1. ANTIPARKINSONS Drugs By
Dr. Mirza Shahed Baig

2. What is Parkinson’s Disease (PD)
Parkinson’s Disease (Paralysis Agitants) is a progressive disorder that affects nerve cells in the brain responsible for body movement. When dopamine-producing neurons die, symptoms such as tremor, slowness, stiffness, and balance problems occur. Treatments focus on reducing symptoms to enable a more active lifestyle and include medication, diet, exercise, and deep brain stimulation surgery.

3. Mohammad Ali Legend of Ring (Boxing) was a Parkinson Patient

5. Symptoms of PD

6. CAUSES OF PD
Age. Since it mostly affects people 60 and older, your risk goes up as the years go by.
Family history. If your parent, brother, or sister has it, you're a little more likely to get it.
Job. Some types of work, like farming or factory jobs, can cause you to have contact with chemicals linked to Parkinson's.
Race. It shows up more often in white people than other groups.
Serious head injury. If you hit your head hard enough to lose consciousness or forget things as a result of it, you may be more likely to get Parkinson's later in life.
Gender. Men get it more than women. Doctors aren't sure why.
Where you live. People in rural areas seem to get it more often, which may be tied to chemicals used in farming.

7. CAUSES OF PD

8. Pathophysiology of PD

9. Imbalance of Neurotransmitters in PD

12. Objectives of antiparkinsonian pharmacotherapy
The dopaminergic/cholinergic balance may be
restored by two mechanisms.
1. Enhancement of DA-ergic activity by drugs which may:
(a) replenish neuronal DA by supplying levodopa, which
is its natural precursor; administration of DA itself is
ineffective as it does not cross the BBB;
(b) act as DA agonists (bromocriptine, pergolide, cabergoline, etc.);
(c) prolong the action of DA through selective inhibition of its
metabolism (selegiline);
(d) release DA from stores and inhibit reuptake (amantadine).
2. Reduction of cholinergic activity by antimuscarinic
drugs; this approach is most effective against tremor and rigidity,
and less effective in the treatment of bradykinesia.

14. Central DA-ergic Drugs
Levodopa
Levodopa
Dopamine
(-)
Selegiline
MAO-B
(-)
Amantadine
Reuptake
Amantadine
(+)
Bromocriptine
Pergolide
(+)
D2-receptors

15. Why DA not given?

16. DA Precursors

19. Peripheral Decarboxylase Inhibitors

23. Drugs Affecting Metabolism of DA

24. Monoamine Oxidase Inhibitors (MAO – B Inhibitors)

26. Catechol -O-methyl transferase (COMT) Inhibitors

27. Catechol -O-methyl transferase (COMT) Inhibitors

28. DA Agonists

29. DA Receptors Agonists
Apomorphine

30. Amantadine DA Facilitator
Weak antagonist of the N-Methyl-D-aspartate receptor (NMDA-type glutamate receptor) 
Increases dopamine release from its Nerve endings,
 Blocks dopamine reuptake.
Amantadine

32. Anticholinergics in Antiparkinsons