Chapter 10 Workbook Questions

Question 1

Experience and expectation of disturbances in the environment contribute to
___________________________ (feed-forward/feedback) control.

Answer 1

Feed-forward control is anticipatory and uses prior knowledge and experience of movement.

Question 2

Smooth control of automatic movement requires the continuous integration of ____________, ________________, and _______________ information.

Answer 2

Visual, somatosensory, and vestibular information is continuously monitored and integrated during movement.

Question 3

Which one of the following proteins is NOT involved in the active process of muscle contraction?
	A. Myosin
	B. Actin
	C. Tropomyosin
	D. Troponin
	E. Titin

Answer 3

E: Binding of Ca2+ with troponin causes tropomyosin to move, exposing active sites on actin for myosin to bind. When the heads of myosin swivel, the sarcomere actively contracts. Titin is a structural protein, not involved in active contraction.

Question 4

Continuous prolonged immobilization of skeletal muscle in a shortened position results in which of the following?
A. Increased muscle tone from hyperactive reflexes
B. Contracture from loss of sarcomeres
C. Increased tensile strength from the addition of titin
D. Both A and B
E. A, B, and C

Answer 4

B: When skeletal muscle is continually immobilized for a prolonged time, the muscle physiologically adjusts to the shortened position by losing sarcomeres from the ends of myofibrils. This length adjustment enables the shortened muscle to contract optimally at the shortened length.

Question 5

Which one of the following produces weak actin-myosin bonding?
A. Active muscle contraction
B. Muscle immobility
C. Physiologic contracture
D. Active contraction in lengthened muscles
E. Reflexive muscle contraction

Answer 5

B: When skeletal muscle is at rest, a small number of myosin crossbridges bind to actin but the crossbridge heads do not swivel. The longer muscle is immobile, the greater the number of actin-myosin weak bonds and the greater the muscle resistance to stretch. The hamstring stiffness upon standing after prolonged sitting is due to weak actin-myosin bonds.

Question 6

Descending pathways

What is the function of this group of neurons?

Answer 6

Convey signals from the brain to spinal interneurons and lower motor neurons.

Question 7

Alpha motor neurons

What is the function of this group of neurons?

Answer 7

Convey signals from the spinal cord to extrafusal muscle fibers.

Question 8

Ascending pathways

What is the function of this group of neurons?

Answer 8

Modulate activity of upper motor neurons.

Question 9

Gamma motor neurons

What is the function of this group of neurons?

Answer 9

Convey signals from the spinal cord to intrafusal muscle fibers.

Question 10

What is the purpose of alpha-gamma coactivation?
A. Prevents simultaneous activation of fast twitch and slow twitch muscles.
B. Coordinates reciprocal reflex innervation.
C. Coordinates the actions of the basal ganglia and cerebellum.
D. Maintain muscle spindle sensitivity when extrafusal muscle fibers contract.
E. Prevents contraction of an antagonist muscle when the agonist is contracting.

Answer 10

D: To maintain muscle spindle sensitivity when the extrafusal muscle fibers contract, when alpha motor neurons fire gamma motor neurons to the spindle in the same muscle also fire. The gamma signals cause the ends of the intrafusal muscle fibers to contract, maintaining the stretch of the central region of intrafusal fibers when the extrafusal muscle fibers actively contract.

Question 11

The term phasic stretch reflex is synonymous with which of the following?
	A. Myotatic reflex
	B. Muscle stretch reflex
	C. Deep tendon reflex
	D. Both A and B
	E. A, B, and C

Answer 11

E: Myotatic reflex, muscle stretch reflex, and deep tendon reflex are all synonymous with phasic stretch reflex.

Question 12

Reciprocal inhibition produces inhibition of the alpha motor neurons to which of the following?
A. Agonist muscle
B. Agonist muscle and its synergists
C. Antagonist muscle
D. Agonist muscle, its synergists and antagonists
E. Homologous muscles in the opposite limb

Answer 12

C: Reciprocal inhibition inhibits the alpha motor neurons to the antagonist muscle.

Question 13

Which of the following is true about the Golgi tendon organ (GTO)?
A. Maximum GTO activation occurs before maximum voluntary contraction.
B. GTO inhibition of the agonist alpha motor neuron causes immediate muscle relaxation via the GTO reflex.
C. Effectiveness of the contract-relax technique for stretching is dependent on GTO input.
D. GTO conveys information via a type IIa afferent to the spinal cord.
E. All of the above are true statements.

Answer 13

B: Maximum GTO activation occurs before maximum voluntary contraction. Because maximum GTO activation occurs prior to maximum voluntary contraction, GTO inhibition of the agonist alpha motor neuron cannot cause immediate muscle relaxation; otherwise, muscle could not continue to contract when GTO signals are maximal. Thus there is no GTO reflex. For the same reason, GTO inhibition cannot explain the effectiveness of the contract-relax technique. GTO information is conveyed via type Ib afferents.

Question 14

Which of the following statements about fast-twitch muscle fibers is true?
A. The neuron innervating the muscle determines twitch characteristics.
B. Alpha motor neurons having large-diameter axons innervate fast-twitch muscle fibers.
C. Using a long train of repetitive contractions identifies twitch characteristics.
D. Both A and B
E. A, B, and C

Answer 14

D: The neuron innervating the muscle determines twitch characteristics and large-diameter axons innervate fast-twitch muscles.

Question 15

Which one of the following contributes to the spinal control of walking?
A. Afferent input from muscle spindles and GTOs
B. Adaptable networks of interneurons that modulate lower motor neuron firing patterns
C. Reciprocal signals crossing in the anterior commissure of the spinal cord
D. All of the above

Answer 15

D: Stepping pattern generators (SPGs) contribute the spinal control of walking. SPGs are adaptable networks of interneurons that receive input from muscle spindles and GTOs and modulate lower motor neuron firing. The cycles of left and right SPGs are coordinated by signals that cross in the anterior commissure, so that the right lower limb hip and knee flex while the left hip and knee extend.

Question 16

Define H-reflex

Answer 16

EMG activity elicited by electrical stimulation of group Ia and Ib afferents that, in turn, stimulate motor neurons

Question 17

Define Muscle synergy

Answer 17

Simultaneous activation of multiple muscles during coordinated, voluntary movement

Question 18

Define M-wave

Answer 18

Electromyographic (EMG) activity elicited by electrical stimulation of motor neuron axons

Question 19

Define Stepping pattern generators

Answer 19

Flexible networks of interneurons that produce reciprocal movements of lower limbs

Question 20

Medial upper neuron tracts

What is the function of this motor neuron group?

Answer 20

Control lower motor neurons that innervate postural and proximal limb muscles.

Question 21

Alpha motor neurons

What is the function of this motor neuron group?

Answer 21

Innervate extrafusal muscle fibers.

Question 22

Lateral upper neuron tracts

What is the function of this motor neuron group?

Answer 22

Control lower motor neurons that innervate distally located muscles.

Question 23

Nonspecific upper neuron tracts

What is the function of this motor neuron group?

Answer 23

Increase interneuron and motor neuron activity in the spinal cord.

Question 24

Which of the medial upper neuron tracts originate in the brainstem?

Answer 24

The reticulospinal and medial and and lateral vestibulospinal tracts originate in the brainstem.

Question 25

Lateral corticospinal tracts encompass axons from neurons in which areas of cortex?

Answer 25

Lateral corticospinal tract originate from neurons in the primary motor, premotor, and supplementary motor cortex. The axons descend through the corona radiata through the internal capsule.

Question 26

What is fractionation of movement and which descending pathway is critical for fractionation?

Answer 26

Fractionation of movement is the ability to activate individual muscles independently of other muscles. Fractionation is dependent on intact signaling of the lateral corticospinal tract.

Question 27

Name the two descending tracts whose activity produces a generalized increase in spinal interneuron and motor neuron activity

Answer 27

The ceruleospinal and raphespinal tracts produce a generalized increase in spinal interneuron and motoneuron activity.

Question 28

Which one of the following involuntary muscle contractions is always abnormal?
	A. Muscle spasms
	B. Cramps
	C. Fasciculations
	D. Fibrillations
	E. All of the above

Answer 28

D: Fibrillations, because the affect only a single muscle fiber, are always abnormal. When an alpha motor neuron fires, all of the muscle fibers it innervates contract, so there is no normal mechanism to fire an individual muscle fiber. Muscle spasms, cramps, and fasciculations can occur in normal and pathologic conditions.

Question 29

Myoclonus is:
A. Severe and painful muscle spasms
B. Quick twitches of a single motor unit
C. Brief involuntary contractions of a muscle or group of muscles
D. Persistent muscle twitching after a spinal or cerebral shock
E. None of the above

Answer 29

C: Myoclonus is brief, involuntary contractions of a muscle or group of muscles. Examples are hiccups and the muscle jerks that some people experience when falling asleep. Myoclonus is not painful, affects the entire muscle, and is not characteristic after spinal or cerebral shock.

Question 30

If the lower motor neurons to a muscle are destroyed, which of the following signs affects the denervated muscles?
	A. Loss of reflexes
	B. Atrophy
	C. Spasticity
	D. Both A and B
	E. A, B, and C

Answer 30

D: Denervated muscles atrophy and lose reflexes because there is no efferent pathway from the spinal cord to the muscles. Spasticity cannot occur because spasticity is neuromuscular overactivity, and there are no signals from the nervous system to the muscles.

Question 31

After lower neuron motor denervation caused by poliomyelitis, how does recovery of some muscle strength occur?
A. Cell division of surviving motor neurons produces new motor neurons.
B. Loss of interneuronal inhibition causes hyperreflexia.
C. Axonal sprouting of surviving neurons innervate muscles fibers.
D. Both A and B
E. A, B, and C

Answer 31

C: Post-polio, some muscle strength recovers when surviving neurons innervate muscle fibers. Hyperreflexia and neural cell division do not contribute to the recovery of strength.

Question 32

Abnormal cutaneous reflexes that occur after an upper motor neuron lesion include which of the following?
A. Emergence of Babinski’s sign
B. Muscle spasms in response to normally innocuous stimuli
C. Paresthesias
D. Both A and B
E. A, B, and C

Answer 32

D: Both Babinski’s sign and muscle spasms in response to normally innocuous stimuli are abnormal cutaneous reflexes that occur after an UMN lesion. Paresthesia is an abnormal sensation, not a reflex.

Question 33

Which one of the following major factors limits movement in individuals who have had a stroke?
A. Paresis caused by decreased agonist activation
B. Loss of ability to fractionate movement
C. Abnormal timing of muscle activation
D. Both A and B
E. A, B, and C

Answer 33

E: Paresis caused by decreased agonist activation, loss of ability to fractionate movement, and abnormal timing of muscle activation limit movement in individuals post stroke.

Question 34

Clonus is characterized by which one of the following?
A. Involuntary, repetitive, and rhythmic muscle contractions in response to muscle stretch
B. Decrease in resistance to passive stretch of a hypertonic muscle
C. Excessive resistance to both passive and active muscle stretch
D. Prolonged contraction of antigravity muscles
E. Brief, involuntary contraction of a single muscle fiber

Answer 34

A: The definition of clonus is involuntary, repetitive, and rhythmic muscle contractions in response to muscle stretch.

Question 35

Decorticate rigidity occurs with which of the following?
A. Lesions of the medulla
B. Vascular lesions of the anterior choroidal artery
C. Lesions superior to the midbrain
D. Lesion to the cerebellar lobes
E. All of the above

Answer 35

C: In decorticate rigidity, the entire brainstem is intact and the lesion is superior to the midbrain.

Question 36

Myoplasticity results from which of the following?
	A. Contracture 
	B. Increased weak actin-myosin binding
	C. Spasticity
	D. Both A and B
	E. A, B, and C

Answer 36

D: Myoplasticity is adaptive changes within a muscle in response to changes in neuromuscular activity level and to prolonged positioning. Contracture and increased weak actin-myosin bonding are forms of myoplasticity. Spasticity is neuromuscular overactivity, so spasticity includes neural effects in addition to muscle effects.

Question 37

In what way are EMG recordings used to analyze the contributions of Hyperreflexia to movement impairment

Answer 37

EMG activity occurring at a specific latency after the onset of muscle stretch

Question 38

In what way are EMG recordings used to analyze the contributions of Cocontraction to movement impairment

Answer 38

Temporal overlap of EMG activity in antagonist muscles

Question 39

In what way are EMG recordings used to analyze the contributions of Contracture to movement impairment

Answer 39

Decreased passive range of motion without EMG output

Question 40

In an individual with paraparesis secondary to an incomplete spinal cord lesion, the increase in Achilles tendon tension during gait coincides with the stretch of the triceps surae during passive dorsiflexion of the foot in the stance phase. The increase in Achilles tendon tension is not correlated with an increase in EMG. What causes the abnormal muscle resistance to stretch?
	A. Spasticity
	B. Contracture
	C. Cocontraction
	D. Hyperreflexia
	E. Atrophy

Answer 40

B: The abnormal triceps surae resistance to stretch is caused by contracture. The shortened muscle cannot stretch as much as a normal length muscle.

Question 41

What is the mechanism by which onabotulinumtoxinA (BOTOX) decreases muscle activation?
A. Blocks the binding of acetylcholine (ACh) to the motor end plate.
B. Inhibits the binding of myosin to active sites on actin.
C. Blocks the release of Ca+2 from the sarcoplasmic reticulum.
D. Inhibits the release of ACh from the presynaptic terminal.
E. None of the above occurs.

Answer 41

D: Botox decreases muscle activation by inhibiting the release of ACh from the presynaptic terminal. With decreased transmitter release from the alpha motor neuron, the muscle membrane does not get the signal to initiate muscle contraction.