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MD4001 - Disease > Basal Ganglia and Parkinson's Disease > Flashcards

Basal Ganglia and Parkinson's Disease Flashcards

1
Q

Striatum =

A

Dorsal striatum and ventral striatum

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2
Q

Dorsal striatum =

A

caudate and lentiform

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3
Q

Neostriatum =

A

caudate nucleus and putamen

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4
Q

Ventral striatum =

A

nucleus accumbens and olfactory tubercle

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5
Q

Lentiform/Lenticular =

A

putamen and globus pallidus

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6
Q

What are the basal ganglia? And name the main components

A
  • Neostriatum (caudate nucleus and putamen)
  • Paleostriatum (globus pallidus)
  • Subthalamic nucleus
  • Substantia nigra
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7
Q

What are the main functions of the basal ganglia?

A
  • Smooth movement
  • Switching behaviour
  • Reward systems
  • Closely linked to thalamus, cortex and limbic system
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8
Q

What sort of patterns do the basal ganglia generate?

A
  • Basal ganglia thought to generate basic patterns of movement (motor programs)
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9
Q

Where do all parts of the cerebral cortex project to?

A
  • All parts of cerebral cortex project to corpus striatum, basal ganglia project to thalamus, thalamus projects to cerebral cortex (the motor loop)
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10
Q

What does cortical activation of the putamen lead to?

A
  • Cortical activation of putamen leads to excitation of supplementary motor area (SMAO by ventrolateral nuclei (VLN) of thalamus
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11
Q

Draw a diagram of the direct pathway of the basal ganglia system

A
  • Cortical excitation of neostriatum leads to distribution of thalamic nuclei
  • Movement follows activation of putamen by cortical areas
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12
Q

Draw a diagram of the indirect pathway of the basal ganglia components

A
  • Cortical excitation of neostriatum leads to inhibition of inhibitory input to subthalamus
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13
Q

What leads to activation of the direct pathway and inhibition of the indirect pathway

A

Activation of the dopamine pathway

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14
Q

What is the MAIN function of the basal ganglia?

A

remove the inhibition on the thalamus

**The thamalus allows information to travel to the cortex and trigger movement with inhibitory signal removed

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15
Q

What are the major clinical problems associated with the basal ganglia? And where does the defect occur

A
  • Parkinson’s disease (substantia nigra deficit)
  • Huntington’s disease (caudate deficit)
  • Hemiballismus (subthalamic deficit)
  • Wilson’s disease (lenticular)
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16
Q

What are the clinical features of Parkinson’s Disease?

A
  • Hypokinetic - decreased bodily movement
  • Tremor at rest
  • Rigidity – cogwheel, limbs > axial
  • Bradykinesia
  • Asymmetry
  • Loss righting reflex
  • 30% cognitive decline
  • Hypomimia (lack of facial expression)
  • Glabellar tap
  • Quiet speech
  • Micrographia
17
Q

What is the pathogenesis of Parkinson’s Disease?

A
  • Bradykinesia, akinesia, rigidity
  • Degeneration of dopaminergic neurons on substantia nigra
18
Q

Describe the features of Huntington’s disease

A
  • Hyperkinetic - increased bodily movements
  • Autosomal dominant
  • CAG triple repeat disease (>40 repeats)
  • Mutant huntingtin accumulates, toxic
  • Chorea, behavioural disorders, dementia
  • Caudate nucleus wasting
19
Q

What is the pathophysiology of the basal ganglia in Huntington’s Disease?

A
  • Degeneration of caudate, putamen and globus pallidus
20
Q

What are the clinical features of Huntington’s disease?

A
  • Hyperkinesia, dyskinesia
  • Characterised by inappropriate or repetitive execution of movement patterns
21
Q

What type of genetic disorder is Wilson’s disease?

A
  • Autosomal recessive
22
Q

What are the clinical features of Wilson’s Disease?

A
  • Abnormal copper accumulation
  • Hepato-lenticular degeneration (liver and brain)
  • Dystonia, ataxia, subcortical dementia
  • Copper transport, protein abnormality
  • Low serum copper and caeruloplasmin
  • Kayser-Fleisher rings
23
Q

What is the main treatment of Wilson’s Disease?

A
  • Treatment = Penicillamine
24
Q

What is the main stratgey in the treatment of Parkinson’s Disease?

A

counteract the deficiency in dopamine in the basal ganglia

25
Q

What are the 5 main drugs used in the treatment of Parkinson’s?

A
  • Levodopa (in combination with carbidopa or benserazide)
  • Dopamine agonists (e.g. pramipexole, ropinirole and bromocriptine)
  • Monoamine oxidases B (MAO-B) inhibitors (e.g. selegiline and rasagiline)
  • Amantadine – releases dopamine
  • Muscarinic Acetylcholine Antagonist (trihexyphenidyl (benzhexol))
26
Q

What are the main sites of action of drugs used in Parkinson’s?

A
27
Q

What is the first line treatment for Parkinson’s?

A
  • First line treatment for PD combined with a dopa decarboxylase inhibitor (cabidopa or benserazide)
  • This combination lowers the dose needed and reduces peripheral system side effects (e.g. nausea, hypotension)
28
Q

Why is there a limited time effectiveness of levodopa?

A
  • Limited effectiveness with time as the neurodegeneration progresses
29
Q

What are the long term side effects of levadopa

A
  • Involuntary writhing movements (dyskinesia) which may appear within 2 years. After face and limbs mainly. Occurs at peak therapeutic effect
  • Rapid fluctuations in clinical state. Hypokinesia and rigidity may suddenly worsen and then improve again. This on-off effect not seen in untreated PD patients or with other PD drugs. Reflects fluctuating receptor dynamics
30
Q

What are the main dopamin agonists that work on the D1 and D2 receptors? And what are their side effects?

A

Bromocriptine, cabergoline and pergolide (ergots) are orally active drugs that work on D1 and D2 receptors.

They have limiting side effects – fibrotic reactions.

31
Q

Name the D2/3 selective dopamine receptor agaonists

A

Pramipexole and roprinole

32
Q

What are the amin MAO inibitiors and why are they used in combination?

A
  • Selegiline & Rasagiline are a selective MAO-B which lacks the unwanted peripheral effects of non-selective MAO inhibitors.
  • Inhibition of MAO-B protects dopamine from extra neuronal degradation.
  • Combination with levodopa is more effective in relieving symptoms and prolonging life.
33
Q

What is amantadine and how does it work?

A
  • Antiviral drug discovered to be beneficial in PD.
  • Increased dopamine release is primarily responsible for its therapeutic effect.
  • Less effective than levodopa or bromocriptine and action declines with time.
34
Q

What are the main acetylcholine anatgonists?

A
  • Muscarinic acetylcholine receptors exert an inhibitory effect on dopaminergic nerves suppression of which compensates for a lack of dopamine.
  • Benzhexol, Orphenadrine and procyclidine can all be used, with usual anti- cholinergic side effects.

MD4001 - Disease (7 decks)

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