Spinal control of motor functions Flashcards

1
Q

corticobulbar tract

A

Pathway carrying motor information from the primary and secondary motor cortices to the brainstem.

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2
Q

corticospinal tract

A

Pathway carrying motor information from the primary and secondary motor cortices to the spinal cord in humans. Essential for the performance of discrete voluntary movements, especially of the hands and feet.

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3
Q

decerebrate rigidity

A

Excessive tone in extensor muscles as a result of damage to descending motor pathways at the level of the brainstem.

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4
Q

medullary pyramids

A

Longitudinal bulges on the ventral aspect of the medulla that signify the corticobulbar and corticospinal tracts at this level of the neuraxis.

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5
Q

premotor cortex

A

Motor association areas in the frontal lobe anterior to the primary motor cortex; thought to be involved in planning or programming of voluntary movements.

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6
Q

primary motor cortex

A

A major source of descending projections to motor neurons in the spinal cord and cranial nerve nuclei; located in the precentral gyrus (Brodmann’s area 4) and essential for the voluntary control of movement.

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7
Q

reticular formation

A

A network of neurons and axons that occupies the core of the brainstem, giving it a reticulated (“net-like”) appearance in myelin-stained material; major functions include control of respiration and heart rate, posture, and state of consciousness.

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8
Q

spinal shock

A

The initial flaccid paralysis that accompanies damage to descending motor pathways.

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9
Q

superior colliculus

A

Laminated structure that forms part of the roof of the midbrain; plays an important role in orienting movements of the head and eyes.

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10
Q

upper motor neuron syndrome

A

Signs and symptoms that result from damage to descending motor pathways; these include paralysis, spasticity, and a positive Babinski sign.

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11
Q

What are the differences between red (type 1) and white (type 2) muscle fibers?

A

Red muscle fibers are small, weak, slow to contract but very resistant to fatigue and used for tonic, low force activity. White muscle fibers are the opposite although there are two types (one somewhat more resistant to fatigue but intermediate in strength).

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12
Q

What is the difference between a motor unit and a motor pool?

A

A motor unit is a single alpha motor neuron and all of the muscle fibers to which it is connected. A motor pool is all of the motor neurons that innervate one muscle. Motor pools extend over several spinal segments and the axons of these motor neurons leave the spinal cord in several nerve roots that join to form nerves that go to muscles.

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13
Q

How are motor neurons arranged and distributed in the ventral horn?

A

The more medial motor neurons innervate axial muscles (e.g., paraspinal and very proximal muscles). The most lateral motor neurons innervate distal muscles.

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14
Q

What happens physiologically as a muscle gradually increases its force of contraction?

A

First one motor unit begins firing (generating action potentials) at a slow rate. This rate increases until a second motor unit is added, which increases firing until a third is added, etc.

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15
Q

What is the reflex response to stretch of a muscle?

A

Stretch of extrafusal muscle fibers also stretches intrafusal muscle fibers, which are organized in parallel with the extrafusal fibers. This stretch deforms annulospiral nerve endings, which are activated based on the degree and speed of stretch. The annulospiral endings are continuous with 1a afferent nerve fibers (the largest, most rapidly conducting nerve fibers). These sensory axons enter the spinal cord through the dorsal root (the cell bodies are in the dorsal root ganglion). These muscle spindle afferent terminate directly on motor neurons that return to extrafusal muscle fibers in the muscle that contains the muscle spindle, exciting these motor neurons. They also synapse on interneurons that excite agonist muscles (muscles that have a similar function to the muscle stretched) and inhibit antagonist muscles.

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16
Q

How can activation of a muscle spindle afferent inhibit motor neurons to antagonist muscles?

A

Since all collateral nerve terminals of an axon contain the same neurotransmitter and since the neurotransmitter is glutamate (which is excitatory), these muscle spindle afferent axons synapse on, and excite interneurons that are inhibitory to motor neurons to the antagonist muscles.

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17
Q

How can you recognize hyperactivity of a muscle stretch reflex?

A

Pathologically brisk reflexes are recognized by the speed with which they are elicited and the amplitude. They often jerk to a stop because of overactivity of stretch reflexes in the antagonist muscles. Additionally, there is often contraction of muscles beyond just the agonist muscles, sometimes to include the contralateral muscles.

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18
Q

What is spasticity? How can you test it and what does it do?

A

Spasticity is overactivity of stretch reflexes that makes it difficult to passively move a joint. This resistance is greater the faster the movement is. If spasticity is severe, the resistance may be great at the onset of movement, with a sudden loss of resistance as the Golgi tendon organs are activated (this “inverse myotonic reflex” is also overactive). This give a “clasp knife” feel to the resistance.

19
Q

What would happen if a muscle did not contract intrafusal muscle fibers at the same time as extrafusal muscle fibers are contracted during a movement?

A

As a muscle was voluntarily contracted by activation of alpha motor neurons, the intrafusal muscle fibers would become lax. This would decrease action potential generation in the muscle spindle afferent fibers and decrease the excitation of the alpha motor neurons that are making the muscle contract. Therefore, the muscle contraction would be less than desired. In order to prevent this, the gamma motor neurons are activated at the same time as the alpha, resetting the muscle spindles to the same length as the new position of the muscle (“alpha-gamma coactivation”).

20
Q

What would happen to a muscle if a gamma motor neuron to a muscle spindle in that muscle was activated?

A

The muscle woud contract. This is because of the following sequence of events. Activation of a gamma motor neuron will contract the ends of the muscle spindle intrafusal fibers. This will stretch the center of the intrafusal fiber, deforming the annulospiral nerve endings and generating action potentials in the 1a afferent nerve fibers. These spindle afferent fibers will synapse directly on motor neurons that return to extrafusal muscle fibers of the muscle. These muscle spindle afferent fibers will also synapse on interneurons that polysynaptically excite agonist muscles and inhibit antagonist muscles. Ultimately, the muscle will contract (this process has been called the “gamma loop”).

21
Q

Why do Golgi tendon organs respond mainly respond to muscle tension rather than muscle stretch?

A

During stretch, the muscle itself is much more elastic than tendon (where the Golgi tendon organ is located). Therefore, stretch mostly affects the muscle belly, with much less force being transmitted to the GTO located in the tendon. This is true until the muscle reaches it’s elastic limit, where the GTO will see a rather sudden increase in force (just before the muscle/tendon tears). During muscle contraction, the physical properties of the muscle are changed by contraction of the extrafusal muscle fibers, which exert pull on the tendon. Therefore, the GTO is mainly a sensor of muscle tension.

22
Q

What is the response to sudden activation of Golgi tendon organ afferent fibers?

A

Sudden and massive activation of GTO afferent fibers can result in an “inverse myotonic reflex” in which the muscle attached to the tendon containing the GTO is inhibited, and antagonist muscles are excited (both polysynaptically).

23
Q

What are the advantages of having most motor activity controlled through interneurons?

A

here are patterns of excitation and inhibition of motor neurons produced by pools of interconnected interneurons. Therefore, activation of this pool can create a pattern of coordinated muscle activation and inhibition that allows for smooth movement.

24
Q

What is the reflex response that happens when there is activation of nociceptors in a limb?

A

The nociceptive withdrawal reflex (also known as the flexion reflex) is a coordinated action to remove the body part from harm. It involves a pattern of physiological flexion in a limb (basically all of the movements that would withdraw a digit from harm should it be acutely injured), along with exactly the opposite movements in the contralateral limb.

25
Q

What pathological reflex reflects overactivity of the nociceptive flexor (withdrawal) reflex?

A

The Babinski reflex (also known as an “upgoing toe”) is a sign of overactivity of the withdrawal reflex.

26
Q

hat other patterns of spinal reflexes are there?

A

There are coordinated patterns (through interneurons) of activation and inhibition associated with locomotor patterns integrated into the spinal cord. Unfortunately, these do not produce strong enough reflex action by themselves to permit ambulation after spinal cord injury.

27
Q

What are the functions of descending tracts of the spinal cord?

A

In addition to being predominately involved in motor control (muscle tone, regulation of reflexes and movement) descending tract are also involved in controlling autonomic function and sensory transmission in the spinal cord.

28
Q

What are some fundamental differences in function of tracts in the ventral funiculi versus those in the lateral funiculi (so-called lateral motor systems)?

A

Axial motor neurons and the interneurons that regulate them are in the medial part of the anterior horn. Descending tracts in the ventral funiculus have a greater effect on these axial motor neurons. Motor neurons to the limbs are lateral in the anterior horn of the spinal cord and are more affected by tracts in the lateral funicuus. The descending tracts that are immidiatly anterior to the ventral horn tend to be more involved in regulation of tone.

29
Q

What is the difference between the concept of “upper motor neurons” and the corticospinal tract?

A

Upper motor neurons include all of the connections between the cerebral cortex (both direct and indirect) to the spinal cord. Obviously, this includes the corticospinal tract (a direct pathway), but also includes indirect pathways such as the cortico-reticular, reticulo-spinal pathway (among others).

30
Q

What are the functional differences between the corticospinal tract and the indirect corticospinal pathways?

A

The CST is responsible for fine, rapid and highly skilled motions (particularly of distal limbs and fingers). Damage produces contralateral deficits in distal limb movements. The indirect corticospinal pathways are mostly involved in regulating muscle tone (mostly decreasing it) and generating postures and proximal limb/trunk positions that generally position the limbs in support of the more skilled movements.

31
Q

What is the pathway for the direct corticospinal tracts?

A

The origin is in a somatotopic distribution in the motor cortex (motor homunculus). This tract runs through the posterior limb of the internal capsule, the middle part of the cerebral peduncle, the basal pons, and the medullary pyramid. Most of the tract decussates in the pyramidal decussation at the junction between the upper spinal cord and the medulla (lateral corticospinal tract). These fibers descend in the lateral funiculus of the spinal cord. A small percentage of fibers do not decussate and descend in the anterior funiculus (anterior corticospinal tract).

32
Q

What is the function of the direct corticospinal tracts (lateral and anterior)?

A

The lateral CST is responsible for fine, rapid and highly skilled motions (particularly of the fingers). Damage produces contralateral deficits in distal limb movements. The anterior corticospinal tract is in the ventral funiculus. Therefore, they mostly affect axial muscles (e.g., trunk and very proximal limbs).

33
Q

What properties would be common to all descending tracts in the ventral funiculus?

A

All tracts in the anterior funiculus tend to affect axial motor neurons more and they terminate bilaterally. Therefore, it is difficult to paralyze proximal limb movements by unilateral damage to the CNS.

34
Q

What are the categories of corticobulbar pathways based on their terminations in the brain stem, and what do they do?

A

There are corticobulbar axons terminating in motor cranial nerve nuclei for voluntary control. These axons control the voluntary functions of motor cranial nerves (e.g., chewing, eye movements, speaking, face movement). Of course, there are reflexes affecting each of these. Some corticobulbar axons terminate in sensory nuclei in the brain stem (such as the dorsal column nuclei). These axons modify sensory transmission. There are corticobulbar axons terminating in brain stem regions that project to the spinal cord (forming indirect corticospinal pathways). These include areas like the red nucleus and reticular formation that are able to regulate reflexes and muscle tone and also that provide indirect pathways for control of crude movement. Finally, there is termination in the basal pontine nuclei for relay to the cerebellum.

35
Q

What is the pattern of control of motor cranial nerve nuclei by corticobulbar axons?

A

There are bilateral connections between the cerebral cortex and the motor trigeminal nucleus (i.e., from both hemispheres to each trigeminal motor nucleus). Therefore, unilateral strokes will not paralyze chewing. The connections between the cortex and the hypoglossal and vagal nuclei are bilateral, but more are crossed. Therefore, extensive damage to one hemisphere will slightly weaken the contralateral tongue and soft palate. The facial nucleus represents the most interesting and important corticobulbar connection. Corticobulbar input to motor neurons controlling lower face is contralateral while corticobulbar input to motor neurons controlling the upper face is bilateral. Therefore, unilateral weakness around the mouth with preserved strength in the upper face (such as forehead muscles) is a pattern indicating damage to corticobulbar axons.

36
Q

What is the clinical concept of “Upper motor neurons”?

A

This is a collective term for corticobulbar and corticospinal tracts that are involved in motor control and regulation of muscle tone and reflexes.

37
Q

What are the classic signs and symptoms of upper motor neuron damage?

A

Upper motor neuron damage produces weakness particularly of fine distal movements (like hands), sparing of proximal movements (such as shrugging the shoulders), increased myotatic (muscle stretch) reflexes, pathological reflexes (such as upgoing toes of Babinski response) and spasticity.

38
Q

following upper motor neuron damage: why are spinal reflexes increased; why do you see pathological reflexes (e.g., Babinski sign); and why is there increased muscle tone?

A

The corticobulbar tracts activate pates of the reticular formation (especially medullary reticular formation) that have a strong inhibitory effect on muscle tone and reflexes at the spinal cord. Increased reflexes are due to a decrease in this inhibitory effect. Therefore, deep tendon reflexes are overactive, there may be clonus and pathological reflexes may appear (the Babinski sign is an exaggerated withdrawal reflex). Increased muscle tone may present as spasticity.

39
Q

What is the difference between an upper and lower motor neuron?

A

The upper motor neurons originate in the cerebral cortex and travel down to the brain stem or spinal cord, while the lower motor neurons begin in the spinal cord and go on to innervate muscles and glands throughout the body.

40
Q

What are the major components of a stretch reflex?

A

The pathway can be described as a ‘reflex arc’ which is made up of 5 components:

  1. A receptor – muscle spindle.
  2. An afferent fibre – muscle spindle afferent.
  3. An integration centre – lamina IX of spinal cord.
  4. An efferent fibre – α-motoneurones.
  5. An effector – muscle.
41
Q

Primary motor cortex (M1)

A

Anterior wall of central sulcus (Brodmann area 4)

→Very few granular cells in layer IV

→Many large pyramidal cells (Betz cells) in layer V

Direct connections with motor neurons and interneurons in the spinal cord and brainstem

→Low current stimulation evokes movements

Rough topographic representation of body (‘homunculus’)

Coordinated movements of trunk and extremities→Population coding of movement direction

42
Q

Dorsal premotor cortex involvement in movement

A

Dorsolateral surface of precentral gyrus (BA 6)

Externally (sensory) guided behavior

Selection of behavior based on external cues(choice reaction time tasks)

Visuo-motor integration

▪Reaching

▪Targeting of movements in space

▪Spatial structure of sequences

43
Q

Supplementary motor area

A

Medial surface of precentral gyrus(BA 6)

▪Internally generated movements

▪Movement sequences

▪Both ordinal (spatial) and temporal aspects

▪Motor imagery

▪Bimanual coordination

44
Q

Ventral premotor cortex (PMV)

A

Ventrolateral precentral gyrus (Brodmann area 6)

▪First region where mirror neurons were found

→Neurons that fire during performance of an act and during observation of someone else performing the same act

▪Mirror neurons found also in other motor areas and in the inferior parietal cortex (‘the mirror system’)