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632: Neuroanatomy-Neuroscience > Spasticity and UMN Lesions > Flashcards

Spasticity and UMN Lesions Flashcards

1
Q

What does the mechanism of spasticity depend on?

A

The site of the lesion and whether the lesion occurs prenatally

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2
Q

Describe the development of a lesion in spastic CP patients

A

The lesion affects the corticospinal and corticobrainstem tracts during the perinatal period, interfering with development of the brain and spinal cord

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3
Q

What does damage to the corticospinal tracts during development result in?

A

It eliminates some competition for synaptic sites during a critical period, causing persistence of inappropriate connections and abnormal development of spinal motor centers which in turn lead to abnormal cocontraction

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4
Q

What is abnormal cocontraction?

A

the simultaneous activation of antagonist muscles that interferes with task performance

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5
Q

What 3 things lead to movement dysfunction in developmental spasticity (CP) patients?

A
  • cocontraction
  • hyperreflexia
  • brainstem UMN overactivity
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6
Q

What does a typical stroke interrupt?

A

The corticospinal and corticoreticular tracts on one side of the brain

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7
Q

What is the primary cause of stroke spasticity?

A

Brainstem UMN overactivity which results in excessive muscle contraction

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8
Q

What happens when UMN tracts are severed in the spinal cord?

A

Interneurons are disinhibited and LMNs below the lesion develop enhanced excitability, which causes hyperreflexia

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9
Q

What are the positive aspects of hyperreflexia?

A
  • people can intentionally trigger hyperreflexia to elicit involuntary muscle contraction during transfers
  • muscle contractions triggered by hyperreflexia help maintain muscle mass and assist in venous return
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10
Q

What are the 5 clinical signs of spinal spasticity?

A
  • velocity-dependent increase in tonic stretch reflexes
  • brisk deep tendon reflexes
  • exaggerated cutaneous reflexes
  • involuntary flexor and extensor spasms
  • clonus
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11
Q

In people post stroke or with spastic cerebral palsy, what 3 things contribute to hypertonia?

A
  • reticulospinal tract overactivity
  • contracture
  • increased number of weak actin-myosin bonds
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12
Q

In post stroke patients does hyperreflexia contribute to hypertonia during active movements?

A

Not typically

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13
Q

After SCI what contributes to the increased resistance to stretch?

A

tonic stretch hyperreflexia

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14
Q

What are the contributors to hypertonia in spastic cerebral palsy?

A

vestibulospinal tract overactivity and abnormal muscle development

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15
Q

What 2 tools are used to assess hypertonia?

A
  • electromyographic (EMG) recordings

- Ashworth scale

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16
Q

Surface EMGs are used to reveal what?

A

the mechanisms of hypertonia and to assess effects of interventions on tone and motor impairment

17
Q

EMGs are used to determine what factors are contributing to movement impairment. List the 4 factors

A
  • Contracture
  • Hyperreflexia
  • Cocontraction
  • Inappropriate timing of muscle activity
18
Q

What is the difference in EMG readings between phasic and tonic stretch hyperreflexia?

A

Phasic stretch hyperreflexia is indicated by excessive EMG amplitude occurring 30 to 50 msec after initiation of muscle stretch.
Tonic stretch hyperreflexia is indicated by excessive EMG amplitude occurring 80 to 100 msec after initiation of muscle stretch.

Increased muscle membrane depolarization registers as increased amplitude

19
Q

How does cocontraction effect EMG readings?

A

It produces temporal overlap of EMG activity in antagonist muscles

20
Q

What is the Ashworth Scale?

A

a subjective clinical assessment of resistance to passive stretch

21
Q

What is a downfall to the Ashworth scale?

A
  • it cannot be used to distinguish between contracture and hyperreflexia
  • there is no relationship between it and functional activity
22
Q

What are high Ashworth scores associated with?

A

Contracture, not spasticity

23
Q

What are the 3 types of UMN lesions that are not due to trauma?

A
  • Spastic cerebral palsy (CP)
  • Stroke or cerebrovascular accident (CVA)
  • Spinal cord injury (SCI)
24
Q

What leads to movement dysfunction in spastic CP?

A
  • abnormal supraspinal influences
  • failure of normal neuronal selection
  • consequent aberrant muscle development
25
Q

What are the motor disorders included in spastic CP?

A
  • Problems with coordination
  • Abnormal tonic stretch reflexes both at rest and during movement
  • Reflex irradiation which is the spread of reflex activity
  • Lack of postural preparation before movement
  • Abnormal cocontraction of muscles
26
Q

Where does stroke most frequently affect?

A

The middle cerebral artery (MCA)

27
Q

Stroke affecting the MCA causes damage to what?

A

Corticospinal, corticoreticular and corticobrainstem neurons and thus disrupting cortical connections with the spinal cord, brainstem and cerebellum

28
Q

What are the most common impairments in MCA stroke patients?

A

paresis and decreased fractionation of movement in both the upper and lower limbs contralateral to the lesion

29
Q

What 2 things cause excessive resistance to stretch in paretic muscles following a stroke?

A
  • contracture

- increased weak binding of actin and myosin

30
Q

In patients with hemiparesis, the gastrocnemius on the weak side is 50% less active than the normal side during pushoff, so why is there an increase in gastrocnemius resistance to stretch in the paretic limb during the stance phase?

A

There is a large, early increase in the Achilles tendon force despite very little EMG activity of the gastrocnemius

31
Q

What is the only factor that limits upper limb activity after stroke?

A

weakness

32
Q

Weakness in upper extremity function following stroke is due to what 2 things?

A
  • voluntary activation failure

- muscle atrophy

33
Q

What tract provides voluntary control of paretic limb muscle post stroke?

A

Reticulospinal

34
Q

What are the 3 conditions that occur following SCI?

A

1) phasic stretch reflexes and the withdrawal reflex involving intact spinal segments below the lesion can still be elicited
2) the amount of contracture significantly correlates with the amount of resistance to muscle stretch
3) type IIb muscle fibers predominate and the number of type I muscle fibers is reduced

35
Q

What 3 things produce excessive resistance to muscle stretch after a SCI?

A
  • excessive stretch reflexes
  • muscle contracture
  • increased cross-bridge binding
36
Q

What 3 things limit active movement in people with incomplete SCI?

A
  • paresis
  • hyperreflexia
  • contracture
37
Q

In summary what are the 4 common signs of UMN lesions?

A
  • Paresis
  • Abnormal timing of muscle activity
  • Babinski’s sign
  • Myoplasticity
38
Q

In summary what are the 4 common signs of chronic SCI?

A
  • hyperreflexia of the phasic stretch reflex
  • clonus
  • abnormal cutaneous reflexes
  • the clasp-knife phenomenon
39
Q

In summary what are the 2 things that accompany UMN syndromes that arise during nervous system development?

A
  • reflex irradiation

- abnormal cocontraction of antagonist muscles

632: Neuroanatomy-Neuroscience (26 decks)

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