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Recapping > EDX > Flashcards

EDX Flashcards

1
Q

Types of neurons in DRG?

A

Sensory bipolar ( one extends to dorsal horn, other to skin)

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2
Q

Dorsal column pathway

A

light touch/ pressure

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3
Q

Spinothalamic pathway

A

pain/ temperature

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4
Q

Where are alpha motor neurons located

A

ventral horn of spinal cord

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5
Q

motor unit

A

alpha neuron and associated muscles

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6
Q

muscle contraction pathway

A

frontal lobe to primary motor cortex to corticospinal tract decussate in medulla synapse at anterior horns. alpha motor neurons in ant horn project to muscles cells at NMH to depolarize

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7
Q

innervation ratio

A

muscle fibers/ LMN

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8
Q

Myelin made by

A

schwann cells

(oligodendrcytes in cns)

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9
Q

Endoneurium

A

tissue around axon

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10
Q

perineurium

A

bundles axons

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11
Q

epineurium

A

connect fascicles together

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12
Q

MEPPs

A

mini depolarization caused by regular quantas

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13
Q

resting charge or neuron

A

-70mv

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14
Q

SNAP

A

sensory n. action potential

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15
Q

CMAP

A

compound muscle action potential

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16
Q

normal orientation of 2 pronged device

A

Cathode (-) towards stimulating

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17
Q

black bar/ ring on fingers

A

recording electrode g1/ black

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18
Q

electodes 4cm apart over bone or tenden

A

reference electrode g2 (to subtract background noise

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19
Q

green electrode

A

placed between stimulator and active electrode (dissipates current)

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20
Q

Conduction velocity

A

how fast a wave is

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21
Q

latency

A

how fast is the wave conducting

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22
Q

CMAP measuring

A

baseline to peak amp

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23
Q

SNAP measuring

A

peak to peak

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24
Q

onset latency

A

time before starting negative (upward) deflection

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25
Q

peak latency

A

time from start to peak negative deflection

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26
Q

temporal dispersion

A

the distribution of action potentials

27
Q

orthodromic

A

physio direction of AP

28
Q

antidromic recording

A

against physio direction of AP (SNAP studies)

29
Q

UE and LE temp for EDX. what if too cold?

A

UE 32C
LE 30C
too cold = increase amp, conduction velocity will slow with prolonged latency, duration increased (slower atoms longer opened channels)

30
Q

Ranges for Sensory and Motor NCS
Hi frequency filter
Lo frequency filter

A

Sensory 20-2000hz

Motor 10-10000hz

31
Q

Effects of lowering and raising filters

A

lowering filter = lower amp and prolonged onset of peak latency

Raising lo = peak early, low amp

32
Q

Normal and Aging on AP conduction velocity

A 
Normal 
UE 50 m/s
LE 30 m/s
>50yo
-2m/s per decade
33
Q

Normal range apply to stim and duration?

A

1-100 mAmps

0.1-1.0 ms

34
Q

h- reflex (true reflex)
nerve?
direction of AP?
what if prolonged?

A

Ia sensory afferent n.
AP towards spinal cord -> spinal reflex arc -> motor nerve -> muscle contracts
prolonged= pathology (radiculopathy)

35
Q

F wave (not a true reflex)
stim n?
direction?
prolonged/absent?

A

record at mus, stim motor n at distal location in proximal direction.
AP is antidromic towards ant horn, depolarize back to axon of motor n.

Prolonged/ absent f wave can be GBS

36
Q

A wave (not a true reflex)

A

predictable, stable waveform (in amp and latency) between F wave and direct motor response when recording F wave. Means that there was a reinnervation in the past.

37
Q

EMG
Concentric electrode
vs
Monopolar electrode

A

Concentric- reference electrode attached to needle
con- small recording area

Monopolar- broad listening area, needs separate reference electrode

38
Q

insertional activity

A

TV static when entering muscle (AP caused by ripping thru muscle)
Decreased- fibrosis
increased- active denervation/ irritated

39
Q

MEEPs

A 
Normal Resting
Seashell noise (painful, at motor end plate, move needle away)
40
Q

Complex repetitive discharge CRD

A

Abnormal Resting
involuntary serrated complex (similar to myokymia but wider)
Motor unit denervated and reinnervated by another motor neruon which was denervated.
“Ephaptic transmission”
Seen in chronic radiculopathy, ant horn cell dz, and nl pt

41
Q

Fasciculation

A

Normal Resting

involuntary MUAPs

42
Q

fibs/sharps

A 
Abnormal Resting
positive (downward) depolarization
axon loss (scale 0-4+) denervation of muscle.
43
Q

Fasciculation + Fibs/sharps

A

Abnormal Resting

ant horn cell dz

44
Q

Myokymia

A

Abnormal Resting
involuntary, abrupt, regular “marching”
upper trunk plexopathy, tumor, radiation

45
Q

Myotonic Discharge

A

Abnormal Resting
Dive-bombers, amp steady
any myotonia: myotonic dystrophy, paramyotonia, myotonia congenita, kyperkalemic periodic paralysis, acid maltase deficiency

46
Q

Recruitment

A

increasing motor units to activate more contraction of muscle fibers

47
Q

Est Hz of a MUAP

A

MUAP/screen x 5

48
Q

Decreased recruitment

A

increased firing (machine gun)- making up for lack of axons 30-50hz. neuropathic recruitment pattern

49
Q

Decreased recruitment, LDLA

A

Large amp, long duration MUAPs

50
Q

Polyphasic MUAPs

A

during collateral sprouting (MU taking over another’s) polyphasic, crosses baseline >x5.

Eventually myelinate and become a LDLA

51
Q

Increased recruitment

A

Small duration, small amp SDSA
muscle is weak due to myopathy, more motor units need to be recruited to allow activation.
Myopathic recruitment pattern

52
Q

Demyelination
causes
EMG
NCS

A

causes: focal compression, stretched, systemic dz (AIDP/GBS)
EMG: nl
NCS: prolonged latency, decreased CV, increased temporal dispersion

53
Q

Axonal loss
Causes
EMG
NCS

A

focal crush, transection, stretch, systemic dz, ant horn cell dz. Few healthy axon exist to summate into a CMAP
EMG: decreased recruitment
NCS decreased amp (possible decreased CV)

54
Q

Axonal vs wallerian degenderation

A

Retrograde/systemic
vs
Anterograde, complete in 5 (motor) or 10 (sensory) days

55
Q

Conduction block

A

failure of AP to propagate past a focal spot in peripheral nervous system.

Usually focal demyelination- GBS or focal compression (CTS/ saturday night palsy)

56
Q

Seddon classification:
Neurapraxia

timeline findings

A

focal pressure/ focal demyelination

EMG nl, CMAP nl
stimulate proximally, may see decreased amp- nl in a few weeks

great prognosis

57
Q

Seddon classification:

Axonotmesis

A

crush/ stretch nerve- axon die, epineurium intact

Axons can reheal 1 inch/ month.

immediately: decreased amp proximally, nl CMAP distally

After a few weeks: decreased amp prox and distally with fibs and sharps, decreased recruitment

after a few months: Reinnervation potentials (polyphasic MUAPs)

58
Q

Seddon classification: Neurotmesis

A

complete severed/ transection of nerve

absent CMAP

May attempt to regrow but form neuromas (painful, can inject with steroids)

59
Q

Blink Reflex Study (NCS)

what nerves?

How it works?

A

detect lesion of trigeminal n., facial n., and pons/medulla

useful in strokes/ MS/ trauma

Stimulates facial sensory n (trigeminal) V1 to Pons Vm nuclei that stimulates facial nerve (CN VII) output in pons leading to blink response by VII orbicularis oculi muscle on ipsilateral side AKA R1 response

At the same time the Vm nuclei also stimulates the Vs nucleus in the medulla which sends a b/l signal to blink via the same orbicularis oculi muscle AKA R2 response

60
Q

Blink Reflex Study (NCS) pathology
Trigeminal lesion
Facial nerve lesion

A

Trigeminal n lesion
no R1 and no R2 on lesion side
R1 and R1 of contralateral side

Facial lesion
no R1 and R2 present
R1 and only R2 response on contralateral side

61
Q

Synkinesis in blink reflex study

A

syn together
kinesis move

a complication of facial n. regeneration

inappropriate sprouting during regeneration leading to more than just one muscle innervation

62
Q

nl findings in

A

steroid myopathy 2B fibers cant be seen on edx
disuse myopathy
congenital
mitochondrial, GSD V GDS VII, carnitine defi

63
Q

characteristic in waveform shows potential for ongoing functional recovery in deinervation and clinically weak muscle

A

stability- shows mature recovery

Recapping (4 decks)

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