Eduovisual
Nervous System & Special Senses
Essential tremor vs Parkinson tremor
— Prevalence ~1% overall, rising to 4–5% in adults >65; bimodal age onset (teens/20s and again in 60s).
— Bilateral, largely symmetric, action (postural + kinetic) tremor of hands/forearms; may involve head ("yes-yes" or "no-no") and voice; legs spared.
— Frequency 8–12 Hz, often improves transiently with alcohol (~50–70%).
— Family history positive in ~50–70% (autosomal dominant pattern).
— Part of PD, prevalence ~1% over age 60; mean onset ~60 years.
— Asymmetric resting tremor ("pill-rolling"), 4–6 Hz, that dampens with action and reemerges after a latency when arms held outstretched (re-emergent tremor).
— Accompanied by bradykinesia, rigidity, postural instability, hypomimia, micrographia, hyposmia, REM sleep behavior disorder, constipation.
— Patient complains: "I can't hold a coffee cup or sign my name" → think ET (action tremor interferes with fine motor tasks).
— Patient or spouse says: "His hand shakes when sitting watching TV, but stops when reaching" → think PD.
— Tremor + slow shuffling gait, stooped posture, soft voice → PD until proven otherwise.
— Tremor + alcohol relief + father had it → ET.
Board pearl: The single most discriminating bedside feature is activation state — ET worsens with action and posture, PD tremor is maximal at rest. A patient whose tremor disappears when reaching for a target almost always has Parkinson, not essential, tremor.
Step 3 management: In the ambulatory setting, do not start empiric levodopa or propranolol before completing a focused exam — misclassification at the first visit drives years of wrong therapy and unnecessary referrals.
— ET: insidious, often present for years to decades, slowly progressive; patient may say "I've always shaken a little, but now I can't drink soup."
— PD: subacute over months, unilateral hand or foot tremor noticed first; spouse often notices before patient.
— ET: worse with sustained posture (holding a newspaper) and goal-directed action (pouring, writing, spooning); absent at rest.
— PD: worse at rest (hands in lap, arms hanging while walking); diminishes when patient grabs an object.
— ET: bilateral upper extremities (dominant hand often worse but both involved); head and voice common; jaw rare.
— PD: unilateral onset, may involve hand, foot, jaw, lip, or chin; head tremor is unusual — if present suggests ET or dystonic tremor.
— ET: alcohol improves, caffeine/stress/fatigue worsen; beta-agonists (albuterol) and valproate, lithium, amiodarone, SSRIs exacerbate.
— PD: emotional stress and cognitive load (counting backward) dramatically worsen resting tremor.
— Hyposmia, constipation, REM sleep behavior disorder (acting out dreams), orthostatic lightheadedness, depression often precede motor symptoms by 5–10 years.
— ET may have mild gait ataxia and subtle cognitive slowing but lacks the autonomic/olfactory signature.
— ET: difficulty with writing, eating, drinking, fine tasks — embarrassment in public.
— PD: difficulty initiating movement, turning in bed, buttoning shirts, smaller handwriting.
Key distinction: A patient whose handwriting got bigger and shakier has ET (megalographia of tremor); a patient whose handwriting got smaller and tighter has PD (micrographia). This single history item is repeatedly tested.
Board pearl: Ask every tremor patient about REM sleep behavior disorder — its presence shifts the diagnosis strongly toward an alpha-synucleinopathy (PD, DLB, MSA), not ET.
— Watch the patient sit in the waiting room with arms in lap — a tremor visible here is resting → PD.
— Note facial expression (hypomimia in PD), blink rate (reduced in PD), voice (hypophonic monotone in PD; tremulous wavering voice in ET).
— Have patient hold arms outstretched, palms down, fingers spread.
— ET: immediate symmetric tremor.
— PD: initially still, then re-emergent tremor after a 4–10 second latency — classic.
— Finger-to-nose and pouring water between cups: ET worsens at the target (terminal accentuation); PD tremor diminishes.
— Patient walks while you observe hands hanging — unilateral pill-rolling rest tremor while walking is pathognomonic for PD.
— Finger taps, hand opening/closing, foot taps — look for decrement in amplitude and speed (sequence effect); this is the defining feature of parkinsonism.
— Passive wrist/elbow movement reveals cogwheel (PD) vs normal tone (ET).
— PD: stooped, shuffling, reduced arm swing on affected side, en bloc turning; pull test positive later in disease.
— ET: normal gait early; mild tandem ataxia possible.
— ET produces large, irregular, oscillating loops; PD produces small, cramped spirals (micrographia).
CCS pearl: Document on physical exam: "tremor at rest / with posture / with action," handedness asymmetry, presence/absence of bradykinesia, rigidity, gait abnormality. These fields determine whether you order DaT scan, refer to neurology, or trial therapy — the CCS engine rewards specificity.
Board pearl: No bradykinesia = no Parkinson disease. Tremor alone, even if asymmetric, is insufficient — the UK Brain Bank criteria require bradykinesia plus rigidity or tremor.
— TSH — hyperthyroidism causes a fine, fast (10–12 Hz) postural tremor that mimics ET.
— Serum ceruloplasmin and 24-hour urine copper in any patient <40 with tremor, even if ET-pattern, to screen for Wilson disease (also check LFTs, slit-lamp for Kayser-Fleischer rings).
— CBC, CMP, BUN/Cr, glucose to rule out metabolic contributors.
— B12 if neuropathy or cognitive complaints.
— Medication and toxin review: beta-agonists, valproate, lithium, amiodarone, SSRIs/TCAs, stimulants, caffeine, metoclopramide and prochlorperazine (drug-induced parkinsonism), antipsychotics.
— Routine MRI brain is NOT required for classic ET or PD with a typical history and exam.
— Obtain MRI if red flags: abrupt onset, stepwise progression, focal deficits, age <40, prominent gait/cerebellar/pyramidal signs, suspicion of vascular parkinsonism, NPH, or stroke.
— Use a standardized scale (e.g., Fahn-Tolosa-Marin or MDS-UPDRS Part III) at baseline to track response.
— Assess handwriting sample, drinking from a cup, ADL impact to guide whether to treat.
Step 3 management: In a 70-year-old with bilateral symmetric action tremor, family history, normal TSH, and no bradykinesia, the workup is complete — diagnose ET clinically and discuss treatment. Ordering an MRI or DaT scan here is low-value care and a wrong answer on Step 3.
Board pearl: Always screen tremor patients <40 years old for Wilson disease — missing it is a classic malpractice and exam trap; treatment (chelation) reverses neurologic damage if caught early.
— Visualizes presynaptic dopamine transporter density in the striatum.
— Abnormal (reduced uptake, "comma → period") in PD and other neurodegenerative parkinsonisms (MSA, PSP, CBD, DLB).
— Normal in ET, drug-induced parkinsonism, psychogenic tremor, and dystonic tremor.
— Indication: clinically ambiguous cases — e.g., older patient with asymmetric tremor but no clear bradykinesia, or distinguishing tremor-predominant PD from ET.
— Does NOT distinguish PD from atypical parkinsonisms (MSA/PSP/CBD all show reduced uptake).
— Look for vascular lesions in basal ganglia (vascular parkinsonism), hummingbird sign (PSP), hot-cross-bun sign (MSA-C), putaminal rim (MSA-P), hydrocephalus (NPH).
— Not routine for ET (polygenic, low yield).
— PD genetic testing (LRRK2, GBA, PARK7, parkin) considered if onset <50, strong family history, Ashkenazi Jewish or North African Berber ancestry — relevant for clinical trial enrollment and family counseling.
— Sustained, robust response to levodopa supports idiopathic PD; minimal response suggests atypical parkinsonism or ET.
— In practice, a therapeutic trial of carbidopa-levodopa (e.g., 25/100 TID titrated) for 4–8 weeks is both diagnostic and therapeutic.
— Hyposmia present in >90% of PD, generally normal in ET — useful adjunct when DaTscan unavailable.
— Confirms REM sleep behavior disorder, a strong prodromal marker of alpha-synucleinopathy.
Key distinction: DaTscan separates ET from PD, NOT PD from atypical parkinsonism. If a question stem describes early falls, vertical gaze palsy, or autonomic failure, the answer is MRI and clinical phenotyping, not DaTscan.
Board pearl: A normal DaTscan in a patient with clinical "tremor" essentially rules out neurodegenerative parkinsonism — reframe diagnosis toward ET, drug-induced, or functional tremor.
— ET: treat when tremor causes functional impairment (writing, eating, drinking, occupational tasks) or social embarrassment. Mild tremor noted only on exam → observation and reassurance.
— PD: treat when motor symptoms interfere with function, work, or quality of life. There is no proven disease-modifying therapy, so timing is symptom-driven, not protective.
— Reduce caffeine, stress, sleep deprivation.
— Review medication list for tremorgenic drugs (beta-agonists, valproate, lithium, amiodarone, SSRIs, stimulants) and dopamine blockers (metoclopramide, prochlorperazine, antipsychotics).
— Avoid recommending alcohol for ET despite symptomatic benefit — rebound worsening and dependence risk.
— ET first-line: propranolol or primidone (roughly equivalent efficacy, ~50% reduction in tremor amplitude).
— PD first-line in younger (<65, cognitively intact): consider MAO-B inhibitor (rasagiline, selegiline) or dopamine agonist (pramipexole, ropinirole) to delay levodopa-related motor fluctuations.
— PD first-line in older (≥65) or significant disability: carbidopa-levodopa — most effective, best tolerated.
— Combine ET drugs if monotherapy partial; add topiramate or gabapentin.
— In PD, add COMT inhibitors, amantadine for dyskinesia, deep brain stimulation for refractory cases.
Step 3 management: A retired schoolteacher with bilateral hand tremor making it hard to sign checks and her father had the same — start propranolol 10 mg BID, titrate to 60–120 mg/day, recheck in 4–6 weeks with a handwriting sample to document response.
Board pearl: Levodopa is not protective and is not "saved for later" out of fear of tolerance — modern guidelines treat motor symptoms when they impair life, regardless of age.
— Propranolol (non-selective beta-blocker)
— Start 10 mg BID, titrate to 60–320 mg/day (often 80–160 mg/day).
— Long-acting once-daily formulation improves adherence.
— Contraindications: asthma, decompensated heart failure, high-degree AV block, severe bradycardia; caution in diabetes (masks hypoglycemia) and depression.
— Primidone (barbiturate, metabolized to phenobarbital)
— Start 12.5–25 mg qHS (very low) to avoid acute sedation/ataxia ("first-dose reaction"), titrate to 250–750 mg/day divided.
— Useful when beta-blocker contraindicated (asthma, bradycardia) or as adjunct.
— Side effects: sedation, ataxia, nausea, behavioral changes.
— Second-line: topiramate (start low for cognitive/word-finding side effects, paresthesias, weight loss, kidney stones), gabapentin.
— Botulinum toxin for head and voice tremor refractory to oral therapy.
— Carbidopa-levodopa — gold standard.
— Start 25/100 mg TID with meals (or 30 min before for max effect); titrate by symptoms.
— Side effects: nausea (carbidopa mitigates), orthostasis, somnolence, hallucinations, eventual motor fluctuations and dyskinesia after 5–10 years.
— Dopamine agonists (pramipexole, ropinirole, rotigotine patch)
— Useful in younger patients to delay levodopa; reduce dyskinesia risk.
— Side effects: somnolence/sleep attacks, orthostasis, peripheral edema, impulse control disorders (gambling, hypersexuality, compulsive shopping/eating) — counsel explicitly and screen at every visit.
— MAO-B inhibitors (rasagiline, selegiline) — modest benefit, well tolerated; mind serotonin syndrome risk with SSRIs/meperidine.
— Anticholinergics (trihexyphenidyl) — tremor-specific but avoid in elderly (confusion, urinary retention, falls).
— Amantadine — mild tremor and dyskinesia benefit.
Board pearl: A PD patient on pramipexole who develops new gambling losses — this is impulse control disorder, taper the agonist, do not just add a psych medication.
— Indicated for medication-refractory tremor in both ET and PD.
— ET target: ventral intermediate nucleus (VIM) of thalamus — dramatic suppression of contralateral tremor.
— PD target: subthalamic nucleus (STN) or globus pallidus interna (GPi) — improves tremor, rigidity, bradykinesia, motor fluctuations, dyskinesia; allows medication reduction with STN.
— Best candidates: clear levodopa-responsive PD, age <70 preferred, no significant cognitive impairment, no severe depression/psychosis, no axial-predominant disease.
— Does NOT improve speech, gait freezing, postural instability, or non-motor symptoms reliably.
— Risks: infection, hemorrhage (1–3%), hardware issues, mood changes, dysarthria.
— Incisionless lesioning of VIM thalamus; FDA-approved for medication-refractory ET (unilateral) and tremor-dominant PD.
— Good option for patients unwilling or unfit for DBS surgery (anticoagulation, comorbidities).
— Single-session; risks include gait imbalance, paresthesias.
— Carbidopa-levodopa enteral suspension (Duopa) via PEG-J for advanced PD with motor fluctuations refractory to oral therapy.
— Newer subcutaneous levodopa/carbidopa infusion approved as alternative.
— For head tremor, voice tremor, task-specific tremors in ET; targeted dystonic tremor.
— Diagnostic uncertainty, age <50, atypical features, inadequate response to two first-line agents, consideration of advanced therapy.
Step 3 management: A 68-year-old with PD on levodopa 5×/day with 2 hours of "off" time daily and peak-dose dyskinesias has reached advanced disease — refer to movement disorders neurology for DBS evaluation rather than adding another oral adjunct indefinitely.
Board pearl: DBS works best for symptoms that respond to levodopa — the best predictor of DBS success in PD is a clear levodopa-responsive phenotype.
— Essential tremor
— Propranolol risks: orthostatic hypotension, bradycardia, fatigue, depression, falls. Start 10 mg BID, titrate slowly; check BP and HR at every visit.
— Primidone risks: sedation, ataxia, falls; start 12.5 mg qHS, titrate weekly.
— Avoid anticholinergics (Beers criteria) — trihexyphenidyl, benztropine cause delirium and urinary retention.
— Parkinson disease
— Levodopa is first-line in elderly — better tolerated than dopamine agonists, which cause somnolence, hallucinations, orthostasis, and impulse control disorders.
— Screen for orthostatic hypotension at every visit; PD itself causes autonomic failure compounded by dopaminergic drugs.
— Monitor for levodopa-induced hallucinations and psychosis — first reduce/eliminate anticholinergics, amantadine, dopamine agonists, then reduce levodopa, then add pimavanserin or low-dose quetiapine/clozapine (avoid typical antipsychotics — worsen parkinsonism).
— Primidone and phenobarbital are renally cleared — reduce dose in CKD.
— Pramipexole is renally excreted — dose-adjust in eGFR <60; many alternatives prefer ropinirole (hepatically cleared).
— Topiramate — caution with nephrolithiasis risk and acidosis in CKD.
— Amantadine — renally cleared; avoid or dose-adjust in CKD; risk of livedo reticularis, ankle edema, confusion.
— Propranolol is hepatically metabolized — reduce dose in cirrhosis.
— Ropinirole, rasagiline, selegiline — hepatic metabolism, use with caution.
— Carbidopa-levodopa generally safe in mild–moderate hepatic disease.
Board pearl: New visual hallucinations in an elderly PD patient on multiple agents — first stop anticholinergics and amantadine, not levodopa. Cutting levodopa worsens motor function and is usually the last lever.
Step 3 management: Always perform a fall risk and orthostatic vitals assessment in tremor patients before titrating propranolol or starting levodopa in the elderly.
— Essential tremor
— Propranolol: category C; associated with fetal growth restriction, neonatal hypoglycemia, bradycardia — use lowest effective dose; coordinate with OB.
— Primidone: teratogenic risk (orofacial clefts, cardiac defects) — avoid; counsel folate supplementation if used.
— Topiramate: avoid — cleft palate risk and reduced oral contraceptive efficacy.
— For mild ET, often defer pharmacotherapy until postpartum/post-lactation.
— Parkinson disease in pregnancy (rare but possible in young-onset PD)
— Levodopa-carbidopa has the most reassuring pregnancy safety data; preferred.
— Avoid dopamine agonists, amantadine, MAO-B inhibitors when possible.
— Higher likelihood of genetic etiology (LRRK2, GBA, parkin) — refer for genetic counseling.
— Greater risk of motor fluctuations and dyskinesia with chronic levodopa — start with MAO-B inhibitor or dopamine agonist, add levodopa later.
— DBS candidacy is often favorable.
— Higher rates of depression, anxiety, dystonia; address holistically.
— Onset in teens is well described; family history nearly always present.
— Propranolol preferred (avoid primidone-related sedation affecting school).
— Counsel on school accommodations (extra time for writing, laptop use).
— Surgeons, dentists, musicians, microelectronics workers with ET may need earlier, lower-dose propranolol specifically before high-stakes tasks (situational dosing 30–60 min before).
— Propranolol is banned in precision sports (shooting, archery, golf at elite level) — disclose.
Key distinction: Young-onset PD requires genetic counseling and a different drug ladder, but young-onset ET is treated identically to adult ET with attention to occupational/academic demands.
Board pearl: A pregnant patient with disabling ET — preferred symptomatic option is as-needed low-dose propranolol in 2nd–3rd trimester after OB co-management, not primidone or topiramate.
— Functional disability: progressive worsening of fine motor tasks — writing, dressing, feeding, drinking; up to 25% retire early or change occupation.
— Social withdrawal and depression from embarrassment about visible shaking.
— Falls less common than in PD unless coexisting cerebellar features or medication side effects.
— Cognitive changes: mild executive dysfunction in long-standing ET; modestly increased risk of dementia in elderly ET, though much less than PD.
— Drug toxicity: propranolol-induced bradycardia, bronchospasm, depression; primidone sedation and falls.
— Motor:
— Motor fluctuations ("wearing off," on-off phenomenon) after 5–10 years of levodopa.
— Levodopa-induced dyskinesias — choreiform movements at peak dose.
— Freezing of gait, festination, falls — leading cause of injury.
— Non-motor:
— Orthostatic hypotension (combined disease + drug effect) → syncope, falls, hip fractures.
— Dementia: PD dementia in 30–80% over disease course; if cognitive impairment precedes or starts within 1 year of motor symptoms, consider dementia with Lewy bodies (DLB).
— Psychosis and hallucinations — often drug-induced.
— Depression (40%), anxiety, apathy.
— REM sleep behavior disorder — injuries to self/bedpartner.
— Constipation, urinary urgency, sialorrhea, dysphagia → aspiration pneumonia (leading cause of death).
— Impulse control disorders with dopamine agonists.
CCS pearl: In an advanced PD patient hospitalized for aspiration pneumonia, order speech/swallow evaluation, head-of-bed elevation, dysphagia diet, continue home PD meds on schedule, and screen for depression and constipation — missed home-dose timing causes "off" states and prolonged length of stay.
Board pearl: Aspiration pneumonia is the leading cause of death in advanced PD — proactively screen for dysphagia annually.
— Diagnostic uncertainty between ET, PD, atypical parkinsonism, dystonic tremor, or functional tremor.
— Age <50 with tremor (Wilson disease, genetic PD, dystonia).
— Red flag features: abrupt onset, stepwise progression, early falls, vertical gaze palsy, severe autonomic failure, rapid cognitive decline, pyramidal or cerebellar signs.
— Failure of two first-line agents at adequate doses.
— Consideration of DBS, focused ultrasound, or advanced PD therapies.
— Pregnancy planning with active medication needs.
— PD patients NPO (perioperative, GI illness): rapid dopamine withdrawal can precipitate parkinsonism-hyperpyrexia syndrome (NMS-like: hyperthermia, rigidity, altered mental status, autonomic instability, elevated CK). Restart dopaminergic therapy via NG tube or rotigotine patch within 24 hours.
— Acute deterioration with fever, rigidity, AMS in a PD patient → check for infection (UTI, pneumonia), drug holiday, recent neuroleptic exposure (e.g., metoclopramide for nausea).
— Hallucinations or delusions unmanageable at home → admit, work up infection/metabolic causes, adjust meds.
— Recurrent falls or fracture → inpatient PT/OT evaluation, home safety, possibly skilled nursing rehab.
— Neurology, PT, OT, speech therapy (LSVT BIG and LSVT LOUD are evidence-based), social work, mental health, palliative care in advanced disease.
— Sudden-onset tremor or asymmetric severe ET — image for stroke, MS, structural lesion.
Step 3 management: A PD patient admitted for elective hip surgery — never write "hold home meds" generically. Continue carbidopa-levodopa on schedule, use rotigotine transdermal patch as a bridge if NPO, and consult neurology for perioperative planning.
Board pearl: Metoclopramide and prochlorperazine are the classic inpatient antiemetics that precipitate or worsen parkinsonism — use ondansetron, trimethobenzamide, or domperidone (where available) instead.
— Fine, fast (10–12 Hz) postural tremor in normal individuals exacerbated by anxiety, caffeine, fatigue, hyperthyroidism, hypoglycemia, beta-agonists, stimulants, alcohol withdrawal.
— Reversible — treat the trigger; no chronic therapy needed.
— Irregular, jerky, position-dependent tremor in a body part affected by dystonia (e.g., head tremor with cervical dystonia — "null point" exists where tremor disappears in a specific head position).
— Geste antagoniste (sensory trick) relieves the dystonia.
— Treat with botulinum toxin, not propranolol.
— Low frequency (<5 Hz), worsens at the target (terminal intention), large amplitude.
— Accompanied by ataxia, dysmetria, dysdiadochokinesia, nystagmus.
— Causes: MS, stroke, tumor, spinocerebellar ataxia, alcohol-related degeneration.
— Combination of rest + postural + intention tremor, low frequency, large amplitude.
— Lesion in midbrain/thalamus (stroke, MS); responds variably to levodopa, clonazepam, anticholinergics.
— Abrupt onset, variable frequency, distractibility, entrainment to tapping at a different rate, bizarre incongruent features.
— Normal DaTscan; treat with physical therapy, CBT, address psychosocial stressors.
— High-frequency (13–18 Hz) tremor of legs while standing, relieved by sitting or walking; patient describes unsteadiness when standing still.
— Treat with clonazepam, gabapentin.
— Primary writing tremor — only when writing; otherwise normal exam.
Key distinction: Head tremor + null point + neck posturing = dystonic tremor, not ET — botulinum toxin, not propranolol, is the answer.
Board pearl: Distractibility and entrainment during exam are the bedside hallmarks of functional tremor — ask the patient to tap a complex rhythm with the unaffected hand and watch the tremor frequency change or disappear.
— Most common PD mimic; caused by dopamine receptor blockers: typical antipsychotics, risperidone, metoclopramide, prochlorperazine, and to a lesser extent SSRIs, valproate, amiodarone.
— Typically symmetric, rapid onset, no resting tremor (or symmetric tremor); resolves over weeks–months after withdrawal.
— Normal DaTscan.
— Lower-body parkinsonism — gait abnormality, falls, urinary incontinence, less tremor, poor levodopa response.
— MRI shows subcortical white matter disease, lacunes.
— Manage vascular risk factors.
— Triad: gait apraxia ("magnetic gait"), urinary incontinence, dementia ("wet, wobbly, wacky"); tremor is uncommon.
— MRI: ventriculomegaly out of proportion to atrophy; large-volume LP improves gait → confirms; treat with VP shunt.
— Early postural instability and falls (within 1 year), vertical supranuclear gaze palsy (downgaze first), axial rigidity, pseudobulbar affect, frontal cognitive changes; little tremor, poor levodopa response.
— MRI: midbrain atrophy ("hummingbird sign").
— Severe early autonomic failure (orthostasis, urinary retention/incontinence, erectile dysfunction) + parkinsonism (MSA-P) or cerebellar signs (MSA-C).
— MRI: hot-cross-bun sign (pons), putaminal rim.
— Minimal/transient levodopa response.
— Asymmetric rigidity, apraxia, alien limb phenomenon, myoclonus, cortical sensory loss; poor levodopa response.
— Cognitive impairment within 1 year of parkinsonism, fluctuating cognition, visual hallucinations, RBD, neuroleptic sensitivity.
Board pearl: Early falls + vertical gaze palsy + poor levodopa response = PSP. Early autonomic failure + cerebellar or pyramidal signs = MSA. Memorize these one-liners — they reliably appear on Step 3.
— Set realistic expectations: medications reduce amplitude ~50%, don't eliminate tremor.
— Annual review of efficacy, side effects, functional impact; titrate or switch agents.
— Encourage occupational adaptations: weighted utensils, wide-grip pens, voice-to-text software, button hooks.
— Genetic counseling for autosomal dominant family history (no formal screening yet).
— Address co-existing anxiety/depression that amplify tremor perception.
— Pharmacologic optimization as disease progresses: shorter dosing intervals, COMT inhibitors (entacapone, opicapone), MAO-B inhibitors, amantadine for dyskinesia.
— Non-motor symptom management:
— Constipation: hydration, fiber, polyethylene glycol.
— Orthostatic hypotension: hydration, salt, compression stockings, midodrine, fludrocortisone, droxidopa.
— Depression/anxiety: SSRIs/SNRIs; avoid MAO-B + SSRI combos that risk serotonin syndrome.
— RBD: melatonin first-line, clonazepam second; bedroom safety counseling.
— Sialorrhea: glycopyrrolate, botulinum toxin to salivary glands.
— Cognitive impairment: rivastigmine for PD dementia; treat sleep, mood, hearing, vision first.
— Vaccinations: annual influenza, pneumococcal, COVID-19, RSV (age-appropriate), shingles — aspiration risk magnifies infection consequences.
— Bone health: PD increases osteoporosis and fracture risk — DEXA, vitamin D, calcium, weight-bearing exercise, bisphosphonates as indicated.
— Advance care planning early — establish health care proxy, POLST, hospice criteria.
— Driving evaluation if tremor or bradykinesia affects vehicle control.
— Medication reconciliation at every visit — purge tremorgenic and dopamine-blocking drugs.
Step 3 management: In any PD patient, include annual DEXA, fall risk assessment, depression screening (PHQ-9), and advance directive discussion as standard preventive care.
Board pearl: Exercise is the only intervention with disease-modifying signal in PD — prescribe aerobic + resistance training ≥150 min/week, ideally including tai chi or dance.
— Newly diagnosed ET on therapy: recheck in 4–6 weeks — assess tremor reduction, BP/HR (propranolol), sedation/ataxia (primidone), adherence; titrate.
— Stable ET: every 6–12 months.
— Newly diagnosed PD: 1 month after starting therapy, then every 3–6 months initially; transition to every 3 months once on advanced therapy with fluctuations.
— Propranolol: resting HR (>55), BP, asthma symptoms, mood, blood glucose in diabetics.
— Primidone: sedation, ataxia, mood; no routine drug levels needed.
— Topiramate: weight, cognition, paresthesias, kidney stones, serum bicarbonate (metabolic acidosis).
— Levodopa: efficacy (UPDRS, patient diaries), timing of doses relative to protein meals (large meals delay absorption), orthostatic vitals, hallucinations, dyskinesias, sleep.
— Dopamine agonists: screen for impulse control disorders at every visit (gambling, shopping, sexual behavior, binge eating), daytime sleepiness, edema.
— MAO-B inhibitors: check for serotonergic drug interactions.
— Physical therapy — gait, balance, freezing strategies; LSVT BIG is PD-specific evidence-based.
— Speech therapy — LSVT LOUD improves hypophonia; swallow evaluation for dysphagia.
— Occupational therapy — ADL adaptation, home safety, adaptive equipment.
— Exercise prescription — aerobic, resistance, balance, flexibility; boxing programs, tai chi, dance have RCT support in PD.
— Mental health — CBT for tremor-related anxiety; treat depression aggressively.
— Support groups — IETF (ET), Michael J. Fox Foundation, Parkinson Foundation patient networks.
CCS pearl: When advancing the clock on a PD patient, schedule a follow-up neurology visit within 4–6 weeks of any medication change and obtain PT/OT/speech referrals as standing orders — these are explicitly rewarded order entries.
Board pearl: A PD patient whose levodopa "isn't working anymore" — first check timing with protein meals; advise levodopa 30–60 min before or 1–2 hours after meals.
— Both ET and PD can impair driving (reaction time, motor control, cognition, visual scanning).
— Obtain a formal driving evaluation when tremor affects steering control, when bradykinesia/rigidity slows reactions, or when cognition declines.
— State reporting laws vary — some states (e.g., California, Pennsylvania) mandate physician reporting of conditions affecting driving (dementia, lapses of consciousness); know your state.
— DBS and focused ultrasound require capacity assessment, discussion of irreversibility (especially MRgFUS lesioning), risks (hemorrhage, infection, dysarthria), and realistic expectations — DBS does not improve gait freezing, postural instability, or non-motor symptoms.
— Dopamine agonists: document explicit counseling about impulse control disorders; patients have sued over undisclosed gambling losses.
— PD patients admitted to hospital: do not automatically hold home dopaminergic regimens; use rotigotine patch as a bridge if NPO. Missed doses cause parkinsonism-hyperpyrexia syndrome, falls, aspiration.
— Avoid contraindicated medications in PD on admission: metoclopramide, prochlorperazine, haloperidol, risperidone. Place EMR alerts.
— Discharge reconciliation — confirm exact dose timing (often non-standard, e.g., q3h), refer to neurology within 2–4 weeks, ensure pharmacy can compound or supply.
— Address early, before cognitive decline impairs capacity. Document health care proxy, advance directive, code status, preferences regarding feeding tubes for dysphagia.
— Document functional limitations objectively (handwriting samples, timed tasks) for FMLA, ADA accommodations, disability applications.
Board pearl: A common Step 3 stem: PD patient post-op on metoclopramide for nausea, develops worsened rigidity and confusion — answer is discontinue metoclopramide, switch to ondansetron, and ensure home PD meds resume on schedule.
— Most common adult movement disorder; autosomal dominant in ~half.
— Bilateral, symmetric, action tremor; head + voice common; legs spared.
— Improves with alcohol in 50–70% (do not prescribe).
— First-line: propranolol or primidone.
— Handwriting: large and tremulous.
— Modest association with increased dementia risk in elderly.
— Unilateral resting pill-rolling tremor 4–6 Hz, re-emergent tremor on posture.
— TRAP: Tremor, Rigidity (cogwheel), Akinesia/bradykinesia, Postural instability.
— Lewy bodies (alpha-synuclein) in substantia nigra pars compacta.
— Hyposmia, RBD, constipation, depression precede motor symptoms.
— Handwriting: micrographia.
— First-line elderly: carbidopa-levodopa; younger: agonist or MAO-B inhibitor.
— Aspiration pneumonia is leading cause of death.
— DaTscan: abnormal in PD, normal in ET — does NOT distinguish PD from atypical parkinsonism.
— Levodopa response: robust in PD, absent in PSP/MSA/CBD/vascular parkinsonism.
— MRI hummingbird sign = PSP; hot-cross-bun sign = MSA-C.
— Wilson disease in any tremor patient <40.
Board pearl: When you see asymmetric tremor + reduced arm swing + hyposmia + acting out dreams, the diagnosis is Parkinson disease — no further testing needed before initiating treatment.
Step 3 management: Recognize and act on the handwriting clue — micrographia → PD; megalographic tremor → ET — it is the single most reliable history pearl.
— 68-year-old retired accountant with 5 years of bilateral hand shaking when reaching for coffee, improves with wine at dinner, father had the same; exam shows postural and kinetic tremor, normal gait, no bradykinesia.
— Answer: Essential tremor → propranolol (or primidone if asthma/HFrEF).
— 70-year-old with 6 months of right-hand shaking at rest, stops when reaching, decreased right arm swing, hypomimia, soft voice, wife reports he acts out dreams and has lost his sense of smell.
— Answer: Parkinson disease → carbidopa-levodopa.
— 65-year-old with asymmetric arm tremor unclear whether rest or action; mild slowness on finger taps but ambiguous bradykinesia; clinician unsure.
— Answer: DaTscan to distinguish ET from neurodegenerative parkinsonism.
— 60-year-old on metoclopramide for gastroparesis develops symmetric bradykinesia and mild tremor.
— Answer: Discontinue metoclopramide; expect resolution over weeks.
— 68-year-old with falls in the first year, vertical gaze palsy, minimal tremor, no levodopa response.
— Answer: PSP; MRI for hummingbird sign.
— 28-year-old with bilateral tremor, dysarthria, elevated LFTs, brownish corneal ring.
— Answer: Ceruloplasmin and 24-hour urine copper; not propranolol.
— 62-year-old PD patient on pramipexole with new gambling debts and compulsive online shopping.
— Answer: Reduce/discontinue dopamine agonist, substitute levodopa.
— Hospitalized PD patient given prochlorperazine for nausea develops rigidity, confusion, fever.
— Answer: Stop prochlorperazine, switch to ondansetron, resume home levodopa.
— Patient with "no-no" head tremor that disappears when she turns her head to the right (null point).
— Answer: Dystonic tremor → botulinum toxin, not propranolol.
Board pearl: The clue is almost always in a single sentence — "tremor while reaching" (ET), "tremor when hands rest in lap" (PD), "metoclopramide" (drug-induced), "falls in first year" (PSP), "Kayser-Fleischer ring" (Wilson). Train pattern recognition.
Essential tremor is a bilateral, symmetric action tremor often familial and alcohol-responsive treated first with propranolol or primidone, while Parkinson disease is an asymmetric resting pill-rolling tremor accompanied by bradykinesia, rigidity, and non-motor features (hyposmia, RBD, constipation) treated with carbidopa-levodopa as first-line in older adults.
— ET → propranolol (60–320 mg/day) or primidone (start 12.5–25 mg qHS, titrate to 250–750 mg/day); add topiramate or gabapentin as adjuncts; botulinum toxin for head/voice tremor; DBS of VIM or MR-guided focused ultrasound thalamotomy for medication-refractory cases.
— PD → carbidopa-levodopa first-line in elderly or significantly disabled; MAO-B inhibitor or dopamine agonist in younger patients to delay levodopa; treat non-motor symptoms (constipation, orthostasis, depression, RBD, dementia) proactively; DBS of STN/GPi for advanced motor fluctuations.
Board pearl: When in doubt between ET and PD on a Step 3 stem, scan for three discriminators in order — tremor activation state, asymmetry, and presence of bradykinesia — and the diagnosis (and therefore the management answer) becomes nearly automatic.