Dr. med. Fabian Sinowatz is a freelance contributor to NetDoktor’s medical editorial team.
Martina Feichter studied biology with pharmacy as an optional subject in Innsbruck and also immersed herself in the world of medicinal plants. From there it was not far to other medical topics that still captivate her today. She trained as a journalist at the Axel Springer Akademie in Hamburg and has been working for NetDoktor since 2007 – first as an editor and since 2012 as a freelance writer.
At Parkinson’s disease certain nerve cells in the brain die. Patients can only move slowly, their muscles become stiff. Arms and legs begin to tremble in silence. Many patients also develop problems thinking and become demented. Read here: What is Parkinson’s exactly? Who is Affected? How he expresses himself? What treatment options are available?
Parkinson’s disease: brief overview
- Typical symptoms: Slowed movements, lack of movement, muscle stiffness, trembling at rest, lack of stability in upright posture, rigid facial expressions
- Causes: In Parkinson’s disease: death of dopamine-producing cells in the brain; in secondary Parkinson’s disease: other diseases, drugs, or poisoning; in genetic Parkinson’s disease: genetic changes
- Examinations: Physical and neurological examination, L-dopa test, computer tomography (CT), keratin spin tomography (magnetic resonance imaging, MRI)
- Treatment: Medication (such as levo-dopa), physiotherapy, speech therapy, occupational therapy, deep brain stimulation (THS)
Parkinson’s disease: symptoms
Stiff muscles, slowed movements and trembling hands are typical features of Parkinson’s disease.
Parkinson’s early symptoms
Signs of the progressive brain disease can appear years before the main symptoms. Such early Parkinson’s symptoms are:
- REM sleep behavior disorder: normally a person is "paralyzed" during dream sleep. In REM sleep behavior disorder, the dreamed movements are partially performed (speaking, laughing, gesticulating, etc.).). This can be dangerous for the affected person and the sleeping partner.
- The sense of smell is diminished or fails completely (hyposmia/anosmia).
- Pain in muscles and joints (dysesthesias), often in the shoulder and arm area
- The arms vibrate diminished when walking.
- Standing up, washing, dressing, eating, etc. take longer than before.
- Visual disturbances (such as impaired color vision)
- Handwriting appears cramped and becomes smaller, especially at the end of a line or page.
- Tiredness, fatigue
- stiff, unsteady feeling, shakiness
- The patient withdraws and neglects his hobbies.
Many of these early Parkinson’s symptoms are very unspecific. So they can also have many other causes (such as advanced age). Therefore, they are often not recognized as early signs of Parkinson’s disease.
Driving with Parkinson’s disease
Three questions to
Can you still drive a car with Parkinson’s?
This question is asked very often by Parkinson’s patients and is unfortunately not so easy to answer. Essentially, it depends on the stage of the disease and the patient’s symptoms. If a patient has only few limitations after the initial diagnosis and is well controlled with medication, there is no reason not to drive. If fluctuations in effect or relevant concentration and memory disorders occur, I advise against it in principle.
How do I tell if I can still drive a car??
Interestingly, the first clues are often given by the partners of the affected person, who no longer feel safe as a passenger. I then like to advise to take a driving lesson. That’s when you get feedback from the driving instructor, who can assess the situation well. Of course, patients can also take an official test for fitness to drive – but if they fail, they must surrender their driver’s license.
Can you, as a doctor, forbid the affected person to drive??
No, to pronounce a restricted fitness to drive as z.B. in patients with epileptic seizures is usually not possible in patients with Parkinson’s disease. It is always a difficult decision for the doctor; on the one hand, one does not want to restrict the patient’s independence, but on the other hand, one also does not want to endanger anyone in traffic. I always actively discuss this with patients – but ultimately this is based on their voluntary choice.
Senior Physician at the Neurology Clinic and Polyclinic in Cologne, Head of the Movement Disorders and Deep Brain Stimulation Unit there, Head of the Cologne Parkinson’s Network
REM sleep behavior disorder
REM sleep behavior disorder is considered the most important early sign: those who exhibit this form of sleep disorder are generally at increased risk for so-called neurodegenerative diseases. These are progressive diseases associated with the loss of nerve cells. Most people with REM sleep behavior disorder later develop PD. Others develop a specific form of dementia (Lewy body dementia).
Parkinson’s disease: main symptoms
The symptoms of Parkinson’s disease usually develop gradually. Relatives and friends often notice them earlier than the patient himself.
Most often, Parkinson’s signs begin on one side, that is, on only one side of the body. Later they spread to the other side as well. In the course of the disease, they also become more pronounced.
The typical Parkinson’s symptoms are:
- slowed movements (bradykinesis) up to a lack of movement (hypokinesis) resp. immobility (akinesia)
- Stiff muscles (rigor)
- Muscle tremor at rest (Parkinson’s tremor)
- Lack of stability of the upright posture (postural instability)
Slowed movements (bradykinesis): All body movements occur unnaturally slowly. This means, for example, that people with Parkinson’s disease walk remarkably slowly and in small steps. Over time, the gait becomes shuffling, and patients walk bent forward. This is one of the most noticeable symptoms. Parkinson’s patients can also sit down and stand up 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" (Engl. for "freezing").
PD symptoms also affect gestures and facial expressions: the face increasingly looks like a rigid mask. The affected person usually speaks quietly and monotonously, making it more difficult to understand them. They often have problems swallowing, for example when drinking or eating. Another Parkinson’s sign is impaired fine motor skills: for example, those affected have difficulty writing, buttoning their coat, or brushing their teeth.
If the body movements are particularly slowed down or the patient is partially completely motionless, physicians speak of akinesia (akinesia).
Stiff muscles (rigor): In Parkinson’s disease, there is no paralysis, but muscle strength is largely preserved. But the muscles are permanently tense, even at rest. This is painful for those affected. Especially the shoulder and neck area can hurt.
The muscle stiffness can be detected by the so-called "Parkinson’s disease" test cogwheel phenomenon: If the doctor tries to move the patient’s arm, this is prevented by the stiff muscles. This is why the arm can only be moved a little at a time and jerkily. It almost feels as if there is a cog in the joint, allowing movement only until the next notch at a time and then locking in place. The cogwheel phenomenon is usually tested in the elbow or wrist joint. It is a typical sign of Parkinson’s disease, but can also occur in other diseases.
muscle tremor at rest (resting tremor): In Parkinson’s disease, arms and legs typically begin to tremble in resting situations. That is why the disease is also called "shaking palsy". One side of the body is usually more affected than the other. In addition, the arm usually trembles more than the leg.
Parkinson’s tremor characteristically occurs at rest. This is how Parkinson’s can be distinguished from other diseases with tremor. If, for example, the hand does not tremble at rest, but as soon as one wants to make a specific movement, physicians speak of the so-called intention tremor. Its cause is damage or dysfunction in the cerebellum.
By the way, most people who tremble do not have Parkinson’s disease or any other identifiable neurological disorder. The cause of this "essential tremor" is unknown.
Lack of stability of upright posture: Unconsciously, everyone corrects their posture at all times when walking or standing upright. The whole thing is controlled by so-called positional and retentive reflexes. Reflexes are automatic movements triggered by certain stimuli. These are unconscious, involuntary movements or muscle tensions. The holding and positioning reflexes of the human body are responsible for automatically balancing the body and not falling, even when moving.
In Parkinson’s disease, the position and hold reflexes are typically impaired. Affected persons therefore have difficulty keeping themselves upright in a stable manner. This is called postural instability. This is the reason why Parkinson’s patients can no longer "catch" sudden, unpredictable movements without problems can occur, for example, when stumbling or in the event of a sudden gust of wind. Therefore, they are unsteady when walking and fall easily.
These symptoms often indicate Parkinson’s disease. Especially the bent forward posture and small steps can be easily recognized as an outsider.
Parkinson’s disease: accompanying symptoms
The main Parkinson’s symptoms are sometimes accompanied by other complaints:
Parkinson’s patients are more likely to have Depression as healthy people and as people with other chronic diseases. Sometimes depression develops during the course of Parkinson’s disease. In other patients, it precedes the motor symptoms (slowing of movement, etc.) ahead.
In addition, Parkinson’s disease can cause intellectual performance decreases and a Dementia arise (see below). The affected person has increasing difficulty thinking. But it’s important to remember that most healthy people also think more slowly and have a harder time remembering things as they age. This does not necessarily have to be a sign of Parkinson’s.
In many Parkinson’s patients, the facial skin produces excessive sebum. This makes it appear greasy and shiny. Doctors speak of the so-called "ointment face." The patient’s face looks as if he or she has 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. Thus it can happen that urinate involuntarily (incontinence) and the patients may experience Wetting themselves at night (enuresis). But the opposite is also possible: some patients have Problems urinating (urinary retention).
The intestine is often sluggish in Parkinson’s, so that a Constipation develops. Such constipation can also occur as an early sign of Parkinson’s disease.
In men sometimes show potency problems (Erectile Dysfunction). This impotence can be caused by the disease itself as well as by the Parkinson’s medication.
All of the above-mentioned accompanying symptoms can also be triggered by other diseases, not only by Parkinson’s disease.
Parkinson’s patients are more susceptible to dementia than the general population: about one-third of patients also develop dementia during the course of 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 primarily include a disturbed attention and a slowed thinking. This is an important difference from Alzheimer’s disease – the most common form of dementia. Alzheimer’s patients mainly suffer from memory disorders. In Parkinson’s dementia, however, these only occur in the later stages of the disease.
You can read more about this topic in the article Dementia in Parkinson’s disease.
Doctors also call Parkinson’s disease "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. To be distinguished from this are the rare genetic forms of Parkinson’s disease, that"secondary parkinsonism" and that"Atypical Parkinson’s syndrome". They are described briefly below.
Parkinson’s disease – the first warning signals
Christiane Fux studied journalism and psychology in Hamburg, Germany. Since 2001, the experienced medical editor has been writing magazine articles, news and non-fiction on every conceivable health topic. In addition to her work for NetDoktor, Christiane Fux is also involved in prose writing. Her first crime novel was published in 2012, and she also writes, designs and publishes her own crime games.
First signs of "shaking palsy
shoulder and neck pain
Pills against tremor& Co.
Substitute for dopamine
Idiopathic Parkinson’s: Dopamine deficiency
Parkinson’s disease originates in a specific region of the brain, the so-called "black substance (substantia nigra) in the midbrain. This brain region contains a lot of iron and the pigment melanin. Both color the substantia nigra conspicuously dark (compared to the otherwise light brain tissue).
In the substantia nigra there are special nerve cells that produce the nerve messenger (neurotransmitter) dopamine. Dopamine is very important for the control of movements. In idiopathic Parkinson’s, more and more dopamine-producing nerve cells die off. Why, is not known.
As a result of this progressive cell death, the level of dopamine in the brain continues to drop – a Dopamine deficiency. 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, in some cases, no longer at all (akinesia).
But dopamine deficiency in itself is not the sole cause of Parkinson’s: it also causes the sensitive Balance of nerve messengers out of balance: Because less and less dopamine is present, the amount of the neurotransmitter acetylcholine, for example, increases in relative terms. Experts suspect that this is the reason for the tremor and rigidity in Parkinson’s disease.
The neurotransmitter dopamine in the brain is essential for movement coordination in humans. In idiopathic Parkinson’s there is too little dopamine present. Therefore, there cannot be sufficient signal transmission to perform movements normally.
The imbalance of neurotransmitters in Parkinson’s disease could also be responsible for the fact that many patients also become depressed. Because it is known that generally in depression the balance of the nerve messengers is disturbed. However, the connection between Parkinson’s disease and depression has not yet been conclusively clarified.
Parkinson’s causes: Many assumptions, little evidence
Why in Parkinson’s disease nerve cells in the "substantia nigra" are damaged die off, is still unclear. Research suggests that several factors are involved in the development of Parkinson’s disease.
For example, scientists have found that the nerve cells in Parkinson’s patients are 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 in Parkinson’s patients are not capable of breaking down these dangerous substances before they cause damage. Or the detoxification capacity of the cells is normal, but an excessive number of "free radicals" produced in Parkinson’s disease. In both cases, the cell-damaging substances could accumulate in the nerve cells and cause them to die off.
In addition, there are other possible causes of Parkinson’s that are currently being discussed and researched.
Genetic forms of Parkinson’s disease
When a family member has Parkinson’s disease, it is upsetting for many family members. They wonder whether Parkinson’s is hereditary. In the vast majority of cases, however, Parkinson’s is the idiopathic Parkinson’s described above. Experts believe that heredity is not an issue in this sporadic form of the disease.
The so-called monogenetic forms of Parkinson’s disease are different: each of them is caused by a mutation in a specific gene. These gene mutations can be passed on to the offspring. Monogenetic forms of Parkinson’s disease are thus hereditarily. They are often referred to as familial Parkinson’s syndrome designated. Fortunately they are rare.
Secondary Parkinson’s disease
In contrast to idiopathic Parkinson’s, symptomatic (or secondary) Parkinson’s syndrome has clearly identifiable causes. These include:
- Medications: Inhibitors of dopamine (dopamine antagonists) such as neuroleptics (to treat psychosis) or metoclopramide (to treat nausea and vomiting), lithium (to treat depression), valproic acid (to treat seizures), calcium antagonists (to treat high blood pressure)
- other diseases such as brain tumors, inflammation of the brain (e.g., as a result of AIDS), parathyroid hypofunction (hypoparathyroidism) or Wilson’s disease (copper storage disease)
- Poisoning, for example with manganese or carbon monoxide
- Injuries of the brain
Atypical Parkinson’s 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 does not only affect the substantia nigra, but also other brain regions. Therefore, in Atypical Parkinson’s Syndrome, in addition to Parkinson’s-like symptoms, other symptoms also occur.
Neurodegenerative diseases that can cause atypical Parkinson’s syndrome include:
- Lewy body dementia
- Multisystem atrophy (MSA)
- Progressive supranuclear palsy (PSP)
- Corticobasal degeneration
Such diseases have a much worse prognosis than the "real" one (idiopathic) Parkinson’s syndrome.
By the way: The drug "L-Dopa, that work very well in idiopathic Parkinson’s, help little or not at all in atypical Parkinson’s.
Parkinson’s therapy is adapted individually to each patient. Because the symptoms of the disease can vary from person to person and progress at different rates.
Mostly Parkinson’s is treated with Medication treated, with mild symptoms sometimes requiring no therapy at all in the beginning. Which agents are used depends above all on the age of the patient. Sometimes a neurosurgical intervention can also be useful – the so-called "L-Dop" Deep brain stimulation (deep brain stimulation, DBS).
In addition to medication and, if necessary, surgical measures, individual Parkinson’s treatment can include other building blocks. This includes for example Physiotherapy, Speech therapy and Occupational therapy. In any case, it makes sense to seek treatment in a special Parkinson’s clinic.
Parkinson’s therapy: medication
There are different medications for Parkinson’s therapy. They help against symptoms such as slowed movements, rigid muscles and tremors. However, they cannot prevent the death of nerve cells and thus the progression of the disease.
The typical Parkinson’s symptoms are triggered by a lack of dopamine in the brain. They can therefore be alleviated either by supplying the neurotransmitter as a drug (for example, in the form of L-dopa) or by preventing the breakdown of the dopamine present (MAO-B inhibitors, COMT inhibitors). Both mechanisms compensate for the lack of dopamine. It largely eliminates the typical Parkinson’s symptoms.
It makes no sense to give Parkinson’s patients the missing dopamine directly as an injection or tablet: the neurotransmitter is transported to the brain via the bloodstream. But it can’t cross the protective blood-brain barrier, so it can’t get directly into nerve tissue. The precursor of dopamine but is able to do so: this L-dopa (levodopa) is therefore suitable for the treatment of Parkinson’s disease. Once in 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 hardly any side effects. It is usually taken in the form of tablets, capsules or drops. Physicians prescribe it primarily for patients over the age of 70. Year of life. In younger patients, on the other hand, L-dopa is used only very cautiously. The reason is that treatment with L-dopa can cause movement disorders (dyskinesias) and fluctuations in effect (fluctuations in effect) after a few years (see side effects).
L-dopa is always combined with another active ingredient, a so-called Dopa decarboxylase inhibitors (like benserazide or carbidopa). This prevents L-dopa from being converted into dopamine in the blood before it reaches the brain. The dopa decarboxylase inhibitor itself is unable to cross the blood-brain barrier. In the brain, L-dopa can therefore be easily converted into dopamine.
Every Parkinson’s patient responds differently to L-dopa. Therefore, the dosage is determined on an individual basis: Therapy is started at a low dose and then gradually increased until the desired effect occurs.
Usually L-dopa has to be taken several times a day. This should always be at the same times, if possible. Here’s how to prevent a fluctuating effect.
It is also important that L-dopa be taken at least one hour before or after a high-protein meal. Protein-rich foods actually 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, especially at the beginning of the therapy Nausea occur. However, this can be alleviated well with the active ingredient domperidone. On the other hand, other anti-nausea drugs, such as metoclopramide, may not be used: They also cross the blood-brain barrier and can cancel out the effect of L-dopa.
Other possible side effects of L-dopa include lack of appetite, dizziness, increased drive and Depression. Older people in particular sometimes react to treatment with L-dopa with Hallucinations, Confusion and compulsive behavior. The latter manifests itself, for example, as an addiction to gambling or shopping, a constant urge to eat or have sex, or a compulsive ordering of objects.
Also Movement disorders (dyskinesias) are possible side effects of L-dopa: the affected patients twitch involuntarily or make jerky movements, which they can not prevent. The longer someone is treated with L-dopa, the more frequent and severe such movement disorders become.
Long-term treatment with L-dopa may also cause the drug’s effects 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 lower the Change dosage regimen of L-dopa. Alternatively, the patient may increase to a retarded L-dopa preparation The retard tablets release the active ingredient more slowly and over a longer period than "normal" tablets (unretarded) L-dopa preparations. The treatment then usually has a more uniform effect again.
If there are fluctuations in the effect of L-dopa (ON-OFF phases) and/or movement disorders, the doctor can also give the patient a portable Drug pump The levodopa is automatically administered via a thin tube directly into the duodenum, where it is absorbed into the blood (duodenal tube). The active ingredient is therefore administered to the patient continuously. In this way, very uniform levels of active ingredient can be achieved in the blood. This lowers the risk of fluctuations in effect and movement disorders. However, a duodenal tube also carries risks, for example for peritonitis. That is why it is used only in selected cases and by experienced physicians.
An alternative to pump therapy is deep brain stimulation (see below).
In patients younger than 70, Parkinson’s therapy is usually started with so-called dopamine agonists. Only later is there a switch to the more effective L-dopa. This delays the onset of movement disorders caused by the prolonged use of L-dopa.
Dopamine agonists are chemically similar to the neurotransmitter dopamine. They easily cross the blood-brain barrier and dock at the same binding sites (receptors) of the nerve cells as dopamine does. Therefore, they also have a similar effect.
Most dopamine agonists used in Parkinson’s therapy are taken orally (such as tablets). This is true, for example, of pramipexole, piribedil and ropinirole. Other representatives are administered as an active ingredient patch (rotigotine) or as an 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), Clog, Drowsiness, Dizziness And Nausea. Like L-dopa, dopamine agonists can cause side effects, especially in the elderly Hallucinations, Confusion and Obsessive-compulsive behavior trigger.
With prolonged use, dopamine agonists can also Fluctuations in effect (fluctuations with ON-OFF phases) triggered. But that 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 the tablets to a drug patch (with rotigotine).
There is another option for fluctuations in effect: The patient receives in addition to the tablets Injections with apomorphine into the subcutaneous fatty tissue (subcutaneous). Apomorphine can quickly relieve Parkinson’s symptoms that remain bothersome despite taking the tablets. Possible side effects include nausea, vomiting, increased or new movement disorders (dyskinesias), dizziness, hallucinations, etc.
If all these attempts fail to compensate for the fluctuations in effect, the patient may be given a portable drug pump (Apomorphine pump). It delivers the active substance continuously (usually over 12 to 18 hours) into the subcutaneous fatty tissue on the abdomen or thigh via a thin tube and a fine needle.
So far, comprehensive studies on this apomorphine pump therapy are still missing. Studies show that it can significantly shorten daily OFF periods (when the patient can hardly move). Movement disorders (dyskinesias) may also decrease with apomorphine pump.
Possible side effects are mainly skin reactions at the injection site of the needle, which can be severe in some cases (painful redness, nodule formation, death of tissue = necrosis, etc.).). Some patients also complain of nausea, vomiting, circulatory problems, and hallucinations.
MAO-B inhibitors (such as 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 in the case of 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 (reversible) side effects. They include sleep disturbances, because the drugs increase drive. MAO-B inhibitors should therefore be taken earlier in the day. Then the sleep in the evening is not disturbed.