Motor System Flashcards

1
Q

What is the motor unit?

A

[the lower motor neuron and all of the muscle fibers it innervates]

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2
Q

What is an alpha motor neuron?

A

[the power guys, they innervate extrafusal muscles]

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3
Q

Can single muscle fibers be innervated by more than one alpha motor neuron?

A

[no]

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4
Q

If I work out really, really hard, using heavy weights over months, my muscles get big. Am I increasing the number of muscle fibers?

A

[No, you’re increasing the size of the muscle fibers you have… you may also be adding more mitochondria for them]

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5
Q

Are there different types of muscle fibers (cells)?

A

[Yes. Slow twitch, fast twitch fatigue-resistant, and fast twitch fatigueable]

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6
Q

Do lower motor neurons innervate multiple muscle fibers?

A

[Yes, but all are of the same type. Innervating only a few fibers is associated with dexterity. Motor units involving hundreds, if not thousands of fibers, are typically postural muscles]

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7
Q

Do muscle fibers vary in strength?

A

[Yes, it’s specified as force. A slow twitch fiber only generates ~4 dynes, whereas a fast twitch fatigue resistant generates about 28 dynes, and a fast twitch fatigueable ~70 dynes. However, the slow twitch can go forever, and have lots of mitochondria for efficient energy management. Fast-twitch fatigueable have no mitochondria, pooping out in seconds and generating lactic acid]

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8
Q

How do I get muscles to increase force?

A

[normally the slow twitch are always active. They can increase force if the LMN increases firing rate. If more force is needed they start recruiting other LMNs, from other slow twitch to fast twitch fatigue-resistant to fast twitch fatigueable]

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9
Q

Can I change my ratio of muscle fibers I have?

A

[Not much… although one does read stories about it every now and then. Suffice to say, if you’ve never dunked a basketball, you probably never will]

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10
Q

What is the size principle?

A

[recruitment of muscles goes from small alpha motor neurons to large motor neurons, also from slow-twitch to fast-twitch fatigue-resistant to fast-twitch fatigueable]

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11
Q

What’s the difference between a fibrillation and a fasciculation?

A

[both are ‘twitches’, triggering of muscle fiber contraction; fibrillation is single muscle fibers (usually need EMG), fasciculation is motor units and visible to naked eye]

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12
Q

Ia fibers are the fastest axons we have. How fast are they? How big are they?

A

[120 m/sec; 20 um (includes myelin)]

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13
Q

Ia fibers innervate which sensory structure?

A

[muscle spindle]

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14
Q

Gamma motor neurons are lower motor neurons but only innervate intrafusal muscles on which structure?

A

[muscle spindle]

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15
Q

Identify the ‘sensor’ for the inverse myotatic reflex?

A

[Golgi tendon organ]

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16
Q

What does the inverse myotatic reflex do?

A

[activation inhibits the homonymous muscle via a disynaptic circuit, yielding decreased contraction of that muscle. Sensor is Golgi tendon organ which innervates muscle tendons (considered ‘in series’ with the muscle vs muscle spindle considered ‘in parallel’]

17
Q

What is the myotatic reflex?

A

[the prototype, ‘knee-jerk’ reflex. Stretch of a muscle stretches the muscle spindle organ (which is set in parallel with the extrafusal ‘power’ muscle) on which the Ia afferent fiber resides and is activated by the stretch. This activation causes monosynaptic activation (and contraction) of the muscle (leg extension due to contraction of the quads in the knee-jerk reflex) and its ilk (referred to as homonymous muscles) and disynaptic inhibition of antagonistic muscles via a specific inhibitory interneuron, the Ia inhibitory interneuron. In the knee jerk reflex, this mean inhibiting the hamstring muscles]

18
Q

What seems to be the ‘normal’ use of the myotatic reflex?

A

[this is the most important reflex in everyday life because it is powerful with a constant interplay between flexors and extensors, and information coming back via the Ia fibers. The Ia output specifies muscle length and its dynamics… the sum of this will specify postural position, as well as our kinesthetic sense, position in space. Second, it has a safety function… should you suddenly trip while walking, the induced stretch will provide a powerful signal to contract the muscle and keep you from falling (course, the linear acceleration of your trip will also activate your otoliths which will then correct the sudden perturbation in your balance ]

19
Q

What are the properties of a reflex?

A

[Reflexes are locally autonomous, depend only on a simple spinal (or cranial nerve circuit). They have a sensory component to initiate the reflex, may or may not have local inhibitory neurons to change sign, and effectors, or lower motor neurons to drive the response. Spinal reflexes occur in the absence of any upper motor neuron involvement. Normally, upper motor neurons can alter the gain (intensity) of the reflex, and some can even drive the reflex with or without the sensory input.

20
Q

How do reflexes decrease the computational load on programming movement?

A

[Reflexes are referred to as ‘the building blocks of behavior’, they are little, and very useful pieces of behavior that we can press into service to accomplish motor tasks. Similar to a computer software sub-routine, instead of forcing the upper motor neuron to specify every muscle length and action, the upper motor neuron can simply press this reflex or that reflex into service. Upper motor neurons and local circuits can adjust the intensity of the expressed reflex. Reflexes can also be chained into useful repetitive behaviors, e.g., locomotion is the chaining of spinal reflexes in a very adaptive manner, and apparently, under the control of a single locus in midbrain (the ‘locomotor center’). Basically, ‘push a button’ and we start walking, and the numbers of neurons active in that ‘center’ specify speed which also modifies the step cycle and phase relations between the extensors/flexors of each leg. Such chaining of reflexes for everyday behaviors are referred to as central pattern generators]

21
Q

What’s so interesting about the fact that a brainless frog can scratch where it itches?

A

[It tells us interspinal circuits can program kinematics of a ‘reflex’ without use of any upper motor neurons… ‘intelligent’ behavior whose topological accomplishment is ‘scratch where it itches’. Investigators fixed the posture of the frog, put vinegar on the frog’s ‘elbow’ and it scratched where the vinegar was placed (producing one set of kinematics which are the product of certain muscles contracting at certain times). Investigators then changed the frog’s posture, put vinegar on the same spot, and the frog scratched where it itched. But the change in posture necessitated a different motor program (producing different kinematics)… the interspinal circuits solved the problem, showing they are capable of high level motor control … i.e., tailoring a motor trajectory based on current posture]

22
Q

Who are the upper motor neurons and what do they do?

A

[Upper motor neurons ‘control’ lower motor neurons, but as we’ve seen, they are largely ‘idea’ guys that drive a behavior without specifying kinematics, which are left largely to local circuits (i.e., reflexes). The upper motor neurons are the corticonuclear (aka, corticobulbar) fibers that drive the cranial nerve motor nuclei (III, IV, V, VI, VII, IX, X, XI, XII), and the corticospinal, rubrospinal, vestibulospinal, and reticulospinal tracts. The oculomotor system is particularly sneaky as there are several sets of upper motor neurons. Layer V neurons in the frontal eye fields, neurons in the intermediate layers of the superior colliculus, and neurons in the vertical and horizontal gaze ‘centers’]

23
Q

What does the corticospinal tract do?

A

[Absolutely critical in humans; especially the lateral corticospinal tract which, when damaged, renders the person nearly paralyzed on the contralateral side. This is probably because it is common in human for the corticospinal tract to make monosynaptic contact with lower motor neurons; something uncommon in non-primates, and even other primates. The tract is dominant on distal muscles; for the upper musculature it appears extensor dominant to counteract rubrospinal influence, for the lower limbs, it seems flexor dominant to counteract the extensor dominance of reticulospinal and vestibulospinal influence].

24
Q

Where does the corticospinal tract originate?

A

[about half the fibers come out of layer V cells in Brodmann’s area 4 (primary motor strip), about 35-40% come out of Brodmann’s area 6, and, oddly, 10-15% emerge from primary somatosensory cortex. The tract descends topographically with the foot posterior in in the internal capsule and lateral in the cerebral peduncle. ~90% of the fibers cross at the pyramidal decussation to become the lateral corticospinal tract, the remaining 10% form the anterior corticospinal tract (which is proximal muscle dominant).

25
Q

Where does the rubrospinal tract originate?

A

[in the red nucleus of midbrain. Axons decussate immediately as the course posterior, and the rubrospinal tract runs with the lateral corticospinal tract in the spinal cord, but, in humans, only extends through cervical level. It is flexor dominant, and, in the absence of cortex can be driven just fine from activity in the cerebellum (e.g., flexion of upper limb observed in decorticate rigidity).]

26
Q

In decorticate posturing, what drives the rubrospinal neurons?

A

[With cortex gone, they can do just fine with cerebellar circuits. The direct drive comes from deep nuclei cells (e.g., interpositus, dentate) in the contralateral cerebellum.

27
Q

Where does the vestibulospinal tract originate?

A

[in the vestibular nuclei. There are 2 tracts: medial and lateral with medial originating mostly in the medial vestibular nucleus, and the lateral mostly in the lateral vestibular nucleus. The medial tract is the caudal extension of the medial longitudinal fasciculus and only extends through cervical level, is uncrossed and extensor dominant. The lateral tract runs the length of the spinal cord, is uncrossed, extensor dominant and tends to target proximal muscles. The lateral tract makes the ‘spots’ or fascicles of axons one can see in the inferior vestibular nucleus. Because both tracts are driven by vestibular inputs, they contribute to decorticate and decerebrate rigidity. Both tracts are critical for balance, and the lateral tract in particular is critical for maintaining muscle tone.]

28
Q

Where does the reticulospinal tract originate?

A

[There are 2 tracts: medial and lateral. The medial originates among large cells in the pons, descends uncrossed, is extensor dominant (mainly proximal muscles), and can be driven by either cortex or spinal inputs. As such, it contributes to decorticate and decerebrate rigidity. The lateral reticulospinal tract originates among large cells in the medulla, inhibits extensors (dominant on proximal muscles), is both crossed and uncrossed, and is driven by cortical influence. As such, it does not contribute to decorticate or decerebrate rigidity]

29
Q

What does the primary motor cortex (area 4) do?

A

[It is apparently critical to movement in the contralateral musculature. It contains a topographic map of the contralateral musculature with the foot represented along the medial wall of the hemisphere, and the face laterally. Electrical stimulation at very low intensities yields simple movement. Selective damage to area 4 yields a profound contralateral paresis without apraxia. This region is critical for encoding discrete movements]

30
Q

What does the supplementary motor area (medial area 6) do?

A

[this area contributes corticospinal neurons and appears to encode sequences of movements, becoming active during movement sequences, but not during simple flexion or extension. Damage here yields a contralateral apraxia without paresis]

31
Q

What does the pre-motor cortical area (lateral area 6) do?

A

[this area contributes corticospinal neurons and appears to encode movement sequences, especially if they involve bimanual coordination (e.g. the monkey was impaired in a task in which all he had to do was poke a raisin through a hole with one hand and catch it in the other. Damage here yields an apraxia without paresis]

32
Q

Where is the foot represented in the cerebral peduncle?

A

[laterally]

33
Q

What drives decerebrate rigidity?

A

[decerebrate rigidity is an extensor dominance of all 4 limbs associated with loss of corticospinal and rubrospinal tracts, resulting in unchecked influence of vestibulospinal and medial reticulospinal tracts on extensors; curiously, it is a gamma rigidity, preferentially driving gamma motor neurons… proof of this is that cutting dorsal roots (rhizotomy) relieves the rigidity. Apparently, gamma motor neurons were ‘tricking’ the muscle spindle organ and Ia fibers into thinking the muscle was being stretched when it wasn’t, tripping the myotatic reflex and pathologic extensor rigidity]