Spinal Cord, Descending Tracts & Reflexes Flashcards

1
Q

Where is the primary motor cortex?

A

Pre-central gyrus (Brodmann Area 4) anterior to the central sulcus in the frontal lobe

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2
Q

What is the primary motor cortex?

A

The site of origin of 80-80% of UMNs of the corticospinal tract that controls contralateral body motor functions

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3
Q

What does the primary motor cortex receive input from?

A

Pre-motor cortex + SMA which lie anterior to it (Brodmann Area 6) which help fine motor movements

Cerebellum via the thalamic nuclei VLP

Somatosensory cortex involved in +ve feedback from muscle spindles

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4
Q

What does injury to the primary motor cortex result in?

A

Contralateral paralysis and paresis (weakness)

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5
Q

What input does the supplementary motor area have and what does it do?

A

Basal ganglia and pre-frontal cortex so is critical for planning motor tasks being activated by internally generating intention from the pre-frontal cortex

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6
Q

What does injury to the supplementary motor area result in?

A

Unilateral akinesia (including speech loss) on contralateral side of body

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7
Q

What are the inputs and outputs of the pre-motor cortex?

A

Similar inputs to SMA

Outputs mainly to primary motor cortex, reticular formation (influences reticulospinal activity) + contributes outflow to corticospinal tract

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8
Q

What does the pre-motor cortex rely on to release one of its motor programs?

A

External stimuli i.e. visual, auditory or somatosensory cue

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9
Q

What does pre-motor cortex damage result in?

A

Paresis (weakness) of contralateral postural muscles due to its influence on the reticulospinal tract

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10
Q

What is a motor unit?

A

A LMN and the extrafusal muscle fibres it innervates (NOT the same as a myotome)

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11
Q

What is a myotome?

A

Muscle fibres innervates by a single spinal nerve

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12
Q

What is the difference between muscles with unrefined and refined control?

A

Unrefined e.g. knee extensors have a large no. of muscle fibres per motor unit (1000+)

Muscles with fine control e.g. hand digit movement have few muscle fibres per motor unit (10)

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13
Q

What do α lower motor neurons (LMN) innervate?

A

Motor neurons with large myelinated axons that innervate motor units of EXTRAFUSAL fibres making muscles contract directly

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14
Q

What do ϒ LMNs innervate?

A

Motor neurons will small diameter axons that innervate Intrafusal fibres found inside the muscle spindle keeping it under load during muscle contraction/stretchby sensing this

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15
Q

What are the different types of motor system disorders?

A
Monoplegia
Hemiplegia
Diplegia
Paraplegia
Quadraplegia
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16
Q

What are some causes of infarction of the spinal cord?

A
Embolus
Ruptured plaque/atheroma
Dissecting AAA
Trauma to vessels
Tumor
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17
Q

What are some causes of damage to the spinal cord?

A
Ventral root damage
Spinal cord lesions
Motor neuron disease
Parkinsons
MS
ALS
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18
Q

What is amyotrophic lateral sclerosis (ALS)?

A

Degeneration of the corticospinal tracts and ventral horn of the spinal cord so it shows UMN/LMN symptoms where there is a limb onset first then spread to other body areas

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19
Q

What are symptoms of amyotrophic lateral sclerosis (ALS)?

A

Fasciculations
Spasticity/cramps
Weakness (limbs, neck, diaphragm)
Dysarthria, dysphagia + dyspnoea

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20
Q

What are the descending tracts?

A
  1. Lateral corticospinal
  2. Lateral vestibulospinal
  3. Ventral corticospinal
  4. Rubrospinal
  5. Reticulospinal
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21
Q

What does the reticulospinal tract mainly function to do?

A

Helps to inhibit LMNs so you do not have overactive spastile/hyper-flective muscles

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22
Q

What is the function of the rubrospinal tract?

A

May contribute to limb flexor muscle control but it is small and not very relevant in humans

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23
Q

What is the pathway of the lateral corticospinal tract?

A

Pyramidal tract outputs from primary motor cortex, pre-motor cortex + SMA travels down the lateral corticospinal tract and causing MAJOR voluntary skilled motor movement

24
Q

What is the pathway of the ventral corticospinal tract?

A

Pyramidal tract (10-15% corticospinal neurons) outputs from primary motor cortex, travels along the ventral corticospinal tract and causing MINOR motor movement

25
Q

What is the pathway of the lateral vestibulospinal tract?

A

Extrapyramidal system (80-90% corticospinal neurons) outputs from vestibular nuclei of pons + medulla, travels along the lateral vestibulospinal tract and causing extensor muscle control (anti-gravity action) to keep you upright

26
Q

What is the main function of the corticospinal tracts in general?

A

Main motor track to body: controls the speed, direction and agility of movements involved in rapid, skilled, fine movement (ventral can restore some movement if some of the lateral tract is knocked out)

27
Q

___ neurons of the corticospinal tract do not decussate.

A

~2%

28
Q

Describe the lateral corticospinal tract.

A
  1. UMN cell body located in primary motor cortex
  2. Axons form pyramids of brainstem decussating at lower medulla
  3. Travel down tract
  4. Synapse with LMN in ventral grey horn
29
Q

Describe the ventral corticospinal tract.

A
  1. UMN cell body located in primary motor cortex
  2. Travel down tract
  3. Decussate at level of synapse with LMN
  4. Synapse with LMN in ventral grey horn
30
Q

Where do upper motor neuron (UMN) lesions occur?

A
Cortex 
Internal capsule
Corona radiata
Descending tracts
Brainstem e.g. medulla
Spinal cord
31
Q

Where do lower motor neuron (LMN) lesions occur?

A

Spinal cord (at level of LMN cell body)
Spinal nerve
Cauda equina
Peripheral nerve damage e.g. radial nerve

32
Q

What are some causes of motor neuron damage?

A
Stroke
Motor neuron disease
MS
CNS tumour
Meningeal tumour
Spinal tumour
Trauma
Penetrating injury
Fracture
Dislocation
Stenosis
IV disc prolapse
33
Q

What will the symptoms of upper motor neuron (UMN) lesion?

A

Initially patient presents with LMN symptoms

After a few days UMN symptoms present and take over:

  • Spastic paralysis
  • Hyper-reflexia
  • No muscle wasting
  • Extensor plantar response
34
Q

What will be the symptoms of lower motor neuron (LMN) lesion?

A

Flaccid paralysis
Hypo-reflexia (or absent)
Muscle wasting (atrophy)
Fasciculations (twitches)

35
Q

What is clonus?

A

A rhythmic series of contractions (oscillations) caused by the alternative stretching and unloading of muscle spindles in a patient with spastic muscles e.g. if foot is dorsiflexed (toes towards ceiling), flexor muscle clonus is observed

36
Q

What is a normal and abnormal plantor reflex?

A

Stroke side of foot on outside edge towards toe

Normal: digit plantarflexion (flexor plantar response)

Abnormal: great (big) toe extension + digit splaying (newborns/2 years + adults with UMN lesions)

37
Q

What symptoms would occur in Brown-Sequard syndrome (hemi-section of the spinal cord)?

A

LMN symptoms at level of injury on relevant side

UMN symptoms below injury on relevant side(but not to LMN at levels below as multiple neurons/pathways/tracts influence a single LMN cell body compensating)

38
Q

What questions can you ask yourself to determine what symptoms a lesion will cause in a patient?

A
  1. What tracts are affected?
  2. What types of sensation/motor fibres do they carry?
  3. Where do they decussate?
39
Q

What is the corticobulbar tract?

A

Major motor pathway to the FACE initially running next to the corticospinal tract as they both descend from the cortex

40
Q

What is the rule for innervation in the corticobulbar tract?

A

Primary UMN innervation for left face comes from right contralateral cortex (minor innervation from left too) bilaterally

APART FROM unilateral contralateral supply to CN VII to lower face

41
Q

If a brainstem lesion caused lower motor neuron (LMN) in the head/neck, would you see any upper motor neuron (UMN) motor loss in the body? If so, where?

A

You would lose most motor movement of the body bilaterally too due to both sides of the corticospinal tract coming through the brainstem

42
Q

Describe the lateral vestibulospinal tract.

A
  1. Tract comes from vestibular nucleus in brainstem (pons/medulla) down the spinal cord
  2. Tract NEVER decussates
  3. Excites extensor LMN and inhibits flexor LMN to keep upright posture + balance (antigravity)
43
Q

What is a important influence on lower motor neuron (LMN) modulation?

A

Reticulospinal tract originating from brainstem nuclei in the pons/medulla with fibres running ipsilaterally

44
Q

What does the reticulospinal tract do to modulate lower motor neuron (LMN) activity?/

A

Normally UMN motor pathway (releases glutamate) excites LMN releasing ACh

However, this tract activates Renshaw cells (release glycine) which are inhibitory interneurons affecting the LMNs inhibiting the hyper-excitable LMNs

45
Q

What will happen if you reduce reticulospinal tract function?

A

Lost ability to inhibit hyper-excitable LMNs so muscle spasticity

46
Q

What are the main roles of the reticulospinal tract?

A

Locomotion, posture + moderating LMN activity:

  • Inhibit or excite LMNs (α and ϒ)
  • Modulate sympathetic activity
  • Modulate muscle activity/tone (especially in antigravity muscles)
  • Control emotional movement of facial expression muscles
47
Q

How can the reticulospinal tract act as a compensatory tract?

A

Locomotion centres may be involved in the partial recovery of motor function following spinal cord lesions e.g. patients can smile even if they have a bilateral corticobulbar lesion to CN VII due to this tract

48
Q

What are the 2 parts of the reticulospinal tract?

A
  1. Medullary

2. Pontine

49
Q

What does the medullary tract of the reticulospinal tract do?

A

Medullary tract and nucleus help to control sympathetic chain where reticulospinal neurons innervate preganglionic sympathetic fibres in lateral grey horn so cervical cord damage can lead to Horners syndrome with symptoms such as pupil constriction (miosis), vasodilation, ptosis + lack of sweating (anhidrosis)

50
Q

What are symptoms of lower motor neuron (LMN) disease?

A

Muscle weakness
Wasting
Areflexia
Fasciculations

51
Q

How does muscle wasting come about in lower motor neuron (LMN) disease?

A

It does NOT simply result from not using the muscle - the UMN and LMN are mutually dependent so patients can get neurogenic atrophy as well as denervation atrophy

52
Q

Why do upper motor neurons (UMNs) have opposite symptoms to lower motor neurons (LMNs)?

A

In UMN lesions, the LMN is typically hyper-excitable due to loss of inhibitory input from reticulospinal tract Renshaw cells so hyper-reflexia and spasticity occur whereas LMN lesions show the opposite symptoms e.g. hypo/are-flexia

53
Q

What is a disease that can cause lower motor neuron (LMN) disease?

A

Polio

54
Q

Describe the myotatic/muscle stretch/patellar tendon reflex.

A
  1. Passive muscle stretch sensed by muscle spindle of quadricep when hit with a reflex hammer
  2. Afferent neurons carry sensory information up + feeds into conscious/unconscious proprioceptive pathways
  3. Efferent motor neurons travel back down
  4. Reflex arc stimulates contraction of stretched muscle + inhibits antagonist muscle (reciprocal inhibition) relaxing the hamstring (corrective response)
55
Q

Describe the inverse myotatic/Golgi tendon reflex.

A
  1. GTO detects stretch in tendons of agonist muscle
  2. Reflex arc inhibits agonist muscle + stimulates antagonist muscle contraction
  3. If tension is great enough, this reflex will OVERIDE the myotatic reflex for protective reasons
56
Q

What is the flexor withdrawal reflex?

A

Quick withdrawal of a limb from a noxious stimuli mediated by free nerve endings with synaptic connections spanning several spinal cord levels:

  • Stimulates ipsilateral flexors of limb
  • Inhibits ipsilateral extensors of limb
57
Q

What is the crossed extensor reflex?

A

Ipsilateral flexor withdrawal + contralateral extensor activation