Parkinson’s disease is one of the most common neurodegenerative diseases. There are about 10 million people worldwide with Parkinson’s disease. There are over 15,000 of them in Switzerland. An increase is expected in the next few years. Most are over the age of 60 when diagnosed. Men are affected somewhat more often than women.
In rare cases (less than 10%), the disease is inherited and traced to a certain genetic defect.
People’s life expectancy with Parkinson’s disease is approximately the same as that of healthy people.
What happens in the body
Parkinson’s disease is a neurodegenerative disease in which there is progressive damage to dopamine-producing nerve cells in the brain (substantia nigra). The resulting lack of dopamine information substance leads to various motor disorders. You can treat these disorders with L-Dopa’s treatment, the precursor of the substance dopamine.
At the onset of the disease, nerve cells in other parts of the brain that have nothing to do with dopamine production also die. This leads to several symptoms (e.g., autonomic disorders, pain, sleep disorders, psychological symptoms), which become more stressful and extensive for those affected as the disease progresses.
Causes of Parkinson’s disease
Although Parkinson’s disease was first described by the English physician James Parkinson in 1817, years and research have been looking for causes ever since. They are still unknown.
The interaction between genetic predisposition and the influence of environmental factors is discussed. So far, no single factor has been identified as the sole driver.
Symptoms can be alleviated, but disease progression cannot be slowed or stopped.
Symptoms of Parkinson’s disease
The symptoms of Parkinson’s disease are very individual. The disease does not progress at the same rate in all patients. Therefore, each affected person has “his” Parkinson’s disease with its own individual symptoms.
Slowing down (bradykinesia, akinesia)
Movements and movements become increasingly difficult. Particularly affected are automatic movements such as walking or swallowing, which healthy people perform without thinking. But it also affects facial expressions and fine motor skills (closing keys, using mobile phones). Akinesia increases as the disease progress.
The tension of the entire musculature is constantly increasing. Patients have the impression that their limbs are “paralyzed.” Bending posture is also an expression of increased muscle stiffness.
Tremor at rest
Shivering at rest, which occurs in about two-thirds of those affected, is usually one-sided at first. The arms are usually more affected than the legs. With targeted movements, the tremor temporarily disappears.
Postural instability (postural instability)
Human balance is provided by a complex system of regulation in which the automatically running retention and adjustment reflexes play a central role. The balance in Parkinson’s disease is disturbed, especially in the disease’s latter stages. Fall is a dangerous consequence.
Other common symptoms of Parkinson’s disease are non-motor symptoms: neuropsychiatric problems (e.g., Depression, anxiety), vegetative-autonomic disorders (e.g., blood pressure regulation, digestion, bladder function, and temperature regulation), sleep and wakefulness rhythm disorders, and sensory disorders (e.g., sense of smell disorder, pain). In the advanced stage, cognitive changes are not uncommon.
Development of Parkinson’s disease
Parkinson’s disease begins insidiously and with individual, not always clearly differentiated symptoms. Typical early symptoms include trembling in one arm, recurrent cramps in some limbs, chronic neck tension, sleep disturbances, general fatigue and lethargy, persistent constipation, odor disturbances, and discomfort when walking, and depression.
As cell loss in the substantia nigra progresses steadily, the symptoms also increase steadily. As you walk, the stairs become smaller and smaller. Fine work (brushing teeth, closing buttons, writing, handicrafts) becomes increasingly difficult; speech often becomes quieter and more obscure, facial expressions are reduced, the upper body can be tilted forward.
It is important to know that the disease’s progression – and therefore the picture of the symptoms – is very individual. The course and severity of the disease vary greatly from patient to patient.
The first stage of the disease
In the first two to five years of the disease, the so-called “honeymoon phase,” drug treatment is simple and reliably effective so that most patients can lead an almost normal life. At this stage of the disease, the medication’s effects are balanced throughout the day. There is little or no fluctuation.
Unfortunately, as the disease progresses, the drug’s duration of action decreases. Symptom control becomes more unbalanced and fluctuates throughout the day. Fluctuations also result in involuntary excessive movement (dyskinesia), which alternates with pronounced immobility phases. It is not uncommon for non-motor symptoms (depression, cognitive disorders, digestive disorders, fluctuations in blood pressure, etc.) to increase significantly.
Due to fluctuations in strength, the intervals between medications must be shortened, or medications with a prolonged effect must be combined. To achieve the best possible setting, the neurologist must give the sick person enough time to describe the symptoms and time. Active cooperation between doctor and patient is necessary.
Hospital settings in specialized Parkinson’s disease centers may be useful in later stages. There, the drug’s effect and the symptoms can be precisely monitored over a longer period, and the therapy can be adjusted accordingly. Neurorehabilitation is also very important, where speech therapy, occupational, and physiotherapy are used. Targeted exercise and therapy plans help those affected to cope more easily with their daily lives.
If control of symptoms is no longer possible with tablet drugs, pumps (apomorphine or droxidopa) or surgical methods (deep brain stimulation / DBS or focused ultrasound / FUS) are increasingly being used. These machine treatments have been shown to improve quality of life.
Parkinson’s disease almost always starts with a disorder. They are uncharacteristic and only gradually take shape. The contact person at this stage is the family doctor.
Important: Observe changes and symptoms over a period of time and write them down in a diary. Show the doctor. He needs as much information as possible from you: the earlier the diagnosis, the better.
The diagnosis of idiopathic Parkinson’s syndrome is primarily made clinically, based on symptom history and neurological examination. Additional examinations such as MRI of the skull, SPECT brain, DAT scan, and ultrasound support the diagnosis.
For a clinical diagnosis, bradykinesia and at least 1 additional symptom such as tremor or numbness must be detected. The L-dop response is an important supporting diagnostic criterion.
Atypical Parkinson’s syndrome
Nearly four of the five classic Parkinson’s symptoms listed above are included in diagnosing Parkinson’s disease. Significantly rarer atypical Parkinson’s syndromes are therefore less well known.
In addition to the most common and well-known Parkinson’s disease – another term: idiopathic Parkinson’s disease (iPS) – there are several atypical Parkinson’s syndromes (APS). The demarcation is difficult. A distinction is made between:
- multiple system atrophy (MSA) with subtypes
- progressive supranuclear palsy (PSP) with subtypes
- corticobasal degeneration (CBD) with subtypes
- dementia with Levi’s bodies (Levi body dementia, LBD)
Only a pathological diagnosis from brain tissue (biopsy or autopsy) is a reliable diagnosis of atypical Parkinson’s syndrome (APS). This cannot be reported in a living patient. Thus, the diagnosis is now based solely on clinical criteria with an error rate of up to 30 percent. Uncertainty in the diagnosis is reflected in the fact that in the case of several atypical Parkinson’s syndromes, there are different lists of criteria for the same syndrome. It should be considered when diagnosing that periodically international revisions of valid clinical diagnostic criteria (CBD, PSP) are performed. These criteria have never been prospectively confirmed or clinically pathologically confirmed for each APS. Studies in recent years have also shown an expansion of the possible spectrum of clinical symptoms and findings so that early diagnosis of all APS is increasingly difficult.
Differentiation of different APS
Differentiation of different APS from each other and idiopathic Parkinson’s syndrome (iPS) would be significant in the disease’s early stages. This is due to the prognosis and the corrector adequate therapy. Also, early and unambiguous diagnosis for scientific reasons, such as investigating the cause or looking for new therapeutic options, would greatly benefit. Because despite decades of research, the causes and mechanisms of APS disease are still unexplained. On the therapeutic side, the current possibilities are also minimal.
Currently, available imaging procedures (MRI) and laboratory diagnostic methods do not contribute to a very reliable and early diagnosis. Accordingly, research moves towards the search for new biomarkers (measured values specific to a particular APS). Biomarkers are used, for example, in genetic analyzes or special laboratory methods in the examination of serum and nerve water, as well as in special functional imaging processes.