Nerve conduction studies and EMG learning Flashcards
What is dispersion?
Increased duration of CMAP with proximal stimulation compared with distal. Amplitude decreases but area under the waveform is preserved.
What causes a conduction block?
demyelination
What is an F wave?
A small late potential in the muscle seen because when stimulate distally, impulse also travels up to the spinal motor neurone then reflected back along motor axon to the muscle
USED TO ASEESS PROXIMAL SEGMENT CONDUCTION
In demyelination see? (5)
Slow conduction velocity but minimal functional deficit
Conduction block- THIS correlates with weakness
Temporal dispersion
Lower amplitudes (not as much as axonal though)
Delayed or absent F wave
Axonal pathology see?
Low amplitudes
Normal conduction velocities (or mild decrease)
Takes 10-14 days post injury to show up and differentiate between this and NCS for demyelination (if initial cut, distal seg still works!!) Motor takes 3-7 days, sensory 6-10
Carpal tunnel pattern?
Sensory distal latencies first
Then decrease size sensory response (amplitude)
Increase motor distal latencies
Decreased motor amplituees
Last of all evidence on EMG of demyelination
What is a motor unit potential?
MUP is sum of all APs in motor unit
What is recruitment?
In EMG, assessing number of functional units in relation to generated force
In myopathy- early recruitment
In neruopathy- late recruitment
What is interference pattern?
The extent of muscle activity at full force
What are fibrillation potentials and when do you see them?
Rhythmic firing of non innervated muscle fibres
Suggests denervation
Fasciculations represent???
Spontaneous firing of a whole motor unit
What do positive sharp waves mean?
similar to fibrillation potentials in significance
Suggests denervation
Acute denervation EMG changes?
Before 6 weeks
At rest have fibrillation potentials and positive sharp waves
Surviving MUPs are normal
Recruitment reduced as have lost motor units (EARLIEST sign)
Chronic denervation EMG changes?
MUPs increase amplitude and duration, are polyphasic adn unstable (vary in shape) because muscle fibres have either died or been haphazardly reinnervated)
No fibrillation potentials or positive sharp waves
Recruitment reduced in proportion to motor units lost
Myopathy changes on EMG?
At rest silent
Polyphasic MUPs with reduced amplitude and duration
Early recruitment
If inflammatory- some fibrillation potentials
In MD- myotonia
MND NCS?
Normal
EMG in MND?
EMG large motor units
Fibrillation + pos sharp waves in active denervation
Similar changes in multiple segments and in weak and non weak muscles
How does Riluzole work?
Inhibit glutamate release from presynaptic nerve terminals
Stabilise inactive state of voltage dependent sodium channels
Inhibit GABA uptake
3-6 month survival benefit
and have to have over 60% FVC, be under 75, no resp failure, able to walk and swallow, disease under 2 years
early PEG and NIV increase QOL and possibly duration
NCS for multifocal motor neuropathy?
proximal conduction block with normal distal latencies
What is the autoAb in multifocal motor neuropathy with conduction block?
Anti GM1 in 80% (but non specific)- also seen in ALS LMN form, GBS, axonal motor neuropathies.
Respond VERY well to IVIG 5 days
Signs in anterior interosseous nerve palsy?
Cannot make OK sign
Cannot pick up coin from flat surface
Causes of mononeuritis multiplex
Diabetes HIV, leprosy CTS/vascultis Trauma Sarcoid Malignancy
Order of severity…. neurotmeses, axonotmesis, neuroprazia
Neuropraxia mildest- conduction block but no loss axons
Then
Axonotmesis- intact connective tissues but axonal loss
Then
Neurotmesis- three different grades (3,4,5)
What do you NOT get in MND?
Ocular involvement
Sensory loss
Bladder or bowel involvement
Autonomic
