Spasticity Flashcards

1
Q

What happens soon after a spasticity-causing event?

A

Key characteristics of spasticity emerge after the neurogenic shock stage, including hyperreflexia, reflex cascade, and reversion to early motor system patterns.

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2
Q

What is hyperreflexia in spasticity?

A

Hyperreflexia is the primacy of basic excitatory protective reflexes (e.g., stretch reflex, withdrawal reflex, joint protective reflexes) operating with poor or absent HMC modulation.

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3
Q

How does hyperreflexia affect reflex responses?

A

It causes exaggerated responses to both normal and noxious stimuli, such as a larger-than-normal reaction to touching something hot.

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4
Q

What is Reflex Cascade (Domino Reflex/Reflex Spillover/Spastic Reaction)?

A

It is when one stimulus activates a sequence of reflex responses that spreads in either or both directions from the original activation, often including clonus at affected joints.

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5
Q

What happens during reversion to early motor system patterns in spasticity?

A

The motor system reverts to primitive patterns, often showing flexion dominance or abnormal reflexes like Babinski’s Sign.

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6
Q

What is Flexion Dominance in spasticity?

A

It is when the lesion causes the motor system to revert to a flexed, “fetal position,” where flexion becomes the normal and comfortable resting position for affected joints.

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7
Q

What is Babinski’s Sign?

A

Babinski’s Sign occurs when the primitive Babinski reflex re-emerges abnormally in adults, causing reflex toe extension and ankle dorsiflexion in response to plantar stimulation.

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8
Q

Why is Babinski’s Sign abnormal in adults?

A

In normal CNS maturation, the infantile Babinski reflex is replaced by a functional toe flexion and ankle plantarflexion response for standing and walking.

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9
Q

What is clonus?

A

Clonus is the alternating activation of agonist and antagonist stretch reflex responses acting on a joint, causing a “reverberating” back-and-forth action.

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10
Q

What are spastic co-contractions?

A

Abnormal antagonist contractions occur during voluntary agonist effort, creating a rigidity-like appearance during clinical observation.

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11
Q

What is spastic dystonia?

A

It is a muscle contraction present at rest, leading to a holding position that is very sensitive to stretch.

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12
Q

What are the key muscle tone abnormalities seen in spasticity?

A
  1. Resting tone can be too high, too low, or fluctuate.
  2. Abnormal tone setting occurs with posture changes, walking, etc.
  3. Tone can change dramatically with emotion, pain, etc.
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13
Q

What motor control abnormalities are associated with spasticity?

A
  1. Diminished fine motor control.
  2. Synergistic stabilization patterns become stereotyped.
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14
Q

What are the effects of contractures in spasticity?

A
  1. Reduced range of motion (ROM) and specificity of movements.
  2. Early activation of protective reflexes.
  3. Ischemia and pain add to muscle irritability.
  4. Develop within 6 months after the spasticity-causing event.
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15
Q

What is 1a neuronal sprouting?

A

It is when 1a neurons add telodendria (axon terminal branches), increasing their number of synapses on their partner alpha motor neuron in the stretch reflex arc.

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16
Q

How does 1a neuronal sprouting intensify spasticity?

A

The increased synapses cause a much larger amount of acetylcholine to be released at the alpha motor neuron, resulting in an exponentially more intense reflex contraction in response to muscle elongation.

17
Q

What happens with reduced spinal cord availability of GABA in spasticity?

A
  1. Reduces the strength and duration of the GTO reflex response.
  2. Weakens the GTO’s ability to counteract the stretch reflex.
18
Q

How do neuronal sprouting and reduced GABA together affect spasticity?

A

They make the stretch reflex significantly stronger/hyperreflexic and the GTO reflex weaker, disrupting their homeostatic relationship and causing spastic hypersensitivity to stretch.