NCS/EMG

Question 1

effects of adjusting high/low frequency filters on NCS

Answer 1

adjusting frequency filters squishes the action potential down

“I’m late because I was high”
lowering the high frequency filter will prolong onset and peak latencies

“I peaked early at a low point in my life”
“amp-low-tude”
raising the low frequency filter will shorten the peak latency

Question 2

temperature effects on action potential

Answer 2

if limb is too cold

1. amplitude will increase
2. CV will be slow with prolonged latency
3. duration will increase

sodium channels remain open longer → beefier amplitude and longer time of depolarization

Question 3

age effects on action potential

Answer 3

normal CV is at least 50 m/s in UE and 40 m/s in LE

after age 50, CV will decrease ~2 m/s per decade; this is normal

Question 4

H reflex

Answer 4

true reflex

stimulate Ia afferent sensory nerves → AP travels to spinal cord → stimulates spinal reflex arc → travels back down to make muscle contract → record over muscle belly

should have symmetric latencies from side to side

prolonged latency → damage somewhere along the reflex pathway; non specific

usually to evaluate S1 radiculopathy

Question 5

H reflex evaluates

Answer 5

S1 radiculopathy

non specific

true reflex

Question 6

F wave

Answer 6

not actually a true reflex

record from muscle → stimulate nerve distally in proximal direction → AP antidromically to anterior horn → depolarization of random population fo anterior horn cells → depolarization travels back down axons of motor nerve → recorded by G1 over muscle belly

normally F wave on 80% or more of stimulations and all similar in terms of latency

prolonged/absent F waves are first sign of Guillain Barre syndrome

Question 7

F wave clinical signficance

Answer 7

prolonged/absent F waves are first sign of Guillain Barre syndrome
AKA acute inflammatory demyelinating polyneuropathy AIDP

Question 8

A wave

Answer 8

not a true reflex

predictable, stable waveform that shows up somewhere between the F wave and the direct motor response

exact same waveform with every stimulation - same latency and amplitude

indicates there has been reinnervation of the nerve to that muscle (i.e., prior nerve damage occurred at some point in the patient’s life)

Question 9

An wave clinical signficance

Answer 9

usually means there has been reinnervation of the nerve to that muscle
i.e., prior nerve damage at some point in the patient’s life

Question 10

insertional activity clinical significance

Answer 10

normal

decreased - fibrosis

increased - active denervation

Question 11

resting activity clinical significance

Answer 11

normal: total silence, MEPPs (seashell noise) bc near end plate → very painful, EPPs d/t needle causing EPPs to be produced

abnormal spontaneous activity → fibs and sharp waves (regular popping sound) → active denervation (axonal loss)

denervation can be from root-level injury, plexus injury, peripheral n. injury, etc.

abnormal spontaneous activity (fibs and sharps) can be graded 0 (nml) to +4 (whole screen filled w fibs/sharps)

Question 12

fasiculations EMG clinical significance

Answer 12

seen in anterior horn cell disease (e.g., ALS) and normal patients w spasms

involuntary MUAPs d/t spontaneous muscle contractions, irregular

Question 13

EMG myokymia clinical significance

Answer 13

involuntary, abrupt, fairly regular, “marching” potential (sounds like soldiers marching), tightly grouped together

seen in upper trunk radiation plexopathy

Question 14

EMG complex repetitive discharge clinical significance

Answer 14

involuntary, similar to myokymic discharged (tightly grouped) except whole discharge is much wider → very serrated like saw → complex in appearance and repetitive in firing

d/t motor unit becoming denervated, reinnervated by another motor n, which then also becomes denervated

Question 15

ephaptic transmission clinical signifcance

Answer 15

process by which muscle fibers w CRDs all fire regularly together

seen in chronic radiculopathy, anterior horn disease, normal patients

Question 16

EMG myotonic discharges clinical significance

Answer 16

involuntary APs when you move the needle into an affected muscle fiber

amplitude steadily decreased as fiber continues to fire

sounds like a divebomber

seen in anything with “myotonia” or similar in its name
e.g., myotonic dystrophy, paramyotonia, myotonia congentia, hyperkalemic periodic paralysis, acid maltase deficiency

Question 17

EMG recruitment

Answer 17

voluntary activation of alpha motor neurons w gradually increasing intensity

one MUAP at 5Hz

increasing contraction intensity → firing at 10Hz and recruitment of 2nd MUAP at 5Hz

should be able to get 4 MUAPs on screen firing at 20/15/10/5Hz

Question 18

EMG decreased recruitment clinical significance

Answer 18

axonal damage → fewer remaining axons do all the work to achieve muscle contraction → sounds like machine gun

AKA neuropathic recruitment pattern → some kind of neuropathy going on (rather than muscle problem e.g., myopathy)

Question 19

decreased recruitment MUAPs

Answer 19

more scarce, each one firing faster, but also large and long

large amplitude, long duration MUAPs = neuropathic MUAPs

large bc axons that have not died demonstrate collateral sprouting that are new and not uniformly myelinated → variations in how consistently APs are transmitted to neuron’s muscle fibers

polyphasic MUAPs AKA reinnervation potentials

Question 20

EMG increased recruitment clinical significance

Answer 20

d/t myopathy → small muscle contraction requires recruitment of many muscle fibers → many many small, short MUAPs

AKA myopathic recruitment pattern

small duration, small amplitude motor units (SDSA) = myopathic motor units

Question 21

NCS findings demyelination

Answer 21

prolonged latency, decreased CV, increased temporal dispersion

Question 22

EMG findings demyelnation

Answer 22

normal (no conduction block) v. decreased recruitment (conduction block)

Question 23

NCS findings axonal loss

Answer 23

decreased amplitude (possibly decreased CV if fastest fibers are destroyed)

very few axons exist to summate into the CMAP

Question 24

EMG findings axonal loss

Answer 24

decreased recruitment

Question 25

demyelination 2/2

Answer 25

focal compression (e.g., CTS), stretching (on exam), systemic disease (e.g., AIDP), etc.

Question 26

axonal loss 2/2

Answer 26

focal crush, transection, stretching, systemic disease, anterior horn cell disease, etc.

Question 27

axonal v wallerian degeneration

Answer 27

retrograde v anterograde processes

wallerian degeneration is complete by 5 days (motor) or 10 days (sensory)

Question 28

conduction block 2/2

Answer 28

focal demyelination d/t compression (CTS, Saturday night palsy, any prolonged n. compression)

sometimes GBS can cause conduction block at typically non-entrapment sites → clue for GBS

DDx conduction block v axonal loss: stimulate distally to see if amplitude is normal → implies conduction block

Question 29

DDx NCS conduction block v axonal loss

Answer 29

stimulate very distally to see if amplitude is normal → conduction block

Question 30

Seddon n. injury classification

Answer 30

Neurapraxia: focal pressure on n. → focal demyelination → conduction block → resolves w removal of compression

Axonotmesis: crush or stretch injury → axonal death with epineurium still intact → axonal regeneration (~1 in/mo)

Neurotmesis: completely severing/transecting nerve all the way through epineurium d/t trauma → nerve death

Question 31

Seddon n. injury classification

Answer 31

Neurapraxia: focal pressure on n. → focal demyelination → conduction block → resolves w removal of compression

Axonotmesis: crush or stretch injury → axonal death with epineurium still intact → axonal regeneration (~1 in/mo)

Neurotmesis: completely severing/transecting nerve all the way through epineurium d/t trauma → nerve death

Question 32

Neurapraxia

Answer 32

focal n. compression → focal demyelination → conduction block (decreased proximal amplitude, normal distal CMAP)

remove compression → after few wks will see everything normal d/t remyelination

Question 33

Axonotmesis

Answer 33

crush/stretch injury to n. → axonal death w epineurium intact → axonal regeneration (~1 in/mo) along intact epineurium → biggest motor neuron w strongest NMJ connection will “win” control of muscle fiber

NCS/EMG:

1. immediately decreased proximal amplitude, normal distal CMAP
2. after few weeks, decreased proximal and distal amplitudes (axons take 5-10 days to die) with fibs and sharps (active dennervation) and decreased recruitment (axonal loss)
3. weeks to months later: reinnervation potentials (polyphasic MUAPs)

Question 34

Neurotmesis

Answer 34

complete nerve transection → loss of epineurium → no way for axons to regrow → possible neuroma formation (painful, local paresthesias) → MRI/US for resection or lido/steroid injection

NCS/EMG:

1. immediately: absent proximal CMAP, normal distal CMAP
2. after weeks (5-10 days for wallerian degeneration): absent CMAP both proximally and distally
3. after weeks-months: CMAPs still absent, fibs and sharps w absent recruitment on EMG

Question 35

Blink Reflex

Answer 35

CN V sensory input
CN VII motor output

sensory input CN V → CN V nucleus in pons → output to CN VII in pons → R1 response ipsilaterlaly
CN V nucleus in pons → output to V(s) nucleus in medulla → output to CN VII bilaterally → R2 response bilaterally

think of lesions to CN V or VII on each side and findings with R1/R2 responses

Question 36

NCS components

Answer 36

NCS: amplitude, CV, onset/peak latency, duration/dispersion

SNAP: peak latency

CMAP: onset latency → only look at distal latency
theoretically amplitude should be same at all stimulation points
CV should be similar at various stimulation sites; otherwise could reflect focal demyelination (conduction block)

normal CV 50 m/s UE, 40 m/s LE

Question 37

Demyelination EDX findings

Answer 37

focal compression, stretching, systemic disease → focal or diffuse removal of myelin around an axon → APs don’t travel as fast

NCS: prolonged latency, decreased CV, increased temporal dispersion

EMG: normal (no conduction block) v decreased recruitment (conduction block)

Question 38

Axonal loss EDX findings

Answer 38

focal crush, transection, stretching, systemic disease, anterior horn cell disease, etc → axon degeneration → few axons remain to summate CMAP

NCS: decreased amplitude (possibly decreased CV if fastest fibers are destroyed)

EMG: decreased recruitment

Question 39

Conduction block EDX findings

Answer 39

focal compression → focal demyelination → AP cannot cross proximal to lesion

NCS: zero amplitude (total conduction block), reduced amplitude (partial conduction block); can’t really measure amplitude, CV, latency proximal to lesion

Don’t confuse with axonal loss → Be sure to stimulate distally to see if amplitude is normal

Question 40

EMG myopathic motor units

Answer 40

SDSA, early recruitment, decreased insertional activity

Question 41

EMG myotonic discharged

Answer 41

sound like divebomber

anything with “myotonia” in name