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Neurorehab > Basal Ganglia/Parkinson's Disease > Flashcards

Basal Ganglia/Parkinson's Disease Flashcards

1
Q

Another name for the basal ganglia

A

Basal nuclei

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2
Q

What does the basal ganglia consist of?

A

Caudate nucleus, putamen, globus pallidus (internus and externus)

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3
Q

What other 2 nuclei make up the basal ganglia?

A

Subthalamic nucleus, substantia nigra

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4
Q

What 2 nuclei make up the striatum?

A

Caudate nucleus, putamen

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5
Q

What 2 nuclei make up the lentiform nucelus?

A

Putamen, globus pallidus (internus and externus)

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6
Q

Where does the striatum get its name?

A

From its grey appearance which is due to white fibres of the corona radiata piercing through it

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7
Q

What kind of matter are the putamen and caudate nucleus made of?

A

Grey (unmyelinated) matter

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8
Q

What kind of matter is the corona radiata made of?

A

White (myelinated) matter

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9
Q

What is the function of the white fibres of the corona radiata?

A

They carry information from the cortex to the basal ganglia, internal capsule and thalamus and from the thalamus back to the cortex

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10
Q

What are the 2 key functions of the basal ganglia?

A

The basal ganglia regulates motor and psychological functions

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11
Q

What 3 aspects of psychological functions does the basal ganglia influence?

A

Decision-making - uses past information to inform decision-making
Social behaviour - it filters out unacceptable behaviour
Emotion - regulates reward-seeking behaviour e.g. gambling

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12
Q

What are the main functions of the basal ganglia?

A

Filters unnecessary information that arrives from the primary motor cortex such as inhibiting antagonistic movement
Has a role in starting, stopping and monitoring intensity of movements

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13
Q

What parts of the basal ganglia is responsible for filtering movement information before the information goes back to the cortex?

A

Globus pallidus and substansia nigra

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14
Q

Name 1 excitatory and 1 inhibitory neurotransmitter associated with the basal ganglia.

A

Excitatory: glutamate
Inhibitory: GABA (gamma-amino-buteric acid)

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15
Q

Is the neurotransmitter dopamine excitatory or inhibitory?

A

Both. It has 2 components: D1 which is excitatory and D2 with is inhibitory.

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16
Q

Where is dopamine released from in the brain?

A

The substantia nigra pars compacta

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17
Q

How many different types of dopamine receptor exist in the central nervous system?

A

5

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18
Q

What happens when D1 (dopamine) is released from the substantia nigra pars compacta?

A

D1 increases the inhibitory output from the striatum (via the direct pathway)

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19
Q

What happens when D2 (dopamine) is released from the substantia nigra pars compacta?

A

D2 decreases the inhibitory level of the striatum (via the indirect pathway)

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20
Q

What are the structures involved in the direct pathway?

A

cortex

  • > striatum (caudate & putamen)
  • > globus pallidus internus & substantia nigra & pars reticulata
  • > thalamus
  • > cortex
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21
Q

What are the structures involved in the indirect pathway?

A

cortex

  • > striatum (caudate+putamen)
  • > globus pallidus externus
  • > subthalamic nucleus
  • > globus pallidus internus, substantia nigra & pars reticulata
  • > thalamus
  • > cortex
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22
Q

What neurotransmitter does the cortex release when synapsing to the striatum?

A

Glutamate

23
Q

What neurotransmitter does the striatum release when synapsing onto the output nuclei (globus pallidus internus & substantia nigra & pars reticulata)?

A

GABA

24
Q

What neurotransmitter does the output nuclei (globus pallidus internus & substantia nigra & pars reticulata) release when synapsing onto the thalamus?

A

GABA

25
Q

What neurotransmitter does the thalamus release when synapsing with the cortex?

A

Glutamate

26
Q

What is the end result of the indirect pathway?

A

The production of movement

27
Q

What neurotransmitter does the striatum emit when synapsing with globus pallidus externus?

A

GABA

28
Q

What neurotransmitter does globus pallidus externus release when synapsing with the subthalamic nuclei?

A

GABA

29
Q

What neurotransmitter does the subthalamic nuclei release when synapsing with the output nuclei (globus pallidus internus & substantia nigra & pars reticulata)?

A

Glutamate

30
Q

What is the end result of the direct pathway?

A

The inhibition of movement

31
Q

What is the difference between Parkinson’s and Huntington’s disease?

A

Parkinson’s - too little movement
Huntington’s - too much movement
Both a disease of the basal ganglia

32
Q

What is the difference between Parkinson’s disease and Parkinsonism?

A

Parkinson’s disease is idiopathitic with genetic and environmental links
Parkinsonism occurs due to known damage to the basal ganglia e.g. professional boxing, ingesting a toxic drug

33
Q

What is the pathology of Parkinson’s disease?

A

Cell death in the substantia nigra pars compacta causing a severe reduction in dopamine from it.

34
Q

What are the 3 cardinal signs of Parkinson’s disease?

A

Bradykinesia
Rigidity
Tremor

35
Q

What is bradykinesia?

A

Slowness/poverty of movement due to reduced dopamine and a decrease in level of functioning of the basal ganglia
Its a difficulty in selecting and initiating movement

36
Q

What is festination? Give an example

A

A progressive reduction in speed and amplitude of repetitive actions
Reduction in step length during walking

37
Q

What does bradykinesia cause?

A

Lack of automatic movements/responses such as;

  1. Saving reactions during loss of balance
  2. High risk of falls
  3. Swallowing, emotional expression on the face
38
Q

What is rigidity in PD?

What are the two types?

A

Increased muscle activity causing resistance to passive movement felt throughout range of movement. Is present in opposing muscle groups

  1. Lead pipe rigidity - smooth resistance
  2. Cog wheel rigidity - intermittent catch and release of the muscle
39
Q

What is the difference between resting and intension tremor?

A

Intention tremor - tremor gets worse as the movement progresses
Resting tremor - is slow, coarse and present at rest

40
Q

Describe tremor in relation to PD.

A

More commonly seen in upper limbs

Tremor increases with anxiety and at the beginning of the movement

41
Q

4 ways PD impacts the patient functionally.

A

Communication - limited non-verbal, slow & quiet voice
Swallow - reduced control of swallow, drooling and difficulty chewing, high risk of aspiration
ADL’s - gait, bed transfers
Posture - flexes trunk, hips and knees

42
Q

Name 3 pharmaccologics that address hypokinesia in PD patients

A

L-Dopa
Dopamine agonists
Anticholinergics

43
Q

How does L-Dopa work?

A

Synthetically increases dopamine levels
L-Dopa is the precursor to dopamine (which cannot cross the BBB) so it synthetically makes dopamine once it has crossed the BBB.

44
Q

List the pros of L-Dopa.

A

Dramatic improvements in motor function

Improves physical functioning/independence

45
Q

List the cons of L-Dopa. (4)

A
  • End of dose decline in function
  • On/off oscillations - drug reaches its optimal level 30min after ingestion
  • Effectiveness diminishes with time as its neurotoxic to remaining dopaminergic cells
  • Dyskinesia (hyperkinetic, uncontrolled movements)
46
Q

How do dopamine agonists work?

A

Are an artificial form of dopamine mimicking the hormones endogenous action
Act on dopamine receptors.
They cross the BBB, bind to D1 and D2 receptors

47
Q

Pros of dopamine agonists? (1)

A

Can be used to delay start of L-Dopa treatment

48
Q

Cons of dopamine agonists?

A

Doesn’t bind to D1/D2 as well as L-Dopa
Many of the same side effects of L-Dopa (hallucinations, nausea, dizziness)
Long term effects not known

49
Q

What is the mechanism of action of anticholinergic drugs for PD?

A

There is a balance between dopamine and acetylcholine in the brain
Anticholinergics block acetylcholine to readjust the balance between them

50
Q

Pros of anticholinergic drugs for PD?

A

Effective for tremor as it doesn’t bind to D1/D2 receptors

51
Q

Cons of anticholinergic drugs for PD?

A

Not effective for symptoms of bradykinesia (as it doesn’t bind to D1/D2)
Side effects can cause early onset dementia in the older population

52
Q

What cues help reduce hypokinesia in PD patients?

A

Auditory - music with a strong beat so they can walk to the beat
Visual - markers on floor

53
Q

What can cause falls in PD patients?

A

Physical problems - muscle tone becomes more rigid, change in posture, problems initiating movement/freezing

Effects of medication used to treat PD - side effect of med= they cause low blood pressure - increases dizziness

Hazards around the home - pets, rugs, loose carpet

Neurorehab (13 decks)

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