NCS/EMG Flashcards
effects of adjusting high/low frequency filters on NCS
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
temperature effects on action potential
if limb is too cold
- amplitude will increase
- CV will be slow with prolonged latency
- duration will increase
sodium channels remain open longer → beefier amplitude and longer time of depolarization
age effects on action potential
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
H reflex
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
H reflex evaluates
S1 radiculopathy
non specific
true reflex
F wave
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
F wave clinical signficance
prolonged/absent F waves are first sign of Guillain Barre syndrome
AKA acute inflammatory demyelinating polyneuropathy AIDP
A wave
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)
An wave clinical signficance
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
insertional activity clinical significance
normal
decreased - fibrosis
increased - active denervation
resting activity clinical significance
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)
fasiculations EMG clinical significance
seen in anterior horn cell disease (e.g., ALS) and normal patients w spasms
involuntary MUAPs d/t spontaneous muscle contractions, irregular
EMG myokymia clinical significance
involuntary, abrupt, fairly regular, “marching” potential (sounds like soldiers marching), tightly grouped together
seen in upper trunk radiation plexopathy
EMG complex repetitive discharge clinical significance
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
ephaptic transmission clinical signifcance
process by which muscle fibers w CRDs all fire regularly together
seen in chronic radiculopathy, anterior horn disease, normal patients
EMG myotonic discharges clinical significance
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
EMG recruitment
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
EMG decreased recruitment clinical significance
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)
decreased recruitment MUAPs
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
EMG increased recruitment clinical significance
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
NCS findings demyelination
prolonged latency, decreased CV, increased temporal dispersion
EMG findings demyelnation
normal (no conduction block) v. decreased recruitment (conduction block)
NCS findings axonal loss
decreased amplitude (possibly decreased CV if fastest fibers are destroyed)
very few axons exist to summate into the CMAP
EMG findings axonal loss
decreased recruitment
demyelination 2/2
focal compression (e.g., CTS), stretching (on exam), systemic disease (e.g., AIDP), etc.
axonal loss 2/2
focal crush, transection, stretching, systemic disease, anterior horn cell disease, etc.
axonal v wallerian degeneration
retrograde v anterograde processes
wallerian degeneration is complete by 5 days (motor) or 10 days (sensory)
conduction block 2/2
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
DDx NCS conduction block v axonal loss
stimulate very distally to see if amplitude is normal → conduction block
Seddon n. injury classification
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
Seddon n. injury classification
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
Neurapraxia
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
Axonotmesis
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:
- immediately decreased proximal amplitude, normal distal CMAP
- 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)
- weeks to months later: reinnervation potentials (polyphasic MUAPs)
Neurotmesis
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:
- immediately: absent proximal CMAP, normal distal CMAP
- after weeks (5-10 days for wallerian degeneration): absent CMAP both proximally and distally
- after weeks-months: CMAPs still absent, fibs and sharps w absent recruitment on EMG
Blink Reflex
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
NCS components
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
Demyelination EDX findings
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)
Axonal loss EDX findings
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
Conduction block EDX findings
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
EMG myopathic motor units
SDSA, early recruitment, decreased insertional activity
EMG myotonic discharged
sound like divebomber
anything with “myotonia” in name
