. Heredity is not an issue in this sporadically occurring form of the disease, experts believe.
The situation is different with the so-called monogenetic forms of Parkinson’s disease: each of them is caused by a change (mutation) in a specific gene. These gene mutations can be passed on to the offspring. Monogenetic forms of Parkinson’s disease are therefore inheritable. They are often referred to as familial Parkinson’s syndrome. Fortunately they are rare.
Secondary Parkinson’s syndrome
In contrast to idiopathic Parkinson’s disease, symptomatic (or secondary) Parkinson’s syndrome has clearly identifiable causes. These include:
- Drugs: Inhibitors of dopamine (dopamine antagonists) such as neuroleptics (for the treatment of psychosis) or metoclopramide (for nausea and vomiting), lithium (for depression), valproic acid (for seizures), calcium antagonists (for high blood pressure)
- other diseases such as brain tumours, inflammation of the brain (for example as a result of AIDS), hypothyroidism (hypoparathyroidism) or Wilson’s disease (copper storage disease)
- Poisoning, for example with manganese or carbon monoxide
- Brain injuries
Atypical Parkinson syndrome
Atypical Parkinson’s syndrome develops in the context of various neurodegenerative diseases. These are diseases in which nerve cells in the brain die off progressively. In contrast to idiopathic Parkinson’s syndrome, this cell death affects not only the substantia nigra, but also other regions of the brain. Therefore, in Atypical Parkinson’s Syndrome, other symptoms occur in addition to Parkinson-like symptoms.
Neurodegenerative diseases that can trigger an atypical Parkinson’s syndrome include
- Lewy Body Dementia
- Multisystem atrophy (MSA)
- Progressive supranuclear gaze paresis (PSP)
- Corticobasal degeneration
Such diseases have a significantly worse prognosis than the “real” (idiopathic) Parkinson’s syndrome.
By the way: The drug “L-Dopa”, which works very well in idiopathic Parkinson’s disease, has little or no effect in atypical Parkinson’s disease.
Parkinson therapy is individually adapted to each patient. This is because the symptoms of the disease can vary from person to person and progress at different speeds.
Parkinson’s disease is usually treated with medication, although mild symptoms sometimes do not require therapy at all at first. Which active ingredients are used depends mainly on the age of the patient. Sometimes a neurosurgical intervention can also be useful – the so-called Deep Brain Stimulation (DBS).
In addition to medical and, if necessary, surgical measures, individual Parkinson’s treatment can also include other components. These include, for example, physiotherapy, speech therapy and occupational therapy. In any case, it makes sense to be treated in a special Parkinson’s clinic.
Parkinson therapy: Medications
There are different medications for Parkinson’s therapy. They help against complaints such as slowed movements, stiff muscles and trembling. However, they cannot prevent the nerve cells from dying and thus the progression of the disease.
The typical Parkinson symptoms are caused by a lack of dopamine in the brain. They can therefore be alleviated either by administering the messenger substance as a drug (e.g. in the form of L-dopa) or by preventing the breakdown of the existing dopamine (MAO-B inhibitors, COMT inhibitors). Both mechanisms compensate for the dopamine deficiency. They thus largely eliminate the typical Parkinson’s symptoms.
There is no point in giving Parkinson’s patients the missing dopamine directly as a syringe or tablet: the messenger substance is transported to the brain via the bloodstream. However, it is unable to cross the protective blood-brain barrier, i.e. it cannot directly enter nerve tissue. However, the precursor of dopamine is able to do this: this L-dopa (levodopa) is therefore suitable for the treatment of Parkinson’s disease. Once it reaches the brain, it is converted into dopamine by the enzyme dopa-decarboxylase. This can then unfold its effect in the brain and alleviate Parkinson’s symptoms such as muscle stiffness (rigor).
L-Dopa is very effective and has few side effects. It is usually taken in the form of tablets, capsules or drops. Doctors prescribe it mainly for patients over 70 years of age. In younger patients, on the other hand, L-dopa is only used very cautiously. The reason is that treatment with L-dopa can trigger movement disorders (dyskinesias) and fluctuations in effect (fluctuations in effectiveness) after several years (see side effects).
L-dopa is always combined with another active substance, a so-called dopa decarboxylase inhibitor (such as benserazide or carbidopa). This prevents L-dopa from being converted into dopamine in the blood, i.e. before it reaches the brain. The dopa-decarboxylase inhibitor cannot even cross the blood-brain barrier. In the brain, L-dopa can therefore easily be converted into dopamine.
Every Parkinson’s patient responds differently to L-dopa. Therefore the dosage is determined individually: The therapy is started with a low dose and then gradually increased until the desired effect is achieved.
Usually L-Dopa must be taken several times a day. This should always be at the same times if possible. In this way a fluctuating effect can be prevented.
It is also important that L-Dopa is taken at least one hour before or after a high-protein meal. Protein-rich foods interfere with the absorption of the active ingredient into the blood.
Side effects: Parkinson’s therapy with L-dopa is generally very well tolerated, especially at low doses. However, nausea can occur especially at the beginning of the therapy. However, this can be alleviated well with the active ingredient domperidone. Other drugs for nausea, such as metoclopramide, may not be used: They also cross the blood-brain barrier and can cancel the effect of L-dopa.
Other possible side effects of L-Dopa are lack of appetite, dizziness, increased drive and depression. Especially older people sometimes react to treatment with L-dopa with hallucinations, confusion and compulsive behaviour. The latter manifests itself, for example, as an addiction to gambling or buying, as a constant urge to eat or have sex, or as a compulsive ordering of objects.
Movement disorders (dyskinesias) are also possible side effects of L-dopa: the affected patients twitch involuntarily or make jerky movements that they cannot prevent. The longer someone is treated with L-Dopa, the more frequent and severe such movement disorders become.
Long-term treatment with L-dopa can also cause the effect of the drug to begin to fluctuate (fluctuations in effect): sometimes Parkinson’s patients can no longer move at all (“OFF phase”), then again completely normally (“ON phase”).
In such cases it may help to change the dosage scheme of L-Dopa. Or the patient switches to a retarded L-dopa preparation: the retard tablets release the active substance more slowly and over a longer period of time than “normal” (unretarded) L-dopa preparations. The treatment then usually works more evenly again.
In the event of fluctuations in the effect of L-dopa (ON-OFF phases) and/or movement disorders, the doctor can also give the patient a portable medication pump: this automatically channels the levodopa through a thin probe directly into the duodenum, where it is absorbed into the blood (duodenal probe). The active substance is therefore administered continuously to the patient. In this way, very even levels of the active ingredients in the blood can be achieved. This reduces the risk of effect fluctuations and movement disorders. However, a duodenal tube also carries risks, for example for peritonitis. Therefore, it is only used in selected cases and by experienced doctors.
An alternative to pump therapy is “deep brain stimulation” (see below).
In patients younger than 70 years, Parkinson’s therapy is usually started with so-called dopamine agonists. Only later does the switch to the more effective L-Dopa take place. This delays the occurrence of movement disorders such as those caused by prolonged use of L-Dopa.
Dopamine agonists are chemically similar to the messenger substance dopamine. They easily pass the blood-brain barrier and dock at the same binding sites (receptors) of the nerve cells as dopamine. That is why they also have a similar effect.
Most dopamine agonists used in Parkinson’s therapy are taken orally (for example, as tablets). This applies, for example, to pramipexole, piribedil and ropinirole. Other agents are administered as a patch (rotigotine) or by injection or infusion (apomorphine).
Side effects: Dopamine agonists are less well tolerated than L-dopa. For example, they cause water retention in the tissue (edema), constipation, drowsiness, dizziness and nausea. Like L-dopa, dopamine agonists can cause hallucinations, confusion and compulsive behavior, especially in the elderly.
Dopamine agonists can also trigger fluctuations in effect (fluctuations with ON-OFF phases) during prolonged use. But this happens much less often than with L-dopa. The fluctuating effect can be compensated for by adjusting the dosage of the dopamine agonists or by switching the patient from tablets to an active ingredient patch (with rotigotine).
There is another possibility in case of fluctuations in effect: In addition to the tablets, the patient receives injections of apomorphine into the subcutaneous fatty tissue (subcutaneously). Apomorphine can quickly relieve Parkinson’s symptoms, which remain disturbing despite taking the tablets. Possible side effects are nausea, vomiting, increased or newly occurring movement disorders (dyskinesia), dizziness, hallucinations, etc.
If all these attempts cannot compensate for the fluctuations in effect, the patient may be given a portable drug pump (apomorphine pump). Via a thin tube and a fine needle, it releases the active ingredient continuously (usually over 12 to 18 hours) into the subcutaneous fatty tissue on the abdomen or thigh.
So far, comprehensive studies on this apomorphine pump therapy are still lacking. Studies show that it can significantly shorten the daily OFF phases (in which the patient can hardly move at all). Movement disorders (dyskinesia) can also be reduced by the apomorphine pump.
Possible side effects are mainly skin reactions at the needle insertion site, which may be severe (painful redness, boils, tissue death = necrosis, etc.). Some patients also complain of nausea, vomiting, circulation problems and hallucinations.
MAO-B inhibitors (like selegiline) inhibit the enzyme monoaminooxidase-B (MAO-B), which normally breaks down dopamine. In this way, the dopamine level in the brain of Parkinson’s patients can be increased.
MAO-B inhibitors are less effective than levodopa or dopamine agonists. They are therefore only suitable as sole Parkinson’s therapy for mild symptoms (usually in the early stages of the disease). However, they can be combined with other Parkinson’s drugs (such as L-dopa).
Side effects: MAO inhibitors are considered to be well tolerated. They have only mild and reversible side effects. These include sleep disorders, because the drugs increase the drive. Therefore, MAO-B inhibitors should be taken earlier in the day. Then sleep in the evening will not be disturbed.
COMT inhibitors (such as entacapone) are prescribed together with L-Dopa. They also block an enzyme that breaks down dopamine (the so-called catechol-O-methyl transferase = COMT). In this way COMT inhibitors prolong the effect of dopamine.
The active ingredients are mainly prescribed to reduce fluctuations in efficacy (fluctuations) under therapy with L-dopa. So they are drugs for advanced stages of Parkinson’s disease.
Side effects: COMT inhibitors are usually well tolerated. Possible adverse effects include diarrhoea, nausea and vomiting.
The so-called anticholinergics were the first drugs used for Parkinson’s therapy. Today they are not prescribed so often.
Due to the dopamine deficiency in Parkinson’s disease, other nerve messengers are – relatively speaking – in surplus. This applies to acetylcholine, for example. This causes, among other things, the typical tremor in patients. It can be relieved with anticholinergics because these inhibit the action of acetylcholine in the brain.
Side effects: Anticholinergics can have various side effects. These include, for example, dry mouth, dry eyes, reduced (rarely increased) sweating, bladder emptying disorders, constipation, palpitations, light-sensitive eyes, thinking disorders and confusion.
Especially older people often do not tolerate anticholinergics very well. Therefore, the drugs are preferably prescribed to younger patients.
Just like acetylcholine, the messenger substance glutamate is also present in a relative surplus in Parkinson’s disease due to dopamine deficiency. So-called NMDA antagonists (amantadine, budipine) help against this. They block certain docking sites of glutamate in the brain and thus reduce its effect.
NMDA antagonists are used in early stages of primary Parkinson’s disease.
Side effects: Possible adverse effects of amantadine include restlessness, nausea, loss of appetite, dry mouth, reticular reticular bluish skin changes (livedo reticularis), confusion and psychosis (especially in elderly patients). Budipine can cause dangerous cardiac arrhythmia.
Deep Brain Stimulation (DBS)
Deep Brain Stimulation (THS) is a surgical procedure in the area of the brain. It is sometimes performed in idiopathic Parkinson’s syndrome. The English term is “Deep Brain Stimulation” (DBS).
Deep brain stimulation involves the insertion of small electrodes into specific areas of the brain during an operation. They are supposed to positively influence (either stimulate or inhibit) the pathological activity of nerve cells. Deep brain stimulation thus functions in a similar way to a pacemaker. It is therefore sometimes called a “brain pacemaker” (although this term is not quite correct).
Deep brain stimulation comes into consideration when:
- fluctuations in effectiveness (fluctuations) and involuntary movements (dyskinesia) cannot be alleviated with medication, or
- the tremor cannot be eliminated by medication.
In addition, the patient must also meet other requirements. For example, he must not show early symptoms of dementia. His general physical condition must be good. In addition, Parkinson’s symptoms (except tremor) must respond to L-dopa.
Experience shows that the procedure can effectively relieve the symptoms of many patients and significantly improve their quality of life. The effect seems to continue in the long term. This does not mean, however, that deep brain stimulation can cure Parkinson’s – the disease continues to progress even after surgery.
By the way: Originally, deep brain stimulation was mainly used for advanced Parkinson’s disease. In the meantime, however, studies have shown that it is also well suited for patients under 60 years of age in whom L-dopa therapy has only recently begun to show fluctuations in effect and cause movement disorders.
How does the procedure work?
Deep brain stimulation is performed in specialized clinics (THS centers). Before the operation, a stable metal frame is firmly fixed to the patient’s head. During the actual operation, the frame is firmly attached to the operating table. This keeps the head in exactly the same position the whole time. This is necessary to be able to work with the medical instruments as precisely as possible (“stereotactic brain surgery”).
Now a computer tomography (CT) or magnetic resonance imaging (MRT) of the head clamped in the frame is performed. The computer can be used to calculate the exact angle and depth at which the electrodes need to be inserted into the brain so that the electrode tips are in the right place. The “right place” is usually a tiny area in the brain called the nucleus subthalamicus (NST).
Next comes the actual operation: the neurosurgeon drills two small holes in the skull using a special drill bit in order to insert the tiny electrodes above them. This sounds brutal, but is not associated with pain for the patient. He’s awake during the whole operation. This is necessary so that the surgeon can check the correct placement of the electrodes in a test.
The next day, the pulse generator is implanted under general anaesthetic under the skin on the collarbone or upper abdomen. It is connected to the electrodes in the brain via small cables. The cables run under the skin.
The pulse generator continuously emits current to the electrodes. Depending on the current frequency, this stimulates or inhibits the areas at the ends of the electrodes. This immediately relieves the main motor symptoms of Parkinson’s disease, i.e. slowed movement, muscle stiffness and tremor. If necessary, the current frequency can be readjusted with a remote control.
If the intervention does not have the desired effect, the electrodes can be removed again or the pulse generator switched off.
Possible complications and side effects
In general, deep brain stimulation seems to be more successful in patients before the age of 50 and to cause fewer complications than in older people.
The most important complication that can result from the brain surgery itself is bleeding in the skull (intracranial bleeding). In addition, the insertion of the pulse generator and cables can cause an infection. Then the system usually has to be temporarily removed and the patient treated with antibiotics.
In almost every patient, temporary side effects occur after the procedure, when the system is still adjusted. These can be, for example, paraesthesias. However, these often only occur directly after the pulse generator is switched on and then disappear again.
Other mostly temporary effects are, for example, confusion, increased drive, a flattened mood and apathy. Sometimes so-called impulse control disorders also occur. This includes, for example, an increased sexual desire (hypersexuality). In some patients, deep brain stimulation also triggers mild speech disorders, ataxia, dizziness, and gait and standing insecurity.
Further therapy methods
Various treatment concepts can also help Parkinson’s patients to retain their mobility, speech ability and independence in everyday life for as long as possible. The most important procedures are:
Physiotherapy: Physiotherapy includes many different techniques. For example, patients can use suitable exercises to train their balance and safety when walking. Strength and stretching exercises are also useful. The speed and rhythm of the movements can also be specifically trained.
Speech therapy: Many patients develop a speech disorder during the course of Parkinson’s disease. For example, they speak in a remarkably monotonous and very quiet way or repeatedly experience blockages when speaking. A speech therapy can help here.
Occupational therapy: The aim of occupational therapy is to enable Parkinson’s patients to remain independent in their personal environment for as long as possible. For example, the living space can be adapted so that the patient can find his way around better. In addition, stumbling blocks such as carpets are removed. The occupational therapist also develops strategies together with the affected person to help them cope better with their everyday life with the disease. For example, he shows patients how to use aids such as stocking pullers or buttoning aids. In addition, the therapist advises the relatives how they can support the Parkinson’s patient in everyday life.
Treatment of concomitant diseases
Parkinson’s syndrome often affects older people. They usually also suffer from other diseases such as high blood pressure, heart failure (cardiac insufficiency), elevated blood lipid levels or diabetes. These concomitant diseases must also be treated professionally. This has a positive effect on the quality of life and life expectancy of patients.
Parkinson therapy: What can you do yourself?
As with most chronic complaints and diseases, the same applies to Parkinson’s disease: those affected should actively deal with their disease and inform themselves about its causes and treatment options. In many cases, it is the fear of uncertainty that puts a particular strain on patients. The more you learn about the disease, the sooner the feeling of powerlessness over progressive Parkinson’s disappears.
Unfortunately, the disease is currently not curable. With the right treatment, however, a largely normal life is possible for many patients.
You can read here what you yourself can contribute to an effective therapy:
“Be open about your illness. Many people with Parkinson’s disease initially find it very difficult to accept the disease and deal with it openly. Instead, they try to hide the symptoms. But in this way you put yourself under unnecessary pressure. Talking openly about your condition with friends, family and work colleagues will take a tremendous burden off your shoulders.
“Find out about the disease. The more you know about PD, the less scary it may seem to you. Even as a relative of a Parkinson’s patient you should inform yourself about the disease. In this way you can support your relatives effectively and meaningfully.
“Join a Parkinson’s support group. Those who are able to communicate regularly with other affected people often cope better with the disease.
” Keep fit. You can maintain a good general condition, you will remain physically active. Regular exercise (such as walking) and light endurance sports are sufficient. The relatives can support the patient in this.
“Use small aids in everyday life. Many Parkinson’s symptoms make everyday life difficult. This includes the so-called “freezing” – the person concerned can no longer move. This is where visual stimuli on the floor, such as glued-on footprints, or acoustic rhythm generators (“left, two, three, four”) help. Important for fellow human beings: It makes no sense to rush or pull the patient. This rather prolongs the “freezing” episode.
“Eat a healthy diet. People with PD often eat and drink too little because they are clumsy and slow. Some people also want to avoid the strenuous trip to the toilet if possible. For a healthy general condition, however, it is very important that you drink enough fluids (about two litres a day) and eat a balanced diet.
Parkinson: Specialist clinics
People with Parkinson’s syndrome should be treated in a specialist clinic if possible. Doctors and other staff there are specialised in the disease.
Parkinson: examinations and diagnosis
If you suspect that you or a relative has Parkinson’s disease, it is advisable to consult a specialist doctor. The specialist for diseases of the nervous system is the neurologist. It is best to see a neurologist who specialises in the diagnosis and treatment of Parkinson’s disease. Some neurological clinics also have their own consultation hours or outpatient clinics for Parkinson’s patients.
During the first visit, the neurologist will take the patient’s medical history (anamnesis) in consultation with you or the affected relative. This discussion is extremely important for the diagnosis of Parkinson’s disease: If the patient describes his or her symptoms in detail, the doctor can assess whether it could actually be Parkinson’s disease. Possible questions from the doctor are, for example:
- Since when approximately does the tremor of the hands/legs exist?
- Do you have the feeling that your muscles are constantly tense?
- Do you have pain, for example in the shoulder or neck area?
- Do you find it difficult to keep your balance when walking?
- Do you find fine motor activities (e.g. buttoning a shirt, writing) increasingly difficult?
- Are you having trouble sleeping?
- Have you noticed that your sense of smell has deteriorated?
- Have relatives already been diagnosed with Parkinson’s disease?
- Are you taking any medication, for example because of psychological problems? (antipsychotics, “dopamine antagonists” like metoclopramide)
Physical and neurological examination
In addition to the medical history interview, a physical and neurological examination will follow. In this process, the doctor generally checks the function of the nervous system: for example, he tests the patient’s reflexes, the sensitivity (sensitivity) of the skin and the mobility of muscles and joints. He pays particular attention to the main symptoms of Parkinson’s disease:
Slowed movements (bradykinesis) are very characteristic of Parkinson’s disease. The doctor recognizes them by observing your gait, gestures and facial expressions. He may ask you to walk a few feet into the examination room. He can also assess whether you are “shaky on your feet” (postural instability).
To determine whether your muscles are noticeably stiff (rigor), the doctor will check whether your joints can be moved smoothly. In Parkinson’s disease, muscle tension is greatly increased, so that the muscles resist when the doctor tries to move a joint (such as the elbow). This phenomenon is also known as the cogwheel phenomenon (see above: “Parkinson: symptoms”).
During the physical examination, the doctor will determine whether you have a tremor at rest (rest tremor). Important for the diagnosis of Parkinson’s disease is the distinction between rest tremor (as occurs in Parkinson’s disease) and other types of tremor. This includes, for example, the so-called intention tremor: When the cerebellum is damaged, the hand begins to tremble as soon as the person concerned tries to perform a targeted movement with it. At rest, however, the hand does not tremble.
Parkinson test (L-dopa test)
To support the diagnosis of Parkinson’s disease, sometimes the so-called L-dopa test is performed. Patients receive the dopamine precursor L-dopa (levodopa) once. This is the drug that belongs to the standard therapy for Parkinson’s disease. In some patients the movement disorders and stiff muscles improve shortly after taking the product (about half an hour later). Then there is probably an idiopathic Parkinson’s syndrome (note: rest tremor cannot always be alleviated with levodopa).
However, the L-dopa test has only limited value in the diagnosis of Parkinson’s disease. Because some people have Parkinson’s disease but do not respond to the test. Then the result is false negative. Conversely, the L-dopa test can also be positive for diseases other than Parkinson’s disease. This is true, for example, for some (but not all) patients with so-called multisystem atrophy. In this progressive disease, nerve cells in various regions of the brain die off. This can cause atypical Parkinson’s syndrome.
Because of these problems, the L-dopa test is not routinely recommended in Parkinson’s disease diagnosis. Another reason is that it can have side effects such as nausea and vomiting. To prevent this, patients are usually given the anti-emetic Domperidone before the test.
The L-dopa test can also help in planning therapy for Parkinson’s disease: if Parkinson’s disease is detected, the test can be used to check how well the patient responds to L-dopa. But here again, one should not expect a clear test result. Some patients do not respond to the test (negative result), but can still be treated well with L-Dopa later.
By the way: Instead of the L-dopa test, the apomorphine test is occasionally used to diagnose Parkinson’s disease. Here it is tested whether the movement disorders improve after an apomorphine injection. If so, this speaks for an idiopathic Parkinon syndrome. However, the same applies here as for the L-dopa test: not every Parkinson’s patient is tested positive. Side effects such as nausea, vomiting or drowsiness may also occur.
Computer tomography (CT) or magnetic resonance imaging (MRT) can be used to visualize the patient’s brain. This may help to rule out other possible causes for the suspected Parkinson’s symptoms, such as a brain tumour. Brain imaging therefore helps to distinguish idiopathic Parkinson’s syndrome from secondary Parkinson’s or other neurodegenerative diseases (such as atypical Parkinson’s).
Special examinations may also be carried out for this purpose. This includes, for example, SPECT (Single Photon Emission Computed Tomography), a nuclear medical examination: the patient is first administered a radioactive substance. This can be used to visualise those nerve endings in the brain that are receding in Parkinson’s disease (DAT-SPECT). This can provide information in unclear cases.
If the diagnosis of Parkinson’s is unclear, the doctor sometimes orders a special variant of positron emission tomography (PET): FDG-PET. The abbreviation FDG stands for fluorodeoxyglucose. This is a radioactively marked simple sugar. It is administered to the patient before the brain is imaged using PET. This examination can especially help to clarify an atypical Parkinson’s syndrome. However, the investigation is not officially approved for this purpose. It is therefore only used in justified individual cases (“off-label use”).
Less complex and cheaper than these special examinations is the ultrasound examination of the brain (Transcranial Sonography, TCS). It helps to detect idiopathic Parkinson’s syndrome at an early stage and to differentiate it from other diseases (such as atypical Parkinson’s syndromes). However, the doctor should have extensive experience with this examination. Otherwise, he may not be able to interpret the results of the investigation correctly.
How is the diagnosis of Parkinson’s finally made?
It is still often difficult to make a clear diagnosis of Parkinson’s without doubt. One reason for this is that there are many different diseases that cause similar symptoms to Parkinson’s disease.
The doctor-patient consultation (anamnesis interview) and the physical-neurological examination are essential for the diagnosis of Parkinson’s disease. The further examinations serve primarily to rule out other reasons for the symptoms. Only if the symptoms can be well explained by Parkinson’s disease and no other causes can be found, the Parkinson’s diagnosis (Idiopathic Parkinson’s syndrome) can be made.
Special case: Genetically caused Parkinson’s
As mentioned in the “Causes” section, genetically determined forms of Parkinson’s disease are very rare. However, they can be determined with a molecular genetic examination. Such an investigation may be considered if:
- the patient develops Parkinson’s disease before the age of 45 or
- at least two first-degree relatives suffer from Parkinson’s.
In these cases it is suspected that Parkinson’s disease is caused by a gene mutation.
Healthy relatives of a patient with genetic Parkinson’s disease can also undergo a genetic test. In this way, it can be determined whether they too have the triggering gene mutation. However, such a genetic test to assess the personal risk of Parkinson’s disease may only be carried out after the person concerned has received detailed genetic advice from a specialist.
Course of disease and prognosis
The idiopathic Parkinson’s syndrome is a progressive disease that has not yet been cured. Depending on the symptoms, physicians differentiate between four forms of the disease:
- akinetic-rigid type: motionlessness and muscle stiffness are the most common symptoms, while tremor is hardly or not at all present.
- Tremordominant type: The main symptom is tremor.
- Equivalence type: Motionlessness, muscle stiffness and tremor are approximately equally pronounced.
- monosymptomatic rest tremor: tremor at rest is the only symptom. Very rare progressive form.
In addition to the form of progression, the age at which the disease develops plays an important role in Parkinson’s disease: progression and prognosis are influenced by whether the disease breaks out at a relatively young age (for example, from the age of 40) or at a later age.
It is much more likely that the Parkinson’s drugs trigger movement disorders (dyskinesias) and fluctuations in effect (fluctuations) in younger patients. This is especially true for the akinetic-rigid type of Parkinson’s disease, for which an early age of onset is typical. On the other hand, L-dopa is very effective in these patients.
The tremor dominance type is different: those affected respond relatively poorly to L-dopa. On the other hand, Parkinson’s progresses more slowly in them than in the other forms of the disease. Thus, the tremor dominaz type has the most favorable prognosis.
Parkinson: life expectancy
In the mid-1970s, modern Parkinson’s drugs such as levodopa were developed. This changed the prognosis for “real” (idiopathic) Parkinson’s disease: life expectancy and quality of life of patients improved thanks to the new active ingredients. According to statistics, an optimally treated Parkinson’s patient today has almost the same life expectancy as a healthy person of the same age: If someone is diagnosed with Parkinson’s disease today at the age of 63, he can expect to live another 20 years. For comparison: in the middle of the last century, patients lived on average just over nine years after diagnosis.
The increased life expectancy in idiopathic Parkinson’s syndrome is due to the fact that modern medications largely eliminate the patients’ essential complaints. In the past, such complaints often led to complications, which then caused the patient to die prematurely. An example: Parkinson’s patients who could hardly move (akinesia) were often bedridden. This confinement to bed increases the risk of dangerous diseases such as thrombosis or pneumonia massively.
The improved life expectancy as described here refers only to idiopathic Parkinson’s syndrome (= “classical Parkinson’s”). Atypical Parkinson’s syndromes, in which the affected persons do not respond or hardly respond at all to treatment with L-dopa, usually progress more rapidly. They usually have a much worse prognosis.
- Parkinson – the exercise book: Staying active with movement exercises (Elmar Trutt, 2017, TRIAS)
- Parkinson: A guide for those affected and their families (Willibald Gerschlager, 2017, Facultas / Maudrich)