EDX Flashcards
Types of neurons in DRG?
Sensory bipolar ( one extends to dorsal horn, other to skin)
Dorsal column pathway
light touch/ pressure
Spinothalamic pathway
pain/ temperature
Where are alpha motor neurons located
ventral horn of spinal cord
motor unit
alpha neuron and associated muscles
muscle contraction pathway
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
innervation ratio
muscle fibers/ LMN
Myelin made by
schwann cells
(oligodendrcytes in cns)
Endoneurium
tissue around axon
perineurium
bundles axons
epineurium
connect fascicles together
MEPPs
mini depolarization caused by regular quantas
resting charge or neuron
-70mv
SNAP
sensory n. action potential
CMAP
compound muscle action potential
normal orientation of 2 pronged device
Cathode (-) towards stimulating
black bar/ ring on fingers
recording electrode g1/ black
electodes 4cm apart over bone or tenden
reference electrode g2 (to subtract background noise
green electrode
placed between stimulator and active electrode (dissipates current)
Conduction velocity
how fast a wave is
latency
how fast is the wave conducting
CMAP measuring
baseline to peak amp
SNAP measuring
peak to peak
onset latency
time before starting negative (upward) deflection
peak latency
time from start to peak negative deflection
temporal dispersion
the distribution of action potentials
orthodromic
physio direction of AP
antidromic recording
against physio direction of AP (SNAP studies)
UE and LE temp for EDX. what if too cold?
UE 32C
LE 30C
too cold = increase amp, conduction velocity will slow with prolonged latency, duration increased (slower atoms longer opened channels)
Ranges for Sensory and Motor NCS
Hi frequency filter
Lo frequency filter
Sensory 20-2000hz
Motor 10-10000hz
Effects of lowering and raising filters
lowering filter = lower amp and prolonged onset of peak latency
Raising lo = peak early, low amp
Normal and Aging on AP conduction velocity
Normal UE 50 m/s LE 30 m/s >50yo -2m/s per decade
Normal range apply to stim and duration?
1-100 mAmps
0.1-1.0 ms
h- reflex (true reflex)
nerve?
direction of AP?
what if prolonged?
Ia sensory afferent n.
AP towards spinal cord -> spinal reflex arc -> motor nerve -> muscle contracts
prolonged= pathology (radiculopathy)
F wave (not a true reflex)
stim n?
direction?
prolonged/absent?
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
A wave (not a true reflex)
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.
EMG
Concentric electrode
vs
Monopolar electrode
Concentric- reference electrode attached to needle
con- small recording area
Monopolar- broad listening area, needs separate reference electrode
insertional activity
TV static when entering muscle (AP caused by ripping thru muscle)
Decreased- fibrosis
increased- active denervation/ irritated
MEEPs
Normal Resting Seashell noise (painful, at motor end plate, move needle away)
Complex repetitive discharge CRD
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
Fasciculation
Normal Resting
involuntary MUAPs
fibs/sharps
Abnormal Resting positive (downward) depolarization axon loss (scale 0-4+) denervation of muscle.
Fasciculation + Fibs/sharps
Abnormal Resting
ant horn cell dz
Myokymia
Abnormal Resting
involuntary, abrupt, regular “marching”
upper trunk plexopathy, tumor, radiation
Myotonic Discharge
Abnormal Resting
Dive-bombers, amp steady
any myotonia: myotonic dystrophy, paramyotonia, myotonia congenita, kyperkalemic periodic paralysis, acid maltase deficiency
Recruitment
increasing motor units to activate more contraction of muscle fibers
Est Hz of a MUAP
MUAP/screen x 5
Decreased recruitment
increased firing (machine gun)- making up for lack of axons 30-50hz. neuropathic recruitment pattern
Decreased recruitment, LDLA
Large amp, long duration MUAPs
Polyphasic MUAPs
during collateral sprouting (MU taking over another’s) polyphasic, crosses baseline >x5.
Eventually myelinate and become a LDLA
Increased recruitment
Small duration, small amp SDSA
muscle is weak due to myopathy, more motor units need to be recruited to allow activation.
Myopathic recruitment pattern
Demyelination
causes
EMG
NCS
causes: focal compression, stretched, systemic dz (AIDP/GBS)
EMG: nl
NCS: prolonged latency, decreased CV, increased temporal dispersion
Axonal loss
Causes
EMG
NCS
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)
Axonal vs wallerian degenderation
Retrograde/systemic
vs
Anterograde, complete in 5 (motor) or 10 (sensory) days
Conduction block
failure of AP to propagate past a focal spot in peripheral nervous system.
Usually focal demyelination- GBS or focal compression (CTS/ saturday night palsy)
Seddon classification:
Neurapraxia
timeline findings
focal pressure/ focal demyelination
EMG nl, CMAP nl
stimulate proximally, may see decreased amp- nl in a few weeks
great prognosis
Seddon classification:
Axonotmesis
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)
Seddon classification: Neurotmesis
complete severed/ transection of nerve
absent CMAP
May attempt to regrow but form neuromas (painful, can inject with steroids)
Blink Reflex Study (NCS)
what nerves?
How it works?
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
Blink Reflex Study (NCS) pathology
Trigeminal lesion
Facial nerve lesion
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
Synkinesis in blink reflex study
syn together
kinesis move
a complication of facial n. regeneration
inappropriate sprouting during regeneration leading to more than just one muscle innervation
nl findings in
steroid myopathy 2B fibers cant be seen on edx
disuse myopathy
congenital
mitochondrial, GSD V GDS VII, carnitine defi
characteristic in waveform shows potential for ongoing functional recovery in deinervation and clinically weak muscle
stability- shows mature recovery
