This document discusses Parkinson's disease and its treatment. Parkinson's is caused by the death of dopaminergic neurons in the substantia nigra. Dopamine functions include reward behavior, motor control, memory, sleep, mood and cognition. Common Parkinson's symptoms include tremors, rigid muscles, slowed movement, impaired posture and loss of automatic movement. While there is no cure, treatments aim to reduce symptoms by replenishing dopamine through levodopa/carbidopa or MAO inhibitors like selegiline. Levodopa crosses the blood brain barrier and is converted to dopamine, while carbidopa prevents peripheral breakdown and increases levodopa's effects. Amantadine is also used though less effective than levodopa

1. PREPARED BY PHILIP RAPHAEL
PHARMACEUTICAL TECHNICIAN

2. NEURODEGENERATIVE DISORDER
 Parkinson’s Disease
 Alzheimers Disease

3.  Parknison’s disease common cause of parkinson’s disease
is uknown to many patients but is correlated with death of
doparminergic neurons in the substantia nigra .
 Roles of dopamine are as follows to mention a few of them
 Functions in reward-motivated behavior
 Motor controll
 Memory
 Sleep
 Mood
 Cognition

4. Mnemonic “LISTS”
L-Loss of Automatic Movement
I-Impaired posture and Movement
S-Slowed Movement (Bradykinesia)
T-Tremor
R- Rigid Muscles (Muscles Stiffness)

5.  There is no total cure for parkinson’s disease
but it can be managed and the symptoms can
be relieved or reduced the treatment goals
are as follows:
 Reduce rigidty
 Improve posture , gait, balance, speech and
writing skills
 Reduce tremors and Reversed slowed
movement

6.  Levodopa and Carbidopa
 Mechanism of action (MOA) :Levodopa is a
precussor of dopamine that is used to
replenish the dopamine defficiency since
dopamine itself doesn’t cross the blood brain
barrier (BBB) due to being polar, so levodopa
is trasnported in the CNS and converted into
dopamine in the brain

7.  Levodopa is highly metabolized peripherally
and in the GIT hence it’s amount required to
reach the brain is reduced
 What is Carbidopa?
Carbidopa is a dopa decarboxylase inhibitor

8. • Carbidopa reduces the metabolism of
levodopa in the GIT and Peripheral tissues
• Carbidopa reduces the dose of administered
levodopa to four to five times
• Carbidopa reduces the severity of peripherally
formed dopamine
NOTE:Carbidopa on it’s own doesn’t cross the
the blood brain barrier (BBB)

9.  Vitamin B6 (Pyridoxine) increases peripheral
breakdown of levodopa and diminishes its
effectiveness
 Administration of levodopa and Monoamine
Oxidase Inhibitor (MAOI’s) such as Phenelzine
produce hypertensive crisis caused by enhanced
catecholamine therefore caution is required
 Antpsychotics are contraindicated in
parkinsonian patients since they block dopamine
receptors and produce parkinsonian syndrome
themselves

10.  Mnemonic “VAN” For peripherall effects
 V-Vomiting
 A-Anorexia
 N-Nausea
 All these occurs due to stimulation of
chemoreceptor trigger zone (CTZ) in the
medulla

11. Mnemonic “ HI DAMP”
H-Hallucinations (Visual and Auditory )
I-Involuntary movements (Dyskinesia)
D-Depression
A-Anxiety
M-Mood Changes
P-Psychosis

12.  Selegline and Rasalgine these selectively
inhibits MAO type B which metabolize
dopamine at low moderate doses,selegiline
has been found to increase the level of
levodopa in the brain when administered
together but when administered in low doses

13.  Methylation of Levodopa to 3-O-Methyldopa
is a minor pathhway for levodopa metabolism
 Concentration of 3-O-Methlydopa is formed
which competes with levodopa for active
transport in the CNS therefore COMT such as
entecapone and tolcapone decrease
competition between 3-O-methyldopa and
Levodapa hence incresease levodopa CNS
uptake

14.  It’s an antiviral drug specifically antiinfluenza
but it has been observed it contains
antiparkinson action by causing increase of
release of dopamine by blocking cholinergic
receptors and N-methyl-D-Aspartate
(NMDA) Amantadine is less efficaous to
Levodopa but is tolerated more readily and
contains fewer side effects