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Quadrupedal Motor Systems

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Quadrupedal Motor Systems 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 Neuromuscular junction 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 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 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 9 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 (midbrain) • Affect timing, amplitude and pattern • Efferents via reticular formation, 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 -> interneuron -> g MN (most UMN) -> stretches muscle spindle 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, red nucleus, 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 – Rubrospinal tract 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 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 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: vestibulospinal tract is facilitatory to ipsilateral side Fig. 13.2 King 25 Why do we get spasticity with of UMN spinal cord lesions? 26 Pyramidal Motor System • Mammals only – Output from motor cortex: – Via crus cerebri (A) – longitudinal fibres of the pons (B) A • Corticopontine – To cerebellum and back to motor cortex • Corticonuclear A – e.g. to CNN nuclei of B brainstem B • Corticospinal tract, C – via medullary pyramids D (C,D), to spinal cord – Tracts decussate – Spinal cord C • 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 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-stroke Pyramidal Motor Where is the Lesion? System – Clinical significance of pyramidal lesions • Humans vs quadrupeds 29 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 = 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 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
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