Lesson 14: Voluntary Movement - From the Cerebral Cortex Flashcards Preview

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Flashcards in Lesson 14: Voluntary Movement - From the Cerebral Cortex Deck (53)
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1
Q

What are the two main types of damage to the motor system?

A

Loss of voluntary movement (pyramidal system) and movement disorders of motor control (extrapyramidal system).

2
Q

What are motor control centres?

A

(for example the basal ganglia) that send their input into the extrapyramidal tracts

3
Q

How is a LMNL caused?

A

Caused by damage to the alpha motor neuron at the cell body or anywhere along the axon

4
Q

In a LMNL how is the final common pathway affected? What does this cause?

A

Because it interrupts the final common pathway, there is no means for voluntary or reflex muscle activation to occur. This will produce hypo- or a a-reflexia, hyptonia, muscle flaccidity and rapid muscle atrophy

5
Q

How is an UMNL caused?

A

Loss of circulation or trauma involving the voluntary motor pathway at the level of the upper motor neuron
- Stroke involving the motor cortex or the internal capsule, a tumour, an arteriovenous malformation, traumatic brain injury (TBI).

6
Q

What does the clinical picture depend on for an UMNL?

A

Depends on both the extent of the damage and the location.

Could include the pyramidal tracts, the extrapyramidal tracts, the sensory tracts and motor control centres.

7
Q

How are UMNL of the pyramids different than the extrapyramidal tracts?

A

In most cases, an UMNL of just the pyramidal tracts (corticospinal and corticobulbar) really can’t be separated from the extrapyramidal tract influence (rubrospinal, olivospinal tectospinal, vestibulospinal, and reticulospinal).

8
Q

In strokes, how does one encounter pyramidal and extrapyramidal effects?

A

One encounters a combination of loss of voluntary movement (the pyramidal tract deficits) and extrapyramidal effects such as spasticity, hyperreflexia, hypertonia and the reappearance of primitive reflexes including the Babinski reflex and clonus

9
Q

What is clonus?

A

Alternating stretch reflex due to hyperreflexia in both agonists and antagonists (opposing muscle groups) which after being triggered stretch their antagonist producing a repeating reciprocal activation

10
Q

In CNS and PNS lesions from the motor or sensory system, which (CNS/PNS) has better potential for recovery? Why?

A

PNS has better potential for recovery

The CNS has factors that inhibit this regeneration (transneuronal degeneration)

11
Q

In a complete spinal cord lesion, which pathways are severed?
What does this cause in the body?

A

ALL of the pyramidal and extrapyramidal pathways to the body are severed
-All voluntary movement is lost below the (spinal cord) level of the lesion.

12
Q

Does a spinal cord lesion produce language-processing problems?

A

No

13
Q

What are motor control disorders?

A

Diseases that directly affect the motor control centres, such as injury to the cerebellum, damage to the brainstem form head injury, or disorders of the basal ganglia such as Parkinson’s and Huntington’s disease

14
Q

What is cerebral palsy?

A

Loose term to include a collection of disorders that occur at or around birth. Some of these are similar to strokes; others involve damage to areas of motor control.

15
Q

What is dysarthria?

A

Difficulties with respiration, phonation, articulation, resonance and/or prosody due to impaired voluntary movement (LMNLs and UMNLs) and/or disorders of programming of speech (motor control disorders)

16
Q

In the mechanisms that cause loss of quality of voluntary movement, where does it originate and target?

A

Originating in the motor cortex, carried out along the corticospinal or corticobulbar tracts targeting the alpha motor neuron

17
Q

In the mechanisms that cause loss of quality of voluntary movement, what is the role of the primary motor cortex?

A

Primary motor cortex the command post (instructions). In this analogy, the programming of voluntary movement is represented by a program of firing the missiles, such as the number and general target for the missile. This is the job of the “planning subcommittee”, the basal ganglia.

18
Q

In the mechanisms that cause loss of quality of voluntary movement, what does the basal ganglia do?

A

Responsible for programming the instructions.

19
Q

In the mechanisms that cause loss of quality of voluntary movement, what is the role of the cerebellum?

A

Quality control - is responsible for keeping the missile directly on target. A missile guidance system does not fire the missile, nor does it decide how many missiles or where they are directed; it just guides it smoothly, making path corrections.

20
Q

What does the input of the cerebellum and basal ganglia do in the mechanisms that cause loss of quality of voluntary movement?

A

Their input to the motor cortex (command post), or through their influence on inter-neurons that in turn affect the probability of the alpha motor neurons to fire, they produce minor adjustments that influence movement quality

21
Q

Influences on the final common pathway: where does the alpha motor neuron travel to and what does the gamma motor neuron do?

A

Alpha motor neuron going to the extrafusal fibres and the sensory
Gamma motor neurons innervating intrafusal fibres traveling in the peripheral nerve

22
Q

Influences on the final common pathway: Which three routes does sensory info from the muscle spindle have?

A

To the higher centres through the dorsal columns (conscious proprioception), to the spinocerebellar pathways (unconscious proprioception), or to produce reciprocal innervation.

23
Q

Influences on the final common pathway: Where does the primary descending neuron travel, what does it do to the alpha motor neurons?

A

Goes directly to the alpha motor neuron from the motor cortex. There is a negative feedback loop through the Renshaw cell, which has a dampening (inhibitory) influence on the alpha motor neuron.

24
Q

Influences on the final common pathway: What are the 5 descending extrapyramidal tracts?

A

Reticulospinal, vestibulospinal, olivospinal, rubrospinal, tectospinal

25
Q

What does the reticulospinal and vestibulospinal tract do in the final common pathway?

A

Send constant signals from the reticular and vestibular systems. These tracts produce postural responses and produce extension of the arms and legs

26
Q

What do the olivospinal and rubrospinal tracts do in the final common pathway?

A

Modify quality of movement

27
Q

What does the tectospinal tract do in the final common pathway?

A

Modifies responses to auditory and visual responses from the superior and inferior tectum in the midbrain

28
Q

What is the type of input from the extrapyramidal tract in the final common pathway?
What is the constant activity that the extrapyramidal tract does?

A

Their input is indirect through interneurons
There is constant adjustment of the intrafusal fibres through the gamma motor neurons being constantly stimulated by extrapyramidal tract input. There are both (+ve) and (-ve) effects

29
Q

How does the gamma motor neuron reset the muscle spindle?

A

Changes in extrapyramidal input (as with an UMNL), cause the gamma motor neurons to reset the spindle to be extra sensitive or less sensitive to stretch

30
Q

What does extra input to the gamma motor neurons cause?

A

Causes a hyper-responsive muscle spindle and muscle lengthening is resisted.

31
Q

How does normal muscle have a small amount of resting tone?

A

Due to the constant response to various forms of input, sensory, postural, or reflex

32
Q

What are the two types of hypertonicity?

A

Spastic hypertonicity and rigid hypertonicity

33
Q

What is spasticity? (spastic hypertonicity)

A

Velocity-dependent increased resistance to passive movement and therefore depends on the speed at which the passive movement occurs.

Velocity-dependent resistance to passive movement

34
Q

What are the two features of spastic paralysis?

A

Increased resistance to passive movement and loss of voluntary movement.
If the velocity is increased, the resistance increases (spasticity).

35
Q

When is a muscle considered flaccid?

A
  • In fact, there isn’t even the normal resistance of innervated muscle. Even when handled there is no resistance, hence it is flaccid (floppy
36
Q

What is rigid hypertonicity?

A

Is the velocity-independent hypertonicity, is less common and occurs in the motor control disorders such as Parkinson’s disease.

37
Q

What is tone?

A

Normal tone, hypotonic (reduced tone), or hypertonic (increased tone).
Based on the ongoing stimulation of the muscle caused by the constant input from the extrapyramidal tracts,

reflex responsiveness is influenced by both the extrapyramidal influence and lack of normal inhibition from higher centers on the stretch reflex responsiveness.

38
Q

What is reflex responsiveness influenced by?

A

Influenced by both the extrapyramidal influence and lack of normal inhibition from higher centres on the stretch reflex responsiveness.

39
Q

Why is there hypertonia if the activity of the extrapyramidal tract is lost?

A

Because there are both inhibitory and facilitatory influences all the way along the brainstem, the actual picture depends on where the lesion has occurred. Depending where the lesion occurs, there may still be some input to the muscle from the extrapyramidal trac

40
Q

What is the difference between areflexia and hyporeflexia?

A

Muscles are usually innervated by a number of neurons that may come from different levels of the spinal cord. If only one source is damaged, testing will not produce areflexia, but hyporeflexia because some motor units remain intact.

41
Q

What does a lesion in the upper motor neuron cause?

A

The instructions of voluntary movement to the lower motor neuron (paralysis).

42
Q

What are the the basal ganglia, reticular formation, inferior olivary nucleus, red nucleus, visual and auditory reflex centers in the tectum of the midbrain, vestibular input from the brainstem and local reflexes – local stretch reflex and central pattern generators into spinal cord mediated by?

A

Interneurons

43
Q

How is the alpha motor neuron influenced to increase/decrease the likelihood of firing?

A

The sum of their inhibition or excitation input to the interneuron will decrease or increase the probability of the alpha motor neuron firing

44
Q

Which tract gives constant input to the muscles to respond to vestibular info?

A

Vestibulospinal tract

45
Q

Which tract gives constant input for the reticular system?

A

Reticulospinal tract

46
Q

What does the red nucleus do?

A

Modifying information it collects from the cerebrum and from the cerebellum and which it integrates and descends as the rubrospinal tract.

47
Q

What is spastic hemiplegia?

What are some symptoms?

A

Paralysis with hypertonia, hyperreflexia, and clasp-knife ridigity. Posture – flexed upper arm, thumb and fingers with the neck bent toward the affected side; when walking, the patient usually circumvents the affected leg.

48
Q

What are some symptoms of spastic hemiplegia?

A

Profound weakness and flaccidity in contralateral distal muscles and a loss of delicate and manipulative skills; loss of abdominal and cremasteric reflexes, positive Babinski reflex, flaccid tone in the affected muscles. Muscle becomes spastic

49
Q

In spastic hemiplegia, how is the gradual emergence of spasticity developed?

A

Outgrowth of local stretch afferents, which fill the depopulated synapses on the α-motor neurons after a cortical lesion. Growth may subsequently promote increased afferents on type Ia fibres form the muscle spindles, causing greater activation of the motor neurons.

50
Q

How does pseduobulbar palsy develop?

A

Bilateral involvement of the corticonuclear pathways and is associated with a bilateral spastic paralysis of the speech musculature

51
Q

What are some symptoms of pseudobulbar palsy?

A

Patient has difficulty controlling facial muscles for delicate and discrete motor control, such as in speech.
- Facial emotional response pattern remains intact. When patient attempts to move the facial muscles in voluntary motor activities, they respond poorly.

52
Q

How does alternating hemiplegia arise?

Which structures does it usually involve?

A
  • Lesion on one side of brainstem affects the ipsilateral cranial nerve motor nuclei and/or nerves (motor units) extending to target facial muscles on the same side. This leads to LMN signs unilateral to the side of the lesion.
  • mostly involving arteries that supply the pons and medulla
53
Q

If there is a brainstem lesion, causing alternating hemiplegia, what are the symptoms?

A

Ipsilateral pharyngeal, lingual, facial, and/or ocular palsy (LMN) and contralateral spastic hemiplegia (UMN)