Week 11 - Drugs for Parkinson's Disease

Question 1

What dopamine pathway is important in Parkinson’s Diseases (PD)?

Answer 1

Nigrostriatal system (Striatum and Substantia nigra)

Question 2

What is Nigrostriatal system responsible for?

Answer 2

Fine motor control

Prepares motor system for next movement in a sequence of movements

Question 3

What are pathological changes that occur in PD

Answer 3

loss of dopamine in striatum and of neurons in substantia nigra

Question 4

What is the pathway of making dopamine?

Answer 4

Tyrosine –> Dopa –> Dopamine

Enzymes = Tyrosine hydroxylase, Dopa decarboxylase

Question 5

What is Levadopa?

Answer 5

A dopamine pre-cursor -> helps increase dopamine pathway -> more dopamine

Question 6

What must Levadopa be combined with to preserve its levels in the body?

Answer 6

Must be combined with peripheral DDC inhibitors that do not cross the blood-brain barrier -> More Levadopa to CNS

Eg. DDC inhibitors -> Carbidopa, Benserazide

Question 7

What are AEs of Levadopa?

Answer 7

Dyskinesias
Nausea
Hallucinations

Question 8

How are drugs that directly activate the dopamine receptor advantageous to dopamine pre-cursors?

Answer 8

• bypass enzymatic conversion to dopamine
• less dyskinesiaas than levadopa
• longer half life than levadopa

Question 9

What are drugs that directly activate the dopamine receptors? and what are AEs?

Answer 9

Pramipexole
Rotigotine

AEs:
- nausea
- hallucinations
- impulse control disorders

Question 10

How can Dopamine be metabolised?

Answer 10

Can undergo reuptake into pre-synaptic neuron -> then metabolised by monoamine oxidase (MAO)

If MAO can be inhibited -> more dopamine bc less is broken down

Question 11

What are MAO inhibitors and examples?

Answer 11

inhibit MAO enzyme

eg - Selegiline

Question 12

What are Catechol-O-methyl-transferase (COMT) inhibitors? Eg?

Answer 12

COMT inhibitors preserve levodopa and dopamine levels

Eg - Entacapone, Tolcapone

Question 13

What are key cortical regions for speech and language?

Answer 13

Broca’s Area
Wernicke’s Area
Arcuate Fasciculus

Question 14

What are Broca’s and Wernicke’s areas functions?

Answer 14

Broca’s:
- Speech prod
- Receives input from Wernicke’s area
- Near motor cortex
Wernicke’s:
- Speech understanding
- Near auditory cortex

Question 15

What are the 7 components of the Wernicke-Geschwind Model

Answer 15

• Primary Motor Cortex
• Broca’s Area
• Primary Auditory Cortex
• Wernicke’s Area
• Angular Gyrus
• Primary Visual Cortex
• Arcuate Fasciculus

Question 16

What does Angular gyrus do?

Answer 16

Converts info from prim. visual cortex into an auditory type signal that can be processed by Wernicke’s

For looking at written word

Question 17

What is Aphasia?

Answer 17

= partial or complete loss of language abilities following brain damage

Question 18

What is Dysarthria?

Answer 18

= group of motor speech disorders -> slow/poor coordination of speech muscles

Question 19

What is Apraxia?

Answer 19

= Motor speech disorder

Question 20

What categories can you split Aphasia into?

Answer 20

Nonfluent & Fluent

Nonfluent:
- Struggle to produce speech but can relay meaning/theme still

Fluent:
- Can speak properly but speech lacks meaning

Question 21

What is Broca’s Aphasia? What is the cause? What does it affect?

Answer 21

= Motor/expressive Aphasia

• Caused by lesions of left frontal lobe -> associated w damage to prim motor cortex and post frontal lobe
• Affects ability to prod language efficiently but language comprehension is fine

Question 22

What is Broca’s Aphasia? What is the cause? What does it affect?

Answer 22

= Sensory/Receptive Aphasia

• Caused by damage to left temporal lobe over Wernicke’s area
• Can speak in long sentences but has no meaning

Question 23

What is Conduction Aphasia?

Answer 23

• Lesion located at arcuate fasciculus
• difficulty or unable to repeat what is spoken
• Could say ‘hosical’ or ‘hotel’ instead of ‘hospital’

Question 24

Summary of all types of Aphasia

Answer 24