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Mechanistic Deep Dive
α-Synuclein in DLB
- Lewy bodies cortical + brainstem (vs PD mostly brainstem early)
- Diffuse cortical spread
- Often + AD co-pathology
Antipsychotic Sensitivity Mechanism
- D2 receptor blockade in already depleted dopaminergic system
- Severe EPS, mutism, rigidity
Subcortical Ischemic Vascular Disease (SIVD)
- Lipohyalinosis of small penetrating arteries
- Lacunes + white matter changes
- Chronic ischemia
- Often HTN-related
Recent Trials & Updates
Pimavanserin for DLB Psychosis
- Selective 5HT-2A inverse agonist
- Avoids dopaminergic blockade
- FDA-approved for PD psychosis (off-label for DLB)
- HARMONY trial
Lewy Body RT-QuIC
- α-synuclein seed amplification assay
- CSF, skin biopsy
- High accuracy for synucleinopathies
- Distinguishes DLB from AD
Plasma Biomarkers
- Phosphorylated α-synuclein
- Emerging
High-Yield Specialist Points
Lewy Body Pathology Spread (Braak)
- Brainstem â limbic â cortex
- DLB has prominent cortical involvement
- PD typically more brainstem early
Cingulate Island Sign
- FDG-PET DLB
- Preserved posterior cingulate
- Surrounded by reduced metabolism (especially precuneus)
REM Sleep Behavior Disorder Importance
- Strong predictor of synucleinopathy
- 80%+ develop within 15 years (PD, DLB, MSA)
- Counsel patients
Differential of Visual Hallucinations
- DLB (well-formed, animals, people, often non-threatening)
- Drug-induced (anticholinergics, dopaminergics)
- Delirium (variable)
- Charles Bonnet (visual loss)
- Schizophrenia (less well-formed in elderly)
- AD with psychosis
Charles Bonnet Syndrome
- Visual loss â vivid hallucinations
- Insight preserved
- Not DLB
- Sensory deprivation phenomenon
Sundowning in DLB
- Worsening evening/night
- Similar to AD
Cognitive Fluctuations Distinguishing
- DLB classical
- Delirium (acute, identifiable cause)
- Sleep disorders (especially OSA)
- Medication side effects
Vascular Cognitive Impairment Imaging
- White matter hyperintensities
- Lacunar infarcts
- Cortical infarcts
- Microbleeds
- CAA features
Hypertensive Encephalopathy
- Severe HTN
- Confusion, seizures, vision changes
- PRES on MRI
- Treat HTN
CADASIL Details
- NOTCH3 mutation
- Cysteine substitution
- Granular osmiophilic material on skin biopsy
- White matter (anterior temporal characteristic)
- Migraine + recurrent strokes + cognitive
- Genetic testing
CARASIL
- AR
- HTRA1 mutation
- Asian populations
- Similar to CADASIL
Fabry Disease
- α-galactosidase
- White matter changes
- Strokes
- Renal, skin, cardiac
Pearls
- DLB: 4 core (fluctuation, visual hallucinations, RBD, parkinsonism)
- DLB vs PDD: timing distinction
- DLB: severe antipsychotic sensitivity â AVOID typical antipsychotics
- Rivastigmine, donepezil: very effective in DLB
- Pimavanserin for psychosis
- VCI: stepwise (multi-infarct) or gradual (subcortical)
- Mixed dementia very common
- NPH: wet, wobbly, wacky â shunt
- CADASIL: AD, NOTCH3, anterior temporal white matter