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Neuroscience > Motor System > Flashcards

Motor System Flashcards

1
Q

Where does movement emerge from

A
  • emerges from the interactions of individual, task, & environment
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2
Q

Describe feedforward and feedback mechanism of sensory contribution to motor control

A
  • Feedforward: anticipatory use of sensory information (ex. shaping hand when seeing a cup prior to grabbing it)
  • Feedback: use of sensory information during & after movement to make corrections/adjustments (misjudging the weight of an object & then immediately using more muscle force to correct it)
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3
Q

Describe the pyramidal system

A
  • corticospinal & corticobrainstem
  • UMN pathways (upper motor neurons)
  • controlled by primary motor cortex
  • directly connect to the motor neurons, whereas extrapyramidal tracts do not have direct connections, but connect indirectly via interneurons
  • drive voluntary movements by activating ventral horn lower motor neurons directly
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4
Q

Describe the extrapyramidal system

A
  • tracts outside of the pyramids
  • tracts that originate in various nuclei of brainstem (reticulospinal, vestibulospinal, rubrospinal, ect.)
  • these tracts are modulated/regulated by connections from motor cortex, basal ganglia, cerebellum
  • not part of the UMN pathways
  • indirectly control background tone, stretch sensitivity
  • modulate voluntary movements by regulating the motor neurons indirectly
  • act in the background to regulate involuntary reflexive postural responses to make voluntary movements look natural, coordinate complex movements, locomotion
  • regulate muscle tone
  • under the influence of motor cortex, basal ganglia, & cerebellum for motor planning & coordination system
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5
Q

What tracts are 2-neuron pathways

A
  • corticospinal tract
  • corticobulbarr tract
  • extrapyramidal
  • AKA corticobrainstem & corticonuclear tract
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6
Q

Describe the different motor tracts (MT) in the spinal cord

A
  • Medial MTs: innervate axial/proximal girdle muscles to control posture & perform gross movements
  • Lateral MTs: innervate distal limb muscles for fine motor control & perform fractionated movements
  • Non-specific Mts: contribute to background levels of excitation in spinal cord & facilitate reflex arcs
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7
Q

Describe the medial motor tracts

A
  • for adjusting posture & gross movements by regulating postural reflexes & muscle tone
  • control of posture usually occurs automatically without much conscious effort
  • involuntary coordinated responses that are mostly initiated in brainstem centers, conveyed through these tracts
  • includes reticulospinal tracts, medial & lateral vestibulospinal, & medial/anterior corticospinal from cortex
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8
Q

Describe the medial reticulospinal tracts

A
  • from reticular formation in brainstem to motor neurons to regulate muscle activity in trunk & proximal limb muscles for following purposes
  • helps with gross movements needed during walking
  • help with automatic anticipatory postural adjustments during movements like reaching/carrying objects
  • control of autonomic functions (HR, respiratory rate)
  • pontine RST has extensor bias to cause tonic activation of antigravity muscles LE extensors & UE flexors
  • medullary RST are inhibitory for antigravity muscles via inhibitory interneurons
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9
Q

Describe the vestibulospinal tracts

A
  • receives information about head position in space from vestibular nuclei
  • descends only up to cervical & upper thoracic levels
  • regulates motor neurons bilaterally to control neck & upper back muscles extensors
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10
Q

Describe the lateral vestibulospinal tract

A
  • receives gravity information from vestibular nuclei
  • descends all the way down the spinal cord
    regulates motor neurons ipsilaterally to activate trunk paravertebrals & proximal LE extensors while inhibiting flexors to maintain upright antigravity posture within base of support
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11
Q

Describe the medial/anterior corticospinal tracts

A
  • tract descends from pyramidal neurons in motor cortex through internal capsule, anterior brainstem to connect to spinal motor neurons bilaterally to activate neck, shoulder & trunk muscles
  • these are a minor portion (2%) of the total corticospinal fibers descending from the motor cortex
  • role is to probably to prepare the postural system for intended movements & coordinate posture with the other medial tracts
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12
Q

Describe lateral motor tracts

A
  • voluntary control of movements
  • active proximal 7 distal muscles in the limbs
  • provides ‘fractionation’ ability in distal muscles ability to isolate specific muscles for fine movements without activating other neighboring muscles for fine motor control
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13
Q

Describe lateral corticospinal tracts

A
  • most important tract controlling voluntary movements
  • primary motor cortex -internal capsule- cerebral peduncles-pyrimids of medulla-spinal motor neurons
  • at lower medulla, 88% fibers decussate to contralateral side, 10% keep running ipsilaterally, 2% run with medial corticospinal tract
  • unique ability to generate fractionated movements by using interneurons to inhibit unwanted neighboring muscles
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14
Q

describe rubrospinal tract

A
  • arises in red nucleus in midbrain, decussates & descends to innervate contralateral motor neurons that activate wrist/finger extensors
  • in humans it is small & makes minor contribution to control of distal upper limb muscles
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15
Q

Describe nonspecific motor tracts

A
  • ceruleospinal tract & raphespinal tract
  • facilitate all types of motor neurons across spinal cord
  • do not activate any specific movements not connected directly to motor neurons
  • activated during intense stress & emotions, may contribute to decreased motor control when anxiety is high
  • involved in sending descending pain-regulating information
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16
Q

Describe the corticobulbar/corticobrainstem tracts

A
  • control of muscles in the head
  • activate cranial motor nerve nuclei that innervate muscles of the face, mastication, tongue, pharynx, larynx, & some neck muscles (CNs V, VII, IX, X, XI, XII)
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17
Q

Describe the cortical motor areas

A
  • somatotopic arrangement from M1 (motor homunculus) to corticospinal/corticobrainstem tracts
  • premotor & supplementary motor area plan for complex movements in association with M1
  • stimulation of premotor area activates several muscles
  • supplementary motor area involved in movements that require coordination of both hands, or sequential movement
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18
Q

Describe lower motor neurons

A
  • neurons in spinal cord that convey signals to extrafusal & intrafusal muscles
  • cell bodies located in ventral horn, axons leave through ventral root
  • Motor pools: cluster of motor neurons that connect to single muscle belly
  • Motor pools innervate separate groups of muscles
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19
Q

Describe the myotome actions

A
  • C5: elbow flexion/shoulder abduction
  • C6: wrist extension
  • C7: elbow extension
  • C8: finger flexion
  • T1: finger abduction
  • L2: hip flexion
  • L3: knee extension
  • L4: ankle dorsiflexion
  • L5: great toe extension
  • S1: ankle plantar flexion
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20
Q

Describe the two types of motor neurons

A
  • Alpha: large cell bodies, large myelinated axons, and connect to extrafusal muscles
  • Gamma: medium cell bodies, medium myelinated axons, and connect to intrafusal spindle muscle fibers
  • type Ia and type II sensory neurons activate both motor neuron types during stretch reflex
  • presynaptic inhibition from cortico-spinal fibers keeps motor neuron excitability in check
  • loss of presynaptic inhibition contributes to increase in tone & reflex responses
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21
Q

Describe motor unit recruitment properties during contraction

A
  • can be small or large
  • vary in number of fibers innervated (muscles for large movements have a higher numbers of fibers per motor neuron)
  • can be classified as slow (small) or fast (large) twitch
  • slow twitch motor units constitute majority of postural muscles
  • more motor units need to be recruited with increasing force of contraction
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22
Q

Describe the Henneman’s size principle for motor neurons

A
  • order to motor neuron recruitment from small to larger
  • less force to more force
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23
Q

Define reflex

A
  • involuntary motor response to external sensory stimulus conveyed via spinal cord
  • no inputs from higher levels
24
Q

Steps in a phasic stretch reflex

A
  • quick phasic response, monosynaptic reflex
  • afferent arm: Ia/II afferents from muscle spindles or GTOs
  • efferent arm: alpha motor neurons to same muscle
  • deep tendon reflex/myotactic reflex
25
Q

Steps in a withdrawal reflex

A
  • reflexive withdrawal from stimulus
  • elicited by painful cutaneous stimuli
  • needs synaptic interactions between neurons at various spinal cord levels
26
Q

Steps in a crossed extension reflex

A
  • reflexive extension of the other LE to support posture & prevent falling
27
Q

Describe reciprocal inhibition

A
  • during agonist muscle contraction or reflex activity, inhibition of antagonist is achieved by activating interneurons in spinal cord that inhibit motor neurons of the antagonist group
28
Q

Describe spinal region motor control

A
  • most purposeful movements occur from voluntary motor activity or automatic postural activity & are not reflexive
  • mechanisms at the spinal cord level contribute to automatic smooth coordination of movements using: muscle synergies, central pattern generators (CPG), and modification of spinal motor activity by sensory inputs & reflexes
29
Q

Define muscle synergies

A
  • coordinated contraction of different muscles to produce movements
30
Q

Steps in synergy involving muscles at the same joint

A
  • activate other muscles at same joints
  • phasic synergy: modulated in both amplitude & timing
  • used type Ia afferents
  • monosynaptic
31
Q

Steps in synergy involving muscles at neighboring joints

A
  • activate muscles at other neighboring joints
  • tonic synergy: modulated only in amplitude
  • use type II afferents
  • bisynaptic/polysynaptic
32
Q

Describe complex automatic movement control at the spinal cord level

A
  • spinal cord controls motor activity via network of motor neurons & interneurons based on information received from descending motor transmitters
  • motor activity can be modified by afferent/sensory input
  • descending motor activity can also be modified to change activation patterns of spinal networks
33
Q

Describe the Jendrassik maneuver

A
  • distracts person which decreases the effects of descending inhibitory control and enhances the deep tendon reflex response
34
Q

Describe central pattern generators (CPG)

A
  • adaptable network of spinal interneurons that activate motor neurons to elicit alternating flexion & extension of hips & knees
  • each LE has a dedicated CPG
  • MTN –> neuron 1 activated/extensor muscles activated –> interneuron 2 activated which inhibits neuron 3 –> once fatigued neuron 3 is activated/flexor muscles activated –> interneuron 4 activated which inhibits neuron 1
  • this only occurs during gait
35
Q

Describe somatosensory input affects CPG processing

A
  • various types of sensory input modify CPG processing such as proprioceptive information from muscle spindles/GTOs/joint receptors, touch, pressure, & pain receptors
  • CPG output is adapted to the task, the environment, & the stage of gait cycle for successful walking/running under different conditions
36
Q

Influence of GTOs reflexive input on CPG activity

A
  • responds to tension changes during contraction or passive stretch
  • info conveyed through type Ib edited or inhibits synergistic motor neurons through activity of interneurons depending on weight bearing status of the limb during gait cycle
  • GTO in Achilles tendon excited gastroc during stance & inhibits during swing
  • GTOs never work alone but in conjunction with spindles, joints, & skin
37
Q

Influence of withdrawal reflex on CPG activity

A
  • electrical stimulation to sole of foot during various phases of gait cycle activated different muscle groups & changed ROMs
  • stem during swing phase increased Tib Ant. activity but at end of swing decreased activity & increased antagonist activity
  • max increase in joint ROMs during swing phase stimulation
38
Q

Describe how CPG can be activated/modulated even in the absence of descending MT activity

A
  • complete SCI patients showed rhythmic step-like EMG activity in LE muscles on application of electrical stimulation to posterior lumbar spinal cord
  • attempted E-stim + manually assisted treadmill gait training enhanced/amplified the electrically induced CPG activity at lumbar levels but not enough for independent walking
39
Q

Steps to a muscle contraction

A
  • action potential reaches NMJ
  • Ach released in synapse & binds to receptors on motor end plate
  • sodium inflow causes local depolarization
  • depolarization spreads through T-tubules
  • ER releases Ca2+
  • Ca2+ binds to troponin in actin which moves to expose binding sites with myosin
  • myosin uses ATP to bind to actin
  • myosin head swivels causing actin to slide relative to myosin
  • myosin uses ATP to detach from actin
40
Q

Describe muscle tone

A
  • normal is the minimal resistance to stretch provided by titan and/or weak actin-myosin bonds
  • controlled by various mechanisms: stretch reflex activity by proprioceptive afferent inputs, descending control of various MTs on motor neurons, pre-synaptic inhibition on motor neurons by spinal interneurons, muscle length, & contracture
41
Q

Effects of different Mts on muscle tone

A
  • Corticospinal tract: inhibit tone
  • Pontine (Medial) Reticulospinal tract: facilitate tone
  • Medullary (Lateral) Reticulospinal tract: inhibit tone
  • Corticoreticular/Corticobulbar fibers: connect to medullary reticular formation & facilitate tone
  • Vestibulospinal tract: facilitate tone
42
Q

Signs of a upper motor neuron lesion

A
  • paresis (partial paralysis)/paralysis
  • abnormal tone
  • abnormally high reflexes activity (hyperreflexia)
  • loss of fractionated movements
  • abnormal synergies
  • myoplasticity
  • abnormal co-contractions
43
Q

Describe hemiplegia or -paresis

A
  • occurs high up in the brain and causes symptoms on one side of the body
  • lesion of corticospinal tracts
  • stroke, CP, TBI
44
Q

Describe quadriplegia or - paresis

A
  • SCI
  • lesion of Mts in higher spinal levels
45
Q

Describe paraplegia or -paresis

A
  • SCI
  • lesion of MTs in lower spinal levels
46
Q

Describe spasticity and rigidity for types of hypertonia

A
  • Spasticity: velocity dependent & in MT lesions like stroke or SCI
  • Rigidity: velocity independent & in basal ganglia lesions like extrapyramidal lesions
47
Q

Cause of Clonus abnormal reflex

A
  • lack of descending MT control allowing activation of oscillating neural networks in spinal cord
48
Q

Describe phasic stretch hyperreflexia

A
  • quick muscle activity seen as exaggerated deep tendon reflexes due to loss of descending inhibitory control of nTs regulating information conveyed by afferent type Ia fibers from muscle spindles to motor neurons
49
Q

Describe tonic stretch hyperreflexia

A
  • continued muscle activity in response to continued passive stretch at slow/moderate velocities
  • due to absence of presynaptic inhibition on sustained stretch information being conveyed by both type Ia & type II fibers from muscle spindles to motor neurons mostly in SCI
50
Q

Describe Clasp-Knife response

A
  • resistance to passive stretch decreases after a certain point in ROM conveyed by type II fibers
51
Q

Loss of fractionated movements & abnormal muscle synergies

A
  • mostly after stroke
  • loss of fractionated movements due to loss of lateral corticospinal activity
  • abnormal synergies due to pontine reticulospinal overactivity
52
Q

Describe myoplasticity

A
  • adaptive changes in muscles in response to changes in neuromuscular activity level
  • occurs after MT lesions from stroke/SCI
  • occurs due to increased number of weak actin-myosin bonds & contracture
53
Q

Main factors that limit functional activities after stroke

A
  • paresis
  • loss of fractionated movement
  • abnormal synergies
  • myoplastic changes
54
Q

Main factors that limit functional mobility after SCI

A
  • paresis/paralysis
  • stretch hyperreflexia (mostly tonic)
  • myoplastic changes
55
Q

Describe abnormal co-contractions

A
  • occur in CP
  • lesion in corticospinal or corticobrainstem tracts during perinatal period
  • failure of normal circuit connection during development
  • initially corticospinal axons connect to both agonist & antagonist
  • during development weaker synapses to antagonist are removed by competition & “synaptic pruning”
  • damage to MTs during development eliminates some of that competition allowing connections to both agonist & antagonist to remain causing abnormal co-contractions
56
Q

Signs of lower motor neuron lesions

A
  • paralysis or paresis: flaccidity
  • decrease in muscle tone: hypotonia/flaccidity
  • decrease or loss of reflexes: hyporeflexia
  • neurogenic atrophy due to lack of trophic support to muscles

Neuroscience (10 decks)

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