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Nursing Field Notes / Neuro · Degenerative · Med-Surg
🧠 NEURO SET NG-255 Neuro Overview NG-069 Alzheimer's NG-244 Dementia vs Delirium NG-258 Parkinson's NG-253 MS NG-245 Guillain-Barré

Parkinson's Disease 🧊

No dope in the park — dopamine DOWN, acetylcholine relatively UP

NG-258 NEURO · MOVEMENT ADHD-friendly visual edition

Parkinson's is a movement disorder caused by the progressive death of dopamine-producing neurons in the substantia nigra of the midbrain. Less dopamine means acetylcholine is left relatively dominant, and the result is the classic tetrad — Tremor at rest, Rigidity, Akinesia/bradykinesia and Postural instability. It affects gross subconscious movement of skeletal muscle: the automatic things you never think about — swinging your arms, blinking, swallowing your own saliva, making a facial expression. For the underlying neuroanatomy, see NG-255 Neuro Overview.

📄 Simple Nursing original — opens in Drive →

🧬 LOW DOPAMINESubstantia nigra neurons die. By the time symptoms show, 60–80% are already gone. ACh is relatively HIGH.
🎯 T · R · A · PTremor at rest · Rigidity (cogwheel) · Akinesia/bradykinesia · Postural instability.
🚨 FALLS + ASPIRATIONShuffling festinating gait and dysphagia with drooling. Suction at the bedside.
💊 LEVODOPA–CARBIDOPAGive it ON TIME. Watch for wearing-off and on–off. Nothing cures it.
🧬

WHY IT HAPPENS

CAUSE

Dopamine neurons die in the substantia nigra and the see-saw tips.

FIGURE 1 · WHERE PARKINSON'S STARTS — the substantia nigra goes paleRead LEFT (normal) → RIGHT (Parkinson's) · same slice, same magnification① NORMAL MIDBRAINSubstantia nigra is DARK — full of pigmented dopamine neurons② PARKINSON'S MIDBRAINSubstantia nigra is PALE — the pigmented neurons have diedSUBSTANTIA NIGRALatin for “black substance” —it is black because it is full ofpigmented dopamine neuronsRed nucleusSUBSTANTIA NIGRA — PALEBy the time symptoms appear, roughly60–80% of these neurons are alreadygone. Damage is not recoverable.anterior (front)AXIAL SLICE through the midbrainfront of the head at the TOPDOT COLORsurviving pigmented neuronlost / depigmented neuron

This is why a scan cannot diagnose Parkinson's early: the loss is microscopic and enormous before the first tremor appears.

🧪 Definition in one sentence

Parkinson's disease is a chronic, progressive movement disorder caused by the death of dopamine-producing neurons in the substantia nigra, producing tremor at rest, rigidity, bradykinesia and postural instability.

It primarily affects gross, subconscious movement of skeletal muscle — the automatic movements you never plan.

🧠 “No DOPE in the PARK.” Low DOPamine in PARKinson's.
FIGURE 2 · THE SEE-SAW — dopamine DOWN, acetylcholine relatively UPSchematic · ball SIZE = how much of each transmitter · read LEFT (normal) → RIGHT (Parkinson's)① NORMAL — balancedDopamine and acetylcholine hold each other in check② PARKINSON'S — tippedDopamine falls, so acetylcholine is relatively HIGHDAAChDAAChSmooth, controlled movementTremor · rigidity · slow movement · droolingSO THE TREATMENT WORKS FROM BOTH ENDSPUSH DOPAMINE UPLevodopa–carbidopa — replaces dopaminePramipexole, ropinirole — dopamine agonistsSelegiline, rasagiline — MAO-B inhibitors,stop dopamine being broken downEntacapone — COMT inhibitorPULL ACETYLCHOLINE DOWNBenztropine, trihexyphenidyl —anticholinergics, mainly for TREMORAmantadine — helps tremor and dyskinesiaAnticholinergic cautions: dry mouth, blurredvision, constipation, urinary retention, confusion+

This single picture explains the whole drug list. If dopamine is down and acetylcholine is relatively up, you either add dopamine or block acetylcholine — and often both.

🧬 Why acetylcholine matters too

Dopamine and acetylcholine normally balance each other in the basal ganglia. Lose dopamine and ACh is left unopposed — which is why the picture includes tremor and a lot of wet: excess saliva and drooling.

🧠 High acetylCCCholine = lots of seCCCretions. That is the drooling.

⚠️ Risk factors and causes

  • Age — most commonly diagnosed after 60.
  • Male sex; family history in a minority of cases.
  • Exposure to some pesticides, herbicides and heavy metals.
  • Repeated head trauma.
  • Drug-induced parkinsonism — antipsychotics and metoclopramide block dopamine receptors and produce the same picture. It can improve when the drug is stopped, so always check the medication list.
🧠 If a “new Parkinson's” appears within weeks of starting an antipsychotic, suspect the drug, not the disease.

🧪 Diagnosis — clinical, not a single test

  • Diagnosis is made on the history and the physical exam — the TRAP signs, especially asymmetric onset.
  • A positive response to a trial of low-dose carbidopa–levodopa supports the diagnosis.
  • CT/MRI may show cerebral atrophy but is mainly used to rule out other causes (stroke, tumor, hydrocephalus).
  • Decreased motility through the upper GI tract is common — swallowing, gastric emptying and bowel transit all slow down.
🧠 No blood test, no scan finding, no biopsy. The diagnosis is made by watching someone move.
🎯

T · R · A · P

CLUES

The four cardinal signs, plus the gait, the face and the handwriting.

FIGURE 3 · T · R · A · P — the four cardinal signs, drawn on one patientStanding, side-on · read the cards TOP → BOTTOM · every card points at the drawingcenter of gravity falls IN FRONT of the feetTTREMOR at REST“Pill-rolling” — thumb rolls across the fingersPRESENT at rest, BETTER with purposeful movementWorse with stress · disappears in sleepRRIGIDITYStiff, resistant to passive movement“COGWHEEL” — a ratcheting catch-and-releaseAching muscles, stooped postureAAKINESIA / BRADYKINESIASlow to START and slow to moveMasked face, soft monotone voice, less blinkingMICROGRAPHIA — handwriting shrinksPPOSTURAL INSTABILITYStooped forward, small shuffling stepsLoses balance easily → HIGH FALL RISKFestination: steps get faster and shorterT — pill-rolling tremorR — rigid, flexed elbows held inA — masked, expressionless faceP — trunk stooped FORWARD

Learn TRAP as a picture of one patient, not a list. Onset is usually asymmetric — one hand, one side, first.

⭐ The 3 signs the NCLEX asks about again and again

1 · Shuffling gait + decreased arm swingAlso written “propulsive shuffling gait”. The lost arm swing is often the very first thing a family notices.
2 · Pill-rolling tremorThumb rolls across the fingertips as if rolling a pill. Present at rest.
3 · Tremors AT RESTImprove with purposeful movement, disappear in sleep, worsen with stress and fatigue.

“Tremors decrease when attention is diverted by activity.” — that exact statement is a correct answer.

🧠 Rest tremor rests when you move. The opposite of the cerebellar intention tremor, which gets worse as you reach.
FIGURE 4 · THE GAIT — shuffling, no arm swing, festination, freezingFive frames, read LEFT → RIGHT · pink brackets show step LENGTH shrinkingTHE PARKINSONIAN GAIT — five frames, left to right12345steps start SHORT……and get SHORTER + FASTERDOORWAYFREEZING① SHUFFLINGFeet barely leave the floorSmall, flat, dragging steps② NO ARM SWINGArms hang still at the sides— an early, easily-missed sign③ FESTINATION + FREEZINGSteps speed up and shorten as ifchasing the center of gravity;feet stick at doorways and turnsCue them OVER the freeze: “step over my foot”, a line of tape on the floor, or count “1-2, 1-2” out loud.

Freezing is not stubbornness and it is not weakness — the motor program stalls. Visual and verbal cues restart it far better than pulling on the person's arm.

FIGURE 5 · THE FACE AND THE HANDWRITING — two signs you can SEEFaces: read LEFT (normal) → RIGHT (Parkinson's) · handwriting sample reads LEFT → RIGHT along one line① NORMAL FACEExpressive · blinks 15–20 times a minute② MASKED FACIESFlat · rare blinking · mouth open · drooling✓ Eyebrows move✓ Blinks normally✓ Smiles, frowns, reacts✓ Swallows saliva without thinking• Eyebrows fixed · staring• Blinking almost stops• No expression — people read it as• rude, depressed or “not listening”MICROGRAPHIA — the handwriting shrinks as the line goes onstarts normal size…ends tiny and cramped

Masked facies is one of the most misread signs in nursing: a flat face gets charted as “withdrawn”, “depressed” or “uncooperative”. The person inside is usually fully aware.

🧊 Rigidity — what “cogwheel” actually feels like

Passively bend the patient's elbow or wrist. Instead of moving smoothly, it gives way in small catch–release steps, like turning a ratchet or a cogwheel.

Rigidity is present at rest and throughout the range of movement, and it is not velocity-dependent (unlike the spasticity of MS or stroke).

🧠 Cog-WHEEL = clicks like a wheel. Spasticity = a spring. Different feel, different disease.

🗣️ The other signs worth knowing

  • Hypophonia — soft, monotone, hard-to-hear voice.
  • Dysphagia and drooling (sialorrhoea) — not more saliva, just fewer automatic swallows.
  • Constipation — often present years before the motor signs.
  • Orthostatic hypotension — from the disease itself and from the drugs.
  • Sleep disturbance, acting out dreams, daytime sleepiness.
  • Depression and anxiety — very common and treatable; do not write it off as “understandable”.
  • Parkinson's disease dementia in later disease.
  • Seborrhoea (oily skin), reduced sense of smell, small cramped handwriting.
🧠 The non-motor symptoms are often what the patient minds most. Ask about them.
🚨

FALLS AND AIRWAY

CARE 1

The two complications that actually harm patients. Everything else comes after these.

🚨 Airway is priority #1 — the aspiration bundle

  • Suction set up at the bedside before meals — this is the answer when the question asks what to prepare.
  • High Fowler's / sit fully upright to eat and for 30–60 minutes afterwards.
  • Pureed or soft diet, small bite-sized pieces, and a thickening agent added to fluids when ordered.
  • Tissues within reach during meals for drooling.
  • Monitor the swallow every meal; stop if the voice becomes wet or the person coughs.
  • Give plenty of time — a Parkinson's meal is slow, and rushing causes aspiration.
  • Watch weight — eating is exhausting and intake often falls.

Never leave a patient with dysphagia to eat unsupervised, and never give oral medications without checking that the swallow is safe.

🧠 Upright · Thick · Small · Slow · Suction.

🚨 Falls — the other thing that hurts them

  • Postural instability + festination + freezing + orthostatic hypotension = a very high fall risk.
  • Change position slowly; dangle the legs before standing.
  • Clear the floor: no throw rugs, no clutter, no trailing cords. Good lighting.
  • Grab bars, raised toilet seat, a firm chair with arms they can push up from.
  • Cue over a freeze: “step over my foot”, a line of tape on the floor, a rhythm to march to.
  • Teach a wide-based turn — turn in a small arc, not by pivoting on the spot.
🧠 Feet stick, hips break. A freeze at a doorway is a fall waiting to happen.

✅ Promote independence — the neuro rule

1
Gait training FIRST
↓
2
Cane
↓
3
Walker
↓
4
Wheelchair last

Never perform all the ADLs for the client. Allow extra time and assist only where needed.

Realistic goal for a care plan: “Maintain optimal function within the client's limitations.”

🧠 Do WITH, not FOR.

🏃 Exercise and therapy actually change outcomes

  • Physical therapy — big-amplitude movement training, stretching, balance work, treadmill.
  • Occupational therapy — adaptive utensils with built-up handles, plate guards, button hooks, elastic laces, weighted cups.
  • Speech-language pathology — loud-voice training and formal swallow assessment.
  • Daily walking with deliberate heel-toe steps and swinging arms; march to a beat.
  • Warm baths and massage for muscle stiffness and cramps.
  • Constipation: fluids, fiber, movement, a toileting routine.
🧠 Consciously do what used to be automatic. That's the whole of PD rehab.
💊

THE DRUGS

CARE 2

Push dopamine up, pull acetylcholine down — and give levodopa on the clock.

FIGURE 6 · WHY IT IS LEVODOPA AND CARBIDOPASchematic · read TOP (levodopa alone) → BOTTOM (the combination) · see the key, bottom left① LEVODOPA ALONEMost of the dose is converted to dopamine BEFORE it reaches the brainBLOODSTREAMBLOOD–BRAIN BARRIERBRAINDADAL crossesLLLDDCDAconverted early → wasted, and it causes nausea + low BP② LEVODOPA + CARBIDOPACarbidopa blocks the peripheral enzyme, so far more levodopa gets throughBLOODSTREAMBLOOD–BRAIN BARRIERBRAINDADADADADAL crossesLLLDDCCARBIDOPA blocks itKEYLEVODOPA — CAN cross the barrierDOPAMINE — CANNOT cross the barrierDDC = the enzyme that converts levodopa → dopamineCARBIDOPA — blocks DDC in the body onlyCarbidopa does not treat Parkinson's itself.It is a bodyguard: it stops levodopa being used up before it reaches the brain,which means a smaller dose and far less nausea and orthostatic hypotension.

Carbidopa is not a second treatment — it is a bodyguard for the levodopa. That is the whole reason the two come in one tablet.

💊 The drug table

Drug / classWhat it doesKey nursing points
Carbidopa–levodopaLevodopa crosses the blood–brain barrier and is converted to dopamine. Carbidopa stops that conversion happening in the body first. Most effective drug available. Give ON TIME. Take on an empty stomach if tolerated. AVOID high-protein meals — protein competes for absorption. Watch for orthostatic hypotension, nausea, dyskinesia, and darkened sweat/urine (harmless).
Dopamine agonists
pramipexole · ropinirole		 Stimulate dopamine receptors directly — they do not need surviving neurons Sudden sleep attacks, hallucinations, orthostatic hypotension, and impulse-control problems (gambling, shopping, hypersexuality) — ask about them directly
MAO-B inhibitors
selegiline · rasagiline		 Block the enzyme that breaks dopamine down, so what is there lasts longer Selegiline is an MAOI — watch for interactions, and with some antidepressants/opioids the risk of serotonin syndrome. Insomnia if given late in the day.
COMT inhibitors
entacapone		Extends each levodopa dose Always given with levodopa. Harmless brown-orange urine. Diarrhea.
Anticholinergics
benztropine · trihexyphenidyl		 Pull acetylcholine down — mainly to help tremor Classic anticholinergic effects: dry mouth, blurred vision, constipation, urinary retention, and confusion in older adults — use cautiously
AmantadineHelps tremor and drug-induced dyskinesia Livedo reticularis (mottled skin), ankle edema, confusion

A patient on carbidopa–levodopa + selegiline + pramipexole has Parkinson's disease — that combination is a give-away in exam stems.

🧠 LEAVE the protein with LEVOdopa. High-protein meals block its absorption.
FIGURE 7 · ON–OFF and WEARING-OFF — why the CLOCK mattersMovement on the vertical axis, one whole day on the horizontal · pill icons = dose timesMOVINGWELLFROZENTIME OF DAY →“ON” — the drug is working“OFF” — rigid, slow, frozen💊08:00💊12:00💊16:00💊20:00WEARING-OFFBenefit fades BEFORE the next dose.Fix: smaller doses, more often.PEAK-DOSE DYSKINESIAToo much dopamine → writhing,involuntary movements at the peak.“ON–OFF” PHENOMENONSudden, unpredictable switchesbetween moving and frozen.Give levodopa ON TIME, to the minute — this is one of the few oral drugs where a 30-minute delay is a real clinical problem.

After several years on levodopa most patients develop motor fluctuations. This is disease progression, not the drug “stopping working” — do not let a family conclude it should be stopped.

🚨 Levodopa nursing — the non-negotiables

  • Administer on schedule, to the minute. A late dose can leave a patient frozen and unable to move or swallow.
  • Never stop levodopa abruptly — abrupt withdrawal can precipitate a severe parkinsonism–hyperpyrexia crisis with rigidity, fever and altered mental status.
  • Check orthostatic blood pressures; teach slow position changes.
  • Effects build over weeks — teach patience.
  • Report new dyskinesias, hallucinations, or sudden sleep attacks.
  • Separate the dose from high-protein food by about an hour where possible.
🧠 On time, every time, and never stopped suddenly.

🔪 When drugs are not enough

Deep brain stimulation (DBS) — electrodes are implanted in the basal ganglia and connected to a pulse generator under the collarbone. It can dramatically reduce tremor and motor fluctuations in carefully selected patients.

It does not cure the disease and it does not help the non-motor symptoms. Patients still take medication, usually at a lower dose.

🧠 DBS is a pacemaker for movement — it manages symptoms, it does not replace dopamine neurons.
🗣️

TEACH AND LIVE WITH IT

CARE 3

What to say, what they must not believe, and how to set up the house.

⭐ The “needs further teaching” answers

  • ❌ “This treatment will CURE my disease.” — the single most common wrong statement on this topic.
  • ❌ “I'll take my levodopa with a big steak so it doesn't upset my stomach.”
  • ❌ “If I feel stiff I'll just skip a dose and take a double one later.”
  • ❌ “I should rest in bed most of the day to save my energy.”
  • ❌ “My tremor means I'm getting anxious — it's not the disease.”
  • ✅ “Tremors decrease when my attention is diverted by an activity.”
  • ✅ “I'll sit upright for half an hour after I eat.”
🧠 Any option containing cure, skip a dose, protein with levodopa or rest all day is wrong.

✅ Communication with a masked face

  • Assume full comprehension. A blank face is a motor sign, not a cognitive one.
  • Allow long pauses — bradykinesia slows speech and thought output, not thought itself.
  • Ask yes/no questions if speech is very soft; consider a communication board or an amplifier.
  • Face the person, reduce background noise, and be patient with the volume.
  • Explain the masked face to the family so they stop reading it as rejection.
🧠 The face is frozen. The person is not.

🏠 Home and safety teaching

  • Remove rugs and clutter; add night lights and grab bars; use a raised toilet seat.
  • Electric razor and electric toothbrush; Velcro fastenings; elastic shoelaces.
  • Weighted or built-up utensils; a plate guard; a cup with a lid and a wide base.
  • A firm mattress and a bed rope/rail to help with turning.
  • Set alarms for medication times.
  • Keep a symptom diary of “on” and “off” times to bring to appointments.
  • Involve the caregiver, arrange respite, and refer to a Parkinson's support organization.
🧠 Every gadget replaces one automatic movement they've lost.

🔀 Don't confuse it with these

FeaturePARKINSON'SConfused with…
TremorAt REST, better with movement Cerebellar/MS intention tremor — worse as you reach for something
ToneCogwheel rigidity, whole range Stroke/MS spasticity — velocity-dependent, clasp-knife
MovementToo little (hypokinetic) Huntington's — too much (chorea, writhing)
WeaknessStrength is preserved — it is slow, not weak Myasthenia gravis / Guillain-Barré — genuinely weak
🧠 Parkinson's = slow and stiff. Huntington's = fast and writhing. MG/GBS = weak.
🧬 SUBSTANTIA NIGRADopamine neurons die in the midbrain. 60–80% gone before symptoms. Dopamine ↓, acetylcholine relatively ↑.
🎯 T R A PTremor at rest (pill-rolling) · Rigidity (cogwheel) · Akinesia/bradykinesia · Postural instability.
🚶 THE 3 NCLEX SIGNSShuffling gait with decreased arm swing · pill-rolling · tremors at rest that ease with activity.
🍽️ AIRWAY FIRSTSuction at the bedside · upright to eat · pureed, small bites · thickened fluids · tissues to hand.
💊 LEAVE the PROTEINHigh-protein meals block LEVOdopa absorption. Give doses ON TIME. Never stop it abruptly.
❌ “IT WILL CURE ME”Needs further teaching. Nothing cures it — we slow it and manage symptoms. Goal: optimal function within limitations.