Motor systems

Chris Thomson BVSc(Hons), Dip ACVIM (Neurol), Dip ECVN, PhD Associate Professor Neurobiology, Dept. of Vet. Med., University of Alaska, Fairbanks, 1 Alaska. Quadrupedal Motor Systems

What are their functions?

1. Antigravity support 2. Postural platform for movement 3. Movement initiation, maintenance and

termination Fig 5.3 Thomson and Hahn

2 Motor hierarchy

• Motor unit – LMN and NMJ • Reflexes • Central pattern generators (CPG) • UMN – Semiautomatic function – brainstem – Skilled/learned function – forebrain EMG study Kiwi chick • Motor planning centres

3 Motor unit = MN + innervated muscle cells Size determines degree of fine control Examples A B

B

Fig 1.4 Thomson and Hahn

A

4 UMN and LMN: the confusing couplet

Upper motor neurons (UMN) – central MN • Location: confined to brain and – ‘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

5 Motor systems

LMN also in CNN and visceral efferents (autonomic)

Picture of ‘Stephie’ By Catie, aged 6 6 Reflexes

• What is their physiological role in posture and locomotion? – Agonist-antagonist muscle interaction – Antigravity – Gait switch between retraction and protraction Fig 4.3 Thomson and Hahn 7 Fig 5.3 Thomson and Hahn

Appendicular muscle reflexes – Agonist-antagonist muscle interaction • Intersegmental connection propriospinal tract – Antigravity – Gait switch between retraction and protraction

8 Axial muscle myotatic reflex Effect on posture?

Fig 5.2 Thomson and Hahn

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http://www.vcahospitals.com/ Locomotion and reflexes

• Reflex wiring – Basis of locomotion in quadrupeds – Muscle stretch induces reflex contraction – Extensor postural thrust reflex – Crossed extension reflex

– Diagonal stepping reflex Fig 9.1 Thomson and Hahn

10 Movement facilitates movement Using reflex circuits Gait initiation Movement 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 11 Central Programme/pattern Generators • Basic motor control for rhythmical movement – Alternating contraction / relaxation – Locomotion, flying, scratching, breathing, chewing, micturition • CPG – Trigger neurons () • Affect timing, amplitude and pattern • Efferents via , reticulospinal tract to oscillator neurons http://almirah.deviantart.com/art/Moki-Run-Cycle – Oscillator neurons (spinal cord) • Alternating support (extensor) and swing (flexor) phase • Alternating limbs – Influence LMN

12 How can this dog still walk?

13 Spinal reflexes and amplification • UMN Connection to LMN – UMN -> -> g MN (most UMN) -> stretches Amplification stage -> reflex a MN firing

• Clinical significance 1. Few UMN required to trigger oscillator neurons in intumescence 2. Amplification of signal via ɣ motor neurons

14 What about Spinal Walking? Fig 5.2 Thomson and Hahn 15 UMN centres

• Brainstem – origin of semi-automatic movements • Forebrain – skilled/learned movements

Fig 9.4 Thomson and Hahn Fig 4.15 Thomson and Hahn

16 Divisions of Motor Systems

• Extrapyramidal – Most important in quadrupeds • Pyramidal – Highly important in humans

Fig 8.50, Dyce, Sack and Wensing, 4th ed.

17 Extrapyramidal System

• Origin – All brain divisions • e.g. basal nuclei, , pontine and medullary reticulospinal, vestibulospinal, tectospinal tracts • Multisynaptic • Ipsi- and contralateral projection • Termination – a and g MN brainstem and spinal cord

18 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 Fig 4.2 Thomson and Hahn – Extensor spasticity after TL lesion

19 Spinal cord motor tracts

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

Fig 4-5 Thomson and Hahn

20 Extrapyramidal Tract Function

• Rubrospinal • Important in dogs and cats • Semiskilled and postural (flexor) activity

• Reticulospinal – Medullary • Suppresses antigravity muscle activity – Pontine • Standing posture

21 http://www.releasethehounds.com/media Extrapyramidal Tract Function

• Vestibulospinal tracts (VST) • Lateral VST – From lateral (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 Fig 8.5 Thomson and Hahn • 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 22 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’ 23

https://s-media-cache-ak0 Corpora quadrigemina • Rostral colliculus • Caudal colliculus

Thomson and Hahn Fig A7 24 Extrapyramidal system • Red lines are facilitatory • Black lines are inhibitory

• NOTE: is facilitatory to ipsilateral side

Fig. 13.2 King

25 Why do we get spasticity with of UMN spinal cord lesions?

26 Pyramidal • Mammals only – Output from : – Via crus cerebri (A)

– longitudinal fibres of the (B) A • Corticopontine – To and back to motor cortex • Corticonuclear A

– e.g. to CNN nuclei of B brainstem B • , C – via medullary pyramids D (C,D), to spinal cord – Tracts decussate – Spinal cord C • 75% decussate at C1-2 into (LF) • rest in VF, decussate just b/4 termination Fig A3 Thomson and Hahn Dog brain, ventral aspect 27 D Motor cortex output

• Function http://www.horsenation.com/ – Skilled /learned movement • Humans/primates – 30% spinal cord WM • Quadrupeds – Dogs 10% spinal cord WM – c/w ungulates – Note » horses, camelids » raccoons

28 Fig 8.50, Dyce, Sack and Wensing, 4th ed. Human Pons XS: 30 years post- Pyramidal Motor Where is the Lesion? System – Clinical significance of pyramidal lesions • Humans vs quadrupeds

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th Fig 8.50, Dyce, Sack and Wensing, 4 ed. Ovine pons, Thomson and Hahn Fig A30 30 31 Why the difference with a forebrain lesion?

http://graphics8.nytimes.com 32 Fig 4-10, Thomson and Hahn Fig 8-14 deLahunta and Glass 33 Basal nuclei - components

Note red = , blue = .

A. Caudate nucleus B. C. D. Putamen E. External capsule F. Claustrum G. Extreme capsule

Corpus = basal nuclei and intervening WM

FE C

34 Basal nuclei – What’s this dog’s presenting sign? function

• Humans – disease affecting BN? • Feedback circuits – modify motor output – Ritual movements? • ‘Ordering the component parts of Photo courtesy Kate Hill complex movement’ (Jenkins) – Lesions • putamen – propulsive activity • globus pallidus – hypoactive • caudate n. – athetoid movements • Effect of unilateral lesion?

Forebrain neoplasia Differentiating disease in UMN versus LMN

NeuroRAT Reflexes Atrophy Tone

Fig 5.6 Thomson and Hahn Sign UMN – central MN dz LMN – peripheral (damaged UMN) MN dz (damaged LMN)

Reflexes Intact (increased) Decreased/absent

Atrophy Disuse: mild Neurogenic: severe, generalised specific muscles

Tone Intact (increased) Decreased/absent

36 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 Fig 9.6 Thomson and Hahn hypoactivity) – Schiff-Sherrington – acute thoracolumbar lesion

37 Henry 7 yo MN Corgi, LMN lesions Hx 1 mo progressive RPL lameness

• ↓/0 Reflexes • neurogenic atrophy • ↓/0 tone

38 Coordination of movement

39 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 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 42 • Forebrain motor centres Postural platform

• Planned motor activity – Inform cerebellum – Cerebellum checks body posture

(SCP) Fig 7.9 Thomson and Hahn – 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 – 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 Evans, 18-4 and 18-41 • Cerebellovestibular Cerebellar peduncles – bilaterally paired • Cerebelloreticular Name for their position of attachment to the brainstem • Rostral – 12 (upper image); 6 – lower image • Middle 10 • Caudal 11; 3 44 Sequential images

Caudal CP (?) Lateral aperture Caudal and rostral CP (?) Rostral CP Middle CP (?) Transverse fibres of the pons Cerebellar Efferents

Purkinje (pyramidal) cells – May be stimulated or inhibited

http://image.slidesharecdn.com/ – They are inhibitory histologyofnervesystem • to vestibular nuclei – direct inhibition • to excitatory cerebellar nuclei – Decrease their facilitation of motor activity

– indirect inhibition Fastigial CN – Lateral cerebellar nucleus Interposital CN

» To forebrain Lateral CN – Interposital nucleus » To red nucleus and reticular formation – » To vestibular nucleus and reticular formation

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Fig 7.6c Thomson and Hahn 47 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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