Unit 2D: Parkinson's Disease

Front 1

A disease of the basal ganglia characterized by slowness in the initiation and executive of movement (bradykinesia), increased muscle tone (rigidity), tremor at rest, and impaired postural reflexes:

Back 1

-Parkinson's Disease

Front 2

Describe the pathophysiologic process of PD:

Back 2

-Involves degeneration of the dopamine-producing neurons in the substania nigra of the midbrain, which in turn disrupts the normal balance between dopamine (DA) and acetycholine (ACh) in the basal ganglia

Front 3

Why is dopamine so important for a patient with PD?

Back 3

-It is a neurotransmitter that is essential for a normal functioning motor system, including control of posture, support, and voluntary smooth movement

Front 4

Describe s & s for a patient experiencing PD:

Back 4

-Onset is gradual and insidious, with gradual progression
-May involve only one side initially
-Tremor, rigidity, bradykinesia
-Begins with tremor, slight limp, or decreased arm swing
-Later is shuffling, propulsive gait with arms flexed and loss of postural reflexes

Front 5

What is the triad of PD?

Back 5

1.) Tremor

2.) Rigidity

3.) Bradykinesia

Front 6

Describe Tremors:

Back 6

-First sign of PD
-Minimal initially
-Patient is the first to notice
-More prominent at rest and is aggravated by emotional stress or increased concentration
-"Pill Rolling"
-Tremor can involve the diaphragm, tongue, lips, and jaw, but rarely the head

Front 7

Describe Rigidity:

Back 7

-The second sign
-Increased resistance to passive motion when the limbs are moved through their range of motion
-Typified by a jerky quality
-"Cogwheel rigidity": caused by sustained muscle contraction and consequently elicits a complaint of muscle soreness; feeling tired and achy; or pain in the head, upper body, spine, or legs
-Slowness in movement

Front 8

Describe Bradykinesia:

Back 8

-Particularly evident in the loss of autonomic movements
-Secondary to the physical and chemical alteration of the basal ganglia and related structures in the extrapyramidal portion of the CNS
-Lack of spontaneous activity
-Accounts for the stooped posture, masked face, drooling, and shuffling gait

Front 9

Describe complications of PD:

Back 9

-Depression
-Anxiety
-Apathy
-Fatigue
-Pain
-Constipation
-Impotence
-Short-term memory impairment
-Hallucinations
-Psychosis
-Dementia occurs in up to 40%
-Dysphagia
-Malnutrition
-UTI
-Skin breakdown
-Orthostatic hypotension
-Sleep disorders

Front 10

How is PD diagnosed?

Back 10

-At least 2 of the 3 characteristic signs of the classic triad are present

-Ultimate confirmation of PD is a positive response to antiparkinsonian drugs

Front 11

Describe PD drug therapy:

Back 11

-Antiparkinsonian Drugs: drugs either enhance the release or supply of DA or antagonize or block the effects of the overactive cholinergic neurons in the striatum (Levodopa with carbidopa [Sinemet])

-Anticholinergic drugs act by decreasing the activity of ACh, thus providing balance between cholinergic and DA actions

-Antihistamines and Beta blockers manage tremors

-Antiviral agent: amantidine

-Apomorphine: given SQ, needs to be taken with antiemetic (not Zofran) can severely lower BP and LOC

Front 12

Describe surgical treatment for PD:

Back 12

-Ablation Sx: involves stereotactic ablation of areas in the thalamus; recently replaced by DBS

-Deep Brain Stimulation (DBS): involves placing an electrode in the brain, connecting it to a generator placed in the chest and programmed to deliver a specific current to the targeted brain location; can be adjusted to control symptoms better and is reversible

-Transplantation: fetal neural tissue into the basal ganglia is designed to provide DA-producing cells in the brains of patients with PD

**Both DBS and ablative therapy reduce the increased neuronal activity by DA depletion