Chapter 8 Neurophysiologic Testing for Pain Flashcards Preview

Essentials of Pain Medicine > Chapter 8 Neurophysiologic Testing for Pain > Flashcards

Flashcards in Chapter 8 Neurophysiologic Testing for Pain Deck (73):
1

Electrophysiologic studies indication

are a very sensitive indicator of central and peripheral nervous system involvement but do not indicate underlying disease

2

Conventional Electrophysiologic Tests

Electromyography (EMG), Short-Latency Somatosensory-Evoked Potentials (SSEPs), quantitative sensory testing (QST),
Laser-Evoked Potentials (LEPs), and
Contact Heat–Evoked Potentials (CHEPs)

3

EMG

EMG indicates only a needle examination of muscles. However, EMG is often used to include both needle studies and nerve conduction studies

4

Nerve conduction studies are often referred to by

the letters NCV, with “V” standing for velocity, although nerve conduction
studies measure more than velocity. For clarity, EMG/NCV to indicate the combination of needle electromyography
and nerve conduction studies

5

three most common diagnoses in EMG laboratories

peripheral neuropathy, carpal tunnel syndrome, and lumbosacral radiculopathy

6

EMG/NCV can identify

the anatomic site of injury (anterior horn cell, spinal
root, plexus, nerve, neuromuscular junction, or muscle), the type of neurons or fibers involved (motor, sensory, or autonomic), the nature of pathologic alteration (demyelination,
or axonal degeneration), time course (acute, subacute, or chronic), and severity of injury

7

What is recorded when stimulating a peripheral nerve with supramaximal intensity?

Compound muscle action potential (CMAP) for motor nerve and sensory nerve action potential (SNAP)
for sensory nerve are recorded. The amplitude of action potentials as well as the time from stimulation to response is recorded

8

Latency

the interval between the onset of a stimulus and the onset of a response, expressed in milliseconds.

9

Conduction velocity

obtained by dividing the
distance between two stimulation points (mm) of the same nerve by the difference between proximal and distal latencies (ms). This calculated velocity, expressed in meters per second (m/s) represents the conduction velocity of the fastest nerve fibers between two points of stimulation. It is important to note that studies may be normal if a disorder is limited to small nerve fibers such as Ad and C-fibers.

10

Amplitude of CMAP
Amplitude of SNAP

The amplitude of CMAP is measured from baseline to
negative peak in millivolts, and the amplitude of SNAP is measured from the first positive peak to negative peak in microvolts.

11

Effect of lower temperature on distal latencies, conduction velocities, amplitude of CMAP and SNAP

will prolong distal latencies, reduce conduction velocities, and increase the amplitude of CMAP and SNAP

12

Amplitude of a response when the same nerve is stimulated proximally and distally

The amplitude of a response should be similar when the same nerve is stimulated proximally and distally. A 20% to 50% reduction between distal and proximal stimulation of a motor nerve suggests an abnormal
block in conduction between two stimulation points

13

Conduction block on EMG

Greater than 20% to 40% reduction in area also suggests conduction
block.

14

Temporal Dispersion on EMG

A significant reduction in amplitude from proximal to distal stimulation sites without a reduction in area under the response curve, and a significant increase in
duration (>15%) suggest temporal dispersion resulting
from a relative desynchronization of the components of an action potential, which is due to different rates of conduction
of each nerve fiber. This also suggests nerve pathology
between the proximal and distal stimulation sites.

15

H-reflex

The H-reflex is the electrophysiologic equivalent of a muscle stretch reflex. A sensory nerve is stimulated with submaximal intensity, and a late motor response is recorded owing to reflex activation of motor neurons

16

In adults, H-reflexes are easily obtained from

Soleus muscle and less easily from flexor carpi radialis muscle following the stimulation of tibial and median nerves, respectively. The tibial H-reflex is useful in identifying S1 radiculopathy.

17

F-waves

F-waves are late response recorded from muscle after
supramaximal stimulation of a motor nerve. F-waves represent a response to a stimulus that travels first to and then from the cord via motor pathways; thus, F-waves are useful in studying the proximal portion of motor nerves

18

Repetitive nerve stimulation (RNS) studies

are used primarily for evaluation of neuromuscular junction disorders like myasthenia gravis.

19

Needle examination electrical activity

The electrical activity is evaluated by sight and sound, as specific activities have specific wave forms and characteristic sounds

20

Insertion activity

Insertion activity, also referred to as injury potential, is caused by movement of the needle electrode, resulting in mechanical damage to the muscle fibers. Increased insertion activity consists of unsustained fibrillation potentials and positive sharp waves. A muscle at rest should be electrically silent. Spontaneous activity in a resting muscle usually suggests a pathologic condition

21

What happens as a muscle contracts?

motor unit action potentials
(MUAPs) are observed. MUAP represents the summation of muscle fiber action potentials of a given motor unit. With increasing voluntary muscle contraction, individual
motor units fire more frequently, and more motor units are recruited to fire. The term “onset frequency” is used to describe the firing rate of a single MUAP maintained at the lowest voluntary muscle contraction (normally ,10 Hz).

22

Recruitment frequency

defined as the frequency of first MUAP when the second MUAP is recruited (normally ,15 Hz). A reduced number of MUAPs (high recruitment frequency) can be seen in neuropathic processes. An increased
number of MUAPs (low recruitment frequency),
however, can be seen in myopathic disorders or defects of the neuromuscular junction

23

MUAPs are analyzed in terms of

amplitude, duration, number of phases, and stability.

24

The morphology of the MUAPs is affected by

the type of needle electrode used, location of the needle within the motor unit territory, age, temperature, and specific muscle being examined.

25

In general, changes in conduction, either a prolonged distal latency or a low velocity, suggest a

pathologic lesion between the site of stimulation and the recording site.

26

PATHOPHYSIOLOGY: IS THE LESION AXONAL
OR DEMYELINATING?

If an injury occurs at the cell body or axon, axonal degeneration results. If an injury is directed against the myelin, demyelination ensues

27

Demyelinating neuropathies

Demyelinating neuropathies
can be further divided into segmental (acquired) and
uniform (hereditary) types. In the former, nonuniform
slowing in individual myelinated nerve fibers results in conduction block and temporal dispersion. In the latter, prolonged latency and slowing of conduction predominate as a result of uniform involvement of all myelinated fibers

28

FIBER TYPE SPECIFICITY: IS THE LESION MOTOR, SENSORY, OR AUTONOMIC?

In a case of distal sensory or motor neuropathies,
amplitudes as well as velocities are abnormal.
With a dorsal root ganglia lesion or anterior horn cell disease, NCV studies show small amplitude SNAP or CMAP, respectively, and as a rule normal velocity. Routine EMG/ NCV studies do not test the integrity of the autonomic nervous
system

29

DISTRIBUTION: IS THE LESION FOCAL, MULTIFOCAL, OR DIFFUSE?

neuropathy, for example, can be further divided into mononeuropathy, multifocal neuropathy, and polyneuropathy

30

A multifocal disorder is suggested

If the same nerve is affected disproportionately in
the opposite limb or one nerve is affected more than the other in the same limb,

31

In a fully developed polyneuropathy,

motor and sensory
nerves in both upper and lower extremities are affected in equal and symmetrical fashion

32

CHRONICITY: HOW OLD IS THE INJURY?

Following an axonal injury, the nerve distal to the lesion undergoes Wallerian degeneration. For the first 2 to 3 days, motor conductions distal to a lesion will be normal. Then CMAP amplitude drops progressively, reaching a
nadir at about 7 days. SNAP amplitudes distal to a lesion
are unaffected for 5 to 6 days but by day 10 to 11, the nadir is reached.

33

What happens after an axonal motor nerve injury?

EMG findings will change slowly. Initially, insertional activity is increased. Positive sharp waves and fibrillation potentials may not occur for 2 to 3 weeks following a nerve injury, depending on the length between site of nerve injury and corresponding muscles. The abnormal spontaneous activity can resolve in 3 to 6 months. Therefore needle studies performed less than 2 to 3 weeks after injury, or later than 3 to 6 months after injury, may be normal.

34

Large-amplitude,
long-duration polyphasic MUAPs seen in

denervation and reinnervation develop 3 to 6 months after an injury

35

SEVERITY AND PROGNOSIS: HOW BAD
IS THE INJURY?

The amplitude difference
between the same nerve on affected and unaffected sides gives an idea of extent of injury and potential recovery if they are determined sequentially.

36

A paucity of spontaneous activity in affected muscles 3 weeks after injury indicates

an excellent outcome for the return of muscle function.

37

Markedly reduced recruitment of MUAPs indicates

severe lesion except for neurapraxia.

38

The quantitative sensory test (QST)

provides a quantitative
measure to detect large and small fiber dysfunction.

39

“sensory detection threshold”

define as “the smallest stimulus that can be detected at least 50% of the time.” By increasing and decreasing stimulus intensity from the predetermined level, “appearance” and “disappearance” thresholds can be determined.

40

Sensory modalities commonly used are

vibration and thermal senses—warm, cold, heat pain, and cold pain. The vibration threshold measures large myelinated fiber function, whereas warm, heat pain, and cold pain thresholds reflect the function of unmyelinated C-fibers. The cold threshold measures small myelinated Ad fiber function

41

QST measures

not only peripheral nerve fiber function but also central pathway function. Vibratory sense is carried by the dorsal columns and thermal senses via the spinothalamic tract

42

a feature of complex regional pain syndrome.

Cold or heat hyperalgesia

43

Features of the CCC syndrome

Cold hypoesthesia, cold hyperalgesia, and cold limb are features of the CCC syndrome

44

typical manifestations of postherpetic neuralgia

whereas thermal hypoesthesia and hyperalgesia (anesthesia dolorosa) are typical manifestations of postherpetic neuralgia

45

Advantages and Disadvantages of QST

QST allows early detection of disease. Sequential testing
can be used to monitor disease progression and therapeutic
efficacy. However, QST is not objective and relies on patient cooperation. QST does not localize a lesion, as it tests the integrity of the entire sensory pathway from nerve ending to cortex

46

Conventional sensory NCV vs. SSEPs

Conventional sensory NCV studies assess a lesion distal to
the dorsal root ganglion. SSEPs provide a quantitative
measure to study the entire sensory pathway

47

SHORT-LATENCY SOMATOSENSORY- EVOKED
POTENTIALS

Stimulations are mediated by

Stimulations are mediated by Type Ia and II sensory
afferents, dorsal root ganglion (neuron I), dorsal columns,
gracilis and cuneatus nuclei (neuron II), contralateral
medial lemniscus, ventroposterolateral nucleus of the thalamus (neuron III), and sensory cortex

48

Factors that may alter latency and amplitude

Age, temperature, limb length, medications, level of attention, and sleep may alter latency and amplitude

49

Useful obligate potentials after median nerve stimulation include

EP (Erb’s point), N13 (dorsal column of the cervical cord), P14 (caudal medial lemniscus), N18 (thalamus), and N20 (sensory cortex)

50

Identifiable potentials
after tibial nerve stimulation are

PF (popliteal fossa), LP (lumbar potential), P31 (caudal medial lemniscus), N34 (thalamus), and P37 (sensory cortex)

51

LASER-EVOKED POTENTIALS AND CONTACT HEAT–EVOKED POTENTIALS

A CO2 laser can be used to generate pain-related cerebral
potentials. The laser stimulator produces radiant heat quickly
and activates Ad and C nociceptors. Twenty to 40 stimuli are delivered at the intervals of 6 to 10 s. The late component, which occurs at approximately 220 to 340 ms following stimulation of the hand, corresponds to Ad fiber conduction and the ultra-late component at 800 to 1000 ms corresponds to C-fiber; both components are maximum in amplitude (10–50 mV) at the vertex (Cz).

52

LEPs provide an objective
measure to

assess the function of pain and temperature pathways in patients with neuropathic pain.

53

SSEPs and LEPs in a lesion involving the spinothalamic tract

In a lesion involving the spinothalamic tract including small fiber neuropathy, SSEPs are usually normal but LEPs are abnormal

54

SYMPATHETIC SKIN RESPONSE

A standard method of obtaining SSR is to place a recording electrode on the palmar and plantar surfaces, because these recording sites yield higher amplitudes. A stimulator is placed on either the median or the tibial nerve of the opposite limb, and the stimulus is given randomly at a rate of less than one per minute, and with a
stimulus intensity that is sufficient to cause mild pain. A
minimum of 5 to 10 responses should be recorded, and
SSR responses are obtainable 60% to 100% of the time
in normal subjects.

55

SYMPATHETIC SKIN RESPONSE
waveform

Waveforms are usually triphasic, with an initial small negativity followed by a large positive wave, and a subsequent prolonged negative wave. Waveforms can also be monophasic or diphasic with an initial negative or positive peak.

56

SYMPATHETIC SKIN RESPONSE
amplitude
latencies

Maximal peak-to-peak amplitudes and mean latencies are measured. Amplitude and latency variability can be minimized by reducing stimulus frequency, increasing stimulus intensity, and/or changing stimulus site or mode

57

Factors that attenuate the response of SYMPATHETIC SKIN RESPONSE

Low skin temperature, low level of attention, medication (especially anticholinergics),
age, and habituation will also

58

The somatic afferent
limb

The somatic afferent
limb depends on the stimulus type (electrical shock, loud
noise, visual threat, deep breathing); with the electrical
stimulation, the afferent limb occurs via large myelinated
fibers.

59

The efferent limb

The efferent limb is a sympathetic pathway, originating
in the posterior hypothalamus, descending through the spinal cord to the intermediolateral cell column (T1 to L2), and paravertebral ganglia and then to the sweat gland via small unmyelinated fibers

60

Low amplitude or absent response indicates

abnormal sympathetic reflex arc, and the lesion can be central or peripheral, preganglionic or postganglionic

61

SSR in axonal neuropathies

As a rule, SSR is abnormal in
axonal neuropathies. An exception is the demyelinating
neuropathy with prominent autonomic features, such as
Guillain-Barre syndrome

62

SSR in entrapment neuropathy and radiculopathy.

The SSR is usually normal in
entrapment neuropathy and radiculopathy.

63

QUANTITATIVE SUDOMOTOR AXON REFLEX TEST AND RESTING SWEAT OUTPUT TEST

This is a sensitive, reproducible, and quantitative method to
test sudomotor function. A multicompartment plastic “sweat cell” is tightly secured to the skin. The outer compartment is filled with acetylcholine solution, and nitrogen gas flows constantly to an inner compartment through an instrument that measures the change of humidity (sudorometer). A direct current is applied and the water content
in the inner compartment is continuously measured before,
during and after the stimulus.

64

The basis of the QSART

The basis of the test is that
the axon terminal of the sweat gland under the outer compartment is activated by acetylcholine iontophoresis; the
impulse travel centripetally to a branch point and then distally
to the axon terminal under the inner compartment where acetylcholine is released and a sweating response results

65

In the QSART after the induction of the stimulus, what happedns to the sweat output

With a latency of 1 to 2 min after the induction of the
stimulus, sweat output increases rapidly while stimulation continues; then the stimulator is turned off, and sweat output returns to its prestimulus baseline within 5 min

66

In the QSART the area under the curve represents

the total amount of sweat output expressed in microliter per square centimeter, and the normal value varies depending on the site of testing, gender, and age of the subject.

67

Result of QSART

Reduced or absent response indicates postganglionic disorder.
Normal response does not rule out preganglionic
involvement. Excessive and persistent sweating is also considered
abnormal. Comparison is made between the two
limbs, and an asymmetry of more than 25% is considered
to be abnormal

68

The RSO test compared to the QSART

The RSO test is basically similar to the QSART; a capsule with one chamber is attached to the skin, and the rate of water evaporation is continuously recorded for 5 min. The presence of RSO indicates that the sweat gland is spontaneously activated by the sympathetic fibers

69

Findings of RSO test and QSART in a patient with painful diabetic neuropathy,

In a patient with painful diabetic neuropathy, RSO studies show the presence of increased sweat activity, and QSART exhibits short latency, excessive, and persistent sweat patterns, which is evidence of sympathetic overactivity.

70

Findings of RSO test and QSART in a patient with symptoms of CRPS/RSD-related pain

Sweat test abnormalities correlate well with the
symptoms of CRPS/RSD-related pain, for which the
pathophysiologic mechanism is uncertain; perhaps a lower
firing threshold, or an increased firing frequency due to
denervation hypersensitivity of the sudomotor axons may
produce excitation of the sweat gland

71

NOCICEPTIVE REFLEXES- The blink reflex

The blink reflex is recorded by electrically stimulating the
supraorbital branch of the trigeminal nerve. Ipsilateral R1
(10–13 ms) and bilateral R2 potentials (30–41 ms) are
obtained from the orbicularis oculi muscles.

72

NOCICEPTIVE REFLEXES- The masseter inhibitory reflex

The masseter inhibitory reflex is recorded from the masseter muscles bilaterally with stimulation of the mentalis nerve while the muscle is fully activated by clenching teeth. Ongoing EMG activity is interrupted by two silent periods—an early phase with a latency of 10 to 15 ms and a late phase with 40 to 50 ms

73

NOCICEPTIVE REFLEXES- Trigeminal Reflexes

These trigeminal reflexes have been reported normal in tic douloureux, but abnormal in facial pain due to neuropathy, multiple sclerosis, and cerebellopontine angle tumor

Decks in Essentials of Pain Medicine Class (80):