The development of Parkinson’s disease – what happens in the body?

When suffering from idiopathic Parkinson’s (without discernible cause), the dopamine-producing nerve cells in the mesencephalon (substantia nigra) slowly die. The reason for this is still unknown. The falling dopamine level in the brain results in impaired communication between nerve cells and an imbalance of neurotransmitters. The body can compensate for this deficiency sufficiently for quite some time so that it goes unnoticed by the patient. The first typical symptoms occur once approximately 60 % of dopamine-producing nerve cells have died. It is hypothesized that this causes the shaking (tremor) that is so typical for Parkinson’s disease.

Nonspecific early symptoms of Parkinson’s disease

Even years before apparent symptoms appear, there may be unspecific symptoms indicating Parkinson’s:

• Changes in dream phases: Usually, the body is limp while we dream, almost as if paralyzed. It has been shown that years before Parkinson’s was diagnosed, patients would actually perform the actions they dreamt of (talking, laughing, gesturing).
• Sense of smell might be reduced or disappears completely.
• Inexplicable joint pain, especially in the arms
• Interference with color perception
• Change in handwriting: The longer the patient writes, the smaller and more illegible the writing becomes.
• Depression, fatigue, exhaustion
• Unspecific digestive issues

The most common symptoms of Parkinson’s disease

Slowness of movements (bradykinesia):

The patient’s movements become slower and the range of motion decreases (hypokinesia), which may worsen to total loss of motion (akinesia). Both voluntary and autonomic muscle control may be affected. All movements are unnaturally slow. The posture is stooped, steps are small, and/or patients scuttle or shuffle when they walk. Starting or stopping a movement is also difficult. Sudden stopping of a movement, so-called “freezing“, occurs frequently. This increases the risk of falling. Facial expressions and gestures are reduced; laughing and crying seem delayed and look like a grimace. The face seems to become an unmoving mask. The abilities to speak and swallow may also be affected. Fine motor function worsens: manipulating buttons or opening/closing zippers becomes difficult; writing becomes illegible; brushing teeth becomes impossible.

Reactions and accompanying movements are also affected. The patient doesn’t move his or her arms when walking or simply “falls” into a seat due to poor balance. Parkinson’s disease also reduces the speed of thought processes.

Stiff muscles:

Parkinson’s disease increases muscle tone, causing the body to become stiffer. Both contracting and stretching muscles may be affected. Deliberate relaxation is not possible. Passively moving parts of the body results in the so-called “cogwheel” phenomenon. The muscles relax in bursts, like a cogwheel. Typical for this stiffness of the muscles is the “floating pillow” sign. When the patient lies down on their back, they cannot put their head down. The muscles are so tense that the head seems to “float” above the pillow.

Shaking (tremor):

When relaxed, arms or legs may shake. One half of the body is often more severely affected than the other. Shaking usually occurs in the hands and arms.

Insufficient stability of posture (postural control):

Righting and postural reflexes are continuously and unconsciously correcting the position and posture of our body. This balancing process prevents falls. In patients with Parkinson’s disease, the righting and postural reflexes are interrupted. Patients struggle to remain upright. Sudden, unforeseen changes in movement can no longer be countered and corrected in time. Their gait becomes insecure, and they tend to fall more often.

Other symptoms:

Patients may also have difficulties swallowing or suffer from incontinence, insomnia, depression, and dementia. Hallucinations, delusions, and paranoia often accompany dementia.

Does Parkinson’s start in the intestines?

It is becoming more evident that the nervous system in the abdomen is closely linked to the brain. Animal studies were able to show that incorrectly shaped proteins (alpha-synucleins) form in the digestive tract and can spread along the vagus nerve into the brain. Whether Parkinson’s actually starts in the digestive tract and the consequences for treatment options remain open at this time.

How is Parkinson’s disease diagnosed?

Parkinson’s disease is often diagnosed based on its typical symptoms. The severity of the disease is assessed based on the Hoehn and Yahr Scale, amongst others. It records the disruption of movements. The Unified Parkinson’s Disease Rating Scale (UPDRS) is another standardized tool for recording clinical symptoms. 

Physicians and therapists may perform additional active and passive movement tests to get a clearer picture of the disease presentation and progression:

• Quick movements like screwing in a lightbulb are no longer possible (dysdiadochokinesis).
• Passive movement, such as of the elbow joint, results in the cogwheel phenomenon, i.e. the relaxation of muscles in short bursts.
• Tests to check balance and posture stability are also performed (Berg Balance Scale, Timed Up and Go Test).

Imaging technology such as CT or MRI can be used to exclude other diseases with similar symptoms.

If Parkinson’s is suspected but not confirmed, specific medication can be used to clarify the diagnosis. If the symptoms improve with medication, the patient likely has Parkinson’s. If no change is observed, there may be other causes for the Parkinson’s-like symptoms (secondary or atypical Parkinson’s syndrome).

Therapy options for Parkinson’s disease

Treatment for Parkinson’s disease must be tailored to the individual patient. Good success can be achieved with medication, physiotherapy, occupational therapy, speech therapy, and psychological support.

Medication

The goal of medication is to reduce the lack of dopamine in the brain. The neurotransmitter is either administered directly as medication or the breakdown of existing dopamine is inhibited. The active agents used depends mainly on the age of the patient. The goal of medication is symptom reduction.

Deep Brain Stimulation, DBS

If certain conditions are met, deep brain stimulation may be the method of choice for treating the symptoms of Parkinson’s. In a surgical procedure, small electrodes are implanted into certain areas of the brain. The so-called “leads” generate electrical impulses that control abnormal brain activity.

Non-medication based treatment

Physiotherapy, occupational therapy, speech therapy, and psychological support are essential parts of treating Parkinson’s. Interdisciplinary cooperation of different therapeutic and medical disciplines can considerably alleviate symptoms.Physiotherapy knows several techniques to improve agility, balance, coordination,  strength, and endurance. Technology-based therapy equipment can supplement other treatments.

When living with Parkinson’s disease, independent practice, continued participation in daily life, and support through therapeutic aids can improve the quality of life of patients. The goal is to maintain the independence of the patient in everyday situations for as long as possible.

Sources:

Parkinson Disease, 2020

Physiotherapy in Parkinson’s Disease: A Meta-Analysis of Present Treatment Modalities, 2020

In vivo distribution of α-synuclein in multiple tissues and biofluids in Parkinson disease, 2020

Deep Brain Stimulation in Parkinson’s Disease, 2019

Initiation of Parkinson’s disease from gut to brain by δ-secretase, 2019

Chronic stress-induced gut dysfunction exacerbates Parkinson’s disease phenotype and pathology in a rotenone-induced mouse model of Parkinson’s disease, 2018

Motor assessment in Parkinson’s disease, 2017