Parkinson Disease in the Elderly
Parkinson's disease is a progressive neurodegenerative disorder affecting approximately 150,000 people in the UK, characterised by bradykinesia, rigidity, and rest tremor, managed with levodopa as the mainstay of treatment.
Key Facts
Parkinson's disease affects approximately 150,000 people in the UK; prevalence increases with age (1-2% >65) Cardinal features: bradykinesia (must be present) + at least one of: rest tremor, rigidity Levodopa (co-careldopa/co-beneldopa) is the most effective symptomatic treatment; start when symptoms affect quality of life NICE NG71: do not delay levodopa to prevent motor complications; refer to specialist before starting treatment Non-motor symptoms are common and disabling: depression, constipation, REM sleep behaviour disorder, anosmia, cognitive impairment, orthostatic hypotension Never abruptly stop Parkinson's medications (risk of neuroleptic malignant-like syndrome / parkinsonism-hyperpyrexia) Avoid dopamine-blocking drugs: metoclopramide, haloperidol, prochlorperazine (worsen Parkinson's); use domperidone for nausea Falls are common in Parkinson's disease: multifactorial (postural instability, freezing, orthostatic hypotension, cognitive impairment)
Overview
Key Facts
Parkinson's disease is the second most common neurodegenerative disease after Alzheimer's. Management is complex, requiring specialist input and multidisciplinary care.
Epidemiology
- ~150,000 affected in the UK; ~18,000 new diagnoses/year
- Prevalence: 1-2% of >65; mean age of onset: 65 years
- Male:female ratio 1.5:1
- Young-onset Parkinson's: <50 years (~5-10%)
Aetiology
- Idiopathic (most common)
- Loss of dopaminergic neurons in the substantia nigra pars compacta
- Lewy bodies: α-synuclein protein aggregates (hallmark pathology)
- Genetic: LRRK2, SNCA, Parkin, PINK1, GBA mutations (5-10% familial)
- Risk factors: age, male sex, pesticide exposure, head trauma, family history
- Protective: smoking (paradoxical), caffeine (epidemiological association)
Pathophysiology
- Progressive loss of dopaminergic neurons in substantia nigra → striatal dopamine depletion → loss of inhibition of indirect pathway and loss of excitation of direct pathway → excessive inhibitory output from GPi → thalamic suppression → hypokinesia
- Symptoms appear when >60-80% of striatal dopamine is lost
- Lewy body pathology spreads via Braak staging: enteric/olfactory → brainstem → midbrain → cortex (explains non-motor symptoms preceding motor symptoms)
Clinical Presentation
Motor Features
- Bradykinesia (essential for diagnosis): slowness of movement, progressive fatiguing/decrement on repetitive movements, reduced amplitude
- Rest tremor (70%): 4-6 Hz, "pill-rolling", worse at rest, suppressed by action, unilateral onset
- Rigidity: lead-pipe ± cogwheeling (superimposed tremor); increased tone throughout range of movement
- Postural instability (late feature): retropulsion, falls
- Gait: shuffling, reduced stride length, reduced arm swing, festination, freezing of gait
Non-Motor Features
- Anosmia (often earliest symptom)
- REM sleep behaviour disorder (may precede motor symptoms by years)
- Constipation (common, may be prodromal)
- Depression and anxiety (40-50%)
- Cognitive impairment/dementia (80% develop PDD eventually)
- Orthostatic hypotension
- Urinary urgency/frequency
- Pain (musculoskeletal, dystonic, central)
Red Flags (Suggest Atypical Parkinsonism)
- Symmetrical onset
- Early falls (PSP)
- Poor/no response to levodopa
- Early severe autonomic failure (MSA)
- Cerebellar signs (MSA-C)
- Vertical gaze palsy (PSP)
- Rapid progression
- Early dementia (DLB)
- Alien limb phenomenon (CBD)
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| Essential tremor | Action/postural tremor, bilateral, family history, improves with alcohol | Clinical, trial of propranolol |
| Drug-induced parkinsonism | Symmetrical, no rest tremor; dopamine blockers | Medication history |
| Vascular parkinsonism | Lower body predominant, stepwise progression, vascular risk factors | MRI brain |
| Progressive supranuclear palsy (PSP) | Early falls, vertical gaze palsy, poor levodopa response | Clinical, MRI (midbrain atrophy) |
| Multiple system atrophy (MSA) | Early autonomic failure, cerebellar signs, poor levodopa response | Clinical, MRI (hot cross bun sign) |
| Lewy body dementia | Early dementia, visual hallucinations, fluctuating cognition | DaTSCAN, clinical |
Diagnosis / Investigation
Bedside
- Neurological examination: bradykinesia testing (finger tapping, hand movements, toe tapping), tremor assessment, rigidity, gait, postural reflexes
- Lying/standing BP (orthostatic hypotension)
- Cognitive assessment (MoCA — screens executive function well)
- Anosmia testing (UPSIT)
Bloods
- Routine bloods to exclude secondary causes (TFTs, copper studies if Wilson's suspected in <40)
Imaging
- MRI brain: not diagnostic of PD but excludes structural causes, vascular parkinsonism, NPH
- DaTSCAN (FP-CIT SPECT): confirms dopaminergic deficit; differentiates PD from essential tremor or drug-induced parkinsonism (NICE NG71 — only if diagnosis uncertain)
- PET imaging: research
Special Tests
- Levodopa challenge: improvement confirms dopaminergic responsiveness (not diagnostic of PD specifically)
- MIBG cardiac scintigraphy: reduced uptake in PD/DLB (differentiates from MSA); not widely used in UK
- Genetic testing: if young-onset (<50) or strong family history
Management
Non-pharmacological
- MDT approach: Parkinson's nurse specialist, physiotherapy, OT, SALT, psychology
- Exercise: regular aerobic and resistance exercise (improves motor function, balance, mood)
- Physiotherapy: gait training, balance, cueing strategies for freezing
- SALT: swallowing assessment (aspiration risk in advanced disease), speech therapy (LSVT LOUD)
- OT: home adaptations, maintaining independence
- Patient education and support: Parkinson's UK
Pharmacological
- Levodopa (most effective; first-line in most elderly patients):
- Co-careldopa (Sinemet) or co-beneldopa (Madopar): start 50/12.5 TDS → titrate to effect
- Modified-release preparations for nocturnal symptoms or fluctuations
- Dopamine agonists: ropinirole 0.25mg TDS → up to 8mg TDS; pramipexole 88mcg TDS → up to 1.1mg TDS; rotigotine patch 2-16mg/24h
- Beware impulse control disorders (gambling, hypersexuality, compulsive shopping — affects 15-20%)
- MAO-B inhibitors: rasagiline 1mg OD, selegiline 5-10mg OD, safinamide 50-100mg OD (adjunct)
- COMT inhibitors: entacapone 200mg with each levodopa dose, opicapone 50mg OD (adjunct to levodopa)
- Motor fluctuations (wearing off/dyskinesia):
- Add COMT inhibitor, MAO-B inhibitor, or dopamine agonist
- Adjust levodopa dose/frequency
- Amantadine 100mg BD-TDS for dyskinesia
- Advanced therapies: apomorphine SC infusion, levodopa-carbidopa intestinal gel (LCIG/Duodopa), deep brain stimulation (DBS)
- Non-motor management: treat depression (SSRIs, SNRIs), orthostatic hypotension (midodrine, fludrocortisone), constipation (macrogol), dementia (rivastigmine — only AChEI licensed for PDD)
Surgical/Interventional
- Deep brain stimulation (DBS): subthalamic nucleus or GPi; for motor fluctuations/dyskinesias despite optimised medication; improves motor function by ~50%
- Focused ultrasound thalamotomy: emerging for tremor-predominant PD
Referral Criteria
- All suspected PD: refer to specialist (neurologist or geriatrician with PD interest) before starting treatment (NICE NG71)
- Complex motor fluctuations: specialist review
- Advanced therapies: specialist PD centre
- Cognitive decline: dementia assessment
- Falls: falls prevention service + PD specialist review
Prognosis
- Life expectancy: reduced by approximately 2-5 years compared to age-matched population
- Motor complications (wearing off, dyskinesia): develop in 50% within 5 years of levodopa
- Dementia: develops in ~80% of patients over 20-year course
- Falls: affect >60% of PD patients; leading cause of hospital admission
- Aspiration pneumonia: leading cause of death in advanced PD
- Quality of life significantly impacted by non-motor symptoms
- Individual prognosis varies widely; tremor-predominant has better prognosis than postural instability-gait difficulty (PIGD) phenotype
Other Relevant Information
Hoehn and Yahr Staging
| Stage | Description |
|---|---|
| 1 | Unilateral involvement only |
| 2 | Bilateral involvement, no balance impairment |
| 3 | Bilateral, mild-moderate disability; impaired postural reflexes |
| 4 | Severely disabled; able to walk/stand unassisted |
| 5 | Wheelchair-bound or bedridden unless aided |
Drugs to Avoid in Parkinson's Disease
| Drug | Reason |
|---|---|
| Metoclopramide | D2 antagonist; worsens PD |
| Haloperidol | D2 antagonist |
| Prochlorperazine | D2 antagonist |
| Chlorpromazine | D2 antagonist |
| Use domperidone | Does not cross BBB; safe antiemetic |