Chapter 13: Motor system Flashcards
The motor system
Movement starts out with the decision to move (frontal decision-an executive decision).
Motor planning areas-what it is that we are going to do (frontal lobe- what we need to do to achieve the goal that we set) (pre-central cortex=just in front of the central gyrus)
Control circuits- peripheral inputs (basal ganglia and the cerebellum- help with motor plan by detecting things like trajectory and speed.
Motor tracts (UMN)- neurons that extend from motor cortex down to the spinal cord. Motor neuron part of efferent motor system that start in the cortex and end in the spinal cord.
Motor neurons (LMN)- neurons that start in the spinal cord and end in a muscle. Ventral horn of spinal cord and end at a muscle
Skeletal muscles- are the target of all of this activity. A-alpha actually make the muscles move and A-gamma maintain tension to let brain know info about muscle.
Myofibrils
Muscle is nothing but proteins- some structural and some contractile
Composed of a bunch of myofibrils- a bunch of muscle fibers
Sarcomeres
a bunch of proteins that help a muscle contract.
-contractile unit of a muscle. Contains all of the structural and all of the active proteins for one little contractile unit
Z line
the structural end of a sarcomere (protein that defines boundaries of a sarcomere)
M line
a structural protein that myosin is hung on. Anchors in place in a sarcomere.
Titin
Final structural protein (light brown) extends from one end of sarcomere to another and is like a rubber band, big job is to resist a stretch that would pull the sarcomere apart. is elastic.
Skeletal muscle
When action potential arrives and calcium spills down into sarcomeres and both z lines come towards the middle and then they relax (actin climbs on the jungle gym of myosin and shortens the muscle.
Calcium makes actin climb and shortens the muscle.
A-alpha neuron brings an action potential to neuromuscular junction and creates an EPSP so it contracts (only has a gas pedal so you either step on the gas or don’t and let the muscle relax)
Acytocholine creates the EPSP opens the membrane and lets calcium get down and activates actin and actin climbs myosin and the muscle shortens/contracts.
contracture
try to lengthen a muscle but it wont let go
Cross bridges
When active crawls on to the base of myosin. When actin and myosin are in contact.
4 things that makes a muscle stiff.
Titin- Can be stiff because we reach the elastic limit of titin (feels stiff to stretch further) stiffness of titin is important when the muscle is pathologically short (contracture)
Active contraction- actin is pulling on myosin and we cannot stretch out arm because cross bridges are being formed. Active contractions can be voluntary (an active contraction) or involuntary (Parkinson’s disease- involuntary contractions of core muscles that make muscles stiff all the time due to damage to the brain telling the muscles to contract even when they don’t want to or need to.
Weak actin-myosin bonds- slight initial resistance (lightly stuck Velcro) happens when the muscle doesn’t move. As we sit muscles get stuck together (just need to move to break up the weak bods) pull bonds apart and make the muscle move again. Some of the stiffness when we try to move them is due to immobility (after moving them for a bit the stiffness will go away).
Proprioceptive information- spindle sends more signals to spinal cord and makes a connect to contract the muscle. Muscle spindles can influence the stiffness of a muscle by depolarizing motor neurons. Stretching spindle with deep tendon reflex
Muscle resistance to stretch
1) active contraction (descending motor commands)
2) Proprioceptive information
3) Weak actin-myosin bonds
4) Titin
Number of sarcomeres adapts to length
muscles are dynamic- they respond to the position and stretch. Arm is put in a sling when out of commission. Body says those sarcomeres are always shortened and the brain remodels the arm to the structure it is stuck in. When trying to stretch the muscle titin gets stretched out and the muscle cant go any further. Leads to contracture. Body has to add sarcomeres.
Therapy- maintain stretch and body will put some sarcomeres back in to reduce the constant stretch of muscle.
Cocontracture
Static- two muscles contracting at the same time (biceps and triceps will cocontract and lock joint in place)
Dynamic cocontraction- play one side of the body segment against another (pelvis) gluteus Medius swaying from side to side. adductors are contracting in both ways. One lengthening and one actively stretching under control to stabilize movement.
LMN
start in spinal cord and go out to a muscle, second in line. Has its cell bodies in the spinal cord and it synapses in a muscle.
Cell body pools
cell bodies in the ventral horn of spinal cord. (both horizontal and vertical organization of motor neurons).
Horizontally across any level of spinal cord the cell bodies that control core and proximal muscles are closer to the midline. Lateral cell bodies of motor neurons that make distal muscles contract are located more laterally in the ventral horn.
Anterior- cell bodies of extensors
Posterior- cell bodies of flexors
Vertical organization- All of the cells that contribute to controlling one particular muscle cluster themselves in a little pool. (vertical pool) each of the vertical tapered purple shapes. to a muscle or number of muscles.
Myotomes
Every spinal nerve contribute to more than one muscle besides the intrinsic of the hand. Every muscle gets input from more than one spinal nerve.
Representative muscle actions that are indicated by being represented by a spinal level (C5 best represents elbow flexion action). If patient able to flex elbow then C5 must be in tact
Lower motor neurons A-alpha and A gamma
connection of every spinal cord to every muscles has 3 neurons (2 are efferent and 1 is afferent)
At every level of the spinal cord we have an extrafusal LMN (A-alpha) and A-gamma is a smaller cell body that goes out to the muscle spindle (intrafusal muscles)
Afferent neuron- pseudounipolar and cell body in dorsal root (sensory part of a muscles spindle) is a Ia class fiber. Has a connection to a motor neuron at the same level.
Alpha-gamma coactivation
when we think to move our brain recruits Alphas to contract the muscles and simultaneously contracts A-gammas to keep the muscle sensitive
Motor unit
A lower motor neuron an all the muscle fibers it innervates.
Motor unit-slow twitch
need oxygen for contraction, generate lower amounts of tension but can go for a long time (more fatigue-resistant) sometimes called red
Small alpha turns into slow twitch
Smaller diameter A-alpha
Motor unit- fast twitch
innervated by the biggest of the A-alphas that send big signals, need to burn glucose for fuel (needed for flight or fight), generate high amounts of tension but for a short period of time.
Motor units-order of recruitment
Henneman’s size principle- brain recruits slow twitch motor units first and it only recruits fast twitch if it needs more power, more speed, or more strength.
It is easier for brain to depolarize a small A-alpha, unless the functional activity allows the order to be reversed.
-fighting a bear, when called for the brain can switch the order of recruitment because of the demands of the task
Brain does not recruit all the motor units of one class at the same time. Brain has 3 different motor units and wants to make sure the motor units stay functional for as long as possible so the brain cycles which motor units are active and inactive throughout the task to help delay the fatigue.
Motor neuron disease- loses some of motor units and motor neurons, brain has a decreased ability to switch and has to call the same motor unit over and over again.
Muscle fibers per motor unit
Gastroc (gross motor control) have many muscle fibers per every axon. Gets 2,000 muscle fibers per one axon. a lot of strength but not much control
Small muscles of the hand (fine motor control)- 3 muscle fibers per 1 axon. Every new motor unit does not add much strength of action but adds a lot of fine control for an action. Fine movements of tension.
Convergence of information
Any one A-alpha motor neuron gets converging information from multiple sources. Activity of the alpha represents the balance/sum of all of the incoming information.
Alpha motor neuron- gets information from the brain and it gets info from the muscle spindle (sensory receptor) converge on the same alpha motor neuron.
Deep tendon aims to have the pressure inhibit the alpha motor neuron that says to contract (top down) with the sensory input that says to relax.
Reciprocal inhibition
Comes as a result of muscle contraction. Contraction can be active (from the brain down) or can be a result of a reflex (quick stretch). Signal to contract a muscle can be top down or outside in. We are wired such that if a muscle (the agonist) is facilitated (shortened), its antagonist is inhibited so that it can be lengthened.
We can defeat this reciprocal inhibition through cocontraction.
Those with a stroke have too much flexion which then inhibits the extensor side (help relax flexors to allow for the extensor to actively contract so then the extensor facilitation inhibits the flexors.
Muscle synergies
Usually mean bad, abnormal, nonfunctional.
Normal- a group of muscle tat work together under food voluntary control in any pattern desired for function.
Abnormal- A group of muscles that work together under limited voluntary control in a limited number of patterns that may or may not contribute to function.
Spinal region coordination
-proprioceptive Body schema
an internal body map- I know where my body parts are in relation to another
Role of the GTO- autoinhibit the muscles they are in (they report tension)
Stepping pattern generators
Believed that we are wired in the spinal cord, brainstem, and brain we have a neural network that when you start the walking pattern it self perpetuates. Doesn’t require anymore input. Why we can walk and pay attention to other things.
Spinal reflexes
for every reflex there is a stimulus and a response.
Sensory organ- gest stimulus there is a pathway to the spinal cord, there is a response in the spinal cord.
Sensory stimulus and motor response and the spinal cord is where the switch takes place.
Phasic stretch reflex (muscle spindle)
momentary stimulation that produces a momentary muscular response.
stimulus is the stretch of the spindle- reflex hammer gives tendon a short sharp tap and tendon deforms the muscle then gets quickly stretched apart, the spindle also gets stretched apart and send more signals to the spinal cord. Spindle makes a direct synaptic connection to the alpha motor neuron to the same muscle that was stretched. Depolarizes alpha motor neuron and the response is a contraction in the same muscle that was tapped/stretched.
Stretch any muscle quickly and the same muscle is facilitated to contract.
Facilitation
motor neuron is brought closer to action potential
Activation
motor neuron, action potential was achieved.
Withdrawal reflex (cutaneous receptors
activation of free nerve endings (a-delta) sharp pain, get away this is hurting you.
Response- withdrawal (multisegment)=not only do you flex your knee to get foot away from Lego but you also flex your hip automatically at the same time.
When A-delta fibers come in from the periphery they branch above and below before they get into the dorsal horn. The branches help facilitate the automatic multimuscle multi-segment muscle response. Create framework of automatic withdrawal.
Muscle cramps
is a muscular phenomenon- contraction of muscular units without neural input. Sudden involuntary contraction of a motor unit. (can be an electrolyte imbalance and lactic acid imbalance are a result of over work.
Brain cycles its motor units, in ALS not as many units so brain calls on units every day, contraction after contraction. Report calf cramps over night, overuse has set up a metabolic reaction that causes the cramps.
Fasciculations
Have a little bit of a neural origin- little muscle in corner of eye that twitches like crazy. Small repetitive muscle spasm, spontaneous depolarization of an entire motor unit (all of its muscle fibers), when the whole motor unit contract we see it as a twitch.
Benign-no comorbid signs or symptoms. No signs of damage to the NS
Pathologic- comorbid signs and symptoms, often in calf muscles, see rippling fasciculations but also has 4/5 strength and atrophy of those calf muscles.
Myoclonus
just about to fall asleep and your whole body contracts/jerks
Fibrillations (always pathologic)
involuntary muscle contractions, spontaneous depolarization of one little muscle fiber. When axon is gone it can depolarize on its own and is always pathologic because they only contract on their own if the have lost their nerve. Sign of denervation. Single muscle fiber=not able to see it through surface of the skin.
Tremors
involuntary muscle contraction. An oscillating type of movement (back and forth type movement) of a body part or limb.
Resting- typically of hands or feet
Action: postural-
Action: Orthostatic-
Action: Intention- when not moving they are fine, When they move is when they demonstrate the tremor. Only when they move. (cerebellar dysfunction)
Potential sources of damage
- trauma- (sharp or blunt) compression of median nerve by transverse ligament, or gross leg and foot falls asleep (fibular never) or sharp (cuts peripheral motor neurons)
- Infection- (polio) attacks the cell body in the ventral horn, kills cell body and the axon degenerates all the way to the muscle (viral infection)
- Degenerative disorders-(Glutamate excitotoxicity problem)- people leak a little too much glutamate which causes degeneration.
- Vascular disorders- Rich blood supply, oxygen, sugar, and trash taken out is not available to nerves that need it.
- Tumors- grow and press on a nerve.
Denervation
from point of axon death, degeneration of distal axon and denervation typically means a muscle fiber loses its axon.
Decrease or loss of reflexes
denervation leads to a loss of reflexes (muscle deep tendon reflex) stretch of a muscle and goes to spinal cord (Ia class peripheral sensory neuron) and goes out of the ventral horn and fails at the point of neuron damage.
If spinal nerve is completely cut there is a decrease of spinal reflex because the stretch that gets into the spinal cord cannot come back out in the form of a response. Because every muscle gets supply from more than one spinal level the reflex will be decreased/weakened. Cut peripheral nerve completely and there will be no reflex at all.
Paresis or paralysis
paresis would happen if one spinal nerve were cut.
Paralysis would occur if one peripheral nerve is cut.
Atrophy
Muscle shrinks
Disuse= muscle is a little bit smaller than normal but still has bulk
Denervation=muscles wither away to nothing. It will completely atrophy away. Very visible and pronounced. Is marked atrophy.
Abnormal muscle tone
Resistance to passive stretch
Hyponia/hypotonic- Loses some of its alpha neurons-loss of some muscle tone
Flaccidity- If it loses musculocutaneous (peripheral nerve) “flaccid paralysis”- loss of muscle tone, inability to contract=paralysis due to an injury due to LMN A-alpha motor neurons.
