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97 Cards in this Set
- Front
- Back
what is feedforward |
the anticipatory use of sensory info to prepare for movement |
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feedback |
provide info during and after movement |
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where is a decision first made |
in the anterior part of the frontal lobe |
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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 |
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what regulates activity in descending pathways |
motor control circuits: cerebellum and basal ganglia |
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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 |
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after signal reaches the spinal interneurons and LMN's what happens |
the LMN's deliver the signal directly to skeletal muscle, eliciting contraction |
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in the spinal cord, what determines the information conveyed by the LMNs to the muscles |
interactions among neurons |
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what are the classifications of UMN tracts |
- postural/gross movement tracts - fine movement tracts |
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what do postural/gross movement tracts control |
automatic skeletal muscle activity |
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what do fine movement tracts control |
fractionated movements of the limbs and face |
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the control circuits adjust activity in the descending tracts resulting in _______ or _______ |
excitation or inhibition of motor neurons |
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what is the sarcolemma |
the membrane of a muscle cell |
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what are t tubles |
projections on the sarcolemma which extend into muscle |
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what is the sarcoplasmic reticulum and where is it located |
- a series of storage sacs for Ca ions - adjacent to T tubules |
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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 |
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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 |
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what do individual muscle fibers consist of |
myofibrils arranged in parallel to the long axis of the muscle fiber |
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what do myofibrils consist of |
proteins arranged in sarcomeres |
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what are the functional units of muscle |
sarcomeres |
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sarcomeres are composed of two types of proteins _______ and _______ |
structural and contractile |
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what are the contractile proteins in a sarcomere (myofilaments) |
actin, myosin, troponin, tropomyosin |
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what are the structural proteins of a sarcomere (myofilaments) |
Z line, M line, tintin |
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what is the Z line |
fibrous structure at each end of a sarcomere |
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what is the M line |
it anchors the fibers in the center of the sarcomere |
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what is tintin |
large elastic protein, connects Z line with the M line |
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what is the function of tintin |
it maintains the position of myosin relative to actin and prevents the sarcomere from being pulled apart |
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myosin filaments have specialized projections called ___________ ending in _________ |
- cross bridges - myosin heads |
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myosin head are capable of |
binding with active sites on actin |
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a thin protein attached to the Z line |
actin |
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a thick filament attached to the M line |
myosin |
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muscle contraction is produced when |
actin slides relative to myosin |
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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 |
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the amount of tension generated by contracting muscle depends on |
length of the sarcomeres |
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what determines the total resistance to muscle stretch |
active contraction, tintin, weak actin myosin bonds |
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what is the definition of muscle tone |
the resistance to stretch in resting muscle |
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clinically, what is used to asses muscle tone |
passive range of motion |
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normal resting muscle tone is provided by |
tintin and weak actin myosin bonds |
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weak actin myosin bonds are formed when |
when myosin attaches to actin but myosin heads do not swivel so there is not power stroke |
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force generated by muscles is determined by muscle |
stiffness |
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what is stiffness technically defined as |
change in force per change in length |
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what determines total stillness of a muscle |
active, intrinsic, and passive factors |
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what is active stiffness generated by |
neural activity ( UMN firing and reflexes) |
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when innervated mm is immobilized in a shortened position what happens |
structural adaptation - sarcomeres are lost |
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stiffness is |
resistance to stress
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tone is |
amount of tension (stiffness) in resting muscle |
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what makes up the motor unit |
the alpha motor neuron and all the muscle fibers it innervates |
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the activity of the motor unit depends on the convergence of information from these three areas: |
peripheral sensory afferents interneurons descending pathways |
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what is the function of slow twitch mm fibers |
majority of postural and slowly contracting muscles |
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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 |
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what do spinal region reflexes require |
1. sensory receptors 2. primary afferents 3. connections between primary afferents and LMN 4. effectors (muscles or glands) |
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what are the diff. names of the phasic stretch reflex |
1. myotatic reflex 2. muscle stretch reflex 3. deep tendon reflex |
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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
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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 |
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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 |
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tonic stretch reflex is _______synaptic |
multisynaptic
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phasic stretch reflex is _____synaptic |
monosynaptic |
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what is a normal muscle synergy |
elbow and wrist flexion combined with forearm supination to get food to mouth when eating |
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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 |
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what are the pathways in the medial activation system |
1. tectospinal 2. medial reticulospinal 3. medial vestibulospinal 4. lateral vestibulospinal |
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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 |
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what does the term fractionation of movement mean |
ability to activate individual muscles independently of other muscles |
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where do corticospinal fibers come from |
1. primary motor cortex 2. lateral premotor area 3. supplementary motor area |
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what is the function of the lateral premotor area |
preparing to move - produces muscle activity that spans several joints |
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what is the function of the supplementary motor area |
preparing to move - active prior to bimanual and sequential movements |
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what is the function of the lateral corticospinal tract |
- controls fine distal movements |
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what is the function of the rubrospinal tract |
primarily innervates upper limb flexors |
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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 |
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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) |
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what are the signs of lower motor neuron lesion |
1. loss of reflexes 2. atrophy 3. flaccid paralysis 4. fibrillations |
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what is the difference between paralysis and paresis |
paralysis is complete loss of voluntary contraction paresis is partial loss of voluntary contraction |
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what is the difference between disuse atrophy and neurogenic atrophy |
disuse- due to lack of use neurogenic- due to damage of nervous system |
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what kind of atrophy do you see with upper motor neuron lesion |
disuse atrophy - skeletal muscle continues to receive stimulation, slower rate of atrophy
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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 |
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what are the different types of involuntary muscle contraction |
1. muscle spasm 2. cramps 3. fasciculations 4. fibrillations 5. abnormal movements |
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define muscle spasm |
sudden involuntary contraction |
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define crams |
severe and painful muscle spasms |
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define fibrillations |
brief contractions of single muscle fibers, not visible |
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define fasciculations |
quick twitches of muscle fibers of single motor unit, visible under skin |
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what are abnormal movements due to |
basal ganglia disorders |
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what is flaccidity |
hypotonia - abnormally low resistance to passive stretch |
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what are the causes of flaccidity |
- cerebellar disorders - lower motor neuron lesions - temporarily following UMN lesion |
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what is hypertonia and what causes it |
abnormally strong resistance to passive stretch - chronic UMN lesions - some BG disorders |
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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 |
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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 |
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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 |
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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 |
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what is clonus |
involuntary, repeating, rhythmic contractions caused by mm stretch, cutaneous and noxious stimuli and attempts at voluntary movement can induce clonus |
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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 |
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what is the cause of muscle hyperstiffness post stroke?
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1. loss of sarcomeres 2. inc. weak actin myosin bonds 3. atrophy of type 2 muscle fibers |
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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 |
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what is the modified ashforth scale? and how is it used? |
subjective assessment of the resistance to passive stretch |
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what tract is most damaged from stroke? |
corticospinal tract |
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what is the most common site of stroke |
middle cerebral artery |
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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
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besides movement consequences what other consequences of stroke are there |
emotional lability |
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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. |