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
Paraparesis/plegia
-Injury caudal to T1
26
-Quadriparesis/plegi
-Neck injury
27
Immediate acute consequences of SCI
- Weakness - Sensory loss - Sensory abnormalities--parasthesia, neuropathic pain - Hypotension (low BP) - Spinal cord ischemia - Urinary retention - Orthopedic pain
28
Long-term chronic consequences of SCI
- 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
Spastic (neurogenic bladder)
- 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
Male sexual dysfunction after SCI
- Erection unlikely, ejaculation rare - Sperm viability impaired - Fertility reduced
31
Female sexual dysfunction after SCI
- Fertility largely unaffected | - C-section strongly recommended due to autonomic dysreflexia
32
Autonomic dysreflexia
- 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
Possible causes of autonomic dysreflexia
- 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
ASIA A Complete
-No motor or sensory function below injury
35
ASIA B Incomplete
-Sensory only below the injury, including S4-S5 segment
36
ASIA C Incomplete
-Sensation and limited motor function below the injury level
37
ASIA D Incomplete
-Sensation and significant motor function below the injury level
38
ASIA E Normal
-Sensory and motor function normal
39
Factors that may damage nerves within region of injury
- Interrupted blood flow--ischemia - Local toxins - Glutamate release (excitotoxicity) - O2 radicals (membrane breakdown)
40
3 approaches to SCI treatment
- Protect surviving cells and axons--neuroprotection - Replace cells, establish a growth-permissive environment--neurorestoration - Strengthen existing systems--neurorehabilitation
41
CPG for stepping in humans
- 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
Interlimb reflex characteristics
- In ALL personals with chronic cervical SCI - Common in distal limb muscles - Excitatory response - Appear months to years later
43
Plasticity and SCI--Interlimb reflexes mechanism
-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 -