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Motor systems
Chris Thomson
BVSc(Hons), Dip ACVIM (Neurol), Dip ECVN, PhD
Associate Professor Neurobiology,
Dept. of Vet. Med.,
University of Alaska, Fairbanks,
Alaska.
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Quadrupedal Motor Systems
What are their functions?
1. Antigravity support
2. Postural platform for
movement
3. Movement initiation,
maintenance and
terminationFig 5.3 Thomson and Hahn
Motor hierarchy• Motor unit – LMN and NMJ
• Reflexes
• Central pattern generators
(CPG)
• UMN
– Semiautomatic function
– brainstem
– Skilled/learned function
– forebrain
• Motor planning centres
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EMG study Kiwi chick
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Neuromuscular junction
Fig 1.4 Thomson and Hahn
Motor unit = MN + innervated
muscle cells
Size determines degree of fine
control
Examples
A
B
A
B
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UMN and LMN:
the confusing couplet
Upper motor neurons (UMN) – central MN• Location: confined to brain and spinal cord
– ‘Management’
– Control motor activity
» Initiate, regulate, terminate
– Lower motor neurons (LMN) – peripheral MN• Location – nerve cell body in CNS, axon in PNS
– ‘Workers’
– Connect to muscle of body, limb or head
– Key part of the reflex
– Spinal and cranial nerves
» Cause muscle to contract
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Motor systems
Picture of ‘Stephie’ By Catie, aged 6
LMN also in CNN and visceral efferents (autonomic)
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Reflexes
• What is their
physiological role in
posture and locomotion?
– Agonist-antagonist
muscle interaction
– Antigravity
– Gait switch between
retraction and
protractionFig 4.3 Thomson and Hahn
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Appendicular muscle
reflexes– Agonist-antagonist
muscle interaction• Intersegmental connection
propriospinal tract
– Antigravity
– Gait switch between
retraction and protraction
Fig 5.3 Thomson and Hahn
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Axial muscle myotatic reflex
Fig 5.2 Thomson and Hahn
Effect on posture?
http://www.vcahospitals.com/
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Locomotion and reflexes
Fig 9.1 Thomson and Hahn
• Reflex wiring
– Basis of locomotion in quadrupeds
– Muscle stretch induces reflex
contraction
– Extensor postural thrust reflex
– Crossed extension reflex
– Diagonal stepping reflex
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Movement facilitates movement
Using reflex circuits
Gait initiationMovement changes sensory (proprioceptive) input
motor neuron excitation
• Sensory input stimulates reflex function
• Same limb e.g. hip extension reflex hip flexion
• Other limbs e.g. limb flexion crossed extension, diagonal stepping
• Spinal reflexes are the basis of movement
• Used by central pattern generators
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Central Programme/pattern
Generators• Basic motor control for rhythmical movement
– Alternating contraction / relaxation
– Locomotion, flying, scratching, breathing, chewing, micturition
• CPG
– Trigger neurons (midbrain)
• Affect timing, amplitude and pattern
• Efferents via reticular formation, reticulospinal tract to oscillator neurons
– Oscillator neurons (spinal cord)
• Alternating support (extensor) and swing (flexor) phase
• Alternating limbs
– Influence LMN
http://almirah.deviantart.com/art/Moki-Run-Cycle
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How can this dog still walk?
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Spinal reflexes and
amplification
• UMN Connection to LMN
– UMN
-> interneuron
-> g MN (most UMN)
-> stretches muscle spindle
Amplification stage
-> reflex a MN firing
• Clinical significance1. Few UMN required to trigger oscillator neurons in
intumescence
2. Amplification of signal via ɣ motor neurons
What about Spinal Walking?Fig 5.2 Thomson and Hahn
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UMN centres
• Brainstem – origin of semi-automatic movements
• Forebrain – skilled/learned movements
Fig 4.15 Thomson and HahnFig 9.4 Thomson and Hahn
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Divisions of Motor Systems
• Extrapyramidal
– Most important in
quadrupeds
• Pyramidal
– Highly important in
humans
Fig 8.50, Dyce, Sack and Wensing, 4th ed.
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Extrapyramidal System
• Origin
– All brain divisions
• e.g. basal nuclei, red nucleus, pontine and
medullary reticulospinal, vestibulospinal,
tectospinal tracts
• Multisynaptic
• Ipsi- and contralateral projection
• Termination
– a and g MN brainstem and spinal cord
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Extrapyramidal System
• Function
– Posture and locomotion
– Synapses primarily onto g-MN
– Inhibitory
• Medullary reticulospinal tract
– Loss -> UMN spasticity
– Excitatory
• Extensor muscle facilitation
– Vestibulospinal, tectospinal, pontine reticulospinal tracts
• Flexor muscle facilitation
– Rubrospinal tractFig 4.2 Thomson and Hahn
Extensor spasticity after TL lesion
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Spinal cord motor tracts
Fig 4-5 Thomson and Hahn
ID Name
A Propriospinal (spino-spinal)
H Rubrospinal
I Lateral corticospinal
J Lateral tectotegmentospinal
K Medullary (lateral) reticulospinal
L Pontine (ventral) reticulospinal
M Lateral vestibulospinal
N Tectospinal
O Ventral corticospinal
P Medial vestibulospinal and medial
longitudinal fasciculus
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Extrapyramidal Tract Function
• Rubrospinal• Important in dogs and cats
• Semiskilled and postural
(flexor) activity
• Reticulospinal– Medullary
• Suppresses antigravity muscle activity
– Pontine • Standing posture
http://www.releasethehounds.com/media
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Extrapyramidal Tract Function
• Vestibulospinal tracts (VST) • Lateral VST
– From lateral vestibular nuclei (VN)
– Stimulated by static head position
– Ipsilateral antigravity muscles whole body
• Medial VST– From medial, rostral and caudal VN
– Stimulated by head acceleration
– Output to neck/shoulder muscles
» Maintains head posture
• Medial longitudinal fasciculus– Medial VN (and other brainstem nuclei)
– VF – neck and cranial thoracic cord
– Brainstem to CN III, IV, VI nuclei
– Coordination eye, neck and TL posture during head movement
Fig 8.5 Thomson and Hahn
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Extrapyramidal Tract Function
• Tectospinal tracts – Lateral (tectotegmentospinal)
• UMN for sympathetic output to eyes– To T1/T2 spinal cord segments
• Active pupillary dilation in response to dim light
– Medial • From the corpora quadrigemina
– Rostral and caudal colliculi
• Function – head/neck movement in response
visual/auditory stimuli
» ‘Visual grasp’, ‘auditory grasp’
https://s-media-cache-ak0
24Thomson and Hahn Fig A7
Corpora quadrigemina
• Rostral colliculus
• Caudal colliculus
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Extrapyramidal system
• Red lines are facilitatory
• Black lines are inhibitory
• NOTE: vestibulospinal tract is
facilitatory to ipsilateral side
Fig. 13.2 King
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Why do we get spasticity with of
UMN spinal cord lesions?
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Pyramidal Motor System• Mammals only
– Output from motor cortex:
– Via crus cerebri (A)
– longitudinal fibres of the pons (B)
• Corticopontine
– To cerebellum and back to motor cortex
• Corticonuclear
– e.g. to CNN nuclei of brainstem
• Corticospinal tract,
– via medullary pyramids (C,D), to spinal cord
– Tracts decussate
– Spinal cord
• 75% decussate at C1-2 into lateral funiculus (LF)
• rest in VF, decussate just b/4 termination Fig A3 Thomson and Hahn
Dog brain, ventral aspect
A
A
B
C
D
D
C
B
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Motor cortex output• Function
– Skilled /learned movement
• Humans/primates
– 30% spinal cord WM
• Quadrupeds
– Dogs 10% spinal cord WM
– c/w ungulates
– Note
» horses, camelids
» raccoons
http://www.horsenation.com/
Fig 8.50, Dyce, Sack and Wensing, 4th ed.
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Pyramidal Motor
System
– Clinical significance
of pyramidal lesions
• Humans vs
quadrupeds
Human Pons XS: 30 years post-stroke
Where is the Lesion?
Ovine pons, Thomson and Hahn Fig A30Fig 8.50, Dyce, Sack and Wensing, 4th ed.
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Why the difference with a forebrain
lesion?
http://graphics8.nytimes.com
Fig 4-10, Thomson and Hahn
33Fig 8-14 deLahunta and Glass
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Basal nuclei - components
Note red = grey matter,
blue = white matter.
A. Caudate nucleus
B. Globus pallidus
C. Internal capsule
D. Putamen
E. External capsule
F. Claustrum
G. Extreme capsule
Corpus striatum = basal nuclei
and intervening WM
CEF
Basal nuclei –
function
• Humans
– disease affecting BN?
• Feedback circuits
– modify motor output
– Ritual movements?
• ‘Ordering the component parts of
complex movement’ (Jenkins)
– Lesions
• putamen – propulsive activity
• globus pallidus – hypoactive
• caudate n. – athetoid movements
• Effect of unilateral lesion?
Forebrain neoplasia
Photo courtesy Kate Hill
What’s this dog’s presenting sign?
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NeuroRATReflexesAtrophy Tone
Differentiating disease in UMN versus LMN
Fig 5.6 Thomson and Hahn
Sign UMN – central MN dz
(damaged UMN)
LMN – peripheral
MN dz (damaged
LMN)
Reflexes Intact (increased) Decreased/absent
Atrophy Disuse: mild
generalised
Neurogenic: severe,
specific muscles
Tone Intact (increased) Decreased/absent
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UMN lesions
• Clinical effect of UMN lesions
– Depends on lesion location
• Rigidity/spasticity
– Loss of inhibitory input
» From forebrain – decerebrate rigidity
» From medullary reticular formation – limb and trunk hypertonus
• Paresis/paralysis
– Loss of movement initiation
– Decreased facilitation LMN
– Loss of skilled motor activity/control
» Motor cortex (visual placing is a good test)
• Postural abnormalities
– Decerebrate rigidity – mesencephalic lesion
– Pleurothotonus – mesencephalic lesion
– Decerebellate rigidity – rostral cerebellum
– Head tilt – vestibular dysfunction
– Torticollis – forebrain or neck LMN (hyper or hypoactivity)
– Schiff-Sherrington – acute thoracolumbar lesion
Fig 9.6 Thomson and Hahn
LMN lesions
• ↓/0 Reflexes
• neurogenic atrophy
• ↓/0 tone
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Henry 7 yo MN Corgi,
Hx 1 mo progressive RPL lameness
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Coordination of movement
Cerebellar Function– To coordinate posture and movement
• Receives input information about
– Position and movement of body
parts
» Spinocerebellar
» Vestibulocerebellar tracts
– Planned motor activity
» Forebrain
» Extrapyramidal system
• Send output to
– Brainstem UMN centres
– Forebrain
» motor planning centres
Cerebellar function
• Continual input from
– Muscles and joints (SCP) – head,
neck, trunk, limbs, tail
– Vestibular system – head position
– Motor planning centres
• Modifies output from UMN centres
– Forebrain (skilled) and brainstem
(semi-automatic)
– Coordinate agonist-antagonist muscle
function
– At rest and during locomotion
• Sets the postural platform
– On which motor activity can occur
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Functional connections of the cerebellum
Cerebellar afferents:
•Proprioceptive information from trunk, limbs and head
•Motor planning
• Motor cortex (voluntary) – via cortiocpontocerebellar
• Extrapyramidal from forebrain and midbrain, via olivary nucleus
•Cerebellar efferents• Brainstem UMN nuclei
• Forebrain motor centres
Postural platform
Fig 7.9 Thomson and Hahn
• Planned motor activity
– Inform cerebellum
– Cerebellum checks body posture
(SCP)
– Cerebellar efferents to UMN centres
sets postural platform (UMN
coordination)
– New SCP to cerebellum
– Cerebellum informs motor cortex
– Motor activity occurs
• Cerebellar dysfunction Postural
paralysis
Cerebellar peduncles
• Rostral CP– Afferent
• ventral spinocerebellar tract
– Efferent • cerebellar nuclei to midbrain and forebrain UMN centres
• Middle CP– Afferent only
• corticopontocerebellar tract
• Caudal CP– (restiform and juxtarestiform bodies)
– Afferent • Spinocerebellar (dorsal, cranial, cuneocerebllar),
• vestibulocerebellar,
• olivocerebellar,
• reticulocerebellar (pontine and medullary)
– Efferent• Cerebellovestibular
• Cerebelloreticular
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Evans, 18-4 and 18-41
Cerebellar peduncles – bilaterally paired
Name for their position of attachment to the brainstem
• Rostral – 12 (upper image); 6 – lower image
• Middle 10
• Caudal 11; 3
Sequential images
Lateral aperture Caudal and rostral CP (?) Rostral CP Middle CP (?)Caudal CP (?)
Pontine nuclei
Transverse fibres of the pons
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Cerebellar
Efferents
Purkinje (pyramidal) cells
– May be stimulated or inhibited
– They are inhibitory
• to vestibular nuclei
– direct inhibition
• to excitatory cerebellar nuclei
– Decrease their facilitation of motor activity
– indirect inhibition
– Lateral cerebellar nucleus
» To forebrain
– Interposital nucleus
» To red nucleus and reticular formation
– Fastigial nucleus
» To vestibular nucleus and reticular formation
Fig 7.6c Thomson and Hahn
http://image.slidesharecdn.com/
histologyofnervesystem
Lateral CN
Fastigial CN
Interposital CN
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Locomotion Summary
• Spinal reflexes and CPG
– Foundation of movement
• Supraspinal input
– Initiates
– Terminates
– Coordinates
– Modulates spinal reflexes
-> many, varied patterns
of movement
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