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COM: Neuro - Exam 2 > Lecture 4: Corticospinal Pathways/LMN > Flashcards

Lecture 4: Corticospinal Pathways/LMN Flashcards

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1
Q

Where is the corticospinal tract versus the lateral corticospinal tract located?

A

Corticospinal tract is in the brain and the lateral corticospinal tract is int he spinal cord

**Need to know this

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2
Q

Upper motor neuron paralysis is commonly due to interruption of what?

A

Motor cortex, corticospinal and/or corticobulbar tracts

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3
Q

What is the function of upper motor neurons and where do they start and synapse?

A

UMN’s influence the activity of lower motor neurons to control voluntary movement of the body

Start in primary motor cortex and end synapsing with interneurons or directly with lower motor neuron cell bodies

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4
Q

UMN paralysis is classically referred to as ______________________________________. What are the signs and symptoms of UMN lesions?

A

Spastic paralysis of the antigravity muscles

Sx = hypertonia, varying degrees of spastic paralysis, hyperreflexia, babinski sign, clonus, rigidity, disuse atrophy

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5
Q

What are the 3 phases of physical events following UMN lesions?

A

Initially, the pt is in spinal shock with areflexia, atonic and flaccid paralysis

After a few weeks or months, return of basic spinal reflexes indicates pts recovery from spinal shock -> due to reactivation of the intrinsic circuits of the spinal cord distal to lesion

After 1-2 years, the affected muscle groups will exhibit spasms of the extensors, or flexors, or remain flaccid

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6
Q

What occurs as a result of a unilateral lesion of the corticospinal tract?

A

Contralateral spastic hemiplegia or spastic hemiparesis

**85% of strokes happen in the internal capsule

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7
Q

What occurs as a result of unilateral lesions to the lateral corticospinal tract?

A

Ipsilateral paralysis or paresis of muscles innervated by spinal segments below the level of the lesion

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8
Q

What are signs and symptoms of LMN disorders?

A 
Flaccid paralysis 
Areflexia 
Atonia
Atrophy
Fasciculations
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9
Q

What is the function of lower motor neurons and where do they start and end?

A

They are the final effectors of the motor systems

Starts at LMN motor nuclei in the ventral horn of spinal cord and ends at muscle

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10
Q

What are the 2 types of lower motor neurons?

A

Somatic efferents -> directly innervate skeletal muscles, cell bodies in ventral horn, exit in ant root and pass into spina nerve, synapse directly with skeletal muscle

Special visceral efferents (autonomics) -> preganglionic fiber synapse on cell bodies in peripheral visceromotor ganglion and postganglionic fibers innervate smooth muscle, cardiac muscle and glandular epithelium

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11
Q

What is the difference between alpha and gamma fibers in terms of what they innervate?

A

Alpha innervates skeletal muscle fibers (extrafusal) -> voluntary, postural and reflex motion

Gamma innervates muscle spindles (intrafusal)

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12
Q

What is the topographic arrangement of LMN cell bodies in the ventral horn from most lateral to most medial?

A

Distal musculature -> proximal musculature -> axial muscles

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13
Q

Spinal segments ______-______ and _____-_____ innervate extremities. What is the location of extensor versus flexor innervation?

A

C4-T1; L1-S2; Extensors = anterior and flexors = posterior

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14
Q

Define flaccid paralysis

A

Muscle completely limp with inability to contract

**Seen with LMN lesion

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15
Q

What is Atonia?

A

Loss of gamma motor neuron activity leading to loss of tone

**LMN lesion

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16
Q

What are fasciculations?

A

Denervation leading to increased sensitivity of motor end plates causing “twitching”

**Seen in LMN lesion

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17
Q

What deficits are seen with damage to motor neuron and ventral root?

A

Motor signs ONLY, sensation intact

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18
Q

What is radiculopathy?

A

Damage to nerve roots which are mixed motor and sensory -> cuases decreased sensation in specific dermatomal pattern, weakness in muscles innervated by the level involved, and +/- decreased DTRs depending on level

Ex. Herniated disc

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19
Q

What is neuropathy?

A

Damage to peripheral nerves causing weakness n specific muscle groups and decreased sensation in specific peripheral nerve distribution

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20
Q

What is poliomyelitis?

A

Poliovirus infection leading to destruction of the ventral horn motor cell bodies -> pts present with paresis and paralysis in an asymmetrical pattern

Decreased or absent tone and reflexes

Sensory exam almost always normal

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21
Q

Where does the corticospinal tract originate?

A

In grey matter of precentral gyrus in the primary motor cortex

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22
Q

What structures do the fibers of the corticospinal tract descend thorugh?

A

Internal capsule in cerebrum
Peduncles in midbrain
Anterior pons
Medullary pyramids

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23
Q

Where do 85% percent of the fibers of the corticospinal tract decussate?

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A

Pyramidal decussation at the spinomedulary junction

24
Q

Betweeen the lateral and anterior corticospinal tracts which has crossed fibers and which has uncrossed fibers?

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A

Lateral corticospinal tract = crossed fibers

Anterior corticospinal tract = uncrossed fibers

25
The most common form of amyotrophic lateral sclerosis (ALS) involves a combination of which structures?
LMN: anterior horn cells, hypoglossal nucleus, nucleus ambiguous, facial motor nucleus UMN: chronic, progressive degeneration of the corticospinal tract
26
What symptoms does amyotrophic lateral sclerosis (ALS) was to?
LMN paresis and atrophy of the intrinsic muscles of the hands followed after by the arms and shoulder musculature Pts may develop dysarthria, dysphagia and paresis of tongue Involvement of the corticospinal tract leads to spastic paralysis, hyperreflexia and a babinski sign **There are NO sensory deficits
27
T/F: There are no sensory deficits seen in amyotrophic lateral sclerosis (ALS)
True
28
What condition causes destruction of the anterior white commissure due to compression by a cyst, therefore causing a bilateral loss of pain and temperature sensation to the UE?
Syringomyelia
29
A 70yo woman with a cc that her left leg tended to “catch” when walking. ONe month later, complained of burning sensation in right leg and within 2 months was unable to walk. On admission she had trouble urinating and a T8 lesion was discovered. What is at the top of your differentials?
Brown-sequard syndrome **Whenever you see proprioception and pain and temperature deficit on one side and motor deficit on the other side it should be a dead give away that its brown-sequard syndrome
30
What is tabes dorsalis?
A meningovascular inflammation of the blood vessels as they pierce through the pia mater at the junction of the dorsal rootlets and posterior columns resulting in bilateral ischemic necrosis of the posterior columns and dorsal roots at this level The lumbosacral nerves and spinal cord segments are most frequently affected **Occurs during the tertiary (late) stage of syphilis
31
What are the signs and symptoms of tabes dorsalis?
Pt complains of “lightning pains” or “rheumatic pains” from the LE for the last several years (probably due to irritation of the epicritic (type A) pain fibers in dorsal roots) Involvement of dorsal roots in sacral region results in atonic bladder and painless retention of urine Locomotor ataxia -> pronounced slapping of the feet Positive Romberg test -> suggests involvement of post columns and/or cerebellum
32
Where is the lateral corticospinal tract located?
Posterior half of the lateral funiculus of the spinal cord
33
Where does the lateral corticospinal tract terminate?
At synapses with interneurons or directly on LMNs in the ventral horn -> influences and modulates LMN activity to control motion of the body
34
The anterior corticospinal tract is made up of the remaining 15% of uncrossed fibers from the corticospinal tract and continue in the anterior funiculus of the spinal tract. Where do they synapse and terminate?
Preferentially synapse and terminate to nuclei of axial skeletal muscle **Isolated damage of these fibers typically doesnt result in obvious signs
35
What is spastic paralysis/paresis?
Velocity dependent increase resistance to passive movement, typically in a specific direction
36
What is hypertonia as seen with UMN lesion?
Increased resting muscle toned due to loss of inhibition from corticospinal tract
37
What is hyperreflexia as seen with UMN lesions?
Increase in reflex due to loss of inhibition from corticospinal tract
38
What is clonus?
Rapid series of alternating muscle contractions in response to sudden stretch **Can never grade a reflex a 4/4 unless clonus is present! **Seen with lesions of UMNs
39
What is rigidity?
Non-velocity dependent increase in resistance to passive motion in ALL directions **seen in UMN lesions
40
What is a (+) babinski sign and this is a sign of a lesion where?
Upward (extension) motion of the hallux when plantar surface of foot is stroked -> this is sign of UMN lesion
41
What are common causes of lesions to the corticospinal tract?
Cerebrovascuar accidents (strokes) Spinal cord trauma
42
Signs of lesion to the motor cortex are dependent to area of cortex damaged. What are the signs of ACA occlusion affecting motor cortex versus MCA occlusion?
ACA = contralateral LE MCA = contralateral face and UE
43
What artery is responsible for blood supply to the posterior limb of the internal capsule and what deficits are seen when its occluded?
Lenticular striate a; contralateral complete hemiparesis of LE and UE and possibly some face
44
What is cerebral palsy?
Group of disorders of the CNS characterized by aberrant control of movement or posture Clinical presentation based on area of CNS affected **Present early in life and NOT result of progressive or degenerative disease
45
What are the subtypes of cerebral palsy and the structures affected?
``` Spastic = cerebral cortex Dyskinetic = basal ganglia Ataxia = cerebellum Mixed = multiple areas ```
46
What are the causes of cerebral palsy?
``` Neonatal stroke Prenatal circulatory disturbances Congenital infections Brain maldevelopment Perinatal asphyxia ``` **anything that affects the baby in utero or during childbirth
47
Spastic cerebral palsy is the most common subtype of cerebral palsy. What are the subtypes of spastic cerebral palsy?
Spastic hemiplegia = only one side affected Spastic diplegia = LEs affected with little to no UE involvement Spastic quadriplegia = all limbs affected, children often severely handicapped; increased risk of complications
48
What is the most common subtype of cerebral palsy and what are the signs and symptoms of this subtype?
Spastic cerebral palsy -> spasticity, hyperreflexia, clonus, babinski
49
What condition is due to damage in both UMNs and LMNs?
Amyotrophic lateral sclerosis (ALS)
50
What is the function of the medullary reticulospinal pathway?
Mediate cortical control of reflexes -> inhibits postural or flexor reflexes that may interfere with execution of voluntary motor actiity
51
What is the function of the pontine reticular pathway?
Activates antigravity reflexes in erect person
52
What is the function of the rubrospinal tract?
Mediates oluntary motion, most notably flexor movement of the arms -> originates in red nucleus of midbrain **Small in humans
53
What is the function of the tectospinal tract?
Coordinates movement of head with eyes -> originates in superior colliculus
54
What is the function of the vestibulospinal tract?
Maintains posture against gravity, most notably, trunk and UE/LE extensors -> originates in vestibular cortex
55
Nucleus tractus solitarius contains viscerotopic fibers that contain fibers that control what functions?
Control autonomic and somatic nuclei associated with salivation, respiration, cardiovascular and GI functions
56
Distinguish between spasticity and rigidity
Spasticity = VELOCITY dependent increase in resistance to passive moement in a SPECIFIC direction Rigidity = NON-VELOCITY dependent increase in resistance to passive movement in ALL directions

COM: Neuro - Exam 2 (19 decks)

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