muscle spindle and gto Flashcards

(18 cards)

1
Q

What are muscle spindles?

A

“Proprioceptive receptors within muscles that detect changes in length and rate of stretch. Composed of intrafusal fibers (nuclear chain/bag) with Ia/II afferents.”

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2
Q

What are Golgi tendon organs (GTOs)?

A

“Proprioceptive receptors at muscle-tendon junctions that detect muscle tension (force). Innervated by Ib afferents.”

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3
Q

Compare spindle vs. GTO function:

A

“Spindles: Monitor LENGTH/STRETCH (Ia/II). GTOs: Monitor TENSION/FORCE (Ib). Spindles excite homonymous muscle; GTOs inhibit it.”

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4
Q

What is the structure of muscle spindles?

A

“1. Intrafusal fibers (nuclear chain: static; nuclear bag: dynamic). 2. Sensory endings: Ia (velocity+length)

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5
Q

How do GTOs work?

A

“Muscle contraction → Tendon stretch → Ib afferents fire → Inhibitory interneurons → Relaxation (autogenic inhibition).”

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6
Q

What is the role of gamma (γ) motor neurons?

A

“Innervate INTRAFUSAL fibers to: 1. Maintain spindle sensitivity during muscle shortening. 2. Enable α-γ coactivation for smooth movement.”

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7
Q

How does γ activity affect muscle tone?

A

“↑γ drive → ↑spindle sensitivity → ↑Ia firing → ↑α motor neuron activity → ↑muscle tone (e.g.

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8
Q

Clinical: Hyperreflexia?

A

“UMN lesion → Loss of γ inhibition → ↑spindle sensitivity → Exaggerated DTRs (e.g.

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9
Q

Clinical: Clasp-knife rigidity?

A

“GTO override: Initial resistance (spindles) → Sudden release (GTO inhibition) - seen in UMN lesions.”

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10
Q

Climber with poor balance: Which structure is faulty?

A

“Muscle spindles (Ia afferents). Poor stretch detection → clumsiness.”

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11
Q

Parkinson’s rigidity: Role of γ neurons?

A

“↑γ drive → overactive spindles → constant Ia firing → hypertonia.”

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12
Q

Weightlifter drops barbell: Which reflex acted?

A

“GTO reflex (Ib inhibition) to prevent tendon damage.”

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13
Q

Stroke patient with hyperreflexia: Why?

A

“UMN lesion → ↑γ activity → exaggerated spindle responses.”

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14
Q

Clasp-knife phenomenon: Mechanism?

A

“Initial spasticity (spindles) → sudden GTO-mediated inhibition (Ib).”

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15
Q

How does LMN lesion cause flaccidity?

A

“α motor neuron damage → no extrafusal contraction → muscle limp/paralyzed.”

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16
Q

Why are reflexes absent in LMN lesions?

A

“No α output to extrafusals → areflexia.”

17
Q

What happens to muscle spindles in LMN lesions?

A

“γ neurons often damaged → spindles slack → no Ia feedback.”

18
Q

LMN vs. UMN flaccidity?

A

“LMN: Flaccid IMMEDIATELY (α dead). UMN: Flaccid only initially (spinal shock).”