Neuro8&9 - Motor System

Question 1

3 general features of upper motor neurones (UMNs)

Location
Synapses
Lesion Causes x2

Answer 1

1. ) Location - CNS only
   - cell bodies found in the primary motor cortex (M1)
   - axons are projection fibres
   - not found in the cerebellum and basal ganglia
2. ) Synapses - inhibitory interneurones or LMNs
   - majority of UMNs synapse to inhibitory interneurones so only a few cause excitation of the LMN
3. ) Lesion Causes - brain or white matter of spinal cord
   - brain: stroke, infection, tumour, trauma, MS,
   - white matter: trauma, trans/hemisection of spinal cord

Question 2

5 general features of lower motor neurones (LMNs)

Location
Synapses w/ Sensory Neurones
Synapses w/ UMNs
Relation w/ Cranial Nerves
Lesion Causes x2

Answer 2

1. ) Location - CNS and PNS
   - cell bodies in the ventral horn of the spinal cord or:
   - also in the cranial nerve motor nuclei in the brainstem
   - axons found in the PNS going to the muscles
2. ) Synapses w/ Sensory Neurones
   - stimulated by primary afferent muscle spindles
   - can also be inhibited to cause certain reflexes (e.g. inhibition of antagonist hamstrings in patellar reflex)
3. ) Synapses w/ UMNs
   - inhibitory interneurones and excitatory UMNs
   - net inhibition of LMNs by UMNs via interneurones
   - LMNs then go on to synapse to the muscle
4. ) Relation w/ Cranial Nerves
   - cranial nerve motor nuclei are specialised LMNs
   - extension of the VH into the brainstem
   - other: extension of DH = sensory nuclei, extension of lateral horn = autonomic nuclei
5. ) Lesion Causes
   - injury to axons leaving the spinal cord
   - injury to the ventral grey matter of the spinal cord
   - e.g. GBS, polio, botulism, cauda equina syndrome etc.

Question 3

4 signs of LMN lesions

Flaccid Paralysis
Fasiculations
Fibrillation
Denervation Atrophy

Answer 3

1.) Flaccid Paralysis - muscle weakness with hypotonia and areflexia due to denervation

2. ) Fasiculations - small, involuntary muscle contractions which can be seen underneath the skin
   - due to up-regulation of muscle nAChRs to try to compensate for the denervation
3. ) Fibrillations - rapid, uncoordinated contraction of muscle fibres due to uncoordinated electrical activity
   - spontaneous action potientials due to lack of LMNs
   - not seen underneath skin, needs to be measured
4. ) Denervation Atrophy - muscle loses LMN innervation
   - loss of growth/trophic factors –> muscle wasting
   - greater amount of atrophy than disuse atrophy

Question 4

6 signs of UMN lesions

Spinal Shock
Spasticity
Babinski Sign
Clonus
Clasp-Knife Rigidity
Disuse Atrophy

Answer 4

1. ) Spinal Shock - flaccid paralysis followed by spasticity
   - must wait to see if a patient w/ flaccid paralysis gets spasticity to differentiate UMN or LMN lesion
2. ) Spasticity - hypertonia and hyperreflexia
   - due to loss of inhibitory interneurones
   - overstimulation of lower motor neurones
3. ) Babinski Sign - extension of the hallux when sole of the foot is stimulated with a blunt instrument
   - in healthy adults, the plantar reflex is hallux flexion
   - Babinski sign also seen as a primitive reflex in infants

4.) Clonus - involuntary, rhythmic muscle contractions and relaxation when a reflex is initiated

5. ) Clasp-Knife Rigidity - rapid ↓ in resistance when attempting to flex a joint when sufficient force is applied
   - strong stretch stimulates golgi tendon organs which inhibit the LMN that was previously hyperactive

6.) Disuse Atrophy - muscle weakness leads to less use of the muscle which leads to muscle wasting

Question 5

2 other features of UMN and LMN lesions

Sharp Transection
Complete Destruction (Blunt Transection)

Answer 5

1. ) Sharp Transection - UMN symptoms caudally
   - LMNs spared because the no of LMN cell bodies damaged is too small to create LMN symptoms
   - UMNs affected at cord level and below because the ascending and descending tracts are sliced through
2. ) Complete Destruction - LMN symptoms only in affected level
   - LMNs affected because large amount of LMN cell bodies are damaged so creates LMN symptoms
   - UMNs also affected since the tracts are destroyed
   - DO NOT get UMN symptoms because the LMN are also damaged so UMN symptoms CANNOT appear

Question 6

3 main motor tracts

Lateral Corticospinal Tract (LCT)
Ventral Corticospinal Tract (VCT)
Corticobulbar Tract (CBT)

Answer 6

1. ) Lateral Corticospinal Tract - UMN once it has decussated at the inferior/caudal medulla
   - controls fine movements of upper/lower limbs
   - found in the lateral funiculus of the spinal cord
2. ) Ventral Corticospinal Tract
   - decussates at the relevant spinal level (not medulla)
   - controls the movement of axial (spinal) muscles
   - found below the VH in the spinal cord
3. ) Corticobulbar Tract - UMNs of cranial nerves
   - synapses to LMNs of cranial nerves at the appropriate level in the brainstem, controlling motor function of CNs
   - CNs V, VII, IX, X, XI (not eye ones: III, IV, VI)
   - corticobulbar UMNs innervate the LMNs bilaterally (except lower half of face and CNXII)

Question 7

Pathway of the 3 main motor tracts (UMNs)

Primary Motor Cortex
Internal Capsule
Cerebral Peduncles
Decussation of Pyramids
Synapses to LMN

Answer 7

1.) Primary Motor Cortex - cell body of the UMN

2. ) Internal Capsule - convergence of white matter fibres of corona radiata, encapsulating the thalamus
   - UMN axons moves through the internal capsule to enter the cerebral peduncles
3. ) Cerebral Peduncles - found in the midbrain
   - contains UMN axons travelling from cortex –> pons
4. ) Decussation of Pyramids
   - CBT terminates in the brainstem, only 50% decussate
   - LCT decussate at the caudal medulla (85% of UMNs)
   - VCT decussate at the level of the spinal cord
5. ) Synapses to LMNs
   - CBT synapses to LMNs of cranial nerves
   - LCT to LMNs controlling distal muscles (limbs)
   - VCT to LMNs controlling proximal postural muscles

Question 8

3 regions in the internal capsule

Genu
Anterior Limb
Posterior Limb

Answer 8

1. ) Genu - the flexure of the internal capsule
   - contains UMNs of the corticobulbar tract (face)
2. ) Anterior Limb - in front of the genu
   - between lentiform nucleus and caudate
3. ) Posterior Limb - behind the genu
   - between lentiform nucleus and thalamus
   - anterior 2/3s has UMN axons of the corticospinal tract
   - contains motor and sensory for the arms and legs

Question 9

5 features of controlling the muscles of facial expression

Motor Neurones
Upper Half of Face
Lower Half of Face
Facial Nerve Lesions
UMN Lesions

Answer 9

1. ) Motor Neurones
   - UMNs (CBT) arise from the primary motor cortex
   - synapse to LMN axons of the facial nerve
2. ) Upper Half of Face - receives UMNs from the ipsilateral and contralateral side of the brain
3. ) Lower Half of Face - receives UMNs only from the contralateral side of the brain
4. ) Facial Nerve Lesions - transection of LMN axons
   - paralysis of all muscles of facial expression on ipsilateral side (Bell’s Palsy)
5. ) UMN Lesions - paralysis of lower half of the face on the contralateral side (due to unilateral innervation)
   - forehead is spared due to ipsilateral innervation

Question 10

A patient who previously had breast cancer presents with:
weakness and paresthesia in the right lower limb
loss of pain and temperature in the right lower limb
no other sensory features
wasting and fasciculations in the left quadriceps
up-going planters on the left foot

Where is the lesion?
What is the most likely cause of the lesion?
What other causes of the lesion could there be?

Answer 10

1. ) loss of spinothalamic modalities from L2/3 downwards on right side
   - lesion must appear in the ventral white commissure on the left side of the L2/3 spinal cord
2. ) no loss dorsal column modalities
   - lesion not in dorsal aspect of the spinal cord
3. ) LMN signs from L2/3 downwards on left side
   - cell bodies of LMNs appear in the VH
   - LMN signs appear ipsilaterally
4. ) Babinski sign on left side suggests UMN lesion
   - UMNs run through the lateral funiculus
   - appears on ipsilateral side because the UMN axons have already decussated (lateral corticospinal tract)
5. ) Location of Lesion - VH, ventral white commisure and lateral funiculus on the left side of the L2/3 spinal cord
6. ) Most Likely Cause - bone metastases from the breast cancer
7. ) Other Causes
   - motor neurone disease e.g. multiple sclerosis
   - vertebral/anterior spinal artery occlusion (supplies anterior 2/3 of the spinal cord)