Week 6 Notes On Control Of Movement by Central Motor Pathways Flashcards
somatomotor pathways
originate from UMNs in cerebral cortex and brainstem; axons from UMNs travel to brainstem and spinal cord to influence activity in LMNs
role of descending somatomotor pathways
- maintain appropriate body position (posture)
- permit the animal to move around in their environment (locomotion)
- control directed movement of the body relative to external environment
effective motor output acomplished
by coordination of efforts of multiple somatomotor pathways and cerebellum and basal ganglia which interact w/ somatomotor pathways to facilitate coordination
final common pathway for motor system
LMN in brainstem or spinal cord; LMN damaged UMN rendered useless
hierarchical organization of neural circuitry
- Spinal cord (lowest)
- Brainstem
- Motor cortex (highest)
spinal cord responsible for
- most basic or automatic behaviors ie maintenance of muscle tone, reflexes, and v limited ability to generate some movement involved in locomition
sensory input to spinal cord
- directly relayed to LMNs
- indirectly relayed via network of interneurons
which brainstem nuclei give rise to motor pathways
vestibular nuclei, red nucleus, UMNs of pontine and Medullary Reticular Formation and Rostral Colliculus
brainstem nuclei contain
UMNs which project to spinal cord or brainstem to influence LMNs or spinal cord reflex circuits
motor nuclei in brainstem receive and integrate info from
spinal cord, cerebellum, basal ganglia, thalamus, cortex, and special sense
without inputt from cerebral cortex brainstem can
mediate much more coordinated and useful motor fxs than spinal cord alone maintaining posture and basic locomotion
motor cortex location
frontal lobe of neocortex
motor cortex receives and integrates
highly processed information from association cortical areas, basal ganglia and cerebellum
descending pathways from motor cortex can
influence LMNs in brainstem and spinal cord for precise, specific movements
cortical UMNs can control movements by
influencing UMNs in Red Nucleus or Reticular formation of brainstem
UMNs in motor cortex required for
postural runs and complex highly coordinated and/ or visually guided movements
central motor pathways
- corticospinal
- rubrospinal
- reticulospinal
- vesitbulospinal
- tectospinal
LMNs in brainstem in which nuclei
- Trigeminal motor nucleus
- Facial nucleus
- Hypoglossal nucleus
- Nuclei of CN III, IV, VI
- axons from UMNs in motor cortex can terminate on these nuclei*
single UMN can accomplish useful combination of muscle activation
by synapsing on multiple LMNs
interneurons
allow UMNs to synapse on multiple LMNs
- also hardwire compensatory postural movements like crossed extensor reflex
what converge on spinal networks or directly on LMNs to control ovement
multiple descending somatomotor pathways along with local reflex pathways
postural rxns in spinal cord primarily facilitated by
vestibulospinal and reticulospinal tracts
various inputs to LMN
- Reticulospinal Tract
- Vestibulospinal tract
- contralateral interneurons
- Rubrospinal tract
- proprioceptive afferent
- nociceptor afferent
- corticospinal tract
reticulospinal tract
UMN activates LMNs for locomotion and postural compensation
vestibulospinal tract
UMN activates ipsilateral extensor LMNs for balance and posture
contralateral interneurons
involved reflex activity such as crossed extensor response
rubrospinal tract
UMN mediates cortically controlled movements and locomotion and modulates activity in reflex circuits via excitatory and inhibitory interneurons
proprioceptor afferent
ex. spindle afferents directly excite extensor LMNs to maintain muscle ton and weight bearing for postural compensation
nociceptor afferent
will excite ipsilateral flexor LMNs (not shown) and inhibit ipsilateral extensor LMNs via interneurons (withdrawal reflex)
corticospinal tract
UMN controls voluntary and complex movements of distal limbs and modulates activity in reflex circuits via excitatory and inhibitory interneurons
medial pathways
include reticulospinal and vestibulospinal pathways
medial pathways primarily influence
axial and proximal limb muscles especially extensors
axons from medial pathways
descend spinal cord ipsilaterally or bilaterally in ventral white matter of spinal cord to influence LMNs in more medial aspect of VH (LMNs to proximal limb muscles)
UMNs medial pathways
often branch to terminate on many if not all spinal cord segments; not uncommon for some branches to cross midline and innervate contralateral LMNs
bilateral and far reaching projections of medial pathways permit
coordination of many muscles to maintain posture, regulate muscle tone, and control locomotion
lateral pathways
include corticospinal pathway and rubrospinal pathway
lateral pathways primarily influence
muscles of limb and distal limb especially flexors
axons from lateral pathways descend spinal cord in
dorsolateral funiculus
axons from lateral pathways synapse on
interneurons or directly on LMNs in lateral aspect of ventral horn
- these pathways have few synaptic interuptions
UMNs lateral pathways terminate
unilaterally on limited number of spinal cord segments
lateral pathways important for
voluntary directed movements of limbs for interacting with objects in the enivonrment; pattern of UMN projections and synapses on LMNs reflects their control of specific and limited muscle groups and therefore specific targeted movements
motor pathways that originate in cd brainstem
medial and lateral vestibulospinal pathways, pontine and medullary reticulospinal tracts, tectospinal tract, rubrospinal tract
rubrospinal tract UMNs and LMNs
UMNs in red nucleus; LMNs in spinal cord
rubrospinal pathway
afferent input to ipsilateral cerebellum -> decussate -> somatosensory cortex -> motor cortex -> red nucleus -> decussate -> reticulospinal UMNs -> LMNs to limbs
afferent input to rubrospinal pathway
DC-ML and spinocerebellar pathways
summarized pathway rubrospinal pathway
- UMNs in red nucleus in midbrain
- UMNs decussate in midbrain
- Descend the spinal cord in lateral funiculus
Rubrospinal pathway controls
- movements at various joints of limbs, excluding digits
- voluntary targeted movements of limbs
- red nucleus and midbrain motor circuits: important role in initiating and coordinating locomotion
motor cortex and red nucleus
motor cortex synapses on red nucleus and exerts control over gait modification and postural rxn by synapsing on red nucleus
resotral midbrain lesions that damage red nucleus can
result in contralateral gait and postural rxn deficits
lesions where can interrupt rubrospinal tract to ipsilateral limb
lesions of cd midbrain, pons or medulla interrupt rubrospinal pathway to ipsilateral limb
UMN deficits from lesion interrupting rubrospinal tract on ipsilateral side
spastic paresis +/- hyperreflexia
corticosponal pathway (aka pyramidal tract) fx
- predominant pathway for voluntary control of movement especially in distal limbs and digits in primaries not super important in cats and dogs we should not involve this for anything clinical
coritcospinal pathway pathway
- motor cortex in frontal lobe
- UMNs travel in
- Internal capsule
- Crus Cerebri
- Longitudinal fiber of the pons
- pyramids
3a. Cd medulla most axons decussate and descend spinal cord in dorsolateral funiculus
4a. Synapse on interneurons or LMNs in lateral VH (where LMNs to distal limb muscles are located)
3b. axons that did not decussate descend in ventral funiculus; will influence LMNs -> axial and ipsilateral proximal limb muscles (which play role in feed forward postural adjustments associated with voluntary movement)
ischemic event knocking out motor cortex fx
acute loss of motor cortex function if ischemic event effects frontal lobe may produce clinical signs consistent with UMN lesion like contralateral spastic paresis, deficits in postural runs and sometimes hyper-reflexia but these are usually short lived b/c other pathways in motor system are able to compensate for loss of motor cortex; postural rxn deficits will persist
animals with gradual progressive lesion of motor cortex
show little or no evidence of this lesion in its muscle tone, reflexes, or gait, unless gait is assessed on uneven terrain or with obstacles or if animal is circled; postural rxn deficits will persist
corticospinal pathway UMNs and LMNs
UMNs- in cerebral cortex
LMNs- in spinal cord
* UMNs synapse directly on LMNs)
* can be contralateral or bilateral*
vestibulospinal pathway
- important for maintaining muscle tone, balance, and posture
vestibulospinla pathway activity
depends predominantly on input from vestibular apparatus and cerebellum
- medial and lateral vestibulospinal tracts
cerebral cortex and vestibulospinal pathway
cerebral cortex has no direct control over activity in vestibulospinal pathway
medial vestibulospinla pathway projection
-bilateral projection to cervical spinal cord via MLF and ventromedial funiculus
medial vestibulospinal pathway provides innervation to
neck muscles controlling head position, therefore controls movements of head for maintaining posture and balance
lateral vestibules spinal pathway projects
mostly ipsilaterally to all levels of spinal cord via ventromedial funiculus
Lateral vestibulspinal pathway excites and inhibits
LMNs to ipsilateral axial and proximal limb extensors, inhibits LMNs innervating ipsilateral flexors
activity in lateral vestibular nucleus
on either side; pushes body in opposite direction
lateral vestibulospinal pathway facilitates and inhibits
facilitates ipsilateral stretch reflex for extensor muscles and inhibits contralateral stretch reflex therefore lesions involving vestibular nuclei can affect general muscle tone and stretch reflexes
vestibulospinal pathway UMNs and LMNs
UMNs in rostral medulla
LMNs in spinal cord
if ____bulbar pathway not ____spinal pathway
then LMNs are in brainstem if bulbar in spinal cord if spinal
pontine and medullary reticulospinal tracts fx
posture and locomotion; particularly controlling axial and proximal limb muscles
reticulospinla tracts and cortical input
get cortical input but don’t require it to stimulate locomotion; getting pushed or pulled can -> locomotion
- motor cortex UMNs control locomotion circuits that reaction to conscious awareness of wanting to move toward something like a cookie ect.
medullary reticulospinal UMNs
largely facilitate flexor muscles; receive signficiant amount of excitatory input form motor cortex and red nucleus
pontine reticulospinal UMNs
facilitate extensor muscles
- these neurons important in support phase of locomotion of in stabilizing posture via ipsilateral extensors during a movement of contralateral limb
neurons of pontine reticulospinal UMNs receive input from
- can be corticaly controlled by UMNs for anticipatory postural adjustments
- also receive input including input from spinal cord proprioceptive afferents and vestibular afferents and are v active in absence of cortical input
motor cortex projects onto pontine and medullary reticulospinal tract to
control activity in reticulospinal UMNs to
- Make gate adjustments based on visually detected obstacles or terrain irregularities
- control postural rxns
- mediate “voluntary” directed locomotion such as approaching a visual stimulus
* motor cortex tells reticulospinal neurons what it wants to accomplish and reticulospinal neurons create motor pattern required for locomotion*
lesions affecting reticulospinal UMNs in brainstem or spinal cord
produce ipsilateral spastic paresis or paralysis which will be manifested in gait
Tectospinal tract arises from
rostral colliculus and controls muscles in neck
tecetospinal tract important for
orienting movement
isolated lesions of rostral colliculus
would affect tectospinal tract but isolated lesions of rostral colliculus are rarely observed clinically but may result in ipsilateral turning and circling
tectum projects to
brainstem circuitry that controls eye movements which must be coordinated with movements of head when animal is turning to look at something
rubrospinal tract midbrain lesion ipsi or contralateral
could affect both sides bc a lot of decoration here
rubrospinal tract motor cortex and red nucleus
contralateral then decoration in midbrain then ipsilateral
sensory circuits going through cerebellum vs those going through cd brainstem
can knock out the ones in cd brainstem and everything is fine bc ones going to cerebellum sufficient but if knock out ones in cerebellum will have deficits bc ones in cd brainstem are not sufficient
red nucleus
can control input from cortico-rubrospinal tract; red nucleus gets a lot of input from cerebellum
motor cortex is essential for
certain limb movements including postural runs, navigating obstacles or uneven terrain during locomotion, and making targeted movements of limbs
to coordinate movements of limbs motor cortex is essential for
axons from UMNs in motor cortex can terminate on UMNS in brainstem
cortical UMNs can synapse in reticular formation to
influence reticulospinal tracts for voluntary locomotion and feed forward implementation of postural adjustments
in domestic animals motor cortex exterts control of
motor function predominantly by synapsing on UMNs of rubrospinal and reticulospinal tracts rather than by making direct synapses on LMNs via corticospinal tract
When evaluating patients consider lesions of
- cerebral cortex
- midbrain
- pons
- medulla
- spinal cord zone
- L vs R side
ability to asses motor fxs test
- Muscle tone
- Reflexes
- Postural rxns
- Locomotion (looking for paresis/ paralysis)
most fundamental nervous system requirement for muscle contraction and therefore movement of anytype
LMN
if LMNs damaged in CNS, ventral roots, or peripheral nerves animal will demonstarate
decreased or absent muscle tone, reflexes, and postural runs as well as flaccid paresis/ paralysis; muscle will also undergo profound atrophy
damage to UMNs in spinal cord
- results in normal or increased muscle tone/ reflexes
- postural rxn deficits and spastic paresis or paralysis of gait
damage to lesion in c1-c5 spinal cord vs in brain
c1-c5 lesion may impact all UMNs thet control a limb but lesions in brain may spare some UMNs depending on how far rostral lesion is
lesion in cd medulla vs in pons
lesion in cd medulla has potential to impact all UMNs to the limbs; lesion in pons will impact many UMNs but leave those that originate cd to lesion intact
cortical UMNs originate
in motor cortex in cerebral hemisphere contralateral to the limb
acute lesion of the of motor cortex may result in
transient hypertonia and hyperreflexia and spastic hemiparesis. but not complete paralysis of contralateral limbs
animal in lesion with motor cortex paralysis
an animal with a lesion in motor cortex will never be completely paralyzed bc brainstem UMNs are able to mediate gait and some other movements without cortical input
acute forebrain lesion
will lead to tone, reflex, and gait deficits; usually these are relatively mild and resolve quickly as intact elements of somatomotor system reorganize to compensate
cortical lesions may cause enduring deficits in
locomotion in face of obstacles or on irregular terrain and will cause permanent deficits in ability to perform postural rxns b/c motor cortex is required for performing these tasks and brainstem UMNs cannot “learn” to compensate
rostral midbrain lesions
- damaging red nucleus and descending pathways from motor cortex will manifest as UMN deficits in contralateral thoracic and pelvic limns
- lesions more severe and enduring than cortical lesions bc both cortical and rubrospinal UMNs are impacted by the lesion and the red nucleus and surrounding midbrain plays important role in locomotion
lateralized lesion spanning rostral to cd extent of midbrain
UMNs to both ipsilateral and contralateral limbs will be impacted (bc decoration of rubrospinal tract) and UMN signs will be seen in the limbs on both sides
unilateral lesion of pons or medulla
will manifest as hypertonia, hyperreflexia, postural rxn deficits and spastic hemiparesis, or hemiplegia of ipsilateral limbs; similar to lesions of C1-C5 spinal cord segments
medullar lesion severity
medullary lesions can produce most severe UMN deficits of all regions of brain bc all UMN pathways are present in medulla
lesion that is large or affects both sides of brainstem will affect
motor function of limbs on both sides
vestibulospinal pathway extensors or flexors
generally largely extensors
organization of motor pathways
they are topographically organized; can be seen in md to lat organization of VH in every tract and nucleus up to cortex; neurons that are adjacent to each other influence the same or nearby muscles and muscles of body are represented in spatially continuous way across nucleus or axon tract
paresis
weakness to generate voluntary movement
paralysis
inability to generate voluntary movement
locomition
fx that minimally requires brainstem UMN control of spinal cord LMNs
spastic paresis/ paralysis
occurs when UMNs in cervical or lumbar enlargement damaged; muscle ton present or even increased bc LMNs in myotactic reflex loops in tact -> characteristic of opacity
spastic hemiparesis could be caused by
lesion in pons, medulla, or C1-C5 spinal cord lesion ipsilateral to affected limb
flaccid paresis/ paralysis
occurs when LMNs are damaged; muscle tone is decreased or absent bc LMNs are damaged
no lmn
no lmm -> no muscle contraction -> no muscle tone
flaccid paresis/ paralysis most easily IDed in gait as
decreased or lack of ability to bear weight on limb
in locomotion flaccid paresis manifests
similar to lameness affected limb demonstrating shortened weight bearing phase
