Descending motor tracts Flashcards

1
Q

Motor plan

A

blueprint or module for movement

from premotor cx (lateral BA6&8) along with supplementary cortex

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2
Q

alpha LMNs

A

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

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3
Q

baseline activity

A

of alpha LMNs
can be changed by excitatory or inhibitory inputs
*what causes normal resting muscle tone

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4
Q

Lateral motor systems

A

control distal limb mm.

precise fractionated movements

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5
Q

medial motor systems

A

axial/proximal limb mm.
postural movements
i.e. from non-cortical UMNs

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6
Q

Cortical UMN systems

A

Corticospinal tract and corticobulbar tract

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7
Q

LCST

A

largest motor tract of humans
contralateral projection
some UMNs synapse directly on LMNs
critical for complex, fractionated movements

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8
Q

origins of LCST

A

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

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9
Q

Somatotopy of the internal capsule

A

all within the posterior limb:
facial expression in genu
UL is more anterior
trunk and LL are more posterior

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10
Q

Pre-motor cortex

A

Lateral BA6 &8

involved with motor planning and starting a movement

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11
Q

supplementary motor cx

A

medial BA6&8 located within the longitudinal fissure

interconnected with contralateral side, involved with bimanual movements

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12
Q

corticobulbar tract

A

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.)

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13
Q

LMN damage

A

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

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14
Q

UMN damage

A
normal - hyperreflexia 
hypertonia 
pathological reflexes (babinski) 
spastic 
disuse atrophy 
few EMG changes 
** all due to denervation hypersensitivity 

signs occur inferior to lesion

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15
Q

denervation hypersensitivity

A

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

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16
Q

Non-cortical UMN systems

A

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)

17
Q

Rubrospinal tract

A

cell bodies in the red nucleus
axons decussate in MB, descend in c/l lateral funiculus
innervate arm and forearm flexor (distal

18
Q

MVST

A

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

19
Q

LVST

A

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

20
Q

medial longitudinal fasciculus

A

ascending portion (MLF)
cell bodies in the medial/inf vestibular nuc.
ascends to innervate motor nuc of III, IV VI
b/l

21
Q

Medial RST

A
medial reticulospinal tracts 
aka pontine RST
cell bodies in the reticular formation 
ipsilateral 
backup pathway for voluntary movement if the corticospinal tract is damaged
22
Q

lateral RST

A
lateral reticulospinal tract 
aka medullary RST 
cell bodies in the reticular formation 
bilateral 
backup pathway for voluntary movement if the corticospinal tract is damaged
23
Q

Tectospinal tract

A

cell bodies in the superior colliculus
decussates in the c/l midbrain
synapse on neck mm. (tract terminates in cervical cord

**visual grasp reflex