parkinson's disease by me ..........prakash mahala p.g. medical surgical nursing at himalayan college of nursing dehradun.......prakashjpmmahala@gmail.com

1. Parkinson’s
Disease
BY:- PRAKASH MAHALA
M.SC.NURSING 1STYEAR

2. Introduction:-
 Dr. James Parkinson (1755-1828)
 “involuntary tremulous motion”
 “shaking palsy”
 London home

3. The disease was first
described in 1817 by a British
physician
named James Parkinson
He wrote "An Essay on
Shaking Palsy"

4.  Progressive loss of substantia nigra
dopaminergic neurons; loss of 70% before one is
symptomatic, >90% loss at death
 Disorder that affects the central nervous
system:
 Progressively
 Debilitating
 Degeneratively
 Easily characterized by decreased
movement, muscular rigidity, resting
tremors, and postural instability

5.  Progressive neurodegenerative disorder that
causes motor and nonmotor dysfunction
– Characterized by loss of dopaminergic neurons
in substantia nigra .
– Can affect other areas of the nervous system
including the autonomic and enteric nervous
systems.
 Second most common neurodegenerative
disorder after Alzheimer’s disease

6. Definition :-
 Parkinson's disease is a progressive,
neurodegenerative disorder that affects
movement, muscle control, and balance as
well as numerous other functions. It is part of
a group of conditions known as motor
systems disorders.
 it is always chronic and progressive, meaning
that the symptoms always exist and always
worsen over time.

7. Incidence :-
 Prevalence Rate : 200 per 100,000
Rare for individuals < 40 years of age
1% for individuals > 60 years of age
2% for individuals > 85 years of age
Men > Women
Incidence rate : 20 per 100,000 (annually)
The National Parkinson’s Foundation
estimates that up to 1.5 million
Americans have the disease
Approximately 50,000 new cases are
diagnosed each year

8. Type :-
 There are three types of Parkinson's disease
and they are grouped by age of onset:
 Adult-Onset Parkinson's Disease - This is the
most common type of Parkinson's disease.
 The average age of onset is approximately 60
years old.
 The incidence of adult onset PD rises
noticeably as people advance in age into their
70's and 80's.

9.  Young-Onset Parkinson's Disease - The age
of onset is between 21-40 years old. Though
the incidence of Young-Onset Parkinson's
Disease is very high in Japan (approximately
40% of cases diagnosed with Parkinson's
disease).
 Juvenile Parkinson's Disease - The age of
onset is before the age of 21. The incidence of
Juvenile Parkinson's Disease is very rare.

10. STAGES OF
PARKINSON’S DISEASE
EARLY - no functional impairment
MILD - honeymoon period
MODERATE - multiple drugs,
occupational and social activities affected
SEVERE - side effects from drugs,
resistant to therapy, reduced quality of life
LATE - wheelchair or bed bound

11. Etiology:-
 Increasing age (rare in those < 50; early or
young onset)
 2 times more common in men than
women
may be more common in whites
 1.4 to 3.5 more often to occur in families
with relatives with PD
 Environmental factors (pesticides, rural
residence)

12.  Head trauma
 Encephalitis has been clearly associated with
parkinsonism.

13. Pathophysiology:-
 The basal ganglia is an important part of the
motor system. It is made up of the caudate
nucleus, the putamen, and the globus
pallidus. The caudate nucleus and the
putamen connect with the globus pallidus
which connects with the motor cortex
through the ventral anterior and ventrolateral
nuclei of the thalamus.

14. The basal ganglia receives its most important
input from the substantia nigra.
The substantia nigra has dopaminergic neurons
that release dopamine to the caudate and the
putamen.
In normal movement, the substantia nigra
releases dopamine to the caudate and
putamen which then produce a balance
between excitatory and inhibitory effects to
the globus pallidus internal and glosbus
pallidus external, respectively.

15. Overall, for both pathways there is an excitatory
effect, so the input of dopamine from the
substantia nigra is very important for facilitating
movement.
When there is damage to the dopaminergic
neurons of the substantia nigra the above
pathways are disrupted and the symptoms of
Parkinson’s comes up.

17. Symptoms:-
 Due to the lack of dopamine (neurotransmitters)
brain signals to the body are hindered. Therefore
symptoms may include:
 Tremores occurring in the limbs, jaws and face
 Bradykinesia (slow movement)
 Impaired balance and coordination
 Stiffness of the limbs and trunk

18.  Secondary Symptoms: Varies for different
persons caused by eventual loss of both
voluntary and involuntary controls of the
nervous system.
 Small, cramped penmanship (micrographia)
 Scaling of the skin (seborrhea)
 Loss of bodily waste management
(incontinence)
 Dementia

19.  Feelings of anxiety, depression and loneliness.
 Excessive salivation (hypersalivation) and
excessive sweating
 Constipation
 Soft, whispery voice (hypophonia)
 Slow response to questions (bradyphrenia)

21. Common Treatments:
Medication:-
 Levodopa and Carbidopa
 this substance is converted into dopamine by an
enzyme dopa decarboxylase (DDC) that exists in the
nervous system. Unfortunately, most of the levodopa
is metabolized before reaching the brain1.
 Actual dopamine can’t be used because it is unable to
cross the cell walls into the brain.
 Carbidopa is used in conjuction with Levodopa to
increase the amount of Levodopa to enter the brain.
 Most effective against bradykinesia and rigidity
 Ineffective against balance problems

22. COMT = catechol-O-methyltransferase; MAO-B = monoamine oxidase B

23.  Amantadine
 An antiviral drug with dopamine agonist properties
 Increases the release of dopamine
 Used for early treatment
 loses effectiveness in 3-4 months
 Selegiline
 Prevents the breakdown of natural and levodopa
dopamine by inhibiting the enzyme monoamine
oxidase B (MAO-B, metabolizes dopamine in the
brain)
 Delay the need for levodopa and carbidopa treatment
for a year

24.  Anticholinergics
 Main treatment for tremors before levodopa but the
side effects overwhelmed the benefits
 Side effects include dry mouth, urine retension,
nausea, and mental problems.

25. Common Treatments: Surgery
 Thalamotomy
 Destruction of small amounts of thalamus tissue
 Done on one half of the brain because it usually cause slurred
speech and lack of coordination
 Controls tremors
 Pallidotomy
 Electric current is used to destroy a little bit of tissue in the
globus pallidus
 May improve tremor, rigidity and slowed movement by
interrupting the neural pathway between the globus pallidus and
the thalamus
 Counter involuntary movements caused by drug treatments
 Not a cure, benefits may not last
 The surgery carries a number of risks like slurred
speech, disabling weakness and vision problems2

26.  Deep Brain Stimulation
 There is an extravagant amount of PD research going on. Alot of
it centers around Deep Brain Stimulation.
 A brain implant device that is now widely used to help control
many of the symptoms of Parkinson's disease
 This procedure rarely causes brain hemorrhage and stroke-like
problems
 Infection is a risk and may require parts of the device to be
replaced. For example, the batteries requires replacement every
few years.
 Deep brain stimulation isn't beneficial for people who don't
respond to carbidopa-levodopa. And the device isn't for people
who already have serious difficulty with thinking and memory
because it may make those symptoms worse.

27.  Picture of electrode in sub-thalemic
nucleus

28. Sources http://www.themedicaldirectory.org/essays/parkinsons

29. Nursing management :-
 Nursing interventions for each of the
symptoms of Parkinson's disease, muscle
rigidity, bradykinesia, tremors at rest and
postural reflex abnormalities, are designed to
increase the patient's quality of life by
minimizing symptoms.
 Nurses are responsible for planning patient
medication schedules to maximize drug
effectiveness.

30.  Constipation is addressed by increasing the
patient's fibre and fluid intake and by
increasing the patient's mobility.
 Patient mobility is increased when the
patient is taught purposeful activities and to
concentrate on the way he walks.
 Communication is facilitated if the patient
takes deep breaths before speaking and uses
diaphragmatic speech.

31.  Dietary implications include a low-protein
regimen for the patient during the day, eliminating
foods high in Vitamin B6, high caloric foods, and
soft-solid foods offered at frequent feedings.

32. COMPLICATIONS:-
 Motor fluctuations
 Dyskinesis
 Posture, gait, falling
 Neuropsychiatric problems
 Sleep disorders
 Sensory phenomena
 Dysautonomias
 Speech disturbances

33. Summary:-
 Because PD is a progressive disorder, early diagnosis
and treatment intervention with neuroprotective
therapies to slow or prevent further degeneration
and to promote neuronal repair are current goals in
the management of PD
 The development and validation of diagnostic
markers in symptom recognition and neuroimaging
will aid in early diagnosis of PD
 Advances in neuroimaging and development of
quantitative diagnostic biomarkers will also improve
evaluation of potential neuroprotective therapies

34. References:-
 Cosgrove, G. Rees, Eskandar, Emad
N., Shinobu, Leslie A. “Surgical Treatment of
Parkinson Disease.” JAMA December
26, 2001;286:3056-3059.
 Dipiro, Joseph T., ed. Pharmacotherapy Fourth
Edition. Stamford, Connecticut: Appleton &
Lange, 1999.
 “Early Parkinson’s Disease: Dopamine Agonists
Have Increasingly Important Role in Symptom
Management.” Drug Ther Perspect 2001;17(17).
 Hermanowiez, Neal. “Management of Parkinson’s
Disease.” Postgraduate Medicine 2001;110(6):15-
28
 Korczyn, Amos D. “Hallucinations in Parkinson’s
Disease.” Lancet 2001;358(9287):1031-1032.

35. Thank you