Electro diagnostics Flashcards
5 normal EMG findings?
What causes increased or decreased/prolonged insertional activity?
Amplitudes and duration of miniature endplate potentials (MEPPs)?
Low amplitude: 5-50 mcV
Short duration: 1-2 msec
MEPPs abnormalities (3)
1) complete absence (denervation)
2) reduced frequency, normal amplitude (botulism) - fewer vesicles are released, but when AcH is released it is normal (hence normal amplitude)
3) reduced amplitude, normal frequency (myasthenia gravis) - fewer receptors on the postsynaptic membrane
End-plate spikes; amplitude and duration
Amplitude: 100 - 300 mcV
Duration: 2-4 ms
they are biphasic, with a initial negative (upwards) deflection
Amplitude and duration of motor unit action potentials (MUAPs)
Amplitude: 100-3000 mcV
Duration: 1-12 msec
MUAPs abnormalities (6)
1) reduced amplitude with normal density: reduced number of myofibers per motor unit - myopathy, distal neuropathy, defect NM transmission
2) reduced density, normal amplitude: - axonopathy
3) polyphasia (more than 3 or 4 phases)
- loss of myofibers or different conduction times along muscle
4) doublets or triplets - tetanus, MN hyperexcitability, radiculopathy
5) giant MUAPS (eg > 5 mV)
- re-innervation by axonal spouting (increased numbers of myofibers in new motor unit)
- often poliphasic as new branches have thinner myelin and slowe NCV
6) absence of inducable MUAP in a specific muscle - severe motor axonal damage/denervation
4 possible EMG abnormalities?
1) fibrilation potential (fibs)
2) positive sharp waves (PSWs)
3) complex repetetive discharges (CRDs)
4) myotonic potentials
Amplitude and duration of fibs and PSWs
Fibs (initial positive aka downwards deflection in comparison to endplate spikes)
amplitude: 10-200 mcV
duration: 0.5-3 msec
PSWs
amplitude: 50 mcV - 4 mV
duration: < 5 msec
How many days post denervation do the fibs/PSWs occur?
- small animals: appear 4-5 days post denervation, max 8-10 days
- (12-16 in large animals)
Pathology associated with fibs/PSWs (3)
1) denervation
2) myopathy
3) long-lasting NMJ blockade (like with MG) - rare
Amplitude and duration of CRDs
Amplitude: 100 mcV - 1 mV
- come from multiple myofibers - hence the complex waveforms)
Myotonic discharges - difference in comparison to CRDs?
Come from a single myofiber (in comparison toCRDs which come from multiple muscle fibers)
- waveforms change over time (size and frequency differs - have a waxing/waning dive bomber sound)
EMG-abnormalities of which muscles may be sensitive for prediction of vertebral canal invasion by PNSTs in dogs?
Epaxial muscles
EMG and CK levels?
rise in about 4 hours post EMG (you can take blood samples during EMG study) and should be normal in 2-3 days again
Continuous motor unit activity can be abolished by general anaesthesia if the cause stems from the:
1) CNS
2) nerves
3) muscles?
CNS
Where should the cathode be positioned when doing nerve conduction studies?
closest to the recording site to avoid anodal conduction block (the negative cathode depolarises, whereas the positive anode hyperpolarises thereby inhibiting the action potential)
Which stimulus intensity do we use for nerve conduction studies?
Supramaximal stimulus (30-50% grater than maximal - to be sure we stimulate all the available axons)
What is a CMAP?
compound muscle action potential - summation of individual myofiber potentials we measure in nerve conduction studies
CMAP - what is shown?
peak to peak amplitude
CMAP - what is shown?
duration of CMAP
CMAP - what is shown?
area of CMAP
CMAP - what is shown?
latency (time difference between the stimulus artefact and first deflection of CMAP from the midline)
What does latency consist of?
MNCV formula (m/sec)
Distance mm/(prox latency msec - distal latency msec)
What is residual latency?
How is residual latency measured?
Residual latency = observed distal latency - (distance/MNCV)
Formula to calculate limb length using residual latency?
Distance = (CMAP onset latency - residual latency) x distal conduction velocity
What are common normals for amplitude and MCVN in dogs?
amplitude: 20 +/- 5 mV
MCVN: 65-70 m/sec
What are common normals for amplitude and MCVN in cats?
amplitudes larger than dogs: 20-30 mV
MCVNs faster than dogs, around 90 m/sec
Which named nerves have a faster MNCV?
peronel > tibial > ulnar
What is physiological temporal dispersion?
as the nerve gets longer we see a lag in slower conducting fibers
Effect of age on amplitude and MNCV?
increased duration and amplitude with age, peaks with 6 months, as the dogs get older the MNCV drops again
cats reach adult values around 3 (-6) MO and MNCV starts dropping after 10 YO
Horses MNCV starts dropping after 18 YO
Influence of limb temperature on MNCV and amplitude?
decreased temp -> increased amplitude
decreased temp -> decreases the MNCV 1.7-1.9 m/sec for every 1 C
Influence of limb lenght on MNCV and amplitude
- temporal dispersion (physiologic)
- increased length -> decreased amplitude, longer duration, decreased MNCV
Abnormalities in interpretation of a trace (5)
1) CMAP amplitude
2) temporal dispersion
3) polyphasia
4) MNCV
5) conduction block
Causes of a decreased CMAP amplitude?
1) reduced number of axons (axonopathy)
2) reduced release of Ach at end-plate (botulism)
3) reduced number of functional myofibers (myopathy)
4) (conduction block)
5) (waveform dispersion and phase cancellation)
Findings in axonopathies?
1) severe EMG abnormalities
2) decrease of amplitude (> 50% decrease)
3) MNCV may be normal (if fastest axons are conducting normally) or slower (if there is loss of fastest conducting axons (<20-50% decrease)
Findings in demyelination?
1) no EMG abnormalities if axons are unaffected
2) +/- normal amplitudes
3) marked decrease in MNCV (>50-60% decrease) eg DM in cats and globoid cell leukodystrophy in dogs
4) temporal dispersion and polyphasia if involved fibers are of different diameters eg. feline Niemann-Pick disease
- markedly reduced amplitude by up to 50% points to a concurrent axonopathy
What is conduction block?
Mimics of conduction block?
Axonopathy vs. demyelination findings
Generalised decrease in CMAP amplitudes without temporal dispersion, ddx? (3)
1) axonal disease
2) botulism (decreased NMJ transmision)
3) severe myopathy (decreased number of activated myofibriles)
A decrease in proximal vs distal CMAP amplitude of >50%, without significant dispersion, ddx?
conduction block
The depolarization of one node produces depolarization of adjacent regions for only a limited distance (2 internodes) - if the loss of myelin occurs over a greater distance than 2 internodes, conduction block will occur even though more distal regions of the nerve still remain conductile.
Prolonged latency or slowed conduction velocity without a decrease in CMAP amplitude, ddx?
1) myelin disease (demyelination) +/- axonal neuropathy (loss of the fastest conducting fibers) - usually an accompanying CMAP amplitude to less than 40-50% occurs
Temporal dispersion +/- polyphasia? Most likely disease entity?
demyelination
Which modalities can we use to assess nerve roots? (3)
- F wave,
- H reflex,
- cord dorsum potentials
What is the F-wave?
F wave is a late response that follows the motor response (M-wave) and is elicited by supramaximal electrical stimulation of a mixed or a motor nerve. F-waves provide a means of examining transmission between stimulation sites in the extremity and the related motor neurons in the cervical and lumbosacral cord.
F-wave is 3% of the M-wave amplitude - around 200-300 mcV
Benefits/reasons for testing the F-waves?
Cons of F-waves?
Pros (see image)
Cons: time consuming, only 1-5% of axons backfire giving a small CMAP, we need to record more than 10 so we can average to overcome the variabilty
Changes in F-waves with disease
Axonopathies - F waves might be normal or increased
Demyelination - F waves can be significantly prolonged
- if demyelination is segmental and proximal and patchy, F wave abnormalities can be seen before MNCV
E-dx findings in dogs with acute polyradiculoneuritis?
1) EMG changes (100%)
2) decreased CMAP amplitudes (75-100%)
3) increased minimum F-wave latencies (67%), ratios (92%) and decreased F-wave amplitudes (67%)
Formula for predictive determination of proximal F-wave latency
Latency F prox + Latency M prox = Latency F dist + Latency M dist
—> from this formula
Latency F prox = (Latency F dist + Latency M dist) - Latency M prox
Variation of limb length on F latencies in dogs?
Ulnar nerve - 6.03 + (0.22 x limb lengths in cm)
Sciatic tibial nerve - 3.45 + (0.33 x limb length in cm)
What is the central latency? Formula?
(lat F - lat M - 1 msec) / 2
The F wave latency (F) represents
the conduction time in the proximal part of the nerve fibre in two directions, the time needed for a successful reflection (1 ms) and the latency of the direct muscle response (M).
What is the F-ratio + formula, what does it mean?
The ratio of conduction time in the proximal part of the nerve to conduction time in the distal part of the nerve is known as the F ratio and can be calculated as (F-M-1)/2M.
F-ratio > published reference = proximal segment more involved
F-ratio < published reference value = distal segment more severely involved
F-ratio = reference + an abnormality has been found in your motor nerve conduction study = even distribution
Normal reference values have been
calculated for the sciatic-tibial nerve in the dog:
(1) Stimulation at the hock: F ratio : 1.954 + 0.086
(2) Stimulation at the stifle: F ratio : 0.883 t 0.052
What is the axon reflex?
E-dx test that can be used to test neuromuscular trasmision (3)?
1) supramaximal repetetive nerve stimulation (RNS)
2) single fibre EMG (SF-EMG) - very rarely performed, needs special equipment
3) RNS after Tensilon
What stimulation rate do we need to use when testing for NMJ disease in RNS?
<5 Hz (2-3 preferred) due to a normal expected decremental response when testing at high stimulation rates
When does the NM transmission mature and we can do RNS eg. for congenital myasthenic syndromes
ca. 2 MO
Diseases for which we can use RNS?
1) MG
2) botulism
3) (polymyositis)
4) (motor neuropathies)
RNS findings for MG?
> 10% decrement in CMAP amplitude/area with stim. rate < 3Hz
RNS findings for botulism?
- CMAP amplitude typically decreased from the start
- decremental response to RNS at low freq. stim. (eg. 3 Hz) - ca. 20%
- RNS at high stimulation rates (eg. 50 Hz) can override competetivive blockade of Ach -> incremental response
Which percentage of foals with botulism has an decremental and which an incremental response at low/high frequency stimulation on RNS?
Incremental response in all affected foals at 50 Hz!!!
Techniques for SF-EMG?
What is “jitter” in SF-EMG?
- variation in the latencies
- measure of the safety factor of NM transmission
- mean value of consecutive differences in latency differences in latency (50-100 potentials) from time of stimulus to response
- in humans a highly sensitive test for MG (since 33% of them are AchR-Ab negative) - around 90% of human patient with MG have abnormalities in jitters
Jitter and disease?
What does the following image show?
jitter in a normal dog vs. dog with MG
Which nerve fibers are stimulated in the H-reflex?
1A sensory > synapse > alpha-motor neuron (no interneurons)
- relies on stimulation of 1A fibers at a lower threshold to stimulation of motor fibers
- H-reflex reaches maximal amplitude at a submaximal stimulus strength for the M-wave
Formula for SNCV?
SNCV = distance from stimulation to recording site / latency R1
or
SNCV = distance between recording sites / latency R2 - latency R1
Which nerves can we use for SNCV?
We can use mixed nerves:
- Proximal tibial nerve
- Ulnar nerve
Sensory nerves:
- lateral superficial radial n. (runs with accessory cephalic vein)
- superficial peroneal n. (frequently has a polyphasic waveform)
- saphenous n. (runs with saphenous artery)
- trigeminal (palperal or infraorbital) nerve
Which agent can be used for neuromuscular blockade whilst doing SNCV to reduce recording the contamination by reflexively triggering muscle potentials?
Non-polarizing muscle relaxant like
atracurium 0.2 mg/kg i.v (competitive Ach R antagonist)
Pre-ganglionic lesions - effect on the SNCV?
- watch out - pre-ganglionic means between ganglion and SC
Post-ganglionic lesions - effect on the SNCV?
- watch out - post-ganglionic means between ganglion and extremity
SNCV values for dogs?
ca. 40-58 m/s
SNCV values for cats?
faster than dogs, ca 80-90 m/s
Which nerves do we test with the blink reflex?
Trigemino-facial reflex
stimulate supraorbital nerve and record from both orbicularis oculi muscles at the same time
4 recordable potentials in a sedated animals whilst testing the blink reflex
R1, R2, R3, Rc
What is stimulated with the trigemino.trigeminal reflex?
How will the recordable potentials look like in a blink reflex if we have a complete L sided trigeminal nerve lesion?
How will the trigemino-trigeminal reflex look like?
What about the facial nerve stimulation?
How will the recordable potentials look like in a blink reflex if we have an incomplete L sided trigeminal nerve lesion?
How will the trigemino-trigeminal reflex look like?
What about the facial nerve stimulation?
What is being stimulated and what depolarised in cord dorsum potentials (CDP)?
Stimulation of a mixed/sensory nerve causes depolarisation of the dorsal horn interneurons in the SC segments receiving the nerve being stimulated –> “near field potentials” (we measure activity of synapses in the proximity to the recording electrodes
3 parts of a CDP trace?
1) A component (small triphasic wave before the CDP waveform) - extracellular events associated with propagation of a sensory action potential (+/-) antedromic motor) into the SC
Aa+ = axonal capacitance current at the node of Ranvier
Ab- = depolarisation of the cell membrane at the next node Na+ enters the axon -> (-) charge in the extracellular space
Ac+ = efflux of K+ into the extracellular space
2) B component -
- True cord dorsum potential . can contain 1-2 smaller subpeaks
- change in the extracellular environment resulting from depolarisation of the dorsal horn interneurons in the grey matter of the SC
- negative peak as Na+ enters the dorsal interneuronal cell bodies during depolarisation - (-) extracellular charge
3) C component
- prolonged return in + direction to baseline
- (+) charge in dorsal aspect of SC at excited dorsal horn synapses
- extracellular representation of primary afferent depolarisation
Where is the CDP classically recorded?
In dogs the clearest waveform is L4-5 or L5-6
In cats L4-5 and L5-6 for pelvic limb, C7-T1 for the thoracic limb
What do we measure in CDP?
1) onset latency
2) onset-peak latency difference
Which different electrophysiological events do we record in SSEP?
The appearance of a typical SSEP waveform?
Initial mild positive deflection followed by 3 or more high amplitude negative peaks
Is it possible to get a scalp or spinal SEPs in nociception-negative dogs with SC injury?
Yes, see paper
Waves in BAER?
Wave I: ipsilateral cochlear nerve
Wave II: ispilateral cochlear nuclei (ventral and dorsal)
Wave III: superior olivary complex/trapezoid body
Wave IV: lateral lemniscus
Wave V: caudal colliculus (midbrain) ipsi- +/- contralateral
Wave VI: medial geniculate nucleus
Wave VII: thalamo-cortical auditory radiation
Wave analysis in BAER?
The EEG signal is generated by which cells?
Cerebral pyramidal neurons located in different layers of the neocortex
**Pyramidal neurons are constantly influenced by synaptic activity (excitatory and inhibitory postsynaptic potentials): an excitatory synapse acts like a battery, driving current into the pyramidal cell and then outward to the extracellular space, and the reverse holds true for an inhibitory synapse. This generates a variation in potential difference between the intracellular and extracellular space.
Which waves are found in a normal ERG?
a-wave: the first negative deflection (It reflects a cumulative response of the retinal photoreceptor cells)
b-wave: the next positive peak (generated by the Muller glial cells and bipolar ON cells stimulated by the flow of potassium ions)
- the c-wave, d-wave and i-wave are present only in some dogs under special measuring conditions
What is measured in a normal ERG?
1) amplitude of a and b wave
2) implicit time (time to peak) of the a and b wave
The amplitude of the a-wave is measured from the baseline to the negative trough of the a-wave and the b-wave amplitude is measured from the trough of the a-wave to the following b-wave peak. The implicit times of the a-wave and the b-wave are measured from the flash onset to the trough of the a-wave and to the peak of the b-wave, respectively
How is the rod- and how the cone-driven response generated in ERG?
The rod-driven response is generated during an ERG under scotopic conditions when the dark-adapted retina is exposed to light stimulus with an intensity of 0.01 or 0.02 cd·s/m2.
An increase in the intensity of the stimulus to 3 cd·s/m2 activates the cones and provides a mixed rod-cone-type response.
The cone-driven response is generated under photopic conditions, when the retina is exposed to a light intensity of 30 cd/m2.
Differentiating optic neuritis from SARDS with ERG?
In the case of SARD, the ERG traces are non-recordable, the so called “silent retina”, whereas inoptic neuritis, the ERGs are essentially normal
