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Neuroscience > Session 6 Motor disorders > Flashcards

Session 6 Motor disorders Flashcards

1
Q

What is the source of dopamine in the brain?

A

Substantia Nigra pars compacta (SNc)

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2
Q

What makes up the striatum?

A

Caudate nucleus + Putamen

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3
Q

What makes up the lentiform nucleus?

A

Putamen + Globus pallidus

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4
Q

What does the caudate nucleus line?

A

It is a C shaped nucleus lining the lateral ventricle

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5
Q

Is the striatum functionally or anatomically related?

A

Functionally

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6
Q

Is the lentiform nucleus functionally or anatomically related?

A

Anatomically

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7
Q

How do the basal ganglia communicate with the the motor cortex?

A

Via the thalamus

Increased thalamic activity causes increased cortical activity and vice versa

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8
Q

What is the normal function of the basal ganglia?

A

Unclear but probably has a role in reinforcing appropriate movements and removing inappropriate movements

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9
Q

Do direct pathways reinforce appropriate or inappropriate movements?

A

Appropriate movements (excitatory to motor cortex)

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10
Q

Do indirect pathways reinforce appropriate or inappropriate movements?

A

They edit out inappropriate movements (inhibitory to motor cortex)

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11
Q

How does dopamine facilitate movement?

A

By exciting the motor cortex
* excites the direct pathway by stimulating excitatory D1 receptors on striatal neurones taking part in the direct pathway

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12
Q

How does dopamine inhibit the indirect pathway?

A

By activating inhibitory D2 receptors on striatal neurones taking part in the indirect pathway

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13
Q

Do basal ganglia regulate the ipsilateral or contralateral motor cortex? What side of signs if the SNc is affected unilaterally and why?

A

Ipsilateral motor cortex
If SNc if affected unilaterally (this is rare) there will be contralateral signs due to decussation of the corticospinal tract

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14
Q

What causes Parkinson’s disease?

A

Degeneration of dopaminergic neurones in SNc

Therefore, have LOST the dopamine-driven facilitation of movement via both pathways

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15
Q

What are the symptoms and signs of Parkinson’s disease?

Mechanisms for each (8)

A
  1. Tremor: may be related to dysfunction of indirect pathway which would normally suppress unwanted movements
  2. Rigidity: may be related to lack of coordination between agonists and antagonists
  3. Bradykinesia: slow movements due to loss of cortical excitation
  4. Hypophonia = quiet speech: due to bradykinesia of the larynx and tongue
  5. Decreased facial movement: due to bradykinesia of the face
  6. Micrographia = small handwriting: due to bradykinesia in hands
  7. Dementia: possible progression of currently unknown causative agent
  8. Depression: basal ganglia also have a role in cognition and mood
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16
Q

What type of disorder is Huntington’s Chorea?

A

Autosomal dominant, progressive disorder with an early onset around 30-50 years old

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17
Q

What are the early stages of Huntington’s Chorea associated with and what does this lead to?

A

Associated with loss of inhibitory projections from striatum to GPe

This leads to hyperkinetic features (increased movement as the brakes have been taken off the thalamus)

18
Q

What are the features of Huntington’s Chorea? 4

Mechanisms

A
  1. Chorea = dance-like movements : due to increased motor cortex activation
  2. Dystonia = uncomfortable contractions of agonists and antagonists simultaneously leading to odd postures CAUSED BY over activity in agonist/antagonist muscle circuits and loss of coordination between these
  3. Loss of coordination: mechanism similar to above
  4. Cognitive decline and behavioural disturbances: related to role of basal ganglia in higher mental functions
19
Q

What can Hemiballismus be caused by? 3 things!

A

N.B. Rare disorder

  1. Damage to sub thalamic nucleus which normally inhibits the thalamus via GPi
  2. Sub-cortical stoke = lacunar infarct
  3. Unilateral explosive (ballistic) movements
20
Q

How does the cerebellum communicate with the rest of the CNS?

A

Via cerebellar peduncles

Superior - connects to midbrain
Middle - connects to pons
Inferior - connects to medulla

21
Q

Why can cerebellar lesions (e.g. tumours) cause hydrocephalus?

A

Cerebellum sits above the 4th ventricle

22
Q

Normal functions of the cerebellum?

A

Clear role in the sequencing and coordination of movements

Uses sensory information to decide upon the most appropriate sequence of movements to perform an action

23
Q

How does the cerebellum perform its role?

A

Works with basal ganglia which decide most appropriate movements

Cerebellum then sequences these movements

An example: to develop the picking up of a cup of tea

Basal ganglia say that elbow flexion, shoulder flexion, finger flexion and wrist flexion are most appropriate
Cerebellum then puts these in most appropriate sequences based upon current position of the limb - hence, the cerebellum has profuse sensory inputs from proprioceptive neurones and sensory cortices

24
Q

Where does cerebellum receive sensory input from?

A

Form ipsilateral spinal cord an contralateral sensory cortices

25
Q

Where do the cerebellum outputs go to? What does this mean in terms of signs of damage?

A

To the contralateral motor cortex

Hence, ipsilateral signs of cerebellar damage are due to decussation of corticospinal pathway

26
Q

What are the signs of cerebellar disease and what are they due to (if known)? DANISH!

A 
Dysdiadochokinesia = difficulty with rapidly alternating movements: probably as a result of a problem with sequencing 
Ataxia = unsteady gait: a result of difficulty sequencing lower limb muscle contractions as well as loss of unconscious proprioception from lower limbs 
Nystagmus = flickering eye movements: due to malcoordination of extraocular muscles 
Intention tremor = a tremor that worsens as a target is approached 
Slurred speech (dysarthria): caused by malcoordination of laryngeal and tongue musculature 
Hypotonia: unclear mechanism
27
Q

What would be the effect of stimulation of GPi?

Refer to diagram

A

Increased inhibition of the thalamus

Decreased movement

28
Q

What would be the effect of destruction of GPi?

A

Would lead to decreased inhibition of the thalamus

Increased thalamic activity so increased movement

29
Q

What would be the effect of destruction of the sub thalamic nucleus (STN)?

A

Decreased stimulation/activity of GPi and SNr

Decreased inhibition of thalamus

Increased thalamic activity

= hemiballismus
Increased movement

30
Q

What condition can destruction of STN (subthalamic nucleus) lead to?

A

Hemiballismus

31
Q

What would be the effect of stimulating the subthalamic nucleus (STN) ?

A

Increased stimulation / activity of GPi and SNR

Increased inhibition of thalamus

Decreased thalamic activity

Decreased movement

32
Q

In the internal capsule, where would fibres representing

A) the lower limbs be found?
B) the face be found?

A

A) posterior limb - contains UMN’s for most of the body
B) the genu - contains UMN’s destined for the face

NB: anterior limb contains fibres that aren’t relevant to us right now

33
Q

Which structure in the MIDBRAIN is important for motor control?

A

Red nucleus

  • participates in some complex circuits with the cerebellum and motor cortex
  • red nucleus is the origin for the rubrospinal tract
34
Q

How might damage to the thalamus affect movement?

A

Decreased movement

NB: this is theoretical and not normally seen

Decreased activation of the motor cortex hence decreased movement

35
Q

Destruction of the STN (subthalamic nucleus) would result in what?

A

Increased movement

  • Hemiballismus
36
Q

What defines hemiballismus (movement wise)?

A

Involuntary, explosive movements

Damage to the STN leads to decreases stimulation of GPi and SNr, hence decreased inhibition of the thalamus and ultimately increased motor cortical activity

37
Q

Parkinson’s disease is characterised by which triplet of signs?

A
  • Tremor, rigidity and bradykinesia
38
Q

Hyporeflexia, fasciculation and wasting are characteristic of what?

A

LMN lesions

39
Q

Hypotonia, nystagmus and intention tremor are characteristic features of what?

A

Cerebellar lesions (DANISH)

40
Q

Why do UMN lesions lead to spasticity?

A

Both flexors and extensors are affected equally in UMN lesions but flexors are more powerful, hence flexed spastic posture

Spasticity occurs due to loss of descending inhibitory tone on the LMNs

(NB: There is usually decreased overall activity in the corticospinal tract)

41
Q

Why would a stroke affecting the lateral aspect of the motor cortex compromise swallowing?

A

Denervation of cranial nerve nuclei which distribute LMNs in the vagus nerve

There would be an UMN lesion affecting the nucleus ambiguus

42
Q

A patient has suffered a stroke affecting the internal capsule near the genu. How will his facial weakness manifest?

A

Weakness of the contralateral lower face

(The upper face has bilateral UMN innervation, hence is spared in strokes)

The lower face receives a contralateral UMN innervation

Neuroscience (17 decks)

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