Electrodiagnostics

Question 1

EMG electrodes:

The active electrode is the electrode attached to the (negative or positive) terminal?

Answer 1

Negative terminal

Question 2

EMG:
Insertion activity will be decreased in?
Insertion activity will be increased in?

How long should insertion activity last?

Answer 2

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)

Question 3

EMG:

_____ is the small depolarization of the postsynaptic membrane induced by the sustained random release of a single quantum of ACh

Answer 3

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)

Question 4

EMG:

Miniature End Plate Potentials (MEPPs)

How are they affected by denervation? Myasthenia? botulism?

Answer 4

Miniature end plate potentials MEPPs:

Cease after denervation
Normal frequency, decreased amplitude in MG
Decreased Frequency, normal amplitude in botulism

(Cuddon)

Question 5

EMG:

_______ is spontaneous EMG activity that results from the discharge of a single muscle fiber

Answer 5

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)

Question 6

EMG:
____ are EMG discharges seen associated with mild voluntary muscle contraction

Answer 6

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)

Question 7

EMG:

What is an interference pattern associated with motor unit action potentials?

Answer 7

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)

Question 8

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?

Answer 8

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)

Question 9

EMG:

4 causes of doublet/triplet MUAP:

What causes smaller amplitude MUAP?

Answer 9

1. latent tetani
2. metabolic states associated with motor neuron pool hyperexcitability
3. motor neuron disease or radiculopathy
4. myotonic dystrophy

Smaller amplitude MUAP = myopathy

(Cuddon)

Question 10

EMG:

What abnormality results in a decreased amplitude and duration of MUAP?

Answer 10

Primary myopathy (myofiber destruction)

(Cuddon)

Question 11

EMG:

Decreased amplitude and short duration MUAP likely cause? (2)

Long duration MUAP likely cause?

Answer 11

Decreased amplitude and short duration MUAP

1. distal neuropathy –> damaged axon terminals –> random loss of myofibers
2. reinnervation –> immature motor units with only a few fibers

Long duration MUAP

1. myopathy with regenerating fibers

(Cuddon)

Question 12

EMG:

How does reinnervation/neuropathy affect MUAP?

Answer 12

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)

Question 13

EMG:

________ is caused by the spontaneous action of a single myofiber which is abnormal

Answer 13

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)

Question 14

EMG:

Causes for fibrillation potentials (3)

Answer 14

1. 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
2. polymyositis
3. muscular dystrophy

(Cuddon)

Question 15

EMG:

A marked decrease in the density of fibrillation may indicate?

Answer 15

Successful motor neuron reinnervation

replacement of myofibers by fibrous tissue

(differentiated by clinical evaluation)

(Cuddon)

Question 16

EMG:

_____ is an abnormal EMG potential that consists of an initial positive spike, followed by a shorter, slow, and small negative potential

Answer 16

Positive sharp waves

• Thought to originate from irritated muscle membrane with the potential stopping at an area immediately adjacent to the needle electrode

(Cuddon)

Question 17

Positive sharp waves:

• # of fibers?
• Amplitude? Duration?
• Firing pattern?
• Sound?
• Morphology?

Answer 17

• 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

Question 18

EMG:

__________ are polyphasic or serrated action potential with a uniform frequency, shape and amplitude

Answer 18

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)

Question 19

EMG:

______ are abnormal repetitive discharges at a rate of 20 - 80Hz

Answer 19

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)

Question 20

EMG:

What diseases cause myotonic potentials?

Answer 20

injured single myofibers –> independent, repetitive discharges

• caused by primary muscle disease
• cased by steroids

(Cuddon)

Question 21

How does EMG influence serum CK?

Answer 21

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)

Question 22

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?

Answer 22

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)

Question 23

_____ are electrical events recorded when:

peripheral nerve stimulated –> electrical events elicited from neurons, synapses or axons

Answer 23

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)

Question 24

What is the most significant source of artifact in somatosensory evoked potentials? How can it be eliminated?

Answer 24

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)

Question 25

What are the neural generators of the SSEP?

Answer 25

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 * Ventral quadrant: SSEP is propagated in CROSSED and UNCROSSED pathways (in dogs) (Cuddon)

Question 26

How does the stimulation site affect SSEP?

Answer 26

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)

Question 27

What are the 2 types of SSEP elicited and what causes them?

Answer 27

1. 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 2. Field potentials * Arise from spinal cord gray matter or nucleus synapse * The source is stationary (Cuddon)

Question 28

How does bilateral vs. unilateral stimulation affect SSEPs?

Answer 28

* 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)

Question 29

Where should recording electrodes (active, reference, ground) be placed for SSEP?

Answer 29

* 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)

Question 30

How are onset latencies measured for SSEP?

Answer 30

Measured from the onset of the stimulus artifact to the first positive (downward) peak (Cuddon)

Question 31

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?

Answer 31

Sharp downward displacement of the entire SSEP Dorsal and ventral nerve roots of the cauda equina produce potentials at L6/7 (Cuddon)

Question 32

What are normal causes of peak segregation of SSEP?

Answer 32

1. Distal stimulation sites (especially mixed nerve) --\> leave time for peak segregation 2. Polyphasia in sensory nerves is physiologic in dogs 3. Antidromic conduction along motor nerves (slower conduction velocities) will also be recorded at these sites (Cuddon)

Question 33

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?

Answer 33

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: 1. Species 2. Which nerve roots contribute to the sciatic nerve 3. Where those nerve rooes are located within the spinal canal SSEP * Cat: L3/4 * Dog L2/3 (Cuddon)

Question 34

What is the morphology of SSEP?

Answer 34

Initial positive (downward) deflection followed by at least 1-2ms duration negative peaks (of relatively high amplitude) (

Question 35

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?

Answer 35

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)

Question 36

What kind of potential is recorded at C1 after stimulation of pelvic or thoracic limb nerves?

Answer 36

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)

Question 37

What comprises the SSEP at the AO region?

Answer 37

Dorsal spinocerebellar tract (Cuddon)

Question 38

What contributes to SSEP conduction velocity and latency? (6)

Answer 38

1. 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 2. 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 3. 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 4. Age (dog - CV reaces adult values at 9-9.5 mos, then remains static) 5. Body temp ( decrease by 1 degree C --\> slows velocity by 3 m/sec) 6. 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 Anesthesia/sedation - does not affect latency (but should use consistent protocol?) (Cuddon)

Question 39

How do compressive spinal cord lesions alter SSEP? How to concussive injuries affect SSEP SSEP?

Answer 39

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

Question 40

What muscles should be routinely evaluated in EMG? (18)

Answer 40

1. Pelvic and thoracic interosseous muscles 2. Cranial tibial 3. Gastrocnemius 4. Vastus lateralis 5. Semitedinosus 6. Gluteal 7. Paraspinalis (Cervical, thoracic, lumbar, sacral and coccygeal) 8. Temporalis 9. Masseter 10. Tongue 11. Anal sphincter 12. Supraspinatus 13. Infraspinatus 14. Triceps 15. Biceps 16. Extensor carpi radialis 17. Flexors (?) 18. (special cases - pharynx, larynx, esophagus) (Brain Camp)

Question 41

End plate spikes: * # of fibers? * Amplitude? * Duration? * Firing pattern? * Sound? * Morphology?

Answer 41

* 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)

Question 42

Insertion activity: * represents how many fibers? * Amplitde? * Duration? * Sound?

Answer 42

Multiple fibers Variable amplitude \<300ms obnoxious sound \*\* secondary to mechanical disruption of muscle fibers (Brain Camp)

Question 43

Miniature end plate potentials (MEPP) * Number of fibers? * Amplitude? * Duration? * Firing pattern? * Sound? * Morphology?

Answer 43

* Multiple end plates * 10-50uV, last 0.5 - 2ms * Irregular firing pattern * Sound like seashore * Morphology - monophasic/negative * ABSENT in denervation (Brain Camp)

Question 44

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?

Answer 44

* 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)

Question 45

Fibrillation potentials: * Arise from how many fibers? * Amplitude? Duration? * Firing pattern? * Sound? * Morphology?

Answer 45

* 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

Question 46

Complex repetitive discharges: * Number of myofibers * Amplitude? Duration? * Firing pattern? * Sound? * Morphology?

Answer 46

* 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)

Question 47

Myotonic potentials * # of myofibers? * Amplitude/Duration? * Firing pattern? * Sound? * Morphology

Answer 47

* 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)

Question 48

What kind of EMG artifact is most common? How can it be avoided? What are the limitations of EMG?

Answer 48

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)

Question 49

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)

Answer 49

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)

Question 50

What is threshold (submaximal) vs. maximal vs. supramaximal stimulus?

Answer 50

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)

Question 51

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)

Answer 51

Thoracic limb: 1. Radial nerve 2. Ulnar nerve 3. Median nerve (less frequently) Pelvic limb 1. Sciatic-tibial nerve 2. Common peroneal nerve (less common) Cranial nerves 1. Recurrent laryngeal nerve 2. Facial nerve (Vet Clin N America)

Question 52

What are causes of decreased CMAP amplitude? (3) What is the morphology of normal CMAP?

Answer 52

1. Myopathy 2. Prejunectional neuromuscular disease (ex/ botulism) 3. 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)

Question 53

\_\_\_\_\_\_\_\_\_\_\_\_ 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

Answer 53

**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)

Question 54

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?

Answer 54

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)

Question 55

How does excessive stimulus intensity affect MCNV? How does temp affect MNCV?

Answer 55

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)

Question 56

How does limb length affect CMAP and MNCV? (and why) How does age affect MNCV in dog vs. cat?

Answer 56

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)

Question 57

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?

Answer 57

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

Question 58

EEG: what is a phase reversal?

Answer 58

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)

Question 59

EEG: Using referential montage, what is used to localize a lesion?

Answer 59

Maximal amplitude (Brain Camp)

Question 60

\_\_\_\_\_\_\_\_ has been shown to activate epileptiform activity in patients with seizures and should be included in recordings

Answer 60

Sleep (Brain Camp)

Question 61

\_\_\_\_\_\_\_\_\_ is associated with the appearance of sleep spindles and vertex sharp waves \_\_\_\_\_\_\_\_\_\_\_ is associated with activity that is low in amplitude, high in frequency

Answer 61

Slow-wave sleep - sleep spindles and vertex sharp waves REM sleep and arousal - low amplitude, high frequency (Brain Camp)

Question 62

\_\_\_\_\_\_\_\_\_\_ are patterns commonly seen with sedation/anesthetic drugs, but when naturally occurring indicate a grave prognosis

Answer 62

Burst suppression Isoelectric (flatline) (Brain Camp)

Question 63

EEG: How should background activity and paroxysmal events be characterized?

Answer 63

Focal, lateralized, or generalized (Brain Camp)

Question 64

EEG: What are the 3 types of paroxysmal events? How are they characterized?

Answer 64

1. Spikes (duration \< 70ms) 2. Sharp waves (70 - 200ms) 3. 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)

Question 65

What is the source of the signal recorded in EEG?

Answer 65

1. Synaptic activity of cortical neurons * Pyramidal cells of the cerebral cortex - most important neuronal source of EEG 2. Glial cells The extracellular currents give rise to the surface recorded EEG (Holliday, Williams)

Question 66

When as EPSP occurs near the surface, what is recorded at the surface electrode? Deep electrode?

Answer 66

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)

Question 67

When IPSP is applied at surface, what is recorded from surface electrode? Deep electrode?

Answer 67

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)

Question 68

How is the electrooculogram recorded?

Answer 68

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

Question 69

What 3 things can induce epileptic discharges in dogs that have epilepsy?

Answer 69

Sleep Chlorpromazine Photic stimulation (Holliday and Williams)

Question 70

What kind of electrical activity does muscle artifact cause?

Answer 70

Intermittent or continuous relatively high frequency activity that can partially or completely obscure the background rhythm If persistent, SQ lidocaine may help

Question 71

Sources of EEG artifact?

Answer 71

1. Muscle artifact 2. Movement artifact 3. Respiratory artifact 4. Eye movements 5. ECG artifacts (Holliday and Williams)

Question 72

When does EEG background rhythm reach maturity in puppies?

Answer 72

BGR of puppies reach mature forms around 5 mos of age (occasionally up to 10 mot) (Holliday and Williams)

Question 73

What are the frequencies associated with: * Delta waves * Theta * Alpha * Beta * Gamma DINOSAURS - THEY ALWAYS BE GREEN

Answer 73

Delta: \<4 Hz Theta: 4-\<8 Hz Alpha: 8-\<13 Hz Beta: 13 – 30 Hz Gamma: 30 – 60 Hz (Holliday and Williams)

Question 74

EEG background activity of full arousal:

Answer 74

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)

Question 75

EEG background activity of relaxed state

Answer 75

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)

Question 76

What is the EEG activity associated with drowsiness

Answer 76

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)

Question 77

What is the EEG activity associated with nonREM sleep?

Answer 77

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**

Question 78

EEG activity of REM sleep

Answer 78

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)

Question 79

What are the 3 normal EEG transient events? How can they be distinguished as normal?

Answer 79

1. Sleep spindles 2. K complexes 3. 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)

Question 80

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)

Answer 80

Sleep spindles * Recorded from some dogs during REM sleep - possibly a drug effect (Holliday and Williams)

Question 81

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)

Answer 81

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)

Question 82

EEG: * Response to stimulation, usually during drowsiness or sleep (especially drowsiness) * Normal EEG wave

Answer 82

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)

Question 83

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

Answer 83

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)

Question 84

What is photic driving?

Answer 84

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

Question 85

What are the 7 ways to characterize deafness

Answer 85

1. Unilateral or bilateral 2. Partial or total 3. Syndromic (linked to another disorder) or nonsyndromic * There are no syndromic causes of deafness in the dog and cat 4. Peripheral or central * Central deafness is difficult to produce without other severe CNS signs due to multiple decussations of the central auditory pathway 5. Congenital or Later onset 6. Hereditary or acquired 7. Conductive/sensorineurial (Brain Camp)

Question 86

What are the 3 ways to characterize peripheral deafness

Answer 86

1. Sensorineural vs. conductive 2. Inherited vs. acquired 3. Congenital or later-onset (Brain Camp)

Question 87

Cochlear damage causes what type of peripheral deafness?

Answer 87

Sensorineural deafness * Primary - initial pathology is loss of hair cells * Secondary - dysfunction of stria vascularis --\> secondary loss of hair cells (Brain Camp)

Question 88

A process that blocks sound transmission through the outer or middle ear causes ______ deafness

Answer 88

Conductive deafness (due to external ear disease, middle ear disease) (Brain Camp)

Question 89

At what age do the ear canals open in dogs and cats? T/F: nearly all congenital deafness is hereditary

Answer 89

Ear canals are closed until 12-14 days in dogs, 5 days in cats TRUE: nearly all congenital deafness is hereditary (Brain Camp)

Question 90

Around what age do dogs with congenital, inherited, sensorineural deafness develop strial degeneration? Congenital deafness can occur in any cat carrying the __________ gene

Answer 90

Around 3 weeks of age in dogs Congenital deafness can occur in any cat carrying the **dominant allele of the white (W) gene**

Question 91

In dogs, which 2 genes can cause deafness?

Answer 91

Recessive alleles of the piebald gene, or the dominant allele of the merle gene can cause congenital, inherited, sensorineural deafness (Brain Camp)

Question 92

What is the affected cell type in Doberman Pinschers that are deaf?

Answer 92

Hair cells die, stria is unaffected * Deafness is NOT associated with white pigmentation * Usually bilateral and is accompanied by vestibular signs - dogs usually adapt to vestibular signs (Brain Camp)

Question 93

What dog breeds develop later onset sensorineural deafness? What dogs develop later onset conductive deafness?

Answer 93

Later onset sensorineural - Rhodesian ridgeback, border collie Later onset conductive - CKCS w/ PSOM (Brain Camp)

Question 94

What are the components of the auditory evoked response and where does BAER fall?

Answer 94

Auditory evoked response = averaged time-locked recordings of brain activity in response to externally applied acoustic stimuli. Consists of: * Early latency (0-10ms) * Middle latency (10-80ms) * Late latency (80 - 250) * Long latency (\>250) BAER early latency Middle latency potentials - series of positive waves in the 8-80ms range with amplitudes ranging from 0.5 - 3uV (Cuddon)

Question 95

What are the neural generators of waves I - VII of the BAER?

Answer 95

Wave I - ipsilateral cochlear nerve Wave II - ipsilateral cochlear nucleus and unmyelinated central terminals of the cochlear nerve Wave III - Dorsal nucleus of the trapezoid body (ipsilateral and/or contralateral) Wave V - ipsilateral and/or contralateral caudal colliculus Wave IV, VI, and VII - generators not clearly defined (Cuddon

Question 96

Auditory reflex: is the efferent response unilateral or bilateral?

Answer 96

Bilateral! (Cuddon)

Question 97

What kind of sound is used as auditory click stimulus for BAER?

Answer 97

High frequency sound --\> stimulates receptors at the base of the cochlea (Cuddon)

Question 98

What are the 3 kinds of stimulus polarity? How does it alter the BAER recording?

Answer 98

Stimulus polarity: 1. Rarefaction - initially produce depolarization and generates response of shorter latency * Initial outward deflection of the tympanum * Better separates waves III and IV in dogs 2. Condensation - initially produces hyperpolarization of the cochlear hair cells, followed by depolarization * Results in longer latencies * Produces inward deflection of the tympanum 3. Alternating - alternate between rarefaction and condensation * Makes the peaks more round, makes latency identification harder, may introduce spurious abnormalities * Reduces stimulus artifact and cochlear microphonics preventing distortion of wave I (Brain Camp) (Cuddon)

Question 99

What stimulus factor has the greatest effect on latency and amplitude of BAER?

Answer 99

Stimulus intensity Stimulus intensity should be \> 70dB (Cuddon)

Question 100

The waves produced in BAER reading have an amplitude in the ______ range

Answer 100

microvolt range

Question 101

What are the 2 types of transducer that can be used for BAER?

Answer 101

Ear phone (most common) Bone vibration transducer Held behind the temporal bone/pinna. Vibrations travel through bone to the inner ear (bypassing the outer and middle ear) (Brain Camp)

Question 102

Where are the electrodes placed for BAER recording?

Answer 102

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)

Question 103

What BAER peak is large and positive, present at about 1ms?

Answer 103

Peak I * Peak I for bone conductor stimulus will be sooner than earphone stimulus * Each successive peak occurs at \< 1ms intervals * Latency is measured from the beginning of the stimulus to the positive peak of the wave * Amplitude is measured from the peak of the wave to the nadir of the following negative trough (Brain Camp)

Question 104

What is the BAER central conduction time?

Answer 104

Interpeak latency between peak I and V = central conduction time * Interpeak latency for I and III - approximate time required for the activity created in the auditory nerve to arrive at the level of the pons (Brain Camp)

Question 105

For most BAER stimulus intensities/rates, what three waves will have a lg amplitude

Answer 105

For most stimulus intensities and rates, waves I, II and V in dogs have lg amplitudes Waves III, IV and VII have smaller amplitdes Same basic pattern occurs in cats (except that wave II may be larger than wave I) (Brain Camp)

Question 106

How does the BAER produced from bone transducer differ from air conducted?

Answer 106

Bone conducted - same basic waveform configuration as air conducted BAER with some reduction in amplitude Wave latencies of the responses to bone-conducted clicks may vary somewhat more between animals than air conducted clicks Skull impedance differences account for differences in attenuation of the bone conduction from the mastoid process to the cochlea Useful in predicting auditory capabilities following resection of external ear canals in dogs (Brain Camp)

Question 107

What changes are seen associated with postnatal maturation of the canine BAER?

Answer 107

Altricial species - significant postnatal maturation of the BAER * Ear canal opening at day 12-13 * Prior to this, essentially conduction deafness * During maturation, peak latencies shorten, amplitude increases * Waves I and II are the first to appear after birth, particularly well developed during maturation * Wave V is later about 40 days * BAER is mature by about 8 weeks (Brain Camp)

Question 108

How does head size affect BAER peaks?

Answer 108

Head size has a minor effect on peak amplitudes (larger peak amplitude with small head) Head size does not affect latencies (Brain Camp)

Question 109

How does body temperature affect BAER recording?

Answer 109

Body temp changes within normothermic zone - no effects Hypothermia prolongs peak latencies and responses disappear in mammals at 20C (Brain Camp)

Question 110

BAER - if the stimulus intensity is gradually lowered, which peak will be the last to disappear?

Answer 110

Peak V - most reliable peak

Question 111

What BAER wave will be absent in conductive hearing disorder?

Answer 111

Wave I \*\* Wave I can still be present, can be at a longer latency or reduced amplitude The interpeak latencies may be within normal limits - once the activity gets started, it travels through the neuroaxis at a normal pace (Brain Camp)

Question 112

Cochlear agenesis - What will BAER look like?

Answer 112

Cochlear agenesis -- organ of Corti not present at birth BAER is not recordable (Brain Camp)

Question 113

5 breeds with high prevalence of congenital sensorineural deafness?

Answer 113

Dalmation Dogo argentino Australian Cattle Dog Bull Terrier English Setter (Brain Camp)

Question 114

What is the term for age-related hearing loss?

Answer 114

Presbycusis * High frequencies affected first, then lower frequencies * Decrease in the BAER click stimulus threshold can be detected * Effects are more noticeable with tone burst BAER or otoacoustic emissions testing * BAER at typical screening intensities will not show clear aging effects * BAER latencies can increase and amplitudes eventually decrease (changes are subtle) * Studies of aging cats have shown little if any presbycusis (Brain Camp)

Question 115

What medication is the most common cause ototoxicity?

Answer 115

Gentamicin - Toxicity is unpredictable, does not appear to be dose dependent Hearing loss may result from a single exposure, or not until some weeks after the termination of treatment BAER will be flat (Brain Camp)

Question 116

What are the OFA guidelines for BAER?

Answer 116

Question 117

What anatomic structures are believed to generate the middle-latency potentials of the auditory evoked response?

Answer 117

Medial geniculate nucleus Thalamic nuclei Auditory cortex The middle latency response is more labile than the brainstem response, and is greatly affected by anesthesia Nearly all the studies of MLR in animals have been directed toward defining the neural generators, less attention on waveform characteristics ((Brain Camp)

Question 118

What is the otoacoustic emission test?

Answer 118

Test of hearing Otoacoustic emission = sound emitted by the ear either spontaneously or evoked by a stimulus sound Sound stimulus introduced into the ear canal --\> the machine contains a speaker to emit the stimulating sound, and a microphone to record the returning OAE 2 types can be measured: distortion product (DOAE) or transient evoked OAE Benefits: quick, handheld, low cost Requires unobstructed ear canal/middle ear, functioning cochlea, quiet recording environment (Brain Camp)

Question 119

What test can be used to evaluate the condition of the middle ear, mobility of the tympanic membrane and ossicles?

Answer 119

Tympanometry This is NOT an electrodiagnostic test

Question 120

BAER - positive activity at the vertex should produce an (upward/downward) deflection

Answer 120

Upward (Cuddon)

Question 121

What BAER amplitude ratio can be used to determine the presence of brainstem disease?

Answer 121

Wave V/wave I amplitude ratio (Cuddon)

Question 122

What differences are seen between BAER waves from mastoid vs. T1 reference?

Answer 122

Mastoid reference: * I, II, and V have lg amplitude * III, IV, and VI have smaller amplitudes * Dogs - waves III and IV - commonly form a single wave (III predominates) * sometimes IV and V form a single wave (V predominates) * VII infrequently identified T1 reference * I and II are smaller in amplitude * I has slightly longer latency - 1.12msec * Wave II for T1 reference occurs at about same time as wave III for mastoid reference - debatable if this wave is II or III * V is much larger, deep trough following peak * IV almost always separate peak (Brain Camp) * Subpeaks are very common (waves IIa, IIIa, IVa)

Question 123

How does changing the BAER stimulus rate affect the tracing?

Answer 123

Increase in rate --\> decrease in wave amplitude and increase in latency Waveform latencies of BAER are very stable from /sec - 50/sec

Question 124

What is the postnatal maturation for cat BAER?

Answer 124

Hearing occurs at a mean age of 5 days, cochlea functionally mature at 1 month * Evoked response appear in auditory cortex at 5-10d of age * Click stimulus - BAER latency decrease linearly from 7-18 days, followed by an exponential stage * Adult latency reached at 3 weeks * Wave I latency reaches maturity first (Cuddon)

Question 125

What are the possible findings on BAER with brain death? (3)

Answer 125

* Complete loss of all waves * Most common finding * Loss of wave I probably due to cessation of intracranial blood flow * Supratentorial lesion --\> isoelectric BAER --\> confirms brain death * Infratentorial lesion --\> isoelectric BAER - does NOT confirm brain death * Wave I preserved * Wave I and II preserved

Question 126

Where should the auditory evoked response middle latency potentials be recorded from? What are the most common waves identified in dogs?

Answer 126

Recorded from the vertex Referenced to the ipsilateral mastoid region Most common waves: N_o, P_o, N_a, P_a, N_b, P_b P means positive, N means negative A positive peak Px with a latency of 28 - 33msec occurs between Pa and Pb in 50% of dogs (Cuddon)

Question 127

What factors can influence the waveform of middle latency potentials of the auditory evoked response

Answer 127

Stimulus rate Ambient background noise Conscious state of the animal In dogs, wave amplitudes are more variable from dog to dog than latencies Stimulus intenSITY does not have as great of an effect on waves when compared to BAER (Cuddon)

Question 128

What is a term that describes the electrical responses occurring in different parts of the cochlea?

Answer 128

Cochlea microphonics Does NOT include the acoustic nerve (Cuddon)

Question 129

When do cochlear microphonics appear on the BAER How are they best eliminated? How are they best observed?

Answer 129

Occur just prior to waveform I Alternating stimulus polarity cancels out cochlear microphonics Pure tone stimulus with condensation or rarefaction stimulus polarity will make them easiest to see \*\* Cochlear microphonics are not affected by anesthesia and MAY BE present after death Cochlear microphonics are absent in animals with congenital deafness where the cochlea is lacking an organ of Corti and hair cells (Cuddon)

Question 130

How can you determine if an wave on the BAER is cochlear microphonics or wave I?

Answer 130

Reverse stimulus polarity --\> wave I will not change polarity but cochlear microphonics will (Cuddon)

Question 131

NCV - What strength of stimulus do you want? F wave - what strength of stimulus do you want? M wave and H wave?

Answer 131

MNCV and F wave - All waveforms should be recorded at supramaximal stimulus strength (50% over the stimulus that is required to activate all neurons) - to ensure the entire pool of axons in a particular nerve is being evaluated M wave and H wave - submaximal stimulus (Cuddon)

Question 132

What are the primary sites of motor nerve conduction studies in the thoracic limb and pelvic limb?

Answer 132

Thoracic limb: ulnar or radial (sometimes median) Pelvic limb: Sciatic-tibial (sometimes peroneal) Cranial nerves: Facial, recurrent laryngeal (Cuddon)

Question 133

What 4 measurements should be evaluated for motor nerve conduction studies?

Answer 133

1. Motor nerve conduction velocity 2. CMAP amplitude (peak to peak) 3. CMAP duation 4. CMAP area (Cuddon)

Question 134

Dog with myopathy * CMAP amplitude? Duration? area? * MNCV?

Answer 134

MNCV will be normal CMAP amplitude and area will be decreased, duration will be increased (Cuddon)

Question 135

Causes of CMAP amplitude decrease?

Answer 135

Myopathy Prejunctional neuromuscular disease (botulism) Primary axonopathy (Cuddon)

Question 136

\_\_\_\_\_\_\_\_\_\_ is used to assess the degree of myelination of the fastest conducting fibers

Answer 136

Motor nerve conduction velocity Know how to do this by hand!! (Cuddon)

Question 137

\_\_\_\_\_\_\_\_\_\_\_\_\_\_ is electrodiagnostic calculation used to assess the distal aspect of the nerve and the intramuscular branches

Answer 137

Residual latency Measure of the collective delay through the fine intramuscular motor branches and neuromuscular junction (Cuddon)

Question 138

MNCV: A proximal stimulus gives rise to an evoked potential of longer duration and lower amplitude than a distal stimulus What is this called?

Answer 138

Physiologic temporal dispersion * Occurs as the 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 the slow fibers) (Cuddon)

Question 139

How does age influence motor nerve conduction velocity? Temp? Limb length?

Answer 139

Age: significant influence on MNCV * MNCV reaches adult value @ 6mos - 1yr * 10x increase in MNCV during maturation, greatest increase occurring during birth and 4-5 weeks of age * Gradually slows after about 7 years old, 10y - MNCV is 10-15% slower Temp - 1C decrease I'm temp --\> decrease MNCV of 1.7 - 1.8m/s (dog) Limb length - longer limb length --\> longer tapered segment of nerve --\> slower MNCV and smaller CMAP amplitude, longer CMAL duration (Cuddon)

Question 140

Which calculation, CMAP amplitude or area, is a better index of the number of available functioning axons?

Answer 140

CMAP area - takes into account the width of the CMAP and thus includes the contribution of slower conducting motor axons (Cuddon)

Question 141

Causes of decreased CMAP amplitude (generalized, w/o temporal dispersion) (3)

Answer 141

1. Generalized axonopathy (CHP/APN) 2. Severe myopathy (polymyositis, lipid storage myopathies) 3. Decreased neuromuscular transmission (botulism) (Cuddon)

Question 142

3 causes of slow MNCV with normal CMAP?

Answer 142

1. Demyelination * Fel diabetic neuropathy * Globoid cell leukodystrophy 2. Severe demyelination involving many myelinated fibers of varying diameters also commonly produces temporal dispersion and polyphasia of CMAPs (desynchronization) * Cats with Niemann-Pick disease-associated polyneuropathy 3. Axonopathy in which there is a complete loss of fastest conduction fibers --\> slowed conduction velocity * Usually also an accompanying decrease in CMAP amplitude of \> 40-50%, in addition to severe EMG abnormal spontaneous activity (Cuddon)

Question 143

\_\_\_\_\_\_\_\_\_\_\_ is decreased proximal vs. distal CMAP amplitude (\>50%) without significant temporal dispersion and polyphasia

Answer 143

Conduction block * Causes: * Demyelination - loss of 2+ consecutive internodes * Seen in cats with diabetic neuropathy * Neuropraxia - metabolic disturbance of nerve with preservation of the axon * Axonotmesis - incomplete Wallerian degeneration * Nerve impulses are prevented from traversing this area, even though more distal regions still conduct * Conduction is possible below the point of the block (Cuddon)

Question 144

Nerve conduction study: CMAP temporal dispersion + polyphasia indicates?

Answer 144

Demyelination (Cuddon)

Question 145

Causes of conduction block?

Question 146

Supramaximal antidromic motor nerve activation, and the resulting long-latency muscle action potential - this describes what electrodiagnostic test?

Answer 146

F wave * When the antidromically conducted nerve impulse reaches the ventral horn cell body, it initiates a secondary orthodromically conducted signal --\> Arrives at the muscle several ms after the M wave * F waves represent a purely MOTOR event – they are a means of assessing the VENTRAL ROOT and the most proximal portion of mixed/motor nerves * Also provides a measure of motor neuron excitability (Cuddon)

Question 147

What are the 3 benefits of F wave over M wave? Downside to the M wave?

Answer 147

1. When assessing F waves, borderline abnormalities in motor nerve function are magnified * Longer pathway being tested compared with that of the M wave 2. F wave latencies have a narrower normal range than routine MNCVs * More subtle conduction changes can be found 3. F-wave assessment is a much more precise tool to assess polyneuropathies or injuries that affect proximal segments only * And to assess functionally abnormal ventral horn cell utilization time Downside to F-wave assessment: Inherent variability in wave latency and configuration - makes direct assessment of F-wave latency and amplitude between dogs less precise than that of the M wave (Cuddon)

Question 148

Why is it believed that the F wave represents larger motor neurons with faster conducting axons?

Answer 148

These nerves are less likely to have failure of the orthodromic impulse to pass back through the axon (Cuddon)

Question 149

How does a proximal nerve stimulation site influence the latency of M wave and F wave?

Answer 149

Latency of M wave - increases Latency of F wave - decreases (Cuddon)

Question 150

What is the formula for F ratio? What does increased vs. decreased vs. normal ratio indicate?

Answer 150

F ratio = [Lat (F) - Lat (M) - 1] / [2x Lat (M)] Measurement of conduction of the proximal segment time / distal segment Does not require measurement of limb length * F ratio \> reference value --\> more severe involvement of the proximal segment * F ratio \< reference value --\> more severe involvement of the distal segment * F ratio = reference (but abnormalities have been found in nerve root/peripheral nerve function) --\> neuropathy is distributed equally between the proximal and distal nerve segments (Cuddon)

Question 151

What causes F wave chronodispersion?

Answer 151

* Variable latency between F waves * Caused by demyelinating neuropathies (Cuddon)

Question 152

What is the axon reflex?

Answer 152

Also called A wave Intermediate latency response that occurs between the M and F wave Most likely represents the presence of collateral sprouting in the proximal portion of the nerve Usually will be seen with submaximal stimuli (sufficient to excite one branch of an axon, not the other) Antidromic impulse travels up to the branching point --\> turns distally along the second branch Abolished by supramaximal stimulus (Cuddon)

Question 153

CDP: recording site for hind limb vs. forelimb? Where is the reference?

Answer 153

Peroneal/tibial stimulation --\> record @ interarcuate ligament of L4/5 (or dorsal lamina) Radial/ulnar stimulation --. record @ interarcuate ligament of C7/T1 (T1 dorsal lamina) Reference - SQ at same spinal cord level, contralateral side (Cuddon)

Question 154

What is the neural generator of the initial triphasic spike of the CDP?

Answer 154

Extracellular events associated with propagation of sensory AP into the spinal cord Proximal mixed nerve stimulation – antidromic motor component may have some involvement in this wave 1) Positive capacitance current generated at node of ranvier --\> initial positivity 2) Depolarization of axolemma --\> influx of Na into the axon --\> extracellular space negatively charged --\> negative component of triphasic spike 3) Efflux of K+ from the axon into the extracellular space --\> final small positive phase (Cuddon)

Question 155

What are the neural generators of the large negative peak of CDP, then prolonged positive wave?

Answer 155

* Lg negative peak = actual CDP * Often contains 1-2 smaller sub peaks * Represents changes in the extracellular environment produced by dorsal horn interneuron activity * Na enters the cell bodies at the synapses and exits into the extracellular space along their ventrally projecting axons * Produces a negative charge at the dorsal horn and a positive charge at the ventral horn * In some recordings, there is a small spike on the initial upward deflection of the large positive peak * This is the intramedullary spike – represents propagation of action potentials from the primary afferent fibers to the afferent termini * Final prolonged positive wave = extracellular representation of primary afferent depolarization * Positive current exits the extracellular space at the excited axo-axonal (dorsal nerve root-interneuron) synapses and reenters along the primary dorsal nerve root afferents * Produces a positive charge in the dorsal aspect of the spinal cord (Cuddon)

Question 156

How does stimulation of a more proximal nerve influence the waveform of CDP?

Answer 156

Stimulation of a more proximal nerve --\> recruits more axons --\> larger waveform Disadvantages of proximal stimulation: * Increase in limb motion and muscle contraction (can use paralytic) * Greater ascending compounding AP obscuring the CDP * Latency difference between the orthodromic sensory, and antidromic motor conduction volleys becomes negligible --\> false representation of antidromic motor nerve AP in the initial triphasic peak

Question 157

What kind of stimulus intensity is used for CDP?

Answer 157

Supramaximal stimulus (Cuddon)

Question 158

What parameters are evaluated for CDP?

Answer 158

CDP latency CDP onset to peak latency difference (Cuddon)

Question 159

The largest sensory fibers in a mixed peripheral nerve are the?

Answer 159

1A fibers originating from the muscle spindle In a monosynaptic arc, these fibers synapse directly with the LMN (Cuddon)

Question 160

What strength of stimulus is used to elicit the H reflex?

Answer 160

Submaximal stimulus As stimulus becomes supramaximal, the H reflex is cancelled and replaced by the F wave Optimal elicitation of the H reflex requires maximum stimulation of the group 1A afferents, without spontaneous stimulation of motor fibers The F wave can only be recorded from the palmar interosseous muscles (ulnar nerve) or plantar interosseous muscles (tibial, caudal cutaneous sural nerve) (Cuddon)

Question 161

What factors does the amplitude of the H reflex depend on?

Answer 161

H reflex depends on: * Strength of electrical stimuli * Excitability of the alpha motor neurons Variations in the H reflex amplitude provide a measure of excitability changes in the motor neuron (if constant stimuli are delivered) (Cuddon)

Question 162

What kind of electrodes need to be used for sensory nerve conduction?

Answer 162

Needle electrodes - significantly reduce signal to noise ratio (Cuddon)

Question 163

How does the amplitude of a SNAP compare to the CMAP?

Answer 163

SNAP is much smaller amplitude than CMAP (Cuddon)

Question 164

How is SNCV calculated?

Answer 164

SNAP latency - distance from cathodal stimulating electrode to active electrode divided by time measured from the onset of the stimulus artifact to the initial positive peak expressed as m/s (Cuddon)

Question 165

What are the most common sensory and mixed nerves studied in animals for SCNV?

Answer 165

Lateral superficial radial nerve Superficial peroneal nerve Saphenous nerve Distal tibial nerve Proximal tibial and ulnar nerves (Cuddon)

Question 166

How does age affect SNCV?

Answer 166

Dog: SNCV reduced by 10m/s in animals \> 9 years of age Cat - SNCV remain stable at least until 10y of age (published data later than that very limited) (Cuddon)

Question 167

Peripheral sensory nerve injury below the DRG --\> what kind of SNCV and CDP will be recorded? Sensory nerve avulsion from the spinal cord above the DRG --\> what kind of SNAP and CDP will be recorded?

Answer 167

Injury below the DRG --\> SNAP and CDP absent Injury above DRG --\> intact SNAP, absetn CDP (Cuddon)

Question 168

What is the general protocol for repetitive nerve stimulation?

Answer 168

Stimulate nerve @ 1, 2, 3, 5, 10, 20Hz --\> record CMAP Compare area of CMAP #1, to area of CMAP 3 or 4, 5 and 10 --\> express as @ decrement \* important to use AREA instead of AMPLITUDE due to pseudofacilitation % decrement \> 10 --\> abnormal (MG)

Question 169

What is the best choice of muscle/nerve for repetitive nerve stimulation?

Answer 169

Small motor units are more susceptible to transmission failure (since they have \> % of low-efficiency synapses) Recommended: ulnar-palmar interosseous muscle + tibial-plantar interosseous combination More proximal muscles have greater safety factor - ability of neuromuscular transmission to remain effective under various physiological conditions and stresses. This is a result of the amount of transmitter released per nerve impulse being greater than that required to trigger an action potential in the muscle fiber (Cuddon)

Question 170

What are the criteria for RNS facilitation?

Answer 170

Both amplitude and area of CMAP increase Associated with botulism in horses and humans Botulism: Lower RNS rate --\> decremental response High RNS rate --\> facilitation (Cuddon)

Question 171

How does RNS response change with age?

Answer 171

Maturation of neuromuscular transmission in the dog is largely completed by 2 mos of age No age-related differences in 2-18 mos in the function of the neuromuscular end plate Same criteria for determination of determination of neuromuscular blockade (decrement \> 10% at low frequency stimulation) should be used in young dogs suspected of having congenital MG (Cuddon)

Question 172

What test is the best technique for assessing neuromuscular transmission?

Answer 172

Single-fiber EMG * Concentric stimulating needle electrode w/ recording site consisting of a small port, positioned 2mm from the tip * Axonal stimulation --\> record individual myofiber action potentials * Calculate the mean of consecutive differences in latency * Peroneus longus has been used because of the ease in locating its motor point (just distal to the head of the fibula) (Cuddon)

Question 173

What affects jitter of single fiber EMG?

Answer 173

1. Variation in axonal conductance velocity 2. Variation in myofiber propagation velocity 3. Variation in neuromuscular transmission time (largest contribution) Neuromuscular junction disease with decrease in the end plate potential amplitude --\> increased jitter (Cuddon)

Question 174

Facial reflex testing: what nerves are stimulated and what response is monitored?

Answer 174

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)

Question 175

What are the components of the facial reflex evoked response and what contributes to them?

Answer 175

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)

Question 176

What is direct facial nerve stimulation?

Answer 176

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)

Question 177

What is the trigemino-trigeminal reflex?

Answer 177

Stimulation of the middle mental nerve or infraorbital nerve --\> CMAP in the rostral digastricus measured A polyphasic potential will be produced (Cuddon)

Question 178

What are the electrode sites for the canine facial reflexes?

Answer 178

Question 179

What are the neural generators of the cortical SSEP?

Answer 179

Field potentials arising from the cerebral cortex around the cruciate sulcus and parietal region Pathway: White matter of the spinal cord ipsilateral to the stimulation site --\> decussates in the medulla --\> contralateral medial lemniscus --\> thalamus --\> cerebral cortex Later waves of the cortical SSEP - little clinical use since their presence and amplitudes are strongly influenced by responsiveness of the animal and sedative or anesthetic drugs (Cuddon)

Question 180

What is the morphology of the cortical SSEP? How does the size of the animal influence the amplitude and latency of the cortical SSEP?

Answer 180

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)

Question 181

Stimulating sites for cortical SSEP?

Answer 181

Cat – results published for tibial, pudendal, median, sural, and sciatic nerves Dog – results published for tibial, ulnar, median, and radial nerves * Tibial nerve – hock * Pudendal nerve – caudal rectal branch of the pudendal nerve * Median nerve – medial to the flexor tendons on the caudo-medial surface of the antebrachium (just above the carpus) * Lateral and medial superficial radial nerves – medial to the lateral cephalic vein just above the carpus * Ulnar nerve – lateral to the flexor tendons on the caudolateral surface of the antebrachium, just above the carpus Stimulus intensity should be just sufficient to produce a small twitch of the foot/sphincter (Cuddon)

Question 182

Where should the recording electrodes be placed for cortical SSEP?

Answer 182

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)

Question 183

What parameters of the cortical SEP are analyzed?

Answer 183

Amplitude and latency (although vary based on size of the animal) Body temp will also significantly influence these parameters

Question 184

What parts of the nervous system do cortical SEPs evaluate?

Answer 184

Cortical SSEPs evaluate the central conduction time and integrity of the somatosensory system Clinical application: * Detection of central demyelinating disorders * Indicator of the level of anesthesia * Cortical function following head trauma * Spinal cord integrity * Cortical SSEP can provide information only about the laterality of a lesion, limited use in locating the level of the lesion (Cuddon)

Question 185

What are the 2 circumstances that create voltage? What is Ohm's Law?

Answer 185

Charge is separated (capacitance) Current flows through an impedance Ohm's law: voltage = current \* impedance Impedance may be resistance or capacitance The voltage across a resistor = current \* resistance (Strain Brain Camp)

Question 186

What are the causes of biologic impedance?

Answer 186

1. Current flow in the tissue 2. At the electrode-tissue interface 3. In the electrodes 4. In the input to the amplifier (Strain Brain Camp)

Question 187

How does the electric field increase/decrease in relation to the distance from the source?

Answer 187

The electric field decreases as the square of the distance from the source (decreases by 1/r²) Hypothetical charge in the cortex recorded either @ cortex surface (r = 2mm), or on the scalp (r = 10mm), the ratio of the electric field measurements would be 1/25 --\> a 5x increase in measurement distance (from 2 --\> 10mm) causes a 25x decrease in amplitude from a charge in free space (Strain Brain Camp)

Question 188

How does distance from the source influence voltage amplitude?

Answer 188

The further the measurement from the source, the smaller the measured voltage amplitude @ 1/r² where r is the distance from the dipole This will influence the required signal amplification, and if averaging of multiple responses is being performed, will increase the number of necessary averages to unmask the buried response (Strain Brain Camp)

Question 189

How does tissue surrounding the electrical signal influence the voltage?

Answer 189

There are voltage drops across intervening tissues because the charges are not in free space Ex/ EEG recording - the cerebral cortex, CSF, skull, and scalp have an approximate resistance of 12k-ohm This resistance, combined with the impedance of the electrode-tissue interface and the resistance of the electrode, will act as a voltage divider with the input impedance of the system amplifier The input impedance of the amplifier needs to be significantly greater than the combined other resistances, so that the voltages across them are small compared to the voltages across the amplifier (which is the portion of the signal we ultimately will be measuring) (Strain Brain Camp)

Question 190

Recording artifact causes disruption of \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_

Answer 190

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

Question 191

What are possible causes of artifact in electrodiagnostics? What 2 techniques greatly reduces artifacts?

Answer 191

1. Patient induced artifacts such as muscle artifact, blink, movements, sweating 2. Electrophysiologic activity from tissues not under investigation (EKG) 3. Electrode artifacts from improper electrode application or defects 4. "Airborne" electrical signals such as electric monitors, heating pads, cautery other 5. AC line interference caused by improper grounding and other nearby poorly shielded electrical instruments 6. Instruments electrically connected to the patient such as a respirator, pacemaker, IV pump, and others Techniques to reduce artifact 1. Implementation of differential recording in clinical electrodiagnostic systems - 2 electrodes from a subject are connected to an amplifier which subtracts the signal at one electrode from the signal at the other * Any signal common to both electrodes (such as 60Hz artifact) cancels or is greatly reduced * Only the activity that differs between the electrodes is amplified 2. Band-pass filter * High pass filter - permits passage of frequencies above the filter value (or exclude frequencies below the filter value) * Low pass filter - permits passage of frequencies below the filter value (excludes frequencies above the filter value) (Strain Brain Camp)

Question 192

How does signal-to-noise ratio change with the number of averages?

Answer 192

The signal to noise ratio improves with the square root of the number of averages, but there is a practical limit to the improvement seen with increasing the number of averages In general, the smaller the signal, the more averages will be needed (Strain Brain Camp)

Question 193

What is the advantage to bipolar needle electrodes?

Answer 193

They detect signal activity from a greatly reduced tissue volume, allowing a more precise localization of the signal (Strain Brain Camp)

Question 194

Electrodiagnostic findings in feline diabetic neuropathy?

Answer 194

* Decreased thoracic and pelvic limb MNCV and SNCV * Increased F wave latency * Increased cord dorsum potential latencies * EMG abnormalities In general PL worse than TL and motor worse than sensory (VCNASAP Dickinson)

Question 195

What 3 components does the F ratio calculation involve?

Answer 195

M latency Min F latency Ventral horn cell utilization time (Brain Camp)

Question 196

\_\_\_\_\_\_\_\_ is an antidromic motor potential that triggers a second orthodromic potential

Answer 196

F wave (Brain Camp)

Question 197

What is pseudofacilitation in regards to CMAP?

Answer 197

When performing RNS - synchronization of individual fiber potentials --\> increased CMAP amplitude but the area remains the same (Brain Camp)

Question 198

T/F: CDP are mixed potentials consisting of a conductive volley + field potential

Answer 198

True (Brain Camp)

Question 199

The biological signal with the largest signal frequency range, and thus requiring the highest low pass filter setting, is the:

Answer 199

Evoked potential (Brain Camp)

Question 200

Ways to reduce 60Hz artifact? (5)

Answer 200

1. Using a ground electrode 2. Notch filtering 3. Using a differential amplifier 4. Balanced and low electrode impedances 5. Do not place the animal on a metal surface (Brain Camp)

Question 201

Sensorineural deafness: * Congenital * 2 hereditary causes * 3 acquired causes * Later onset * 2 hereditary causes * 7 acquired causes

Answer 201

Sensorineural deafness: Congenital hereditary - pigment associated (long-list), non-pigment associated (Doberman, Puli) Congenital acquired - perinatal anoxia, dystocia, intrauterine ototoxin exposure Later onset hereditary - non-pigment associated (Rhodesian Ridgeback, Border Collie) Later onset acquired - Ototoxin, otitis interna, presbycusis, noise trauma, physical trauma, anesthesia associated, undetermined (Brain Camp Strain)

Question 202

Conductive deafness * Congenital * 1 acquired cause * (0 congenital) * Later onset * 1 hereditary cause * 7 acquired causes

Answer 202

Conductive deafness: 1 congenital acquired cause - ear canal atresia 1 later onset hereditary cause - PSOM 7 later onset acquired - otitis externa, otitis media, cerumen impaction, ear canal inflammation, ear canal foreign body, middle ear polyp, otosclerosis (Brain Camp)

Question 203

Ototoxic drugs/chemicals?

Answer 203

1. Aminoclygoside antibiotics 2. Diuretics - furosemide 3. Anti-neoplastic agents - actinomycin, cisplatin, nitrogen mustard, vinblastine, vincristine 4. Non-aminoglycoside antibiotics - see pic 5. Antiseptics - see pic (chlorhexidine, iodine) 6. Misc agents - ceruminolytic agents, digoxin, insulin, KBr, prednisolone, (Brain Camp - strain)

Question 204

What test can be used to evaluate the size of the internal ear, integrity and compliance of the tympanic membrane, and function of the middle ear components?

Answer 204

Impedance audiometry-tympanometry (Dewey)

Question 205

What is measured in impedance audiometry tympanometry and how is it measured?

Answer 205

Tube is inserted into the externa auditory canal --\> delivers an auditory stimulus and pressure changes Ear canal is sealed and the changes in pressure reflected back from the tympanic membrane inside the sealed cavity are measured The curve of the tmpanogram will tell the examiner information aout the COMPLIANCE of the tympanic membrane Damage to ossicles --\> abnormally high compliance (flabby tympanic membrane) Otosclerosis --\> abnormally low compliance (stiff TM) (Dewey)

Question 206

EEG artifact?

Answer 206

Muscle (Brain Camp)

Question 207

EEG artifact?

Answer 207

MUAP (Brain Camp)

Question 208

EEG artifact?

Answer 208

Eye movement (Brain Camp)

Question 209

EEG artifact?

Answer 209

Electrode out (Brain Camp)

Question 210

EEG artifact?

Answer 210

60hz (Brain Camp)

Question 211

EEG artifact?

Answer 211

ECG (Brain Camp)

Question 212

EEG - what is the state of consciousness?

Answer 212

Awake OR REM sleep (Brain Camp)

Question 213

EEG - what is the state of consciousness?

Answer 213

Drowsy (Brain Camp)

Question 214

EEG - what is the state of consciousness?

Answer 214

Slow-wave sleep = non REM sleep (Brain Camp)

Question 215

EEG - what kind of PD?

Answer 215

Sleep spindles Normal PD (Brain Camp)

Question 216

EEG - what kind of PD?

Answer 216

Vertex sharp wave - normal PD (Brain Camp)

Question 217

EEG - what kind of PD?

Answer 217

Burst suppression (Brain Camp)

Question 218

EEG diagnosis?

Answer 218

Generalized seizure (Brain Camp)

Question 219

The following is an acceptable sedation protocol for EEG for which species? meperidine 5 mg/kg SQ -or- hydromorphone 0.05 mg/kg SQ + acepromazine 0.1 mg/kg IV  OR dexmedetomidine, 5 µg/kg IV

Answer 219

Canine (Brain Camp)

Question 220

The following is an acceptable sedation protocol for EEG for which species? dexmedetomidine, 5 µg/kg IV, alone or with butorphanol 0.1 mg/kg IM

Answer 220

Feline (Brain Camp)

Question 221

The following is an acceptable sedation protocol for EEG for which species? detomidine 5 mg IV for most, may give an additional 2 mg IV, as needed

Answer 221

Equine 2 - 3 mg IV for most ponies (Brain Camp)

Question 222

EEG - what kind of PD?

Answer 222

Multiple spike complex (abnormal PD) (Brain Camp)