Session 6: Motor Disorders Flashcards

1
Q
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2
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3
Q

What is the basal ganglia made of?

A

Substantia nigra pars compacta

Striatum

Lentiform nucleus

Subthalamic nucleus

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4
Q

What makes up the striatum?

A

The caudate and putamen

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5
Q

What makes up the lentiform nucleus?

A

The putamen and the globus pallidus

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6
Q

What are the parts of the globus pallidus?

A

Globus pallidus interna

Globus pallidus externa

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7
Q

Function of the basal ganglia.

A

Communicates with the motor cortex in order to reinforce appropriate movements and also inhibit inappropriate movements.

An example is raising a glass:

Need to reinforce appropriate movements which would be elbow flexion and shoulder flexion.

Need to inhibit inappropriate movements which would be elbow extension and shoulder extension.

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8
Q

Basal ganglia communicates with the motor cortex via two pathways.

Which?

A

Direct pathway

Indirect pathway

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9
Q

Function of direct pathway.

A

Reinforces appropriate movement.

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10
Q

Function of indirect pathway.

A

Inhibit inappropriate movement

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11
Q

Explain the functions of the cerebellum.

A

Communicates with the motor cortex as well as with proprioception.

Proprioception receptors send an afferent ascending signal via the spinocerebellar tract to the cerebellum. This is in order for the cerebellum to know the position of the limbs in space.

This is important in order for what the cerebellum is about to do next:

Select the appropriate sequence of movements.

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12
Q

Where is dopamine produced?

A

Substantia nigra pars compacta

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13
Q

Explain the action of dopamine in the basal ganglia.

A

Dopamine acts on D1 receptors on striatal neurones in order to excite the direct pathway.

Dopamine also acts on D2 receptors which inhibits the indirect pathway (leading to a net excitatory signal)

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14
Q

What will a basal ganglia lesion affect?

A

It will affect the contralateral side of the body.

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15
Q

Why does a basal ganglia lesion lead to a contralateral presentation?

A

Because the basal ganglia circuit where it communicates with the motor cortex communicates with the ipsilateral side.

This means that there is no decussation in the communication between basal ganglia and motor cortex.

When a motor signal is then sent down via the corticospinal tract it will cause a contralateral presentation.

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16
Q

Are most basal ganglia lesions usually contralateral?

If not, what are they?

A

No, they are usually bilateral due to neurodegeneration.

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17
Q

What will a cerebellar lesion affect?

A

The ipsilateral side of the lesion.

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18
Q

Explain why a cerebellar lesion present with ipsilateral symptoms.

A

Because the cerebellum communicates with the contralateral cerebral hemisphere. This is via the corticopontine pathway where the afferent fibre synapse in the pontine nucleus and then in the pons the fibres will decussate and communicate with the contralateral cerebellum.

There is then a signal going back to the motor cortex via the cerebello-thalamo-cortical pathway where there is decussation again.

Lastly the response is via the corticospinal pathway which also decussate to the same side as the lesion.

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19
Q

What is Parkinson’s disease?

A

Caused by degeneration of dopaminergic neurones in SNc leading to lower levels of dopamine.

20
Q

What is the consequence of the lower levels of dopamine?

A

There is less excitation of the direct pathway and also less inhibition of the indirect patway.

This leads to less motor activity.

21
Q

Symptoms and signs of Parkinson’s disease.

A

Pill rolling tremors

Lead pipe rigidity aka cog-wheel rigidity

Bradykinesia where there are problems with initiating and terminating movement.

Hypophonia

Decreased facial movement / mask-life facies

Micrographia

Dementia

Depression

22
Q

Why does bradykinesia happen in Parkinson’s?

A

Due to loss of cortical excitation

23
Q

Treatment of Parkinson’s.

A

Levodopa which is converted into dopamine in the brain.

Deep brain stimulation (e.g. of subthalamic nucleus)

24
Q

What is Huntington’s chorea?

A

An autosomal dominant and progressive disorder that usually presents in 30-50 years of age.

This is due to the loss of the inhibitory projections from striatum to GPe.

25
Q

What are the consequences of the loss of inhibitory projections from stiatum to GPe?

A

Hyperkinetic features since the ‘brakes’ have been taken off the thalamus.

26
Q

Signs and symptoms of Huntington’s chorea.

A

Bilateral chorea (dance-like movements)

Dystonia

Loss of co-ordination

Cognitive decline and behavioural disturbances

27
Q

Why does chorea occur in Huntington’s?

A

Increased motor cortex activation

28
Q

Why does dystonia occur in Huntington’s?

A

Uncomfortable contractions of agonists and antagonists simultaneously leading to odd postures and pain.

29
Q

What is hemiballismus?

A

Usually caused by damage to subthalamic nucleus.

30
Q

What is the consequence of damage to the subthalamic nucleus?

A

It normally inhibits the thalamus by stimulation of GPi.

If there is damage there will be increased excitation of the motor cortex.

31
Q

What can hemiballismus be caused by?

A

Sub-cortical stroke also called a lacunar infarct.

32
Q

Symptoms and signs of hemiballismus.

A

Similar to Huntington’s where there is involuntary commonly called ballistic movements.

The difference here is that the ballistic movements are unilateral.

33
Q

Anatomy of the cerebellum.

A

Midline vermis and two laterally placed hemispheres

34
Q

Functions of the vermis.

A

Deals with cerebellar movements of the trunk.

35
Q

Functions of the cerebellar hemispheres.

A

Deals with cerebellar movements of the ipsilateral sides of the body.

36
Q

How does the cerebellum communicate with the cerebrum?

A

Via the cerebellar peduncles.

There are three peduncles:

Superior, middle and inferior which communicate with the midbrain, pons and medulla respectively.

37
Q

What does the cerebellum sit on top of?

A

The 4th ventricle

38
Q

What is the relevance of the cerebellum sitting on top of the 4th ventricle?

A

A lesion of the cerebellum can cause hydrocephalus due to compression of the 4th ventricle.

39
Q

Signs of cerebellar disease/lesion.

A

DANISH

Dysdiadochokinesia

Ataxia

Nystagmus

Intention tremor

Slurred speech

Hypotonia

40
Q

What is dysdiadochokinesia?

A

Difficulty with rapidly alternating movements

41
Q

Explain the cerebellar ataxia.

A

Unstead gait as a result of difficulty sequencing lower limb muscle contractions.

42
Q

How do you distinguish between sensory and cerebellar ataxia?

A

By doing Rhomberg’s test.

43
Q

Explain Rhomberg’s test.

A

Tell the patient to close their eyes.

If the patient falls over that is a positive Romberg’s test and a sign of sensory ataxia.

If the test is negative then it can be cerebellar ataxia.

44
Q

What is nystagmus?

A

Rapidly moving eyes with vertigo

This is due to malcoordination of the extraocular muscles.

45
Q

What are intention tremors?

A

Low frequency tremors

46
Q

Why does slurred speech occur in cerebellar lesions?

A

Malcoordination of laryngeal and tongue musculature.

47
Q
A