Peripheral Nerve Flashcards
Which one of the following type of nerve fiber carries fast pain and temperature sensation?
a. Type A alpha
b. Type A beta
c. Type A delta
d. Type A gamma
e. Type B
f. Type C
c. Type A delta
Which one of the following tests is best for confirming an isolated cervical radiculopathy?
a. Compoundmuscle action potential (CMAP)
b. F-wave
c. H-reflex
d. Insertional activity on EMG
e. Sensory Nerve Action Potential (SNAP)
d. Insertional activity on EMG
Over 1-2 weeks denervated muscle fibers
becomes progressively more mechanically irritable such that electrical discharges provoked by
movement of the needle can be prolonged
(increased insertional activity). Muscle fibers also
become chemically sensitive to their microenvironment and their membranes can also become unstable enough to produce spontaneously activity (fibrillation potentials and positive sharp
waves; disappear with complete degeneration of
the denervated muscle fiber). The finding of
fibrillations and positive sharp waves is the most
reliable and objective test that there is for damage
to motor axons to the muscle after 1 week at least
up to 12 months after the damage. If there is
ongoing damage such as in amyotrophic lateral
sclerosis one can see ongoing denervation. Reinnervation of muscle is an ongoing process, occurring whenever a muscle is partially denervated.
This process typically involves the development
of sprouts from adjacent, unaffected motor nerve
fibers that ultimately contact at least some of the
denervated muscle fibers. These reinnervated
muscle fibers cluster right in the area of other,
normally innervated muscle fibers. This process
results in the development of clumps of reinnervated muscle fibers attached to individual motor neurons, producing larger motor units more
irregular potentials (polyphasic).This process
takes months to develop and indicates the presence of chronic denervation.
EMG abnormalities in which one of the following muscles is LEAST specific for C5 radiculopathy?
a. Infraspinatus
b. Levator scapulae
c. Pronator teres
d. Rhomboids
e. Supraspinatus
c. Pronator teres
The typical needle EMG examination requires
sampling several muscles. Its ability to localize a
lesion depends on sampling muscles innervated
by the same nerve but different nerve roots, muscles innervated by the same nerve root but different nerves and muscles innervated at different
locations along the course of the nerves. Paraspinal muscles can be very useful in this regard
because nerve root damage will tend to produce
abnormalities in these muscles as well as within
the muscles of the limbs (helping to distinguish
a radiculopathy from a plexopathy or peripheral
neuropathy, for example). Sometimes precise
localization can be difficult due to the overlap
in innervation of the various nerve root levels.
Fibrillation potentials are an indicator of:
a. Dorsal root ganglion injury
b. Motor axon loss
c. Muscle necrosis
d. Reinnervation
e. Sensory axon loss
b. Motor axon loss
Which one of the following is the earliest electrophysiological change seen in radiculopathy?
a. Fibrillation potentials
b. Increased number of motor unit
potentials
c. Positive sharp spikes
d. Reduced CMAP
e. Reduced interference pattern
e. Reduced interference pattern
During EMG assessment of a muscle during contraction, the electrical activity should fully obscure the baseline (termed a full interference
pattern). Incomplete interference pattern is considered to be a reflection of loss of motor units in a muscle, though it can also be seen with diminished effort. The table below shows the sequence of EMG changes in radiculopathy
Which one of the following best describes a motor unit potential?
a. Sum of conduction velocities of motor neurons
b. Seen during muscle necrosis
c. Reinnervation potential
d. Sensory axon loss
e. Sum of electrical activity from muscle fibers supplied by the same motor neuron
e. Sum of electrical activity from muscle fibers supplied by the same motor neuron
MUP is the sum of the electrical signals
arising from the discharge of the several muscle fibers within recording distance of the tip
of the needle that innervated by the same
motor neuron. The amplitude of the MUP
is dependent on the density of the muscle
fibers attached to that one motor neuron
(also to the proximity of the MUP). As the
degree of contraction is slowly increased,
more motor units are recruited.
The F-wave is useful when trying to confirm which one of the following:
a. Bilateral carpal tunnel syndrome
b. Isolated C7 nerve root lesion
c. Isolated S1 nerve root lesion
d. Multiple proximal motor root compromise
e. Multiple sensory root compromise
d—Multiple motor root compromise
The F-wave (originally recorded in the foot,
hence the name) is a late response that occurs
in muscles during a motor nerve conduction
study long after the initial contraction of the muscle (CMAP). CMAP usually appears within several milliseconds but another response can be
normally recorded in the muscle slightly later
(25-55 ms). The electrical impulse is transmitted
proximally along the motor axon from the site of
initiation of the action potential. When this antidromic depolarization reaches the motor neurons in the spinal cord, a percentage of these motor neurons are activated a second time. This results in an electrical signal being conducted in the normal (orthodromic) direction from the spinal cord
to the muscles innervated by the nerve. This second, later activation produces a small muscle contraction that is termed the F-wave. Because the
number of motor neurons that are re-activated is somewhat unpredictable, the amplitude of this
signal is variable and, therefore, amplitude measurements are usually not used. However, delay in the F-wave indicates some slowing of conduction of the motor axon. Since the F-response
traverses more proximal portions of the motor
axons (twice) it may be useful in the investigation
of proximal nerve pathology. Since the antidromic impulse in motor axons in a single peripheral nerve will test the multiple nerve roots
forming it, F-wave is not useful for isolated
radiculopathy but is valuable where multiple
roots may be involved (e.g., Guillain-Barre syndrome, or chronic inflammatory demyelinating
polyradiculopathy).
The H-reflex is used in which one of the following scenarios:
a. Suspected common peroneal nerve palsy
b. Suspected L4 radiculopathy
c. Suspected L5 radiculopathy
d. Suspected lumbar plexopathy
e. Suspected S1 radiculopathy
e—Suspected S1 radiculopathy
H-reflex is named in honor of Hoffmann, who
first described this response in 1918. The
H-reflex is most commonly tested by electrical
stimulation of the tibial nerve, with recordings
from the gastrocnemius/soleus muscle complex
(triceps surae). Therefore, this response utilizes
the same neural pathway as the ankle jerk reflex.
Electrical stimulation will depolarize the largest,
most heavily myelinated nerve fibers at a lower
stimulus intensity than is required to activate
other smaller nerve fibers. Since the largest
nerve fibers in a peripheral nerve are those arising from muscle stretch receptors, there should
be a stimulus intensity that activates muscle
stretch afferent nerve fibers without directly activating many motor nerve axons eliciting a monosynaptic reflex contraction in the muscle.
Because this response must traverse the sensory axon all the way back to the spinal cord before
synapsing on the motor neuron, and since the
motor response must then traverse the length
of the motor axon to reach the triceps surae
muscle, this reflex takes a long time (i.e., late).
Theoretically, this reflex can be elicited from virtually any muscle but only the triceps surae muscle produces H-reflexes that are reliable enough to be clinically useful. Therefore H-reflex evaluates the integrity of the reflex arc from the tibial nerve, sciatic nerve, S1 sensory root, spinal cord, S1 motor root and back to the triceps surae.
Damage to any portion of the reflex arc can
result in loss or slowing of the reflex response.
Since the H-reflex is mediated primarily over
the S1 nerve root (just like the ankle jerk reflex),
it is a sensitive test for S1 radiculopathy. However, once the reflex arc has been damaged, it
often does not return to normal (making the test
less useful in investigating the question of recurrent radiculopathy).
Which one of the following are features of a primarily demyelinating neuropathy?
a. Fibrillation potentials
b. Increased insertional activity
c. Polyphasic waves
d. Positive sharp spikes
e. Reduced conduction velocity
e—Reduced conduction velocity (or
conduction block)
The table below shows general patterns of
peripheral neuropathies due to demyelination
versus those due to axonal degeneration, though
in reality each can cause secondary damage to
the other and electrophysiology may be mixed.
Pathology which may affect both myelin and
axons equally include diabetes, uremia and paraproteinemia. Radiculopathies (root lesions) and
neuropathies (e.g., MND, herpes zoster) are
not included in this table, although they may
mimic peripheral neuropathy
A 76-year-old woman presented with numbness and tingling of the hands that had persisted for the previous 5 weeks. Examination revealedmildlimitation of neckmovements. Strength and reflexeswere normal. She hadmild atrophy of the right thenar muscles. Pain sensationwas decreased in the radial 3½ digits; Phalen’s test was positive bilaterally. Neurologic examination was otherwise negative and the EMG was done.
Which one of the following explains her symptoms?
a. C6 and C7 radiculopathy
b. C6 radiculopathy
c. Carpal tunnel syndrome
d. Musculocutaneous nerve entrapment
e. Ulnar nerve entrapment
c. Carpal tunnel syndrome
It showed prolonged median nerve distal motor
latency on the right with low-amplitude compound muscle action potential (CMAP). The
elbow to wrist conduction velocity was normal.
The right ulnar conduction velocity, CMAP
amplitude, and distal latency were normal. The
right median sensory nerve action potential
(SNAP) had a prolonged latency and slow conduction velocity. The left median CMAP distal
latency was mildly prolonged and of normal
amplitude; the conduction velocity was normal.
The left median SNAP was prolonged and had
slow conduction velocity. The ulnar SNAP was
normal. The F-response on the right median
nerve was prolonged, likely secondary to the prolonged distal motor latency. The needle test
showed large motor units potentials only in the
abductor pollicis brevis muscle. There was thus
distal median nerve demyelination and chronic
axonal degeneration in the right, causing a lowamplitude CMAP and large motor unit potentials
with reduced recruitment. It was concluded that
this patient had carpal tunnel syndrome from
RA and likely also from a compression from the
use of a walker.
A 57-year-old man presented with an 8 week history of progressive weakness and wasting in the left hand and mild numbness in the little finger. His past medical history was positive for poliomyelitis as a child, which left residual weakness in both legs. He had an almost complete recovery except for a mild deformity of the left foot. He did have occasional fasciculations in the leg. On examination, the left hand interossei muscles were wasted but without fasciculations. He had a positive Froment’s sign and a Tinel’s sign below the left elbow. When extending his fingers, the last two digits had a tendency to remain flexed. He could not “cup” the left hand. Adson’s maneuver was negative. There was decreased pain sensation in the left little finger and the ulnar half of the ring finger with equivocal decreased pain sensation in the ulnar aspect of the dorsum of the hand. All reflexes were mildly depressed.
Which one of the following explains his acute symptoms?
a. Bilateral carpal tunnel syndrome
b. Diabetic neuropathy
c. Lower trunk brachial plexopathy
d. Poliomyelitis
e. Ulnar nerve entrapment below the elbow
e. Ulnar nerve entrapment below the elbow
Absent were the left digital ulnar and dorsal cutaneous SNAPs. The motor ulnar nerve conduction
velocity from elbow to wrist was normal but was
slow at 39 m/s across the elbow. Conduction
velocity of less than 50 m/s, or 10 m/s slower than
the elbow-wrist segment, or 10 m/s slower than
the velocity across the elbow in the opposite side,
are considered abnormal. The “inching,” or short
(1 cm) segment increment study, revealed a significant prolongation of 0.7 ms (normal, 0.5 ms) at
2 cm distal to the medial epicondyle where there
was also a drop in amplitude over 50%. The needle
EMG showed denervation potentials in the left
ulnar-innervated intrinsic hand muscles, but not
in the median-innervated muscles. There were
also denervation potentials in the flexor digitorum
profundus although not in the flexor carpi ulnaris.
The test also showed electrophysiologic evidence
of bilateral median neuropathy at the wrist. In
addition, there were electrophysiologic findings
consistent with the previous history of polio, characterized by large motor unit potentials in the
lower extremities with mild active denervation in
the gastrocnemius muscle.
A 46-year-old woman had a 4-month history of left shoulder and arm pain, and a 3-week history of numbness in the dorsum of the hand with some arm weakness and now wrist drop. She had severe weakness of the brachioradialis muscle, wrist, and finger extensors on the left. Strength of the triceps muscle was difficult to evaluate because of severe pain. The left brachioradialis reflex was
absent, and ankle reflexes were diminished bilaterally; other reflexes were normal. There was decreased sensation in the left hand first web space. The remainder of her neurologic examination
was normal.
Abnormalities can be localized to which one of the following?
a. C7 nerve root
b. C8 nerve root
c. Median nerve
d. Radial nerve
e. Ulnar nerve
d. Radial nerve
The left median and ulnar nerve SNAPs conduction velocities and amplitudes were normal,
whereas the superficial radial SNAP was absent.
Radial nerve motor conduction could not be studied because of discomfort. The needle test
showed denervation potentials in radialinnervated muscles, including wrist extensor
and the brachioradialis, indicating that the lesion
occurred above the elbow. The normal median
and ulnar-innervated muscles negate a C7 radiculopathy or a lesion of the middle trunk of the brachial plexus. The normal EMG of her deltoid is
evidence against a posterior cord lesion. Denervation in the brachioradialis and extensor carpi radialis and the absent radial SNAP indicate that the main trunk of the radial nerve was affected
with axonal degeneration.
A 65-year-old woman developed pain in the right arm and shoulder with some neck discomfort. A few days later, she presented with a rash on the arm and could no longer raise the arm. Examination revealed an erythematous vesicular rash in the outer aspect of the right arm, and she had weakness of the right deltoid of 2/5. Supraspinatus were 5-/5 and brachioradialis was 3/5. Biceps strength was 3/5; triceps, forearm, and hand muscles were normal. The left arm and leg strength were normal. The right biceps and brachioradialis reflexes were absent; the triceps was normal. Reflexes in the legs and left arm were normal. Sensory examination showed diffuse hypoalgesia in the right lower arm; the affected dermatome was hard to localize. The rest of the neurologic examination was normal.
Which one of the following is most likely?
a. C5 radiculopathy
b. C6 radiculopathy
c. Musculocutaneous mononeuritis
d. Suprascapular neuropathy
e. Upper trunk brachial plexopathy
b. C6 radiculopathy
The sensory and motor nerve conduction studies
were normal. The needle test showed denervation potentials with reduced recruitment of
motor units in the deltoid, biceps, brachioradialis,
and cervical paraspinal muscles, indicating axonal
degeneration of the C6 roots sparing the infraspinatus and rhomboids, as well as forearm and intrinsic hand muscles.
A 44-year-old woman came with nearly a year long history of neck pain radiating to the right arm. Neurologic examination showed normal mentation and cranial nerves. There was no weakness, but there was diminished brachioradialis reflex on the right compared with the left. Sensory examination was normal. The rest of the examination was also normal. EMG findings are shown.
Which one of the following is most likely?
a. Axillary nerve pathology
b. C5 radiculopathy
c. C6 radiculopathy
d. Dorsal scapular nerve pathology
e. Musculocutaneous nerve patholog
b. C5 radiculopathy
The median and ulnar motor conduction velocities, distal latencies, compound muscle action
potential amplitudes, F-responses, and sensory
nerve action potentials were normal. Needle
EMG showed denervation potentials in the right
biceps, deltoid, and rhomboids, and complex
repetitive discharges in the supraspinatus muscle.
The motor units appeared normal in these muscles. Paraspinal muscles were normal. This EMG
was suggestive of a C5 radiculopathy (despite no
paraspinal denervation). This was concluded
because there was involvement of muscles innervated only by C5; in particular, the rhomboid that is innervated by the dorsal scapular nerve that
originates directly from the C5 root and not the
brachial plexus
Which one of the labels in the image below corresponds to the innervation from the lateral plantar nerve?
appears to be superficial peroneal
Which one of the following segments is responsible for finger extension?
a. C4,C5
b. C5,C6
c. C6,C7
d. C7,C8
e. C8,T1
d. C7,C8
Long thoracic nerve
20
Musculocutaneous nerve
8
Radial nerve
10
Suprascapular nerve
3
Ulnar nerve
12
Femoral nerve
F
Genitofemoral nerve
D
Lateral cutaneous nerve of the thigh
E
Common peroneal part of sciatic nerve
5
Nerve to piriformis
4
Inferior gluteal nerve
3
Pudendal nerve
14
Tibial part of sciatic nerve
7
Weakness of elbow extension, wrist extension (wrist drop), finger extension and sensory loss in 1st web space.
Upper limb nerve injuries:
a. Anterior interosseous nerve syndrome
b. Carpal tunnel syndrome
c. Cheiralgia paresthetica
d. Cubital tunnel syndrome
e. Erb-Duchenne palsy
f. Guyon’s canal syndrome
g. Klumpke’s palsy
h. Pronator syndrome
i. Radial tunnel syndrome
j. Saturday night palsy
k. Supinator syndrome
l. Thoracic outlet syndrome
j. Saturday night palsy
Weakness in FPL, pronator quadratus and FDP (Digits 2 + 3); Abnormal pinch sign; no sensory loss
Upper limb nerve injuries:
a. Anterior interosseous nerve syndrome
b. Carpal tunnel syndrome
c. Cheiralgia paresthetica
d. Cubital tunnel syndrome
e. Erb-Duchenne palsy
f. Guyon’s canal syndrome
g. Klumpke’s palsy
h. Pronator syndrome
i. Radial tunnel syndrome
j. Saturday night palsy
k. Supinator syndrome
l. Thoracic outlet syndrome
a. Anterior interosseous nerve syndrome
Sensory loss in palmar ulnar 1½ fingers and hand (dorsal sensory branch arises before wrist); weakness and wasting of hypothenar, all interossei, lumbricals 3 + 4, deep head of FPB, adductor pollicis. Froment’s sign due to weak thumb adduction (flexes IPJ instead).
Clawing of 4 + 5th digits when attempting to extend fingers.
Upper limb nerve injuries:
a. Anterior interosseous nerve syndrome
b. Carpal tunnel syndrome
c. Cheiralgia paresthetica
d. Cubital tunnel syndrome
e. Erb-Duchenne palsy
f. Guyon’s canal syndrome
g. Klumpke’s palsy
h. Pronator syndrome
i. Radial tunnel syndrome
j. Saturday night palsy
k. Supinator syndrome
l. Thoracic outlet syndrome
f. Guyon’s canal syndrome
Entrapment of lateral cutaneous nerve of thigh (femoral n) under inguinal ligament. Sensory loss, burning dysesthesias in anterolateral thigh; no motor weakness
Lower limb nerve entrapment:
a. Anterior tarsal tunnel syndrome
b. Deep peroneal nerve entrapment
c. Distal tarsal tunnel syndrome
d. Exertional compartment syndrome
e. Femoral nerve compression syndrome
f. Fibular tunnel syndrome
g. Meralgia paresthetica
h. Obturator syndrome
i. Piriformis syndrome
j. Proximal tarsal tunnel syndrome
g. Meralgia paresthetica
Sensory loss anteromedial thigh; weakness and wasting of quadriceps femoris; point tenderness in groin; impaired knee jerk. Pain and numbness in saphenous nerve distribution (anterior knee, medial leg).
Lower limb nerve entrapment:
a. Anterior tarsal tunnel syndrome
b. Deep peroneal nerve entrapment
c. Distal tarsal tunnel syndrome
d. Exertional compartment syndrome
e. Femoral nerve compression syndrome
f. Fibular tunnel syndrome
g. Meralgia paresthetica
h. Obturator syndrome
i. Piriformis syndrome
j. Proximal tarsal tunnel syndrome
e. Femoral nerve compression syndrome
Pain and parasthesias in toes and sole of foot (heel spared as sensory branches arise proximal to tunnel), clawing of toes due to weakness of intrinsic foot muscles, typically worse at night. Tinel’s test positive. Ankle eversion+dorsiflexion combined with toe dorsiflexion can reproduce pain (dorsiflexioneversion test).
Lower limb nerve entrapment:
a. Anterior tarsal tunnel syndrome
b. Deep peroneal nerve entrapment
c. Distal tarsal tunnel syndrome
d. Exertional compartment syndrome
e. Femoral nerve compression syndrome
f. Fibular tunnel syndrome
g. Meralgia paresthetica
h. Obturator syndrome
i. Piriformis syndrome
j. Proximal tarsal tunnel syndrome
j. Proximal tarsal tunnel syndrome
Obliquely from lateral thigh, lateral aspect of knee/calf, anterior shin and dorsum of foot including medial four toes and sole of foot including heel.
Dermatomes:
a. C4
b. C5
c. C6
d. C7
e. C8
f. T1
g. L2
h. L3
i. L4
j. L5
k. S1
l. S2
m. S3
j. L5
Medial arm, forearm and dorsal and palmar aspects of hand and ring +little fingers.
Dermatomes:
a. C4
b. C5
c. C6
d. C7
e. C8
f. T1
g. L2
h. L3
i. L4
j. L5
k. S1
l. S2
m. S3
e. C8
Lateral shoulder, arm, forearm, anatomical snuff box, thenar eminence and whole thumb.
Dermatomes:
a. C4
b. C5
c. C6
d. C7
e. C8
f. T1
g. L2
h. L3
i. L4
j. L5
k. S1
l. S2
m. S3
c. C6
Ulnar nerve
L
Median nerve
K
Lateral cutaneous nerve of forearm
H
Superficial branch of radial
J
Diminished brachioradialis reflex with reflex contraction of finger flexors.
Clinical signs:
a. Ape hand
b. Claw hand
c. Froment’s sign
d. Hand of benediction
e. Hoffman’s sign
f. Hoover test
g. Inverted radial reflex
h. Lasegue’s sign
i. Lhermitte’s sign
j. Phalen’s test
k. Spurling’s sign
l. Tinel’s test
m. Volkman’s contracture
g. Inverted radial reflex
On attempting to make a fist, only 4th and 5th digits flex at IPJs.
Clinical signs:
a. Ape hand
b. Claw hand
c. Froment’s sign
d. Hand of benediction
e. Hoffman’s sign
f. Hoover test
g. Inverted radial reflex
h. Lasegue’s sign
i. Lhermitte’s sign
j. Phalen’s test
k. Spurling’s sign
l. Tinel’s test
m. Volkman’s contracture
d. Hand of benediction
Loss of thumb opposition and abduction.
Clinical signs:
a. Ape hand
b. Claw hand
c. Froment’s sign
d. Hand of benediction
e. Hoffman’s sign
f. Hoover test
g. Inverted radial reflex
h. Lasegue’s sign
i. Lhermitte’s sign
j. Phalen’s test
k. Spurling’s sign
l. Tinel’s test
m. Volkman’s contracture
a. Ape hand
Saphenous nerve
8 & 21
Sural nerve
10 & 22
Obturator
5 & 17
