3. Parkinson’s disease is a progressive
neurodegenerative disorder that results in
deterioration of neurons in basal ganglia.

4. EPIDEMIOLOGY
 Incidence
=
0.2 / 1000
 Prevalence
=
1.5 / 1000
 The incidence and prevalence both increase
with age.
 Sex incidence is almost equal.
 It is less common in smokers.

5. Typical Age of Onset
 Average age of onset is 60 yrs.
 5-10% of cases occur under the age of 40.
Referred to as Young-Onset Parkinson
Disease.
 Rarely seen under age 30.

6. Famous Faces of Parkinson
Michael J. Fox
Katharine Hepburn
Muhammad Ali
Mao Tse Tung
Pope John Paul II
Johnny Cash

7. Etiology
 Parkinson’s disease is referred to as
idiopathic (unknown cause).
 Genetic link is seen in a small number of
Parkinsons cases.
 Larger genetic link is found in youngonset Parkinsons disease.
 MPTP cause severe parkinsonism in
young drug users

8. Risk factors
 Positive family history
 Male gender
 Head injury
 Exposure to pesticide
 Consumption of well water
 Rural living

10. Factors which decrease incidence of
PD
 Smoking
 Coffee drinking
 Use of NSAIDS
 Estrogen replacement in postmenopausal
women

11.  Repeated head trauma
 Infectious & post infectious disease
 Drugs (neuroleptics, antipsychotics , alpha
methyldopa, lithium carbonate , fluoxetine )
 Toxins
MPTP
Cyanides
Methanol

12. Unilateral Parkinsonism
 Vascular
 Traumatic
 Neoplasm
Lower body Parkinsonism
It may represent a form of vascular
parkinsonism

13. Parkinsonism plus syndrome
 Features of parkinsonism associated with
complex clinical presentation
 Failure to respond to treatment
 Worse prognosis
Examples include :
1. Shy Dragger syndrome
2. Steel Richardson syndrome
3. Parkinsonism-dementia plus

14. PATHOLOGY
There is depletion of pigmented
dopaminergic neurons in the substantia
nigra, atrophic changes in substantia nigra
and depletion of neurons in locus
coeruleus.

16. PATHOLOGY
Reduced dopaminergic output from the
substantia nigra to globus pallidus leads to
reduced inhibitory effect on subthalamic
nucleus, neurons of which become more
active in inhibiting activation of cortex
resulting in bradykinesia.

18. CLINICAL FEATURES
 Tremors
 Rigidity
 Akinesia / Bradykinesia
 Postural instability
T
R
A
P

19. Head bent forward
Tremors of head
Maslike facial expression
Drooling
Rigidity
Stooped posture
Weight loss
Akinesia
tremors
Loss of postural
reflexes
Propulsive gait
CLINICAL FEATURES

20. General Features
 Expressionless face (mask like)
 Greasy skin
 Soft rapid indistinct speech, monotonous
 Glabellar tap sign / Myersons sign
 Flexed posture
 Impaired postural reflexes

21. Gait
 Slow to start walking
 Shortened stride
 Rapid small steps tendency to turn en bloc
 Reduced arm swing
 Impaired balance on turning

22. Tremors
 Resting
(4 - 6 Hz)
 Postural
(8-10 Hz)

23. Rigidity
 Cogwheel :
mostly in upper limbs
 Plastic / lead-pipe:
mostly in lower limbs

24. Bradykinesia
 Slowness in initiation or repeating
movements
 Impaired fine movements

25. Hoehn & Yahr Scale
 Stage I: Unilateral involvement only, usually with
minimal or no function impairment.
 Stage II: Bilateral or midline involvement w/o
impairment of balance.
 Stage III: 1st signs of righting reflex impairment;
functionally restricted in his/her activities but can
lead independent life. Disability mild/moderate.
 Stage IV: Severely disabled. Able to walk &
stand unaided but is markedly handicapped.
 Stage V: Confined to bed.

28. Investigations
 There is no specific medical test used to
diagnose Parkinson disease.
 However, MRIs and blood tests are used
to rule out other possible conditions that
have similar symptoms to Parkinson
disease.

29. TREATMENT
 Drug therapy
 Surgerical Treatment
 Physiotherapy
 Speech therapy

30. LEVODOPA
 It is the oldest and most effective treatment of
PD.
 Brain enzymes modify the drug to create dopamine.
 It reduces slowness and stiffness of muscles.
 Given in combination with peripheral decarboxylase
inhibitors, carbidopa & benserazide.
 Combinations are called Sinemet & Madopar
respectively.

31. Adverse effects:
Nausea, vomiting, hypotension,orofacial
dyskinesias, dystonias, hallucinations.
 Two important phenomenon associated
with levodopa use are:
1) end- of- dose deterioration
2) on-off phenomenon

33. Anticholinergic agents
 Useful effects on tremors & rigidity but
do not help bradykinesia.

Adverse effects :
Dry mouth , blurred vision , difficult
urination , constipation, confusion,
hallucinations

34. Amantadine
 Useful in controlling dyskinesia produced
by dopaminergic treatment later in the
disease.
 Adverse effects:
livedo reticularis , peripheral edema,
confusion , seizures

35. Dopamine receptor agonists
Bromocriptine , lisuride , pergolide
,cabergoline , ropinirole & pramipexole

36. OTHER DRUGS
 COMT inhibitors:
Catechol-O-methyl transferase inhibitors
 Selegeline

37. Surgical procedures are now available for
specific patients who no longer respond to
drug treatments.

38. PALLIDOTOMY
It is a neurosurgical procedure that can
reduce many of the symptoms of Parkinson
Disease
Performed by a neurosurgeon, who inserts a
hallow probe into the globus pallidus and then
liquid nitrogen is circulated in the probe.
 The probe destroys part of the globus
pallidus by creating a scar .

39. The patient is awake during the procedure
which takes about 6 hours.
It can permanently eliminate
dyskinesias
Reduces tremor, rigidity, bradykinesia
and shuffling gait.
It is not a cure.

40. Stereotatic thalamotomy
Used to treat tremors

41. Deep Brain Stimulation
An electrode is placed in one of several parts
of the brain (thalamus, globus palladus, or
subthalamic nucleus).
The electrode is attached to a computerized
pulse-generator which is put under this skin in
the chest.
Symptoms are relieved through the regulation
of electrical impulses from those three areas
of the brain.

42. Deep Brain Stimulation

43. Current Research
 Neural grafting, or transplantation of nerve
cells, is an experimental technique
proposed for treating the disease.
Investigators have shown in animal
models that implanting fetal brain tissue
from the substantia nigra into a
parkinsonian brain causes damaged nerve
cells to regenerate.
 Gene Therapy

44. General Treatment Strategies
 Develop routine for self care
 Help family/care partner, along with patient,
create ideas for adapting home environment to
meet the patient’s needs.
Modified kitchen
Modified bathroom
Full bathroom and bedroom on first floor
Lift chair
Remove rugs/carpet/furniture that could be
easily tripped over

46. Social Participation
 Support groups
 Important to encourage continued
involvement in activities important to their
life.
 Participation in activities which are not
physically taxing.
 Introduce techniques for enhancing voice
volume.

47. job
Educate & inform co-workers
Explore work-at-home options
Adapt job requirements as disease
progresses

48. Prognosis
 Depends upon the age of onset
 If symptom starting in middle life ,the
disease is usually progressive & likely to
shorten lifespan.
 After 70 is unlikely to shorten life or
become severe.