Parkinson's disease is a progressive neurological disorder that results from the loss of dopamine-producing neurons. The document discusses the causes, symptoms, diagnosis and treatment of Parkinson's disease. It presents a case study of a 70-year-old male farmer diagnosed with the disease. His symptoms included tremors, rigidity and bradykinesia. He was diagnosed through neurological exams and SPECT imaging. His treatment plan included starting levodopa and dopamine agonists to manage his symptoms.

1. Parkinson’s Disease

2. Content
 Introduction
 Cause and pathogenesis
 Case Study:
Symptoms
Diagnosis
Treatment
Conclusion

3. oIntroduction
 It is a progressive neurological condition
 Results from the degeneration of dopamine-
producing neurons in the substantia nigra
 Afflicted 25,000 people in Malaysia
 Various types of Parkinson’s disease
 Risk factors:
Middle aged and increased risk with age
Hereditary
Men (1.5 times more)
Environmental exposure to toxins

4. Symptoms
 4 major symptoms:
Rigidity – muscles are tensed and contracted
Resting tremor – trembling which is most obvious
when the patient is at rest or when stressed
Bradykinesia – slowness in initiating movement
Loss of postural reflexes or instability – poor
balance and coordination
 Non-motor symptoms
Anxiety disorders, depression, sleep disturbances,
orthostatic hypotension, olfaction dysfunction,
dysphagia, sialorrhoea, dementia, psychosis and
visual hallucinations

5. Diagnosis and Treatment
 Diagnosis:
Neurological examination
Autopsy of brain to find lewy bodies (trademark
characteristic)
Judgement of physicians
 Treatment:
Medications
Diet
Exercise, physical and speech therapy
Surgery
 Cryothalamotomy
 Pallidotomy
 Deep brain stimulation

6. oCauses and Pathogenesis
 Degradation of dopaminergic neuron.
 Free radicals.
 Neurotoxin - MPTP
 Genetic factors.

7. Degradation of Dopaminergic Neuron
 Substantia nigra pars compacta.
 Death of neuron.
 Symptoms of PD don’t appear until 50-80% of the
neurons in the pars compacta have died.
 Cause of death of neuron is not known.

8. Free Radicals
 Unpaired electrons that can easily react with
surrounding molecules and destroy them.
 Metabolism of dopamine by MAO produce
hydrogen peroxide.
 Glutathione normally breaks down the hydrogen
peroxide quickly.
 Reduced glutathione = loss of protection against
free radicals  cell damage

9. Neurotoxin - MPTP
 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
(MPTP) – neurotoxin.
 MPTP crosses the blood-brain barrier and
oxidized to 1-methyl-4-phenylpyridinium (MPP+)
by monoamine oxidase B (MAO)-B
 MPP+ selectively enters dopamine neurons via
the dopamine transporter.
 MPP+ inhibiting Complex I  leads to cell death
via energy deficit.

10. Genetic Factors
• Mutation of SNCA genes in chromosome 4.
• 2 types of alterations:
• Alanine is replaced with
threonine.
• Cause alpha-synuclein to
misfold.
• SNCA genes is
inappropriately duplicated
or triplicated.
• Extra copies of the gene
lead to an excess of alpha-
synuclein.
• Aggregate (Lewy bodies) and attract other protein.
• Clog neuron and impair the function of neuron.

11. oCase Study:
• 70 year-old male
• Farmer
• Referred to a movement disorders outpatient clinic

12. Symptoms
1. Nondisabling intermittent resting tremor of left
hand
 Result of pallidal dysfunction
 Triggered by specific loss of dopa minergic
projections from retrorubral area

13. 2. Present of myerson
 Eyes blinking when tapped on glabella (glabellar
reflex)
 Involuntary reflex disorder

14. 3. Mild signs of asymmetrical cogwheel rigidity and
bradykinesia (left > right)
 Cause to muscular aches and sensation of fatigue
 Face become masklike, opened mouth, drooling
and reduced blinking
 Underscaling of movement commands in internally
generated movements
 Reflect the role of the basal ganglia in selecting
and reinforce appropriate patterns of cortical
activity during movement preparation and
performance

15. 4. Normal gait and balance and postural reflexes
 Under activity in the left cerebellar hemisphere with
contrast of over activity in vermis
 Associated with loss of lateral gravity shift in
parkinsonian gait
 Loss of postural reflexes
 No tendency of falling forward
 No difficulty of walking, turning and stopping

16. Diagnostic Test
 No specific test.
 Usually based on present of symptoms.
 Referral time should not be more than 6 weeks
and not exceed two weeks in severe case.
 No specific lab test used for diagnosis.
 Follow – up= every 6 to 12 months.

17.  Suggested method include:
Neurologic examination
Oculomotor examination
Electroencephalograms (EEG)
Single photon emission computed tomography
(SPECT)

18.  Neurological examination
Patient’s medical and family history
Observe sign and symptoms present.
Suggested symptoms include:
 Bradikinesia
 Tremor
 Hypokinesia
 Rigidity
Patient had normal cognition and myerson sign is
present.
Intermittent mild tremor was observed as well as
cogwheel rigidity and bradykinesia.

19.  Oculomotor examination
To check abnormalities of eye movement, generation,
and control.
Normal in patient.
 Single photon emission computed tomography
(SPECT)
Show dramatic (50%) loss of striatal uptake in patient
compared to normal individual.
Electroencephalograms
Record patient’s brain electrical activity.

20. Single photon emission computed tomography
(SPECT)

21. Treatment
According to the case study the patient was on
initiation of treatment:In early-stage disease,
the pharmacological options for the treatment
of PD are multiple.
 Levodopa:
 is a medicine that the brain converts to dopamine.
is a medicine used to control symptoms
of Parkinson's disease and used at all stages of the
disease.
Levodopa does not slow the disease process, but it
improves muscle movement and delays severe
disability.
long-term levodopa therapy within 5 to 10 years can
cause complication to occur such as Dyskinesia.

22.  Dopamine agonist:
Example of drugs:pramipexole,ropinirole
directly stimulate the receptors in nerves in the
brain that normally would be stimulated
by dopamine.
used in the early stages of Parkinson’s disease to
reduce symptoms.
effective in people who have been newly diagnosed
with the disease (especially those younger than 60).
Not effective as levodopa in reducing symptom but
can prevent long term effect caused by levodopa.

23.  Monoamine oxidase type B inhibitor
MAO-B is an enzyme in our brain that naturally
breaks down several chemicals in our brain
including dopamine.
Prevent the breakdown dopamine.
they prevent the removal of dopamine between
nerve endings and enhance release of dopamine
from nerve cells.
Example of drug: Rasagiline and selegiline.
used in the early stages, to treat very mild
symptoms (such as resting tremor) and delay the
need for levodopa.
rasagiline or selegiline may be added to levodopa
treatment to reduce motor fluctuations , increase
the time of effect of the levodopa.

24.  Amantadine
 treat people who are in the early stages of
Parkinson's disease.
 It is best used in people who have mild to moderate
symptoms.
cause greater amounts of dopamine to be released
in the brain.
can be used with levodopa in the later stages of
Parkinson's disease to reduce dyskinesias.

25.  Anticholinergic
Example of drugs: benztropine,biperiden
Anticholinergic medicines decrease levels of
acetylcholine to achieve a closer balance with
dopamine levels.
In order to reduce the symptom.

26. Treatment In Malaysia
Decision pathway for the initiation of
medication

27.  Levodopa ( L-Dopa)
the most effective antiparkinsonian medication.
“start low, go slow” approach, L-dopa can be started at
a dose of 50 mg daily (e.g., ¼ tablet of Madopar®
200/50 mg) increasing every 3-7 days by 50 mg to an
initial maintenance dose of 50-100 mg 3x daily.
 Selegiline ( Jumex and Selegos)
usual dose is 10 mg in the morning.
has a mild antiparkinsonian effect.

28.  Dopamine agonist
Next most potent class of drug after L-dopa.
Dopamine
agonist
Usual
Starting Dose
Maximum
recommende
d Dose
Piribedil
(Trivastal
Retard *)
25-50mg 300mg/d
Ropinirole
immidiate
release (
Requip *)
0.25mg 24mg/d
Ropinirole
Prolong
Release
(Requip PD*)
2mg 24mg/d

29.  Anticholinergic agents
 These include trihexyphenidyl or benzhexol (Apo-
Trihex® and Benzhexol®)(1 or 2 mg 2-3x daily) and
orphenadrine (Norflex®) (50 mg 2-3x daily).
 Non-Pharmocologic Management
physiotherapy: stretching and strengthening exercises
and balance training.
occupational therapy: lifestyle adaptations and
assessment of safety in the home environment.
speech therapy: rehabilitation techniques to strengthen
speech for improved communication.
Dietitian: advice from them.

30. Conclusion
 Patient has idiopathic Parkinson’s disease
 There is no cure but therapies are available
 Treatments aim to:
Prevent clinical progression
Improvement of parkinsonism
Delay of motor complications
 Complications: choking, falls and side effects of
drugs
 Prognosis: normal life expectancy for treated
patients

31. Reference
Anonymous. (2012). Tremor Fact Sheet. [Online]. Available from:
http://www.ninds.nih.gov/disorders/tremor/detail_tremor.htm.Nati
onal, Institute of Neurological Disorders and Stroke. Accessed on
2nd March 2013
Dr Ananya Mandal, MD. (2013). Parkinson's Disease
Pathophysiology. [Online]. Available from: http://www.news-
medical.net/health/Parkinsons-Disease-Pathophysiology.aspx.
[Accessed on 1st March 2013].
Dr. Ananya Mandal. (2013). Parkinson’s disease Prognosis.
[Online]. Available from: http://www.news-
medical.net/health/Parkinsons-Disease-Prognosis.aspx.
[Accessed on 2nd March 2013].
Malaysian Parkinson’s Disease Association. (2012). Association
wants Disability Rights for Parkinson’s Patients. [Online].
Available from:
http://mpda.org.my/article.php?type=news&9ja847hd0a1=144.
[Accessed on 2nd March 2013].

32. Mayo Clinic. Parkinson’s Disease: Risk Factors. [Online]. Available
from: http://www.mayoclinic.com/health/parkinsons-
disease/DS00295/DSECTION=risk-factors. [Accessed on 1st
March 2013].
Parkinson’s Disease Society. The professional’s guide to
Parkinson’s Disease. [Online]. Available from:
http://www.parkinsons.org.uk/pdf/B126_Professionalsguide.pdf.
[Accessed on 1st March 2013].
Parkinson’s UK. Types of Parkinson’s and parkinsonism. Online].
Available from:
http://www.parkinsons.org.uk/about_parkinsons/what_is_parkins
ons/types_of_parkinsons.aspx. [Accessed on 2nd March 2013].
Public Health and Genetics Information Series. Parkinson’s
disease. [Online]. Available from:
http://www.hgen.pitt.edu/counseling/public_health/parkinsons.pdf
. [Accessed on 1st March 2013].
Robert A Hauser, MD. (2013). Parkinson Disease . [Online].
Available from : http://emedicine.medscape.com/article/1831191-
overview#aw2aab6b2b1aa.[Accessed 1st March 2013].

33. Takashi Hanakawa. (1999). Mechanisms underlying gait
disturbance in Parkinson's disease. [Online]. Available
from :
http://brain.oxfordjournals.org/content/122/7/1271.full.
[Accessed on 2nd March 2013]
Ted K Koutouzis, MD. (2005). Parkinson's Disease.
[OnlineAvailable from :
http://www.emedicinehealth.com/parkinson_disease/article
_em.htm. [Accessed 1st March 2013].
University of Maryland Medical Centre. Diagnosing
Parkinson’s Disease. [Online]. Available from:
http://www.umm.edu/parkinsons/diagnosis.htm. [Accessed
on 1st March 2013].
Wooten. G.F., Currie. L.J., Bovbjerg. V.E., Lee.J.K. and
Patrie. J. (2013). Are men at greater risk for Parkinson’s
disease than women? J Neurol Neurosurg Psychiatry.
75:637-639.