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Flashcards in 5. The motor system Deck (9):
1

describe the basic neuronal chain in the motor pathway

1. UPPER MOTOR NEURONE
- cell body in primary motor cortex (pre-central gyrus)
- axon extends in CNS to ventral horn grey matter - synapses with LMN

2. LOWER MOTOR NEURONE
- cell body in ventral horn (or brainstem motor nuclei for cranial nerves)
- axon projects through peripheral nerves to skeletal muscle target

2

describe the pathway of UMNs

i. Cell bodies in primary motor cortex...
ii. axons run through corona radiata (white matter sheet), condense into internal capsule (between thalamus and lentiform nucleus) and form cerebral peduncle in midbrain...
iii. axons run through ventral medullary pyramids where they decussate...
iv. join the lateral corticospinal tract down spinal cord...
v. synpase with cell body of LMN in ventral horn of relevant spinal level

3

do all UMNs decussate at the medullary pyramids

no, 15-20% remain ipsilateral and then decussate at relevant spinal level (form anterior corticospinal tract)

4

how do UMNs affect LMNs at synapses

can be:
- excitatory (direct synapse)
- inhibitory (excitatory effect of inhibitory interneurones)

net effect of UMNs on LMNs is inhibitory

5

describe the role of LMNs patellar reflex

1. sensory afferent neurone from muscle spindle runs through dorsal spinal root (L3) to synapse with LMN in ventral horn...

2. LMN conducts impulses from L3 ventral motor horn to quad muscles to stimulate contraction

3. branch of L3 sensory afferent neurone also runs down spinal cord to L5... synapses with inhibitory interneurone... inhibits L5 LMN to hamstrings to prevent hamstring contraction from inhibiting reflex

6

describe 5 signs of LMN lesions

1. WEAKNESS: interrupt info. pathway from neurone to cortex/UMN to muscle

2. AREFLEXIA: cannot complete reflex arc

3. MUSCLE WASTING: LMN provides muscle with trophic factors which cross synapse and interact with muscle cell membrane

4. FASICULATION: uncoordinated muscle contractions

5. HYPOTONIA: decreased muscle tone as no constant low level contraction

7

describe 4 signs of UMN lesions

1. WEAKNESS: loss of LMN activation

Days-weeks later:

2. HYPERTONIA: increased muscle tone (rigid) - as net effect of UMNs on LMNs is inhibitory

3. HYPERREFLEXIA: enhanced reflexes as stimulation from sensory neurones don't need to be strong to activate reflex

4. EXTENSOR PLANTAR REFLEX: big toe extension instead of flexion - revert to less mature descending modulation similar to babies

8

describe the motor pathways controlling facial muscles

Facial motor nuclei containing cell bodies of LMN to facial muscles are separated into 2 halves that supply upper and lower face.

Upper portion of nuclei are controlled by UMNs from both sides of motor cortex (i.e. dual innervation).

Lower portion of nuclei are controlled by UMNs from contralateral cortex (decussate in midline).

9

A lesion in the right UMNs to facial muscles will affect which part of the face

Left lower part of face (upper face will be spared as has dual innervation so still receives stimulation from left UMN)