Short revision bullets only, not a replacement for the full lesson sections below.
Toggle for a short revision list before a mock or question block.
Pathophysiology
Clinical meaning
Parkinson disease involves progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc), with hallmark alpha-synuclein aggregation forming Lewy bodies and Lewy neurites. Dopamine loss disrupts the basal ganglia circuit: normally, dopamine from the SNpc facilitates the direct pathway (D1 receptors → movement initiation) and inhibits the indirect pathway (D2 receptors → movement suppression). In PD, dopamine deficiency causes relative overactivity of the indirect pathway, leading to excessive thalamic inhibition and hypokinesia. Motor symptoms appear after ~60-80% of dopaminergic neurons are lost. The pathology spreads in a caudal-to-rostral pattern (Braak staging): stage 1-2 involves olfactory bulb and brainstem (explaining prodromal anosmia, REM sleep behavior disorder, constipation), stage 3-4 involves the substantia nigra (motor symptoms), and stage 5-6 involves the cortex (cognitive decline, dementia). Non-motor symptoms (depression, autonomic dysfunction, pain) result from alpha-synuclein pathology in non-dopaminergic systems (serotonergic, noradrenergic, cholinergic).
Diagnostics & workup:
- Clinical diagnosis: bradykinesia (cardinal feature, must be present) + rest tremor (4-6 Hz, pill-rolling) and/or rigidity (lead-pipe or cogwheel)
- MDS-UPDRS (Movement Disorder Society-Unified PD Rating Scale): comprehensive assessment of motor and non-motor function, ADLs, motor complications
- DaTscan (ioflupane SPECT): visualizes dopamine transporter density in the striatum — reduced uptake confirms nigrostriatal degeneration; differentiates PD from essential tremor and drug-induced parkinsonism
- MRI brain: primarily to exclude structural causes (normal pressure hydrocephalus, vascular parkinsonism, Wilson disease); may show mild midbrain atrophy
- Olfactory testing (UPSIT): anosmia/hyposmia present in > 90% of PD — absent in essential tremor, PSP, corticobasal degeneration (useful differentiator)
- Autonomic testing: orthostatic vitals (neurogenic orthostatic hypotension common), cardiac MIBG scan (reduced uptake in PD vs. MSA)
- Cognitive screening: MoCA (more sensitive than MMSE for PD cognitive impairment — visuospatial and executive deficits earliest)
- Genetic testing: consider in early-onset PD (< 50), strong family history; GBA, LRRK2, SNCA
Risk factors:
- Age (most significant risk factor — incidence increases dramatically after age 60)
- Male sex (1.5:1 male predominance)
- Pesticide exposure (paraquat, rotenone — mitochondrial complex I inhibition)
- Family history: LRRK2 mutation (most common genetic cause), GBA mutations (strongest genetic risk factor for sporadic PD), SNCA, PINK1, Parkin
- Rural living and well water consumption (pesticide exposure hypothesis)
- Prior head trauma (mild increased risk)
- Protective factors: caffeine consumption, smoking (paradoxical — nicotinic receptor stimulation; NOT a recommendation), vigorous exercise
- REM sleep behavior disorder (80% progress to synucleinopathy within 10-15 years — key prodromal marker)
Management
Additional clinical detail, exam hooks, and takeaways continue in the full lesson.
Prescribing & monitoring
Additional clinical detail, exam hooks, and takeaways continue in the full lesson.
Takeaways
Additional clinical detail, exam hooks, and takeaways continue in the full lesson.
Unlock full lesson + practice questions
3 more sections with scenarios, priorities, and review drills.
We didn’t match sample stems to this lesson in the bank yet. You can still run a topic-scoped drill with the same pathway filters—items load from your live PMHNP pool.
