Last Minute Review
Movement Disorders — Last Minute Review
A last-minute review of high-yield facts — dense tables and one-liners for RITE/Board prep. Not a substitute for the full notes.
Parkinsonism — PD vs Atypical
| Disorder | Key Features | Red Flags / Distinguishing Clues | Pathology | Treatment |
|---|---|---|---|---|
| Parkinson Disease (PD) | Asymmetric rest tremor (4–6 Hz), bradykinesia, rigidity; non-motor prodrome (RBD, anosmia, constipation) | Excellent sustained levodopa response; asymmetric onset; levodopa-induced dyskinesias support diagnosis | α-synuclein Lewy bodies; Braak staging (dorsal motor nucleus of vagus → substantia nigra → cortex) | Levodopa/carbidopa (gold standard); DA agonists; MAO-B inhibitors; DBS (STN or GPi) |
| MSA-P (striatonigral degeneration) | Symmetric parkinsonism + early severe autonomic failure (OH, urinary retention); poor levodopa response | Stridor (laryngeal dystonia); anterocollis; early falls; wheelchair ≤5 yr; putaminal slit sign on MRI | α-synuclein glial cytoplasmic inclusions (GCIs) in oligodendrocytes | Levodopa trial (transient benefit ~30%); midodrine/droxidopa for OH; no disease-modifying therapy |
| MSA-C (olivopontocerebellar atrophy) | Cerebellar ataxia + autonomic failure ± parkinsonism | “Hot cross bun” sign (pons) on MRI; cerebellar/pontine atrophy | α-synuclein GCIs (same as MSA-P) | Supportive; PT/OT; autonomic management |
| PSP (Richardson syndrome) | Early postural instability + falls (backward); vertical supranuclear gaze palsy (downgaze > upgaze); axial rigidity > limb; “surprised” facies | Vertical gaze palsy (downgaze first); “hummingbird” / “penguin” sign on MRI (midbrain atrophy); applause sign | 4R tauopathy; globose neurofibrillary tangles | No effective therapy; levodopa trial (poor response); PT for fall prevention |
| CBS / CBD | Markedly asymmetric rigidity + limb apraxia; cortical sensory loss; alien limb phenomenon; myoclonus | Asymmetric cortical atrophy (parietal); “alien limb”; apraxia of speech; CBD is a pathologic diagnosis | 4R tauopathy; astrocytic plaques; ballooned (achromatic) neurons | Supportive; botulinum toxin for dystonia; clonazepam for myoclonus |
| DLB | Fluctuating cognition; recurrent visual hallucinations; parkinsonism; RBD | Visual hallucinations early; neuroleptic sensitivity (avoid typical antipsychotics!); low DAT uptake on SPECT | α-synuclein Lewy bodies (cortical predominant) | Cholinesterase inhibitors (rivastigmine); pimavanserin or quetiapine for hallucinations; carbidopa/levodopa cautiously |
💎 Board Pearl
- 1-year rule: Dementia within 1 year of parkinsonism onset = DLB; dementia ≥1 year after established PD = PDD. Same α-synuclein pathology, different temporal profile.
- Protein cheat sheet: PD/DLB/MSA = α-synuclein; PSP/CBD = 4R tau. GCIs (oligodendrocytes) = MSA; Lewy bodies (neurons) = PD/DLB.
- DaTscan is abnormal in ALL degenerative parkinsonisms (PD, MSA, PSP, DLB) but normal in ET, drug-induced parkinsonism, and functional tremor — it does NOT distinguish PD from atypical syndromes.
PD Medications
| Drug / Class | MOA | Key Points |
|---|---|---|
| Levodopa/Carbidopa (Sinemet) | DA precursor + peripheral decarboxylase inhibitor | Most effective PD drug; gold standard; motor fluctuations with chronic use; carbidopa blocks peripheral conversion (reduces nausea) |
| DA Agonists (pramipexole, ropinirole, rotigotine) | Direct D2/D3 receptor stimulation | Monotherapy in young-onset PD to delay levodopa; impulse control disorders (gambling, hypersexuality, shopping); daytime somnolence; leg edema |
| MAO-B Inhibitors (selegiline, rasagiline, safinamide) | Block MAO-B → ↓ DA degradation | Mild symptomatic benefit; adjunct to levodopa; selegiline metabolized to amphetamine; avoid with meperidine/SSRIs (serotonin syndrome risk) |
| COMT Inhibitors (entacapone, opicapone, tolcapone) | Block COMT → prolong levodopa half-life | Always used WITH levodopa; extend “on” time; tolcapone = hepatotoxicity (requires LFT monitoring); entacapone = orange urine |
| Amantadine | NMDA antagonist + ↑ DA release | Amantadine ER (Gocovri) is the FDA-approved formulation for LID and OFF episodes in PD; IR amantadine is widely used but does not carry that labeled claim. Also mild antiparkinsonian; livedo reticularis; hallucinations in elderly |
| Anticholinergics (trihexyphenidyl, benztropine) | Block muscarinic receptors (restore DA/ACh balance) | Best for tremor-predominant PD in young patients only; avoid in elderly (confusion, urinary retention, constipation, cognitive worsening) |
| Apomorphine | Potent non-selective DA agonist | SC injection for acute “off” rescue; 5-HT3 antagonists (ondansetron/granisetron) contraindicated — severe hypotension. Trimethobenzamide historically used for prophylactic antiemesis but is no longer reliably US-available (manufacture stopped 2021); many US starts now use monitored titration without prophylactic antiemetic. Continuous SC infusion: Onapgo (FDA-approved 2025). Sublingual apomorphine (Kynmobi) discontinued in the US in 2023. |
| DBS (STN or GPi) | High-frequency stimulation modulates basal ganglia circuits | STN: allows medication reduction; GPi: better for dyskinesias + mood/behavior concerns; requires good levodopa response; no significant cognitive impairment |
PD Treatment Side Effects & Management
| Side Effect | Management |
|---|---|
| Wearing off | Add COMT inhibitor (entacapone) or MAO-B inhibitor; increase levodopa frequency (smaller, more frequent doses); switch to extended-release; add DA agonist |
| Peak-dose dyskinesias | Add amantadine ER (Gocovri — FDA-approved for LID and OFF in PD); IR amantadine commonly used off-label for LID; reduce individual levodopa dose; consider GPi DBS |
| Diphasic dyskinesias | Increase levodopa dose (counter-intuitive — need to reach peak faster); more frequent dosing; consider continuous infusion or DBS |
| “Off” dystonia (early morning foot) | Bedtime long-acting levodopa or DA agonist; early morning rescue dose; botulinum toxin for focal dystonia |
| Impulse control disorders | Reduce or stop DA agonist (most common cause); screen regularly (gambling, hypersexuality, compulsive shopping/eating); can occur with any dopaminergic drug |
| Hallucinations / psychosis | Drug-removal order: anticholinergics → amantadine → DA agonists → MAO-B inhibitors → COMT inhibitors → reduce levodopa last (most effective, most needed). Add pimavanserin (5-HT2A inverse agonist, FDA-approved for PD psychosis) or quetiapine (low-dose). Never use typical antipsychotics or most atypicals (worsen parkinsonism). Clozapine is effective but requires ANC monitoring. |
| Orthostatic hypotension | Reduce antihypertensives; fludrocortisone; midodrine; droxidopa (FDA-approved for neurogenic OH); compression stockings; increase salt/fluid intake |
| Nausea | Take levodopa with food (reduces absorption slightly); add extra carbidopa; trimethobenzamide; domperidone (does not cross BBB). Avoid metoclopramide and prochlorperazine (D2 blockers). Avoid ondansetron specifically with apomorphine (severe hypotension); ondansetron acceptable in other PD nausea contexts. |
| Freezing of gait | Optimize levodopa timing; visual/auditory cues (laser pointer, metronome); PT for gait training; consider DBS if levodopa-responsive freezing |
💎 Board Pearl
- PD psychosis drug-removal order: anticholinergics → amantadine → DA agonists → MAO-B inhibitors → COMT inhibitors → reduce levodopa last (most effective, most needed).
- Pimavanserin = only FDA-approved drug for PD psychosis (no D2 blockade, won’t worsen parkinsonism).
- Never use haloperidol in PD (severe rigidity, NMS risk). Quetiapine and clozapine are the safest antipsychotics in PD.
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