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Neuro Exam 2 > SC Corticospinal Pathways/LMN > Flashcards

SC Corticospinal Pathways/LMN Flashcards

1
Q

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

A

Upper motor neurons (UMN)

Lower motor neurons (LMN)

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2
Q

Function of UMNs

A

Influence lower motor neurons to control voluntary body movements

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3
Q

What tracts do UMNs run in?

A

Corticospinal tracts (aka Pyramidal tracts)

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4
Q

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

A

Precentral

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5
Q

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

A 
Precentral gyrus
Internal capsule in cerebrum
Peduncles in midbrain
Anterior pons
Medullary pyramids
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6
Q

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

A

Spinomedullary

Lateral corticospinal; anterior corticospinal

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7
Q

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 ________

A

Lateral funiculus; interneurons; LMN cell bodies in ventral horn

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8
Q

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

A

Anterior funiculus; axial skeletal muscle

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9
Q

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

A

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

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10
Q

Signs/symptoms of UMN lesion

A

Spastic paralysis/paresis

Hypertonia

Hyperreflexia

Clonus

Rigidity

Disuse atrophy

(+) Babinskis

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11
Q

Define clonus

A

Rapid series of alternating muscle contractions in response to sudden stretch

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12
Q

Difference between rigidity and spasticity

A

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

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13
Q

What is the + babinskis sign seen with UMN lesion?

A

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

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14
Q

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

A

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

Hyperactive DTRs

Absent abdominal cremasteric reflexes

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15
Q

Causes of UMN lesions/damage

A

Strokes

Spinal cord trauma

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16
Q

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

A

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

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17
Q

Define function of LMNs

A

Final effectors of motor system (final common pathway)

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18
Q

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

A

Ventral; skeletal m

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19
Q

2 types of LMN fibers

A

Somatic efferent = directly innervate skeletal m.

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

20
Q

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?

A

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

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

21
Q

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

A

Axial muscles most medially
Distal musculature laterally

Proximal muscles located between axial and distal muscles

22
Q

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

A

C4-T1 and L1-S2 innervate extremities

Extensors are located more anterior
Flexors are located more posterior

23
Q

Symptoms of LMN lesions

A 
Flaccid paralysis
Areflexia
Atonia
Atrophy
Fasciculations
24
Q

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

A

Efferent

25
Q

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

A

Gamma

26
Q

Why do fasciculations occur with lesions to LMNs?

A

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

27
Q

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

A

Paralyzes individual muscles or sets of muscles in root of peripheral nerve distribution

Hypoactive or absent DTRs

28
Q

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?

A

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

29
Q

Primary example of damage to LMN motor neurons in ventral root

A

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

30
Q

Signs/symptoms of damage to LMN nerve roots themselves

A

Mixed motor and sensory = radiculopathy

Decreased sensation in dermatomal pattern

Weakness in muscles innervated by level involved

+/- decreased DTRs depending on level

31
Q

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?

A

ACA —> contralateral LE > UE

MCA —> contralateral face and UE > LE

32
Q

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?

A

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

33
Q

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

A

lower; upper

34
Q

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

A

Cerebral palsy

35
Q

Subtypes of CP and corresponding brain area affected

A 
Spastic = cerebral cortex
Dyskinetic = basal ganglia
Ataxic = cerebellum
Mixed = multiple areas
36
Q

Causes of CP

A 
Neonatal stroke
Prenatal circulatory disturbance
Congenital infection
Brain maldevelopment
Perinatal asphyxia
37
Q

Most common subtype of CP and symptoms

A

Spastic — spasticity, hyperreflexia, clonus, babinskis sign

38
Q

Subtypes of spastic CP

A

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

39
Q

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

A

Amyotrophic lateral sclerosis (ALS)

40
Q

Describe UMN and LMN involvement in ALS

A

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

41
Q

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

A

Reticulospinal tract
Rubrospinal tract
Tectospinal tract
Vestibulospinal tract

42
Q

The reticulospinal tract operates through which 2 motor pathways?

A

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)

43
Q

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

A

Rubrospinal tract

[note: small in humans]

44
Q

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

A

Tectospinal tract

45
Q

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

A

Vestibulospinal tract

Neuro Exam 2 (21 decks)

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