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Parkinson’s syndrome: symptoms, course, therapy

by Josephine Andrews
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In Parkinson’s disease , certain nerve cells in the brain die. Affected people only move more slowly, the muscles become stiff. Arms and legs begin to tremble at rest. Many sufferers also have trouble thinking and become demented. Read here what Parkinson’s is, how the neurological disease manifests and progresses and what treatment options are available.

ICD codes for this disease:

ICD codes are internationally valid codes for medical diagnoses. They can be found, for example, in doctor’s letters or on certificates of incapacity for work.

G21 G22 G20

quick overview

  • Symptoms: Slowed movements, lack of movement, muscle stiffness, tremors at rest, lack of stability in the upright posture, rigid facial expressions
  • Course and prognosis: progressive, incurable disease; Prognosis depends on the course; with optimal treatment, life expectancy is often normal
  • Causes: death of dopamine – producing cells in the brain ; often unknown causes, sometimes medication and toxins or genetic changes are the trigger
  • Investigations: Physical and neurological examination, L-Dopa test, computed tomography (CT), magnetic resonance imaging (magnetic resonance imaging, MRI)
  • Treatment: medication (such as levodopa), physical therapy , speech therapy , occupational therapy , deep brain stimulation (DBS)

What is Parkinson’s?

Parkinson’s syndrome, also known as Parkinson’s disease, Parkinson’s disease or – colloquially – shaking palsy, is one of the most common diseases of the central nervous system. As the neurodegenerative disease progresses, certain nerve cells in the brain that produce the neurotransmitter dopamine die off .

Among other things, dopamine is responsible for controlling movements. If there is a dopamine deficiency, as more and more dopamine-producing nerve cells are lost, the movement disorders typical of Parkinson’s disease occur. These mainly include slow movements, stiff muscles and muscle tremors.

Men and women are about equally affected by Parkinson’s disease. The average age at the time of diagnosis is about 60 years. Only about ten percent of those affected become ill before the age of 40.

What are the symptoms of Parkinson’s?

Parkinson’s disease usually develops gradually. In many people, the disease is initially announced by non-specific early symptoms before the typical movement disorders appear.

Early stage Parkinson’s symptoms

Signs of progressive brain disease appear in some people years before the main symptoms:

  • People talk, laugh, or gesture while dreaming because they are not blocked from doing these activities during dream sleep (REM sleep behavior disorder) like healthy people are.
  • The sense of smell is reduced or lost completely (hyposmia/anosmia).
  • There is discomfort and pain in muscles and joints, especially in the neck, back and extremities.
  • Activities such as getting up, washing or dressing take longer than before.
  • The handwriting looks cramped and gets smaller, especially at the end of a line or page.
  • Affected people feel stiff, shaky and insecure.
  • The facial expressions decrease and the face loses its expression
  • Physical symptoms such as constipation and visual disturbances (eg disturbed color vision) occur.
  • Those affected are often tired and exhausted and move little.
  • Emotional changes occur. For example, those affected are depressed or irritable for no particular reason, withdraw socially and neglect their hobbies.

Many of these early Parkinson’s symptoms are very unspecific. There are also many other causes possible, such as advanced age. Therefore, they are often not recognized as early signs of Parkinson’s.

The most important early sign is the REM sleep behavior disorder: Those who show this form of sleep disorder generally have an increased risk of neurodegenerative diseases. These are progressive diseases associated with the loss of nerve cells. Most people with REM sleep behavior disorder later develop Parkinson’s disease. Others develop a certain form of dementia (Lewy body dementia).

Main symptoms (cardinal symptoms) in Parkinson’s disease

In the advanced stage of Parkinson’s disease, the typical movement disorders come to the fore. Relatives and friends often notice this earlier than the person affected. The symptoms of Parkinson’s usually begin unilaterally, ie on only one side of the body. Later they also spread to the other side. They also become more pronounced as the disease progresses.

The typical Parkinson’s symptoms are:

  • Slowed movements (bradykinesis) up to lack of movement (hypokinesis) or immobility (akinesia)
  • Stiff muscles (rigorous)
  • Muscle tremors at rest (Parkinson’s tremor)
  • Lack of stability in the upright posture (postural instability)

Slowed Movements (Bradykinesia)

All body movements are unnaturally slow. This means, for example, that people with Parkinson’s disease walk conspicuously slowly and in small steps. Over time, the gait becomes shuffling and sufferers walk hunched over. They are also slow to sit up and stand up with difficulty. Sometimes those affected are suddenly blocked in their movements – they seem to freeze. Doctors refer to this as “freezing”.

The changes in the movement sequences also affect gestures and facial expressions. The face increasingly looks like a rigid mask. Those affected usually speak quietly and monotonously, making it difficult to understand them. They often have problems swallowing, for example when drinking or eating. Another sign of Parkinson’s is impaired fine motor skills: those affected find it difficult, for example, to write something, button their coat or brush their teeth .

If the body movements are particularly slow or the person concerned is sometimes completely motionless, doctors speak of akinesia (akinesia).

Stiff muscles (rigorous)

There is no paralysis in Parkinson’s disease. Muscle strength is therefore largely retained. However, the muscles are permanently tense, even at rest. Doctors refer to this condition as rigor. It is painful for those affected. The shoulder and neck areas are particularly affected.

The muscle stiffness can be proven by the so-called gear wheel phenomenon: When the doctor tries to move the arm of the person concerned, the stiff muscles prevent a smooth movement. Instead, the arm can only be moved a little bit and jerkily. It almost feels like there’s a gear in the joint, allowing movement only up to the next notch at a time and then locking into place.

Muscle tremors at rest (resting tremor)

In Parkinson’s disease, arms and legs typically begin to tremble in resting situations. This is why the disease is also known colloquially as “shaking paralysis”. One side of the body is usually more affected than the other. Also, the arm usually trembles more than the leg.

Parkinson’s tremor typically occurs at rest. This makes it possible to distinguish Parkinson’s from other diseases with tremors .

Lack of stability of the upright posture

Everyone unconsciously corrects their posture at any time when walking or standing upright. The whole thing is controlled by so-called positioning and holding reflexes, ie automatic, involuntary movements that are triggered by certain stimuli.

A disturbance of these righting and holding reflexes is characteristic of Parkinson’s disease. Affected people therefore have trouble keeping themselves upright (postural instability), are unsteady when walking and fall easily.

Visible symptoms in Parkinson’s disease
These symptoms often indicate Parkinson’s disease. Especially the bent-over posture and small steps are easy to recognize as an outsider.

Parkinson’s: accompanying symptoms

In addition to the main symptoms of Parkinson’s disease, some people experience other symptoms. However, these are not specific to Parkinson’s disease, but also occur in other diseases. These include, for example:

  • Mental effects and personality changes such as listlessness, depression or anxiety
  • Excessive sebum formation on the face, the skin appears greasy and shiny (ointment face)
  • Speech disorders (often soft, monotonous, slurred speech)
  • Eye movement disorders and eye shaking (eye tremor)
  • dysphagia
  • sleep disorders
  • In advanced disease, disorders of the autonomic nervous system (eg bladder weakness, constipation, erectile dysfunction, drop in blood pressure)

Parkinson’s dementia

People with Parkinson’s are more susceptible to dementia than the general population: around a third of those affected also develop dementia during the course of the disease.

The symptoms of Parkinson’s dementia primarily include impaired attention and slowed thinking . This is an important difference to Alzheimer’s – the most common form of dementia. Alzheimer’s sufferers mainly suffer from memory disorders. In Parkinson’s dementia, on the other hand, these occur only in later stages of the disease.

You can read more about this topic in the article Dementia in Parkinson’s .

Course of the disease and prognosis

Since more and more nerve cells die off over time in Parkinson’s disease, the disease progresses slowly, but not in phases like multiple sclerosis, for example. There is still no cure for Parkinson’s disease. All therapies alleviate the symptoms, but do not stop the destruction of the dopamine-producing nerve cells. Depending on the symptoms, physicians differentiate between four forms of Parkinson’s disease :

  • Akinetic-rigid type: The main symptoms are immobility and muscle stiffness, while there is little or no tremor.
  • Tremor Dominant Type: The main symptom is shaking (tremor).
  • Equivalence Type: Motionlessness, muscle stiffness, and tremors are about equally pronounced.
  • Monosymptomatic tremor at rest: Tremor at rest is the only symptom (very rare form).

The tremor dominance type has the most favorable prognosis: Although those affected respond relatively poorly to therapy with L-Dopa, this form progresses more slowly than the others.

In addition to the course of the disease , the age of onset plays an important role in Parkinson’s disease. The course and prognosis depend on whether the disease breaks out at a relatively young age or at an older age. After about ten years of disease progression, life expectancy in Parkinson’s disease is slightly reduced.

In the final stages of the disease, there is often a need for care. As a rule, however, this is only the case after a long course of the disease from around 20 years of age. In most cases, the cause is dementia, but also a high symptom burden.

Parkinson’s: life expectancy

According to statistics, an optimally treated person with Parkinson’s syndrome today has almost the same life expectancy as a healthy person of the same age. Today, if someone is diagnosed with Parkinson’s at the age of 63, it is estimated that they will 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 medication largely eliminates the main symptoms of those affected. In the past, such complaints often led to complications and premature death. For example, people with Parkinson’s who were unable to move (akinesia) were often bedridden. Being confined to bed massively increases the risk of dangerous diseases such as thrombosis or pneumonia.

The improved life expectancy as described here only relates to idiopathic Parkinson’s syndrome (= “classic Parkinson’s”). Atypical Parkinson’s syndromes, in which those affected do not respond or hardly respond to treatment with L-Dopa, usually progress more quickly. They usually have a much worse prognosis.

Driving with Parkinson’s?

People with Parkinson’s are only allowed to drive a car after successful therapy or in the early stages of the disease. The reason is the sometimes severe motor impairments, but also other symptoms such as dementia, visual and attention disorders. But the drugs used in Parkinson’s also affect driving ability through their side effects, for example through increased tiredness, sleep attacks, loss of impulse control and aggressive behavior.

It is therefore necessary for those affected to have their fitness to drive assessed by a doctor or psychologist every 4 years.

What are the causes of Parkinson’s?

Doctors also call Parkinson’s disease primary or idiopathic Parkinson’s syndrome (IPS) . “Idiopathic” means that there is no tangible cause for the condition. This “real” Parkinson’s makes up about 75 percent of all Parkinson’s syndromes. A distinction must be made between the rare genetic forms of Parkinson’s , ” secondary Parkinson’s syndrome ” and ” atypical Parkinson’s syndrome “.

Idiopathic Parkinson’s: dopamine deficiency

Parkinson’s disease originates in a specific region of the brain called the “black matter” (substantia nigra) in the midbrain . The substantia nigra contains special nerve cells that produce the neurotransmitter dopamine. Dopamine is very important for controlling movement.

The cause of Parkinson’s syndrome is that more and more dopamine-producing nerve cells die off. To this day, however, it is not exactly clear why this happens. It is known that a faulty protein accumulates in the nerve cells and damages them. Recent study results also indicate that – similar to an autoimmune disease – a dysregulation of the immune system may be involved in the development of Parkinson’s disease.

Due to the progressive cell death, the dopamine level in the brain continues to fall – a dopamine deficiency develops. The body compensates for this for a long time: only when about 60 percent of the dopamine-producing nerve cells have died does the dopamine deficiency become noticeable through the movement disorders typical of Parkinson’s.

But the lack of dopamine itself is not the only cause of Parkinson’s: it also disturbs the sensitive balance of the neurotransmitters. Because there is less and less dopamine available, the amount of the messenger substance acetylcholine, for example, increases. Experts suspect that this is the reason for the shaking (tremor) and muscle stiffness (rigor) in Parkinson’s disease.

That’s what happens with Parkinson’s
The neurotransmitter dopamine in the brain is essential for the coordination of movement in humans. In idiopathic Parkinson’s there is not enough dopamine. Therefore, sufficient signal transmission cannot take place to perform movements normally.

The neurotransmitter imbalance in Parkinson’s disease may also be the reason why many sufferers also become depressed. However, the connection between Parkinson’s disease and depression has not yet been conclusively clarified.

Genetic forms of Parkinson’s

When a family member has Parkinson’s disease, many relatives feel insecure. You wonder if Parkinson’s is hereditary. In the vast majority of cases, however, Parkinson’s is the idiopathic Parkinson’s described above. Heredity plays no role in this sporadically occurring form of the disease, experts believe.

The situation is different with the so-called monogenetic forms of Parkinson’s. Each of them is caused by a change (mutation) in a specific gene. Parents pass this on to their children. Monogenetic forms of Parkinson’s are therefore hereditary. They are also often referred to as familial Parkinson’s syndrome . Luckily they are rare.

Secondary Parkinson’s Syndrome

In contrast to idiopathic Parkinson’s, symptomatic (or secondary) Parkinson’s syndrome has clearly identifiable causes. Some important triggers and risk factors include:

  • Drugs that inhibit dopamine (dopamine antagonists), such as neuroleptics (used to treat psychosis) or metoclopramide (for nausea and vomiting), lithium (for depression), valproic acid (for seizures), calcium channel blockers (for high blood pressure). )
  • Other diseases such as brain tumors, inflammation of the brain (eg as a result of AIDS), underactive parathyroid glands (hypoparathyroidism) or Wilson’s disease (copper storage disease)
  • Poisoning, for example with manganese or carbon monoxide
  • brain injuries

The influence of alcohol on the risk of developing Parkinson’s disease has not been conclusively clarified. However, current study data indicate that there is probably no connection. There may be an increased risk with excessive alcohol consumption.

Atypical Parkinson’s Syndrome

The atypical Parkinson’s syndrome develops in the context of various neurodegenerative diseases. These are diseases in which nerve cells in the brain progressively die off. In contrast to idiopathic Parkinson’s syndrome, this cell death does not only affect the “substantia nigra”, but also other brain regions. Therefore, in addition to Parkinson’s-like symptoms, other symptoms also occur in atypical Parkinson’s syndrome.

Examples of neurodegenerative diseases that sometimes trigger an atypical Parkinson’s syndrome are:

  • Lewy body dementia
  • Multiple System Atrophy (MSA)
  • Progressive Supranuclear Palsy (PSP)
  • Corticobasal degeneration

Such diseases have a significantly poorer prognosis than the “real” (idiopathic) Parkinson’s syndrome.

The drug L-Dopa, which works very well in idiopathic Parkinson’s, helps little or not at all in atypical Parkinson’s.

investigations and diagnosis

It is still often difficult to make a definitive diagnosis of Parkinson’s. One reason is that there are many different disorders that cause symptoms similar to Parkinson’s disease.

The doctor-patient conversation (anamnesis conversation) and the physical-neurological examination are indispensable for the diagnosis of Parkinson’s disease. The further examinations serve primarily to rule out other reasons for the symptoms. Parkinson’s disease is only idiopathic if the symptoms can be explained well by Parkinson’s and the doctor can’t find any other causes.

The right person to contact if you suspect Parkinson’s syndrome is a neurologist, ie a specialist in diseases of the nervous system.

medical history

During the first visit, the neurologist will discuss the medical history with the person concerned or their relatives ( anamnesis ). The doctor asks the following questions, for example:

  • How long has the shaking (tremor) in the hands/legs existed?
  • Does the person concerned have the feeling that the muscles are constantly tense?
  • Does the person concerned have pain, for example in the shoulder or neck area?
  • Does the affected person find it difficult to keep their balance when walking?
  • Are fine motor activities (eg buttoning a shirt, writing) becoming increasingly difficult?
  • Are you having trouble sleeping?
  • Has your sense of smell deteriorated?
  • Has a family member been diagnosed with Parkinson’s disease?
  • Does the person concerned take medication, for example due to psychological problems?

Physical and neurological examination

The anamnesis interview is followed by a physical and neurological examination. The doctor checks the general function of the nervous system: He tests, for example, the reflexes, the sensitivity (sensitivity) of the skin and the mobility of the muscles and joints.

He pays particular attention to the main symptoms of Parkinson’s, such as slow movements, an unsteady gait pattern or conspicuous gestures and facial expressions. The doctor also detects the tremors at rest (resting tremor) that are typical of Parkinson’s disease during the physical examination.

Various tests help the doctor to confirm the Parkinson’s diagnosis. These include the following tests:

  • Pull test: The doctor checks the patient’s posture control by gently pulling on their shoulder.
  • Pendulum test: The doctor shakes the arms of the person concerned. pendulum movement is reduced in people with Parkinson’s disease.
  • Wartenberg test: The doctor raises the person’s head in a supine position and then suddenly releases it. In people with Parkinson’s disease, it relapses slowly or not at all.

Parkinson’s test (L-dopa test and apomorphine test)

To help diagnose Parkinson’s, doctors sometimes do what’s called an L-dopa test or an apomorphine test. Those affected receive the dopamine precursor L-Dopa or apomorphine once, ie two drugs that are used in the therapy. In Parkinson’s disease, the symptoms sometimes improve shortly after ingestion.

However, both tests are only of limited value in the diagnosis of Parkinson’s disease. Some people have Parkinson’s but don’t respond to the tests. Conversely, the L-Dopa test is sometimes positive for other diseases. Because of these problems, both tests are not routinely used in Parkinson’s diagnostics.

imaging procedures

The brain can be imaged using computed tomography (CT) or magnetic resonance imaging (MRI). This helps the doctor rule out other possible causes of the symptoms, such as a brain tumor.

The doctor may also carry out special examinations. This includes, for example, SPECT (single photon emission computed tomography), a nuclear medical examination. The affected person first receives a radioactive substance. This can be used to visualize those nerve endings in the brain that regress in Parkinson’s disease.

The ultrasound examination of the brain (transcranial sonography, TCS) is less complex and less expensive. It helps to recognize an idiopathic Parkinson’s syndrome in the early stages and to differentiate it from other diseases (such as atypical Parkinson’s syndromes). However, the doctor should have extensive experience with this examination in order to interpret the result correctly.

Special case: Genetic Parkinson’s disease

The rare genetically determined forms of Parkinson’s can be identified with a molecular genetic test . Such an examination may be considered if:

  • the person concerned develops Parkinson’s disease before the age of 45 or
  • at least two first-degree relatives have Parkinson’s disease.

In these cases, the suspicion arises that Parkinson’s disease is caused by a genetic change.


Parkinson’s is currently not curable. However, the symptoms can be significantly alleviated and the quality of life improved with various treatment options. The doctor adapts the Parkinson’s therapy individually to each person affected. Because the symptoms vary from person to person and progress and at different speeds.

The doctor usually treats Parkinson’s with medication, although mild symptoms sometimes do not require any therapy at all in the beginning. Which active ingredients are used depends primarily on the age of the person affected. Sometimes a neurosurgical intervention is also useful – the so-called deep brain stimulation (DBS or deep brain stimulation, DBS).

The individual Parkinson’s treatment often includes 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’s therapy with drugs

There are various drugs for Parkinson’s therapy. They help against symptoms such as slow movements, rigid muscles and tremors. However, they do not prevent the dopamine-producing nerve cells from dying and the disease from progressing.

The typical Parkinson’s symptoms are triggered by a lack of dopamine in the brain. They can therefore be alleviated by either administering the messenger substance as a drug (eg 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 lack of dopamine. They largely eliminate the typical Parkinson’s symptoms.

L-Dopa (levodopa)

L-Dopa is very effective and has hardly any side effects. Doctors mainly prescribe it for people over the age of 70. In younger sufferers, on the other hand, they only use L-dopa very cautiously. The reason is that treatment with L-Dopa sometimes triggers movement disorders (dyskinesia) and fluctuations in effects after a few years.

L-Dopa is a precursor of dopamine and is always used in combination with another active ingredient, a so-called dopa decarboxylase inhibitor (such as benserazide or carbidopa). This prevents L-Dopa from being converted into dopamine in the blood. This is important because, unlike L-dopa, dopamine is unable to cross the blood-brain barrier and get into the brain. The same applies to the dopa decarboxylase inhibitor, by the way. The conversion of L-Dopa in the brain is therefore not affected.

Fluctuations in the effect of L-Dopa

Long-term treatment with L-Dopa sometimes leads to the effect of the drug beginning to fluctuate (fluctuations in effect): sometimes it is no longer possible for those affected to move (“OFF phase”), then it functions completely normally again ( “ON phase”).

In such cases, it helps to change the dosage or switch to a slow-release L-Dopa preparation: The slow-release tablets release the active ingredient more slowly and over a longer period of time than “normal” (non-retarded) L – Dopa preparations.

A drug pump is also helpful in the event of fluctuations in the effect of L-Dopa (ON-OFF phases) and/or movement disorders. It automatically directs the levodopa directly into the duodenum via a thin tube, where it is absorbed into the blood. The person concerned receives the active substance continuously, which means that there are very even active levels in the blood. This reduces the risk of fluctuations in effect and movement disorders.

dopamine agonists

In those affected who are younger than 70 years of age, the doctor usually starts Parkinson’s therapy with so-called dopamine agonists. In this way, the occurrence of movement disorders, such as those triggered by prolonged use of L-Dopa, can be delayed.

Dopamine agonists are chemically similar to the neurotransmitter dopamine. However, they easily pass the blood-brain barrier and dock at the same binding sites (receptors) of the nerve cells as dopamine. Therefore, they also have a similar effect. Dopamine agonists are available, for example, as tablets, but also as active ingredient patches, injections or infusions .

With prolonged use, dopamine agonists sometimes trigger fluctuations in their effects. But this happens much less frequently than with L-Dopa. The fluctuating effect can be compensated for by the doctor adjusting the dosage, prescribing a different preparation or using a medication pump.

MAO-B inhibitors

MAO-B inhibitors inhibit the enzyme mono-amino-oxidase-B (MAO-B), which normally breaks down dopamine. In this way, the level of dopamine in the brain of people with Parkinson’s disease can be increased. MAO-B inhibitors are less effective than levodopa or dopamine agonists. As sole Parkinson’s therapy, they are therefore only suitable 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).

COMT inhibitors

COMT inhibitors are prescribed along with L-Dopa. They also block an enzyme that breaks down dopamine (the so-called catechol-O-methyl-transferase = COMT). This is how COMT inhibitors prolong the action of dopamine. The active ingredients are mainly prescribed to reduce fluctuations in the effect (fluctuations) during therapy with L-Dopa. So they are drugs for advanced Parkinson’s stages.


The so-called anticholinergics were the first drugs that doctors used to treat Parkinson’s disease. Today they are not prescribed as often.

Due to the dopamine deficiency in Parkinson’s, other neurotransmitters are – relatively speaking – in excess. This applies to acetylcholine, for example. This causes, among other things, the typical shaking (tremor) in those affected. It can be relieved with anticholinergic drugs because they inhibit the action of acetylcholine in the brain.

NMDA antagonists

Like acetylcholine, the neurotransmitter glutamate is also present in relative excess in Parkinson’s due to the dopamine deficiency. So-called NMDA antagonists help against this. They block certain docking points of glutamate in the brain and thus reduce its effect. Doctors prescribe NMDA antagonists, especially in the early stages of Parkinson’s disease.

A change in medication or acute comorbidities rarely lead to an akinetic crisis. This is a sudden worsening of symptoms with total inability to move. Those affected are also no longer able to speak or swallow. Akinetic crisis is an emergency and requires immediate hospital treatment.

The drugs used in Parkinson’s sometimes cause psychosis. It is estimated that up to 30 percent of all those affected experience such a crisis. It first manifests itself through restless sleep with vivid dreams, later also through hallucinations , delusions and states of confusion. In this case, it is important to see a neurologist immediately.

Deep brain stimulation

Deep brain stimulation (DBS) is a surgical procedure in the area of ​​the brain. It is sometimes performed in idiopathic parkinsonian syndrome. During an operation, a doctor inserts small electrodes into certain areas of the brain. They should positively influence (either stimulate or inhibit) the pathological activity of the nerve cells.

This means that deep brain stimulation works in a similar way to a pacemaker . It is therefore sometimes referred to as a “ brain pacemaker ” (although this term is not entirely correct).

Deep brain stimulation can be considered when:

  • Effect fluctuations (fluctuations) and involuntary movements (dyskinesia) cannot be alleviated with medication or
  • the shaking (tremor) does not respond to medication.

In addition, the applicant must meet other requirements. For example, he must not show any early symptoms of dementia. His general physical condition must be good. In addition, the Parkinson’s symptoms (apart from the tremor) must respond to L-dopa.

Experience has shown that the procedure effectively alleviates the symptoms in many of those affected and significantly improves their quality of life. This effect also seems to persist over the long term. However, this does not mean that deep brain stimulation cures Parkinson’s disease: the disease progresses even after the procedure.

Originally, deep brain stimulation was mainly used in patients with advanced Parkinson’s disease. In the meantime, however, studies have shown that it is also suitable for those under the age of 60, in whom the L-Dopa therapy has only recently started to show fluctuations in the effect and causes movement disorders.

Possible complications and side effects of deep brain stimulation

In general, deep brain stimulation appears to be more successful and less likely to cause complications in people under the age of 50 than in older people.

The main complication of brain surgery is bleeding inside the skull (intracranial hemorrhage). Also, inserting the pulser and cables sometimes triggers an infection . Then it is necessary to temporarily remove the system and treat the infection with antibiotics.

Almost everyone affected experiences temporary side effects after the procedure. These include, for example, abnormal sensations (paresthesia). However, these often only appear immediately after switching on the pulse generator and then disappear again.

Other mostly temporary effects are, for example, confusion, increased drive, flattened mood and listlessness (apathy). Sometimes so-called impulse control disorders also occur. This includes, for example, increased sexual desire (hypersexuality). In some people, deep brain stimulation also triggers slight speech disorders, impaired movement coordination ( ataxia ), dizziness and unsteadiness when walking and standing.

Other therapy methods

Various treatment concepts also help people with Parkinson’s syndrome to maintain their mobility, ability to speak and independence in everyday life for as long as possible. The most important procedures are:

  • Physiotherapy (physiotherapy), for example to improve balance and safety when walking and to improve strength and speed
  • Speech therapy for speech disorders, for example in the case of remarkably monotonous and very soft speech or speech blocks
  • Occupational therapy, to better cope with everyday life with the illness and to remain independent in one’s personal environment for as long as possible (for example, the therapist shows the person concerned how to use certain aids and, together with the person concerned, adapts the living space so that they can find their way around better.)

Parkinson’s: treatment in specialist clinics

If possible, people with Parkinson’s disease should be treated in a specialist clinic. Doctors and other employees there specialize in the disease.

There are now numerous clinics in Germany that offer acute treatment and/or rehabilitation for people affected by Parkinson’s. Some of them are certified by the German Parkinson Association (dPV). It is awarded to hospitals and rehabilitation facilities that have special diagnostic and therapeutic offers for people with Parkinson’s and related diseases.

A selected list of specialist clinics for people with Parkinson’s can be found in the Parkinson’s Clinic article .

Living with Parkinson’s: what can you do yourself?

In addition to medical treatment, the behavior of those affected also potentially contributes a lot to effective therapy:

Be open about your illness. Many people with Parkinson’s initially find it very difficult to accept the disease and deal with it openly. Instead, they try to hide the symptoms. This puts you under unnecessary pressure. Talking to friends, family and co-workers about your condition will take a tremendous burden off your shoulders.

Find out about the disease. Because in many cases, the fear of the unknown is particularly stressful. The more sufferers learn about the disease, the sooner the feeling of powerlessness in the face of the progressive disease disappears. As a relative of a Parkinson’s patient, you should also find out about the disease in order to support your relative effectively and meaningfully.

Join a Parkinson’s support group. Those who have the opportunity to regularly exchange ideas with other affected people often cope better with the disease.

stay fit Try to stay in good general health by staying physically active. Regular exercise (such as walks) and light endurance sports are sufficient for this.

Use small help in everyday life. Many Parkinson’s symptoms make everyday life difficult. This includes the so-called “freezing” (freezing) – the person concerned is no longer able to move. Visual stimuli on the floor, such as footprints glued on, or acoustic rhythm generators (“left, two, three, four”) help here. Important for fellow human beings: It makes no sense to hurry or pull the person concerned. This tends to prolong the “freeze” episode.

Eat healthy. People with Parkinson’s often eat and drink too little because they are clumsy and slow. Some 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 liquid (about two liters a day) and eat a balanced diet.


Since the causes of idiopathic parkinsonian syndrome are not known, there are no specific measures to prevent the disease.

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