Electrodiagnostics Flashcards
EMG electrodes:
The active electrode is the electrode attached to the (negative or positive) terminal?
Negative terminal
EMG:
Insertion activity will be decreased in?
Insertion activity will be increased in?
How long should insertion activity last?
Insertion activity decreased in fibrosis (lack of healthy myofibers)
Insertion activity increased in denervation or inflammation
Insertion activity should not last longer than 300ms
Figure: Insertional activity. Note the abrupt onset and termination of activity associated with needle placement
(Cuddon)
EMG:
_____ is the small depolarization of the postsynaptic membrane induced by the sustained random release of a single quantum of ACh
Miniature End Plate Potentials
- spontaneous, subliminal electrical activity in normal muscle
- frequency varies (increases with elev. temp)
- Amplitude 5-50uV (usually 5-15), duration 1-2ms
- (sounds like a seashell)
Figure: Miniature end plate potentials with 2 end plate spikes indicating close proximity of the needle to an end plate
(Cuddon)
EMG:
Miniature End Plate Potentials (MEPPs)
How are they affected by denervation? Myasthenia? botulism?
Miniature end plate potentials MEPPs:
Cease after denervation
Normal frequency, decreased amplitude in MG
Decreased Frequency, normal amplitude in botulism
(Cuddon)
EMG:
_______ is spontaneous EMG activity that results from the discharge of a single muscle fiber
End plate spikes:
- commonly associated with miniature end plate potentials
- Result from the discharge of a single muscle fiber that is excited by activity in nerve terminals
- Intermittent, with an irregular firing rate
- Amplitude 100 - 200uV, duration 2-4ms
- Initial NEGATIVITY and is BIPHASIC
(Cuddon)
EMG:
____ are EMG discharges seen associated with mild voluntary muscle contraction
Motor Unit Action Potentials (MUAPs)
- seen with mild voluntary muscle contraction
- Consist of isolated discharge of 1-few motor units
- A compound action potential of all myofibers in electrode recording range
- Generally biphasic or triphasic with initial NEGATIVE phase
- Occasional polyphasic waves are acceptable as normal
- Semirhythmic with a slowly increasing, then decreasing interspike interval during constant contraction
- Amplitude 100 - 3000uV, rate 5-7Hz, duration 1-12msec
- RECRUITMENT - increasing strength of muscle contraction –> successive activation of the same and new motor units
(Cuddon)
EMG:
What is an interference pattern associated with motor unit action potentials?
Simultaneous discharge of many different MUAPs (precluding individual MUAP recognition)
- Myopathy –> decreased AMPLITUDE of MUAPs (normal density) - same number of functioning motor units, but fewer myofibers/unit
- Partial denervation –> decrease in DENSITY of MUAPs - individual MUAPs still discernible
(Cuddon)
EMG:
What is abnormal activity related to MUAPs that results in differences in conduction time along nerve branch/muscle fiber; or temporal dispersion of muscle fiber potentials?
Polyphasia
- There is a loss of individual myofibers from a motor unit while others survive –> loss of the normal smooth algebraic summation and results in 4-5 phases within the waveform
(Cuddon)
EMG:
4 causes of doublet/triplet MUAP:
What causes smaller amplitude MUAP?
- latent tetani
- metabolic states associated with motor neuron pool hyperexcitability
- motor neuron disease or radiculopathy
- myotonic dystrophy
Smaller amplitude MUAP = myopathy
(Cuddon)
EMG:
What abnormality results in a decreased amplitude and duration of MUAP?
Primary myopathy (myofiber destruction)
(Cuddon)
EMG:
Decreased amplitude and short duration MUAP likely cause? (2)
Long duration MUAP likely cause?
Decreased amplitude and short duration MUAP
- distal neuropathy –> damaged axon terminals –> random loss of myofibers
- reinnervation –> immature motor units with only a few fibers
Long duration MUAP
- myopathy with regenerating fibers
(Cuddon)
EMG:
How does reinnervation/neuropathy affect MUAP?
Giant MUAPs:
- Represents loss of innervation to a group of myofibers –> collateral branch of another motor unit has grown in to innervate those myofibers
- The number of myofibers contributing to a motor unit doubles or triples
- New nerve branches have a thinner myelin sheath –> decreased NCV –> polyphasic/asynchronous Giant MUAP
Collateral sprouting –> Increased MUAP amplitude, +/- increased duration, +/- polyphasia
Regeneration of axons –> increased MUAP amplitude
Histopathologic correlate is fiber type grouping
_** Polyphasic MUAP or increased size of MUAP = neuropathy_
(Cuddon/Brain camp)
EMG:
________ is caused by the spontaneous action of a single myofiber which is abnormal
Fibrillation potentials
- the majority of fibrillation potentials are induced by needle insertion (and are not spontaneous)
- Amplitude 10-200uV, 0.5 - 3ms duration
- Initial deflection is usually POSITIVE (will be negative if recorded within an endplate zone)
- Sound: frying egg, wrinkling tissue paper
(Cuddon)
EMG:
Causes for fibrillation potentials (3)
- hypersensitive, denervated myofibers
- in dogs and cats there is an increase in sensitivity to ACh within a few hours after denervation, although it takes 4-5 days to be able to record increased insertional activity
- This slightly precedes the presence of fibrillation
- The abnormal activity becomes especially prominent at approximately 8-10 day post-injury
- Fibrillations are first reported in lg animals at approximately 12-16 days post denervation
- polymyositis
- muscular dystrophy
(Cuddon)
EMG:
A marked decrease in the density of fibrillation may indicate?
Successful motor neuron reinnervation
replacement of myofibers by fibrous tissue
(differentiated by clinical evaluation)
(Cuddon)
EMG:
_____ is an abnormal EMG potential that consists of an initial positive spike, followed by a shorter, slow, and small negative potential
Positive sharp waves
- Thought to originate from irritated muscle membrane with the potential stopping at an area immediately adjacent to the needle electrode
(Cuddon)
Positive sharp waves:
- # of fibers?
- Amplitude? Duration?
- Firing pattern?
- Sound?
- Morphology?
- Single fiber
- 20uV - 1mV (same as fibrillation potential) , <5ms (+/- neg phase 10-100ms)
- Regular firing pattern 1-50Hz
- Sound like dull thud
- Morphology - initial positive (downward) spike followed by a much shorter, slow negative potential
“mean the same thing as fibrillation potentials,” and can occur with fibrillation potentials
EMG:
__________ are polyphasic or serrated action potential with a uniform frequency, shape and amplitude
Complex repetitive discharges (CRD)
- may begin spontaneously or after needle movement
- ABRUPT onset, cessation, or change in configuration
- Amplitude 100uV - 1mV, frequency 5-100Hz
- represents a group of myofibers firing near synchrony
- Sound like a machine gun
- Seen in a wide range of chronic denervating conditions, and in some myopathies
(Cuddon)
EMG:
______ are abnormal repetitive discharges at a rate of 20 - 80Hz
Myotonic potentials
- 2 types = sustained run for 5-20msec, (resemble positive sharp waves)
- Sustained run of biphasic spike potentials (<5msec) consisting of an initial small positive peak followed by a larger negative peak (resemble fibrillation)
- The amplitude and frequency of the potentials must wax and wane to be classified as myotonic
- DIVE BOMBER
(Cuddon)
EMG:
What diseases cause myotonic potentials?
injured single myofibers –> independent, repetitive discharges
- caused by primary muscle disease
- cased by steroids
(Cuddon)
How does EMG influence serum CK?
For both dogs and horses, mean values for serum Ck do show increases although are still usually within the normal range both at 4-24h after EMG evaluation
The CK returns to baseline 48h after EMG
(Cuddon)
NCV:
Stimulating electrodes consist of an anode (positive or negative pole) and a cathode (positive or negative pole)
Where should the cathode and cathode be placed in relation to the recording site? (and why)
Where should the ground electrode be placed and why?
Anode = positive/red/reference. Should be farthest from recording electrodes
Cathode = negative/black/active. Should be CLOSE to the nerve
The positive charge of the anode hyperpolarizes the nerve - should be placed farthest away to prevent “anodal block” where the positive charge prevents depolarization/propagation
The negative charge of the anode depolarizes the nerve
The ground electrode should be between the stimulating and recording electrodes - important to diminish stimulus artifact
(Cuddon)
_____ are electrical events recorded when:
peripheral nerve stimulated –> electrical events elicited from neurons, synapses or axons
Somatosensory evoked potential (SEP)
- The spinal cord and brain potentials arise from sensory pathways, information about motor pathways can be inferred (because at many points the pathways are adjacent to each other)
(Cuddon)
What is the most significant source of artifact in somatosensory evoked potentials? How can it be eliminated?
Skeletal muscle artifacts
- muscle fibers near the recording electrodes contract spontaneously –> irregular baseline, high voltages
- nerve stimulation causes direct or reflex muscle contraction –> artifact that is TIME LOCKED into the stimulus –> appears in the final SSEP recording
- Eliminated with muscle paralytic
(Cuddon)
What are the neural generators of the SSEP?
Ipsilateral (major contributor) and contralateral sensory pathways
- Dorsal quadrant: SSEP is propagated in UNCROSSED pathways
- Specific ascending pathways:
- Dorsal spinocerebellar tract
- Spinocervicothalamic tract
- Spinomedullothalamic tract
- Dorsolat region of ipsilateral dorsolat funiculus - very important in the propagation of the early, high amplitude negative peaks of the SSEP
- Damage to the DLF –> loss of amplitude of the EARLY phases of the SSEP (especially the first negative peak)
- Damage to the DC –> smaller loss of amplitude in the early phases, no effect on the first negative peak
- Specific ascending pathways:
- Ventral quadrant: SSEP is propagated in CROSSED and UNCROSSED pathways (in dogs)
(Cuddon)
How does the stimulation site affect SSEP?
Proximal stimulation –> larger number of spinal cord neurons and axons stimulated –> higher amplitude (more readily recognizable) waveforms
- Produces more stimulus artifact (since stimulus electrodes are closer to the recording sites)
(Cuddon)
What are the 2 types of SSEP elicited and what causes them?
- Compound action potentials (CAPs)
- Arise from axons in peripheral nerves, cauda equina, and spinal cord white matter
- CAPs are conducted to the area of the recording electrode from a distance, pass by the electrode, and move off into the distance again
- Field potentials
- Arise from spinal cord gray matter or nucleus synapse
- The source is stationary
(Cuddon)
How does bilateral vs. unilateral stimulation affect SSEPs?
- Overall amplitude of the SEP will be increased with bilateral in:
- Initial peaks from the nerve roots/cauda equina
- CDP - first positive and large negative peak
- The only component that did not increase was the 2nd positive peak of the cord dorsum
- SEP - 3rd, 4th, 5th peak components
- Increase in amplitude was approximately 2x that of unilateral stimulation
- SEP: results of bilateral stimulation on the components of the SEP was not uniform
(Cuddon)
Where should recording electrodes (active, reference, ground) be placed for SSEP?
- Electrode impedance should be kept below 5kOhms to ensure that recorded SSEP amplitudes are within acceptable accuracy levels
- Active electrode:
- monopolar needle electrodes with a bare tip, placed percutaneously through the interarcuate ligament into the epidural space
- Thoracic level - recording electrode placed immediately lateral to the base of the spinous process
- C1 - recording electrode placed against the vertebral arch
- Surface recording electrode produces the shortest SSEP < electrode placed on the tip of the dorsal spinous process < electrode on the dorsal lamina < dural electrode
- “In a study in cats, the peak to peak amplitudes of SSEPs recorded from electrodes placed against vertebral laminae was 12% of the peak to peak amplitudes of recordings made at interarcuate ligaments”
- Reference electrode - SQ 1-3cm lateral to the active electrode
- Greater distance will increase EKG and muscle artifacts
- Ground electrode - placed SQ between the stimulating and recording electrodes
(Cuddon)
How are onset latencies measured for SSEP?
Measured from the onset of the stimulus artifact to the first positive (downward) peak
(Cuddon)
Injury potential produced by touching the surface of the spinal cord with the recording electrode - what does it look like?
Sciatic nerve stimulation –> potentials recorded at L6/7. What is responsible for these?
Sharp downward displacement of the entire SSEP
Dorsal and ventral nerve roots of the cauda equina produce potentials at L6/7
(Cuddon)
What are normal causes of peak segregation of SSEP?
- Distal stimulation sites (especially mixed nerve) –> leave time for peak segregation
- Polyphasia in sensory nerves is physiologic in dogs
- Antidromic conduction along motor nerves (slower conduction velocities) will also be recorded at these sites
(Cuddon)
Where is cord dorsum potential recorded in the lumbar region of dog vs. cat?
What contributes to this location?
Where should SSEP be recorded from dog vs. cat?
CDP:
- Cat: L4/5 or L5/6 (L4/5 best)
- Dog: L6/7 to L3/4 (L4/5 or L5/6 best)
CDP depends on:
- Species
- Which nerve roots contribute to the sciatic nerve
- Where those nerve rooes are located within the spinal canal
SSEP
- Cat: L3/4
- Dog L2/3
(Cuddon)
What is the morphology of SSEP?
Initial positive (downward) deflection followed by at least 1-2ms duration negative peaks (of relatively high amplitude)
(
Stimulation of the dorsal ulnar nerve, median nerve, or branches of the superficial radial nerves allows recording of cord dorsum potential at what site? SSEP at what site?
CDP - cervical intumescence
SSEP - mid and upper cervical region
** the relative importance of the various spinal cord pathways in generating these SSEPs is unknown (thank god)
(Cuddon)
What kind of potential is recorded at C1 after stimulation of pelvic or thoracic limb nerves?
Mixed potential (consists of a large field potential with a CAP superimposed)
This mixed potential represents the passage of the SSEP through axons in the region plus a sink source potential arising from nearby nuclei
PL stimulation -> nucleus gracilis, lateral cervical nucleus, nucleus Z
TL stimulation –> medial cuneate nucleus
(Cuddon)
What comprises the SSEP at the AO region?
Dorsal spinocerebellar tract
(Cuddon)
What contributes to SSEP conduction velocity and latency? (6)
- Type of nerve stimulated
- Cutaneous afferents - ascend in the DC without synapse
- Muscle afferents - ascend in the DLF (delay up to 0.5msec/synapse)
- Max CV in cutaneous afferents is 90m/sec in the dog, max CV in muscle afferents is up to 120m/sec
- Taking into account the synaptic delay for DLF axons - spinal cord conduction distance of approximately 100mm from the synaptic region is sufficient to offset this delay
- Stimulation site
- Due to synaptic delay of 0.5msec, dorsal column nonsynaptic pathways will produce the first peak of the SSEP in the lumbar cord
- UNLESS - nerve is stimulated 180mm or more from the synaptic sites in the cord - in this case, the faster conduction of the muscle afferents will offset the synaptic delay and lead to the DLF region being the producer of the first SSEP peak
- Proximal mixed nerve stimulation - first peak of cranial lumbar SSEP will represent activity in the nonsynaptic pathways of the DC
- Location of the recording electrode
- The distance of the recording electrodes to the synapse region will influence the spinal cord region that represents the onset latency of the SSEP
- In the cat, onset of sciatic nerve evoked SSEP recorded from at least as far cranial as the T11/12 interarcuate space will represent activity in the dorsal column fibers
- Age (dog - CV reaces adult values at 9-9.5 mos, then remains static)
- Body temp ( decrease by 1 degree C –> slows velocity by 3 m/sec)
- Signal intensity
- RS = reference effective stimulus = stimulus giving maximal response in the plantar interosseous muscles
- Stimulus intensity of 1/4 RS increased to RS –> induces a small but insignificant decrease in peak latency
- Induces a significant increase in amplitude in the first 3 deflections
- Stimulation intensity > RS –>
- Induces lg potential in the 10-16 ms poststimulus period
- Most likely muscle origin
- Obscures the contributions to the SSEP from small, slower conducting cord fibers
- Muscle paralysis eliminates this
- Modifies waveform (adding further deflections after the initial peaks)
- Interdog variation in this
- Increase stimulus artifact
- Increases amplitude of the first waveform
- Induces lg potential in the 10-16 ms poststimulus period
Anesthesia/sedation - does not affect latency (but should use consistent protocol?)
(Cuddon)
How do compressive spinal cord lesions alter SSEP? How to concussive injuries affect SSEP SSEP?
Compressive lesion –> SEP amplitude and morphologies are affected, latencies remain mostly unchanged (until disappearance)… Then says may cause prolonged latencies…
Concussive injury –> may result in transient or permanent blocking of SSEP
- If conduction is blocked at the same transverse level in a lg number of axons, deep positive potentials arise called injury potentials
- Indicate that CAP has been propagated into the region of the recording electrode, then blocked at the recording site
- SSEP can be superimposed on injury potential (suggesting some axons may have survived the lesion)
- May just indicate the recording electrode has detected activity in some axons recording further into the affected area than others
- Detection of an SSEP cranial to the myelopathy is the most reliable indicator of some degree of spinal cord integrity
Cuddon
What muscles should be routinely evaluated in EMG? (18)
- Pelvic and thoracic interosseous muscles
- Cranial tibial
- Gastrocnemius
- Vastus lateralis
- Semitedinosus
- Gluteal
- Paraspinalis (Cervical, thoracic, lumbar, sacral and coccygeal)
- Temporalis
- Masseter
- Tongue
- Anal sphincter
- Supraspinatus
- Infraspinatus
- Triceps
- Biceps
- Extensor carpi radialis
- Flexors (?)
- (special cases - pharynx, larynx, esophagus)
(Brain Camp)
End plate spikes:
- # of fibers?
- Amplitude?
- Duration?
- Firing pattern?
- Sound?
- Morphology?
- Single fiber
- LARGE 100 - 200uV amplitude
- 3-4ms duration
- Irregular firing pattern
- Sound like bacon frying (similar to fibrillation potentials)
- Morphology - biphasic with negative, then positive deflection
- Can look like fibrillation potentials, but fibrillation potentials are triphasic +/-/+ deflection
Figure: Miniature end plate potentials with 2 end plate spikes indicating close proximity of the needle to an end plate
(Brain camp)
Insertion activity:
- represents how many fibers?
- Amplitde?
- Duration?
- Sound?
Multiple fibers
Variable amplitude
<300ms
obnoxious sound
** secondary to mechanical disruption of muscle fibers
(Brain Camp)
Miniature end plate potentials (MEPP)
- Number of fibers?
- Amplitude?
- Duration?
- Firing pattern?
- Sound?
- Morphology?
- Multiple end plates
- 10-50uV, last 0.5 - 2ms
- Irregular firing pattern
- Sound like seashore
- Morphology - monophasic/negative
- ABSENT in denervation
(Brain Camp)
Motor unit action potentials:
- How many fibers contribute?
- What is the amplitude?
- Duration?
- Firing pattern?
- Sound?
- Morphology?
What is the ratio of 5 regarding MUAP?
- Multiple fibers innervated by the same motor neuron
- Amplitude varies with muscle and electrode proximity (200uV - 2mV)
- Duration varies with muscle (5-15ms)
- Regular firing pattern at 5-20Hz
- Sound like wind up toy
- Triphasic
Ratio of 5?
- 1 motor unit at 5hz, 2nd motor unit should appear at 10hz, 3rd should appear at 15Hz
- Recruitment
- Ratio > 10 – indicates neuropathic disease
- If frequency has to get up to 10Hz before you see a second MUAP, indicates neuropathic disease
- Ratio <5 – myopathic dz
(Brain Camp)
Fibrillation potentials:
- Arise from how many fibers?
- Amplitude? Duration?
- Firing pattern?
- Sound?
- Morphology?
- Single fiber
- 20uV - 1mV amplitude, 1-5ms duration
- Regular firing pattern 0.5 - 20Hz
- Sound like bacon frying or rain on a tin roof
- Morphology - biphasic or triphasic spikes with the initial deflection usually in the positive (downward) direction except if recorded within an end plate region
- Seen in neurogenic, muscle, and NMJ disorders
- Sometimes with PSW
- The DENSITy and CONSISTENCY of observed fibrillation potentials is an accurate representation of the severity of muscle involvement
Complex repetitive discharges:
- Number of myofibers
- Amplitude? Duration?
- Firing pattern?
- Sound?
- Morphology?
- Multiple myofibers
- 50uV - 1mV amplitude, variable duration
- Regular firing pattern (0.3-150Hz, start/stop abruptly)
- Motorcycle idling…
- Morphology - polyphasic with a uniform frequency, shape and amplitude, trains of waves
Commonly mistaken for myotonic potentials
Commonly seen with hyperadrenocorticism
(Brain Camp)
Myotonic potentials
- # of myofibers?
- Amplitude/Duration?
- Firing pattern?
- Sound?
- Morphology
- Multiple single fibers
- 10uV - 1mV
- 500ms and above
- Waxing and waning firing pattern 20-100Hz
- Sound - divebomber
- Morphology 1 of 2 types:
- Sustained run of positive waves (resembling PSWs)
- Sustained run of biphasic spike potentials (initial small + peak then larger negative peak, resembling fibrillation poentials)
Characteristic of myotonia congenita. Also seen in some chronic radiculopathies and polyneuropathies
(Brain Camp)
What kind of EMG artifact is most common? How can it be avoided?
What are the limitations of EMG?
60mHz artifact is most common
- EMG machine should be plugged into its own circuit
- Turn off fluorescent lights
- Turn off anesthesia monitor
- ECG artifact
Limitations:
- Findings are not specific: Myopathy and neuropathy have similar lesions
- Focal lesions can be missed
- Diseases limited to sensory neurons will have normal results
- Findings are normal in neuropathies that are primary demyelinating
- Timing is important - takes days to weeks for a muscle that has lost its nerve supply to exhibit spontaneous activity and end stage muscle will be electrically slient
(Brain Camp)
What kind of recording system is needed for nerve conduction studies?
What kind of electrodes can be used? (pros/cons)
Why do you want to keep the stimulus as low as possible (but still supramaximal)
4 channel system (evoked potential system) with electrical stimulation
Electrodes = monopolar, surface, and ground.
- Typically monopolar needle electrodes that are insulated except for the tip are used.
- Surface electrodes are generally regarded as better than needle electrodes for recording CMAPs because they assess contributions from all discharging units
- Needle electrodes register only a small % of potentially recordable CMAPs
- Positioning is more critical than with surface electrodes - minor displacement can result in a substantial change in the size and shape of the CMAP
- Improve recordings from small atrophic muscles
If you increase the intensity of the stimulus, you could stimulate a distal part of the nerve - which will affect the velocity
(Brain Camp)
What is threshold (submaximal) vs. maximal vs. supramaximal stimulus?
Threshold stimulus = one that barely elicits a response in some, but not all axons in a nerve
Maximal stimulus = one that activates the entire group of axons (so that further increase in stimulus intensity does not cause additional increases in amplitude)
Supramaximal stimulus = An intensity greater than maximal (1.2 - 1.5x)
(Brain Camp)
Most commonly used nerves for motor nerve conduction studies in the thoracic limb? (3)
Most commonly used in the pelvic limb? (2)
Cranial nerves? (2)
Thoracic limb:
- Radial nerve
- Ulnar nerve
- Median nerve (less frequently)
Pelvic limb
- Sciatic-tibial nerve
- Common peroneal nerve (less common)
Cranial nerves
- Recurrent laryngeal nerve
- Facial nerve
(Vet Clin N America)
What are causes of decreased CMAP amplitude? (3)
What is the morphology of normal CMAP?
- Myopathy
- Prejunectional neuromuscular disease (ex/ botulism)
- Primary axonopathies
Morphology: Simple or biphasic with initial negativity (upward deflection). A small positive/downward deflection may precede the negative peak if the recording electrodes are not placed near the motor point of the muscle
(Cuddon)
____________ is used to assess the degree of myelination of the fastest conducting axons
________ is used to assess the most distal aspect of the nerve and the intramuscular nerve branches
Motor nerve conduction velocity is used to assess the degree of myelination of the fastest conducting axons
Residual latency is used to assess the most distal aspect of the nerve and the intramuscular nerve branches. It is a measure of the collective delay through fine intramuscular motor branches and the neuromuscular junction
A direct measurement of a single CMAP latency (from beginning of stimulus artifact to the first deflection of the wave from baseline) is of little value in assessing MNCV. This direct latency measurement accounts for neuromuscular transmission and the time required for generation of the CMAP
(Cuddon)
Motor nerve conduction: A proximal stimulus gives rise to an evoked potential of longer duration and lower amplitude than a distal stimulus - what is this called? What causes it?
Physiologic temporal dispersion
Occurs as a result of the impulses of the slow conducting fibers progressively lagging further behind those of the fast conducting fibers
This increase in latency difference may result in phase cancellation (positive peaks of the fast fibers + negative peaks of slow fibers)
(Cuddon)
How does excessive stimulus intensity affect MCNV?
How does temp affect MNCV?
Excessive stimulus intensity –> spread of stimulus current depolarizes the nerve a few mm distal to the cathode –> erroneously short latency –> affects MNCV
1C dcerease in limb temp –> decrease MNCV of 1.7 - 1.8m/s (dog)
(Cuddon)
How does limb length affect CMAP and MNCV? (and why)
How does age affect MNCV in dog vs. cat?
Dog: greater limb length –> longer tapered segment of the nerve –> slower MNCV, smaller CMAP amplitude, longer CMAP duration
- Peripheral tapering of nerves occurs at the same anatomic level regardless of limb length
Age:
- Dog: MNCV does not reach adult values until the animal is between 6 mos and 1 year of age
- 10x increase in MNCV during maturation, greatest increase occurring between birth and 4-5 weeks of age
- Remain stable from 1-7y, then gradually slows
- ~ 10y old –> MNCV reduced by 10-15% compared with young adult levels
- Cat: MNCV do not reach adult values until the animal is approximately 3m of age
- Effect of advanced age not evaluated
(Cuddon)
EEG:
- An upward deflection is indicative of input terminal 1 becoming more (negative/positive) with respect to input terminal 2
- The number of derivations in a montage are limited by?
- What is the difference between a bipolar vs. referential montage?
Upward deflection - input terminal one becoming more NEGATIVE with respect to input terminal 2
Multiple derivations are limited by the number of amplifiers within the recording system
Bipolar montage - derivations are arranged in saggital or transverse planes
Referential montage - input terminal 1 varies, input terminal 2 stays the same
- A single electrode, pair of electrodes, or all electrodes averaged together are commonly used for IT2
EEG: what is a phase reversal?
Bipolar montage - electrodes are shared, IT2 in one derivation will become IT1 in the next
Phase reversal: Downward deflection (IT1 positive with respect to IT2) in one tracing is upward in the next
In bipolar montage - phase reversal used to localize an event
(Brain Camp)
EEG: Using referential montage, what is used to localize a lesion?
Maximal amplitude
(Brain Camp)
________ has been shown to activate epileptiform activity in patients with seizures and should be included in recordings
Sleep
(Brain Camp)
_________ is associated with the appearance of sleep spindles and vertex sharp waves
___________ is associated with activity that is low in amplitude, high in frequency
Slow-wave sleep - sleep spindles and vertex sharp waves
REM sleep and arousal - low amplitude, high frequency
(Brain Camp)
__________ are patterns commonly seen with sedation/anesthetic drugs, but when naturally occurring indicate a grave prognosis
Burst suppression
Isoelectric (flatline)
(Brain Camp)
EEG: How should background activity and paroxysmal events be characterized?
Focal, lateralized, or generalized
(Brain Camp)
EEG: What are the 3 types of paroxysmal events? How are they characterized?
- Spikes (duration < 70ms)
- Sharp waves (70 - 200ms)
- Slow waves (>200ms)
Paroxysmal events may or may not be epileptiform
They can occur singly or in multiples and can be rhythmic or periodic
The different types of paroxysmal discharges can occur together as in the case of spike-and-wave discharges
(Brain Camp)
What is the source of the signal recorded in EEG?
- Synaptic activity of cortical neurons
- Pyramidal cells of the cerebral cortex - most important neuronal source of EEG
- Glial cells
The extracellular currents give rise to the surface recorded EEG
(Holliday, Williams)
When as EPSP occurs near the surface, what is recorded at the surface electrode? Deep electrode?
EPSP @ surface –> ECF becomes more negative –> upward deflection
EPSP @ surface –> depolarization pulls negative charges rowards the cell membrane –> remaining ECF is positive @ deep electrode –> downward deflection
(Holliday, Williams)
When IPSP is applied at surface, what is recorded from surface electrode? Deep electrode?
IPSP @ surface –> ECF becomes more positive –> downward deflection recorded @ surface electrode
IPSP @ surface –> hyperpolarization pulls positive charges rowards the cell membrane –> remaining ECF is negative @ deep electrode –> upward deflection
(Holliday and Williams)
How is the electrooculogram recorded?
Place a pair of electrodes adjacent to the lateral canthus of each eye or near the medial canthus of one eye, then connecting them to one channel of the polygraph
What 3 things can induce epileptic discharges in dogs that have epilepsy?
Sleep
Chlorpromazine
Photic stimulation
(Holliday and Williams)
What kind of electrical activity does muscle artifact cause?
Intermittent or continuous relatively high frequency activity that can partially or completely obscure the background rhythm
If persistent, SQ lidocaine may help
Sources of EEG artifact?
- Muscle artifact
- Movement artifact
- Respiratory artifact
- Eye movements
- ECG artifacts
(Holliday and Williams)
When does EEG background rhythm reach maturity in puppies?
BGR of puppies reach mature forms around 5 mos of age (occasionally up to 10 mot)
(Holliday and Williams)
What are the frequencies associated with:
- Delta waves
- Theta
- Alpha
- Beta
- Gamma
DINOSAURS - THEY ALWAYS BE GREEN
Delta: <4 Hz
Theta: 4-<8 Hz
Alpha: 8-<13 Hz
Beta: 13 – 30 Hz
Gamma: 30 – 60 Hz
(Holliday and Williams)
EEG background activity of full arousal:
Alert behavior
BGR are usually of very low amplitude (<20mV) and high frequency (15 - 25Hz) = Beta waves
Muscle artifact is common during arousal
(Holliday and Williams)
EEG background activity of relaxed state
Quiet ambience and closed eyes
Stable period of alpha rhythm (8-<13 Hz)
Typically a period of stable alpha rhythm had a duration of 8-15 sec after which it was replaced by:
Higher frequencies if the animal opened its eyes/was aroused,
Lower frequencies as the animal became sleepy
(Holliday and Williams)
What is the EEG activity associated with drowsiness
Dogs are recumbent with their eyes partially or completely closed
At this time, they can be quite readily aroused by minimal stimulation, or small disturbances in the environment
BGR consists of predominant 6-8 or 6-10 Hz waves of 10-20FV amplitude with superimposed random slower and higher frequencies - (Between theta and alpha waves)
If undisturbed during drowsiness, most sedated dogs soon enter non-REM sleep
(Holliday and Williams)
What is the EEG activity associated with nonREM sleep?
During non-REM sleep, dogs are recumbent and apparently unaware of environmental disturbances
Eyes are closed or nearly closed
Stronger stimuli are needed to arouse them than during drowsiness
BGR at this time are predominantly 2-4 Hz with lower amplitude superimposed activity, predominantly in the 6-10Hz range
Amplitudes during non-Rem sleep var from 15-20FV up to 100 FV
Stages of light and deep nonREM sleep are recognizable by the higher amplitudes and lower frequencies
EEG activity of REM sleep
During rem sleep, dogs are recumbent with their eyes partially or completely closed
With the onset of REM sleep, BGR change rapidly losing amplitude and increasing in frequency so the resemble those of arousal
About 5-10 minutes after REM sleep begins, the eye movements begin - very often these are accompanied by movements of the feet, mouth, or other parts of the body and even vocalization
(Holliday and Williams)
What are the 3 normal EEG transient events? How can they be distinguished as normal?
- Sleep spindles
- K complexes
- V waves
HIghest amplitude on midline, also quite evident in electrodes located laterally where they are symmetrical in amplitude and frequency
Distinct asymmetries or absences on one side are more indicative of an abnormality
(Holliday and Williams)
EEG:
- What are repetitive sinusoidal waves, begin at lower amplitude, increase, then decrease
- Often recorded during nonREM sleep
- Bilaterally symmetric and highest amplitude at midline (visible from lateral derivations as well)
Sleep spindles
- Recorded from some dogs during REM sleep - possibly a drug effect
(Holliday and Williams)
EEG:
- Sleep spindle + slow wave
- Spindle may appear before, during or after the slow wave
- Occur during nonREM sleep
- Highest amplitude and most clearly developed on midline (visible in lateral derivations as well)
K complex
- Because the spindle may appear before, during, or after the slow-wave, there is considerable variation in the appearance of K complexes
- Nonpathologic waveform
(Holliday and Williams)
EEG:
- Response to stimulation, usually during drowsiness or sleep (especially drowsiness)
- Normal EEG wave
Vertex waves
- Can be differentiated from paroxysmal discharges by the fact that they do not have spike components, occur only during drowsiness, and are always of highest amplitude on the midline and symmetrically distributed
(Holliday and Williams)
EEG:
- Rhythmic 0.5-1sec bursts of 4-6Hz sinusoidal waves recorded about the same time of the transition from drowsiness to nonREM sleep
- Symmetrically distributed, highest amplitude on midline, frequently associated with eye movements
4-6 per second bursts
- The nature of these discharges is unknown - recorded from normal dogs and clinical patients
- Considered normal EEG waves
(Holliday and Williams)
What is photic driving?
Response to photic stimulation - appearance of symmetrical sinusoidal BGR at the same frequency as the stimulation
Rhythms appear at or within a few seconds of the onset of stimulation and disappear immediately with its cessation
Stimulus frequencies of 2-10Hz are most effective in eliciting photic driving
(Holliday and Williams)
Figure: “Photic driving” in response to flickering light stimulation (PS: stimulus event marker in lowermost channel). Note onset and end of change in BGR rhythms concurrent with onset and end of stimulation; this is normal. High amplitude irregular waves at right of upper panel were movement artifacts; photic stimulation often disturbs the patient, resulting in movements. After stimulation, BGR were those of full arousal. Low amplitude muscle artifact throughout both panels in channel 3
What are the 7 ways to characterize deafness
- Unilateral or bilateral
- Partial or total
- Syndromic (linked to another disorder) or nonsyndromic
- There are no syndromic causes of deafness in the dog and cat
- Peripheral or central
- Central deafness is difficult to produce without other severe CNS signs due to multiple decussations of the central auditory pathway
- Congenital or Later onset
- Hereditary or acquired
- Conductive/sensorineurial
(Brain Camp)
What are the 3 ways to characterize peripheral deafness
- Sensorineural vs. conductive
- Inherited vs. acquired
- Congenital or later-onset
(Brain Camp)
Cochlear damage causes what type of peripheral deafness?
Sensorineural deafness
- Primary - initial pathology is loss of hair cells
- Secondary - dysfunction of stria vascularis –> secondary loss of hair cells
(Brain Camp)
A process that blocks sound transmission through the outer or middle ear causes ______ deafness
Conductive deafness (due to external ear disease, middle ear disease)
(Brain Camp)
Where are the electrodes placed for BAER recording?
Recording electrode (active electrode) - placed at the tragus of the tested ear
Reference electrode - Verte
Ground electrode - nuchal crest (in this picture is interorbital line)
(Cuddon)
What are the OFA guidelines for BAER?
__________ is used to assess the degree of myelination of the fastest conducting fibers
Motor nerve conduction velocity
Know how to do this by hand!!
(Cuddon)
______________ is electrodiagnostic calculation used to assess the distal aspect of the nerve and the intramuscular branches
Residual latency
Measure of the collective delay through the fine intramuscular motor branches and neuromuscular junction
(Cuddon)
Facial reflex testing: what nerves are stimulated and what response is monitored?
SQ stimulating electrode of the trigeminal nerve branches or facial nerve branches –> reflex contractions of the ipsilateral orbicularis oculi muscle
It is considered an evoked potential
Trigeminal: Infraorbital, frontal (supraorbital), zygomatic branches
Facial: middle and caudal internal auricular branches
(Cuddon)
What are the components of the facial reflex evoked response and what contributes to them?
Stimulation of sensory/mixed nerve –> transmits to the brain –> orbicularis oculi contraction
Ipsilateral early (R1) and late (R2) component
- R1 has a lower stimulation threshold and is more stable than R2
- R3 = third ipsilateral wave, inconsistently observed, longer latency than R2
- R1 latency = conduction along trigeminal and facial nerves –> pontine synaptic relay –> neuromuscular delay –> orbicularis oculi fibers
- R2 latency = trigeminal/facial nerve –> polysynaptic reflex pathways involving the trigeminal spinal and sensory nuclei –> contralateral ventral thalamic nucleus –> bilateral facial nuclei
- Essential to determine whether the afferent or efferent arc is primarily involved
- R3 = activation of small diameter, high threshold afferent, unmyelinated fibers (nociceptive fibers?)
Contralateral = Rc
- Stimulation of the supraorbital nerve/frontal nerve –> contralateral reflex muscle potential recorded in the opposite orbicularis oculi muscle
- Has a slightly longer latency than R2
- Polysynaptic reflex
- Depressed by GA
- Rc and R2 show habituation - decreased in amplitude with repeated uniform stimuli
(Cuddon)
What is direct facial nerve stimulation?
Stimulation of the palpebral nerve (motor branch of facial nerve) –> measure CMAP in orbicularis oculi muscle
This reflex has a stable latency, highly variable response
(Cuddon)
What are the electrode sites for the canine facial reflexes?
What is the morphology of the cortical SSEP?
How does the size of the animal influence the amplitude and latency of the cortical SSEP?
Initial positive (upward) deflection, then negative deflection
Larger animal - longer latency and smaller amplitude cortical SSEP
The cortical SEP ipsilateral to the stimulation site will have opposite polarity to the contralateral side, and amplitude significantly decreased
(Cuddon)
Where should the recording electrodes be placed for cortical SSEP?
Active electrode: near the cruciate sulcus, contralateral to the stimulated nerve
- 1-2cm off midline, 1-2cm caudal to the intracanthal line
- This position will vary with head size and shape
Midline location can be used if both right and left nerves will be stimulated
- Some reports placed the active electrode on the midline over the occipital protuberance
- Smaller peaks prior to the primary cortical SEP likely represent brainstem activity
(Cuddon)
Recording artifact causes disruption of __________________
Helmholtz double layer:
- Electrode-tissue interface develops a charge layer, where charges of one polarity on the electrode metal surface attract an opposite charge layer in the electrolyte with an interposed molecular layer of water absorbed on the metal surface
Ototoxic drugs/chemicals?
- Aminoclygoside antibiotics
- Diuretics - furosemide
- Anti-neoplastic agents - actinomycin, cisplatin, nitrogen mustard, vinblastine, vincristine
- Non-aminoglycoside antibiotics - see pic
- Antiseptics - see pic (chlorhexidine, iodine)
- Misc agents - ceruminolytic agents, digoxin, insulin, KBr, prednisolone,
(Brain Camp - strain)
EEG artifact?
Muscle
(Brain Camp)
EEG artifact?
MUAP
(Brain Camp)
EEG artifact?
Eye movement
(Brain Camp)
EEG artifact?
Electrode out
(Brain Camp)
EEG artifact?
60hz
(Brain Camp)
EEG artifact?
ECG
(Brain Camp)
EEG - what is the state of consciousness?
Awake OR REM sleep
(Brain Camp)
EEG - what is the state of consciousness?
Drowsy
(Brain Camp)
EEG - what is the state of consciousness?
Slow-wave sleep = non REM sleep
(Brain Camp)
EEG - what kind of PD?
Sleep spindles
Normal PD
(Brain Camp)
EEG - what kind of PD?
Vertex sharp wave - normal PD
(Brain Camp)
EEG - what kind of PD?
Burst suppression
(Brain Camp)
EEG diagnosis?
Generalized seizure
(Brain Camp)
EEG - what kind of PD?
Multiple spike complex (abnormal PD)
(Brain Camp)
