ð¥ å
§ç§å°ç§èåç
Mechanistic Deep Dive
α-Synuclein
- 140-AA protein
- Normally in synaptic vesicles
- Misfolds â aggregates â Lewy bodies + neurites
- Prion-like spread (cell to cell)
Dopamine Loss
- Loss in nigrostriatal pathway
- Loss of inhibition on indirect pathway
- â Output of GPi â â thalamocortical drive â bradykinesia
Levodopa Pharmacology
- Crosses BBB
- Converted to dopamine in CNS
- Carbidopa blocks peripheral conversion (less nausea)
- Short half-life (1-2 hr) â wearing off
Recent Trials & Updates
Foslevodopa-Foscarbidopa (Vyalev) FDA 2024
- Continuous SC pump (24/7)
- For advanced PD with motor fluctuations
- Alternative to LCIG (less invasive)
- M15-741 trial positive
LRRK2 Inhibitors (Trials)
- For LRRK2-PD
- Multiple in trials
GLP-1 Agonists
- Exenatide (Lixisenatide)
- Lixisenatide trial (LIXIPARK 2024) some neuroprotection signal
- Larger trials planned
Anti-α-synuclein Antibodies
- Prasinezumab (PASADENA) â negative
- Cinpanemab â negative
- BIIB101 (PADOVA) â pending
GBA-Directed Therapies
- For GBA-associated PD (more aggressive cognitive decline)
- Ambroxol increases GCase activity
- Limited evidence
Focused Ultrasound Pallidotomy
Sublingual Apomorphine (Kynmobi)
Inhaled Levodopa (Inbrija)
- For OFF period rescue
- Self-administered
Skin Biopsy for α-Synuclein
- Phosphorylated α-synuclein in peripheral nerves
- Diagnostic accuracy high
CSF + Plasma α-Synuclein RT-QuIC
- Emerging diagnostic biomarker
- Distinguishes synucleinopathies
High-Yield Specialist Points
Early-Onset PD (< 50)
- Genetic more likely
- PARKIN, PINK1, DJ-1, LRRK2, GBA
- Different management considerations
PD vs Atypical Parkinsonism
- Atypical: poor levodopa response, early falls, autonomic failure, bulbar, cerebellar, supranuclear gaze, etc.
- MSA, PSP, CBD, DLB
- See Ch380
REM Behavior Disorder Prodrome
- 80% develop synucleinopathy in 15 yr
- Counsel patients
- Polysomnography for confirmation
- Treat with melatonin or clonazepam + safety
Vascular Parkinsonism
- Lower body more affected (âlower body parkinsonismâ)
- Stepwise progression
- Vascular risk factors
- Normal DaT-SCAN
- Poor levodopa response
- Treatment: vascular risk factor modification
Drug-Induced Parkinsonism
- Antipsychotics, antiemetics (metoclopramide, prochlorperazine), VPA
- Reversible mostly
- Normal DaT-SCAN
Hemiparkinsonism-Hemiatrophy
- Childhood injury
- Asymmetric atrophy + parkinsonism
Wilson Disease
- Young (< 40) with parkinsonism
- dystonia, tremor, dysarthria, psychiatric
- KF rings
- Low ceruloplasmin
- Chelators or zinc
Acquired Hepatocerebral Degeneration
- Cirrhosis + parkinsonism + cognitive
- T1 bright basal ganglia (manganese accumulation)
Manganism
- Welders, miners
- Parkinsonism + behavioral
- Less levodopa response
Genetic PD Testing
- Considered:
- Early onset (< 50)
- Family history
- Specific phenotypes
- LRRK2, GBA, PARK panels
- Genetic counseling
Camptocormia + Pisa Syndrome
- Severe truncal flexion (camptocormia)
- Lateral flexion (Pisa)
- Treatment difficult
- Surgical/orthotic options
Pharmacogenomics
- COMT polymorphisms may affect response
- Limited clinical utility currently
Pearls
- TRAP + non-motor (RBD, hyposmia, constipation)
- α-synuclein pathology
- Levodopa gold standard
- DA agonist ICDs â counsel!
- Pimavanserin for psychosis
- Rivastigmine for PDD
- DBS for motor fluctuations
- LCIG, foslevodopa SC (Vyalev 2024), focused ultrasound advanced therapies
- DaT-SCAN distinguishes from non-PD parkinsonism
- No disease-modifying therapy yet â many trials ongoing