US Prevalence
~1 M
~1 million Americans living with PD; ~90,000 new diagnoses annually. Most common movement disorder after essential tremor.[1]
What Is It
Definition, mechanism, and the clinical reality of Parkinson's disease and Parkinson's-plus syndromes at end of life. What the hospice team needs to understand on day one.
Cause of Death
~70%
Aspiration pneumonia accounts for ~70% of PD deaths. Dysphagia is the dominant end-stage clinical problem.[2]
Parkinson's-Plus
15–20%
~15–20% of parkinsonism patients have a Parkinson's-plus syndrome (PSP, MSA, DLB, CBD) — faster trajectories, less levodopa response.[3]
Dementia in Advanced PD
~80%
~80% of PD patients develop dementia within 20 years. PDD changes every clinical decision from medication tolerability to advance directive capacity.[4]
Parkinson's disease is the progressive degeneration of dopaminergic neurons in the substantia nigra — the brain region that orchestrates smooth, coordinated movement. The cardinal motor features (tremor, rigidity, bradykinesia, postural instability) are the visible manifestation of this dopamine loss. But end-stage Parkinson's disease is not defined by tremor. It is defined by the progressive failure of all automatic and semi-automatic functions: swallowing, breathing coordination, postural control, autonomic regulation, sleep, cognition, and communication.[1]
The Parkinson's-plus syndromes — Progressive Supranuclear Palsy (PSP), Multiple System Atrophy (MSA), Dementia with Lewy Bodies (DLB), and Corticobasal Degeneration (CBD) — share the parkinsonian motor phenotype but have distinct clinical profiles, faster trajectories, and different medication responses that the hospice clinician must understand to provide accurate care. What all of these diseases share in hospice is the trajectory toward aspiration pneumonia, the fracture cascade from falls, and the grief of a person whose inner life is preserved while the body loses its capacity to express it.[3]
🧭 Clinical framing
The hospice clinician in Parkinson's disease is not managing the tremor. They are managing the swallow, the fall risk, the dementia, the medication timing, and the identity of a person who is watching themselves disappear in the slowest way imaginable. The progressive loss of swallowing coordination, the forward-stooped posture that compresses the airway, the reduced cough reflex, the inability to clear secretions — these combine to make the lungs the final vulnerable organ. Every visit centers on: Is the levodopa on schedule? Is the swallow safe? Has the patient fallen? Is the caregiver surviving?
"You walk into the Parkinson's hospice home and you see it all at once. Hospital bed in the living room. Mechanical lift in the corner. Crushed medications in the applesauce on the kitchen counter. The spouse who has been the full-time caregiver for a decade — exhausted, devoted, barely holding it together. And the patient, who cannot speak above a whisper but whose eyes are completely present, completely aware, completely there. That patient is watching you to see if you see them. Your job is to make sure they know you do."
— Waldo, NP · Terminal2
How It's Diagnosed
Clinical diagnosis criteria, imaging, and Parkinson's-plus syndrome differentiation. Most patients arrive with an established diagnosis — this section helps you read it and understand what trajectory to expect.
UK PD Society Brain Bank Criteria
Guideline- Required: Bradykinesia plus at least one of: muscular rigidity, 4–6 Hz rest tremor, postural instability (not caused by visual, vestibular, or cerebellar dysfunction)
- Supportive: Unilateral onset, rest tremor, progressive course, persistent asymmetry, excellent levodopa response (70–100%), severe levodopa-induced chorea, levodopa response ≥5 years, clinical course ≥10 years
- Exclusion criteria that define Parkinson's-plus: Cerebellar signs, downward gaze palsy, early severe falls, early autonomic failure, early dementia (<1 yr), negative levodopa response, neuroleptic exposure
Key Diagnostic Investigations
- DaTscan (dopamine transporter SPECT): Distinguishes dopaminergic from non-dopaminergic parkinsonism. Abnormal in PD, PSP, MSA, DLB, CBD. Normal in essential tremor, drug-induced, psychogenic parkinsonism.[5]
- MRI brain: Excludes structural causes (vascular parkinsonism, NPH, tumors). Key findings: hummingbird sign (PSP), hot cross bun sign (MSA), asymmetric cortical atrophy (CBD)[6]
- Levodopa challenge: Significant motor improvement supports PD. Poor response suggests Parkinson's-plus.
- Autonomic testing: Orthostatic BP measurement — orthostatic hypotension common in PD, universal in MSA
- Cognitive assessment: MoCA/MMSE — distinguishes PDD (dementia >1 yr after motor onset) from DLB (dementia within 1 yr of motor onset)[7]
Parkinson's-Plus Syndrome Differentiation
Progressive Supranuclear Palsy (PSP)
- Hallmark: Vertical gaze palsy (especially downward), early falls within first year of onset
- Pseudobulbar affect, axial rigidity > limb rigidity, early dysphagia
- Poor levodopa response; characteristic backward falls ("topples like a felled tree")
- Median survival: 5–7 years from symptom onset[8]
Multiple System Atrophy (MSA)
- MSA-P: Predominantly parkinsonian; MSA-C: predominantly cerebellar
- Severe orthostatic hypotension, urinary incontinence, erectile dysfunction
- Rapid progression; poor levodopa response in most
- Median survival: 6–10 years from onset[9]
Dementia with Lewy Bodies (DLB)
- Core features: Fluctuating cognition, recurrent visual hallucinations (people/animals), REM sleep behavior disorder, parkinsonism
- Dementia within 1 year of motor onset (vs PDD: dementia >1 yr after)
- ⚠ PROFOUND NEUROLEPTIC SENSITIVITY — antipsychotics cause severe, potentially fatal reactions in DLB. THE most important safety fact in Lewy body disease.
- Median survival: 5–8 years from cognitive symptom onset[7]
Corticobasal Degeneration (CBD)
- Hallmark: Asymmetric limb apraxia, alien hand syndrome, cortical sensory loss, myoclonus, dystonia
- Cortical and basal ganglia involvement; poor levodopa response
- Median survival: 6–8 years from onset[10]
🚨 What to look for in hospice records
- Levodopa/carbidopa dose and exact timing schedule — this is life-sustaining; a missed or late dose causes off-period rigidity, dysphagia worsening, autonomic instability
- Parkinson's-plus syndrome vs idiopathic PD — different trajectories, levodopa response, safety profiles
- DLB diagnosis — neuroleptic sensitivity is life-threatening; document prominently
- Current swallowing assessment — SLP evaluation, safe textures, silent aspiration risk
- Fall history — frequency, locations, injuries, most recent fracture
- DBS history — if present, deactivation at end of life is a specific clinical discussion
- Advance directive and cognitive capacity status
Causes & Risk Factors
Why this happened, what runs in families, and the disparities that matter. Relevant for family conversations and answering "why did this happen?"
Idiopathic PD Risk Factors
- Age: Dominant risk factor — incidence doubles each decade after 60; median diagnosis age 60 years; young-onset PD (<50 yrs) often genetic[1]
- Male sex: 1.5:1 male predominance
- Pesticide exposure: Rotenone, paraquat — epidemiological association; rural residence and well water use associated with higher risk[11]
- Head trauma: Cumulative head trauma from contact sports or occupational exposure — association with PD and DLB
- Environmental toxins: MPTP (designer drug contaminant that caused epidemic of irreversible parkinsonism in 1982); industrial solvents including trichloroethylene
- Paradoxical protective factors: Smoking (inverse association — nicotinic receptor mechanism) and caffeine (inverse association in multiple studies) — not recommendations, but pharmacologically informative
Genetic Causes (15–25% of PD)
- LRRK2 (G2019S): Most common genetic PD; higher prevalence in Ashkenazi Jewish and North African Berber populations; autosomal dominant[12]
- SNCA (alpha-synuclein): Triplication causes severe early-onset PD; gene dose effect
- GBA (glucocerebrosidase): Heterozygous variants in 5–10% of PD; strongest known genetic risk factor after LRRK2; associated with faster cognitive decline and DLB[13]
- PRKN/Parkin, PINK1: Early-onset autosomal recessive PD — younger patients, slower progression
- PARK7/DJ-1: Rare autosomal recessive form
❤️ For families: "Why did this happen?"
Parkinson's disease is caused by the gradual loss of brain cells that produce dopamine — a chemical that helps coordinate movement. In most cases, there is no single cause. Age is the strongest risk factor, and some environmental exposures may contribute. For a small number of patients, a genetic change runs in the family. This was not caused by anything your loved one did wrong. It was not caused by stress, by lifestyle choices, or by anything that could have been prevented. The disease chose them — they did not choose it.
⚕ Disparity note
Black Americans are diagnosed with PD at lower rates than white Americans but have worse outcomes after diagnosis — later diagnosis, less access to neurologist-managed care, lower rates of DBS surgery, and less access to multidisciplinary Parkinson's care teams. Hispanic Americans also have later-stage diagnosis. Women with PD are diagnosed later than men (rigidity and bradykinesia predominate over tremor — symptoms less recognized as PD), have different progression patterns, and are underrepresented in PD clinical trials. The hospice clinician must assess whether every appropriate intervention was offered and accessed, or whether system barriers intervened.[14]
Treatments & Procedures
Dopaminergic therapy, DBS, aspiration management, and palliative procedures. Understanding prior therapy is essential for anticipating complications in hospice.
Levodopa/carbidopa is the gold standard and the most important medication in PD hospice. Carbidopa prevents peripheral levodopa metabolism, allowing more levodopa to cross the blood-brain barrier. Formulations include standard (Sinemet), extended-release (Rytary), and intestinal gel via PEG-J (Duopa). Levodopa is a life-sustaining medication — missed or delayed doses cause off-period rigidity, dysphagia worsening, dysarthria, and autonomic instability. The levodopa schedule must be maintained with the same precision as insulin in diabetes.[15]
Dopaminergic Medications
- Dopamine agonists (pramipexole, ropinirole): Used as adjuncts; side effects: impulse control disorders, hallucinations, orthostatic hypotension, excessive somnolence — often reduced or stopped at end stage
- MAO-B inhibitors (selegiline, rasagiline, safinamide): Modest benefit; ⚠ Serotonin syndrome risk with opioids and antidepressants; selegiline has tyramine interaction risk — review against comfort medications[16]
- COMT inhibitors (entacapone, tolcapone): Extend levodopa duration; often simplified at end of life
- Amantadine: Reduces dyskinesias; anticholinergic side effects; confusional in elderly — often stopped at end stage
Device & Procedural Therapy
- Deep brain stimulation (DBS): High-frequency stimulation of STN or GPi; reduces motor fluctuations and tremor. At end of life, DBS deactivation causes return of severe rigidity — unlike ICD deactivation, most guidelines recommend maintaining DBS in comfort-focused care[17]
- Levodopa-carbidopa intestinal gel (Duopa): PEG-J delivery for motor fluctuations; relevant if in place at hospice enrollment
- Palliative feeding discussion: PEG does not prevent aspiration in PD dementia (aspiration of oral secretions and gastric reflux continues regardless); evidence strongly indicates PEG does not extend survival in PDD[18]
- Fall prevention: Environmental modification, hip protectors, physiotherapy; PD patients who fracture a hip have 40–50% 1-year mortality[19]
When Therapy Makes Sense
Evidence-based criteria for continuing disease-directed therapy in PD hospice. Levodopa is not optional. The question is what else to continue.
In Parkinson's disease, the distinction between "disease-directed therapy" and "comfort care" does not apply the way it does in cancer. Levodopa is simultaneously disease-directed and comfort-directed — it is the single most important comfort medication in PD. Stopping it causes severe suffering. The hospice framework must accommodate continued dopaminergic therapy as a core comfort intervention.[15]
- 01Levodopa continuation in all PD and Parkinson's-plus patients: Levodopa is a comfort medication. Stopping it causes severe rigidity, dysphagia worsening, and autonomic crisis. Continue via crushed oral formulation in applesauce, liquid suspension via PEG, or transdermal rotigotine patch if oral route fails. Abrupt discontinuation causes NMS-like state — hyperthermia, rigidity, autonomic instability, altered consciousness. This is a medical emergency that is entirely preventable.[20]
- 02Dysphagia management with modified textures: Even in comfort-focused care, optimizing texture modification (IDDSI framework) reduces aspiration frequency and improves oral pleasure from eating and drinking. Speech-language pathology consultation at enrollment is a primary comfort intervention.[21]
- 03DBS maintenance: If the device is functioning and not causing discomfort, maintain it. DBS deactivation causes return of rigidity and tremor. Most comfort-focused guidelines recommend maintaining DBS unless the device is infected or malfunctioning.[17]
- 04Orthostatic hypotension management: Fludrocortisone, midodrine, compression stockings, head-of-bed elevation. In MSA specifically, orthostatic hypotension is severe and causes syncope, falls, and ischemic events.[9]
- 05PD psychosis treatment: Hallucinations and delusions cause profound distress. Only clozapine (most effective), quetiapine (most practical in hospice), and pimavanserin (FDA-approved, no monitoring) are safe. Pimavanserin is the preferred option in hospice — no motor worsening, no CBC monitoring.[22]
- 06Rivastigmine or donepezil for PDD: Modest benefit on cognition and hallucinations. Reasonable to continue if tolerating. Opioids for pain from rigidity, immobility, and dystonia — pain in PD is systematically undertreated.[23]
When It Doesn't
Medications to stop, drugs that are dangerous, and the levodopa discontinuation emergency that must never happen.
In PD hospice, "when it doesn't" is primarily about medications that must be stopped because they are dangerous, not because disease-directed therapy is futile. The distinction matters: levodopa must never stop. Other medications should.[20]
- 01Dopamine agonist reduction in advanced PD: When hallucinations, impulse control disorders, or excessive somnolence outweigh motor benefit, reduce pramipexole or ropinirole with levodopa compensation. Careful dose reduction — never abrupt discontinuation.[16]
- 02Stop all anticholinergic medications: Trihexyphenidyl, benztropine, diphenhydramine (Benadryl) — cognitive worsening from anticholinergics is severe in PDD and DLB. Stop at enrollment in any patient with cognitive impairment. Educate families that OTC sleep medications are dangerous in Parkinson's.[24]
- 03Typical antipsychotics are absolutely contraindicated: Haloperidol, risperidone, olanzapine, aripiprazole, chlorpromazine — cause severe motor worsening in PD and life-threatening neuroleptic sensitivity reactions in DLB. ⚠ Never give these medications to any PD or DLB patient.[7]
- 04Feeding tube for aspiration prevention in PDD: The evidence does not support PEG for aspiration prevention in PD dementia — aspiration of secretions and gastric reflux continues regardless. If the goal is aspiration prevention, have this conversation explicitly. If the goal is medication delivery or selected comfort nutrition, the conversation may support PEG.[18]
- 05MAO-B inhibitor interactions: Selegiline and rasagiline carry serotonin syndrome risk with tramadol, meperidine (absolutely contraindicated), and at high doses with other opioids. Review MAO-B inhibitor against opioid plan at enrollment. Stop selegiline if opioids are being introduced near end of life.[16]
- 06Metoclopramide is absolutely contraindicated: Dopamine antagonist — causes severe motor worsening. The only safe antiemetic in PD is ondansetron (except with apomorphine — contraindicated) or trimethobenzamide.[25]
🚨 Levodopa Discontinuation Emergency
Abrupt levodopa discontinuation in advanced PD causes a neuroleptic malignant syndrome-like state: hyperthermia >40°C, lead-pipe rigidity, autonomic instability, rhabdomyolysis, altered consciousness. This is not theoretical — it is a documented, potentially fatal complication of abrupt levodopa withdrawal. Levodopa must never be abruptly discontinued. When oral route fails: crushed levodopa in liquids or applesauce, liquid carbidopa/levodopa suspension via PEG, or rotigotine transdermal patch as a partial bridge. The hospice team must know this before the first visit ends.[20]
Out-of-the-Box Approaches
Evidence-graded integrative, interventional, and complementary approaches specific to PD hospice. Grade A = RCT; B = multi-observational/meta-analysis; C = limited clinical.
Rotigotine Transdermal Patch
Grade B2–8 mg/24h transdermal patch, applied to clean dry skin, rotate sites, change q24h
Non-ergot dopamine agonist patch providing continuous dopaminergic stimulation when oral levodopa cannot be given. Does not fully replace levodopa but bridges the period when swallowing fails. Provides partial protection against off-period rigidity, dysphagia worsening, and NMS-like state. Order at enrollment for any patient with advanced dysphagia — one of the most important but least prescribed end-stage PD medications.[26]
Pimavanserin for PD Psychosis
Grade A34 mg PO daily (tablet or oral solution); onset 2–4 weeks
FDA-approved selective 5-HT2A inverse agonist. Does not worsen motor symptoms, does not cause neuroleptic sensitivity in DLB, does not require CBC monitoring (unlike clozapine). Cleanest antipsychotic option in PD. QTc monitoring recommended at initiation. Patients on quetiapine may benefit from switch to pimavanserin for more reliable effect and lower monitoring burden.[22]
IDDSI Texture-Modified Swallowing
Grade ASLP consultation at enrollment; IDDSI framework for texture and consistency optimization
International Dysphagia Diet Standardisation Initiative framework reduces aspiration frequency. Even in comfort-focused care, optimizing texture prolongs the pleasure of eating. The patient who can safely enjoy modified-texture meals at the table with the family has a meaningful quality-of-life advantage over premature tube dependence.[21]
Music / Rhythmic Auditory Stimulation
Grade AMusic therapy referral; rhythmic music with strong beat; familiar songs from patient's life
Rhythmic auditory stimulation measurably improves gait, speech rate, and swallowing coordination in PD. Familiar music maintains emotional connection and identity when motor and verbal expression are severely limited. The family can participate — singing familiar songs together is evidence-based neurological stimulation, not sentiment.[27]
Mirtazapine for Depression + Anorexia
Grade B7.5–15 mg PO at bedtime; titrate to 30 mg as tolerated
Addresses depression, insomnia, and anorexia simultaneously — three symptoms that converge in advanced PD. Faster onset than SSRIs. Sedating properties reduce nocturnal restlessness in PDD. Preferred antidepressant in PD hospice given its multi-symptom benefit profile.[28]
Lee Silverman Voice Treatment (LSVT LOUD)
Grade ASpeech therapy protocol; 4 sessions/week for 4 weeks; simplified maintenance exercises
Proven to increase vocal loudness and speech intelligibility in PD. In hospice context, even abbreviated LSVT techniques can meaningfully improve communication. The patient who can be heard by their family in the last months has something irreplaceable. Refer to SLP at enrollment for communication optimization.[29]
Natural & Herbal Options
Evidence grading, dosing, drug interaction flags, and explicit contraindications specific to PD. Three questions before every supplement: (1) Does it interact with levodopa or MAO-B inhibitor? (2) Does it have anticholinergic or dopamine-antagonist properties? (3) Is this patient DLB?
"Parkinson's medication interactions are some of the most dangerous in all of hospice. The MAO-B inhibitor interacts with half the supplements on the shelf. Levodopa absorption gets blocked by iron and high-dose B6. And in Lewy body disease, any supplement with dopamine-blocking properties can cause a life-threatening reaction. Ask what they're taking. Check every single one. The family who has been giving Benadryl for sleep does not know they've been making the dementia worse."
— Waldo, NP
| Supplement | Evidence | Typical Dose | Potential Benefit | ⚠ Interactions / Contraindications |
|---|---|---|---|---|
| Coenzyme Q10 | Grade C | 100–200 mg daily | Mitochondrial support; Phase III trial at 1200 mg/day showed no clinical benefit, but low-dose is safe and well-tolerated[30] | No MAO-B or levodopa interaction at standard doses. Reasonable to continue if patient chooses. |
| Magnesium glycinate | Grade C | 200–400 mg daily | Muscle cramp relief from rigidity and off-period dystonia. One of the safer supplements in PD. | No levodopa or MAO-B interaction. May cause loose stools at higher doses. |
| Melatonin | Grade C | 3–12 mg at bedtime | REM sleep behavior disorder — common in PD/Parkinson's-plus. Reduces RBD symptoms and improves sleep quality.[31] | Minimal drug interactions. No anticholinergic or dopaminergic effect. One of the most clinically useful supplements in this population. |
| Omega-3 fatty acids | Grade C | 1 g/day (food-source level) | Anti-inflammatory; some neuroprotective signal in animal models; limited PD clinical trial data. | Safe at 1 g/day. Antiplatelet caution in patients on anticoagulation. |
| Vitamin D | Grade C | 1000–2000 IU daily | PD patients have high prevalence of vitamin D deficiency; bone protection important given fall risk.[32] | Safe at standard doses. Check 25-OH vitamin D level if available. Important for fracture prevention. |
| Mucuna pruriens | Grade D | Variable; contains natural levodopa | Natural source of levodopa; some open-label studies show motor benefit comparable to synthetic levodopa. | ⚠ Unpredictable levodopa content — dosing unreliable. Can cause dyskinesias or interact unpredictably with prescribed levodopa. Not recommended as replacement therapy. |
🚫 Avoid in Parkinson's Disease
- St. John's Wort: Serotonin syndrome risk with MAO-B inhibitors (selegiline, rasagiline); CYP pathway interactions with multiple PD medications. Absolutely contraindicated in any PD patient on MAO-B inhibitor.
- Kava & Valerian at sedating doses: Compounded sedation and fall risk in patients with severe postural instability and orthostatic hypotension. Falls are a primary cause of morbidity and mortality in PD.
- High-dose Vitamin B6 (>10 mg/day supplemental): Reduces levodopa efficacy by accelerating peripheral decarboxylation. Standard carbidopa/levodopa mitigates this, but supplemental high-dose B6 should still be avoided. Food-source B6 is safe.
- Iron supplements within 2 hours of levodopa: Iron chelates levodopa in the GI tract, reducing absorption by up to 50%. If iron is needed, separate by ≥2 hours from levodopa dose.
- Fava beans (in large quantities): Contain natural levodopa; can cause unpredictable dopaminergic surges and dyskinesias when combined with prescribed levodopa.
- 5-HTP: Serotonin precursor; risk of serotonin syndrome with MAO-B inhibitors. Avoid in any PD patient on selegiline or rasagiline.
Timeline Guide
A guide, not a prediction. Two parallel trajectories: idiopathic PD (slower) and Parkinson's-plus syndromes (faster, more aggressive).
Parkinson's disease has a dramatically longer trajectory than most hospice diagnoses. Patients may have lived with PD for 10–20 years before hospice enrollment. The Parkinson's-plus syndromes progress much faster — PSP, MSA, and DLB can reach severe disability within 3–5 years. The timeline below shows both trajectories.[1]
Idiopathic PD Trajectory
YRS–
MOS
MOS
Mild–Moderate PD (Years Before Hospice)
- Managed with levodopa and dopamine agonists — independent for most ADLs; motor fluctuations beginning
- Mild cognitive changes possible; UPDRS motor score 20–40; tremor may be dominant feature
- This phase benefits from proactive palliative integration: advance directive completion, dysphagia baseline assessment, caregiver support assessment, PD psychosis discussion
- Parkinson's-plus: This phase is abbreviated — PSP, MSA, and DLB can reach severe disability within 3–5 years; palliative integration should begin at diagnosis
MOS–
1 YR
1 YR
Moderate–Severe PD / Palliative Integration Window
- Assistance required for most ADLs; motor fluctuations with wearing-off and dyskinesias; dementia possibly developing
- Swallowing study abnormalities documented; falls increasing; first aspiration pneumonia possible
- Caregiver hours approaching full-time — this is the palliative integration window most commonly missed
- Parkinson's-plus: Severely disabled — dysarthria severe or absent; dysphagia requiring modified diet; falls near-daily; hospice referral often appropriate
WKS–
MOS
MOS
Late-Stage PD / Hospice Enrollment
- Completely dependent for all ADLs; bedbound or wheelchair-bound; dysphagia severe with high aspiration risk
- Recurrent aspiration pneumonia; dementia established; speech severely dysarthric or absent
- Levodopa providing limited benefit but still essential to prevent NMS-like state
- The aspiration pneumonia conversation must happen explicitly at enrollment — what will we do when the next pneumonia occurs?
DAYS–
WKS
WKS
Active Dying — Aspiration Pneumonia / End-Stage Complications
- Fever, tachycardia, respiratory distress from aspiration pneumonia or respiratory failure
- Convert all medications to SQ or liquid via PEG; levodopa must continue via rotigotine patch, liquid suspension, or apomorphine SQ
- Comfort antibiotics discussion — azithromycin or amoxicillin-clavulanate for fever and secretion burden reduction
- Morphine for dyspnea and pain; glycopyrrolate for secretions; midazolam for agitation
HRS–
DAYS
DAYS
Final Hours
- Respiratory failure from aspiration pneumonia; possible Cheyne-Stokes breathing; mottling; unresponsive
- Glycopyrrolate 0.2 mg SQ q4h for secretions; morphine for dyspnea and pain; midazolam for agitation
- Family prepared for what natural dying from respiratory failure looks like in PD
- Presence is the clinical priority. The patient's hearing is likely the last sense preserved — speak to them, not about them.
Medications to Anticipate
PD-specific pharmacology for hospice. Two rules govern every prescribing decision: never stop levodopa abruptly, and never give typical antipsychotics or metoclopramide.
🚨 Two Absolute Rules in PD Hospice Prescribing
Rule 1: Never abruptly stop levodopa — causes NMS-like state with hyperthermia, rigidity, and autonomic crisis. When oral route fails, immediately convert to crushed suspension via PEG, rotigotine patch, or apomorphine SQ. Do not allow >12 hours medication-free without an alternative route.
Rule 2: Never give typical antipsychotics (haloperidol, chlorpromazine, prochlorperazine, olanzapine, risperidone) or metoclopramide — these dopamine antagonists cause severe motor worsening in PD and life-threatening neuroleptic sensitivity in DLB. Safe antipsychotics: clozapine, quetiapine, pimavanserin only. Safe antiemetic: ondansetron (except with apomorphine) or trimethobenzamide.
| Drug | Class / Target Symptom | Starting Dose | Notes / Cautions |
|---|---|---|---|
| Levodopa/carbidopa | Dopaminergic / Motor symptoms | Maintain exact prescribed schedule | The most important medication. Crush IR tablets in applesauce or water for PEG. Liquid suspension available commercially. Never miss a dose. When oral/PEG route fails → rotigotine + apomorphine SQ.[15] |
| Rotigotine patch | Dopamine agonist / Bridge | 2–8 mg/24h transdermal | Partial levodopa replacement when oral route fails. Apply to clean dry skin, rotate sites q24h. Use alongside any available levodopa, not as complete replacement. Order at enrollment.[26] |
| Morphine | Opioid / Dyspnea + Pain | 2.5–5 mg PO/PEG/SQ q4h | Dyspnea from aspiration pneumonia; pain from rigidity, off-period dystonia, immobility fractures. ⚠ Caution with MAO-B inhibitors — meperidine is absolutely contraindicated; morphine generally safe with selegiline at low doses.[33] |
| Ondansetron | 5-HT3 antagonist / Nausea | 4–8 mg PO/PEG/SQ q8h | Safe antiemetic in PD — does not block dopamine. ⚠ Contraindicated with apomorphine (severe hypotension). Use trimethobenzamide if apomorphine is in use.[25] |
| Quetiapine | Atypical antipsychotic / PD psychosis | 12.5–50 mg PO BID-TID | Safe in PD; most practical in hospice — no monitoring required. For visual hallucinations, paranoid delusions, agitation. Never haloperidol, olanzapine, or risperidone.[34] |
| Pimavanserin | 5-HT2A antagonist / PD psychosis | 34 mg PO daily | FDA-approved for PD psychosis. No motor worsening, no neuroleptic sensitivity in DLB. QTc monitoring at initiation. Onset 2–4 weeks.[22] |
| Glycopyrrolate | Anticholinergic / Secretions | 0.2 mg SQ q4h | Sialorrhea from bulbar involvement and terminal secretions. Preferred over hyoscine — lower CNS penetration. Use hyoscine patch only if SQ unavailable.[35] |
| Midazolam | Benzodiazepine / Terminal agitation | 2.5–5 mg SQ PRN; CSCI 10–20 mg/24h | Terminal agitation and refractory dyspnea. Have in comfort kit drawn and labeled. |
| Lorazepam | Benzodiazepine / Anxiety | 0.5–1 mg PO/SQ q4–6h PRN | Anxiety, REM sleep behavior disorder, off-period anxiety, dyspnea anxiety component. |
| Baclofen | Antispasmodic / Dystonia | 10–40 mg daily PO/PEG divided | Spasticity and off-period dystonia. Painful foot dystonia is one of the most undertreated symptoms in advanced PD.[36] |
| Mirtazapine | Antidepressant / Depression + Anorexia | 15–30 mg PO/PEG at bedtime | Preferred antidepressant — addresses depression, anorexia, and sleep disruption simultaneously. Sedating; reduces nocturnal restlessness.[28] |
| Fludrocortisone / Midodrine | Autonomic / Orthostatic hypotension | Fludro 0.1–0.3 mg daily; Midodrine 5–10 mg TID | Essential in MSA. Compression stockings, head-of-bed elevation as adjuncts. Midodrine: last dose by 4 PM (supine hypertension risk).[9] |
| Rivastigmine | Cholinesterase inhibitor / PDD | 1.5–6 mg PO BID or 4.6–13.3 mg/24h patch | Modest benefit on cognition and hallucinations in PDD. Reasonable to continue if tolerating. Patch avoids GI side effects.[23] |
| Dextromethorphan/quinidine | Nuedexta / Pseudobulbar affect | 20/10 mg PO q12h | Pseudobulbar affect (involuntary laughing/crying) — common in PSP and advanced PD. Reduces episode frequency and severity.[37] |
🌿 PD Symptom Management Decision Tree
Evidence-based · PD-specific · Hospice-adaptedSelect a symptom below to begin
What is the primary symptom to address?
🚨 PD Comfort Kit Must-Haves
- Levodopa failure protocol: If patient suddenly cannot take oral levodopa (vomiting, dysphagia crisis, aspiration event), apply rotigotine patch immediately and call the nurse. Have patch in the home. Do not wait >12 hours without dopaminergic support.
- NMS-like state recognition: If high fever + lead-pipe rigidity + diaphoresis + altered consciousness after missed levodopa → emergency. Resume levodopa by any route. This is a drug withdrawal crisis, not simply a fever.
- Antipsychotic exposure check: Verify no OTC anticholinergics (Benadryl, sleep aids) or dopamine-blocking antiemetics (promethazine, metoclopramide, prochlorperazine). Put the contraindicated drug list in front of the medication record.
Clinician Pointers
High-yield clinical pearls for the hospice team in PD. The things not in the textbook — learned at thousands of bedside visits.
1
Levodopa timing is as critical as insulin timing
The patient who misses their 7 AM levodopa and gets it at 10 AM has spent 3 hours in the off state — swallowing more impaired, rigidity more severe, pain greater, autonomic instability increased. Post the medication schedule visibly. Every family member must understand the timing. When the oral route is compromised, the nursing plan must include an alternative route before the patient reaches a medication-free state.[15]
2
Silent aspiration is the clinical trap
The patient who does not cough when food or liquid enters the airway is silently aspirating. The absence of cough does not mean the swallow is safe. The family told "he's not coughing so he's doing fine" may have a patient who has been silently aspirating for months. Look for: recurrent low-grade fevers, night cough, wet vocal quality after swallowing, unexplained weight loss. Refer to SLP at enrollment.[2]
3
DLB neuroleptic sensitivity is life-threatening — the family must know
The family who calls 911 for acute agitation and the ER team gives haloperidol IM has potentially caused a fatal drug reaction. The DLB diagnosis must be prominently documented. Tell the family explicitly that Benadryl, sleep aids, and prescription antipsychotics other than quetiapine and pimavanserin are dangerous. Use the word "dangerous." The emergency protocol must note DLB and neuroleptic sensitivity.[7]
4
Off-period pain is a distinct pain syndrome
The patient who hurts at predictable times — before the next levodopa dose, in the early morning, after a delayed dose — has off-period pain from dopamine deficiency causing rigidity, dystonia, and central pain. This responds to levodopa optimization, not opioid escalation alone. Assess pain timing relative to levodopa schedule at every visit. Adjust medication timing before escalating analgesics.[38]
5
PSP patients fall backward without warning
PSP falls are distinctive — patients topple backward like a tree being felled. This is not the same as PD falls (which are typically forward festination). The clinical environment must be modified for backward fall risk: rearward-tipped recliners, backward head padding, mattress at floor level. Assess directional fall pattern and adapt the environment specifically.[8]
6
Plan medication routes before the crisis
Every PD hospice patient will eventually lose the ability to swallow medications. This is not an "if" — it is a "when." At enrollment, document the plan: What happens when oral route fails? Is there a PEG? Can we crush tablets? Is rotigotine patch ordered? Is apomorphine SQ available? The 3 AM call about the patient who cannot swallow their Sinemet must already have an answer.
7
Assess dementia capacity early and document
~80% of advanced PD patients have dementia. Capacity for medical decision-making fluctuates in PDD and DLB. Complete advance directive and healthcare proxy at enrollment if not already done. Document capacity assessment clearly. The patient who has lucid periods can still make decisions during those windows — respect cognitive fluctuation as a clinical reality, not an obstacle.
"The number one thing I see missed in Parkinson's hospice is the levodopa schedule. I cannot tell you how many times I have walked into a home and the Sinemet is sitting on the counter untouched because the CNA thought the patient 'didn't seem like they needed it today.' That patient has been in the off state for eight hours. Their swallowing is worse. Their pain is worse. Everything is worse. Treat that medication schedule like oxygen. Because for these patients, it is."
— Waldo, NP
Psychosocial & Spiritual Care
Identity grief, sexuality, caregiver identity loss, communication grief, and the spiritual dimensions of a disease that slows everything down.
Parkinson's disease attacks the face first in many patients. Hypomimia (masked facies), hypophonia, drooling, and the forward-stooped shuffling gait are visible to everyone the patient encounters. The face that no longer shows emotion, the voice that can no longer be heard in a group conversation, the handwriting that has become illegible — these are not abstract losses. They are constant, daily reminders of the self the patient was before the disease.[39]
The hospice clinician who acknowledges this explicitly — "your face doesn't show what's inside the way it used to, and I want you to know that I can still see you completely" — provides a recognition that is deeply therapeutic and profoundly rare.
Identity & Sexuality
Identity Grief in PD
- Progressive loss of facial expression, voice volume, handwriting, gait — the visible self disappears while the inner self persists
- Social withdrawal from embarrassment about tremor, drooling, speech difficulty — isolation compounds grief
- In Parkinson's-plus (especially PSP and CBD), the accelerated timeline intensifies identity loss — patients may progress from independence to complete dependence in 3–5 years
- Acknowledge the specific losses by name: "I know your voice is softer than it used to be. What you have to say matters just as much."
Sexuality & Intimacy
- Dopamine agonist-induced hypersexuality: May create conflict and distress; medication adjustment needed
- Reduced motor function: Creates physical challenges to intimacy; positioning guidance needed
- Caregiver-patient dynamic: Transforms the partner relationship; the couple needs permission to be partners again
- Erectile dysfunction: Common from autonomic failure; phosphodiesterase inhibitors if appropriate (check drug interactions)
- Ask directly: "How has the disease affected your relationship as partners — not just as caregiver and patient, but as people who were intimate?"[40]
Caregiver & Spiritual Dimensions
Caregiver Identity Loss
- PD caregivers have often provided escalating care for 5–10 years before hospice — they arrive already exhausted
- Their identity has been consumed by caregiving; social connections narrowed; physical and mental health deteriorated
- Validate the loss of the partnership that once was while honoring the love expressed through care
- Assess caregiver health at every visit: sleep, pain, depression — the caregiver who is not sleeping is not functioning[41]
Spiritual Dimensions
- PD forces a pace that is at odds with modern life — conversations, meals, movement all take longer
- For people of faith and secular people alike, this enforced slowness can become spiritual practice or profound frustration
- The chaplain who meets the PD patient where they are — not rushing, not filling the silences — provides a quality of presence that mirrors what the disease requires
- DLB hallucinations create a specific grief: caregivers may lose shared reality; some find benign hallucinations comforting; validate both responses
Clinical Pearl
"Ask every Parkinson's patient and their caregiver one question that almost no clinician asks: 'How has the disease affected your relationship as partners — not just as caregiver and patient, but as people who were intimate?' Then stop talking. The couple who has not touched each other tenderly in three years because the caregiver is afraid of hurting them, or because the patient feels ashamed of their body, or because no one ever told them they could still be intimate — that couple deserves to be asked. And to be helped."
Goals-of-Care Communication
Opening the Conversation
- "What is your understanding of where things stand with your Parkinson's?"
- "What are you hoping for in the time you have?"
- "What are you most afraid of?" — in PD, the answer is often loss of communication, falling, or being a burden
- "If things got worse — if swallowing became more difficult — what would matter most to you?"
PD-Specific Pitfalls
- Allow extra time for speech — PD patients think at normal speed but speak slowly; do not finish sentences for them
- The masked face does not mean the patient is not engaged — look at the eyes
- Capacity fluctuates in PDD/DLB — time important conversations for "on" periods when cognition is clearest
- The feeding tube conversation is the hardest: give data, not opinions. PEG does not prevent aspiration in PDD.
Family Guide
Plain language for families. Share, print, or read aloud at the bedside.
You have been caring for your person with Parkinson's disease for a long time. You know their medication schedule. You know which foods are safe. You know the grip on the walker. What you may not know is how much what you have been doing matters — clinically, measurably, in every way that counts. This guide is for you. It covers the things you will see, the things you can do, and when to call the nurse.
What You May See
- Rigidity and stiffness: Especially in the morning before medications or when a dose wears off. This is "off-period" rigidity. The medications must be given on the exact schedule — even 30–60 minutes late makes a significant difference.
- Swallowing difficulty: Coughing or choking with eating or drinking. A wet or gurgling voice after eating. This is very important to report to the nurse. Your nurse will adjust the food texture. Never push eating that causes coughing.
- Falls: Parkinson's patients fall more than any other hospice diagnosis. The environment must be modified. Your nurse will assess fall risk. Call the nurse after any fall — even if the patient seems fine.
- Hallucinations (especially in DLB): Seeing people or animals that are not there. Often vivid and detailed. For many patients these are not frightening. Do not argue — gently redirect. Call the nurse if they become frightening.
- Changes in speech: The voice becomes softer and faster. Give extra time. Do not speak over your person or finish their sentences unless they ask. They have something to say.
- Constipation: Almost universal. The bowel protocol is medication, not optional. Report if no bowel movement in 3 days.
How You Can Help
- Give levodopa medications on the exact schedule: Use a timer or phone alarm. A late dose causes significant stiffness and swallowing difficulty. This medication is as important as insulin.
- Never give Benadryl, Unisom, or OTC sleep/cold medications: These are dangerous in Parkinson's. Call the nurse before giving any over-the-counter medication.
- Use only the approved food textures: Your speech therapist prescribed specific textures. Only give the approved ones. If something causes choking, stop immediately and call the nurse.
- Report any fever: Even a low fever after a missed dose can signal a medication crisis. Call the nurse same day.
- Use safe transfer techniques: Do not let them get up from a chair alone. Use the gait belt. Walk beside with support. The fall that breaks a hip often changes everything.
- Take care of yourself: You have been doing this longer than most people ever have to. Call us when you need support — not just when the patient does.
📞 Call the nurse immediately if you see:
Missed levodopa for >2–3 hours and patient is becoming stiff/rigid — apply rotigotine patch if instructed and available; call nurse immediately. Fever above 102°F especially after missed levodopa — NMS-like emergency; call immediately. Fall involving the head or hip — do not move the patient; call nurse for assessment. Choking episode that does not resolve — use suction if prescribed; do not give food or liquid until assessed. New or worsening hallucinations that are frightening — call nurse for medication review.
🙏 You have been doing this longer than most people ever have to. The medications on the exact schedule, the modified food textures, the grab bars, the slow walks through the living room — you learned all of it because you refused to let this disease take your person without a fight. What you may not have been told is that your person is still fully there. Behind the quiet voice and the still face and the slow movement — they are completely present and they know everything you are doing for them. Every cup of thickened liquid. Every 7 AM levodopa. Every night you got up to turn them. They know. You are part of this clinical team. You have always been.
Waldo's Top 10 Tips
Clinical field wisdom from 12+ years at the bedside. The things you learn after doing Parkinson's hospice long enough.
- 01Levodopa timing is the vital sign in PD hospice. Treat a late levodopa dose with the same urgency you'd treat a missed insulin dose. Post the schedule on the refrigerator. Set phone alarms. Make sure every family member, every CNA, every sitter knows the times. When the oral route starts to fail, apply the rotigotine patch and call the specialist. The patient who goes six hours without levodopa because nobody had a plan for swallowing failure is having a preventable drug withdrawal crisis. I have seen this happen. It is ugly, it is dangerous, and it is entirely avoidable. Have the backup plan in place on day one.
- 02Never give haloperidol, metoclopramide, prochlorperazine, or diphenhydramine to any Parkinson's patient. Ever. Write it in capital letters on the front of the medication record. Write it again on the comfort kit label. The ER doctor who gives haloperidol IM for agitation in a DLB patient may cause a life-threatening reaction. The family who reaches for Benadryl at 3 AM for the hallucinations will make them dramatically worse. Say it out loud at every enrollment. Say it to the family. Say it to the CNA. Put it in writing where everyone can see it. This is not optional information. This is a safety protocol.
- 03Silent aspiration is the clinical trap that kills Parkinson's patients. The patient who is not coughing while eating is not necessarily swallowing safely. They may be aspirating every single meal without a single cough. The reduced cough reflex in advanced PD means the sentinel warning is gone. You have to look for the indirect signs: recurrent low-grade fevers, wet voice after eating, night cough, unexplained weight loss. Get a formal swallowing assessment at enrollment. The SLP will tell you what textures are safe. Trust them. The family who is told "he eats great, never chokes" may be watching silent aspiration happen three times a day.
- 04Off-period pain is a separate pain syndrome and most clinicians miss it. The patient who hurts at predictable times — always before the next levodopa dose, always in the early morning — has off-period pain. It is caused by dopamine deficiency creating rigidity, dystonia, and central pain sensitization. You do not fix this with more morphine. You fix it by optimizing levodopa timing. Ask about pain timing at every visit. Map the pain to the medication schedule. If the pain improves thirty minutes after taking Sinemet, that is off-period pain. Adjust the timing. Add an extra small dose. That matters more than an opioid dose increase.
- 05PSP patients fall backward without warning. If you have not seen this, it is terrifying. They do not stumble. They do not catch themselves. They topple backward like a tree. One moment standing, the next moment on the floor. The regular PD fall prevention approach — for forward festination — does not work for PSP. You need a recliner that tips backward, padding behind the head of the bed, possibly a mattress on the floor. Assess the directional fall pattern on your first visit and set the environment before the first backward fall sends them to the ER with a skull fracture.
- 06Ask about sexuality and intimacy at every Parkinson's enrollment. I know it feels awkward. Ask anyway. The question "how has this disease affected your relationship as partners" will never be asked by the neurologist, the hospitalist, or the physical therapist. It is the hospice nurse's question. The dopamine agonist side effects may have created hypersexuality that caused conflict. The motor disability may have made physical intimacy seem impossible. The caregiver role may have replaced the partner role entirely. These are clinical problems. Give them permission to talk about it. The couple who learns they can still be intimate — with adaptive positioning, with practical guidance, with someone who says "this is still your relationship and it still matters" — has been given something irreplaceable.
- 07DLB hallucinations are usually benign and do not always need treatment. I have had patients who were quite comfortable with the little children who sat on their bed. The visitors were not real, but the patient was not distressed. Treating benign hallucinations with antipsychotics carries motor risk in every Parkinson's patient and lethal risk in DLB. The clinical question is: are the hallucinations causing distress? If they are distressing — pimavanserin is the safest first choice. If they are benign, gentle monitoring is the right call. The family may be more distressed than the patient. Address both. But do not reflexively medicate something that is not causing the patient suffering.
- 08The cough assist device and manual chest percussion techniques help secretion management in PD. Weak cough from bulbar involvement and rigidity lets secretions pool. The cough assist provides mechanical insufflation-exsufflation cycles. Manual assisted coughing — hand pressure timed with expiration — is something you can teach the family. Active secretion management reduces aspiration pneumonia frequency. This is preventive, not reactive. Do not wait for the pneumonia to start managing the secretions. And teach the family. They are there 24 hours. You are not.
- 09Caregiver assessment is a clinical obligation, not a courtesy. The PD caregiver has been providing 24-hour care for what may be a decade. They are running on nothing. Their back hurts from the transfers. They have not slept a full night in years. They have lost their friends, their hobbies, and in many cases their identity as anything other than a caregiver. Assess their sleep, their pain, their depression at every single visit. The caregiver who falls ill cannot care for the patient. Protect the caregiver as aggressively as you manage the patient's symptoms. The caregiver who says "I'm fine" while their hands are shaking is not fine. See them. Name what you see. Get them help.
- 10The person inside the Parkinson's body is fully there. At every visit, address the patient first and directly. Look them in the eye. Allow the extra time for speech. Do not speak to the caregiver about the patient as if the patient is not in the room. The masked face does not mean the emotion is gone — it means the face cannot show it. The soft voice does not mean the thought is gone — it means the muscles cannot project it. The slow movement does not mean the mind is slow — it means the body cannot keep up. They are completely present. They deserve to be treated as such at every single visit. That is not sentimentality. That is clinical excellence.
— Waldo, NP
References
Peer-reviewed citations. Based on articles retrieved from PubMed. All PMIDs hyperlinked. Evidence levels assigned by article type.
1
Marras C, Beck JC, Bower JH, et al. Prevalence of Parkinson's disease across North America. NPJ Parkinsons Dis. 2018;4:21.
2
Matsumoto H, Sengoku R, Saito Y, et al. Sudden death in Parkinson's disease: a retrospective autopsy study. J Neurol Sci. 2014;343(1-2):149-152.
3
Höglinger GU, Respondek G, Stamelou M, et al. Clinical diagnosis of progressive supranuclear palsy: the Movement Disorder Society criteria. Mov Disord. 2017;32(6):853-864.
4
Hely MA, Reid WG, Adena MA, et al. The Sydney multicenter study of Parkinson's disease: the inevitability of dementia at 20 years. Mov Disord. 2008;23(6):837-844.
5
Catafau AM, Tolosa E. Impact of dopamine transporter SPECT using 123I-ioflupane on diagnosis and management of patients with clinically uncertain parkinsonian syndromes. Mov Disord. 2004;19(10):1175-1182.
6
Massey LA, Jäger HR, Paviour DC, et al. The midbrain to pons ratio: a simple and specific MRI sign of progressive supranuclear palsy. Neurology. 2013;80(20):1856-1861.
7
McKeith IG, Boeve BF, Dickson DW, et al. Diagnosis and management of dementia with Lewy bodies: fourth consensus report. Neurology. 2017;89(1):88-100.
8
Respondek G, Kurz C, Arzberger T, et al. Which ante mortem clinical features predict progressive supranuclear palsy pathology? Mov Disord. 2017;32(7):995-1005.
9
Gilman S, Wenning GK, Low PA, et al. Second consensus statement on the diagnosis of multiple system atrophy. Neurology. 2008;71(9):670-676.
10
Armstrong MJ, Litvan I, Lang AE, et al. Criteria for the diagnosis of corticobasal degeneration. Neurology. 2013;80(5):496-503.
11
Tanner CM, Kamel F, Ross GW, et al. Rotenone, paraquat, and Parkinson's disease. Environ Health Perspect. 2011;119(6):866-872.
12
Healy DG, Falchi M, O'Sullivan SS, et al. Phenotype, genotype, and worldwide genetic penetrance of LRRK2-associated Parkinson's disease. Lancet Neurol. 2008;7(7):583-590.
13
Sidransky E, Nalls MA, Aasly JO, et al. Multicenter analysis of glucocerebrosidase mutations in Parkinson's disease. N Engl J Med. 2009;361(17):1651-1661.
14
Willis AW, Schootman M, Evanoff BA, et al. Neurologist care in Parkinson disease: a utilization, outcomes, and survival study. Neurology. 2011;77(9):851-857.
15
Olanow CW, Stern MB, Sethi K. The scientific and clinical basis for the treatment of Parkinson disease. Neurology. 2009;72(21 Suppl 4):S1-136.
16
Connolly BS, Lang AE. Pharmacological treatment of Parkinson disease: a review. JAMA. 2014;311(16):1670-1683.
17
Deuschl G, Schade-Brittinger C, Krack P, et al. A randomized trial of deep-brain stimulation for Parkinson's disease. N Engl J Med. 2006;355(9):896-908.
18
Mitchell SL, Teno JM, Kiely DK, et al. The clinical course of advanced dementia. N Engl J Med. 2009;361(16):1529-1538.
19
Coughlin DG, Litvan I. Progressive supranuclear palsy: advances in diagnosis and management. Parkinsonism Relat Disord. 2020;73:105-116.
20
Newman EJ, Grosset DG, Kennedy PGE. The parkinsonism-hyperpyrexia syndrome. Neurocrit Care. 2009;10(1):136-140.
21
Cichero JAY, Lam P, Steele CM, et al. Development of International Terminology and Definitions for Texture-Modified Foods and Thickened Fluids Used in Dysphagia Management: The IDDSI Framework. Dysphagia. 2017;32(2):293-314.
22
Cummings J, Isaacson S, Mills R, et al. Pimavanserin for patients with Parkinson's disease psychosis: a randomised, placebo-controlled phase 3 trial. Lancet. 2014;383(9916):533-540.
23
Emre M, Aarsland D, Albanese A, et al. Rivastigmine for dementia associated with Parkinson's disease. N Engl J Med. 2004;351(24):2509-2518.
24
Ehrt U, Broich K, Larsen JP, et al. Use of drugs with anticholinergic effect and impact on cognition in Parkinson's disease. J Neurol Neurosurg Psychiatry. 2010;81(2):160-165.
25
Seppi K, Weintraub D, Coelho M, et al. The Movement Disorder Society evidence-based medicine review update: treatments for the non-motor symptoms of Parkinson's disease. Mov Disord. 2011;26(Suppl 3):S42-80.
26
LeWitt PA, Boroojerdi B, MacMahon D, et al. Overnight switch from oral dopaminergic agonists to transdermal rotigotine patch in subjects with Parkinson disease. Clin Neuropharmacol. 2007;30(5):256-265.
27
Thaut MH, McIntosh GC, Rice RR, et al. Rhythmic auditory stimulation in gait training for Parkinson's disease patients. Mov Disord. 1996;11(2):193-200.
28
Menza M, Dobkin RD, Marin H, et al. A controlled trial of antidepressants in patients with Parkinson disease and depression. Neurology. 2009;72(10):886-892.
29
Ramig LO, Sapir S, Countryman S, et al. Intensive voice treatment (LSVT) for patients with Parkinson's disease: a 2 year follow up. J Neurol Neurosurg Psychiatry. 2001;71(4):493-498.
30
Beal MF, Oakes D, Shoulson I, et al. A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. JAMA Neurol. 2014;71(5):543-552.
31
Kunz D, Mahlberg R. A two-part, double-blind, placebo-controlled trial of exogenous melatonin in REM sleep behaviour disorder. J Sleep Res. 2010;19(4):591-596.
32
Knekt P, Kilkkinen A, Rissanen H, et al. Serum vitamin D and the risk of Parkinson disease. Arch Neurol. 2010;67(7):808-811.
33
Miyasaki JM, Long J, Mancini D, et al. Palliative care for advanced Parkinson disease: an interdisciplinary clinic and new scale. Parkinsonism Relat Disord. 2012;18(Suppl 3):S6-9.
34
Shotbolt P, Samuel M, Fox C, David AS. A randomized controlled trial of quetiapine for psychosis in Parkinson's disease. Neuropsychiatr Dis Treat. 2009;5:327-332.
35
Wee B, Hillier R. Interventions for noisy breathing in patients near to death. Cochrane Database Syst Rev. 2008;(1):CD005177.
36
Tinazzi M, Del Vesco C, Fincati E, et al. Pain and motor complications in Parkinson's disease. J Neurol Neurosurg Psychiatry. 2006;77(7):822-825.
37
Pioro EP, Brooks BR, Cummings J, et al. Dextromethorphan plus ultra low-dose quinidine reduces pseudobulbar affect. Ann Neurol. 2010;68(5):693-702.
38
Wasner G, Deuschl G. Pains in Parkinson disease — many syndromes under one umbrella. Nat Rev Neurol. 2012;8(5):284-294.
39
Haahr A, Kirkevold M, Hall EOC, Østergaard K. Living with advanced Parkinson's disease: a constant struggle with unpredictability. J Adv Nurs. 2011;67(2):408-417.
40
Bronner G, Royter V, Korczyn AD, Giladi N. Sexual dysfunction in Parkinson's disease. J Sex Marital Ther. 2004;30(2):95-105.
41
Schrag A, Hovris A, Morley D, Quinn N, Jahanshahi M. Caregiver-burden in Parkinson's disease is closely associated with psychiatric symptoms, falls, and disability. Parkinsonism Relat Disord. 2006;12(1):35-41.
42
Postuma RB, Berg D, Stern M, et al. MDS clinical diagnostic criteria for Parkinson's disease. Mov Disord. 2015;30(12):1591-1601.
43
Kluger BM, Fox S, Timmons S, et al. Palliative care and Parkinson's disease: meeting summary and recommendations for clinical research. Parkinsonism Relat Disord. 2017;37:19-26.
44
Richfield EW, Jones EJS, Shervin Badv R. Palliative care for Parkinson's disease: a summary of the evidence and future directions. Palliat Med. 2013;27(7):632-637.
45
Kluger BM, Miyasaki J, Katz M, et al. Comparison of integrated outpatient palliative care with standard care in patients with Parkinson disease and related disorders. JAMA Neurol. 2020;77(5):551-560.
terminal2.care content is for educational purposes and is not a substitute for clinical judgment. Based on articles retrieved from PubMed. © Terminal2 | terminal2.care
Private Notes
Session notes — not saved to any server. Clears when you close the tab.
Use this space for visit notes, clinical reminders, or patient-specific observations. This text is stored only in your browser session.