Descending motor tracts Flashcards
Motor plan
blueprint or module for movement
from premotor cx (lateral BA6&8) along with supplementary cortex
alpha LMNs
innervate skeletal muscle
final common pathways (always excitatory)
don’t decussate (usually)
cell bodes in the ventral horn and CN motor nuclei
large diameter and high baseline activity
baseline activity
of alpha LMNs
can be changed by excitatory or inhibitory inputs
*what causes normal resting muscle tone
Lateral motor systems
control distal limb mm.
precise fractionated movements
medial motor systems
axial/proximal limb mm.
postural movements
i.e. from non-cortical UMNs
Cortical UMN systems
Corticospinal tract and corticobulbar tract
LCST
largest motor tract of humans
contralateral projection
some UMNs synapse directly on LMNs
critical for complex, fractionated movements
origins of LCST
1/3 from the Primary Motor Cortex
2/3 from frontal lobes and somatosensory cx and premotor and supplementary motor areas
runs in corticospinal tract
Somatotopy of the internal capsule
all within the posterior limb:
facial expression in genu
UL is more anterior
trunk and LL are more posterior
Pre-motor cortex
Lateral BA6 &8
involved with motor planning and starting a movement
supplementary motor cx
medial BA6&8 located within the longitudinal fissure
interconnected with contralateral side, involved with bimanual movements
corticobulbar tract
terminates in the brainstem
influences CN motor nuclei (LMNs) -bilaterally
and UMN nuclei (vestibular nuclei, reticular nuclei, red nucleus)
**gain voluntary control of medial motor systems (axial proximal mm.)
LMN damage
hypo—>areflexia and atonia —>decreased stretch reflex
paralysis/paresis, flaccid
rapid, severe atrophy (neurogenic atrophy) due to lack of trophic effects
fasciculation and fibrillation due to spontaneous release of NTs
signs occur at lesion level
UMN damage
normal - hyperreflexia hypertonia pathological reflexes (babinski) spastic disuse atrophy few EMG changes ** all due to denervation hypersensitivity
signs occur inferior to lesion
denervation hypersensitivity
occurs when UMN inhibition on LMN is lost
LMNs release trophic factors
increases collateral from primary afferent
increases input on surface of LMN
causes hyperreflexia, hypertonia, sapsticity
Non-cortical UMN systems
origin at sites outside cx
affect axial and proximal limb mm.
**reflex postural movement
also under voluntary control from cx via corticobulbar tract
**axons in the ventromedial cord (medial motor systems)
Rubrospinal tract
cell bodies in the red nucleus
axons decussate in MB, descend in c/l lateral funiculus
innervate arm and forearm flexor (distal
MVST
medial vestibulospinal tracts: aka descending MLF
cell bodies in the medial/inf vestibular nuc.
axons run b/l thru the cervical and upper thoracic in the descending MLF
acts on neck mm.
changes head and neck posture
damage causes less sx due to bilateral inputs
LVST
lateral vestibulospinal tracts
cell bodies in the lateral vestibular nuc.
run ipsilateral in the cord to axial postural/abdomen muscles to help maintain trunk posture
lesions cause ipsilateral loss of muscle activity
medial longitudinal fasciculus
ascending portion (MLF)
cell bodies in the medial/inf vestibular nuc.
ascends to innervate motor nuc of III, IV VI
b/l
Medial RST
medial reticulospinal tracts aka pontine RST cell bodies in the reticular formation ipsilateral backup pathway for voluntary movement if the corticospinal tract is damaged
lateral RST
lateral reticulospinal tract aka medullary RST cell bodies in the reticular formation bilateral backup pathway for voluntary movement if the corticospinal tract is damaged
Tectospinal tract
cell bodies in the superior colliculus
decussates in the c/l midbrain
synapse on neck mm. (tract terminates in cervical cord
**visual grasp reflex
