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