Clinical Movement

Atypical Parkinsonism

Atypical Parkinsonism

What You'll Learn

  • MSA: Cerebellar ataxia + autonomic failure (MSA-C) or parkinsonism + autonomic failure (MSA-P); glial cytoplasmic inclusions (GCIs) with α-synuclein; hot cross bun sign and putaminal rim sign; mean survival 6–10 years
  • PSP: Vertical supranuclear gaze palsy (downgaze first) + early backward falls within the first year + axial rigidity; hummingbird sign and morning glory sign; 4R tauopathy
  • CBD: Asymmetric rigidity + apraxia + alien limb phenomenon + cortical sensory loss + myoclonus; asymmetric frontoparietal atrophy; 4R tauopathy; CBS ≠ CBD
  • DLB: Fluctuating cognition + visual hallucinations + parkinsonism + REM sleep behavior disorder; neuroleptic sensitivity; DaTscan abnormal; the “1-year rule” separates DLB from PDD
  • Common theme: All show poor or absent sustained levodopa response (except DLB with modest benefit); early red flags distinguish these from idiopathic PD
HighYield Pearls
  • Vertical supranuclear gaze palsy + early backward falls (within year 1) = PSP. Single most tested PSP stem — "patient cannot look down at the plate"
  • Cerebellar ataxia + autonomic failure = MSA-C; akinetic-rigid parkinsonism + autonomic failure = MSA-P. Per MDS 2022: clinically established MSA requires autonomic dysfunction plus poorly levodopa-responsive parkinsonism or cerebellar syndrome, supportive features, and an MRI marker; clinically probable MSA requires at least two of autonomic dysfunction, parkinsonism, and cerebellar syndrome, plus at least one supportive feature (MRI not required)
  • Alien limb + asymmetric apraxia + cortical sensory loss = CBS (clinical). Only ~25–50% of CBS patients have CBD pathology at autopsy — CBS ≠ CBD
  • Fluctuating cognition + visual hallucinations + RBD + parkinsonism = DLB. Probable DLB = ≥2 core clinical features OR 1 core feature + ≥1 indicative biomarker; well-formed visual hallucinations are the single biggest distinguisher from AD
  • NEVER give haloperidol/typical antipsychotics in DLB. Severe neuroleptic sensitivity → NMS → death; use quetiapine or pimavanserin if absolutely needed
  • Levodopa response is the key initial filter: excellent + sustained = PD; modest = DLB; poor/transient = MSA-P; absent = PSP/CBD
  • MIBG cardiac scintigraphy: reduced uptake in PD/DLB (postganglionic denervation); preserved in MSA (preganglionic) — can support the distinction between MSA and PD/DLB (performance imperfect; US availability variable)
  • DBS is NOT indicated in MSA, PSP, CBD, or DLB — robust sustained levodopa response is required for PD DBS candidacy
  • 1-year rule: dementia onset ≤1 year of parkinsonism = DLB; >1 year after = PDD (same pathology, clinical distinction)
  • Inspiratory stridor in a parkinsonian patient = MSA until proven otherwise (sudden death risk; ~30% of MSA)
🔍 Quick ReferenceImaging · Clinical · Pathology
Imaging signs
  • Hummingbird sign / penguin sign (sagittal midbrain atrophy) → PSP
  • Morning glory sign (axial midbrain — concave lateral margin) → PSP
  • Midbrain-to-pons ratio <0.52 on midsagittal MRI → PSP (normal ≈0.6)
  • Hot cross bun sign (cruciform pontine T2 hyperintensity) → MSA-C (also seen in SCA2/3/7)
  • Putaminal rim sign (hyperintense lateral putaminal margin on T2) → MSA-P (1.5T more specific)
  • Putaminal atrophy + T2 hypointensityMSA-P
  • Cingulate island sign on FDG-PET (cingulate preservation amid posterior hypometabolism) → DLB
  • Asymmetric frontoparietal atrophy contralateral to affected limb → CBD
  • Hippocampal preservation on MRI (relative to AD) → DLB
Clinical signs
  • Applause sign (cannot stop clapping after 3 claps) → PSP frontal dysfunction
  • Rocket sign (recklessly rising from chair without checking environment) → PSP
  • "Surprised facies" / frontalis overactivityPSP (compensating for limited upgaze)
  • Retrocollis (extended neck) → PSP (vs. flexed posture of PD)
  • Square wave jerks on primary gaze fixation → PSP
  • Doll’s eyes intact despite gaze palsy → PSP supranuclear lesion (VOR bypasses supranuclear pathways)
  • Alien limb phenomenon (limb “acts on its own”) → CBS
  • Pisa syndrome (sustained lateral truncal lean) → MSA, PD
  • Inspiratory stridorMSA (vocal cord abductor paralysis)
  • Neuroleptic sensitivity (severe reaction to low-dose antipsychotic) → DLB
  • REM sleep behavior disorder preceding parkinsonism by years → α-synucleinopathy (DLB, PD, MSA)
Pathology hallmarks
  • Glial cytoplasmic inclusions (GCIs) in oligodendrocytes (α-synuclein) → MSA
  • Tufted astrocytes + 4R NFTs + coiled bodies → PSP
  • Astrocytic plaques + ballooned neurons (4R tau) → CBD
  • Cortical Lewy bodies (neuronal α-synuclein) → DLB
  • Brainstem Lewy bodies in SN pars compacta → PD
Red Flags for Atypical Parkinsonism

When to Suspect “Parkinson-Plus”

  • Early falls (within first year) — especially backward falls (PSP)
  • Poor or absent levodopa response after adequate trial (up to 1000 mg/day, or maximum tolerated dose, for ≥1 month)
  • Symmetric onset — PD is classically asymmetric, but both MSA and PSP can also present asymmetrically; symmetric onset should raise suspicion but does not exclude PD
  • Early severe autonomic failure — orthostatic hypotension, urinary retention/incontinence, erectile dysfunction (MSA)
  • Vertical gaze palsy — especially downgaze limitation (PSP)
  • Alien limb phenomenon — involuntary purposeful movements of a limb (CBD)
  • Early dementia (<1 year from motor onset) with visual hallucinations (DLB)
  • Rapid progression — wheelchair-bound within 5 years
  • Cerebellar signs (gait ataxia, dysarthria, nystagmus) — MSA-C

Red Flags Summary Table

Red FlagMost Suggestive Of
Early backward fallsPSP
Vertical supranuclear gaze palsyPSP
Severe early autonomic failureMSA
Cerebellar ataxia + parkinsonismMSA-C
Alien limb phenomenonCBD
Asymmetric apraxia + cortical sensory lossCBD
Early visual hallucinations + fluctuating cognitionDLB
REM sleep behavior disorder + parkinsonismDLB (also MSA, PD)
Symmetric akinetic-rigid syndromeMSA-P or PSP
Inspiratory stridorMSA
💎 Board Pearl
  • Falls within the first year + poor levodopa response = not PD. In PD, falls typically occur ≥5 years into the disease. Early falls are the single strongest predictor of atypical parkinsonism, especially PSP
Multiple System Atrophy (MSA)

Overview & Subtypes

  • α-Synucleinopathy — deposits in oligodendrocytes (GCIs), not neurons
  • Mean onset: 50–60 years; no sex predominance; mean survival 6–10 years
FeatureMSA-C (Cerebellar)MSA-P (Parkinsonian)
Motor phenotypeCerebellar ataxia (gait > limb), scanning dysarthria, nystagmusAkinetic-rigid parkinsonism, often symmetric; jerky postural/action tremor with a myoclonic component — classic pill-rolling rest tremor is uncommon
PrevalenceMore common in East Asian populationsMore common in Western populations
Key MRI findingHot cross bun sign (cruciform pontine hyperintensity on T2)Putaminal atrophy with T2/iron-related hypointensity and a hyperintense lateral putaminal rim (best at 1.5T; rim alone can be a normal finding at 3T)
Levodopa responsePoor or absentTransient modest response possible; never sustained

Autonomic Failure

  • Required for clinically established MSA (MDS 2022); for clinically probable MSA, autonomic dysfunction is one of three core domains (with parkinsonism and cerebellar syndrome) and only two of three need be present
  • Orthostatic hypotension: ≥20 mmHg systolic or ≥10 mmHg diastolic drop within 3 min of standing (threshold for clinically probable MSA); ≥30/≥15 within 3 min for clinically established MSA
  • Supine hypertension — frequently coexists with OH in MSA; complicates pharmacologic management of orthostasis
  • Urogenital dysfunction: Urinary incontinence/retention (early), erectile dysfunction in men (often presenting symptom)
  • Inspiratory stridor: Vocal cord abductor paralysis; ~30% of MSA; risk of sudden death

Diagnostic Criteria (MDS 2022)

  • Clinically established MSA: Autonomic failure (OH ≥30/15 mmHg within 3 min OR unexplained urinary incontinence with erectile dysfunction in males <60) + poorly levodopa-responsive parkinsonism (MSA-P) or cerebellar syndrome (MSA-C) + ≥2 supportive clinical/imaging features
  • Clinically probable MSA: at least two of three core domains — autonomic dysfunction (lower OH threshold ≥20/10 mmHg within 3 min, or other autonomic feature), parkinsonism, and cerebellar syndrome — plus at least one supportive clinical feature (e.g., stridor, rapid progression). MRI marker is NOT required for clinically probable MSA.
  • Neuropathologically confirmed: GCIs with α-synuclein in widespread CNS distribution
💎 Board Pearl
  • GCIs (glial cytoplasmic inclusions) = MSA. α-Synuclein in oligodendrocytes, not neurons — the defining pathological distinction from PD/DLB (neuronal Lewy bodies)
  • Hot cross bun sign = MSA-C; putaminal rim sign = MSA-P — the hot cross bun sign is highly suggestive of MSA-C but is also seen in some spinocerebellar ataxias (SCA2, SCA3, SCA7)
  • Inspiratory stridor in a parkinsonian patient = MSA until proven otherwise
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