Term
| What is electrophysiological examination? |
|
Definition
| a set of clinical procedures to examine the integrity of the neuromuscular systems including PNS, CNS, and muscles. Performed by neurologists, physiatrists, physical therapists, and also chiropractors; tests to establish the location, nature, and severity of neuromuscular disorder. |
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Term
| How do we study neuromuscular function/dysfunction using clinical electrophysiology? |
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Definition
| Observe the deficits or abnormal activity (done during initial eval), stimulate electrically or voluntarily active tissue and observe the response; monitor nerve or muscle activity in response to voluntary or artificial activation. Clinical electrophysiology employs stimulation and recording techniques to identify the location and nature of neurological or muscular disorders. |
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Term
| What is recorded in electrophysiological examination? |
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Definition
| Electrical activity in nerve or muscle (action potentials from groups of nerve or muscle fibers). |
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Term
| *Where do action potentials occurs in n cells? |
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Definition
Multipolar (motor neurons)
Special sensations (bipolar)
General sensation (pseudo-unipolar) |
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Term
| What are nerve and muscle action potentials? |
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Definition
| Voltage changes associated with ionic mov't across electrically excitable membranes of nerve or muscle. Reflects changes in concentration of ions (Na+ and K+) btwn the inside and outside of n. axons or muscle fibers. |
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Term
| What is happening to produce APs in nerve or muscle? |
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Definition
| APs reflect the permeability changes in the nerve or muscle fiber membrane to sodium (Na+) and potassium (K+) ions. Na+ moves in and then K+ moves out. The changes in charge (+ or -) can be detected w/ voltage meter devices. |
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Term
| What are the 2 techniques for n and muscle action potential recording? |
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Definition
| Intracellular and extracelluar techniques |
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Term
| What is the intracellular technique for recording muscle action potential? |
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Definition
| Monitors electrical activity in single nerve or muscle fibers; One electrode inside the fiber and one electrode outside; records transmembrane voltage changes; used in research lab |
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Term
| What is the extracellular technique for recording muscle action potential? |
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Definition
| Monitors electrical activity of groups of nn. or muscle fibers; Both electrodes are outside of the fibers; records electrical potential difference btwn two electrodes; used in electrophysiological tests |
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Term
| Describe what is happening underneath the electrodes using the extracellular action potential recording technique? |
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Definition
| Sodium enters beneath 1st electrode so it is less positive under 1st electrode; Sodium enters between electrodes so u get an equal net charge under both electrodes; sodium enters beneath second electrode, so u get more positive under first electrode. |
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Term
| What are two ways to activate n or muscle in electrophysiological tests |
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Definition
1. electrical stimulation
2. Voluntary activation of skeletal muscle |
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Term
| How does electrical stimulation activate n or muscle in electrophysiological tests? |
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Definition
| Single short duration stimuli applied with a rectangular monophasic pulsed current generator; Triggers AP initiation and bidirectional propagation from point of stimulation; number of nerve or muscle fibers acticated determined by stimulus amp and duration; applied w/ either surface electrodes or needle electrodes. |
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Term
| *Difference between physiological stimulation/recruitement and electrical stimulation/recruitment? |
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Definition
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Term
| Stimulation amplitude and duration effects on recruitment. |
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Definition
| Higher stimulation & greater duration activates more axons. |
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Term
| Direction of AP propagation in electrophysiological evaluation. |
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Definition
| ES of nerve produces AP propagation in both directions from point of stimulus. |
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Term
| Difference between orthodromic propagation and antidromic propagation? |
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Definition
| Orthodromic propagation is in the "normal direction" for the particular axon (distally for motor axons, proximal for sensory); Antidromic propagation is in the opposite from normal direction (proximal for motor, distal for sensory) |
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Term
| T/F- compound muscle or n. action potentials are recorded w/ physiological examination |
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Definition
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Term
| What is the purpose of clinical nerve conduction studies? |
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Definition
| test the functional integrity of the motor and sensory axons in peripheral nn. Are n axons sending APs normally. |
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Term
| What axons are motor NCV studies looking at? sensory? |
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Definition
Motor- looking at speed of Alphamotor neurons (largest diameter and most susceptible to compression)
Sensory (looking at Abeta neurons) |
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Term
| T/F- When looking at AP propagation, you want to know the direct and speed of conduction? |
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Definition
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Term
| When stimulating UE nerve pathways, where do you place the electrodes? |
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Definition
| Place the cathode closes to point of recording b/v it is better than anode at picking up the signal; generally, u want the electrodes where the n. is exposed and not covered by muscle or fat. |
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Term
| Outline a Motor nerve conduction test schematic |
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Definition
| Supramaximal nerve stimulation --> 100% 100% motor axon activation --> AP propagation --> NMJ activation --> skeletal muscle fiber activation --> record electrical activity in muscle |
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Term
| What does amplitude represent? |
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Definition
| the number and amount of nerve fibers activated. |
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Term
| What is measured in response to each stimulus? |
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Definition
| Compound Muscle Action Potential (CMAP) |
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Term
| What is CMAP latency? What contributes to it? |
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Definition
| CMAP latency is the time btwn stimulating and onset of the waveform. AP initiation time, AP propagation time, NMJ activation time, and MAP propagation time all contribute to CMAP latency, but AP propagation time and NMJ activation time contribute the most to latency. |
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Term
| What does CMAP amplitude mean? |
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Definition
| Reflects the number of muscle fibers activated, proportional to # motor axons activated and transmitting APs to mm; not affected by sensory axon activation. |
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Term
| T/F- u can have a decrease in amplitude w/ problems in motor axons, muscle fibers, or both. |
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Definition
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Term
| How do u determine segmental conduction velocities? |
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Definition
| stimulate at several diff locations, record latencies from each stimulation site, segment conduction velocity equals: length of segment/(latency of prox stim site - latency distal stim site) |
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Term
| Describe the schematic for antidromic techniques for sensory NCV studies |
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Definition
| Stimulate proximally over nerve --> supramaximal nerve stimulus --> 100% sensory recruitment --> Antidromic AP propagation --> Record CSNAP distally. |
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Term
| T/F- a compound nerve sensory AP is about 1000x smaller than muscle response (measured in microvolts rather than minivolts) |
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Definition
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Term
| Schematic for Orthodromic Sensory NCV studies. |
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Definition
| Stimulate distally over nerve or digit --> supramaximal n stimulus --> 100% sensory recruitment --> orthodromic AP propagation --> record CSNAP proximally over nerve. |
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Term
| T/F- sensory NCV studies typically limited to distal segment |
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Definition
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Term
| What does the amplitude of CSNAP amplitude mean? |
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Definition
| Reflects # of sensory fibers activated; proportional to # sensory axons activated and transmitting APs to recording site; recorded over area w/ no muscle or over sensory n bundle; 1000 times smaller than CMAP. |
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Term
| CSNAPSs of lat cut n of forearm and superficial radial to thumb are reduced. Where's the problem? |
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Definition
| UT or C6 (most likely UT and not C6 b/c central processes often not affected in sensory disorders w/ digits) |
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Term
| What are the normal variation in CV values? |
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Definition
| higher in more proximal segments (b/c axons are larger more proximally), higher in UEs than LEs, may be 5-10 m/s different from side-to-side, variation in normal values between labs, lower past 60yrs old or <5yrs old (Not well myelinated yet) |
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Term
| Sources of error in NCV studies (6) |
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Definition
1. lack of temp control (CV drops by 2.4 m/s for each drop of 1 degree C)
2. error in segment length measurement (biggest source of error)
3. Inadequate amp of stim
4. Anatomic anomalies (martin-gruber)
5. Inconsistent limb position (stretching of n)
6. Inappropriate bandpass filter settings |
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Term
| *T/F- neuropraxia will cause latency--- depends |
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Definition
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Term
| T/F- if there is a conduction block, u will get latency |
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Definition
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Term
| What represents abnormal slowing in motor nerve conduction studies? |
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Definition
- Distal motor latencies in a single peripheral nerve that are >1ms longer than that for contralateral normal nerve OR ipsilateral normal n (e.g. median to ulnar)
- segmental conduction velocities that are >10-15 m/s lower than the same segment in contralateral n OR the segments just proximal or distal to reduced CV segment. |
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Term
| *What represents abnormal amplitudes of CMAP responses in motor n conduction studies? |
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Definition
- Values that fall below lower limits of normal
- 30-50% drop in AMP from distal to prox stimulation side
-??? |
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Term
| 2 types of peripheral nerve lesions |
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Definition
|
|
Term
| difference between neuropraxia and axonotmesis |
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Definition
| Neuropraxia is a localized conduction slowing w/ or w/o a conduction block, NO axon degeneration, compression/stretch/inflammation; Axonotmesis is an axon disruption w/ distal degeneration, there may or may NOT be slowing in remaining axons, crush/stretch injuries, like neurotmesis |
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Term
| What effect does demyelination have on partial neuropraxia? |
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Definition
| For those axons not blocked, it will slow their conduction. |
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Term
| MNCV results for partial neuropraxia (partial axonal conduction block and demyelination) |
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Definition
| Some axons get blocked and dont propagate, others will slow down at the segment of compression. You will get a reduced amplitude (b/c some axons are blocked) and increased latency due to slowing. |
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Term
| During a partial neuropraxia w/ conduction slowing and partial conduction block, What will happen to the conduction velocity at the segment of the compression site, the segment proximal to compression and segments distal to compression. |
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Definition
| At segment of compression, you will get reduced CV. At segment proximal, you will get normal CV but reduced amplitude. At segment distal, you will get normal CV and normal distal latency and normal amplitude |
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Term
| During a partial neuropraxia w/ conduction slowing at and distal to injury site, What will happen to the conduction velocity at the segment of the compression site, the segment proximal to compression and segments distal to compression. |
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Definition
| At segments proximal, you will get normal CV. At segment of injury, reduced CV. At segments distal, you get reduced CV and prolonged distal latency. Overtime, u get axoplasmic transport problems which will slow NCV. |
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Term
| What happens to nerve conduction in double crush syndrome? |
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Definition
| Proximal segment nerve compression/compromise may lead to distal compromise at anatomical compression sites. This secondary compression occurs b/c proximal compression impairs axoplasmic transport of proteins so distal membrane function is impaired and distal segments swell against fixed structures. If compression is prolonged, distal axon may degenerate. (note: axoplasmic transport is bidirectional) |
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Term
| Nerve conduction results in double crush syndrome |
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Definition
| You get reduced conduction at initial compression site and then reduced conduction due to axonal swelling and secondary compression somewhere distal |
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Term
| MNCV results for partial axonotmesis (14-21 days after injury), what happens if you stimulate below lesion? |
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Definition
| Reduced amplitude, normal latency |
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Term
| MNCV results for partial axonotmesis (14-21 days after injury), what happens if you stimulate above (before) lesion? |
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Definition
| Reduced amplitude, normal latency (no conduction impairment at site of cut) |
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Term
| Segmental conduction velocity with partial axonotmesis at segment of injury, proximal, and distal. |
|
Definition
At segment- normal or slightly reduced CV
distal- normal latency
Proximal- normal CV. |
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Term
MNCV results for complete neuropraxia with stimulation distal to site of lesion(all axons involved/blocked like saturday night palsy)
Hint: looks exactly like complete axonotmesis in first 10-14 days |
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Definition
| Normal amplitude, normal latency |
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Term
| MNCV results for complete neuropraxia w/ stim proximal (above) site of lesion. |
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Definition
| No response (all axons gone) |
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Term
| MNCV results for complete axonotmesis with stim below lesion (distal) |
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Definition
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Term
| MNCV results for complete axonotmesis with stim below lesion (distal) |
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Definition
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Term
| MNCV results for complete axonotmesis with stimulation proximal (above lesion). |
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Definition
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|
Term
| What can clinical values of NCV tell us (8) |
|
Definition
1. are peripheral nn involved? how many?
2. is lesion of PN, plexus, of n root?
3. Is PN dysfunction localized or widespread
4. Are sensory, motor, or both components involved
5. Is lesion partial or complete
6. Is lesion neuropraxic or axonotmetic?
7. Is lesion neuropathic or myopathic (conduction of nn would be normal)?
8. Is dysfunction changing over time? |
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Term
|
Definition
| An electrophysiological test of conduction in proximal segments of motor nerve fibers |
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Term
| Describe the F-wave testing procedure |
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Definition
| Record CMAP from muscle, stimulate proximally over innervating n, apply supramaximal stimulus to peripheral n, cathode(-) proximal to anode. (done in conjunction w/ basic NCV tests; APs produced in both directions) |
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Term
| T/F - Fwave is not a reflex response |
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Definition
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Term
| *difference between m wave and f wave |
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Definition
| Orthodromic M wave occurs when you stimulate the nerve and the signal travels down to the muscle from that point. The F-wave is the second response which jitters in latency & amp unlike M wave which is constant. The F-wave is derived fvrom the antidromic APs produced by the stimulation that goes to the SC and comes out of the ventral horn as the orthodromic F-wave and goes to the muscle. |
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Term
| T/F- Fwave responses are in the same size, shape, or latency |
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Definition
|
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Term
| what does F-wave amplitude reflect? |
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Definition
| Reflects antidromic activation of small % (1-5%) of alpha MNs |
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Term
| T/F- fwave amp averages 1% of M wave amp |
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Definition
|
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Term
| T/F- Fwave amp is a measure of MN excitability |
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Definition
|
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Term
| We should see (increases/decreases) in amp in spasticity and UMN diseases. |
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Definition
| Increases (F-wave would be higher) |
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Term
| T/F- Fwave latencies are variable and not fixed as in routine NCV studies |
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Definition
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Term
T/F- Fwave latencies are dependent on site of stimulation
T/F- shortest latency is recorded for interpretation |
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Definition
|
|
Term
| T/F- Longer latencies in LE nerve than UE nerve for Fwave latency. Why/why not? |
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Definition
| True because longer nerves in LE and UE is typically faster. |
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Term
| T/F- Fwave latency is prolonged in demyelinating polyneuropathies (e.g. Guillian-Barre syndrome) or brachial plexopathies |
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Definition
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Term
| Is Fwave latency a sensitive indicator of N root pathology/compression in one level? |
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Definition
| No b/c most mm innervated by multiple n root levels so f-wave can go through a diff level. it is a good indicator of n root conduction in brachial plexus or peripheral n. |
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Term
| What do increases in Fwave latency reflect? |
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Definition
| delays in conduction at some point in path not simply in proximal segments. |
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Term
| *If routine motor n studies in PN are abnormal, should Fwave tests be performed? |
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Definition
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Term
| How much should Fwave latencies vary from side to side? |
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Definition
| They shouldnt vary by >1ms for UE and >1.5ms for LE nerves. |
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Term
| *T/F - voluntary muscle contraction increases frequency of F-wave appearance |
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Definition
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Term
| T/F- Failure to evoke F wave is not necessarily an abnormal finding |
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Definition
| True (might be a "low tone" person) |
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Term
| What is H-reflex Testing? |
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Definition
| Examination of the functional integrity of the stretch reflex pathways using electrophysiological assessment. It examines conduction from knee to the foot. No evaluation from spine to knee. |
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Term
| Draw a schematic of the components of a routine stretch reflex test |
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Definition
| Quick muscle stretch --> muscle spindle activation --> 1a afferent AP propagation --> 1a-motoneuron synapse transmission --> motoneuron AP propagation --> NMJ activation --> Skeletal muscle activation --> muscle twitch contraction |
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Term
| *T/F - 1a afferent is the biggest, fastest conducting and most sensitive afferent to compression |
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Definition
|
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Term
| Describe the following 5 point subjective rating scale for stretch reflex response: 4+, 3+, 2+, 1+, 0 |
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Definition
4+ = brisk, hyperactive w/ clonus
3+ = slightly hyperactive
2+ = active, normal expected response
1+ = sluggish, diminished
0 = no response |
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Term
| Draw a schematic of the electrical testing procedure for stretch reflexes |
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Definition
| Stimulate the 1a afferent coming from muscle spindle --> 1a afferent AP propagation --> 1a-motoneuron synapse transmission --> motoneuron AP propagation --> NMJ activation --> skeletal muscle activation --> Record CMAP --> muscle twitch contraction. |
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Term
| How do you guarentee that you stimulate only 1a afferents and not alpha motorneurons during H-reflex testing? |
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Definition
| Use lower amplitude of stimualtion |
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Term
| What does the H-wave latency represent? |
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Definition
| The latency represents the time it takes from the onset of the stimulus from the electrodes to the CNS and back to the muscle. It reflects the speed of conduction/transmission in reflex pathway. |
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Term
| What does increased H-wave latency indicate? |
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Definition
| Impairment in one or more parts of the pathway (usually in proximal segments) |
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Term
| If peripheral sensory and motor conduction is normal, increased H-wave latency suggests what? |
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Definition
| it suggests a disorder in the proximal reflex arc |
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Term
| What factors contribute to H-wave latency? (3) |
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Definition
| Pathway length (arm or leg length), Integrity of conduction path, age of patient |
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Term
| What factors influence Integrity of conduction path in H-wave latency? (5) |
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Definition
| 1a afferent conduction time, 1a/MN synaptic delay, alpha MN conduction time, NMJ transmission time, Muscle conduction time. |
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Term
| *What is the formula for H-wave latency? |
|
Definition
| Hlatency = 9.14 + .46leg length(cm) + .1age(yrs) |
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Term
| If you perform H-reflex test and you find that actual latency is greater than predicted latency using a nomogram, what should you do? |
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Definition
| Find the contralateral H-latency |
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Term
| If you perform H-reflex test and the side-to-side difference in latency > 1.0 msec, what does this suggest? |
|
Definition
| It suggests sacral radiculopathy |
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Term
| If you perform H-reflex test and H latencies on both extremities are greater than the predicted latency value, what should you do? |
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Definition
| find the tibial nerve conduction velocity |
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Term
| What does the amplitude of the Hwave represent? |
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Definition
| It reflects the number of sensory, motor, and/or muscle muscle fibers activated. It reflects the excitability of alpha MNs (increases suggest hyperactive MNs, decreases suggests hypoactive MNs) |
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Term
| T/F- as you increase the applied stimulus, H-wave begins to appear, followed by M-wave, and the magnitude of these 2 waves is inversely proportional. |
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Definition
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Term
| Why does H-wave appear first when testing? Why does M-wave appear while H-wave grows? |
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Definition
| Small applied stimulus stimulates larger diameter 1a's so you get H-wave response. If you increase amplitude, you activate more 1a's and some of the largest alpha MNs thereby producing a small M-wave as well. |
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Term
| T/F - as you increase the amplitude when testing for Hwave, you will activate 1a's from small-to-largest axons and you will activate alpha MNs from largest-to-smallest axons. |
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Definition
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|
Term
| Why does M-wave grow while H-wave declines? |
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Definition
| When you do H-reflex testing, you want to stimulate all 1a fibers. The stimulus that you apply activates APs in alpha MNs that propagate both orthodromically and antidromically. Antidromic APs will meet APs that were created reflexively by the orthodromic stimulus of 1a afferents. These reflexive APs collide w/ antidromic alpha MN APs and cancel each other out, thereby decreasing H-wave. |
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Term
| T/F- it is possible to have delayed H-wave and normal F-wave. Why or why not? |
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Definition
| true because F-wave only looks at alpha MNs while H-wave looks at alpha MNs and 1a's, dorsal root, dorsal horn...etc. |
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Term
| If you have an increased latency of H-reflex but everything else distally is normal, what does this suggest? |
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Definition
| An S1 nerve root problem. |
|
|
Term
| What is the significance of H-reflex testing? |
|
Definition
| It allows quantitative testing of reflex pathways. |
|
|
Term
| What does increases in H-wave latency indicate? |
|
Definition
| Decreased AP conduction and/or transmission at some point in reflex pathway. |
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Term
| Tibial/soleus H-wave is commonly used to evaluate the integrity of which nerve root? |
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Definition
|
|
Term
| Median n/FCR Hwave is used to assess what? |
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Definition
|
|
Term
| Describe the pathway of FCR that H-wave reflex tests. |
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Definition
| Andrew branch of Median n --> Lateral cord --> ADMT --> C7 (also ADUT and C6) |
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Term
| What is clinical needle electromyography? |
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Definition
| Recording the electrical activity of skeletal muscle fibers at rest and during voluntary activation |
|
|
Term
|
Definition
| Electrical activity arising from skeletal muscle fibers at rest and during voluntary muscle contraction, and in response to involuntary spontaneous activation of muscle fibers. |
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|
Term
| What three electrodes are used in EMG? |
|
Definition
| Needle electrode in muscle (active), surface electrode over muscle (reference), and surface electrode over bone (ground). |
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|
Term
| Between which electrodes is muscle AP recorded in needle EMG? |
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Definition
| Between active and reference electrodes. |
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|
Term
| What are the 5 general principles of needle EMG testing? |
|
Definition
| Examine mm above and below suspected lesion site, examine muscles innervated by different nn and n roots, sample full cross section of muscle, examine contralateral UE/LE mm, perform testing in appropriate timeframe (i.e. cant tell diff between neuropraxic and axonotmetic prior to 2 weeks cuz it takes time for distal nn to degenerate.) |
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|
Term
| What should you examine prior to EMG testing? |
|
Definition
| Review medical record and pt hx, interview pt, perform clinical testing of sensory and motor systems. |
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Term
| What are the 4 phases of needle EMG exam? |
|
Definition
| insertional activity (activity of m as you move needle through), Rest activity, mild contraction activity (isometric), Strong contraction activity |
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Term
| What are normal findings for insertional activity of EMG exam? |
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Definition
| brief bursts of electrical activity produced by briskly moving needle electrode in muscle; reproduced by tapping muscle; the activity is due to mechanical stimulation or injury of muscle fibers with needle movement. |
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|
Term
| What are normal findings for skeletal muscles at rest during EMG exam? |
|
Definition
| No electrical activity in muscle other than in NMJ region. |
|
|
Term
| What accounts for NMJ activity when a muscle is at rest? |
|
Definition
| Miniature end-plate potential and end-plate spikes |
|
|
Term
| What are miniature end-plate potentials? |
|
Definition
| Localized, transient muscle depolarization near NMH related to spontaneous ACh release. |
|
|
Term
| What are end-plate spikes? |
|
Definition
| Discharge of single muscle fibers activated by needle electrode. |
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|
Term
| What are Motor Unit Potentials (MUPs)? |
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Definition
| they represent the synchronous activation of the group of muscle fibers innervated by a single alpha motoneuron; represent the activity of the nerve even though they are muscle APs; they occur when MN AP activates fibers within muscle unit in response to motoneuron AP |
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Term
| T/F- you will only see an MUP when you ask the pt to contract. |
|
Definition
|
|
Term
| Which normal MUP patterns do you see with increasing mild contraction? |
|
Definition
Rate coding- individual MUP freq of d/c increases w/ force of contraction (normally starting in 5-10/s range)
Recruitment- greater # of progressively larger, stronger motor units are activated as force of contraction increases (normally smaller MUPs activated before larger MUPs) |
|
|
Term
| What is interference pattern in EMG studies? |
|
Definition
| it is the summated electrical activity of many motor units recruited and discharging asynchronously |
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|
Term
| T/F- interference pattern is associated with muscle activity during strong voluntary contraction |
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Definition
|
|
Term
| if a muscle has normal insertional activity, no activity at rest, Normal motor unit potentials, and a full interference pattern ,it is considered (normal/abnormal) |
|
Definition
|
|
Term
| When observing the interference pattern, motor units are activated in order of (smallest/largest) to (smallest/largest) |
|
Definition
|
|
Term
| T/F- individual motor unit potentials can't be recognized with full normal recruitment pattern. Why/why not? |
|
Definition
| True because the interference pattern obliterates the display screen at normal recording settings for MUP observation. |
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|
Term
| What is the significance of normal EMG findings? (3) |
|
Definition
| It suggests no motor axon pathway conduction block or degeneration, no muscle disease of disorder, and no NMJ dysfunction |
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|
Term
| T/F- if you didn't see an abnormal finding w/ EMG, this doesn't mean that everything is normal. |
|
Definition
|
|
Term
| What are abnormal findings for insertional activity with EMG? |
|
Definition
1. Increased amplitude/prolonged duration of insertional activity (lasts longer than a few hundred ms after needle stops moving, associated w/ denervation, myotonia, or myositis...usually starts like this)
2. Reduced amplitude- associated w/ muscle fiber loss as in fibrotic or denervation atrophied muscle
3. Insertional positive waves |
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|
Term
| What are insertional positive waves as seen during abnormal insertional activity of muscle during EMG studies? |
|
Definition
| it is a sustained series of positive waves after needle movement has stopped, lasting several seconds to minutes. It is associated w/ increased Amplitude and prolonged duration of insertional activity which is common in early (10-14 days) denervation. |
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|
Term
| What are six examples of abnormal spontaneous potentials in resting muscle? |
|
Definition
1. Fibrillation potentials
2. Positive sharp waves
3. Fasciculation potentials
4. Myokymic discharges
5. Complex repetitive discharges
6. Myotonic discharges
Any of these seen when muscle is at rest is abnormal. |
|
|
Term
| T/F - you see a fibrillation potential pattern w/ small amplitudes. It can therefore be interpreted that denervation occurred a long time ago. |
|
Definition
|
|
Term
| What is the origin and clinical significance of Fibrillation potentials? |
|
Definition
Origin- spontaneous activation of single muscle fibers
Significance- associated w/ denervation of muscle fibers as in axonotmetic lesion; seen in myopathy, myositis, and NMJ disease; can be neuropathic or myopathic; won't see this till 10-14 days after injury. |
|
|
Term
| What is the origin and clinical significance of positive sharp waves? |
|
Definition
Origin- spontaneous activation of single muscle fibers.
Significance- associated w/ denervation of muscle fiber as in axonotmetic lesion; seen in myopathy, myositis, and NMJ disease; can be neuropathic or myopathic. |
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Term
| What is the origin and clinical significance of Fasciculation potentials? |
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Definition
Origin- spontaneous activation of motor units or groups of muscle fibers
Significance: associated w/ motoneuron disease (eg post-polio syndrome); seen in radiculopathies and entrapment neuropathies (very common in cervical radiculopathy); appears in myopathies and myositis; NOT linked to denervation of muscle |
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Term
| What is the origin and clinical significance of myotonic discharges? |
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Definition
origin- Cyclical activation of muscle fibers or groups of muscle fibers
Significance- seen in myotonia congenita, myotonic dystrophy, and other related disorders; associated more frequently w/ myopathy (myotonic dystrophy, polymyositis, hyperkalemic periodic paralysis), seen in some neuropathic disorders (chronic radiculopathy, chronic peripheral neuropathy) |
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Term
| Where do you observe myokymic discharges? |
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Definition
| Observed in facial muscles (MS, brainstem neoplasm, bell's palsy, polyradiculopathy), Extremity mm (radiation plexopathy, chronic nerve compression, rattle snake venom poisoning) |
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Term
| What is the origin and clinical significance of complex repetitive discharges? |
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Definition
Origin = >10 muscle fibers discharging in series
Significance = in myopathies, polymyositis;
In neuropathies- associated w/ chronic denervation as seen in chronic nerve compression in CTS (ALS, spinal muscular atrophy, poliomyelitis) |
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Term
| Describe abnormal potentials during mild voluntary contraction in EMG studies. |
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Definition
1. Absence of MUPs in complete neuropraxia (100% conduction block) or axonotmesis (100% axonal breakage)--cant differentiate these 2 in first 10 days; after 10 days, you would see positive sharp waves and fibrillation potentials
2. Changes in MUP characteristics -
a)amplitude larger (sign of axon sprouting) or smaller (most often associated w/ muscle disease; small amp and long duration APs)
b) duration- longer or shorter
c) Numbers of phases - more than 4
d) recruitment- reduced or absent |
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Term
| Describe some abnormal changes in motor unit characteristics in EMG studies. |
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Definition
Reduced amp or duration of MUP (seen in myopathies and early stages of axonal regeneration)
Increased amplitude or duration of MUPs (seen in later stages of muscle reinnervation) |
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Term
| What are polyphasic MUP's? What is their clinical significane? |
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Definition
MUPs w/ more than four phases; from desynchronization of muscle fiber activation within MU
significance- seen in either neuropathy or myopathy; seen in both degenerating and regenerating conditions; must be >15-20% polyphasic MUPs to be of clinical significance; similar to CRDs but CRDs are spontanous while these only happen when person is asked to contract. |
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Term
| What is abnormal MU recruitment? What is its clinical significance? |
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Definition
It is higher than normal initial discharge frequencies; Is also characterized by Large MUPs appearing before small;
Significance: appearance in neuropathic or myopathic disorders |
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Term
| With abnormal MU recruitment in EMG studies, what would is the significance of higher discharge frequencies (i.e. why does it happen)? |
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Definition
| Higher frequency discharges means that motor units have died so ur body is rate coding at higher frequencies to compensate for lack of recruitment. |
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Term
| Describe abnormal activity in strong contractions during EMG studies. |
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Definition
| You will get a reduced interference pattern (which reflects a reduction in # of functional motor units); may result from either neuropathic, NMJ, or myopathic disorders. |
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Term
| What are 5 clinical questions that needle EMG addresses? |
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Definition
1. is muscle normally innervated, partially innervated, or totally denervated?
2. has reinnervation begun?
3. What is the location of the lesion?
4. Is disorder neuropraxic or axonotmetic/neurotmetic or myopathic?
5. Is a pattern of EMG abnormality consistent w/ n root disorder, brachial plexus disorder, peripheral n disorder, myopathic disorder. |
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Term
| Describe needle EMG findings for partial neuropraxia w/ conduction slowing only. (Insertional activity, spontaneous activity at rest, Mild volitional activity, strong contraction recruitment) |
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Definition
Insertional activity- normal (no denervated mm fibers)
Spontaneous activity at rest- none (maybe fasciculations)
Mild volitional activity- normal MUPs (amplitude and duration)
Strong contraction recruitment- Normal (all MUs can be activated).
In other words, EMG does not address conduction slowing. |
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Term
| Describe needle EMG findings for partial neuropraxia w/ conduction slowing and partial conduction block. (Insertional activity, spontaneous activity at rest, Mild volitional activity, strong contraction recruitment) |
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Definition
Insertional activity= normal (no denervated mm fibers)
spontaneous activity at rest= none, maybe occasional fasciculations
Mild volitional activity= normal MUPs (normal amplitudes and duration)
Strong contraction recruitment = decreased (not all MU can be activated..decreased interference pattern) |
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Term
| Describe needle EMG findings for partial axonotmetic/neurotmetic lesion 14-21 days post-injury. (Insertional activity, spontaneous activity at rest, Mild volitional activity, strong contraction recruitment) |
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Definition
Insertional activity= increased/prolonged (some m fibers denervated)
Spontaneous activity at rest = fibrillations and positive sharp waves common, consistent w/ denervation of some mm fibers
Mild volitional activity = normal (remaining MUs are normal), >15% polyphasic MUPs in reinnervation w/ axon sprouting and recovery after 21 days.
Strong contraction recruitment = decreased (reduced # of MUs activated...reduced interference pattern) |
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Term
| Describe needle EMG findings for partial axonotmetic/neurotmetic lesion 1 day post-injury. (Insertional activity, spontaneous activity at rest, Mild volitional activity, strong contraction recruitment) |
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Definition
Insertional activity- normal (m fibers have not yet reacted to denervation) Spontaneous activity at rest- Normal (m fibers have not begun to adapt or degenerate)
Mild volitional activity- normal (remaining MUs are normal)
Strong contraction recruitment- decreased (reduced # MUs activated) |
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Term
| Describe needle EMG findings for complete neuropraxic w/ 100% conduction block, short term duration. (Insertional activity, spontaneous activity at rest, Mild volitional activity, strong contraction recruitment) |
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Definition
Insertional activity= normal
Spontaneous activity at rest= none
Mild volitional activity = no MUPs
Strong contraction recruitment = absent |
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Term
| Describe needle EMG findings for complete axonotmetic/neurotmetic lesion 2-3 weeks post-injury. (Insertional activity, spontaneous activity at rest, Mild volitional activity, strong contraction recruitment) |
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Definition
Insertional activity= increased or prolonged
Spontaneous activity at rest= fibs, +sharps
Mild volitional activity = none, no MUPs
Strong contraction recruitment = none, no MUPs |
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Term
| Describe needle EMG findings for complete axonotmetic/neurotmetic lesion 1 day post-injury. (Insertional activity, spontaneous activity at rest, Mild volitional activity, strong contraction recruitment) |
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Definition
Insertional activity- normal spontaneous activity at rest- none
Mild volitional activity- no MUPs
Strong contraction recruitment- absent
Note: Results are like those seen in acute complete neuropraxia |
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Term
| Describe needle EMG findings for myopathies. (Insertional activity, spontaneous activity at rest, Mild volitional activity, strong contraction recruitment) |
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Definition
Insertional activity= Increased/prolonged
spontaneous activity at rest= fibs, PSW, myotonic d/c, CRDs in many mm
Mild volitional activity= SLAPS (short duration, low amp MUPs b/c fewer muscle fibers per motor unit)
Strong contraction recruitment = reduced b/c fewer functional motor units
Note: found in many mm consistent w/ specific type of muscle disease. Also, no conduction slowing, will appear in mm associated w/ several nn and will be more localized. |
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Term
| T/F- EMG findings will not identify sensory nerve axon disorder |
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Definition
| True- it only gives info on mm and Alpha MNs |
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Term
| T/F- EMG results can not be interpreted in isolation of NCV test results or other clinical test results |
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Definition
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