SC Corticospinal Pathways/LMN

Question 1

Descending pathways control voluntary motion and consist of what 2 types of neurons?

Answer 1

Upper motor neurons (UMN)

Lower motor neurons (LMN)

Question 2

Function of UMNs

Answer 2

Influence lower motor neurons to control voluntary body movements

Question 3

What tracts do UMNs run in?

Answer 3

Corticospinal tracts (aka Pyramidal tracts)

Question 4

UMNs begin their course in gray matter of _____ gyrus which is the primary motor cortex

Answer 4

Precentral

Question 5

From the precentral gyrus, what is the order of UMNs descent?

Answer 5

Precentral gyrus
Internal capsule in cerebrum
Peduncles in midbrain
Anterior pons
Medullary pyramids

Question 6

85% of UMN fibers cross at the pyramidal decussation at the _____ junction

The crossed fibers run in the ____ tract while the 15% of uncrossed fibers run in the _____ tract

Answer 6

Spinomedullary

Lateral corticospinal; anterior corticospinal

Question 7

The lateral corticospinal tract (crossed UMNs) is located in the posterior half of the _____ ____ of the spinal cord; UMNs in this tract synapse at ______ or with ________

Answer 7

Lateral funiculus; interneurons; LMN cell bodies in ventral horn

Question 8

The anterior corticospinal tract (uncrossed UMNs) continues in the _____ ____ of the spinal cord. These UMNs preferentially synapse with nuclei of _________

Answer 8

Anterior funiculus; axial skeletal muscle

Question 9

T/F: isolated damage to the anterior corticospinal tract does not lead to any obvious signs/symptoms

Answer 9

True (bc only 15% of the UMN fibers are in this tract)

Question 10

Signs/symptoms of UMN lesion

Answer 10

Spastic paralysis/paresis

Hypertonia

Hyperreflexia

Clonus

Rigidity

Disuse atrophy

(+) Babinskis

Question 11

Define clonus

Answer 11

Rapid series of alternating muscle contractions in response to sudden stretch

Question 12

Difference between rigidity and spasticity

Answer 12

Rigidity = non-velocity dependent increase in resistance to passive motion in ALL directions

Spasticity = velocity-dependent increase in resistance to passive movement, typically in specific direction

Question 13

What is the + babinskis sign seen with UMN lesion?

Answer 13

Upward extension of hallux and fanning of toes when plantar surface of foot is stroked

Question 14

Other characteristics of UMN damage in terms of distribution of paralysis, DTR changes, and specific reflexes

Answer 14

Paralyzes movements in hemiplegic, quadruplegic, or paraplegic distribution, not just individual muscles

Hyperactive DTRs

Absent abdominal cremasteric reflexes

Question 15

Causes of UMN lesions/damage

Answer 15

Strokes

Spinal cord trauma

Question 16

How would you localize UMN lesions based on location of decussation?

Answer 16

Lesions above decussation —> contralateral signs/symptoms at and below level of lesion

Lesions below decussation —> ipsilateral signs/symptoms at and below the level of lesion

Question 17

Define function of LMNs

Answer 17

Final effectors of motor system (final common pathway)

Question 18

LMNs start at lower motor neuron motor nuclei in the ____ horn of the SC, then synapse directly in ____

Answer 18

Ventral; skeletal m

Question 19

2 types of LMN fibers

Answer 19

Somatic efferent = directly innervate skeletal m.

Special visceral efferent=motor innervation to muscles of pharyngeal arches including CN V, VII, IX, X, and ???

Question 20

Somatic efferent LMNs have cell bodies in ventral horn of SC, exit via anterior root and pass into spinal nerve. Their activity is influenced by UMNs and segmental afferent inputs (reflexes)

What are the 2 types of somatic efferent LMN fibers?

Answer 20

Alpha (extrafusal) = innervates skeletal muscle fibers; voluntary, postural, and reflex motion

Gamma (intrafusal) = innervates muscle spindles; sensitivity and activity reflex threshold adjusted by UMNs

Question 21

Topographic arrangement of LMN cell bodies in ventral horn of SC — what is the location of axial muscles vs. proximal muscles vs. distal muscles?

Answer 21

Axial muscles most medially
Distal musculature laterally

Proximal muscles located between axial and distal muscles

Question 22

Topographic arrangement of LMN cell bodies in ventral horn of SC — which levels innervate extremities? Flexors vs. extensors?

Answer 22

C4-T1 and L1-S2 innervate extremities

Extensors are located more anterior
Flexors are located more posterior

Question 23

Symptoms of LMN lesions

Answer 23

Flaccid paralysis
Areflexia
Atonia
Atrophy
Fasciculations

Question 24

The areflexia seen with LMN lesion is d/t absence of the _____ component of reflex arc

Answer 24

Efferent

Question 25

The atonia seen with LMN lesions is d/t loss of ____ motor neuron activity leading to loss of tone

Answer 25

Gamma

Question 26

Why do fasciculations occur with lesions to LMNs?

Answer 26

Muscles are denervated, causing motor endplates to increase their sensitivity, and any small amounts of ACh floating around can cause slight contraction at the muscle

Question 27

Other characteristics of LMN lesions in terms of paralysis distribution and DTR changes

Answer 27

Paralyzes individual muscles or sets of muscles in root of peripheral nerve distribution Hypoactive or absent DTRs

Question 28

Different types of damage to LMNs can cause different symptoms, what results from damage to motor neurons in ventral root vs. damage to nerve roots themselves vs. damage to entire peripheral nerve?

Answer 28

Damage to motor neurons in ventral root —> motor signs ONLY, sensation intact Damage to nerve roots themselves —> mixed motor and sensory = radiculopathy Damage to peripheral nerve —> weakness in specific muscle groups + decreased sensation in peripheral nerve distribution = neuropathy

Question 29

Primary example of damage to LMN motor neurons in ventral root

Answer 29

Poliomyelitis Poliovirus leads to destruction of ventral horn motor cell bodies Clinical presentation = paresis and paralysis in asymmetric pattern, decreased or absent tone and reflexes, sensory exam almost always normal

Question 30

Signs/symptoms of damage to LMN nerve roots themselves

Answer 30

Mixed motor and sensory = radiculopathy Decreased sensation in dermatomal pattern Weakness in muscles innervated by level involved +/- decreased DTRs depending on level

Question 31

Localizing lesions to the corticospinal tract, specifically the motor cortex, can be done using the homunculus, as well as the arterial supply. What changes would you see with an anterior cerebral artery infarct vs. middle cerebral artery infarct?

Answer 31

ACA —> contralateral LE > UE MCA —> contralateral face and UE > LE

Question 32

Localizing lesions to the corticospinal tract, specifically the posterior limb of the internal capsule, can be done using the arterial supply of this area. What is the arterial supply and what effect would damage to this artery have?

Answer 32

Lenticular striate artery; damage —> face, LE, and UE affected, causing contralateral complete hemiparesis

Question 33

Localizing lesions to the corticospinal tract after a spinal cord injury can be difficult. The patient initially presents with spinal shock, with ______ motor neuron signs/symptoms lasting from about 1 week to 2 months. Tone and reflexes later return, leading to _____ motor neuron symptoms like spastic paresis depending on area of lesion. These can be unilateral or bilateral

Answer 33

lower; upper

Question 34

Group of disorders of the CNS characterized by aberrant control of movement/posture present since early in life and NOT the result of progressive or degenerative disease

Answer 34

Cerebral palsy

Question 35

Subtypes of CP and corresponding brain area affected

Answer 35

``` Spastic = cerebral cortex Dyskinetic = basal ganglia Ataxic = cerebellum Mixed = multiple areas ```

Question 36

Causes of CP

Answer 36

``` Neonatal stroke Prenatal circulatory disturbance Congenital infection Brain maldevelopment Perinatal asphyxia ```

Question 37

Most common subtype of CP and symptoms

Answer 37

Spastic — spasticity, hyperreflexia, clonus, babinskis sign

Question 38

Subtypes of spastic CP

Answer 38

Spastic hemiplegia = one side affected Spastic diplegia = LEs affected with little to no UE involvement Spastic quadruplegia = all limbs affected

Question 39

Rapidly progressive disease with asymmetric mix of UMN and LMN signs; pathophysiology unknown

Answer 39

Amyotrophic lateral sclerosis (ALS)

Question 40

Describe UMN and LMN involvement in ALS

Answer 40

UMN = degeneration of motor neurons in primary motor cortex + axons throughout corticospinal/corticobulbar tracts; causes weakness, hyperreflexia, spasticity LMN = degeneration of ventral horn cells; causes weakness, atrophy, fasciculations

Question 41

Besides the corticospinal tract, what are 4 other descending (extrapyramidal) motor tracts?

Answer 41

Reticulospinal tract Rubrospinal tract Tectospinal tract Vestibulospinal tract

Question 42

The reticulospinal tract operates through which 2 motor pathways?

Answer 42

Pontine reticular pathway = activates antigravity reflexes in erect position Medullary reticulospinal pathway = mediates cortical control of reflexes (inhibits postural or flexor reflexes that may interfere with voluntary motor activity)

Question 43

Which extrapyramidal motor tract mediates voluntary motion, most notably flexor movements of the arms, and originates in the red nucleus of the midbrain?

Answer 43

Rubrospinal tract [note: small in humans]

Question 44

Which extrapyramidal motor tract coordinates movement of the head with eyes and originates in the superior colliculus?

Answer 44

Tectospinal tract

Question 45

Which extrapyramidal motor tract maintains posture against gravity, most notably the trunk and UE/LE extensors, and originates in the vestibular cortex?

Answer 45

Vestibulospinal tract