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CNS -Antiparkinsonian Drugs

Discuss the signs and symptoms exhibited by a


patient with Parkinson’s Disease

Describe the actions and intended effects of


medications used to treat the signs and symptoms of
Parkinson’s Disease
CNS
Antiparkinsonian Drugs

Parkinson’s Disease:
 Disease of the basal ganglia & related neuronal groups +
neurotransmitter deficiencies
 “shaking palsy”
 Bradykinesia – slowing down in the initiation & execution of
movement
 Rigidity – increased muscle tone
 Tremor at rest
 Impaired postural reflexes
CNS
Antiparkinsonian Drugs

Degeneration of dopamine-producing neurons in the


substantia nigra of the midbrain
 Disrupts the balance of:
 dopamine (DA) – neurotransmitter for normal functioning of
the extrapyramidal motor system (control of posture, support, and
voluntary motion)
 Acetylcholine (Ach)
 and the basal ganglia
Symptoms do not occur until 80% of the neurons in
the substantia nigra are lost
CNS Antiparkinsonian Drugs
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Antiparkinsonian Drugs

Five Stages

 Flexion of affected arm - tremor / leaning toward unaffected


side
 Slow shuffling gate
 Increased difficulty walking – looks for support to prevent
falls
 Further progression of weakness – assistance with
ambulation
 Profound disability – may be confined to wheelchair
CNS
Antiparkinsonian Drugs

Tremor

 First sign
 Affects handwriting – trailing off at ends of words
 More prominent at rest
 Aggravated by emotional stress or increased concentration
 “Pill rolling” – rotary motion of thumb and forefinger
 NOT essential tremor – intentional
CNS
Antiparkinsonian Drugs

Rigidity

 Increased resistance to passive motion when


limbs are moved through their range of motion
 “Cogwheel rigidity” -- Jerky quality –
intermittent catches of movement
 Caused by sustained muscle contraction
 Muscle soreness; feeling tired & achy
 Slowness of movement due to inhibition of alternating
muscle group contraction & relaxation in opposing muscle
groups
CNS
Antiparkinsonian Drugs

Bradykinesia

 Loss of automatic movements:


 Blinking of eyes, swinging of arms while walking,
swallowing of saliva, self-expression with facial and
hand movements, lack of spontaneous activity, lack of
postural adjustment

 Results in: stooped posture, masked face, drooling of


saliva, shuffling gait (festination); difficulty initiating
movement
CNS
Antiparkinsonian Drugs

Drug Therapy

 Correcting the imbalance of neurotransmitters within the CNS


 Dopaminergic – enhance release or supply of dopamine (DA)
 Anticholinergic – antagonize or block the effects of overactive
cholinergic neurons in the striatum
 Monoamine Oxidase Inhibitor
 Decreases MAO (the degradative enzyme for DA)
 Results: DA levels are increased
 Catechol-O-Methyl Transferase (COMT) Inhibitor
 Betablocker
 Antihistamine
CNS
Antiparkinsonian Drugs
CNS
Antiparkinsonian Drugs
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Antiparkinsonian Drugs
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Antiparkinsonian Drugs
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Antiparkinsonian Drugs

Anticholinergic Drugs: decrease the activity of


ACh
 Artane, Pagitane, Cogentin
Antihistamines – decreases rigidity
 Benadryl
Betablockers – decreases rigidity
 Inderal
Monoamine oxidase inhibitor (MAO):
 Eldepryl, Carbex
Catechol-O-Methyl Transferase (COMT)
Inhibitor
 Comtan, Tasmar
CNS
Antiparkinsonian Drugs

Drug Therapy

 Sinemet early in disease becomes ineffective

 Early: DA receptor agonist -- directly stimulate DA receptors


 Parlodel, Permax, Requip, Mirapex

 Moderate to severe symptoms:


 Sinemet is added to therapy
CNS
Antiparkinsonian Drugs
CNS -- Antiparkinsonian Drugs
Nursing Process

Assessment
 Head-to-toe
 Neuro
 GI/GU
 Ability to swallow
 Psychological and emotional coping
 Parkinson progression
Medication History
 Length of time on medications
 Changes in medications and effects
Safety
 Ability to perform ADLs independently
CNS -- Antiparkinsonian Drugs
Nursing Process

Nursing Actions

 Exact timing of medication – cannot be administered


late
 Oral doses given with food
 Avoid foods in Vit B6 – reverse effects of levodopa
 Force fluids >2,000 mL/day
 High roughage, high fiber diet
CNS -- Antiparkinsonian Drugs
Patient Education

 “Wearing off” phenomenon – gradual worsening of


symptoms as medication begins to lose effectiveness, despite
maximal doses
 “Drug Holiday” when levodopa no longer working effectively (usually
10-day period of hospitalization)
 Community resources to assist patient and family
 Safety
 Effect on blood pressure –
 Hypotension
 Hypertensive crisis of MAOI accidentally taken
 “Sleep attacks” – newer dopamine agonists (pramipexole &
ropinirole)
 GI: Constipation – high fiber, high roughage, increased fluids
 GU: urine color changes – brownish-orange (entacapone)
CNS – Antiparkinsonian Drugs
Monitoring Therapeutic Effects

Therapeutic Response:
 Improved sense of well being
 Ability to perform ADLs
 Ability to concentrate and think clearly
 Less intense parkinsonian manifestations

Observe for Adverse Effects:


 Confusion, anxiety, irritability, depression, paranoia,
headache, weakness, lethargy, nausea, vomiting, anorexia,
palpitations, postural hypotension, tachycardia, dry mouth,
constipation, urinary retention, blurred vision, dark urine,
difficulty swallowing, and nightmares
CNS – Antiparkinsonian Drugs

Carbidopa in Parkinson’s disease is to be


used:

 a. As successful monotherapy.
 b. In conjunction with levodopa to block peripheral
conversion to dopamine.
 c. To decrease the incidence of gastrointestinal side
effects associated with levodopa.
 d. 2 and 3
CNS – Antiparksonian Drugs

Discuss the normal course of progression of


Parkinson’s disease. Include the rationale for drug
therapy to alleviate the symptoms.

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