12. Motor tracts Flashcards by Priyanka Barad

where do upper MNs (UMN) synapse

cell bodies in cerbal cortex/brainstem –> descend and synapse with lower MN (LMN) or interneurons

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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

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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

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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

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what areas of the brain initiates voluntary movement

primary motor cortex (area 4) in precentral gyrus

-right side controls left & vice versa

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what does the Medial CST control

postural/proximal movements (neck, shoulder & trunk ms)

DONT cross in medulla

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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

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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

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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

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what do indirect pathways activate

antigravity & axial LMNs

–> sitting/standing up right

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medial LMNs recieve input from

tectospinal tract

medial & lateral vestibulospinal tract (VST)

medial reticulospinal tract

medial CST

–> go to medial LMN –> axial ms

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lateral LMNs recieve input from

rubrospinal

lateral retibulospinal

lateral CST

–> lateral MN –> limb Ms

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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

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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

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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

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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) ## Footnote 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