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Unit 4 > Motor units, Spinal relexes, SCI > Flashcards

Motor units, Spinal relexes, SCI Flashcards

1
Q

Alternative names for lower motor neurons

A
  • Lower motor neuron
  • Alpha motoneuron
  • Spinal motoneuron
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2
Q

Characteristics of lower motor neurons

A
  • Large cell body
  • Extensive dendritic tree
  • Large axon
  • Myelinated with schwann cells
  • Rapid conduction velocity (up to 60 m/s)
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3
Q

Spinal somatotopy of motoneurons

A
  • Medial ventral horn: proximal muscles

- Lateral ventral horn: distal muscles

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4
Q

Motor neuron pool

A
  • Total of all lower motor neurons innervating a given muscle
  • Typically distributed over 2-3 neurologic segments
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5
Q

Motor unit components

A
  • Cell body
  • Axon
  • All of the muscle fibers that axon innervates
  • Axon only innervates one muscle
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6
Q

Muscle unit

A
  • Collection of muscle fibers innervated by one axon
  • Properties of muscle fibers within a muscle are about the same
  • Normally simultaneous contraction of muscle unit
  • Great variety of sizes
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7
Q

Neuromuscular junctions transmitter

A

ACh

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8
Q

Force generation in muscle

A
  • Membrane conducts action potential
  • Thick and thin filaments slide past one another–generates force
  • Ca2+ binding leads to rotation of the myosin cross-bridge
  • ATP consumed for cross bridge release
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9
Q

Rigor mortis

A
  • Occurs because there’s not enough ATP present

- Cross bridges don’t release and muscle remains contracted

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10
Q

Slow motor units

A
  • Slow rate of force increase during twitch
  • Small peak force
  • Little or no force loss with repeated twitches
  • Slow to fatigue
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11
Q

Fast fatigue resistant motor units

A
  • Relatively fast rate of force increase during twitch
  • Moderate peak force
  • Moderate force loss with repeated twitches
  • Moderate to fatigue
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12
Q

Fast fatiguable motor units

A
  • Fastest rate of force increase during twitch
  • Large peak force
  • Rapid force loss with repeated twitches
  • Fatigues quickly
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13
Q

Two ways to modulate force generation

A
  • Recruitment: of other motor units

- Rate-coding: of an already firing motor unit

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14
Q

Size principle

A

-Smaller motor units are the first to be activated

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15
Q

Stretch receptor

A
  • Senses changes in muscle length
  • Only afferent in CNS that receives a nerve supply
  • Arranged in parallel with extrafusal (regular) muscle fibers
  • Target for gamma motor neurons
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16
Q

Gamma motor neurons

A
  • Target stretch receptors
  • Smaller soma than A motor neurons
  • Lower conduction velocity
  • Innervate intrafusal muscle fibers
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17
Q

Intrafusal muscle fibers

A
  • Smaller diameter
  • Effectively no force generation
  • Affect stiffness of sensory region
  • Nuclear bag and nuclear chain types
  • Central (bag) region: Ia receptors (fastest)
  • Distal regions: type II receptors
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18
Q

Type Ia axons

A
  • Dynamic, intense firing with a stretch onset and then slows down
  • Nonlinear
19
Q

Type II axons

A
  • Steady firing, increases with increased stretch

- Linear

20
Q

Stretch reflex

A
  • Muscles typically work as agonist/antagonist pairs
  • Increased load causes stretch of intrafusal fibers (spindle)
  • Afferent signals sent to spinal cord, activating alpha motoneurons
  • Original (homonymous) muscle excited
  • Synergist (heteronymous) muscles also excited
  • Antagonist muscle inhibited by Ia inhibitory interneuron
  • Stretch corrected
21
Q

Gamma motoneurons and the stretch reflex

A
  • When extrafusal fibers contract they fire to shorten intra-fusal fibers
  • Afferent endings remain sensitive to further changes in muscle length
22
Q

Golgi tendon organ

A
  • Type Ib receptor in series with muscle extrafusal fibers (ie connects muscle to tendon)
  • Active muscle contraction causes strong GTO firing–can sense force generation
  • Ib afferent fires Ib inhibitory interneuron which inhibits the homonymous muscle
  • Ib afferent also fires disynaptic pathway that excites the antagonist muscle
23
Q

Flexion crossed-extension reflex

A
  • Protective–faster limb withdrawal than voluntary reaction time
  • Opposite activity across the midline
  • ie stimulated leg flexes to withdraw and opposite leg extends to support
24
Q

Central pattern generator

A
  • Distributed network of neurons in spinal cord that can produce coordinated movements in the absence of higher inputs
  • Cat example: flexors activated in swing phase, extensors in stance phase
25
Q

Paraparesis/plegia

A

-Injury caudal to T1

26
Q

-Quadriparesis/plegi

A

-Neck injury

27
Q

Immediate acute consequences of SCI

A
  • Weakness
  • Sensory loss
  • Sensory abnormalities–parasthesia, neuropathic pain
  • Hypotension (low BP)
  • Spinal cord ischemia
  • Urinary retention
  • Orthopedic pain
28
Q

Long-term chronic consequences of SCI

A
  • Involuntary movements (spasticity, myoclonus)
  • Bladder problems–number 1 complaint 5 yrs post SCI
  • Spastic or flaccid bladder
  • Sexual dysfunction
  • Blood clots
  • Pressure ulcers
  • Cutaneous ischemia–repositioning is vital
  • Autonomic dysfunction
  • Thermoregulation largely absent
  • Autonomic dysreflexia
  • Metabolic disorders
  • Chronic hypertension
  • Musculoskeletal breakdown
  • Fractures
29
Q

Spastic (neurogenic bladder)

A
  • Injury at or above T10
  • Voluntary relaxation of external sphincter is lost
  • Detrusor contracts with continued filling
  • Urine flows in dribbles only when detrusor emptying pressure>sphincter closure pressure
  • Incomplete bladder emptying–chronic infections
30
Q

Male sexual dysfunction after SCI

A
  • Erection unlikely, ejaculation rare
  • Sperm viability impaired
  • Fertility reduced
31
Q

Female sexual dysfunction after SCI

A
  • Fertility largely unaffected

- C-section strongly recommended due to autonomic dysreflexia

32
Q

Autonomic dysreflexia

A
  • Crazy high increased in BP (like, 240/160) for some sensory inputs along with bradycardia (40bpm), for no apparent reason
  • Paradoxical hypertension
  • Noxious inputs commonly cause it
  • Typically seen after cervical or high thoracic SCI and in complete SCI
33
Q

Possible causes of autonomic dysreflexia

A
  • Loss of inhibition from brain/brainstem regions
  • Excessive sensory response to stimuli
  • Excessive sympathetic response to normal afferent activity*****Sensory afferents making novel synaptic contacts onto preganglionic sympathetic neurons in high thoracic spinal cord
  • Excessive vascular response to normal sympathetic activity
34
Q

ASIA A Complete

A

-No motor or sensory function below injury

35
Q

ASIA B Incomplete

A

-Sensory only below the injury, including S4-S5 segment

36
Q

ASIA C Incomplete

A

-Sensation and limited motor function below the injury level

37
Q

ASIA D Incomplete

A

-Sensation and significant motor function below the injury level

38
Q

ASIA E Normal

A

-Sensory and motor function normal

39
Q

Factors that may damage nerves within region of injury

A
  • Interrupted blood flow–ischemia
  • Local toxins
  • Glutamate release (excitotoxicity)
  • O2 radicals (membrane breakdown)
40
Q

3 approaches to SCI treatment

A
  • Protect surviving cells and axons–neuroprotection
  • Replace cells, establish a growth-permissive environment–neurorestoration
  • Strengthen existing systems–neurorehabilitation
41
Q

CPG for stepping in humans

A
  • Low gain (high threshold)
  • Spontaneous expression always associated with pathology
  • Noxious input to cord
  • Can’t train to improve voluntary walking in persons with incomplete SCI–not due to neuroplasticity at least
42
Q

Interlimb reflex characteristics

A
  • In ALL personals with chronic cervical SCI
  • Common in distal limb muscles
  • Excitatory response
  • Appear months to years later
43
Q

Plasticity and SCI–Interlimb reflexes mechanism

A

-LMN lose inneveration from UMN
-Sensory fibers from more caudal regions denied targets in higher level, prompts new growth caudal to level or injury
-New contacts made to LMN–regenerative sprouting
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Unit 4 (17 decks)

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