Eduovisual
Nervous System & Special Senses
Parkinson disease: diagnosis and dopaminergic therapy
— Second most common neurodegenerative disorder after Alzheimer disease
— Mean onset ~60 years; men > women (~1.5:1)
— Risk factors: advancing age, pesticide/herbicide exposure, rural living, well-water use, prior head trauma, family history (LRRK2, GBA, SNCA, PARK7, PINK1 mutations)
— Protective associations: tobacco use, caffeine, physical activity (do not recommend smoking; tested as epidemiologic trivia)
— Older adult with asymmetric resting tremor (4–6 Hz, "pill-rolling") that diminishes with action
— New micrographia, stooped posture, decreased arm swing, shuffling gait, hypomimia ("masked facies")
— Soft hypophonic voice, drooling, constipation, REM sleep behavior disorder, hyposmia (premotor features that may predate motor signs by years)
— Spouse reports patient "looks depressed" or "moves slowly" — bradykinesia is the cardinal required feature
— Bradykinesia plus rest tremor and/or rigidity is required
— Supportive: clear, sustained levodopa response; levodopa-induced dyskinesia; olfactory loss; cardiac MIBG denervation
— Diagnosis remains clinical; imaging is adjunctive
Board pearl: A unilateral resting tremor that disappears with voluntary movement and re-emerges after a latency when the arms are held outstretched (re-emergent tremor) is highly specific for PD and helps distinguish it from essential tremor, which is action-predominant and bilateral.
— Tremor: 4–6 Hz resting, asymmetric, "pill-rolling," worsens with stress/mental tasks (serial 7s), improves with action
— Rigidity: cogwheel (tremor superimposed on lead-pipe) on passive movement; activated by contralateral voluntary movement (Froment maneuver)
— Akinesia/bradykinesia: slowness with decrement in amplitude and speed on repetitive movement (finger taps, foot taps); required for diagnosis
— Postural instability: late feature; early falls suggest atypical parkinsonism
— REM sleep behavior disorder (RBD): dream enactment, kicking/punching spouse — single strongest prodromal marker
— Hyposmia (90% of PD patients)
— Constipation, orthostatic lightheadedness, urinary urgency
— Depression, anxiety, apathy
— Medication review for drug-induced parkinsonism (metoclopramide, prochlorperazine, typical antipsychotics, valproate)
— Falls, freezing of gait, hallucinations (early hallucinations → suspect DLB)
— Cognitive complaints (PD dementia typically emerges >1 year after motor onset; DLB <1 year)
— Autonomic symptoms (severe early dysautonomia → MSA)
— Vertical gaze, early falls within 1 year → PSP
— Handwriting changes (micrographia), buttoning, turning in bed, getting out of chairs, driving safety
Key distinction: One-year rule for dementia — cognitive decline preceding or within 1 year of parkinsonism = Dementia with Lewy bodies; cognitive decline arising well after established PD = Parkinson disease dementia. This single timing question is a recurrent Step 3 vignette discriminator and changes prognosis, neuroleptic safety counseling, and family expectations.
— Hypomimia (reduced blink rate <15/min, masked facies), decreased spontaneous swallowing → drooling
— Stooped (simian) posture, decreased arm swing on affected side while walking
— Hypophonic, monotone speech; palilalia (repetition of syllables)
— Finger taps, hand opening/closing, foot taps: look for decrement in amplitude (hallmark) and speed across 10–15 repetitions
— Cogwheel rigidity: passively flex/extend wrist while patient taps opposite hand on thigh (activation maneuver)
— Rest tremor: have patient count backward from 100 with hands resting in lap — distraction unmasks PD tremor
— Re-emergent tremor: arms outstretched; tremor reappears after a 5–10 second latency
— Pull test (retropulsion): stand behind patient, warn them, then a brisk pull on shoulders — taking >2 steps backward or falling = abnormal
— Shuffling, festinating gait, en bloc turning (multiple small steps to turn), freezing at thresholds
— Symmetric onset, early falls (<1 yr), rapid progression, wheelchair within 5 years
— Vertical supranuclear gaze palsy → PSP
— Severe early autonomic failure, cerebellar signs, stridor → MSA
— Cortical signs (apraxia, alien limb, cortical sensory loss) → CBD
— Stepwise progression with vascular risk factors → vascular parkinsonism (lower-body predominant)
— Check supine and after 3 minutes standing; drop ≥20/10 mmHg suggests autonomic involvement (common in PD, severe/early in MSA)
Board pearl: Asymmetry persisting throughout the disease course is one of the most reliable features distinguishing idiopathic PD from atypical parkinsonian syndromes, which tend to become symmetric rapidly.
— Exclude mimics and reversible causes of parkinsonism
— Establish baseline before initiating dopaminergic therapy
— TSH — hypothyroidism mimics bradykinesia/hypomimia
— CBC, CMP — baseline renal/hepatic function before therapy
— B12 and folate — gait/cognitive contributors
— Ceruloplasmin and 24-hr urine copper if age <50 → rule out Wilson disease (mandatory in young-onset parkinsonism, with slit-lamp exam for Kayser-Fleischer rings)
— HIV, RPR in atypical/young presentations
— Consider heavy metals (manganese) with occupational history (welders, miners)
— Stop offending agents and reassess in 4–6 weeks before labeling as PD:
— MRI brain is not required for diagnosis but obtain when atypical features present (early falls, symmetric signs, dementia, vascular risk, age <50)
— Look for: "hummingbird sign" (PSP — midbrain atrophy), "hot cross bun" (MSA-C), putaminal slit/iron deposition (MSA-P), normal pressure hydrocephalus, strokes
Step 3 management: In a 68-year-old on chronic metoclopramide for diabetic gastroparesis presenting with new bradykinesia and tremor, the next best step is to discontinue metoclopramide and reassess in 4–6 weeks before initiating levodopa or ordering advanced imaging.
— Visualizes presynaptic dopamine transporter (DAT) density in the striatum
— Reduced/asymmetric uptake ("comma → period" shape, then absent putaminal signal) supports degenerative parkinsonism
— Cannot distinguish PD from MSA, PSP, or CBD — all show reduced uptake
— Normal DaTscan essentially excludes neurodegenerative parkinsonism
— Distinguishing essential tremor (normal scan) from PD/tremor-dominant parkinsonism (abnormal)
— Distinguishing drug-induced parkinsonism (normal — postsynaptic effect) from underlying PD (abnormal)
— Diagnostic uncertainty in early or atypical presentations
— MIBG cardiac scintigraphy: reduced cardiac sympathetic uptake in PD; preserved in MSA (not widely used in US)
— Transcranial sonography: hyperechogenic substantia nigra in PD (operator-dependent, less common in US practice)
— FDG-PET: helpful in atypical syndromes (specific metabolic patterns for PSP, MSA, CBD)
— α-synuclein seed amplification assay (SAA) in CSF — high sensitivity/specificity for synucleinopathies; increasingly used in research and select clinical settings
— Skin biopsy for phosphorylated α-synuclein deposition
— Sustained, robust response to levodopa is supportive
— Lack of response after ≥1000 mg/day for ≥1 month suggests atypical parkinsonism
— Consider in age <50, strong family history, or Ashkenazi Jewish ancestry (LRRK2 G2019S, GBA)
— Pre-test genetic counseling required
Board pearl: A patient with an action tremor and unclear exam in whom you cannot decide between essential tremor and tremor-predominant PD → DaTscan: normal favors ET (treat with propranolol or primidone), abnormal favors PD (consider dopaminergic therapy).
— Initiate when symptoms cause functional, occupational, or social impairment
— No benefit to delaying therapy "to save" levodopa response — modern data refute the levodopa-toxicity hypothesis (ELLDOPA, LEAP trials)
— Age and cognitive status — strongest determinants
— Functional disability severity
— Dominant symptom (tremor vs bradykinesia)
— Comorbidities (orthostasis, psychosis, sleep, impulse control risk)
— Employment/social demands
— Age >65–70 or cognitive impairment → start carbidopa-levodopa first (efficacy > side effects)
— Age <60, cognitively intact, employed, mild symptoms → consider dopamine agonist (pramipexole, ropinirole) or MAO-B inhibitor (rasagiline, selegiline) to delay levodopa-related motor complications; though levodopa is increasingly used first-line at any age given superior efficacy
— Tremor-predominant, young → anticholinergic (trihexyphenidyl) is an option but avoid in elderly (cognitive/anticholinergic burden)
— Aerobic exercise (≥150 min/week), resistance training, tai chi, dance, boxing programs — evidence for symptom and gait benefit
— Physical therapy (LSVT BIG), speech therapy (LSVT LOUD) for hypophonia/dysarthria
— Nutrition: high-fiber, hydration for constipation; protein redistribution if motor fluctuations emerge
— Sleep hygiene; screen for and treat depression
Step 3 management: A 58-year-old engineer with mild right-hand tremor and bradykinesia affecting his computer work — start carbidopa-levodopa (or a dopamine agonist if motor-fluctuation risk is the dominant concern) plus referral to PT/exercise program; document baseline UPDRS for follow-up.
— Levodopa crosses BBB → converted to dopamine; carbidopa is a peripheral DOPA decarboxylase inhibitor preventing peripheral conversion (reduces nausea, orthostasis)
— Start: 25/100 mg IR, ½ tablet TID with meals initially, then between meals once tolerated; titrate by symptom response
— Take 30–60 min before or 1–2 hr after protein meals (large neutral amino acids compete for absorption)
— Formulations: immediate-release, controlled-release (CR), extended-release capsule (Rytary), enteral suspension (Duopa), inhaled (Inbrija) for "off" episodes, sublingual apomorphine film
— Side effects: nausea, orthostasis, somnolence, dyskinesias (long-term), hallucinations, impulse-control behaviors (less than agonists)
— Direct D2/D3 receptor activation; longer half-life → smoother coverage, less dyskinesia early on
— Higher rates of impulse control disorders (pathologic gambling, hypersexuality, binge eating, compulsive shopping — counsel patient AND family), sleep attacks, leg edema, hallucinations
— Avoid in elderly, demented, or psychotic patients
— Apomorphine SC/SL for rescue of "off" episodes
— Modest monotherapy benefit in early disease; adjunct for motor fluctuations
— Avoid concomitant meperidine, tramadol, SSRIs/SNRIs at high doses (serotonin syndrome risk — typically clinically minor at MAO-B doses but still tested)
— Used as levodopa adjuncts to extend "on" time
Board pearl: Counsel every patient starting a dopamine agonist and a designated family member about impulse control disorders; ask about gambling, online shopping, and sexual behavior at every visit — documentation is exam- and malpractice-relevant.
— Motor fluctuations ("wearing off," delayed/no "on"), troublesome dyskinesias, refractory tremor — despite optimized oral regimens
— Patient retains good levodopa responsiveness (predicts surgical success)
— Targets: subthalamic nucleus (STN) — most common, allows medication reduction; globus pallidus internus (GPi) — better for dyskinesia control, less mood/cognitive risk; VIM thalamus — tremor-only
— Ideal candidate: <70 years, levodopa-responsive, no significant cognitive impairment, no active psychiatric disease, motor complications limiting QoL
— Contraindications: dementia, severe depression/psychosis, atypical parkinsonism, poor levodopa response
— Complications: infection, hemorrhage (~1–2%), lead migration, mood changes, dysarthria, weight gain
— Incisionless lesional therapy; unilateral; option for tremor or asymmetric disease in patients declining or ineligible for DBS
— Continuous jejunal infusion via PEG-J; for advanced motor fluctuations when DBS not appropriate
— Risks: stoma complications, polyneuropathy (monitor B12/homocysteine)
— Wearing off → shorten levodopa interval, add COMT or MAO-B inhibitor, switch to ER formulation
— Dyskinesias → reduce single levodopa dose (more frequent, smaller), add amantadine ER, consider DBS
— Freezing of gait → physical therapy with cueing strategies, optimize levodopa, consider MAO-B; poorly responsive
Step 3 management: A 62-year-old with 8 years of PD on optimized oral therapy now spending >25% of waking hours in "off" state with disabling dyskinesias — refer to a movement disorders center for DBS evaluation; obtain neuropsychological testing as part of workup.
— Higher risk of hallucinations, delirium, orthostasis, falls, cognitive decline with dopaminergic drugs
— Levodopa is the preferred first-line agent; avoid dopamine agonists and anticholinergics whenever possible
— Start low, titrate slowly: 25/100 carbidopa-levodopa ½ tablet BID–TID, increase weekly
— Screen for dementia (MoCA) and depression (PHQ-9) at baseline and annually
— Polypharmacy review — deprescribe anticholinergics (oxybutynin, diphenhydramine, TCAs), benzodiazepines, sedating antihistamines
— Fall prevention: home safety evaluation, PT, vitamin D, vision/hearing optimization, bone health (DXA — PD is associated with increased fracture risk and lower BMD)
— Amantadine is renally cleared — dose-adjust or avoid; toxicity manifests as confusion, myoclonus, livedo
— Pramipexole is renally cleared — reduce dose with CrCl <50 mL/min
— Ropinirole primarily hepatic — preferred over pramipexole in CKD
— Levodopa requires no renal adjustment
— Tolcapone — black-box hepatotoxicity; requires LFT monitoring (q2–4 weeks initially); use only after entacapone failure
— Ropinirole, rasagiline, selegiline — caution in significant hepatic disease
— Entacapone and opicapone — generally well-tolerated
— Never stop levodopa abruptly — risk of neuroleptic malignant–like syndrome (parkinsonism-hyperpyrexia syndrome): fever, rigidity, autonomic instability, elevated CK
— Maintain doses via NG tube or rotigotine patch (~10 mg ≈ levodopa 100 mg, very rough) if NPO
— Avoid antiemetics with D2 antagonism — use ondansetron or trimethobenzamide instead of metoclopramide/prochlorperazine
CCS pearl: For a PD inpatient made NPO for surgery, order "continue home carbidopa-levodopa via NG tube" or apply rotigotine patch; explicitly write "avoid metoclopramide, prochlorperazine, haloperidol" in the order set.
— Higher likelihood of genetic etiology: LRRK2, Parkin (PRKN), PINK1, DJ-1, GBA, SNCA
— Refer for genetic counseling; relevant to family planning and emerging precision therapies (GBA-PD trials)
— Always rule out Wilson disease in PD-like presentation under age 50: ceruloplasmin, 24-hour urinary copper, slit-lamp for KF rings, hepatic panel
— More dystonia, slower progression, but earlier dyskinesias and motor fluctuations
— Psychosocial: employment, disability planning, raising children — engage social work early
— Rare but increasing as YOPD recognized
— Levodopa has the most reassuring pregnancy/lactation data among dopaminergics; generally continued at lowest effective dose
— Dopamine agonists suppress prolactin → may interfere with lactation
— Avoid amantadine (teratogenic in animals), MAO-B inhibitors (insufficient data)
— Multidisciplinary management with MFM and movement disorders
— Common in psychiatric and elderly populations on antiemetics/antipsychotics
— Typically symmetric, postural tremor more than rest tremor, develops weeks to months after starting agent
— Treatment: discontinue or switch offending drug; expect resolution over weeks–months
— Persistent symptoms after 6 months → suspect underlying PD unmasked by the drug → DaTscan helpful
— High caregiver burden; screen for caregiver depression/burnout
— Education on disease trajectory, medication timing, fall prevention, advance care planning
— Connect to Parkinson's Foundation, Michael J. Fox Foundation, local support groups
Key distinction: In a 35-year-old with parkinsonism, hepatic dysfunction, and behavioral change — think Wilson disease, not PD; treatment is chelation (penicillamine, trientine) plus zinc, not levodopa.
— Wearing off: predictable return of symptoms before next dose
— Delayed "on" / no "on": protein meal interference, gastroparesis
— Peak-dose dyskinesias: choreiform movements at maximal plasma levodopa
— Diphasic dyskinesias: dystonia at beginning and end of dose
— Off-period dystonia (often early morning foot dystonia)
— Freezing of gait — often levodopa-unresponsive
— Visual hallucinations (people, animals; often retained insight initially) — first reduce anticholinergics, then amantadine, then dopamine agonists, last reduce levodopa; if pharmacologic treatment needed → pimavanserin, quetiapine, or clozapine (avoid haloperidol, risperidone, olanzapine)
— Depression (~40%); SSRIs/SNRIs first-line; pramipexole has antidepressant properties
— Anxiety, apathy
— Impulse control disorders — agonist-related; reduce/stop agonist
— Dopamine dysregulation syndrome: compulsive self-medication
— Mild cognitive impairment → PD dementia in ~80% over 20 years
— Treat dementia with rivastigmine (FDA-approved for PD dementia)
— Orthostatic hypotension — non-pharm (compression, salt, fluids, head-of-bed elevation); pharm (midodrine, droxidopa, fludrocortisone)
— Constipation, urinary urgency, sexual dysfunction, sialorrhea (glycopyrrolate, botulinum toxin to parotid)
— RBD (clonazepam, melatonin), excessive daytime sleepiness, RLS, insomnia
Board pearl: Hallucinations in PD → first reduce/discontinue PD meds in reverse order of efficacy (anticholinergics → amantadine → MAO-B → agonist → COMT → levodopa); if antipsychotic needed, use pimavanserin, quetiapine, or clozapine.
— Diagnostic uncertainty, atypical features, red flags
— Young-onset PD
— Motor complications refractory to primary care titration
— Consideration of advanced therapies (DBS, infusion therapies)
— Significant neuropsychiatric symptoms
— Parkinsonism-hyperpyrexia syndrome — ICU-level care; hyperthermia, rigidity, AMS, elevated CK after dopaminergic interruption or rapid taper
— Acute psychosis with safety risk
— Severe orthostatic hypotension with syncope/injury
— Aspiration pneumonia, severe dysphagia, failure to thrive
— Recurrent falls with injury or inability to manage at home
— Surgical procedures requiring perioperative coordination
— Continue home PD medications on schedule (time-critical; pharmacy delays cause "off" states and falls) — many institutions have PD med safety protocols
— Order "administer at home times, not standard hospital times"
— NPO/dysphagia → switch to rotigotine patch or NG-administered levodopa solution
— Aspiration precautions, swallow evaluation by SLP
— Fall precautions, bed alarm, PT consult
— Avoid: haloperidol, metoclopramide, prochlorperazine, promethazine
— DVT prophylaxis (immobility risk)
— Delirium screening (CAM) daily
— Advance care planning at diagnosis and revisited annually
— Palliative care referral with dementia, recurrent aspiration, severe disability
— Hospice eligibility: end-stage with FAST ≥7c, recurrent aspiration, weight loss
CCS pearl: First three orders for a PD patient admitted with pneumonia: (1) Continue carbidopa-levodopa at home times via NG if NPO, (2) Aspiration precautions + SLP swallow evaluation, (3) Avoid metoclopramide/haloperidol — flag in allergies as "intolerance."
— Early postural instability with backward falls (within first year)
— Vertical supranuclear gaze palsy (downgaze first), axial rigidity > limb, frontal cognitive/behavioral changes, "surprised" facial expression
— Symmetric, poor/no levodopa response
— MRI: "hummingbird sign" (midbrain atrophy on sagittal)
— Severe early autonomic failure (orthostasis, urinary incontinence, erectile dysfunction)
— MSA-P: parkinsonism predominant; MSA-C: cerebellar predominant
— Symmetric, rapidly progressive, poor/transient levodopa response, inspiratory stridor, REM sleep behavior disorder
— MRI: "hot cross bun" sign in pons, putaminal atrophy/hyperintense rim (MSA-P)
— Markedly asymmetric rigidity and dystonia, apraxia, alien limb phenomenon, cortical sensory loss, myoclonus
— Poor levodopa response
— Parkinsonism + dementia within 1 year of onset
— Fluctuating cognition, visual hallucinations, REM sleep behavior disorder
— Severe neuroleptic sensitivity — avoid antipsychotics; use pimavanserin/quetiapine if essential
— Stepwise progression, lower-body predominant ("lower half parkinsonism"), gait apraxia, vascular risk factors, pyramidal signs
— MRI: extensive white matter disease, lacunes in basal ganglia
— Poor levodopa response; treat vascular risk factors aggressively
— Triad: gait disturbance ("magnetic"), urinary incontinence, dementia ("wet, wobbly, wacky")
— MRI: ventriculomegaly disproportionate to atrophy; large-volume LP improves gait → VP shunt candidate
Key distinction: Levodopa responsiveness is the single most useful clinical separator — robust, sustained response (>30% UPDRS improvement) favors idiopathic PD; minimal/absent response should prompt reconsideration toward PSP, MSA, CBD, or vascular parkinsonism.
— Bilateral action/postural tremor of hands, head ("yes-yes" or "no-no"), voice
— Family history (autosomal dominant in ~50%), improves with alcohol
— No rigidity, bradykinesia, or asymmetric resting tremor
— Treatment: propranolol (first-line) or primidone; topiramate, gabapentin second-line; focused ultrasound or DBS for refractory
Board pearl: Action tremor + family history + alcohol responsiveness = essential tremor; rest tremor + asymmetry + bradykinesia = Parkinson disease. Propranolol treats ET (and PD anxiety) but not PD itself.
— No therapy proven to alter disease progression to date
— Exercise has the strongest evidence for potential disease-modifying effect; prescribe formally
— Anticipate and treat motor fluctuations with regimen adjustments rather than dose escalation alone
— Strategies for wearing off: shorten interval, add COMT inhibitor (entacapone/opicapone), add MAO-B (rasagiline/safinamide), switch to extended-release levodopa (Rytary)
— Dyskinesias: smaller, more frequent levodopa doses; add amantadine ER (Gocovri); consider DBS
— Inhaled levodopa (Inbrija) or sublingual apomorphine for rescue of off episodes
— Bone health: PD patients have higher fall and fracture risk; DXA, vitamin D, calcium, osteoporosis treatment as indicated
— Cardiovascular screening: lipids, BP (note orthostatic readings); BP targets individualized — aggressive BP lowering worsens orthostasis
— Cancer screening per USPSTF — note increased melanoma risk in PD; annual skin checks
— Vaccinations: influenza annually, pneumococcal, RSV (≥60), shingles, COVID — aspiration pneumonia is a leading cause of death
— Dental care — sialorrhea and dysphagia complicate oral hygiene
— Mediterranean or MIND diet; adequate fiber and fluid for constipation
— Avoid high-protein meals at time of levodopa dose
— Driving safety: formal driving evaluation when reaction time, attention, or motor signs raise concern; mandatory reporting varies by state
— Firearm safety, especially with hallucinations or dementia
— Discuss at diagnosis; revisit annually and at major transitions (DBS, dementia onset, recurrent falls)
Step 3 management: In a PD patient with wearing-off after 4 years of levodopa, the next best step is to shorten the dosing interval and/or add entacapone or rasagiline before escalating to invasive therapies; document UPDRS off/on times.
— Stable, early disease: every 6 months in primary care, annual neurology
— Active titration or motor fluctuations: every 3 months
— Advanced disease, cognitive/psychiatric issues: every 1–3 months, often co-managed with neurology and palliative care
— Symptom diary review (off times, dyskinesias, falls, hallucinations)
— UPDRS or MDS-UPDRS for tracking; functional status (ADLs/IADLs)
— Orthostatic vitals (supine and standing after 3 min)
— Cognitive screen (MoCA annually; more frequent if decline)
— PHQ-9, GAD-7 for depression/anxiety
— Screen for impulse control behaviors (especially on agonists); ask family
— REM sleep behavior disorder, daytime sleepiness (Epworth)
— Constipation, urinary, sexual function
— Falls assessment and Timed Up and Go (>13.5 sec = fall risk)
— Medication reconciliation; weight; swallowing
— Physical therapy: LSVT BIG, treadmill training, balance, cueing for freezing
— Occupational therapy: ADL adaptation, home safety, handwriting
— Speech-language pathology: LSVT LOUD for hypophonia; swallow evaluation (video fluoroscopy if aspiration risk)
— Social work for caregiver support, disability paperwork
— Mental health: CBT for depression/anxiety; caregiver counseling
— Medication timing (especially relative to protein meals)
— Recognize and report impulse control symptoms
— Carry a medication list and "do not give" list (metoclopramide, haloperidol, prochlorperazine) — wallet card
Board pearl: A PD patient describing "I can't be heard at family dinners anymore" warrants referral to SLP for LSVT LOUD, not a medication change — speech therapy outperforms pharmacology for hypophonia.
— Bradykinesia, freezing, daytime sleepiness, dementia, and "sleep attacks" (especially with dopamine agonists) impair driving
— Counsel and document at every visit; refer for formal on-road driving evaluation when concern arises
— State-specific mandatory reporting laws (e.g., California, Pennsylvania, Oregon, Nevada, New Jersey, Delaware) require physician reporting of cognitive/neurologic conditions impairing driving — know your state
— Assess capacity early, especially for DBS and advance directives; capacity is decision-specific, not global
— DBS consent: discuss surgical risks (hemorrhage, infection), realistic outcomes (motor symptoms improve; cognition, speech, axial symptoms may not), reversibility, lifestyle changes (MRI restrictions, device management)
— Document explicit counseling about gambling, hypersexuality, compulsive shopping/eating when prescribing dopamine agonists
— Inform a family member with patient permission — patients often lack insight; this is both safety and risk-management practice
— Hospital admission, surgery, SNF placement: medication timing errors cause "off" states, aspiration, falls, and rare parkinsonism-hyperpyrexia syndrome
— Use medication reconciliation with exact home times, allergy-list "do not administer" (metoclopramide, haloperidol, prochlorperazine, promethazine)
— Provide written discharge instructions with med times and emergency "do not give" list
— Elder abuse/neglect — PD patients are vulnerable; report suspected abuse per state law
— Firearm safety — counsel removal/safe storage when hallucinations or dementia present
— Honor advance directives; involve palliative care early
— Withdrawing dopaminergic therapy at end of life must be gradual to avoid hyperpyrexia syndrome unless actively dying
Step 3 management: A PD patient is admitted to a SNF and the formulary substitutes metoclopramide for nausea; the safest next step is to contact the facility, change to ondansetron, and add metoclopramide/prochlorperazine to the allergy list — a documented transition-of-care intervention.
Board pearl: "Sleep attacks" while driving on a dopamine agonist — discontinue/switch the agonist and counsel driving cessation until resolved; this is a recurrent stem.
Step 3 management: When the stem mentions "avoid which medication" in a PD patient, the canonical answers are metoclopramide, prochlorperazine, haloperidol, and risperidone.
Parkinson disease is a clinically diagnosed synucleinopathy defined by asymmetric bradykinesia plus rest tremor and/or rigidity, managed long-term with individualized dopaminergic therapy — carbidopa-levodopa as the most effective agent — while anticipating motor fluctuations, neuropsychiatric complications, and the critical importance of medication timing across every care transition.
Board pearl: Across every Step 3 PD vignette, the highest-yield single intervention is getting the levodopa dose given on time and avoiding D2-blocking antiemetics and antipsychotics — these two actions prevent the majority of inpatient PD harm.