Parkinson’s disease
- Fysiobasen
- Sep 8
- 9 min read
Parkinson’s disease (PD) is a progressive, neurodegenerative disorder that primarily affects the basal ganglia – an area of the brain central to motor control. The condition is classified as a synucleinopathy, due to the accumulation of alpha-synuclein in neurons, and is the second most common neurodegenerative disease after Alzheimer’s. Its prevalence increases with age, and PD is the fastest-growing neurological diagnosis worldwide¹⁻³.
The classic presentation includes slowness of movement (bradykinesia) and either resting tremor or muscle stiffness (rigidity). Many patients also experience reduced sense of smell, sleep disturbances, mood changes, hypersalivation, constipation, and disrupted REM sleep with involuntary movements¹.
About 80% of patients with parkinsonism have Parkinson’s disease, while the remainder have other related neurodegenerative conditions, such as Lewy body dementia⁴.
Clinically relevant anatomy
Parkinson’s disease affects the basal ganglia, a network of nuclei that regulate motor function. The nuclear structures include the striatum (caudate and putamen), globus pallidus, substantia nigra, and subthalamic nucleus⁶⁻⁸.
The striatum receives afferent signals from large parts of the cerebral cortex and thalamus, as well as dopaminergic input from the substantia nigra pars compacta (SNc). Efferent signals then pass through the globus pallidus to the thalamus and motor areas of the cortex.
In Parkinson’s disease, there is a gradual loss of dopaminergic neurons in the SNc, leading to imbalance in this network and thus motor symptoms⁶.
Clinical presentation and course
Parkinson’s disease was first described in Western medicine by James Parkinson in 1817, and is known from ancient Chinese and Indian medicine⁰.
There is no single test that can confirm the diagnosis. The diagnosis is based on clinical criteria, and motor symptoms often appear late in the disease course. Many patients develop early non-motor symptoms many years before diagnosis¹².
The most typical motor symptoms include:
Resting tremor: Often begins on one side and disappears with use of the extremity¹.
Bradykinesia: A sense of slowness in movement and difficulty with daily tasks¹.
Rigidity: Typical “lead-pipe” or “cogwheel” stiffness, often evident during passive movement¹.
Gait disturbances: Small, slow steps, difficulty turning, and increased tendency to fall¹.
The course is often divided into three clinical phases:
Preclinical phase: No symptoms, but pathological changes are underway.
Prodromal phase: Non-motor symptoms may be present for up to 15–20 years before motor signs.
Clinical phase: Motor symptoms dominate and the diagnosis is established¹²⁻¹³.
Pathology and neurodegeneration
Central to the development of PD is the accumulation of alpha-synuclein, forming so-called Lewy bodies in dopaminergic neurons. Although the main focus has long been on the substantia nigra, recent research shows that degeneration occurs in multiple structures:
Striatum and thalamus: Volume loss, particularly in specific nuclei⁶,¹⁴.
Hypothalamus: Reduced gray matter and decreased melatonin production – which in turn affects striatal function⁶,¹⁴.
Cerebellum: Changes in gray matter in both right and left hemispheres, due to afferent dopaminergic connections to and from the basal ganglia¹⁴.
Locus coeruleus: Loss of noradrenergic neurons and Lewy body formation – suggesting broader system involvement⁶,¹⁴.
Such findings support the hypothesis that Parkinson’s disease is a multisystem disorder with both dopaminergic and non-dopaminergic neurodegeneration¹².
Epidemiology
Parkinson’s disease affects approximately 1–2 per 1000 individuals, and prevalence increases to over 1% after the age of 60¹⁵. Globally, between 7 and 10 million people live with the diagnosis. The condition affects men more often than women, and 5–10% of cases are familial¹.
Etiological factors
The cause of Parkinson’s disease is multifactorial:
Environmental factors: Exposure to pesticides, herbicides, and heavy metals (e.g., manganese) has been associated with increased risk¹².
MPTP toxin: A substance known from drug production that induces parkinsonism, used in animal studies to investigate the disease¹².
Head trauma: Repeated injuries, as in boxing and American football, can cause parkinson-like symptoms – though often with differing pathology.
Medication use: NSAIDs, statins, and calcium channel blockers have been studied, but with inconclusive findings.
Oxidative stress: Increased production of free radicals may damage neurons, particularly in the thalamus¹².
Genetic factors: Around 10% of cases have a known genetic component. Siblings of individuals with PD have higher risk. Mutations in genes linked to alpha-synuclein are particularly relevant¹².
Diagnosis and treatment of Parkinson’s disease
Challenges in early diagnosis and differentiation
The diagnosis of Parkinson’s disease (PD) is still made primarily on clinical grounds, often late in the course of the disease when motor symptoms such as bradykinesia, tremor, and rigidity have already developed¹³. At this point, more than 50% of dopaminergic neurons in the substantia nigra are usually lost, underscoring the need for earlier diagnosis¹³.
In recent years, several biomarkers and early symptoms have shown promising results in identifying PD before motor signs become apparent. Such markers are also used to differentiate PD from other parkinsonian conditions.
Early and preclinical indicators of Parkinson’s disease
Several early signs and diagnostic tools have gained increased attention:
Olfactory dysfunction (hyposmia): Reduced sense of smell is common in early PD, but also age-related. It is considered a useful marker when combined with other factors¹¹.
REM sleep disturbances: Involves loss of normal muscle atonia during REM sleep, with dream enactment. This can be an early sign of neurodegeneration¹¹.
Daytime sleepiness: Excessive sleepiness and sudden sleep attacks are frequent in PD patients and may occur before motor symptoms¹¹.
Insomnia: Difficulty falling asleep or frequent awakenings – often multifactorial, and may be related to PD, medications, or psychological factors such as anxiety and depression¹¹.
Constipation: Idiopathic constipation is a strong risk factor and can appear many years before motor symptoms. Possible mechanisms include inflammation, oxidative stress, and alpha-synuclein deposits in the enteric nervous system¹¹.
Depression: May occur 5–10 years before motor onset, but is not specific to PD and must be assessed in the context of other symptoms¹¹.
Mild cognitive impairment: Seen in 15–20% of patients with early PD¹¹.
Visual disturbances: Reduced color vision, contrast sensitivity, and difficulties with visual tasks may be early biomarkers¹¹.
Biological fluids: Changes in the level and type of alpha-synuclein, as well as biomarkers such as uric acid and epidermal growth factor, are being studied – but none yet hold diagnostic status¹¹.
Pathology: Intestinal biopsies often reveal alpha-synuclein deposits. Altered gut microbiota with pro-inflammatory bacteria is also associated with PD¹¹.
Genetics: Mutations in genes such as SNCA and LRRK2 increase risk. Familial PD carries a 3–4 times higher probability of disease¹¹,¹³.
“Omics”-based methods: Modern molecular approaches aim to uncover disease networks and cellular processes leading to PD¹¹.
Inflammation: Protein misfolding may trigger inflammation and activate microglia, contributing to neurodegeneration¹¹.
Imaging and response to treatment
7T-MRI: Can now identify dopaminergic cell loss in the pars compacta – a hallmark feature of PD¹³.
Nuclear medicine methods: SPECT, PET, and transcranial ultrasound are used in certain cases to support the diagnosis¹³.
Levodopa response: Symptom improvement following L-dopa administration remains one of the most practical methods for confirming the diagnosis¹.
Scoring tools
Motor symptoms and disease progression are often assessed with:
Unified Parkinson’s Disease Rating Scale (UPDRS)
MDS-UPDRS – a revised and more sensitive version
Treatment and follow-up
Parkinson’s disease requires long-term and multidisciplinary follow-up due to both motor and non-motor symptoms. Symptoms may be caused by the disease itself or by side effects of medication¹.
Effective treatment requires contributions from a wide range of professionals, including:
Neurologist
Physiotherapist
Occupational therapist
Speech therapist
Psychiatrist
Social worker
Nurse
Gastroenterologist
ENT specialist
Urologist
Clinical nutritionist
Common complications:
Depression and dementia
Postural instability and falls
Autonomic dysfunction
Laryngeal weakness
Kyphosis with subsequent pulmonary impairment¹
Surgical treatment
Deep brain stimulation (DBS): Stimulation of, among others, the globus pallidus interna and thalamus. The procedure is reversible, but its long-term effect is still under investigation¹.
Pharmacological treatment
Currently, no medications slow disease progression. Treatment is purely symptomatic¹⁶.
Levodopa: First-line choice for most patients. Effective against motor symptoms, but side effects include nausea, dyskinesias, postural hypotension, sleepiness, and hallucinations¹⁶.
Dopamine agonists (DA): May be useful in early stages or in younger patients. However, they carry a higher incidence of impulse control disorders and sleep-related side effects. Tapering may cause withdrawal-like symptoms¹⁶.
MAO-B inhibitors: Have some effect but are associated with more side effects and more difficult discontinuation than levodopa¹⁶.
Physiotherapy and functional follow-up in Parkinson’s disease
Early intervention provides better long-term function
Physiotherapists are often first involved in the mid-stage of Parkinson’s disease, when balance and gait begin to decline. However, there is great benefit in initiating advice and interventions early – preferably right after diagnosis – to maintain function, reduce inactivity, and prevent complications.
An active physiotherapeutic approach should include tailored exercise and close monitoring of function, particularly focused on:
Balance
Gait and gait efficiency
Core and postural stability
Maintaining an active daily life¹
Expert practice in physiotherapy for Parkinson’s disease
A large qualitative study has defined four main domains characterizing expert practice in physiotherapy for neurological conditions¹⁷:
Interdisciplinary and contextual knowledge base
The clinician draws knowledge from literature, clinical experience, and the patient’s life situation. Understanding psychosocial factors, social networks, work, and cognition is crucial.
Clinical reasoning and patient-centeredness
The patient’s own goals and challenges form the foundation of clinical problem-solving. The experienced therapist continuously reflects on interventions and progress.
Movement as a core element
Observation, manual approaches, and function-based training are central. Exercises should be directed toward meaningful movement and daily activities.
Engagement and relational commitment
The therapist demonstrates care and time, functioning both as a professional and as an advocate for the patient’s interests and needs.
Common motor challenges in Parkinson’s disease
Parkinson’s disease leads to a range of motor symptoms that often require follow-up from a physiotherapist:
Tremor: Frequent, but not always present.
Bradykinesia: Slowness of movement affecting daily functions.
Rigidity: Muscle stiffness that limits mobility and makes everyday activities challenging.
Gait difficulties: Festination, reduced arm swing, flexed posture, and balance problems.
Effective interventions and training modalities
The following activities have been shown to improve function and quality of life:
Cycling, particularly with rhythmic tempo
Music-based training and dance
Boxing and coordination trainingThese activities activate motor and cognitive pathways simultaneously, enhancing balance, tempo, and initiative¹.
Prognosis and disease course
The course of the disease varies, but some clinical features provide clues to progression¹:
Poorer prognosis is seen in:
Men with postural instability
Patients with higher age at onset
Patients with cognitive impairment and poor response to levodopa
Better prognosis:
Patients with isolated tremor at onset
Younger patients without marked rigidity or hypokinesia
Most patients develop significant functional impairment within ten years after diagnosis. Mortality is approximately three times higher than in the general population¹.
Differential diagnoses
Several conditions may present with symptoms similar to Parkinson’s disease. Important differential diagnoses include¹:
Essential tremor
Huntington’s disease
Lewy body dementia
Progressive supranuclear palsy
Neuroacanthocytosis
Normal pressure hydrocephalus
Patient resources and support services
Parkinson’s Europe
Formerly known as EPDA. The organization unites 45 member countries and works toward common guidelines and quality of life for patients in Europe.
Parkinson’s UK
The largest resource portal in the UK for patients and relatives. Offers support groups, exercise groups, and information on the disease and its treatment.
Move4Parkinson’s
Founded by Margaret Mullarney, herself diagnosed in 2004. The platform focuses on knowledge, inspiration, and personal empowerment, and is based partly on The Five Elements Framework.
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