Lecture 3

Question 1

What are the symptoms of Parkinson’s?

Answer 1

Resting tremor in limbs
Muscle rigidity
Akinesial
Stooped posture
Shuffling gait
Excessive sweating and salvation e
Micrographia

Question 2

What cognitive dysfunctions are seen, in Parkinson’s what are their mechanisms of action

Answer 2

Cognative deficits → mainly under the frond lobe control→ probably related to the loss of dopamine from the mesiolimbic pathway
Mood disturbances → might be reactionary but changes seen in the locus loerules and dorsal raphe
Dementia → 15% → maybe related the degeneration seen in the basal forebrain,

Question 3

What causes drug induced physosis in Parkinson’s

Answer 3

20 to 30.1 of points on dopemonergic medication → probably due to increased dopamine function be and the migrostriatal pathway

Question 4

Is there any genetic recreditary for Parkinson’s

Answer 4

‘No but cannot be ruled out

Question 5

Is there evidence of viral organ for Parkinson’s

Answer 5

No but encephalitis lethargic has full like symptoms and left people with Parkinson’s like symptoms, not identical but did respond to L-dopa treatment.

Question 6

Chemical postings similar to Parkinson’s

Answer 6

Mptp monoamine neurone killer
-manganese or carbon disulfide → causes Parkinson like symptoms
Diffrentpost mortem neuropathology ‘
→ manages → striata’s degeneration
→carbon disulfide → striata’s output degeneration

Question 7

What pathway degenerates in Parkinson’s disease?

Answer 7

Nigrostaital
Substantial nigra → contains newomelanin
Pet scars shows less dopamine in the stratum
Also reduction of dopamine is seen in the substainatnigra ‘

Question 8

How does dopamine modulate basal ganglia cunciutatly

Answer 8

The pataway has Di and D 2 receptors, so increased dopamine inhibits motor curits through both patways.

Question 9

How does dopamine metabolism change in to remaining nigrostriatal neurones?

Answer 9

Ratio of dopamine metabolite todopamine increase/ activity of tyrosinehydroxylose increases Adas this is the rate limiting step more deparire
Also non post synoptic Di and D2 receptors
Leading to 75% loss before lineal symptoms appear

Question 10

What neurogeneration is seen in Parkinson’s

Answer 10

50% loss dopamine neurones
Cell loss in locus coreless (noradrealine) dorsal raphe(s-ht) and basal forebrain (ach)
Also changes in GABA

Question 11

Why can’t we administer doparinto treat Parkinson’s what dome use and why

Answer 11

Doesn’t Cross bib but L-dopa doses

Question 12

Why do we give carbidopa along with ldopa for Parkinson’s

Answer 12

Carbidopa doos not cross the bbb and so only blocks the periodical action → also allows for less L-dopa to be given

Question 13

What are the problems with L-dopa therapy

Answer 13

Sever side effects , (dykineasea psychotic symptoms)
Effectiveness decreases overtime as dopervergic newoneges needed to covert to dopomante c closing of the therapeutic window
Diet must be regulated
May be neurotoxicity → May increase degeneration

Question 14

What is the problem and befit of dopamine agonist treatment)

Answer 14

Less efficacious as L-dopa but lower side effects

Question 15

What are the benifitard problem with monoanine ox dose inhibitors i n treating Parkinson’s

Answer 15

Variable results → May slow profession

Question 16

What is the Main problem with treating Parkinson’s with a amantidine

How doses it work

Answer 16

Limited duration (6-8) months due to tolerance, stimulates release and may block reuptake

Question 17

What are the non pharmacological treatments for Parkinson’s what are their problems

Answer 17

Grafts → dopamine high adrenal medulla cells graphed into striatum → don’t survive well
Foetal substainia nigra cells translated into striatum → improvements but short lived → good for MPTP patients.
Surgery → legions to thalamus substhalanic nucleus ora globus pladious
Deep brain stimulation → electrodes implanted into thalamus subthalamuc nevellous or globus pallidas