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97 Cards in this Set

  • Front
  • Back

what is feedforward

the anticipatory use of sensory info to prepare for movement

feedback

provide info during and after movement

where is a decision first made

in the anterior part of the frontal lobe

after a decision is made in the anterior part of the frontal lobe what happens next

motor planning areas in the frontal lobe are activated followed by control circuits

what regulates activity in descending pathways

motor control circuits: cerebellum and basal ganglia

after a decision is made in the frontal lobe and motor planning areas and control circuits are activated what happens

upper motor neuron tracts ( descending motor pathways) deliver signals to the spinal interneurons and LMN's

after signal reaches the spinal interneurons and LMN's what happens

the LMN's deliver the signal directly to skeletal muscle, eliciting contraction

in the spinal cord, what determines the information conveyed by the LMNs to the muscles

interactions among neurons

what are the classifications of UMN tracts

- postural/gross movement tracts


- fine movement tracts

what do postural/gross movement tracts control

automatic skeletal muscle activity

what do fine movement tracts control

fractionated movements of the limbs and face

the control circuits adjust activity in the descending tracts resulting in _______ or _______

excitation or inhibition of motor neurons

what is the sarcolemma

the membrane of a muscle cell

what are t tubles

projections on the sarcolemma which extend into muscle

what is the sarcoplasmic reticulum and where is it located

- a series of storage sacs for Ca ions


- adjacent to T tubules

what causes the membrane on a muscle cell to depolarize and what happens following this depolarization

- ACh from a LMN binds with receptors on the sarcolemma


- this induces depolarization of T tubules

once sarcolemma and T tubules have depolarized, what does this change in electrical potential elicit and what does this cause

the release of Ca ions from sarcoplasmic reticulum. These ions then bind to receptors inside muscle cells , initiating contraction

what do individual muscle fibers consist of

myofibrils arranged in parallel to the long axis of the muscle fiber

what do myofibrils consist of

proteins arranged in sarcomeres

what are the functional units of muscle

sarcomeres

sarcomeres are composed of two types of proteins _______ and _______

structural and contractile

what are the contractile proteins in a sarcomere (myofilaments)

actin, myosin, troponin, tropomyosin

what are the structural proteins of a sarcomere (myofilaments)

Z line, M line, tintin

what is the Z line

fibrous structure at each end of a sarcomere

what is the M line

it anchors the fibers in the center of the sarcomere

what is tintin

large elastic protein, connects Z line with the M line

what is the function of tintin

it maintains the position of myosin relative to actin and prevents the sarcomere from being pulled apart

myosin filaments have specialized projections called ___________ ending in _________

- cross bridges


- myosin heads

myosin head are capable of

binding with active sites on actin

a thin protein attached to the Z line

actin

a thick filament attached to the M line

myosin

muscle contraction is produced when

actin slides relative to myosin

what initiates the sliding of actin relative to myosin

when Ca binds to troponin, causing a change to troponin. This change induces movement of the tropomyosin to uncover active sites on actin , allowing myosin heads to attach to these exposed active sites



** ca binds/changes troponin = movement of tropomyosin= uncovers active actin sites/myosin binds to

the amount of tension generated by contracting muscle depends on

length of the sarcomeres

what determines the total resistance to muscle stretch

active contraction, tintin, weak actin myosin bonds

what is the definition of muscle tone

the resistance to stretch in resting muscle

clinically, what is used to asses muscle tone

passive range of motion

normal resting muscle tone is provided by

tintin and weak actin myosin bonds

weak actin myosin bonds are formed when

when myosin attaches to actin but myosin heads do not swivel so there is not power stroke

force generated by muscles is determined by muscle

stiffness

what is stiffness technically defined as

change in force per change in length

what determines total stillness of a muscle

active, intrinsic, and passive factors

what is active stiffness generated by

neural activity ( UMN firing and reflexes)

when innervated mm is immobilized in a shortened position what happens

structural adaptation


- sarcomeres are lost

stiffness is

resistance to stress


tone is

amount of tension (stiffness) in resting muscle

what makes up the motor unit

the alpha motor neuron and all the muscle fibers it innervates

the activity of the motor unit depends on the convergence of information from these three areas:

peripheral sensory afferents


interneurons


descending pathways

what is the function of slow twitch mm fibers

majority of postural and slowly contracting muscles

what is alpha gamma coactivation

the simultaneous functioning of alpha and gamma systems which occurs during most movements


gamma maintains stretch on central region of mm spindle intrafusal fibers when the muscle actively contracts

what do spinal region reflexes require

1. sensory receptors


2. primary afferents


3. connections between primary afferents and LMN


4. effectors (muscles or glands)

what are the diff. names of the phasic stretch reflex

1. myotatic reflex


2. muscle stretch reflex


3. deep tendon reflex

describe the phasic stretch reflexs


1. Ia afferents stimulated by quick stretch


2. transmit AP to spinal cord


3. release neurotransmitter at synapses with alpha motor neuron


4. alpha motor neuron depolarizes


5. Ap propagated o neuromuscular junction


6. Ach released, binds with mm receptors, fibers contract


describe the Golgi tendon organ stretch reflex


1. Ib afferents


2. stimulate interneurons that INHIBIT alpha motorneuron to same muscle


3. results in AUTOGENIC INHIBITION


4. may also inhibit synergistic musle

what is the purpose of the GTO reflex

- adjusts the mm activity in concert w/ info from muscle spindle and descending control


- in extreme contraction, prevents muscle from exerting enough force to tear the tendon, can fail if force build up is very rapid

tonic stretch reflex is _______synaptic

multisynaptic


phasic stretch reflex is _____synaptic

monosynaptic

what is a normal muscle synergy

elbow and wrist flexion combined with forearm supination to get food to mouth when eating

what is the difference between the medial and lateral activation system of descending pathways

- medial synapse medially and innervate postural and girdle muscles


- lateral synapse laterally and innervate distal muscles used for fine movement

what are the pathways in the medial activation system

1. tectospinal


2. medial reticulospinal


3. medial vestibulospinal


4. lateral vestibulospinal

where do the pathways in the medial activation system come from

1. tectospinal from tectum ( posterior midbrain)


2. medial reticulospinal from medial reticular formation


3. med & lat. vestibulospinal from vestibular nuclei

what does the term fractionation of movement mean

ability to activate individual muscles independently of other muscles

where do corticospinal fibers come from

1. primary motor cortex


2. lateral premotor area


3. supplementary motor area

what is the function of the lateral premotor area

preparing to move


- produces muscle activity that spans several joints

what is the function of the supplementary motor area

preparing to move


- active prior to bimanual and sequential movements

what is the function of the lateral corticospinal tract


- controls fine distal movements

what is the function of the rubrospinal tract

primarily innervates upper limb flexors

what is the purpose of the non specific activating pathways

enhance activity of interneurons and motor neurons in spinal cord


- motor effects due to release of neuromodulators


- general effects not related to specific movements


- may contribute to motor performance with varying levels of motivation

what are the signs of upper motor neuron lesion

1. paresis


2. loss of fractionation of movement


3. abnormal reflexes


4. muscle hyperstiffness


5. cocontraction ( spastic CP)


6. abnormal muscle synergies ( post stroke)

what are the signs of lower motor neuron lesion

1. loss of reflexes


2. atrophy


3. flaccid paralysis


4. fibrillations

what is the difference between paralysis and paresis

paralysis is complete loss of voluntary contraction


paresis is partial loss of voluntary contraction

what is the difference between disuse atrophy and neurogenic atrophy

disuse- due to lack of use


neurogenic- due to damage of nervous system

what kind of atrophy do you see with upper motor neuron lesion

disuse atrophy


- skeletal muscle continues to receive stimulation, slower rate of atrophy


what kind of atrophy do you see with lower motor neuron lesion

neurogenic atrophy


- muscle doesn't get innervation anymore causing atrophy which is profound and happens quickly

what are the different types of involuntary muscle contraction

1. muscle spasm


2. cramps


3. fasciculations


4. fibrillations


5. abnormal movements

define muscle spasm

sudden involuntary contraction

define crams

severe and painful muscle spasms

define fibrillations

brief contractions of single muscle fibers, not visible

define fasciculations

quick twitches of muscle fibers of single motor unit, visible under skin

what are abnormal movements due to

basal ganglia disorders

what is flaccidity

hypotonia


- abnormally low resistance to passive stretch

what are the causes of flaccidity

- cerebellar disorders


- lower motor neuron lesions


- temporarily following UMN lesion

what is hypertonia and what causes it

abnormally strong resistance to passive stretch


- chronic UMN lesions


- some BG disorders

what is the difference between spastic hypertonia and rigidity

with spastic the amount of resistance to passive movement depends on velocity of movement where as rigidity resistance remains constant it is velocity independent

what is the difference between decerebrate and decorticate rigidity

decerebrate occurs following midbrain lesions


- rigid extension of limbs and trunk, IR of UE, PF



decorticate occurs following lesions superior to midbrain


- UE are flexed, LE extended

what happens when descending motor commands are interrupted

LMN becomes temporarily inactive


no stretch reflexes, muscles hypotonic


After recovery interneurons and LMN usually resume activity but their activity no longer modulated of abnormally modulated by UMNN


In months following UMN injury tone inc. d/t changes w/in mm = ^ resistance to stretch

what is one common abnormal cutaneous reflex? what does it look like?

babinskis sign


extension of big toe and fanning out of other toes, CST tract

what is clonus

involuntary, repeating, rhythmic contractions caused by mm stretch, cutaneous and noxious stimuli and attempts at voluntary movement can induce clonus

what is the clasp knife response? what kind of disorder do you find it in?

when paretic muscle is slowly and passively stretched, resistance drops at a specific point in the range of motion


- type 2 afferents including some joint, cutaneous, subcutaneous, touch, and pressure receptors elicit the response

what is the cause of muscle hyperstiffness post stroke?


1. loss of sarcomeres


2. inc. weak actin myosin bonds


3. atrophy of type 2 muscle fibers

how does muscle hyperstiffness change normal movement

1. abnormal movement


2. delayed initiation of movement


3. slowed rate of force development


4. prolonged mm contraction time


5. disrupted timing of activation of antagonists relative to agonist

what is the modified ashforth scale? and how is it used?

subjective assessment of the resistance to passive stretch

what tract is most damaged from stroke?

corticospinal tract

what is the most common site of stroke

middle cerebral artery

what does damage to the corticospinal tract cause

abnormal motor control and over activity of antigravity mm


- abnormal mm activation: extension from med. reticulospinal and vestibulospinal tract left relatively unopposed


- rubrospinal tract still intact, = UE flex


besides movement consequences what other consequences of stroke are there

emotional lability

what are the interventions for stroke that are best supported by the research

- constraint induced movement


- movements against resistance


- partial body weight support during gait train.