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MD4001 Week 3 > 5. Control of movement 4: The basal nuclei > Flashcards

5. Control of movement 4: The basal nuclei Flashcards

1
Q

What are the 3 functional divisions of the basal ganglia?

A
  1. Input nuclei
  2. Intrinsic nuclei
  3. Output nuclei
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2
Q

What information is transmitted via the input nuclei of the basal ganglia? Involves which structures?

A

Input taken from the cortex and the thalamus

Involves:
Caudate nucleus (including nucleus accumbens)
-Putamen

(Input structures tend to be at the superior aspect of the basal ganglia)

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3
Q

What information is transmitted via the intrinsic nuclei of the basal ganglia? Involves which structures?

A

Relays information between the input and output nuclei

Involves:

  • Globus pallidus (external segment)
  • The subthalamic nucleus
  • The substantia nigra (pars compacta segment)
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4
Q

What information is transmitted via the output nuclei of the basal ganglia? Involves which structures?

A

Sends information to the thalamus

Involves:

  • Globus pallidus (internal segment)
  • The substantia nigra (pars reticulata)

(Output structures tends to be at the base of the basal ganglia)

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5
Q

Different structures that make up the basal ganglia?

A 
Caudate nucleus (input)
Thalamus
Putamen (input)
Globus pallidus external (intrinsic)
Globus pallidus internal (output)
Subthalamic nucleus (intrinsic)
Red nucleus
Substantia nigra (output from reticula part, intrinsic from compacta part)
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6
Q

What structures make up the neostriatum?

Neostriatum = striatum = corpus striatum

A
  1. Caudate nucleus (includes
    nucleus acumbens)
  2. Putamen
  3. Globus Pallidus
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7
Q

The Basal nuclei consists of five sub- cortical (diencephalic) structures…..

A 
1. Caudate nucleus (includes
nucleus acumbens) 
2. Putamen
3. Globus Pallidus
4. Subthalamic nucleus
5. Substantia nigra
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8
Q

Function of the basal nuclei?

A

Concerned with refinement and initiation of motor output (motor loop)
Emotional and reward aspects of motor output (limbic loop)
Influence on behaviour and learning (behavioural loop)

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9
Q

What is the direct pathway in which the medial globus pallidus holts movement?

A
  1. Cerebral cortex excites the neostriatum with glutamate
  2. Neostriatum inhibits the Globus Pallidus medial lobe with GABA
  3. The medial lobe usually inhibits the thalamus (GABA), but as its activity has been reduced, the thalamus activity increases
  4. Increased activity at the thalamus results in increased cerebral stimulation and so, increased movement

So…
Increase cerebral output activity stimulates neostriatum via Glut (i.e. putamen and cordate nucleus). This causes neostriatum to produce GABA which inhibits the medial lobe of GP. The inhibition of the medial lobe of GP allowed the inhibition on the thalamus to be reduced, thus increasing it;’s activity. If the thalamus is stimulated, it increases cerebral stimulation so leads to increased movement.

To increase movement, you want to suppress the medial lobe of the GP via putamen

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10
Q

What is the indirect pathway in which the lateral lobe of the globus pallidus acts as a brake on movement?

A
  1. Cerebral cortex excites the neostriatum with glutamate
  2. Neostriatum inhibits the Globus Pallidus lateral lobe with GABA
  3. The lateral lobe normally inhibits the subthalamic nucleus (GABA) but as it is inhibited, the subthalamic nucleus activity rises
  4. The subthalamic nucleus then increases its normal excitation of the medial lobe of the Globus Pallidus which increases its activity
  5. Increased activity at medial lobe (brake to movement) results in increased inhibition of the thalamus and so a reduction in cerebral stimulation .
  6. This in turn results in reduced movement
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11
Q

Medial lobe of the globus pallidus is the….

A

brake to movement

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12
Q

Role of the substantia nigra and dopamine in movement stimulation?

A

Substantia nigra release dopamine (from pars compacta) which acts on the putamen.
This acts on 2 receptors
1. Enhances the direct pathway (i.e. medial lobe of gp suppression)
2. Inhibits inhibit pathway (i.e. release inhibition on subthalamic nucleus, so stimulate of medial lobe of gp)

Both receptor effect increase movement.

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13
Q

Indirect pathway, you have to ____ to increase movement

Direct pathway, you have to ______ to increase movement

A

Indirect pathway, you have to inhibit to increase movement

Direct pathway, you have to enhance to increase movement

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14
Q

Why are basal ganglia lesion contralateral?

A

Basal ganglia circuit DOESN’T CROSS

but

the corticospinal tract crosses to the contralateral side and the basal ganglia modulate the motor cortex

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15
Q

Example of a hypokinetic disorder i.e. lesions of the direct pathway?

A

Parkinsonism disease

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16
Q

Parkinsonism Disease, Physical manifestation?

TRAP

A 
TRAP
• Tremor (Resting pill-rolling)
• Rigidity (Lead-pipe and cog-wheel) 
• Akinesia
• Posture (Stooped)
17
Q

Physiology of parkinsonism disease?

A

Progressive degeneration of the dopaminergic neurones of the substantia nigra (this produces dopamine remember)

18
Q

Loss of dopamine leads to hypokinesia by…..

A
  1. a decrease in direct pathway activity (decreased movement)
  2. an increase in the indirect pathway activity (decreased movement)
19
Q

5 examples of hyperkinetic disorders that manifest due to the lesions of the indirect pathway?

A
  1. Hemiballismus
  2. Chorea
  3. Athetosis
  4. Wilson’s disease
  5. Dystonia
20
Q

Why is hemiballismus a hyperkinetic disorder?

Presents as?

A

Hyperkinetic disorders – Lesions of Indirect Pathway

Lesion location: Subthalamic nucleus

–> No stimulation of the GPi (i.e. no stimulation to break, thalamus no longer inhibited)

Presentation: Violent projectile movement of limb seen contralateral to the lesion.

21
Q

What is chorea?
How does it act as a hyperkinetic disorder?
Presents as?

A

Hyperkinetic disorders – Lesions of Indirect Pathway

•Lesion of striatum (putamen)

Results in…
•Initially, loss of GABAergic cells in the striatum that project only to GPe (inhibition of indirect pathway)
•Later, striatal cholinergic cells also begin to die

Presentation:
•Rapid, involuntary and purposeless jerks of irregular and variable location on the body

22
Q

What is athetosis?
How does it act as a hyperkinetic disorder?
Presents as?

A

Hyperkinetic disorders – Lesions of Indirect Pathway

Lesion: In the globus pallidus

Presents as:
-Spontaneous and continuous writhing movement of a hand, arm, neck or face

23
Q

What is wilson’s disease ( I.e. Hepatolenticular degeneration)?
How does it act as a hyperkinetic disorder?
Presents as?

A

Hyperkinetic disorders – Lesions of Indirect Pathway

Lenticular dengeneration due to COPPER accumulation (Lenticular or lentiform nucleus = Putamen + Globus pallidus)

Presents as:
Dystonia and Tremor

24
Q

What is dystonia?
How does it act as a hyperkinetic disorder?
Presents as?

A

Hyperkinetic disorders – Lesions of Indirect Pathway

•Lesions in the lentiform nucleus (Putamen > Globus pallidus)

Presents as:
Increased/sustained muscle contractions
Twisting of the trunk or extremities
Abnormal postures.

25
Q

GPi is..

A

Globus pallidus internal lobe (medial lobe)

26
Q

GPe is…

A

Globus pallidus external lobe (lateral lobe)

27
Q

Cause of huntington’s chorea?

A

Huntington’s chorea – due to excessive CAG (trinucelotide) repeats on chromosome 4

28
Q

Cause of huntington’s chorea?

A

Huntington’s chorea – due to excessive CAG (trinucelotide) repeats on chromosome 4 resulting in malformed protein called Huntington’s protein.

–>
Loss of enkephalinergic and GABAergic neurons in the neostriatum (caudate nucleus and putamen), leading to a DECREASE in the activity of the INDIRECT pathway (this leads to INCREASED MOVEMENT)

29
Q

4 characteristics of huntington’s disease?

A
  1. Wildly flailing limbs (chorea = dance) and contorted posture
  2. Reduced ability to saccade
  3. Abnormal emotional responses (later stages)
  4. Reduced cognitive ability (later stages)
30
Q

Onset and prognosis of huntington’s disease?

A

Life expectance is on average 15yrs after onset of symptoms and death is commonly due to respiratory infection. Onset is usually in 50’s but with a juvenile version of the disease

31
Q 
Lesions of the LMN:
Side of lesion
paralysis?
Muscle atrophy?
Tone?
Tendon reflexes?
A 
Side of lesion: Ipsilateral
Paralysis: Flaccid
Muscle atrophy: Present
Tone: Decreased
Tendon reflexes: Suppressed
32
Q 
Lesion of UMN:
Side of lesion?
paralysis?
Muscle atrophy?
Tone?
Tendon reflexes?
A 
Side of lesion: Contralateral or ipsilateral
Paralysis: Spastic
Muscle atrophy: Absent
Tone: Increased
Tendon reflexes: Suppressed
33
Q 
Lesion of basal ganglia:
Side of lesion
paralysis?
Muscle atrophy?
Tone?
Tendon reflexes?
A 
Side of lesion: Contalateral
Paralysis: None
Muscle atrophy: None
Tone: Increased
Tendon reflexes: Normal
34
Q 
Cerebellar lesion:
Side of lesion
paralysis?
Muscle atrophy?
Tone?
Tendon reflexes?
A 
Side of lesion: Ipsilateral
Paralysis: None
Muscle atrophy: None
Tone: Decreased
Tendon reflexes: Normal or suppressed

MD4001 Week 3 (12 decks)

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