I. Basic Concepts of Electricity and Electronics in Clinical EMG
1. What is charge? (Q = C) A property of certain subatomic particles (especially electrons and protons) that gives rise to
and interacts with the electromagnetic force. Symbol is Q. Unit is coulomb (C) which is approximately equal to 6.24 x
10^8 electrons.
2. What is voltage? (E = V) The electromotive force required to make electricity flow through a conductor. Symbol is E.
Measured in volts (V).
3. What is current? (I = A) The flow of electrically charged particles, usually electrons. Symbol is I. Unit is ampere (A),
which is 1 coulomb passing a point in a conductor in 1 second.
4. What is impedance? (Z = ¿) The total opposition to current flow in an AC circuit, including resistance, capacitive
reactance, and inductive reactance. Symbol is Z. Measured in Ohms (¿).
5. What are filters? Electronic circuits that perform the function of processing a signal (i.e. remove unwanted electrical
noise). Electrodiagnositc studies use low-frequency (high-pass) and high-frequency (low-pass) filters to exclude highand low-frequency electrical noise to reproduce the signal of interest.
6. What are amplifiers? Devices that increases the amplitude (i.e. voltage or current) of a signal.
II. Nerve Conduction Studies
1. What is the difference between the anode and the cathode? An anode is the terminal on the stimulator where current
flows in. The cathode is the terminal on the stimulator where current flows out. Depolarization of a nerve occurs
under the cathode, and the depolarization proceeds both orthodromically and antidromically from the cathode. The
cathode should be placed closer to the active recording electrode than the anode because the anode has the potential
to hyperpolarize the nerve and block the depolarization caused by the cathode; this could cause the recorded
potential to be reduced or absent.
2. What are the filter settings and gain settings for sensory and motor NCS?
- Sensory: low-frequency 20 Hz - high-frequency 2-3 kHz.
- Motor: low-frequency 2 Hz - high-frequency 10 kHz.
3. Where should G1 and G2 be placed?
- Sensory: Active recording electrode/RED (G1) over the nerve to be tested with the reference electrode/BLACK
(G2) placed over the nerve 3 - 4 cm distal to the G1 electrode.
- Motor: Active/G1/RED center of the muscle belly with reference/G2/BLACK placed distally over the tendon of
the muscle.
4. What is the signal-to-noise-ratio and when is this important? What can be done to improve the response?
- Signal-to-noise ratio: ratio of the desired signal power to the background noise signal power. The most common
background noise is 60-Hz noise from electrical devices in the surrounding environment.
- Important outside of the EMG lab such as in a ICU setting. Since the signals recorded during NCS and EMG are
based on the differences between the active and reference electrodes, making sure that the two electrodes have
the same impedance will decrease the background noise. This can be done by making sure the electrodes are the
same type, have intact wires and good connections, the underlying skin is clean and intact, a conducting jelly is
used between the skin and electrodes, the electrodes are secured to the skin with tape, a ground is in place
between the stimulator and recording electrodes, and coaxial cables are used.
5. Motor Amplitude
1. What is the physiologic basis of the motor amplitude?
- CMAP amplitude represents the number of muscle fibers that depolarize.
2. What are the units used to measure it?
- Millivolts (mV)
3. Why do we record over the muscle motor point?
- This is the location where muscle depolarization first occurs.
- If the recording electrode is not placed here, nerve conduction studies can be artifically abnormal because
(a) the initial positive defelction makes the onset latency difficult to accurately measures, and (b) the CMAP
amplitude may appear artificially reduced.
4. What types of disorders cause a reduction of the CMAP amplitude and how can these be distinguished
electrodiagnostically?
- Axonal loss (i.e. axonal neuropathy)
- Conduction block from demyelination between stim & recording sites
- Some neuromuscular junction disorders
- Some myopathies.
6. Sensory amplitude
1. What is the physiologic basis of the sensory amplitude?
- Summation of all the individual sensory fibers action potentials.
2. What are the units used to measure it? Microvolts (µV).
3. What is the localization value of a normal versus abnormal sensory amplitude in the setting of both normal
and abnormal motor amplitudes in the corresponding motor nerve?
Amplitude is dependent on the integrity of the axon, the muscle fiber it depolarized and the variability of
conduction velocity.
- Some fibers fast & some slow = long duration (temporal dispersion) and lower amplitude
- NOTE: CMAP w/ low amplitude = temporal dispersion vs. axon loss (reduced area under the curve.
7. Motor latency
1. What is the significance of the motor latency?
(1) Conduction time from the stimulation site to the neuromuscular junctions
(2) Time delay across the neuromuscular junction
(3) Depolarization time across the muscle.
2. Do we look at the onset or peak?
- Onset which represents the fastest fibers of the nerve.
3. What are the units? Milliseconds (ms).
8. Sensory latency
1. What is the significance of the sensory latency?
- The time it takes for conduction through the largest (i.e. fastest) cutaneous sensory fibers.
- The peak latency represents a mix of large and small fibers.
2. Do we look at the onset or peak?
- Peak latency
3. What are the units? Milliseconds (ms).
9. Conduction velocity
1. What is the physiologic basis of a slow conduction velocity?
- Loss of the fastest fibers, such as in an axonal neuropathy
- Loss of saltatory conduction, as with a demyelinating neuropathy.
2. How do you calculate conduction velocity in a motor nerve?
- 1) Stimulate at two different sites alone the motor nerve.
- 2) Measure the distance between the two stimulation sites.
- 3) Divide the distance by difference of proximal latency from the onset latency between the two
responses.
- motor conduction velocity = distance / (proximal latency - distal latency).
- Example: If a median nerve, measured at the abductor pollicis brevis, has an latency of 3.5 ms when
stimulating at the wrist and a latency of 7.5 ms when stimulating at the elbow and the distance between
the two stimulating sites is 200 mm, then the calculation would be 200 mm / (7.5-3.5) ms = 200 mm / 4
ms = 50 mm/ms = 50 m/s.]
3. What are the units? Meters per second (m/s).
4. Why do you need to stimulate at two different sites along the nerve for a motor conduction velocity but not
for a sensory conduction velocity?
- Since a motor nerve study includes the time across the neuromuscular junction and the time for the muscle
to depolarize, the conduction velocity from a single motor nerve study will not represent the true conduction
velocity of the nerve alone. When two sites are used, the distance between the sites divided by the difference
in latency represents the conduction velocity of only that portion of the nerve. Since that portion of the nerve
does not include the neuromuscular junction or the muscle, the calculation will represent the true conduction
velocity of the nerve.
10. What is the difference between and orthodromic and an antidromic study?
- Orthodromic: stimulus directed in the way the nerve normally depolarizes
- Antidromic: Stimulus directed in the opposite direction.
- Most sensory studies are performed antidromically because this results in a higher SNAP amplitude than
orthodromic studies.
11. Pitfalls
1. How can you tell if you’re not over the motor point of the muscle?
- (A) There will be an initial positive deflection of the CMAP, which makes the onset latency difficult to
determine.
-(B) The CMAP amplitude may be artificially reduced.
2. What will happen to the NCS responses if the patient’s skin is too cold (<32C)?
- Lower temperatures  sodium channels depolarize more slowly  greater influx of sodium 
artificially increased amplitude & prolonged latency  slower conduction velocity.
3. What is the significance of supramaximal stimulation?
- It ensures that all intact nerve fibers are depolarized.
- If this is not achieved, amplitudes can be artificially low and latency prolonged.
4. What does 60 Hz interference look like and what can be done to eliminate it?
- 60 Hz interference appears as a regular sine wave tracing.
-
-
Interference can be decreased by ensuring that the recording and reference electrodes appear electrically
identical. This is done by cleaning the skin, applying conductive jelly to the electrodes, and making sure
the electrodes are securely affixed to the skin using tape or pressure if necessary.
12. F-response
1. What is the physiologic basis of the F-response?
- Antidromic peripheral motor nerve stimulation activates the anterior horn cells which then backfires and
causes an orthodromic impulse that passes back down the motor axon leading to a low amplitude CMAP late
response representing 1-5% of muscle fibers.
2. How is the F-response performed?
- Flip stimulator so that cathode faces the antidromic direction of a motor nerve (ulnar or tibial). Use the
same supramaximal voltage used in the orthodromic motor response.
3. Are the afferent and efferent arms of the F-response sensory or motor?
- Both afferent and efferent are motor
4. Is there a synapse in an F-response?
- No synapse. The response is a backfire from the anterior horn cell.
5. What disease states correlate with a prolonged F-response?
- F-response will NOT pinpoint the exact location of a lesion
- Early AIDP, C8-T1/L5-S1 radiculopathy, polyneuropathy, intrapment neuropathy
- If a distal NCS is normal, a prolonged F-response (>32ms median/ulnar, >56ms peroneal/tibial)
may indicate a proximal neuropathy, plexopathy or radiculopathy.
6. Do F-responses detect radiculopathies not found on needle exam?
- ???
7. Do you apply a supramaximal or submaximal stimulus in the F-response?
- Supramaximal
13. H-Reflex
1. Are the afferent and efferent arms of the H-reflex sensory or motor?
- Afferent is sensory via the Ia muscle spindle; Efferent is motor
2. Is there a synapse in the H-reflex?
- Yes
3. What is the best nerve to study the H-reflex?
- Tibial nerve recording the gastroc/soleus to distinguish S1 vs. L5 radiculopathies
4. Do you apply a supramaximal or submaximal stimulus in the H-reflex?
- Submaximal stimulus with a long duration of 1ms
5. What disease states correlate with a prolonged H-reflex?
- S1 Radiculopathy
6. Do H-reflexes detect radiculopathies not found on needle exam?
- ???
14. Physical Skills. How do you set up each of these nerve conduction studies?
1. Sensory nerves
1. Median at the wrist
2. Ulnar at the wrist
3. Median midpalmar
4. Ulnar midpalmar
5. Radial at the forearm
6. Sural at the calf
7. Medial and lateral antebrachial cutaneous
8. Lateral femoral cutaneous
9. Superficial peroneal
10. Medial plantar
11. Lateral plantar
2. Motor nerves
1. Ulnar
2. Median
3. Peroneal
4. Tibial
5. Musculocutaneous
6. Radial
7. Facial
8. Spinal accessory
9. Femoral
10. Phrenic
III. Normal Values
1. Sensory nerves. What are the normal amplitudes and latencies for each of these nerves?
Sensory
Amp
Peak Lat
Cond Vel
Motor
Amp
Onset Lat
Cond Vel (m/s)
(UV)
(ms)
(m/s)
(mV)
Median
>20
<3.7
53
Ulnar
>6
<3.5
>49
Ulnar
>10
<3.5
53
Median
>4
<4.4
>49
Median
>25
<2.1
Peroneal >2
<6.1
>41
midpalmar
Ulnar
<2.1
42
Tibial
>3
<6.1
>41
midpalmar
Radial
>15-20
<2.7
48
Facial
>1
<4
Sural
>6
<4.2
41
1. F-responses
1. What is a normal median/ulnar F-wave value?
- <32 ms
2. What is a normal tibial/peroneal F-wave value?
- <56 ms
2. What is a normal tibial/soleus H-reflex value?
- <34 ms; <1.5 ms difference from other side
3. How are normal values affected by
1. Height (Lower vs. upper extremities; proximal vs. distal)
- Tall/Long: Slower CV distally – Nerves taper & are cooler distally…CV UE > LE
- Important in F-response & H-reflex
2. Age
- Full term infant 50%; 1 year-old 75% normal values for CV
- >60 yo CV reduce 0.5-4.0 m/s/decade; Amp SNAP 50% by age 70 yo
IV. Repetitive Stimulation
1. Which nerves are typically studied with repetitive simulation?
- Ulnar (Hypothenar): Ease of stim & restraint of movement
- Facial (Nasalis): Assess bulbar/facial Sx when abnormality cannot be found peripherally
2. What is the rate of stimulation that is given?
- 4 stims in 2 sec (2/sec)
3. Regarding the physiology of the neuromuscular junction:
1. How is ACh synthesized?
- Combine acetyl-CoA + Choline in the pre-synaptic nerve terminal
2. What are quanta?
- Packet of ACh
3. What is a mini-endplate potential (MEPP)
- In the absence of an action potential, ACh vesicles spontaneously leak into the NMJ and cause very small
depolarizations (~0.5mV) in the postsynaptic membrane = the smallest possible depolarization which can be
induced in a muscle.
4. What is an end-plate potential (EPP)
- ("end plate spikes") Depolarizations of muscle fibers caused by neurotransmitters binding to the
postsynaptic membrane in the NMJ.
5. What is a muscle fiber action potential (MFAP)
- When a muscle fiber depolarizes to threshold, a MFAP is created.
4. Explain the significance of primary, secondary, and tertiary stores of acetylcholine in neuromuscular transmission,
and the ramifications of these various stores on repetitive stimulation testing.
- Tertiary (LT Storage)  Secondary (ST Storage)  Primary (Available)
5. Describe the exercise protocol with repetitive stimulation
- A normal maximum voluntary muscle contraction = 30-50Hz
- POST-SYNAPTIC NMJ DISORDER: Baseline higher EPP
- PRE-SYNAPTIC: Baseline lower EPP - MG suspected with low Amp response (10-15Hz) OR marked decrement
- 1) Baseline Test: Need 3 consistent responses. Decrement indicates abnormal findings
- 2) Exercise Test:
- If MG suspected, but with high Amp or no decrement
- 1 min of maximum effort exercise (20sec w/ 3-4 sec rest x 4
- Post-exercise: repeat stim immediate, 15s, 30s, 60s, 3min
6. What is post-exercise facilitation and in which disorders is this a prominent finding?
- In NMJ Disorder, immediately after 1min of exercise (or RNS), EPPs increase initially, but then decline to fall below
baseline resulting in EPP do not reach threshold to generate muscle fiber action potential.
7.
What are the expected findings with repetitive stimulation in each of the following disorders:
1. Myasthenia gravis: Low Amp at slow stim at rest w/ repair following exercise
2. Lambert Eaton: Low Amp with minimal decrement as slow rate of stim
3. Botulinum intoxication: ???
V. Needle EMG - Resting Muscle
1. How many locations should be evaluated in each muscle?
- 20 (30?) locations per muscle – 5 thrust in 4 quadrants
2. What sweep speed and sensitivity are best for observing spontaneous activity?
- Sweep: 10ms/div
- Sensitivity: 50uV
3. What sweep speed and sensitivity are best for observing voluntary motor units?
- Sweep: 10ms/div
- Sensitivity: 200uV
4. Insertional activity
1. What causes increased insertional activity?
- Neuropathic & myopathic conditions (>300ms)
2. What causes decreased insertional activity?
- Fat or fibrotic tissue
5. Endplate noise
1. What is endplate noise?
- Random spontaneous release of quanta of ACh
2. Are endplate spikes regular or irregular?
- Irregular
3. Is the initial deflection positive or negative?
- Negative (Above baseline)
6. Fibrillation potentials and positive sharp waves
1. What is the physiologic basis of fibrillations and positive sharp waves?
- Spontaneous firing by muscle fibers indicating active denervation
2. How fast do fibrillations fire? How does this compare to normal motor units?
- 0.5 to 10 Hz (Normal motor units are 5-50 Hz)
3. Are fibrillations generally regular or irregular?
- Regular at 0.5 to 10 Hz
4. Is the initial deflection positive or negative?
- Positive
5. What is the significance of tiny fibrillation potentials?
- Occur >6-12 months with Amp <10uV
6. How long after nerve injury do positive waves and fibrillations appear?
- ~30 days after injury (Subacute)
7. What disease states other than nerve injury can produce positive waves and fibrillations?
- Some Myopathies (Inflammatory), muscular dystrophies, severe NMJ disease (Botulism)
8. Fibrillations are graded on a scale of 0-4+. What is the difference between 1+, 2+, 3+, and 4+ fibrillations?
- 1+ Unequivocal evidence or fib (slow, regular, biphasic – p-waves) in at least 2 locations
- 2+ Moderate # of persistent DC’s in >3 locations
- 3+ Large areas of persistent DC’s in ALL locations
- 4+ Profuse/widespread/persistent that fill the baseline in ALL locations
9. Which myopathies can cause fibrillations?
- Inflammatory, infiltrative, MD, Myotonic dystrophies, toxic, metabolic, congenital, infection
10. Which myopathies generally do NOT cause fibrillations?
- Steroid myopathies do NOT have fibs
11. After denervation, please note that fibrillations may continue until COMPLETE reinnervation has occurred.
7.
Complex repetitive discharges
1. What causes complex repetitive discharges
- AP’s of groups of muscle fibers the DC spontaneously in new synchrony of regular/repetitive fashion.
2. What is the appearance of a complex repetitive discharge on needle EMG?
- “Motor boat misfiring” or “Jackhammer”
- Single AP spreading to a group of adjacent motor units.
- Uniform frequency 3-40Hz
- Wave form is variable; typically polyphasic 3-10 spikes; Amp 50-500uV; duration up to 50ms; discrete
start & stop
- Non-specific for neurogenic or myopathic disorders that are chronic
8.
Myotonia
1. What is myotonia?
- Slow relaxation of the muscles after voluntary contraction or electrical stim (Difficult to release gri)
2. What are the features of a myotonic discharge on EMG?
- “Dive bomb” = Muscle fibers wax/wan in frequency and Amp; Spike or positive wave
3. What disease states are associated with myotonic discharges?
- W/ Dystrophic changes on Bx: Myotonic Dystrophy
- W/O: Myotonia congenita, paramyotonia congenita
- Other: Inflammatory, infiltrative, toxic, metabolic, congenital, medications
4. How can complex repetitive discharges be distinguished from myotonic discharges?
- Single fibers that trail off in amplitude vs. CRDS are more regular multiples with abrupt start & stop.
9. Fasciculations
1. What is the physiologic difference between a fasciculation and a fibrillation?
- Random firing AP’s of a group of muscles innervated by the same anterior horn cell.
2. Are fasciculations regular or irregular?
- IRREGULAR
3. At what rate do fasciculations fire?
Few/sec to 1/min
4. What conditions or disease states are associated with fasciculations?
- Normal benign fasciculation syndrome
- Peripheral nerve hyperexcitablity – Cramping
- Neurogenic: Anterior horn disease (ALS, SMA), peripheral neuropathy (axonal), radiculopathy,
mononeuropathy, plexopathy
- Metabolic: Hyperthyroid
- Meds: ACHE inhibitors
10. Myokymia
1. How can myokymia be distinguished from complex repetitive discharges?
- Myokymia: Groups of recurring spontaneous MUAP’s with repetitive burst; “Marching Soldiers”; unaffected
by voluntary contraction.
2. How can myokymia be distinguished from tremor?
- Myokymia: The SAME MUAP with silence in between
- Tremor: Many DIFFERENT MUAP burst with silence in between
3. What disease states cause myokymia?
- Radiation injury (brachial plexus), AIDP (face > limbs), MS (face), Pontine tumors (face), hypocalcemia,
timber rattlesnake >>> CIDP, nerve entrapment, radiculopathy
11. What is the difference between cramp and neuromyotonia?
- Cramp: Abrupt onset, recurrent/buildup, rapid sputtering out
- Neuromyotnia: Rare spontaneous burst of firing MUAP’s of high feq (100-300Hz), unaffected by
voluntary activity, decrement
VI. Needle EMG – Motor Unit Activity
1. How do you know you are recording directly over a motor unit action potential?
- High amplitude waves with sharp sound
2. Duration (5-15ms) correlates with pitch
1. What does the duration of a motor unit action potential (MUAP) reflect?
- # of muscle fibers within a motor unit.
2. What is the physiologic basis for prolonged duration in neurogenic disease?
- Relates to in synchrony of muscle fiber firing the motor unit. Asynchrony = longer duration
3. What does a long duration MUAP sound like?
- Long duration: “Dull” & “Thuddy”
- Short duration: “Crips” & “Static-like”
4. What is the importance of MUAP rise time?
- Indicates the distance of the muscle fiber to the needle; Sharp rise time = closer.
3. Polyphasia
1. How do you calculate the number of phases in a MUAP?
- Count the number of times the wave crosses the baseline & ADD 1
2. In normals, what percent of MUAP’s have 3 or 4 phases?
- <15% (25% in the deltoid)
3. What is the morphological difference between phases and serrations?
- Phases cross the baseline
- Serrations do NOT cross the baseline
4. What is the physiologic basis for increased polyphasia in neurogenic disease?
- Collateral sprouting, reinnervation or increased fiber density.
What is the physiologic basis for increased polyphasia in myopathic disease?
- Relative asynchrony from drop-out of muscle fibers in the motor unit
4. Satellite potential
1. What does a satellite potential look like?
- Time-locked potentials that trail the main MUAP
2. What is the physiologic basis for a satellite potential?
- Early reinnervation when collateral sprouts occur from adjacent intact motor units
5. Amplitude
1. What is the upper limit of normal for the amplitude of a MUAP?
- 100uV to 2mV
2. What does the amplitude of a MUAP reflect?
- The few fibers close to the needle (2-12 fibers)
- Effected by: 1) proximity of needle to motor unit, 2) increased number of motor fibers in the motor unit,
3) Increased diameter of muscle fibers, 4) More synchronicity of muscle fiber firing
3. What is the physiologic basis for high amplitude MUAPs in neurogenic disease?
- Higher motor unit density due to sprouting.
4. What is the physiologic basis for low amplitude MUAPs in myopathic disorders?
- Reduced number and diameter of muscle fibers
5. What does a high-amplitude MUAP sound like?
- LOUD
6. Recruitment
1. What is the slowest frequency at which a voluntary motor unit can fire?
- 4-5Hz
2. In a normal recruitment pattern, what is the ratio of firing frequency (in Hertz) of the fastest motor unit to
number of units firing?
- 5 Hz:# MU firing…>5 suggest reduced number of motor units
3. What is the difference between reduced recruitment and reduced activation?
- Reduced recruitment: Higher frequency or smaller number of MUAP recruited for the
expected 15 Hz
- Reduced activation: Occurs in UMNL, poor cooperation, pain inhibition, excessively strong
muscle, 2-joint muscles (GS)…Not evidence of LMNL.
VII. Electrodiagnostic Findings in Common Clinical Scenarios
1. In each of the following conditions, describe what would be expected on nerve conduction studies (sensory, motor
and F-responses) and needle EMG (including the pattern of abnormal spontaneous activity, MUAP duration,
amplitude, polyphasia, and recruitment): (see http://rehabmanual.com/book/print/443)
5.
Axon Loss
a. Hyper acute <3d
b. >1wk-<3-6wk
c. Subacute >3-6w - <2-3m
d. Sub-Chronic >2-3m - <yrs
e. Chronic >yrs
Demyelinating
a. Aquired Poly
b. Hereditary polu
c. Focal demyel
Myopathy
a. Fiber necrosis
b. w/o fiber necrosis
CNS Disease
NMJ Disorder
2.
Sense
N
Low
Low
Low
Low
Low
Motor
N
Low
Low
Low
Low
Low
F
Spont Act
N
N
-/+ P/Fib
P/Fib
P/Fib
N
What is the electrodiagnostic approach to the diagnosis of:
1. Unsteady gait
2. Painless weakness
3. Rhabdomyolysis
4. Elevated serum CK levels
MUAP
N
AMP
N
N
N
N
Hi
Hi
Polyph
+
+
-
Recruit
Low
Low
Low
Low
Low
Low
Low
+
Early
Low
N
5.
6.
7.
Muscle cramps
Foot drop
Wrist drop/hand weakness
VIII. Pathophysiology of Peripheral Neuropathies
1. What is neurapraxia?
- Focal demyelination, conduction block
2. What is neurotmesis?
- Complete nerve severance
3. What is axonotmesis?
- Axon loss ONLY, myelin is intact
4. What is Wallerian degeneration and how does it occur?
- Degerneration of axon distal to site of transection
5. Describe the histology of normal nerves and connective tissue
- Read a histology book
6. What are the effects on conduction of an axonopathy?
- Reduced CMAP amplitude with stimulation both proximal and distal to the lesion
- >50% reduction in amplitude compared to uninvolved limb is significant
- Latencies and conduction velocities should NOT be affected
- W/ neurotmesis, CMAP or SNAP amplitudes will be unattainable both proximal & distal to lesion.
IX. Normal Anatomy
1. What are the nerve, nerve root, and trunk innervations of the following upper extremity muscles? (See the Muscle
and Nerve Cheat Sheet )
1. Rhomboids
2. Supraspinatus
3. Infraspinatus
4. Deltoid
5. Biceps Brachii
6. Serratus Anterior
7. Pectoralis Major – clavicular
8. Pectoralis Major – sternocostal
9. Brachioradialis
10. Ext carpi radialis longus
11. Triceps
12. Extensor carpi Ulnaris
13. Extensor digitorum communis
14. Extensor indicis
15. Extensor pollicis longus
16. Supinator
17. Pronator teres
18. Flexor carpi radialis
19. Flexor pollicis longus
20. Flexor digitorum profundus 1&2
21. Flexor digitorum superficialis
22. Abductor pollicis brevis
23. Opponens pollicis
24. Flexor carpi ulnaris
25. Flexor digitorum profundus 4&5
26. First dorsal interosseus of the hand
27. Abductor digiti quinti of the hand
2. What are the nerve and nerve root innervations of the following lower extremity muscles?
1. Iliopsoas
2. Sartorius
3. Rectus femoris
4. Vastus lateralis
5. Vastus medialis
6. Adductor longus
7. Gluteus medius
8. Gluteus maximus
9. Quadratus femoris
10. Peroneus longus
11. Peroneus brevis
12. Anterior tibialis
13. Extensor digitorum longus
14. Extensor hallucis
15. Extensor digitorum brevis
16. Internal hamstrings
17. External hamstrings
18. Short head of the biceps femoris
19. Posterior tibialis
20. Medial gastrocnemius
21. Lateral gastrocnemius
22. Abductor hallucis
23. Abductor digitorum (Ped)
24. First dorsal interosseus pedis
X. Compressive Neuropathies 1: Median Nerve
1. What is the difference between compressive neuropathy and entrapment neuropathy?
- Not sure, I think compression is external and entrapment in internal???
2. What are the signs and symptoms of carpal tunnel syndrome?
SYMPTOMS:
- Carpal tunnel contents = Median nerve, FDP, FDS, FPL
- CTS Sx: N/T/Burn/Pain in hand
- Sensory loss thumb, 2nd & 3rd digits
- Mild weakness
- Poorly localized pain – some report pain up the arm
- Worse at night and AM stiffness – Shake hand out
- Worse w/ knitting, driving, hand tools, typing, holding items
SIGNS:
- Sensory loss (touch/pain) digits 1-4.5 (20-50% can be normal)
- APB weakness in abduction…NOTE: Opposition uses some ulnar innervated muscles
- Positive Tinel’s = distal paresthesias that reproduce pain
- Positive Phalan’s (Hold for 30-60sec)
- Negative for other MSK or radicular exam
3. What are the risk factors for carpal tunnel syndrome?
- Obesity, oral contraceptives, hypothyroidism, arthritis, diabetes, and trauma.[
4. What are the AANEM electrodiagnostic criteria for carpal tunnel syndrome (sensory, midpalmar sensory, and motor)?
5. What are our criteria for carpal tunnel syndrome? Note that these relative differences are not considered absolute or
diagnostic.
- Difference between median and ulnar sensory wrist latency >0.5ms
- Difference between medial and ulnar mid-palm latency >0.5ms
- Difference between median and ulnar motor wrist latency >1.7ms
6. Proximal Median mononeuropathy
1. The pronator syndrome
2. What is it and what are the symptoms?
3. What are the expected nerve conduction and EMG findings?
4. Compression at the ligament of Struthers
1. What are the signs and symptoms?
2. What are the expected nerve conduction study and EMG findings?
7. The anterior interosseus syndrome:
1. Which muscles are innervated by the anterior interosseus nerve (MEDIAN)?
- FPL (C7-8)
- FDP (C7-8) – lateral 2 heads flexes the fingers 2&3
- PQ
2. What are the signs and symptoms?
SYMPTOMS
- +/-Pain over flexor surface of forearm; worse at night
- Spontaneous onset or associated w/ exercise
- Weakness
SIGNS
- No sensory loss
- Tender medial forearm flexors
- Weak flexion at the DIP of 2nd & 3rd FPL without thenar weakness (Weak lateral FDP
- Weak pronation w/ elbow flexed (Weak PQ)
- Pinch/OK test (Weak FPL)
3. What are the expected nerve conduction study and EMG findings?
- Abnormal FPL, FDP & PQ sparing all other muscles – Primarily a needle EMG Dx
- NCS may show prolonged latency from elbow to PQ
XI. Compressive Neuropathies 2: Ulnar Nerve
1. What muscles are supplied by the ulnar nerve?
- FCU, FDP (3&4), FDI, ADQ – All hand intrinsics except the LOAF (median)
- C8-T1; lower trunk; medial cord
2. Ulnar mononeuropathy at the elbow
1. What are the clinical features of ulnar mononeuropathy at the elbow?
SYMPTOMS
- Elbow pain, hand weakness, radicular pain prox/dist
SIGNS
- Tinel at cubital tunnel
- Hand intrinsic weakness
- Sensory loss over medial hand and 4/5 digits
2. What are risk factors for ulnar mononeuropathy at the elbow?
- Compression during the perioperative period, Blunt trauma, Deformities (e.g., rheumatoid arthritis),
Metabolic derangements (e.g., diabetes), Transient occlusion of brachial artery during surgery, Subdermal
contraceptive implant, Venipuncture, Hemophilia leading to hematomas, Malnutrition leading to muscle
atrophy and loss of fatty protection across the elbow and other joints, Cigarette smoking
3. What are the expected nerve conduction study and EMG findings in ulnar mononeuropathy at the elbow?
- NCS: Slowing of CV with a drop in the amplitude or no response in the ulnar sensory. Motor drop >25% at
elbow…Slow CV across the elbow is only significant if difference is >10m/s compared to the distal
segment
- EMG: FDP and hand intrinsics abnormalities. Sparing of the FCU possible since innervation is proximal to
the cubital tunnel
4. How are the flexor carpi ulnaris and flexor digitorum profundus 4&5 useful localizing an ulnar
mononeuropathy?
- FCU is inervated proximal to the cubital tunnel & FDP 4/5 are median innervated.
5. How can an ulnar mononeuropathy at the elbow be distinguished from ulnar mononeuropathy proximal to
the elbow?
- FCU would be abnormal
3. Ulnar mononeuropathy at the wrist (Guyon’s Canal)
1. What are the various branches of the ulnar nerve that can be affected at the wrist?
- Palmar branch (pure motor) – Prolonged latency from FDI; OTHER???
2. How do the clinical presentations vary?
- Pain with finger hyperextension; OTHER ????
3. What are the nerve conduction study findings associated with these?
- Denervation of hand intrinisics only; prolong mid-palmar studies, reduced/normal sensory
4. How does evaluation of the dorsal ulnar cutaneous branch help differentiate ulnar neuropathy at the wrist
from ulnar neuropathy at the elbow?
- Dorsal ulnar branch branches proximal to the wrist.
- Ulnar neuropathy at the elbow – both SNAP at the digit 5 & dorsal ulnar nerves will be abnormal
(provided there is NO axonal loss.
- If the lesion is pure demyelination, at the elbow – both distal sensory losses will be normal.
- If the dorsal ulnar SNAP is normal & an abnormal digit 5 SNAP – the lesion is at the wrist
XII. Compressive Neuropathies 3: Peroneal Nerve (fibular nerve)
1. What muscle is supplied directly by the common peroneal branch of the sciatic nerve above the fibular head?
- Short head of the biceps femoris is innervated by the common peroneal nerve (L5-S1)
2. What muscles are supplied by the deep peroneal nerve?
- AT (L45), EDL (L5S1), EH (L5S1), EDB (L5S1), PT & sensory to the 1st web space
3. What muscles are supplied by the superficial peroneal nerve?
- PL & PB (L5S1) & sensory to the ant/lat calf & dosum of the foot.
4. Which of branch or branches of the peroneal nerve are usually involved in an entrapment neuropathy at the fibular
head?
- Deep branch = Motor involvement
5. What are the expected nerve conduction studies and EMG findings in peroneal mononeuropathy at the fibular head?
- NCS: 20% at EDB compared proximal to distal; CV across fibular head 10ms or 20%
- EMG: Superficial = PL, Deep = EDB, Common peroneal above knee = SHB
XIII. Compressive Neuropathies 4: Radial Nerve
1. What muscles are supplied by the radial nerve before the spiral groove? Which is the last one?
- Triceps & Anconeus (C6-8)
2. What muscles are supplied by the radial nerve after the spiral groove but before the branch to the posterior
interosseus? Which is the first one?
- Brachialradialis, ECR, Supinator
3. What muscles are supplied by the posterior interosseus nerve?
- ECU/EDC/EI/EPL/APL (C7-8) & Supinator (C6-7)
4. What is the first muscle innervated by the posterior interosseus nerve as it emerges from the supinator?
5. What are the expected nerve conduction study and EMG findings in a radial neuropathy at the spiral groove?
6. What are the expected nerve conduction study findings and needle EMG findings in a posterior interosseus syndrome?
7. What is the arcade of Frohse?
XIV. Compressive Neuropathies 5: Uncommon Compressive Neuropathies
1. What is the difference between vascular and neurogenic thoracic outlet syndrome?
2. What are the expected nerve conduction study and EMG findings in neurogenic thoracic outlet syndrome?
3. What are the features of digital nerve entrapment of the hand?
4. Sciatic neuropathy:
1. What muscles are supplied by the sciatic nerve?
2. What etiologic factors may contribute to sciatic mononeuropathy?
3. What are the expected nerve conduction and EMG findings?
5. Tarsal Tunnel Syndrome:
1. What are the clinical features of tarsal tunnel syndrome?
2. What etiologic factors may contribute to tarsal tunnel syndrome?
3. What are the expected nerve conduction study and EMG findings?
6. Femoral Neuropathy:
1. What are the sensory branches of the femoral nerve?
2. What is the clinical presentation of lateral femoral cutaneous neuropathy?
3. What muscles are innervated by the femoral nerve?
7. What are the findings in long thoracic neuropathy?
8. What are the findings in dorsal scapular neuropathy?
9. What are the findings in suprascapular neuropathy?
10. What are the findings in musculocutaneous neuropathy?
11. What are the findings in ilioinguinal, genitofemoral, and saphenous neuropathies?
12. What are the findings in obturator neuropathy?
XV. Anomalous Innervation
1. What are the three types of median-ulnar anastomoses?
2. Which is the most common type of median-ulnar anastomosis?
- Marin-Gruber Anastomosis of the median to ulnar nerve = median (or mixed) innervation of the ADM, FDI, FPB,
ADP
1. What nerve conduction study finding suggests the presence of this anastomosis?
- Median motor fibers cross over in forearm to join ulnar nerve
2. How would this anomaly be confirmed?
- Initial positive defection. Ulnar NCS hypothenar CMAP disproportionately HIGH Amp at wrist > elbow
(>1mV or >10%) w/ stim over the APB.
- Stimulation of median nerve at elbow causes larger thenar CMAP amplitude than median nerve
stimulation at the wrist
- Stimulation of median nerve at elbow causes hypothenar or 1st DI CMAP
- stim of ulnar nerve at wrist gives a hypothenar or 1st DI DMAP amplitude that is 120% larger than CMAP
evoked with ulnar stim at the elbow
3. What are the findings in a patient with a median-to-ulnar anastomosis and carpal tunnel syndrome?
4. What muscle may be innervated by an accessory peroneal nerve?
- Branch of superficial peroneal nerve passing posterior to lateral malleolus  Lateral EDB
5. How is an accessory peroneal nerve identified on nerve conduction studies?
XVI. Axonal vs. Demyelinating Neuropathy
1. What types of nerve fibers are involved in conveying pain:
1. Pain
2. Temperature
3. Pressure
4. Vibration
5. Two-point discrimination
6. Proprioception
What physical exam findings may be present in patients with peripheral neuropathy?
What electrodiagnostic findings differentiate peripheral neuropathy from polyradiculopathy?
- Peripheral neuropathy: Demyelinating = Reduced Amp &/or CV: Axon loss = reduced CMAP or SNAP
- Polyradiculopathy: Intact sensory response. Normal SNAP & CMAP; Paraspinal P’ &fibs????
4. What electrodiagnostic findings are suggestive of an axonal peripheral neuropathy?
- Axon loss = reduced CMAP or SNAP
5. Demyelinating peripheral neuropathy
1. What electrodiagnostic findings are suggestive of an ACQUIRED demyelinating peripheral neuropathy?
- Reduced CV disproportionate to Amp loss
- Usually multifocal resulting in abnormal temporal dispersion & partial conduction block
2. What conditions cause an acquired demyelinating peripheral neuropathy?
3. What electrodiagnostic findings are suggestive of a hereditary demyelinating peripheral neuropathy?
4. What conditions cause a HEREDITARY demyelinating peripheral neuropathy?
- HMSN type 1 = CMT
- HMSN III = Dejerine-Sottas hypertrophic neuopathy
- HMSN IV = Refsum’s Disease
- Metachromatic Leukodystrophy
- Krabbe’s globoid cell leukodystrophy
5. How can cool skin temperature be misleading in determining whether a peripheral neuropathy is axonal or
demyelinating?
6. What percentage of patients over 70 years old will have a sural sensory response?
7. How do you define peripheral neuropathy in the geriatric population?
8. Hereditary neuropathies
1. What are the most common hereditary neuropathies and how are they classified?
2. What genetic tests are available for hereditary neuropathies?
3. In approximately what fraction of hereditary demyelinating neuropathies is there no known family history?
9. What is multifocal motor neuropathy and what are the findings on nerve conduction studies?
- Also known at MMNCB (MMN w/ conduction block)
- Associated with anti-ganglioside antibodies (esp GM1)
- Pure lower motor neuron findings (pure motor) c/ conduction block along motor nerves
- Minimal or no sensory difference from CIDP
- Important to Dx due to treatment with Gamma globulin or cyclophosphamide (DDx from ALS)
- Asymmetric, UE predominance, absent sencory, typical lack of response to prednisone (different from CIDP)
- EDx: Conduction block along motor nerves w/ or w/o temporal dispersion; demyelination; prolonged
latencies’ slow CV; prolonged late responses (F’s); DDx include nerve entrapment
XVII. Radiculopathies and Plexopathies
1. Radiculopathy
1. What are the expected findings on motor nerve conduction studies in a radiculopathy?
- Acute 3-10d: no changes in CMAP
- 2-3wks: Wallerian degeneration (Axon injury) reduces CMAP
- 2-4wks: Sprouting causes increase CMAP
- Chronic: Sprouting and then no change in CMAP
- Preferential large fiber loss may result in reduced CV (30%)
2. What are the expected findings on sensory nerve conduction studies in a radiculopathy?
- Increased or Normal…Most lesions are proximal to the DRG
3. After an acute radiculopathy, which muscles (proximal or distal) will show abnormal spontaneous activity
first? Which muscles will show changes of reinnervation first?
- PROXIMAL muscles with show abnormal spont activity 1st
- Reinervation occurs in paraspinals first (MOST PROXIMAL)
- Fibs are acute proximally & chronic distally…Fibs distally in the 1st week indicate pre-existing injury
4. What are the most common cervical and lumbar radiculopathies?
- C7/L5
5. What are the electrodiagnostic findings in lumbar spinal stenosis?
- Typically normal – Sx tend to be intermittent
6. What is the minimum number of muscles that should be tested to screen for radiculopathy in an upper /lower
extremity?
- UE 6 / LE 5
7. What abnormalities do you expect on needle exam in each of the following radiculopathies?
- Reduced recruitment, P’s & fibs, increased Amp, polyphasia
1. L4 radiculopathy: Quads
2.
3.
2.
3.
4.
5.
6.
7.
2.
L5 radiculopathy: EDB
S1 radiculopathy: AH, glut max
C5 radiculopathy: Deltoid, infraspinatus
C6 radiculopathy: BB, ECU, ECR
C7 radiculopathy: T, EDC
C8 radiculopathy: APB, ADQ
Plexopathy
1. How can you differentiate plexopathy from radiculopathy on the basis of nerve conduction studies?
- Plexopathy have motor & SENSORY abnormalities
2. What are the clinical features of an upper trunk brachial plexopathy?
- Weakness in C5-6: Deltiod, B, BR, SS, IS; sensory loss over lateral forearm/arm/lat hand/thumb; Reduced
DTR B & BR; Sensory from Ax & LABC.
3. What are the clinical features of a lower trunk brachial plexopathy?
- All C8T1 (APB, FPL, FDP) & ulnar (FCU, FDP 4/5, FDI, ADQ); Radial C8 (EI, EPB; sensory to medial
forarm/hand/digits 4-5; normal reflexes
4. Which nerves are supplied by the posterior cord?
- Radial & axillary nerve
5. Which nerves are supplied by the lateral cord?
- MC & outer/lateral median nerve (spares hand)
6. Which nerves are supplied by the medial cord?
- Ulnar & medial median nerve; MBC/MABC
7. Draw the brachial plexus. In an upper trunk plexopathy, which of the following sensory nerve action
potentials will be affected?
1. Median at D1
2. Median at D3
3. Ulnar
4. Radial
5. Medial antebrachial cutaneous
6. Lateral antebrachial cutaneous
8. In a lower trunk plexopathy, which of the following sensory nerve action potentials will be affected?
1. Median at D1
2. Median at D3
3. Ulnar
4. Radial
5. Medial antebrachial cutaneous
6. Lateral antebrachial cutaneous
9. In a middle trunk plexopathy, which of the following sensory nerve action potentials will be affected?
1. Median at D1
2. Median at D3
3. Ulnar
4. Radial
5. Medial antebrachial cutaneous
6. Lateral antebrachial cutaneous
10. In a lateral cord plexopathy, which of the following sensory nerve action potentials will be affected?
1. Median at D1
2. Median at D3
3. Ulnar
4. Radial
5. Medial antebrachial cutaneous
6. Lateral antebrachial cutaneous
11. In a medial cord plexopathy, which of the following sensory nerve action potentials will be affected?
1. Median at D1
2. Median at D3
3. Ulnar
4. Radial
5. Medial antebrachial cutaneous
6. Lateral antebrachial cutaneous
12. In a posterior cord plexopathy, which of the following sensory nerve action potentials will be affected?
1. Median at D1
2. Median at D3
3. Ulnar
4. Radial
5. Medial antebrachial cutaneous
6. Lateral antebrachial cutaneous
13. What is diabetic amyotrophy?
14. What is brachial plexitis (Parsonage-Turner Syndrome?)
15. Are paraspinal muscles affected in plexopathy?
- NO
3. Paraspinal Mapping
1. How much paraspinal denervation can one expect in the low back muscles of asymptomatic persons?
2. What is the specificity of needle EMG in differentiating clinically and radiographically apparent spinal
stenosis from low back pain or no symptoms?
3. How does one place an EMG needle in the L5-innervated paraspinal muscles?
XVIII. Cranial Nerve Studies
1. For what clinical situations is a facial motor response a useful study?
2. In the blink reflex, what pathway does the R1 represent?
3. In the blink reflex, what pathway does the ipsilateral R2 represent?
4. In the blink reflex, what pathway does the contralateral R2 represent?
XIX. Motor Neuron Disease
1. What are the different motor neuron diseases that affect adults and children and how are they can be distinguished
clinically?
2. What is the differential diagnosis for weakness with normal sensation?
3. What are the clinical features of amyotrophic lateral sclerosis?
- Upper/Lower motor neuron lesions in ¾ quadrants
- Bulbar/Cervical/Thoracic/Lumbosacral
- Fascicules & Atrophy
4. In motor neuron disease:
1. What are the expected sensory and motor nerve conductions study findings?
- Sensory NC: Should be normal…Most sensitive test to R/O is the sural evoked w/ low Amp for axon
degeneration
- Motor NC: Done in most involved quadrant. Absent response is NOT enough; motor Amp reduced >50%
between sides
- Rep Stim: Decriment motor response at low rates (2Hz) = Poor Px
o Due to immature NMJ from reinnervation OR terminal twig CB
2. What findings may be noted on repetitive stimulation?
- Decriment motor response at low rates (2Hz) = Poor Px
o Due to immature NMJ from reinnervation OR terminal twig CB
3. What findings are expected on needle examination and what is the distribution of involvement?
- Large & small fibs
- Large polyphasic MUAP
- Frequent satellite potentials
- Noted in at lease 3 extremities (including the head)
5. A cervical lesion may cause polyradiculopathy (wasting and weakness of the upper limbs) and myelopathy (spasticity
in the lower limbs). How can this be distinguished from ALS?
- Radics are painful w/ some sensory findings; ALS has brisk reflexes
6. What are the Escorial definitions of definite, probable, and possible motor neuron disease? What are the four body
segments that can be tested to meet these criteria?
7. What does muscle biopsy show in motor neuron disease?
8. Why are thoracic paraspinal muscles useful in the EMG evaluation of ALS?
- Changes seen in ALS, DM, direct trauma & myopathy
XX. Introduction to Muscle Pathology
1. Be able to identify each of the following in muscle tissue, and describe the clinical significance of the findings that are
abnormal:
1. Normal H&E
2. Atrophic muscle fibers
3. Fiber type grouping
4. Increased glycogen storage
5. Split fibers
6. Central nuclei
7. Vacuoles
8. Z band, I band, and A band
2. What are the features of Type I muscle fibers?
3. What are the features of Type II muscle fibers?
4. How do the following relate to each other: Muscle fibers, myofibrils, sarcomeres?
XXI. The Muscular Dystrophies
1. What are the clinical features, mode of inheritance, and EMG findings in:
1. Duchenne muscular dystrophy
2. Becker muscular dystrophy
3. Limb Girdle muscular dystrophy
4. Fascioscapulohumeral muscular dystrophy
5. Oculopharyngeal muscular dystrophy
6. Myotonic dystrophy
2. How are muscular dystrophies classified?
3. For which muscular dystrophies is a gene test available?
XXII. Inflammatory/Metabolic Myopathies
1. What are the clinical features and EMG characteristics of:
1. Dermatomyositis
2. Polymyositis
3. Steroid myopathy
4. Inclusion body myositis
5. Hypokalemic periodic paralysis
6. Hyperkalemic periodic paralysis
7. Statin myopathy
2. What are the limitations of EMG in the diagnosis of steroid myopathy?
3. What are the EMG findings in an incompletely treated inflammatory myopathy?
XXIII. Congenital/Storage Myopathies
1. What are the clinical features and muscle biopsy findings in:
1. Central core myopathy
2. Nemaline myopathy
3. Myotubular (centronuclear) myopathy
4. Mitochondrial myopathy
1. What are the clinical features and muscle biopsy findings in:
1. Acid maltase deficiency (Pompe¿s disease)
2. Myophosphorylase deficiency (McArdle¿s disease)
3. Carnitine palmitoyltransferase deficiency
XXIV. Myotonia
1. What are the clinical features of myotonic dystrophy?
2. What are the clinical features of myotonia congenita?
3. What are the clinical features of paramyotonia congenita?
4. What ion channels are involved in each of the myotonic disorders?
XXV. Neuromuscular Complications of Cancer
1. What conditions can cause facial myokymia?
2. Describe the clinical picture in the various paraneoplastic syndromes of the peripheral nervous system?
3. How can radiation plexopathy be differentiated from plexopathy caused by metastatic tumor?
XXVI. An Approach to the Diagnosis of Neuromuscular Disease in the Floppy Infant 8.19
1. How do the nerve conduction study findings differ between normal infants and adults?
2. What is the most likely diagnosis in a floppy infant with neuropathic motor unit changes on EMG?
3. What is neonatal myasthenia gravis?
XXVII. SFEMG
1. What is jitter and how is it measured?
2. What is the significance of increased jitter?