Parkinson's disease is a neurological syndrome caused by degeneration of dopaminergic neurons in the substantia nigra. This leads to dopamine deficiency in the basal ganglia and symptoms like tremors, muscle stiffness, slow movement, and impaired balance and coordination. Worldwide prevalence is around 6 million people. Primary causes include genetic mutations and environmental toxins. Secondary causes include infections, head injuries, and certain drugs. Treatment involves replacing dopamine or stimulating dopamine receptors to restore balance between dopamine and acetylcholine in the basal ganglia.

1. - a neurological
syndrome.

2. EPIDEMILOGY
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In India there is a low prevalence of
Parkinson’s disease. We find it in Parsi
community of Mumbai.
Even though we find early onset of PD and
may even be seen due to mutations.
In ancient India Mucuna pruriens was in used
in the treatment of PD.
But worldwide PD is found in 6 million people.
Neurological disorders reduce the quality of
life.

3. ETIOLOGY:They are of following types:1.primary75%
2.secondary.25%
1.Primary:
a) They may due to genetic causes. The
mutation in alpha-synuclein, parkin,
UCH1, DJ1, PINK1, LRKK cause PD
cause oxidative stress on mitochondria.
This in turn leads to nigrostriatal death.
b) Some environmental factors.
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5. Secondary causes:1.vascular diseases:-

6. 2.Infectious and post infectious.
Eg:- lyme disease is caused by 3
types of bacteria belonging to
genus borrelia.

7. Neurosyphilis and AIDS.
 Some toxins such as Mn, cyanide,
methanol, carbon monoxide, pesticides.
 And some medications such as
methyldopa, CCB, lithium and dopamine
depleting agents such as reserpine.
 Rarely it is also due hyoparathyroidsm
due to basal ganglia calcification,
repeated trauma , etc.
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8. PATHOPHYSIOLOGY:Basal ganglia consists of:1.corpus sriatum(caudate nucleus
and putamen).
2.Globus pallidus.
3.Substantia nigra.
*They mediate the extrapyramidal motor
activity.
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9. Basal ganglia

10. Extrapyramidal surface of brain:

11. The cerebral
cortex and the
substantia nigra
both project
towards corpus
straitum.

12. The corpus
striatum(caudat
e nucleus and
putmen)
projects into
globus pallidus
to thalamus and
they regulates
involuntary
movement.

13.  The
nigro striatal neurons make motor
connections to corpus striatum by 2
types of neurons which contain D1
(excitatory) and D2(inhibitory)
receptors.
 The D1 (excitatory) are glutaminergic
and D2 (inhibitory) are
GABAminergic.

14.  D1=excitatory
receptors=
acetylcholine as
transmitter=direct.
 D2=inhibitory
receptors=dopamine as
transmitter=indirect.

15. WHAT HAPPENS IN
PARKINSONISM?
Inhibitory component dopamine is
deficient and its concentration on basal
ganglia is low.
 There is a pathological lesion in basal
ganglia and corpus striatum.
 This occurs due to dopaminergic neuron
degeneration.
 The dopamine is deficient so D2
receptors are less stimulated.
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16. Dopamine
deficiency

17. PICTURE SHOWING
SUBSTANTIA NIGRA
DEGENERATION.
As the dopaminergic
neurons have their
cell bodies in
substantial nigra. And
as the corpus
striatum receives
dopamine from
substantia nigra
degeneration of these
neurons causes
decrease in the
functional amount of
dopamine.

18. So eventually
Parkinsonism is due
to imbalance
between
acetylcholine and
dopamine.

19. Normal
levels of
dopamine
and
acetylcholi
ne
balanced.

20. SIGNS AND SYMPTOMS:
 Tremor
when sitting and in rest and
may be present only to one side.
 Stiff muscles and aching muscles of
leg, neck, face and other muscles of
body.
 Slow limited movement i;e
bradykinesia.
 Insomnia and nightmares are seen at
very early stage before tremor.

21. Person
showing
Parkinson's
disease
symptoms.

22. Weakness of face and throat muscles
making it harder to talk or to swallow.
 Difficulty with walking called gait
instability and postural instability.
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23. COMPLICATIONS OF
PARKINSON’S :
 Depression
and anxiety.
 Sexual dysfunction
 Sleep disorders.
 Urinary incontience.