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- sensory nerve action potentials
- stim a sensory nerve, get a recording further along that same nerve
3 rationales for SNAP testing
- 1) most peripheral neuropathies affect sensory before motor
- 2) test the distal segment of a sensory nerve axon
- 3) most sensory neuropathies start distally
amplification needed for SNAPs
5-20 microvolts (uV) or millionths of a volt
--- that's more amplification that needed for muscle
latency for SNAPS for median and ulnar nerves
- norm 3.6
- borderline 3.6-4.0
- prolonged > 4.0
- norm <3.4
- borderline 3.4-4.0
- prolonged > 4.0
amplitued for SNAPs for median and ulnar nerves
- norm >15
- bord 10-15
- low <10
median and ulnar nerve SNAPS -- to which fingers?
- med - 1, 2, or 3
- ulnar - 5
low amplitude in a SNAP means...
azonal degen and/or partial compression
prolonged latency in a SNAP means...
(an absent response of course is more severe trouble)
radial nerve testing .. ___dromic?
always anti never ortho!
UE vs LE, which is affected first in peripheral neuropathies
usually LE -- bc leg nerves are longer, so there's more surface to be affected
for the LE, conduction velocity below 40 m/sec means
- all conducting fibers are impaired and are conducting slower than 40 m/sec
- -- may have demyelination
compression a/o axonal degen of a high percentage of fibers --> what readings?
decreased CV and decreased amplitude
deep fibular nerve, which muscle?
extensor digitorum brevis
extensor digitorum brevis attachments
Proximal dorsal region of middle phalanges 2, 3, 4 --> dorsal lateral calcaneus
deep fibular nerve
tibial nerve - likely to get compressed where?
- popliteal fossa
- tarsal tunnel syndrome
tibial nerve, what muscle?
where do most systemic neuropahties begin?
distal LEs, so must do LE SNAPs
3 possible reasons for low amplitude in a SNAP while velocity is normal
- loss of some axons
- partial compression
- demyelination (with associated conduction block)
reason for prolonged latency in a SNAP
__dromically is SNAP testing done for LEs?
antidromically (not ortho) always
good early test for neurpathy in a diabetic
medial planta and dorsal sural nerves -- amplitudes will be reduced prior to standard nerve conduction studies
somatosensory evoked potentials
record the conduction of an AP (that started in a sensory nerve) when it reaches the posterior columns of the spinal cord
real basics of how to do a SSEP
- stim a sensory nerve (UE or LE)
- record over the sensory cortex, thru the cranium, with subcutaneous EEG needles
- use a specialized amplifier to average multiple APs
- the electrical equiv of a myotatic reflex (DTR)
- records and AP first in sensory fibers going to the SC, then in motor fibers heading to the muscle (so it's all done orthodromically) ... so it looks at conduction along the entire pathway associated with a reflex
use low intensity stim*
brainstem auditory evoked potentials (BAER) -- what's it for?
to evaluate auditory pathways to the primary auditory cortex
I guess it's R rather than P for "response??"
how is a BAER performed?
headphones produce audible clicks (1 per sec) to produce an AP conducted by the cochlea to the ipsilat temporal lobe ... and I guess it's measured there?
most common etiology of involvement for a BAER
visually evoked potentials -- tests what?
visual tracts to the occipital lobe
how is a visually evoked potential test performed?
use strobe stim (1/sec) to evoke and AP from the retina to the optic radiations to the occipital lobe
(demyelination may lead to increased latency of initial peak)
how will UMNL impact an H-reflex?
how will POLIO impact an H-reflex?
decreased H reflex bc ant horn cell is shot
how will motor root compression (like from a disc) impact an H-reflex?
increased latency, decreased amplitude
F wave tests what?
looks at the backfiring of an ant horn cell, testing its conduction and excitability
the ___dromic stuff in an F wave
starts antidromically, running up a motor fiber, ends orthodromically running down the motor fiber
how will spasticity influence an F wave?
how will spinal shock or motor neuron disease impact an F wave?
SSEP vs F vs H wave, what they test
- SSEP -- sensory
- F -- motor, excitability of ant horn cells
- H -- both
drugs for myesthenia gravis?
prim locations and an early symptom of myesthenia gravis
extraocular, cervical, shoulder girdle muscles
how to test for myesthenia gravis
- small needle in intrinsic hand, prox muscles (such as deltoid), and a facial muscle
- stim repeatedly at various frequencies (5,15, 30, 50)
- do a very slow sweep speed (up to 30 sec / sweep), looking for decrease in amplitude of motor unit APs (MUAP)
healthy should show no decrease in amplitude over 5-10 sec or just a 5% decline, while MG should taper sharper >10%
how should spasticity or increased DTRs impact F wave?
flaccidity, polio, Guillian-Barre -- gives what for F-waves?
- flaccidity - absent
- polio - absent
- GB - impaired
ant horn cell problem -- how will it affect F wave?
- latancy -- normal
- amplitude -- decreased (bc it reflects the excitability of the horn cell -- if it's a UMNL it'll be high amp)
You did some MG testing and saw a taper. What should you do next to confirm the diagnosis?
inject a drug that briefly strengthens function at the NMJ and repeat test to see what happens. If the tapering decreases, it looks like it's MG.