Parkinson's Disease
Progressive neurodegeneration — dopamine replacement and symptom management
Parkinson's disease (PD) is a progressive neurodegenerative disorder caused by the loss of dopamine-producing neurons in the substantia nigra. It is the second most common neurodegenerative condition after Alzheimer's disease, affecting around 145,000 people in the UK. While there is currently no cure, treatment can significantly improve quality of life and motor function.
What is Parkinson's Disease?
Parkinson's disease is caused by the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to dopamine deficiency in the striatum — a region of the brain responsible for coordinating movement. The pathological hallmark is the accumulation of Lewy bodies (abnormal aggregates of alpha-synuclein protein) within neurons. The exact cause of neuronal loss is unknown but is thought to involve a combination of genetic susceptibility, environmental triggers, and mitochondrial dysfunction. Around 10–15% of cases have a familial component — known genetic mutations include LRRK2, PARK7 (DJ-1), PINK1 and SNCA. Parkinson's disease must be distinguished from other Parkinsonism syndromes (multiple system atrophy, progressive supranuclear palsy, drug-induced Parkinsonism) as these respond differently to treatment.
Symptoms (TRAP)
The cardinal motor features of Parkinson's disease are summarised by the TRAP acronym: Tremor (resting 'pill-rolling' tremor, typically 4–6 Hz, improves with movement), Rigidity (cogwheel or lead-pipe resistance to passive movement), Akinesia/Bradykinesia (slowness and reduced amplitude of movement — the core disabling feature), and Postural Instability (impaired balance, increased falls risk — typically a later feature). Other motor features include micrographia (small handwriting), hypomimia (reduced facial expression), hypophonia (soft voice), shuffling gait, and festination. Non-motor symptoms are common and often precede motor features: anosmia (loss of smell), REM sleep behaviour disorder, constipation, depression, and orthostatic hypotension. Recognising non-motor symptoms is crucial as they significantly affect quality of life.
Diagnosis (NICE NG71)
Diagnosis is clinical, based on the presence of bradykinesia plus one of rest tremor or rigidity, per the UK Brain Bank criteria. NICE NG71 recommends that people with suspected Parkinson's disease are referred quickly (within 6 weeks) to a specialist with expertise in movement disorders — and are NOT started on dopaminergic therapy until the diagnosis is confirmed by the specialist. There is no definitive diagnostic blood test. DaTscan (dopamine transporter SPECT imaging) can help differentiate Parkinson's disease from essential tremor and drug-induced Parkinsonism by demonstrating dopaminergic deficit, but cannot distinguish between different Parkinsonian syndromes. MRI brain may be used to exclude other causes. Red flags suggesting an alternative Parkinsonian syndrome include early falls, early dementia, autonomic failure, poor levodopa response, and symmetrical onset.
Non-motor Symptoms
Non-motor symptoms in Parkinson's disease are highly prevalent and can be more disabling than motor features in advanced disease. Depression affects up to 40% of patients — SSRIs are commonly used, though care is needed with selegiline (serotonin syndrome risk). Dementia occurs in up to 80% of patients with long-standing disease — rivastigmine is the only licensed treatment for Parkinson's disease dementia. Psychosis (hallucinations, delusions) may be drug-induced — review and reduce dopaminergic medications; quetiapine or clozapine (with CPMS monitoring) may be used with specialist advice. Constipation should be managed with adequate hydration, dietary fibre and macrogol laxatives. Orthostatic hypotension may require fludrocortisone or midodrine. Bladder symptoms are common — oxybutynin is generally avoided due to CNS side effects; mirabegron or solifenacin are preferred.