Spinal control of motor functions Flashcards
corticobulbar tract
Pathway carrying motor information from the primary and secondary motor cortices to the brainstem.
corticospinal tract
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.
decerebrate rigidity
Excessive tone in extensor muscles as a result of damage to descending motor pathways at the level of the brainstem.
medullary pyramids
Longitudinal bulges on the ventral aspect of the medulla that signify the corticobulbar and corticospinal tracts at this level of the neuraxis.
premotor cortex
Motor association areas in the frontal lobe anterior to the primary motor cortex; thought to be involved in planning or programming of voluntary movements.
primary motor cortex
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.
reticular formation
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.
spinal shock
The initial flaccid paralysis that accompanies damage to descending motor pathways.
superior colliculus
Laminated structure that forms part of the roof of the midbrain; plays an important role in orienting movements of the head and eyes.
upper motor neuron syndrome
Signs and symptoms that result from damage to descending motor pathways; these include paralysis, spasticity, and a positive Babinski sign.
What are the differences between red (type 1) and white (type 2) muscle fibers?
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).
What is the difference between a motor unit and a motor pool?
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.
How are motor neurons arranged and distributed in the ventral horn?
The more medial motor neurons innervate axial muscles (e.g., paraspinal and very proximal muscles). The most lateral motor neurons innervate distal muscles.
What happens physiologically as a muscle gradually increases its force of contraction?
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.
What is the reflex response to stretch of a muscle?
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.
How can activation of a muscle spindle afferent inhibit motor neurons to antagonist muscles?
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.
How can you recognize hyperactivity of a muscle stretch reflex?
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.
What is spasticity? How can you test it and what does it do?
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.
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?
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”).
What would happen to a muscle if a gamma motor neuron to a muscle spindle in that muscle was activated?
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”).
Why do Golgi tendon organs respond mainly respond to muscle tension rather than muscle stretch?
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.
What is the response to sudden activation of Golgi tendon organ afferent fibers?
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).
What are the advantages of having most motor activity controlled through interneurons?
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.
What is the reflex response that happens when there is activation of nociceptors in a limb?
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.