Lecture 4: Corticospinal Pathways and Lower Motor Neurons Flashcards

(36 cards)

1
Q

What is an Upper Motor Neuron (UMN), what tract do they utilize and where do they start/synapse?

A
  • Influence the activity of lower motor neurons to control voluntary movement of body
  • Corticospinal Tracts (AKA pyramidal) - Descending Tract
  • Start in Primary Motor Cortex and end synapsing with interneurons or directly with lower motor neuron cell bodies
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2
Q

What is a Lower Motor Neuron; where do they start and end?

A
  • Final Effectors of the motor systems
  • Known as the “final common pathway”
  • Starts at LMN motor nuclei in ventral horn of spinal cord and ends at muscle
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3
Q

What are the 2 types of LMN motor fibers?

A
  1. Somatic Efferent: directly innervate skeletal muscles
  2. Special Visceral Efferent (autonomics)
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4
Q

What are the LMN somatic efferent motor fibers; location of cell bodies and where do they synapse; activity influenced by?

A
  • Directly innervate skeletal muscles
  • Cell bodies in ventral horn of SC, exit in anterior root and pass into spinal nerve
  • Synapse directly w/ skeletal muscle
  • Activity influenced by UMN’s and segmental afferent inputs (i.e., Reflexes)
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5
Q

What are the LMN special visceral afferent fibers; where are the pre- an postganglionic fibers; innervate what?

A
  • Preganglionic fibers synapse on cell bodes in peripheral visceromotor ganglion (short in sympathetic, long in parasympathetic)
  • Postganglionic fibers innervate smooth muscle, cardiac muscle, and glandular epithelium
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6
Q

What are the 2 fiber types of somatic efferent LMN; what does each innervate?

A
  1. Alpha - innervates skeletal muscle fibers (extrafusal)
    - Voluntary, postural, and reflex motion
  2. Gamma - innervates muscle spindles (intrafusal)
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7
Q

How do UMN’s control gamma neurons (fibers); what occurs if UMN control is lost?

A
  • UMNs adjusts sensitivity and activity of Gamma neurons, thus adjusting threshold of muscle spindle to influence reflex (activity dependent)
  • If UMN control is lost, Muscle spindle becomes more sensitive————–> UMN signs and symptoms

*Muscle spindle loves to party and UMN is like the parent. When parent is away, the kids will play!

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8
Q

How are cell bodies of Axial, Proximal, and Distal musculature topographically arranged in LMN?

A
  • Axial muscles - most medial
  • Proximal (deltoid) muscles - medially
  • Distal (fingers) muscles - laterally
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9
Q

Which spinal levels innervate the UE and LE’s, where are the flexors and extensors located in the ventral horn cell?

A
  • C4-T1 for UE

- L1-S2 for LE

- Extensors located Anterior

  • Flexors located Posterior
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10
Q

What are 5 clinical finidings associated with LMN lesions?

A
  1. Flaccid Paralysis
  2. Areflexia
  3. Atonia
  4. Atrophy
  5. Fasciculations
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11
Q

Damage to motor neuron and vental root of LMN will cause what problems?

A

Motor signs ONLY, sensation intact

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12
Q

Damage to nerve roots of LMN will cause what problems; what is a common example of this?

A
  • Mixed motor and sensory (radiculopathy) - i.e., herniated disc
  • Decreased sensation in specific dermatomal pattern
  • Weakness in muscles innervated by the level involved
  • +/- decreased DTRs depending on level
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13
Q

Damage to peripheral nerves (neuropathy) of LMN will cause what problems?

A
  • Weakness in specific muscle groups
  • Decreased sensation in peripheral nerve distribution
  • Commonly seen in nerve entrapment
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14
Q

How can Polio infection lead to Poliomyelitis; what is the common clinical presentation (pattern, decreased what, sensory exam findings)?

A
  • Poliovirus infection can lead to destruction of the ventral horn motor cell bodies
  • Clinical presentation: Paresis and Paralysis in an ASYMMETRIC pattern
  • Decreased or absent Tone and Reflexes
  • Sensory exam almost always NORMAL
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15
Q

Where does the Corticospinal Tract originate and the UMN fibers descend through where?

A
  • Originate in grey matter of precentral gyrus in the Primary Motor Cortex

- Fibers descend through:

  • Internal capsule in Cerebrum
    • Peduncles in midbrain*
    • Anterior Pons*
    • Medullary Pyramids*
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16
Q

85% of the fibers from the Corticospinal tract cross where; what about the other 15%?

A
  • Cross at MEDULLARY Pyramidal Decussation at the Spinomedullary Junction
  • 85% Lateral Corticospinal Tract - Crossed fibers
  • 15% Anterior Corticospinal Tract - Uncrossed fibers
17
Q

Damage above the Pyramidal Decussation of the Medulla leads to deficits on what side?

A

Damage above the crossing point = deficits on contralateral side

18
Q

The lateral corticalspinal tract, consisting of 85% of the crossed fibers are located where in the spinal cord; where do these fibers synapse?

A
  • Located in Posterior half of the lateral funiculus of the spinal cord
  • Terminates at synapses with interneurons or directly on LMNs in the ventral horn
19
Q

UMN fibers from the lateral corticospinal tract synapse directly on LMNs in the ventral horn and modulate what?

A

Influences and modulates LMN activity to control motion of body

20
Q

The remaining 15% of uncrossed UMN fibers in the Anterior Corticospinal tract are found where in the spinal cord and where do they preferntially synapse?

A
  • Continue in the anterior funiculus of the SC
  • Preferntially synapse and terminates to nuclei of axial skeletal muscles
21
Q

Isolated damage to the Anterior Corticospinal Tract usually results in?

A

Typically doesn’t result in obvious signs, becasue this only accounts for 15% of the fibers which went uncrossed.

22
Q

What are 7 common clinical presentations of UMN lesions?

A

1) Spastic Paralysis/Paresis: is velocity dependent increase resistance to passive movement, in specific direction

2) Hypertonia: increased resting muscle tone due to loss of inhibition

3) Hyperreflexia: increase in reflex due to loss of inhibition

4) Clonus: rapid series of alternating muscle contractions in response to sudden stress

5) Rigidity: is non-velocity dependent increase in resistance to passive motion in ALL directions

6) Disuse Atrophy: decreased muscle, less severe than LMN

7) (+) Babinskis: upward (extension) motion of the hallux when plantar surface of the foot is stroked

23
Q

What is the difference between Spastic Paralysis/Paresis and Rigidity?

A

Spastic Paralysis: is velocity dependent increase resistance to passive movement, typically in specific direction

Rigidity: is NON-velocity dependent increase resistance to passive movement in ALL directions

*BOTH can be present at same time, but they are NOT the same. Signs of UMN lesion

24
Q

What are common causes of lesions to the Corticospinal Tract?

A
  • Cerebrovascular Accidents (strokes)
  • Spinal Cord Trauma
25
When localizing a lesion of the Corticospinal Tract what will be seen if above the decussation and what if below the decussation?
**Above:** will be **contralateral** signs and symptoms at, and below level of lesion **Below:** will be **ipsilateral** signs and symptoms at, and below the level of lesion
26
Lesions to the motor cortex of corticospinal tract by the ACA and MCA will effect what parts of body?
- ACA: **contralateral LE\>UE** - MCA: **contralateral face and UE \>LE**
27
Occlusion or lesion to the Lentricular Strate A., will affect what part of the corticospinal tract and ultimately lead to?
- Posterior limb of internal capsule - Face = LE = UE - **Contralateral complete hemiparesis**
28
Spinal cord injuries intially present with what? What occurs over time depending on level and severity of lesion?
- Initially present with **Spinal Shock** - LMN signs and sx's lasting about 1 wk - 2 mo. - Tone and reflexes return leading to spastic paresis depending on level of lesion (severity of sx's depend on extend of damage to SC) - Can be unilateral or bilateral
29
What is Cerebral Palsy, what causes it and when does it present?
- Group of disorders of the CNS characterized by aberrant control of movment or posture - Caused by: neonatal stroke, prenatal circulatory disturbances, congenital infections, brain maldevelopment, perinatal asphyxia - Present **early in life** and **NOT** result of progressive or degenerative disease
30
What is Spastic Cerebral Palsy; what are signs and symptoms; what are 3 subtypes?
- **Most common** subtype of CP - **Presentation:** Spasticity, Hyperreflexia, Clonus, Babinskis **Subtypes:** 1) Spastic Hemiplegia: only **one side affected** 2) Spastic Diplegia: **LEs affected** with **little** to **no UE involved** 3) Spastic Quadriplegia: **all limbs affected,** children are often **severely handicapped**; increased risk of complications
31
Amyotrophic Lateral Sclerosis may be due to a defect in; what are the clinical features of this disease?
- Pathophysiology unknown, may be **defect** in **glutamate metabolism** - Asymmetric **MIX** of **UMN** and **LMN signs** **- UMN:** degeneration of motor neurons in the primary motor cortex as well as axons throughout corticospinal/corticobulbar tracts (**weakness, hyperreflexia and spasticity**) **- LMN:** degeneration of Ventral horn cells (**weakness, atrophy, fasciculations**)
32
What is the extrapyramidal Pontine Reticular pathway used for?
Activates antigravity reflexes in erect position
33
What is the extrapyramidal Medullary reticulospinal pathway used for; how is it related to reflex hypersensitivity in UMN damage?
- Mediate cortical control of reflexes - **Inhibits postural or flexor reflexes** that may interfere with execution of voluntary motor activity - **UMN damage --\> loss of reflex inhibition ---\> Reflex Hypersensitivty --\> UMN signs**
34
What is the extrapyramidal Rubrospinal tract used for; originates where?
- Mediated voluntary motion, **most notably flexor movement** of the arms - Originates in Red nucleus of midbrain (small in humans)
35
What is the extrapyramidal Tectospinal tract used for; originates where?
- Coordinates movement of head with eyes - Originates in **Superior colliculus**
36
What is the extrapyramidal Vestibulospinal tract used for; originates where?
- Maintains posture against gravity, **most notably**, trunk and UE/LE extensors - Originates in **vestibular cortex**