Parkinson’s Disease (PD)

Parkinson Disease-QR

ACKNOWLEDGEMENTS:

Thanks to Dr. Susan Fox, MB ChB, MRCP (UK), PhD, Associate Professor of Neurology, University Health Network, Toronto Western Hospital, University of Toronto, and Suzette Mahabeer, RN, MScN, Nursing Faculty – McMaster University, Hamilton, ON Canada for their expertise with the initial review of this topic.

Definition

Idiopathic progressive, a neurodegenerative disorder characterized by resting Tremor, Rigidity, Akinesia/bradykinesia, and Postural instability (‘TRAP’). Symptoms usually manifest when ~80% of dopamine-producing cells within substantia nigra (SN) become non-functional resulting in dopamine depletion.

Etiology

Proposed Classification Scheme for Parkinsonism. (Ref: Galpern WR, Lang, AE Ann Neurol 2006; 59:449-458)

Classical Parkinsonism

  • Sporadic
    • Idiopathic Parkinson’s disease
  • Genetic
    • LRRK2 mutations
    • SNCA mutations, duplications
    • Parkin mutations
    • PINK1 mutations
    • DJ-1 mutations
    • GBA mutations
    • Others (e.g. SCA2)

Atypical Parkinsonism

  • Sporadic
    • Dementia with Lewy bodies
    • Multiple system atrophy
    • Progressive supranuclear palsy
    • Corticobasal degeneration
    • Others
  • Genetic
    • Frontotemporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17)
    • Others
      • Wilsons disease
      • Huntington’s disease

Secondary Parkinsonism

  • Drug-induced
  • Toxin-induced
  • Vascular/infection

Environmental risk factors for idiopathic PD

  • Unknown, but the following have been suggested as associated with increased risk:
    • Environmental toxins
    • Pesticides/herbicides
    • Head trauma
  • Environmental factors that have been suggested to have a protective effect
    • Smoking
    • Caffeine
    • Elevated urates
    • Use of non-steroidal anti-inflammatory drugs

Epidemiology

Canada:

  • Prevalence: Approx. 160 per 100,000
  • Incidence: 10 to 20/100,000/year

Both prevalence and incidence increase with age.

  • 85% diagnosed are above the age 65 years
    • Approx. 100,000 Canadians affected
    • Approx. 6.3 million worldwide

Pathophysiology

  • Disease probably begins in the olfactory tract and brain stem (early loss of sense of smell) and spreads rostrally and caudally to substantia nigra and eventually to cortical regions
  • Loss of dopaminergic neurons in the substantia nigra leads to dopamine depletion within the basal ganglia. Multiple neurotransmitter abnormalities occur in the basal ganglia circuitry resulting in motor symptoms of PD
  • Non-motor symptoms of PD, such as neuropsychiatric, autonomic, sleep and pain likely result from degeneration of cortical and other brainstem regions
  • Observed pathological abnormalities in patients with PD include:
    • Degeneration of neurons in (SN)
    • Presence of Lewy bodies correlates with symptoms
  • Exact mechanisms of neurodegeneration are unknown, likely involves genetic and environmental factors
  • Mitochondrial dysfunction and oxidative stress as well as misfolding and aggregation of proteins (alpha synuclein) appears to underlie the neurodegenerative process
  • There is growing evidence to suggest a potential link along the gut-brain axis in the pathogenesis of Parkinson’s Disease, whereby disturbances in the gut biome facilitates neuronal toxicity that contribute to increased  aberrant alpha synuclein production and subsequent injury to central neurons and co-ordinated cell death involving the brain stem, nigrostriatal and other pathways that manifest the clinical symptoms of Parkinson’s Disease

Parkinson Disease-Pathophysiology Alogrithm

Clinical Manifestations:

1. Motor Symptoms

Tremor

“Pill-rolling”, resting tremor

  • Usually begins unilaterally in the hand, less often the leg. May spread over several years
  • Tremor can also involve the legs, lips, jaw, and tongue, Rarely involves the head
  • Anxiety, emotional excitement, or stressful situations exacerbate the tremors
  • Not all patients with PD develop tremor

Parkinson Disease-Clinical Presentation-Essential vs Parkinson Tremor

Rigidity

  • May begin unilaterally and spread to involve contralateral side
  • Cogwheel rigidity due to overlay of tremor
  • Lead pipe rigidity is the increased tone that is present throughout the range of movement
  • Will increase with activation (ask subject to open and close opposite hand)

Akinesia / Bradykinesia

  • Slow movements
  • Masked facies (expressionless), decreased blink
  • Speech may be hypophonic, stuttering or dysarthria
  • Ability to initiate voluntary movement is decreased
  • Affects routine tasks (buttoning, writing (micrographia), typing, tying knots, difficulty rising from a seated position)

Postural instability and gait dysfunction

  • Usually appears later in the disease course, but may occur early in some
  • Tendency to fall forward (propulsion) or backward (retropulsion)
  • Loss of postural reflexes
  • Stooped posture
  • Difficulty in starting to walk, turning, and stopping
  • Shuffling gait with short, quick steps (festinating gait)
  • Decreased arm swing
  • Freezing may occur which is sudden inhibition of movements

OTHER SYMPTOMS

Motor fluctuations

  • On/Off phenomenon:
    • May occur with advancing disease due to disease progression and chronic levodopa treatment
    • Periods of satisfactory or good control (on effect) is followed by periods of near immobility (off effect)
    • Symptoms of wearing off are apparent when the duration of levodopa effect subsides
  • Dyskinesia:
    • Over time many patients with PD may develop medication-induced dyskinesia some of which can be disabling
    • Many PD patients may be either unaware of dyskinesia or not have any functional disability with the involuntary movements

Musculoskeletal problems

  • Camptocormia (bent-spine)
  • Head drop (less common)
  • Kyphosis

2. Non-Motor Symptoms

Dementia

  • Dementia can occur later in the course of disease in 10-15% patients
  • Short-term memory and visuoperceptual functions may be affected

Psychosis

  • Sense of presence: Well formed visual and less commonly auditory and tactile hallucinations
  • Paranoid delusions: May be associated with cognitive impairment; Can be triggered by dopaminergic drugs; always rule out other causes of delirium e.g. infection

Mood disorders

  • Depression
  • Anxiety
  • Apathy
  • All very common in PD. Maybe ‘premotor’ features i.e. occur years before the onset of PD

Sleep disorders

  • Excessive daytime sleepiness
  • Insomnia
  • REM sleep behaviour disorder (maybe a ‘premotor’ feature)
  • Sleep disorders are very common and are often drug-induced

Autonomic dysfunction

  • Urinary frequency and nocturia
  • Constipation
  • Postural hypotension

Pain

  • Can be multifactorial due to rigidity or dystonia or ‘central’
  • Sensory symptoms-Numbness/tingling

Workup and Diagnosis

There is no routine/specific diagnostic test for Parkinson’s disease, hence diagnosis is largely based on history and clinical features.

Diagnosis is suggested when two of the three characteristics signs of the classic triad are present:

  1. Tremor
  2. Rigidity
  3. Bradykinesia

Although dementia occurs in approximately 40% of patients with Parkinson’s disease, the intellectual impairment does not occur in the majority of patients.

Confirmation of Parkinson’s disease is assisted by a positive response to anti-Parkinson’s medication (Ref: Dirksen et al., 2010).

History of presenting complains:

  • Early diagnosis may be difficult as many patients can rarely pinpoint when symptoms started. Usually family or friends notices postural changes, tremors, slowness of movements and small handwriting (micrographia)

Family and occupational history:

  • Enquire about Parkinson’s in the immediate family as well as exposure to pesticides, herbicides, or possible exposure to other toxins (illicit drugs)

Neurological examination:

  • Is a systematic process, which includes a variety of clinical tests, observations and assessments, designed to evaluate the characteristic features of Parkinsonism; i.e., tremor, rigidity, slowness of movements and postural instability (tendency to falls)

Response to dopaminergic therapy:

  • Should be carefully evaluated as this may assist with making the diagnosis

CT/MRI brain:

  • Rule out structural abnormalities like hydrocephalus, tumor, or lacunar infarcts (strokes) that may affect the neural pathways within the deep structures of the brain (basal ganglia) that can lead to Parkinsonism
RN/Medical Management:

No known cure and treatment is therefore largely symptomatic:

  • Dopaminergic
  • Non-dopaminergic agents
  • Non-pharmacologic interventions
  • Surgical

1. MEDICATION INITIATION:

Indications

  • Interference with work, activities of daily living (ADL), or social and leisure function
  • Gait disturbance, falls
  • Patient’s preferences-control of non-disabling but socially embarrassing condition such as tremor

Medication options/strategies:

There are a few options available for the treatment of Parkinson’s. Of these, levodopa may be the most efficacious, but the potential for developing disabling dyskinesias, often leads to trial of other agents, particularly in younger individuals. Consequently, there is no standardized approach with a “first line” treatment as such, and treatment is often individualized.

Dopaminergic:

  • Dopamine replacement: Levodopa (highly effective and usual agent of choice for most)
  • Dopamine receptor agonist: Pramipexole, ropinirole, rotigotine patch
  • COMT inhibitors:
    • Entacapone; extends the duration of action of levodopa
    • Opicapone: high binding affinity with the COMT enzyme and strong inhibition over 24 hours – promising data
  • MAO-B inhibitors: Rasagiline, selegiline, safinamide; for early monotherapy and as an add-on to extend the duration of action of levodopa

Non-dopaminergic:

  • Anticholinergics: Benztropine; trihexyphenidyl-rarely used but may help tremor-dominant conditions
  • Antiglutaminergic: Amantadine (most helpful as a treatment for dyskinesia but can have mild antiparkinsonian effects)

Other agents for non-motor symptoms:

  • Low dose atypical neuroleptic: (serotonin/dopamine antagonist): Quetiapine and clozapine (with CBC monitoring) for visual hallucinations and psychosis

NOTE: Typical neuroleptics e.g. haloperidol should not be used in PD due to the risk of worsening motor function, atypical neuroleptics e.g. olanzapine and risperidone should be used cautiously.

  • Clonazepam/lorazepam-may be useful in associated sleep disorders e.g. REM sleep behaviour disorder (RBD), and anxiety
  • Antidepressants: Tricyclics and SSRI, for anxiety and depression
  • Melatonin-for insomnia, and RBD
  • Anticholinergics e.g. oxybutynin-for overactive bladder syndrome
  • Stool softeners and laxatives-for constipation
  • Analagesic use as required for musculoskeletal discomfort
  • Ipratropium spray, sublingual atropine drops-administered topically for drooling saliva

2. NON-PHARMACOLOGIC INTERVENTIONS

  • Rehabilitation with physical and occupational therapy to help improve functional outcomes in subjects with specific gait and balance problems
  • Emotional and psychological support of patient and family
  • Speech therapy for dysarthria
  • Adaptive strategies → adjustments in their homes to reduce the risk of falls and assist mobility; use of cane or walker when required
  • Providing resources about support groups, counsellors, societies

3. SURGICAL OPTIONS

Deep brain stimulation (DBS)

  • Selection criteria for suitable patients are essential. Usually <70 years old; must be levodopa responsive and have no cognitive problems
  • Procedure is Reversible
  • Adjustable for optimal benefit vs side-effects
  • Bilateral procedures are usually performed if STN is the target
  • Following types of stimulation can be done
    • Thalamic stimulation: Relieves tremors only (may be unilateral procedure)
    • Subthalamic nucleus (STN) stimulation: Relieves tremors, rigidity, dyskinesias, and motor symptoms (commonest target)
    • Unilateral Pallidal stimulation: Relieves dyskinesia (rarely used)
  • Potential (infrequent) complications of DBS
    • Hemorrhage, ischemic, seizures, death in 1%
    • Dysarthria
    • Cognitive decline
    • Mood disturbances
Medications:

Dopamine precursor/Dopamine decarboxylase inhibitor

  • Levodopa/Carbidopa
  • Levodopa/Benserazide
  • Levodopa/Carbidopa/Entacapone

Mechanism

  • Dopamine replacement therapy
  • Carbidopa and Benserazide inhibit peripheral breakdown of Levodopa (L-Dopa) by inhibiting decarboxylation, thereby increasing the availability of L-Dopa to cross the blood-brain barrier (BBB)
  • Within the basal ganglia, L-Dopa is then converted to dopamine

Dose:

Levodopa/Carbidopa:

Immediate Release (100/10; 100/25; 250/25)

  • Start 100/10 mg or 100/ 25 mg PO ½-1 tab TID; Adjust dose according to response, increase 100/25 mg (1 tablet) PO every 7 days or 250/25 mg (1/2-1 tablet) PO every 7 days
  • Most will get benefit with 400-600 mg levodopa. No maximum dose but unusual to require >2 g/d

Extended-release (100/25; 200/50)

  • Can use instead of IR however no real advantage as slower, less predictable time of onset. Maybe useful at bedtime for nocturnal akinesia
  • Start 200/50 mg PO BID, then adjust dose according to response, increase dose by 0.5-1 tab/day every 3 days giving dose interval of at least 4-8 hours during the waking day; Max. 600 mg/2400 mg/day

Levodopa/Benserazide (50-12.5; 100-25; 200-50)

  • 100/25 mg PO once daily or BID; May increase every 3-4 days until optimal effect is achieved; optimal dosage 400/100 mg to 800/200 mg/day divided into 4-6 doses
  • Note:
  • May use 200/50 mg form for maintenance therapy once the optimal dosage has been determined
  • May use 50-12.5 mg form when frequent dosing is required to minimize adverse effects

Caveat: Simultaneous ingestion of L-dopa with high protein meals could decrease absorption and may impact on efficacy

Anti-Parkinson’s agent/COMT inhibitor

  • Entacapone
  • Opicapone

Mechanism

  • Entacapone: Reversible and selective inhibitor of peripheral catechol-O-methyltransferase (COMT); multiple doses per day
  • Opicapone: high binding affinity with the COMT enzyme and strong inhibition; once per day dosing
  • When administered with Levodopa, they decrease the peripheral degradation of Levodopa via the COMT mediated pathways, leading to more sustained Levodopa serum levels
  • Enhanced serum concentrations of L-Dopa increases availability for traversing the blood-brain barrier

Dose:

Entacapone:

  • 200 mg PO with each dose of Levodopa/Carbidopa or Levodopa/Benserazide, Maximum up to 8 times/day (1600 mg/day)
  • Note: May require an average decrease of 25% in the daily Levodopa dose if the patient is taking Levodopa ≥800 mg/day or had moderate-to-severe dyskinesias before beginning therapy

Opicapone:

  • A newer COMT inhibitor; Typical dose: 50 mg PO once daily at bedtime

Combination Therapy:

Anti-Parkinsonian dopaminergic agent

  • Levodopa/Carbidopa/Entacapone

Mechanism

  • Dopamine replacement therapy/Catechol-O-methyltransferase (COMT)

Dose:

Carbidopa/Levodopa/Entacapone (Stalevo)

  • Therapy should be individualized and adjusted according to the desired therapeutic response
  • The combination is supplied as tablets in 6 different strengths

Parkinson Disease-Medication-Stalevo Dosage Forms

Anti-Parkinson’s agent/Monoamine oxidase (MAO) B inhibitor

  • Rasagiline
  • Safinamide
  • Selegiline

Mechanism

  • Selective irreversible Monoamine Oxidase B (MAO-B) Inhibitors
  • Inhibition of MAO-B prevent breakdown of dopamine
  • May also increase dopaminergic activity by interfering with dopamine reuptake at the synapse

Dose:

Rasagiline:

  • Oral 1 mg once daily; may have to reduce levodopa dose if taken concurrently

Safinamide:

  • 50 mg orally once a day initially. May increase to 100 mg orally once a day after two weeks as required, and as tolerated. based on individual need and tolerability; Maximum dose: 100 mg per day

Selegiline:

  • Starting dose 2.5 mg PO BID, then 5 mg PO BID daily with meals. Maintenance dose 5 mg PO BID
  • Renal impairment
    • no change
  • Liver disease
    • Moderate: 50 mg daily
    • Severe: contraindicated

Anti-Parkinson’s agent, Dopamine agonist

  • Pramipexole
  • Ropinirole

Mechanism

  • Activates postsynaptic dopamine receptors in the striatum and substantia nigra
  • Longer duration of action compared to levodopa
  • No effect of food on absorption via GI tract

Dose:

Pramipexole:

Immediate-release form

  • Initial 0.125 PO TID; may increase dose gradually every 5-7 days; usual range 1.5-4.5 mg/day divided TID; Max. 4.5 mg/day
  • Renal impairment
    • Clcr 35-59 mL/minute: Initial: 0.125 mg BID; Max 1.5 mg BID
    • Clcr 15-34 mL/minute: Initial: 0.125 mg once daily; Max.1.5 mg once daily

Extended-release form-(USA)

  • Initial: 0.375 mg PO once daily; increase gradually to 0.75 mg once daily; Max. 4.5 mg once daily
  • Renal impairment:
    • Clcr >50 mL/min no dose adjustment required
    • Clcr 30-50 mL/min: Initial: 0.375 mg every other day; may increase to 0.375 mg/dose after 1 week and every week as required; Max: 2.25 mg once daily

Ropinirole:

Immediate-release form

  • 0.25 mg PO (TID); increase by 0.25 mg/dose every 7 days; daily dose may be increased by 0.5 to 1.0 mg/dose after a month until the desired response is achieved; Max. 24 mg/day

Rotigotine:

  • Initially 2 mg/24 hours and increase by 2 mg/24 hours every 1 -2 weeks if required and as tolerated to a maximum 8 mg/24 hours

Anti-Parkinson’s agent/NMDA receptor inhibitor

  • Amantadine

Mechanism

Possibly enhances dopamine action by:

  • Blocking the reuptake of dopamine into presynaptic neurons or by increasing dopamine release from presynaptic fibers
  • Reduces levodopa-induced dyskinesia by antagonism of NMDA glutamate receptors

Dose:

Amantadine:

  • Usual dose 100 mg PO BID; Max. 400 mg/day in divided dose
    • Note: Start 100 mg/day once daily in Patients taking another anti-Parkinson drug or debilitated; may increase dose to 100 mg twice daily after 1-2 weeks, if needed
  • Renal impairment:
    • Clcr 30-50 mL/min: 200 mg on day 1, then 100 mg PO once daily
    • Clcr 15-29 mL/min: 200 mg on day 1, then 100 mg PO every other day
    • Clcr <15 mL/min: 200 mg every week

Anti-Parkinson’s agent/Anticholinergic agent

  • Benztropine
  • Trihexyphenidyl

Mechanism

  • Possesses both anticholinergic and antihistaminic effects
  • May also inhibit reuptake and storage of dopamine, thereby prolonging the synaptic action of dopamine

Dose:

Benztropine:

  • 0.5-1 mg PO/IM/IV once daily at night; increase dose every 5-6 days; usual dose 1-2 mg/day in two divided doses; Max. 6 mg/da

Trihexyphenidyl:

  • 1 mg PO QID on the first day; then increase by 2 mg every 3-5 days; usual dose 6-10 mg/day in divided doses; Max. 15 mg/day
Diagnosis and Goals:

Diagnosis:

  • Impaired physical mobility related to rigidity, tremor, bradykinesia, and akinesia
  • Self-care deficit (feeding, dressing, personal hygiene, and toileting) due to tremors or motor disturbances, and medication side effects
  • Imbalanced nutrition due to difficulty in chewing and swallowing, or tremors
  • Altered nutrition: Less than body requirements related to dysphagia
  • Constipation due to medications or reduced activity/immobility
  • Impaired verbal communication due to slow movement of speech muscle, lower volume of speech and slowness in speech
  • Ineffective coping related to depression and dysfunction due to disease progression

Goals:

After establishing the diagnosis goals should be determined accordingly:

  • Improving functional mobility
  • Maintaining activities of daily living status (ADLs) and achieving normal bowel movements
  • Improve the nutritional status
  • Maintain and achieve effective communication
  • Develop strategies for coping with the disease progression (optimize psychosocial well-being)
Nursing Intervention:

Health teaching and nursing care in Parkinson’s are geared towards the maintenance of good health, independence, and avoidance of complications such as contractures/falls.

Improving mobility

  • Encourage the patient to participate in daily exercises, such as walking, riding a stationary bike, swimming, or gardening. Exercise can limit the consequences of decreased mobility which include: muscle atrophy, contractures, and constipation
  • Patients should be advised to take warm baths and receive messages to help relax muscles
  • Instruct the patient to take frequent rest periods to overcome fatigue and frustration
  • Stretch-hold-relax and range of motion exercises, provide joint flexibility
  • Advise and teach postural exercises and walking techniques to offset shuffling gait and tendency to lean forward
    • Instruct patient to use a broad-based gait
    • Have patient make a conscious effort to swing arms, raise the feet while walking, use a heel-toe gait, and increase the width of stride
    • Tell patient to practice walking to marching music or sound of ticking metronome to provide sensory reinforcement
  • Individualized physical therapy program by a physical therapist can be developed
  • Deep breathing exercises while walking may help aerate lungs

Optimizing nutritional status

  • Patients are at risk of aspirating and developing bronchopneumonia, due to impaired swallowing and accumulation of saliva
  • Nutritional management is required to avoid malnutrition, aspiration, and constipation
  • Appetizing foods that are easily chewed and swallowed are suggested
  • The diet should contain adequate roughage and fruit to avoid constipation
  • Teach patient to think through the sequence of swallowing-close lips with teeth together; lift tongue up with food on it; then move tongue back and swallow while tilting the head forward
  • Instruct patient to chew deliberately and slowly, using both sides of the mouth
  • Tell patient to make a conscious effort to control the accumulation of saliva by holding the head upright and swallowing periodically
  • Have patient use secure, stabilized dishes and eating utensils
  • Prolong eating process causes difficulty in maintaining weight and nutrition, due to slow chewing, swallowing, and dry mouth from medications. Ample time planned for eating will also prevent frustration and encourage independence
  • Suggest smaller meals and additional snacks
  • Monitor weight

Maximizing communication ability

The speech therapist can help develop speech improvement exercise and assist the family and healthcare personnel to use those methods to communicate.

  • Some of the facial exercises and breathing methods to obtain appropriate pronunciation, volume, and intonation are as follows:
    • Take a deep breath before speaking to increase the volume of sound and number of words spoken with each breath
    • Speak in short sentences, and exaggerate the pronunciation
    • Exercise facial muscles by smiling, frowning, grimacing, and puckering

Preventing constipation

Patients may have severe constipation, due to muscle weakness of the muscles used in defecation, lack of exercise, less fluid intake and medications prescribed for the treatment also inhibits normal intestinal secretion are few other contributing factors.

  • Encourage foods with moderate fiber content-whole grains, fruits, and vegetables
  • Increase water intake
  • Obtain a raised toilet seat to encourage normal position
  • Encourage patient to follow regular bowel regimen

Improving coping ability

The disease may lead to withdrawal and depression.

  • A planned program of activity throughout the day prevents too much sleeping and avoids disinterest and apathy
  • Soothing music may help the patient to cope with pain and depression
  • Determine changes in depression, i.e. response to antidepressants
  • Provide emotional support and encouragement
  • Establish realistic goals and determine there execution
  • Open communication and exchange of information about the disease, and feelings associated with it should be encouraged
  • Encourage use of all resources, such as therapists, primary care provider, social worker, and social support network
  • Should always be vigilant of side effects of treatment with dopamine agonists i.e. obsessions such as hypersexuality, gambling, etc.

Community and home care considerations

  • Utilize physical therapy services to improve mobility and reduce the fear of falls
  • Assess the need for occupational therapy aids, such as handrails in the tub or shower, raised toilet seat, handrails on both sides of the stairway, rope secured to foot-board of bed that can be used for pulling into a sitting position. Use of straight-backed wooden chairs with armrests
  • Respite for caregivers through the use of social services, health visitors, mental health counselors, and support groups is advised as needed
  • Skilled assessment of needs of the patient, professional nursing and therapeutic services should all be provided as the disease progress

Patient education and health maintenance

Management is aimed at relieving symptoms.

  • Instruct the patient to avoid sedatives, unless specifically prescribed, which may have an additive effect with other medications
  • Vitamin B preparations, and vitamin-fortified foods, are avoided or should be taken only by prescription, due to known reverse effects of medication, e.g. vitamin B6 (pyridoxine) may interfere with the metabolism of certain Parkinson’s medication and making them less effective)
  • Concomitant ingestion of levodopa/carbidopa with high protein meals may reduce absorption. Hence, patients may be instructed to use this medication prior to or in between meals
  • Instruct the patient in medication regimen and potential adverse reactions, such as orthostatic hypotension, dry mouth, dystonia, muscle twitching, urine retention, impaired glucose tolerance, anemia, and elevated liver function tests
  • Encourage follow-up and monitoring for diabetes, glaucoma, hepatotoxicity, and anemia while undergoing drug therapy
  • Teach patient ambulation cues to avoid “freezing” in place and possibly avoid falls by doing one of the following:
    • Raise head, raise toes, and then rock from one foot to another while bending knees slightly
    • Raise arms in a sudden short motion
    • Take a small step backward, and then start forward
    • Step sideways, and then start forward
  • Instruct the family not to pull the patient during episodes of “freezing,” which increases the problem and may cause falling
  • Refer the patient/family for more information and support to such agencies as:
    • Canadian Parkinson’s Society
    • National Parkinson’s Foundation
    • National Institute of Neurologic Disorders and Stroke
    • The Michael J. Fox Foundation for Parkinson’s Research
  • As the disease progresses patients and families need to be aware of:
    • Fall risk-encourage to use of canes and walkers where appropriate
    • Remove rugs and avoid uneven floors
    • Clothing can be altered/simplified with the use of slip-on shoes and Velcro hook-and-loop fasteners or zippers on clothing instead of buttons and hooks. An elevated toilet seat can also facilitate transfers from the toilet
    • Nearing end-stage be aware of
    • Aspiration risk and ensuing pneumonia
    • Bedsores (due to immobility)
Nursing Alerts:
  • Elderly patients may have reduced tolerance to anti-Parkinson’s drugs and may require smaller doses
  • Watch for and report psychiatric reactions, such as anxiety, confusion, and hallucinations; cardiac effects, such as dizziness, orthostatic hypotension, and pulse irregularity; and blepharospasm (twitching of the eyelid), an early sign of toxicity
  • Other adverse effects may include dry mouth, nausea, drowsiness, and insomnia
  • Be aware of the development of obsessions with some Parkinson’s medications, particularly dopamine agonist
  • Dysphagia may occur in severe cases leading to malnutrition or aspiration
  • General debilitation may lead to pneumonia, urinary tract infections, and skin breakdown
  • The gait slows, and turning becomes quite difficult
  • Decreased Mobility may result in constipation, ankle edema and also contractures

References

Core Resources:

  • Brust JCM (2007) Current Diagnosis and Treatment (Neurology) (2nd ed.) New York: McGraw Hill
  • Compendium of Pharmaceuticals and Specialties (CPS). Canadian Pharmacist Association. Toronto: Webcom Inc. 2012
  • Day RA, Paul P, Williams B, et al (eds). Brunner & Suddarth’s Textbook of Canadian Medical-Surgical Nursing. 2nd ed. Philadelphia: Lippincott Williams and Wilkins; 2010
  • Dirksen, S., Lewis, S., & Collier, I., Heitkemper, M., O’Brien, P., & Bucher, L. (2010). Medical-Surgical Nursing in Canada: Assessment and management of clinical problems (2nd edition) Toronto: Mosby Elsevier.
  • Foster C, Mistry NF, Peddi PF, Sharma S, eds. The Washington Manual of Medical Therapeutics. 33rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2010
  • Gray J, ed. Therapeutic Choices. Canadian Pharmacists Association. 6th ed. Toronto: Webcom Inc. 2011
  • Grimes D, Gordon J, Snelgrove B. et al. Canadian Guidelines on Parkinson’s Disease. Can J Neurol Sci. 2012;39: S1-S30
  • Katzung BG, Masters SB, Trevor AJ, eds. Basic and Clinical Pharmacology. 11th ed. New York: McGraw-Hill; 2009
  • Longo D, Fauci A, Kasper D, et al (eds). Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2011
  • McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis & Treatment. 49th ed. New York: McGraw-Hill; 2010
  • Pagana KD, Pagana TJ eds. Mosby’s Diagnostic and Laboratory Test Reference. 9th ed. St. Louis: Elsevier-Mosby; 2009
  • Rowland LP et al. (2010) Merritt’s Neurology (9th ed.) Philadelphia: Lippincott Williams and Wilkins
  • Skidmore-Roth L. ed. Mosby’s drug guide for nurses. 9th ed. St. Louis: Elsevier-Mosby; 2011
  • Skidmore-Roth L, ed. Mosby’s nursing drug reference. 24th ed. St. Louis: Elsevier-Mosby; 2011
  • National Collaborating Centre for Chronic Conditions. Parkinson’s disease: national clinical guideline for diagnosis and management in primary and secondary care. London: Royal College of Physicians, 2006

Online Pharmacological Resources:

  • e-Therapeutics
  • Lexicomp
  • RxList
  • Epocrates

Journals/Clinical Trials:

  • Angot E, Steiner JA, Hansen c. et al.  Are synucleinopathies prion-like disorders? Lancet Neurol 2010; 9: 1128–38
  • Block, G, Liss, C, Reines, S, et al. Comparison of immediate-release and controlled-release carbidopa/levodopa in Parkinson’s disease: A multicenter 5-year study. Eur Neurol 1997; 37:23
  • Cruz MP,  Xadago (Safinamide): A Monoamine Oxidase B Inhibitor for the Adjunct Treatment of Motor Symptoms in Parkinson’s Disease Pharmacy and Therapeutics  2017 Oct; 42(10): 622-624,637
  • Emre M, Aarsland D, Albanese A, Rivastigmine for Dementia Associated with Parkinson’s Disease N Engl J Med 2004; 351:2509-2518
  • Fahn, S, Bressman, SB. Should levodopa therapy for Parkinsonism be started early or late? Evidence against early treatment. Can J Neurol Sci 1984; 11:200
  • Galpern WR, Lang, AE Interface between tauopathies and synucleinopathies: A tale of two proteins. Ann Neurol 2006; 59:449-458
  • Goedert, M., Spillantini, M. G., Del Tredici, K. & Braak, H. 100 years of Lewy pathology. Nature Rev. Neurol 2012; 9, 13–24
  • Hauser RA, Cantillon M, Pourcher E et al. Preladenant in patients with Parkinson’s disease and motor fluctuations The Lancet Neurology 2011; 10: 221-229
  • Hauser, RA, McDermott, MP, Messing, S. Factors associated with the development of motor fluctuations and dyskinesias in Parkinson disease. Arch Neurol 2006; 63:1756
  • Irwin DJ, Lee VM, Trojanowski JQ. Parkinson’s disease dementia: convergence of α-synuclein, tau and amyloid-β pathologies. Nat Rev Neurosci. 2013;14(9):626-636. doi:10.1038/nrn3549
  • Kumar, N, Van Gerpen, JA, Bower, JH, Ahlskog, JE. Levodopa-dyskinesia incidence by age of Parkinson’s disease onset. Mov Disord 2005; 20:342
  • Lyons KE, Pahwa R. Outcomes of rotigotine clinical trials: effects on motor and nonmotor symptoms of Parkinson’s disease. Neurol Clin. 2013;31(3 Suppl): S51-9
  • Marks MJ, Bartus RT, Siffert J et al. Gene delivery of AAV2-neurturin for Parkinson’s disease The Lancet Neurology 2010; 9: 1164-1172
  • Mizuno Y, Hasegawa K, Kondo T et al. Clinical efficacy of istradefylline (KW-6002) in Parkinson’s disease Mov Disord. 2010; 25:1437-43
  • Olanow C W, Rascol O, Hauser R, et al, A Double-Blind, Delayed-Start Trial of Rasagiline in Parkinson’s Disease ADAGIO Study Investigators N Engl J Med 2009; 361:1268-1278
  • Postuma RB, Lang AE. Homocysteine and levodopa: should Parkinson disease patients receive preventative therapy?. Neurology. 2004;63(5):886-891. doi:10.1212/01.wnl.0000137886.74175.5a
  • Rascol O, Brooks DJ, Korczyn AD, et al, A Five-Year Study of the Incidence of Dyskinesia in Patients with Early Parkinson’s Disease Who Were Treated with Ropinirole or Levodopa. 056 Study Group.N Engl J Med 2000; 342:1484-1491
  • Sampson TR, Debelius JW, Thron T, et al. Gut Microbiota Regulate Motor Deficits and Neuroinflammation in a Model of Parkinson’s Disease. Cell. 2016;167(6):1469-1480.e12. doi:10.1016/j.cell.2016.11.018
  • Shrivastava A The hot cross bun sign Radiology 2007, 245: 606-607
  • The Parkinson Study Group CALM Cohort Investigators. Long-term effect of initiating pramipexole vs levodopa in early Parkinson disease Arch Neurol 2009; 66:563-70
  • The Parkinson Study Group  A Controlled Trial of Rotigotine Monotherapy in Early Parkinson’s Disease. Arch Neurol. 2003;60 (12):1721-1728
  • The Parkinson Study Group. Levodopa and the Progression of Parkinson’s Disease N Engl J Med 2004; 351:2498-2508
  • The Parkinson Study Group. Impact of deprenyl and tocopherol treatment on Parkinson’s disease in DATATOP patients requiring levodopa. Ann Neurol 1996; 39:37-45
  • Williams A, Gill S, Varma T, et al, for the PD SURG Collaborative Group Deep brain stimulation plus best medical therapy versus best medical therapy alone for advanced Parkinson’s disease (PD SURG trial) The Lancet Neurology 2010; 9:581-591