12. Motor tracts Flashcards
where do upper MNs (UMN) synapse
cell bodies in cerbal cortex/brainstem –> descend and synapse with lower MN (LMN) or interneurons
where do LMN synapse and what are the types of LMNs
-synapse at sk. M
gamma MN = medium, myleinated, to intrafusal fibers in m. spindles
alpha MN: large, meylinated, to extrafusal fibers sk. M
How to the corticospinal tract (CST) direct path project
medial CST –> post Ms (10 % of fibers) - stay ipsi
lateral CST –>limb Ms & fractionation = 90% fibers - go contralat @ pyramidal decussation
what is the path of the direct CST (lateral)
cell body of UMN in cortex –>
descent thru post. limb of internal capsule –>
continue in CST , pass thru middle cerebral peduncles, then to ant pons and then to pyramids in medulla –>
cross at the pyramids in lower medulla –>
descend in lat column (fibers = lateral CST)–>
synapse w/ LMN in ventral horn
what areas of the brain initiates voluntary movement
primary motor cortex (area 4) in precentral gyrus
-right side controls left & vice versa
what does the Medial CST control
postural/proximal movements (neck, shoulder & trunk ms)
DONT cross in medulla
what do corticobulbar tracts control
come from ventral part of cortical area 4
go into Br.st and influence Ms innervated by CN 5, 7, 9, 10, 11, 12
-control contralateral side
UMN = CBT fibers ; LMN = CNs
what the flow of the corticobulbar tract
cortex –> descend thru genu of internal capsule –> pass thru cerebral pedeuncles, ant pons and pyramids –> stop at specific motor nuclei –>
pons: CN 5,7
or medulla: CN 9, 10, 12
or sp. cord: CN 11
how are LMNs represented in the sp. cord
= in ant. horn
- medial = axial Ms
- lateral = limbs
LMN innervating:
- extensor M = lie ventral
- & flexor m = lie dorsal
what do indirect pathways activate
antigravity & axial LMNs
–> sitting/standing up right
medial LMNs recieve input from
tectospinal tract
medial & lateral vestibulospinal tract (VST)
medial reticulospinal tract
medial CST
–> go to medial LMN –> axial ms
lateral LMNs recieve input from
rubrospinal
lateral retibulospinal
lateral CST
–> lateral MN –> limb Ms
what is the path and fxn of the lateral vestibulospinal tract
vestibular nuclei to spinal cord = ipsilateral LMNs innervate postural Ms & limb extensors
fxn: faciliate extension agaisnt gravity
what is the path and fxn of the medial vestibulospinal tract
vestibular nuclei to spinal cord = to cervical & thoracic levels (neck/shoulder Ms)
fxn: coordinate head movement
what is the path and fxn of the medial reticulospinal tract
pontine reticular formation to spinal cord = ipsi LMNs innervating postural Ms & limb extensors
fxn = facilitation of postural reflexes
what is the path and fxn of the rubrospinal tract
red nucleus to spinal cord –> innervate upper limb flexors
fxn: help flex limbs
at cervical & thoracic regions
what is the path and fxn of the lateral reticulospinal tract
medullary reticular formation to spinal tract
fxn: help flexor MN & inhibit extensor MNs (inhibit spinal segmental reflexes)
what is the path and fxn of the tectospinal tract
superior colliculus to upper spinal cord to neck Ms
fxn= coordinate head w/ eye movement
what are signs of LMN lesions
- flaccid paralysis
- wasting/atrophy
- hyporeflexia/areflexia (bc denervation)
- hypotonia
- denervation hypersensitivity (fasiculations)
what are UMN signs
- CST:
loss of distal extremity strength & dexterity (
babinski sign (inverted plantar reflex)
- indirect path:
pronator drift
hypertonia: spastic
hyperreflexia
clasp-knife phenomenon/spasticity
what is UMN syndrome
combo of loss of direct CST & loss of regulation from indirect brainstem motor control
how can you different btn the two types of hypertonia
- spastic = UMN lesion - rate dep. resistance; collapsed resistance at end of ROM
- rigidity: basal ganglia disease - no rate/force dep; constant thru ROM
how can you determine location of a lesion
midbrain = CN 3
pons = CN 6 & 7
medulla = CN 10 & 12
compare decorticate vs decerebrate posture in UMN lesions
decorticate: lesion above level of red nucleus –> thumb tucked under flexed finger in fist, pronated forearm, flexion @ elbow, LE extended w/ foot inverted
decerebrate: lesion _below red nucleu_s ; but above reticulospinal & vestibulospinal nuclei –> UE pronated and extended & LE extended
what results form a complete transection of the spinal cord
All sensation 1 or 2 levels below lesion
Bladder and bowel control are lost
Spinal shock –> Loss of tendon reflexes
UMN signs at levels below the lesion –> Hyperactive reflexes, clonus; Babinski; Spasticity
LMN signs at the level of the lesion
What occurs when you have a hemisection of the spinal cord
Pain and temp from contralat side
–> Complete loss of pain sensation occurs 2 to 3 dermatomes below level of lesion (Lissauer’s tract) = ALS tract
Discriminative touch and conscious proprioception on ipsilateral side = PCML tract
LMN signs at level of lesion = Flaccid paralysis (ant horn)
UNM signs on ipsilateral side = Babinski; Hyperreflexia and Clonus; Muscle weakness; Spasticity (CST)
Pattern of loss is called Brown-Sequard’s syndrome
what occurs when a pt has syringomyelia
Formation of cysts w/i spinal cord in central canal
–> 1st Pain and temp (Anterior commissure) = “cape” pattern
Motor also lost
- > LMN signs if ventral horns affected
- > UMN signs if lateral corticospinal tract is affected
- most often C4-C5
what is anterior cord syndrome
Compression/damage to anterior spinal cord
b/c sp. cord infarction, intervertebral disc herniation, and radiation myelopathy
-hit LCST, LMN & ALS bilaterally
what is central cord syndrome
Compression/damage to central sp cord
usually b/c cervical hyperextension
-ex: syringomyelia
what is the presentation of central 7 palsy
Lesion of the corticobulbar tract w/ CN 7
Lesion rostral to facial motor nucleus results in drooping of muscles at the corner of the mouth
-opposite side
what is the presentation of bells palsy
Ipsilateral flaccid paralysis of upper and lower face
what are symptoms of spastic cerbral palsy
Movement dysfxn: Abnormal supraspinal influences, Failure of normal neuronal selection. Consequent aberrant muscle development
Motor disorders: Paresis, Abnormal tonic stretch reflexes (rest & during movement), Reflex irradiation, Lack of postural preparation prior to movement, Abnormal cocontraction of Ms
what happens in ALS (amyotrphic lateral sclerosis)
Destroys only somatic MNs (UMNs and brainstem and spinal cord LMNs)
Leads to paresis, myoplastic hyperstiffness, hyperreflexia, Babinski’s sign, atrophy, fasciculations and fibrillations.
CN involvement –> difficulty breathing, swallowing and speaking
what is polyneuropathy
Involvement of sensory, motor and autonomic
Progressing from distal to proximal
Due to dying-back or impaired axonal transport
Demyelization may also contribute
