Parkinson's Disease

1. Topic Overview

Summary

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterised by the loss of dopaminergic neurons in the substantia nigra pars compacta and the accumulation of α-synuclein-containing Lewy bodies. [1] It is the second most common neurodegenerative disorder after Alzheimer's disease, affecting approximately 1% of adults over 60 years of age and representing the fastest-growing neurological condition globally. [2]

The clinical hallmark is parkinsonism: the combination of bradykinesia (which must be present for diagnosis) with either rest tremor, rigidity, or both. [3] However, PD is now recognised as a multisystem disorder with prominent non-motor features including anosmia, constipation, REM sleep behaviour disorder (RBD), depression, anxiety, autonomic dysfunction, and cognitive impairment — many of which precede motor symptoms by years or decades. [4]

Diagnosis remains clinical, based on the Movement Disorder Society (MDS) Clinical Diagnostic Criteria. Treatment is symptomatic, with levodopa being the most effective agent for motor symptoms. Dopamine agonists, MAO-B inhibitors, and COMT inhibitors provide additional options. Advanced therapies including deep brain stimulation (DBS), levodopa-carbidopa intestinal gel (LCIG), and apomorphine infusions are available for patients with motor fluctuations refractory to oral medications. [5] Management requires a multidisciplinary approach addressing motor symptoms, non-motor features, falls prevention, and caregiver support.

Key Facts Card

Clinical Pearls

"Bradykinesia is Essential": You CANNOT diagnose Parkinson's disease without bradykinesia. It must be present along with at least one of: rest tremor or rigidity. Bradykinesia is not simply slowness — it requires progressive reduction in amplitude AND speed with repetitive movements (decrement). [3]

Asymmetry is a Hallmark: PD classically starts unilaterally and remains asymmetric even in advanced stages. Symmetric onset or early bilateral disease (within 3 years) should raise suspicion of atypical parkinsonism. [1]

Non-Motor Features Precede Motor Symptoms: The prodromal phase of PD can last 10-20 years. Anosmia, constipation, REM sleep behaviour disorder (RBD), depression, and anxiety often precede motor symptoms — and RBD carries an 80-90% risk of conversion to an α-synucleinopathy. [4,6]

Levodopa Response is Diagnostic: A clear, sustained response to adequate levodopa doses is a supportive criterion for PD diagnosis. Poor or absent levodopa response (despite adequate doses/duration) is an exclusion criterion and suggests atypical parkinsonism. [3]

Falls: Timing Matters: Falls within the first year of diagnosis are a red flag for atypical parkinsonism (especially PSP). In idiopathic PD, falls typically occur in moderate-to-advanced disease. [7]

Why This Matters Clinically

PD affects not just the patient but entire families. Early recognition enables timely specialist referral, accurate diagnosis (distinguishing PD from mimics), and initiation of appropriate symptomatic treatment — significantly improving quality of life. Understanding motor complications (wearing off, dyskinesias) allows proactive management adjustments. Recognising non-motor symptoms prevents undertreatment of depression, psychosis, autonomic dysfunction, and cognitive impairment. Finally, falls prevention through physiotherapy, home assessment, and medication optimisation reduces morbidity, hospitalisation, and mortality. [8]

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2. Epidemiology

Incidence and Prevalence

PD is the fastest-growing neurological disorder in terms of prevalence, disability, and deaths — primarily driven by population ageing. [2]

Demographics

Risk Factors

Protective Factors

Genetic Factors

Exam Detail: Genetic Testing Indications:

• Young-onset PD (less than 40-50 years)
• Multiple affected family members
• Ashkenazi Jewish ancestry (LRRK2 G2019S, GBA)
• Research purposes or clinical trials

GBA Mutations:

• Present in 5-15% of PD patients
• Associated with earlier onset, faster progression, higher dementia risk
• Glucocerebrosidase enzyme dysfunction leads to lysosomal impairment and α-synuclein accumulation

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3. Pathophysiology

Neuroanatomy of the Basal Ganglia

Normal Function:

The basal ganglia circuit modulates movement through the balance of direct and indirect pathways:

Key Structures:

• Striatum (caudate + putamen): Input nucleus
• Globus pallidus interna (GPi): Output nucleus
• Substantia nigra pars compacta (SNpc): Dopamine production
• Subthalamic nucleus (STN): Excitatory drive to GPi

Pathological Changes in PD

Step 1: Dopaminergic Neuron Loss

• Progressive degeneration of pigmented (neuromelanin-containing) neurons in the substantia nigra pars compacta
• By the time motor symptoms appear, 50-70% of SNpc neurons and 70-80% of striatal dopamine have been lost [1,9]
• Loss is most severe in the ventrolateral tier of SNpc (projecting to putamen → motor symptoms)

Step 2: Basal Ganglia Imbalance

• Reduced dopamine in striatum (especially putamen)
• Loss of D1 stimulation → underactive direct pathway
• Loss of D2 inhibition → overactive indirect pathway
• Net effect: Excessive GPi inhibitory output → hypokinesia

Step 3: α-Synuclein Aggregation and Lewy Body Formation

α-Synuclein is a presynaptic protein that misfolds and aggregates in PD:

Exam Detail: Molecular Mechanisms of α-Synuclein Toxicity:

1. Protein misfolding: Native α-synuclein → oligomers → protofibrils → fibrils
2. Prion-like propagation: Cell-to-cell spread via exosomes and direct transmission
3. Mitochondrial dysfunction: Impaired Complex I activity; oxidative stress
4. Proteasome/lysosome dysfunction: Impaired protein degradation
5. Neuroinflammation: Microglial activation; inflammatory cytokines
6. Synaptic dysfunction: Impaired vesicle trafficking and neurotransmitter release

The "prion-like" propagation hypothesis explains the stereotyped caudal-to-rostral spread observed in Braak staging and is supported by evidence of Lewy pathology in transplanted fetal dopaminergic neurons. [9]

Braak Staging (α-Synuclein Pathology Progression)

This staging supports the concept of a prodromal phase where non-motor features precede motor symptoms by years. [4]

Other Neurotransmitter Systems Affected

This multi-system involvement explains why PD is far more than a dopamine-deficiency motor disorder.

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4. Clinical Presentation

Motor Features (Cardinal Features)

ESSENTIAL: Bradykinesia must be present, PLUS at least one of rest tremor or rigidity. [3]

Bradykinesia

Examination Technique:

1. Finger tapping: Thumb to index finger, as fast and big as possible (10-15 times)
2. Hand movements: Open/close fist rapidly
3. Pronation-supination: Piano-playing movements
4. Heel/toe tapping: Foot on ground, tap heel then toe

Look for: Speed reduction, amplitude reduction, freezing/arrests, fatiguing

Rest Tremor

Re-emergent tremor: Action tremor that appears after a latency (seconds to minutes) when maintaining a posture — represents rest tremor suppressed by movement, then re-emerging.

Distinguishing from Essential Tremor:

Rigidity

Rigidity is velocity-independent (cf. spasticity — velocity-dependent, clasp-knife phenomenon).

Postural Instability

Pull Test Technique:

• Patient stands with feet slightly apart
• Examiner stands behind, warns patient of pull
• Brisk backward pull on shoulders
• Normal: 1-2 steps to recover
• Abnormal: > 2 steps, or would fall without catching

Important: Postural instability early in disease (within first 3 years) suggests atypical parkinsonism, especially PSP. [7]

Gait Abnormalities

Freezing of Gait (FOG):

• Affects 30-60% of PD patients
• Major risk factor for falls [10]
• Triggers: Doorways, narrow spaces, turning, dual-tasking, approaching a destination
• Often refractory to dopaminergic therapy (but can be OFF-state phenomenon)
• May respond to visual/auditory cueing strategies

Other Motor Signs

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5. Non-Motor Features

Non-motor symptoms affect nearly ALL patients with PD and are often more disabling than motor symptoms. Many precede motor onset (prodromal markers). [4,6]

Prodromal Non-Motor Features

Autonomic Dysfunction

Exam Detail: Orthostatic Hypotension in PD:

• Definition: SBP drop ≥20 mmHg or DBP ≥10 mmHg within 3 minutes of standing
• Prevalence: 30-50% of PD patients
• Causes: Disease (sympathetic denervation) + medications (levodopa, dopamine agonists)
• Cardiac MIBG scintigraphy: Reduced uptake indicates cardiac sympathetic denervation (supports PD vs MSA)
• Management: Non-pharmacological (fluids, salt, compression, rising slowly) → fludrocortisone → midodrine/droxidopa

Sleep Disorders

Neuropsychiatric Features

Exam Detail: PD Psychosis — Management Hierarchy:

1. Identify/treat triggers (infection, dehydration, metabolic)
2. Reduce anticholinergics, amantadine
3. Reduce/stop dopamine agonists
4. Reduce levodopa (if tolerable)
5. Add atypical antipsychotic: Clozapine (first-line, requires monitoring) or quetiapine [11]
6. Pimavanserin (5-HT2A inverse agonist) — approved in some regions

Never use typical antipsychotics (haloperidol) or risperidone/olanzapine — will dramatically worsen parkinsonism

Cognitive Impairment and Dementia

Risk factors for PDD:

• Older age at onset
• PIGD phenotype (vs tremor-dominant)
• Severe motor symptoms
• Hallucinations
• GBA mutations
• Low education

Management of PDD:

• Rivastigmine (cholinesterase inhibitor) — Level I evidence (EXPRESS trial) [13]
• Donepezil — less evidence
• Memantine — limited evidence

Dementia with Lewy Bodies (DLB) vs PDD:

• Same underlying pathology (α-synucleinopathy)
• "1-year rule": If dementia precedes or begins within 1 year of motor symptoms → DLB; if motor symptoms precede dementia by > 1 year → PDD
• Clinically similar; DLB has more prominent fluctuations and visual hallucinations at onset

Pain

Fatigue

• Affects 40-60% of PD patients
• Often independent of motor disability, depression, sleep disturbance
• Difficult to treat; optimise modifiable factors

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6. Clinical Examination

Structured Approach

General Observation (before touching the patient):

• Tremor at rest (hands, legs, jaw)
• Facial expression (hypomimia)
• Blink rate
• Posture (flexed trunk, neck)
• Spontaneous movements

Gait Assessment:

• Observe walking across the room
• Arm swing (asymmetric reduction)
• Stride length (short, shuffling)
• Turning (en bloc, multiple steps)
• Postural stability (pull test — done safely)

Upper Limb Examination:

• Tremor: At rest (hands in lap); re-emergent (arms outstretched)
• Rigidity: Passive flexion/extension of wrist and elbow; Froment's manoeuvre
• Bradykinesia: Finger tapping, hand open/close, pronation-supination

Lower Limb Examination:

• Tremor at rest
• Rigidity: Passive movement at ankle, knee, hip
• Bradykinesia: Heel tapping, toe tapping

Additional Signs:

• Voice assessment (hypophonia)
• Writing sample (micrographia)
• Rapid alternating movements

MDS-UPDRS (Unified Parkinson's Disease Rating Scale)

The MDS-UPDRS is the standard assessment tool: [14]

Hoehn and Yahr Staging

Schwab and England ADL Scale

Quantifies functional independence from 0% (bedridden) to 100% (completely independent).

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7. Differential Diagnosis

Atypical Parkinsonian Syndromes

Other Causes of Parkinsonism

Red Flags for Atypical Parkinsonism

[!CAUTION] Red Flags — Consider Alternative Diagnosis:

• Falls within first year of symptom onset
• Poor or absent response to adequate levodopa (> 1000mg/day for > 3 months)
• Symmetric onset or early bilateral disease
• Early severe autonomic failure (syncope, urinary incontinence, erectile dysfunction)
• Early dementia (within first year)
• Vertical supranuclear gaze palsy
• Early severe bulbar dysfunction (dysarthria, dysphagia)
• Rapid progression (doubling disability in 3 years)
• Cerebellar signs (ataxia, nystagmus)
• Pyramidal signs (spasticity, hyperreflexia, Babinski)
• Inspiratory stridor
• Alien limb phenomenon, apraxia, cortical sensory loss

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8. Investigations

Diagnosis is Clinical

The diagnosis of PD is clinical. There is no diagnostic blood test or routine imaging study. MRI is performed to exclude alternative diagnoses, not to confirm PD.

First-Line Investigations

Specialist Investigations

MDS Clinical Diagnostic Criteria (2015) [3]

Step 1: Parkinsonism is defined as:

• Bradykinesia (ESSENTIAL), AND
• At least one of: Rest tremor, Rigidity

Step 2: Establish criteria for PD:

Diagnostic certainty:

• Clinically established PD: Parkinsonism + ≥2 supportive criteria + no exclusion criteria + no red flags (or red flags counterbalanced)
• Clinically probable PD: Parkinsonism + no exclusion criteria + red flags balanced by supportive criteria

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9. Management

Principles of Treatment

1. Treatment is symptomatic — no proven disease-modifying therapy
2. Individualised — consider age, symptom severity, comorbidities, patient preference
3. Multidisciplinary — neurology, PD nurse specialists, physiotherapy, occupational therapy, speech therapy, psychology
4. Specialist initiation — all patients with suspected PD should be referred untreated to a movement disorder specialist [8]

When to Start Treatment

• When symptoms cause functional impairment or distress
• There is NO evidence that delaying levodopa prevents motor complications
• Early treatment improves quality of life [15]

Pharmacological Treatment — Initial Therapy

Levodopa

Levodopa — Advantages:

• Most effective motor symptom control
• Generally well-tolerated
• No evidence that early use accelerates motor complications (PD MED trial) [15]

Levodopa — Disadvantages:

• Motor complications develop over time (wearing off, dyskinesias)
• Short half-life (~90 mins) necessitating multiple daily doses

Exam Detail: Levodopa Pharmacology:

• L-DOPA crosses the blood-brain barrier via large neutral amino acid transporter (competition with dietary protein)
• Peripheral dopa decarboxylase inhibitor (carbidopa/benserazide) blocks peripheral conversion → reduces nausea, allows more levodopa to reach brain
• Central conversion to dopamine in residual dopaminergic neurons
• Half-life ~90 minutes (hence need for frequent dosing)
• Bioavailability affected by gastric emptying, protein intake

Wearing Off Phenomenon:

• As disease progresses and dopaminergic neurons decline, brain cannot buffer levodopa levels
• "Short-duration response" — symptoms return as plasma levodopa falls
• Manifests as end-of-dose deterioration, morning akinesia
• Management: Increase frequency, add COMT inhibitor, add MAO-B inhibitor, CR formulations

Dopamine Agonists

Dopamine Agonists — Advantages:

• Longer half-life than levodopa → less pulsatile stimulation
• May delay motor complications when used as initial monotherapy (but less effective)
• Patch formulation (rotigotine) for stable delivery

Dopamine Agonists — Disadvantages:

• Less effective than levodopa for motor symptoms
• Higher rate of adverse effects: Nausea, dizziness, somnolence, hallucinations, oedema
• Impulse control disorders (ICDs): Pathological gambling, hypersexuality, compulsive shopping, binge eating (10-20% on DA agonists) [12]
• Sleep attacks — sudden irresistible sleep episodes (driving warning)
• Not preferred in elderly (hallucinations, cognitive effects)

[!WARNING] Impulse Control Disorders: Screen ALL patients starting dopamine agonists for ICDs at baseline and at every visit. Ask specifically about gambling, shopping, eating, sexual behaviour. ICDs may not be spontaneously disclosed due to shame. First-line management is dose reduction or discontinuation of dopamine agonist.

MAO-B Inhibitors

MAO-B Inhibitors — Role:

• Monotherapy: Mild early disease (modest efficacy)
• Adjunct: Add to levodopa to reduce OFF time

Adverse effects:

• Generally well-tolerated
• Headache, nausea, insomnia (selegiline)
• Drug interactions: Avoid with pethidine, tramadol, SSRIs (serotonin syndrome risk — though rare with MAO-B selective doses)

Initial Treatment Choice — Summary

Management of Motor Complications

Motor complications affect most patients after years on levodopa:

Wearing Off (End-of-Dose Deterioration)

Exam Detail: COMT Inhibitors:

• Block catechol-O-methyltransferase → reduce peripheral levodopa degradation → increase half-life and brain delivery
• Entacapone: 200mg with each levodopa dose (or as Stalevo — combination pill)
• Opicapone: 50mg once daily at bedtime (newer; longer acting)
• Tolcapone: More effective but requires LFT monitoring (hepatotoxicity risk)
• Main side effects: Diarrhoea (especially entacapone), discoloured urine, dyskinesias (if levodopa now "stronger")

Dyskinesias

Amantadine for Dyskinesias:

• NMDA antagonist; antidyskinetic properties [16]
• Dose: 100mg OD–TDS (lower in renal impairment)
• Side effects: Livedo reticularis, ankle oedema, confusion, hallucinations
• ADS (amantadine extended-release) formulations available

Advanced Therapies (Device-Aided Therapies)

For patients with motor fluctuations and dyskinesias inadequately controlled by oral medications.

Deep Brain Stimulation (DBS)

Patient Selection for DBS:

DBS Outcomes:

• Reduces OFF time by 4-6 hours/day
• Reduces dyskinesias (STN: via medication reduction; GPi: direct effect)
• Improves quality of life
• Allows reduction in dopaminergic medications (STN > GPi)
• Does NOT improve: Levodopa-resistant symptoms (postural instability, freezing, dementia, speech)
• EARLYSTIM showed benefit of earlier DBS (within 3 years of motor complications) [17]

Complications of DBS:

• Surgical: Haemorrhage (1-2%), infection (3-5%), hardware problems
• Stimulation-related: Speech problems, balance issues, paraesthesias (usually adjustable)
• Cognitive/psychiatric: Depression, apathy, impulsivity (especially with STN)

Levodopa-Carbidopa Intestinal Gel (LCIG / Duodopa)

LCIG Complications:

• PEG-J tube issues: Dislodgement, blockage, infection, leakage
• Polyneuropathy (vitamin B12/B6 deficiency — monitor and supplement)
• Weight loss
• Cost

Apomorphine

• Most potent dopamine agonist (D1/D2)
• Requires pre-treatment with domperidone (antiemetic) for initiation
• Side effects: Nausea (hence domperidone), nodules at injection sites, sedation, confusion, hallucinations

Non-Motor Symptom Management — Summary

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10. Falls Prevention in Parkinson's Disease

Falls are a major cause of morbidity and mortality in PD, affecting 60-70% of patients. [10]

Risk Factors for Falls

Falls Assessment

1. Falls history: Frequency, circumstances, injuries, fear of falling
2. Motor assessment: Postural stability (pull test), freezing of gait, gait speed
3. Cognitive screening: MoCA or similar
4. Orthostatic BP measurement
5. Medication review: Sedatives, anticholinergics, polypharmacy
6. Vision assessment
7. Home hazard assessment (OT referral)
8. Footwear review

Falls Prevention Strategies

Freezing of Gait (FOG) Management

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11. Multidisciplinary Team Management

PD is best managed by a specialist multidisciplinary team (MDT). NICE recommends access to the following: [8]

Physiotherapy in PD

Speech Therapy

• LSVT LOUD: Evidence-based intensive treatment for hypophonia; focuses on loud phonation
• Swallowing assessment for dysphagia risk
• Alternative communication strategies

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12. Prognosis and Outcomes

Natural History

PD is progressive but highly variable. Patients may live 15-20+ years from diagnosis. The rate of progression depends on:

Mortality

• Life expectancy reduced by approximately 2-5 years compared to age-matched controls
• Main causes of death: Pneumonia (aspiration), falls-related injuries, cardiovascular disease
• Dementia is a major determinant of quality of life and mortality in late disease

Motor Complications Timeline

Key Milestones

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13. Exam-Focused Content

Common MRCP Questions

1. "What are the cardinal features of Parkinson's disease?"
2. "How do you differentiate PD from atypical parkinsonism?"
3. "What is the role of DaTSCAN in diagnosis?"
4. "Describe the management of motor fluctuations."
5. "How would you manage PD psychosis?"
6. "What are the side effects of dopamine agonists?"
7. "Which patients are suitable for DBS?"

Viva Points

Viva Point: Opening Statement: "Parkinson's disease is a progressive neurodegenerative disorder characterised by the loss of dopaminergic neurons in the substantia nigra pars compacta, leading to bradykinesia, rigidity, and rest tremor, along with a wide spectrum of non-motor features. It is the second most common neurodegenerative disorder, affecting approximately 1% of people over 60 years."

Key Facts to Mention:

• Diagnosis is clinical: Bradykinesia PLUS tremor or rigidity (MDS criteria)
• Asymmetric onset is typical
• Levodopa is the most effective treatment (PD MED trial evidence)
• Non-motor features are often more disabling than motor symptoms
• Motor complications (wearing off, dyskinesias) develop with disease progression
• DBS is effective for motor fluctuations in appropriate candidates (EARLYSTIM)
• Falls are a major cause of morbidity — multidisciplinary approach essential

Evidence to Cite:

• MDS Clinical Diagnostic Criteria 2015
• PD MED trial (2014) — levodopa first-line
• EARLYSTIM (2013) — early DBS improves QoL

Red Flags to Mention:

• Early falls, poor levodopa response, symmetric onset, early autonomic failure, vertical gaze palsy

Common Mistakes (What Fails Candidates)

❌ Forgetting bradykinesia is essential — cannot diagnose PD with tremor and rigidity alone

❌ Confusing PD with essential tremor — know the differences (rest vs action tremor, DaTSCAN)

❌ Not knowing red flags — miss atypical parkinsonism

❌ Recommending dopamine agonists in elderly/cognitively impaired — high side effect risk

❌ Using typical antipsychotics for PD psychosis — will worsen parkinsonism dramatically

❌ Forgetting impulse control disorders — must screen all patients on dopamine agonists

❌ Not referring to specialist — all suspected PD should be seen by movement disorder specialist

Model Answer

Q: A 68-year-old man presents with a 2-year history of progressive right hand tremor and slowness. How would you approach this case?

"I would approach this systematically. First, I would take a detailed history focusing on:

• Motor symptoms: Tremor character (rest, action, or both), slowness, stiffness, difficulty with fine movements, gait changes
• Non-motor symptoms: Sleep disturbance (RBD), constipation, loss of smell, mood, cognition
• Medication history: Any dopamine-blocking agents (metoclopramide, antipsychotics)
• Family history: PD or tremor

On examination, I would assess the cardinal features:

• Bradykinesia: Finger tapping, hand open/close, looking for decrement
• Tremor: Rest vs postural/kinetic, frequency, pill-rolling character
• Rigidity: Lead-pipe, cogwheel
• Gait: Arm swing, stride length, turning, postural stability

Key examination findings that would support idiopathic PD: asymmetric bradykinesia with decrement, 4-6 Hz rest tremor, cogwheel rigidity, reduced arm swing on affected side.

I would look for red flags suggesting atypical parkinsonism: early falls, symmetric onset, poor response to levodopa, early autonomic failure, vertical gaze palsy.

Diagnosis is clinical using the MDS criteria. I would refer to a movement disorder specialist before initiating treatment, as per NICE guidance.

Investigations: I would arrange an MRI brain to exclude structural causes. DaTSCAN may be considered if there is diagnostic uncertainty (e.g., differentiating from essential tremor or drug-induced parkinsonism).

Treatment would be guided by symptom severity and patient preference. For most patients, levodopa remains the most effective option for motor symptoms, supported by the PD MED trial."

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14. Patient/Layperson Explanation

What is Parkinson's Disease?

Parkinson's disease is a condition where certain nerve cells in your brain gradually stop working. These cells normally produce a chemical called dopamine, which helps control your movements. As these cells are lost, you may experience shaking (tremor), stiffness, and slowness of movement.

Parkinson's also affects other parts of the nervous system, which is why you might experience other symptoms like constipation, sleep problems, low mood, or changes in blood pressure.

Why Does It Matter?

Parkinson's is a progressive condition, meaning it changes over time. However, with the right treatment and support, most people with Parkinson's can maintain a good quality of life for many years. Treatment can significantly improve your symptoms.

What Are the Symptoms?

Main movement symptoms:

• Tremor (shaking) — usually when your hand is at rest
• Slowness of movement
• Stiffness in your arms and legs
• Balance problems (usually later on)

Other common symptoms:

• Loss of smell
• Constipation
• Sleep problems (vivid dreams, acting out dreams)
• Low mood or anxiety
• Tiredness
• Quieter voice
• Smaller handwriting
• Memory and thinking changes (may occur later)

How Is It Diagnosed?

Parkinson's is diagnosed by a specialist (neurologist or geriatrician) based on your symptoms and examination. There is no blood test for Parkinson's, but scans may be used to help in uncertain cases or to rule out other conditions.

How Is It Treated?

Medications:

The main treatments work by replacing or mimicking dopamine:

• Levodopa: The most effective medication; converted to dopamine in your brain
• Dopamine agonists: Mimic the effect of dopamine
• Other tablets: Help make your medications work better or last longer

Therapies:

• Physiotherapy — helps with movement, balance, and preventing falls
• Occupational therapy — helps with daily activities and home safety
• Speech therapy — helps with voice and swallowing

Surgery (for some people): Deep brain stimulation (DBS) involves implanting electrodes in the brain connected to a small device (like a pacemaker). This can help when medications aren't controlling symptoms well enough.

What to Expect

• Parkinson's progresses slowly — most people have many good years
• Medications work well, especially at first; they can be adjusted over time
• You may notice that medications work for shorter periods as years pass — this can be managed with adjustments
• Regular follow-up with your specialist team is important
• A team approach (doctors, nurses, therapists) helps maintain your independence

When to Seek Help

Contact your Parkinson's team, nurse, or GP if:

• Your symptoms are getting significantly worse
• You're having problems with medication timing or wearing off
• You experience hallucinations (seeing things that aren't there) or confusion
• Falls are increasing
• Mood is low and affecting your daily life
• You're struggling with swallowing

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15. Evidence and Guidelines

Key Guidelines

Landmark Trials

Evidence Level Summary

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