EMG/NCS Flashcards
Bipolar neurons
sensory neurons, LT, pin prickproprioception, bipolar have an axon and a dendrite extending from cell body towards opposite poles…
second order neurons of dorsal column pathway (touch/pressure)
cuneate and gracile nuclei of medulla…then decussate and continue as medial lemniscus and then synapse onto thalamus which extend up to PARIETAL sensory cortex
Second order neurons of spinothalamic pathway (pain/temp)
substantia gelatinosa..then cells decussate and rise as spinothalamic tract until they synapse onto thalamus and then project into the PARIETAL sensory cortex
CV upper and lower ext
50 upper ext, 40 m/s lower ext, decr 2 m/s per decade after 50 yo
Low freq filter is aka
high pass filter
If you lower high freq filter or raise low freq one— amplitude is decreased
shortens peak latency
Sensory NCS filter settings
20-2000 Hz
Motor NCS filter settings
10- 10,000 Hz…..another resource says 2Hz-10kHz
H reflex
stim IA sensory afferent nerve in pop fossa, TRUE reflex
submax stim at a LONG duration (f wave is short duration and supramax)
A wave (axon reflex)
somewhere between F wave and actual CMAP motor response, same spot each time……collateral sprouting pathway so means reinnervation has occurred
concentric electrodes
small listening area, reference is attached, larger/more painful…..less interference
monopolar
broad listening area 360 area
Insertional activity
should be static, crisp…so in duchenne insertional activity will be decr bc of fibrosis……if there is active denervation then insertional activity will be increased (its already irritated and youre irritating it more)
normal duration of insertional activity is 300 ms
in demyelinating injuries: normal insertional activity
axonal: abnormal
Resting activity
fibs/sharp waves heard in this state
fasiculations- anterior horn cell dz, or normal human
myokymia- involuntary, abrupt, regular, marching potentials tightly grouped together, seen in upper trunk radiation plexopathy
complex repetitive discharges
similar to myokymia but closer together and very serrated like a saw , due to denervation then reinnervation, ‘‘ephaptic transmission’’, seen in chronic radic, anterior horn dz, normal patients
Myotonic discharges
involuntary, amplitude steadily decr as muscle fiber fires, ‘‘divebomber’’, seen in myotonic dystrophy, paramyotonia, myotonia congenita AND hyperkalemic periodic paralysis, acid maltase deficiency
Recruitment
activating alpha motor neurons, smallest motor units activated first, then huge type II fibers activated with max intensity . normal firing rate 5 hz, if you incr contraction this motor unit will incr firing rate to 10 hz and you will now recruit a second motor unit that starts firing at 5 hz …. you should be able to get 4 MUAPs on the screen firing 20/15/10/5 Hz
Decreased recruitment
if axonal damage, there will now be increased rate of firing, firing rates of 30, 40, 50 Hz with only 1-2 muaps on screen DOING ALL THE WORK, neuropathic recruitment pattern, polyphasia (more than 5 crossing)
LDLA
large amplitude, long duration = neuropathic MUAPs
LDLA
neuropathic MUAPs
SDSA
myopathic recruitment pattern, all muscle fibers to get a contraction, small ants all of them to move one thing
Reduced duration motor unit potentials are specific for myopathies along with small amplitude, polyphasic and early recruitment.
demyelination
NCS prolonged latency, decr CV, incr temp dispersion
EMG: Normal (if no conduction block) vs decreased recruitment (if conduction block present)
axon loss
NCS: Decr amplitude (possibly decr CV if fastest fibers are destroyed)
ENG: Decr recruitment, PW/Fibs, increased insertional activity
Axonal vs wallerian degeneration
wallerian degeneration is anterograde process, complete by 5 (motor) -10 days (sensory)
Axonal is retrograde process- diabetes
Conduction block
distal amplitude higher than proximal
Neurotmesis
Seddon level 5
complete transection of nerve through epineurium, worst prognosis..absent recruitment
Neurapraxia
focal demyelination with conduction block, nerve still intact just no myelin, good prognosis
Axonotmesis
Crush or stretch injury causing axon death with epineurium stilll intact…if axonotmesis ACUTELY will look like condcion block with decr amplitude proximally and normal cmap distally, but if you wait a few weeks there is axonal loss and fibs/sharps which you DONT see in conduction block
Blink reflex
R1 response, eye sensation to Vm to VII (first spike) in pons
R2: Vm (pons) to Vs in medulla which sends dual signal to VII on both sides, causing double blink
Pathology:
L trigeminal lesion (no Vm inital response, and no R2 pathways bilaterally)
If you stimulate right side with the left trigeminal lesion
the response is normal…..R1 and R2 normal
L facial nerve lesion
Stimulate left side- V1 is intact but cant signal to VII so no R1 …but Vm can go to Vs so there is an R2 on right side, but not left side.
Stimulate right side, totally healthy right side, but no facial output on either left side
The blink reflex study tests CN V and CN VII in the brainstem and peripherally. CN V has two nuclei being tested (Vm and Vs). The Vm nucleus lies within the pons. It accepts CN V input from the face and conducts it to the ipsilateral CN VII nucleus, causing an ipsilateral blink (R1 response). It also simultaneously conducts the impulse to the medulla where the Vs nucleus lies. Vs accepts the impulse from Vm and sends the impulse to the bilateral CN VII nuclei, which then causes a bilateral blink via the orbicularis oculi muscles (R2 response).
blink and move mouth at sime time on accident
synkinesis, secondary complication to facial nerve regeneration
cubital tunnel made of
two heads of FCU
Guyons canal components
Roof- ligament , Floor- flexor retinaculum and hypothenar muscles, medial border- pisiform, latearl border- hook of hamate
Types of ulnar neuropathy at wrist
Type I: motor and sensory
Type II: Motor
Type III: Sensory
+ Wartenberg (cannot addut fingers pinky sign) and Froment signs, Normal DUC on SNAP!
Radial nerve compression in arm
between brachialis and brachioradialis
Cheiralgia parasthetica
Superficial radial pain
Monteggia fx (prox third of ulna) usually has proximal radial dislocation… can cause what
a PIN neuropathy
aching forearm pain with impaired finger extension…abnormal EIP cmap
musculocutaneous neuropathy innervates, and what is its distal branch
impaired coracobrachialis, biceps and brachialis , distal branch is LAC
Paralabral cysts can cause what
pinch suprascapular nerve after spinoglenoid notch…spared supraspinatous, impared infraspinatous
Underneath clavicle what part of brachial plexus
cords…
what scalenes does plexus run thru
anterior and middle
Upper plexus injury
Median SNAP abnormal, but median CMAP normal bc c8-t1…abnormal LAC , emg findings in deltoid, supraspin, infraspin, teres minor, biceps, brachialis, BR, supinator, ECRL, ECRB
Lower trunk palsy
Claw hand lumbrical weakness, + OK sign, wartenberg sign , froment sign , impaired sensory medial arm, medial forearm and hand
Neurogenic TOS compressed by what
clavicle and first cervical rib, anteerior and middle scalenes, pec minor , worse with overhead activity and swimming
median snap normal, but MAC is abnormal
Roos and Adson test
Roos lift hand sup and open and close and reproduce symptoms
Adson– extend right arm look to the right and bring arm posteriorly back should reproduce symptoms and diminish radial pulse
Commonly affected nerves in parsonage turner syndrome
mostly suprascapular nerve, also long thoracic nerve and AIN
Martin Gruber Anastomosis
median nerve fibers cross over to the ulnar nerve in the arm….so now it innervates ADM and FDI as well….so distal snap is larger ….so ulnar stim at elbow is smaller bc only ulnar fibers…..must stim median nerve at cubital fossa while electorde at ADM/FDI and youll get a small response that when added to the other cmap will be a normal cmap
Riche cannieu anastomosis
median nerve crosses to join ulnar nerve at hand….it appears ulnar nerve innervates the entire hand..if you record cmap from apb you will see no cmap if you record cmap from apb and stimulate ulnar nerve at wrist you will see a normal CMAP
The Riche-Cannieu anastomosis is a communication between the deep branch of the ulnar nerve and the recurrent branch of the median nerve in the hand. It can produce an all-ulnar hand. Therefore, if the ulnar nerve is injured proximally, the muscles normally innervated by the median nerve (but now innervated via the ulnar nerve anastomosis) may show signs of injury.
Conversely, if the patient has a complete laceration of the median nerve at the wrist, he or she may still retain thenar function via the anastomosis.
baxters nerve
calcaneal nerve
femoral nerve breaks up into saphenous nerve at hat structure
vastus medialis and sartoriius
lateral femoral cutaneous neuropathy
L2-3, inguinal ligament attaches to ASIS and what sits under that is LAC….so tight inguinal ligament can entrap it
Lumbosacral plexopathy
L1-S4 nerve roots, ventral RAMI not dorsal (that would be radic)
Lumbar plexus L1-4 anterior div obturaor, post femoral
sacral plexus L4-S4- anterior is tibial, posterior common fibular
superior and inferior gluteal nerve directly off of sacral plexus
Ideal temp for lower and upper ext
Upper limb 32
Lower limb 30 C
Compression at arcade of Frosche
PIN neuropathy – Compression by the Arcade of Frohse can cause posterior interosseous neuropathy (PIN-opathy) - a pure motor neuropathy that would spare brachioradialis (not a PIN-innervated muscle) and show normal radial SNAPs. Normal SNAPs to digits 1,2,5, snuffbox. Normal EMG to BR. Abnormal EMG to EIP
biceps, brachialis, coracobrachialis, pronator teres, flexor carpi radialis, flexor digitorum superficialis, pronator quadratus, flexor pollicis longus, pectoralis major, and lateral antebrachial cutaneous nerve are all affected in what
lateral cord brachial plexopathy
CMT1A and HNPP gene alterations
CMT: PMP 22 duplication
HNPP: Deletion of PMP 22
polyphasia is from what, and large MUAPs are from what
Polyphasic potentials represent ongoing reinnervation due to collateral sprouting of existing axons. The polyphasic property arises due to non-uniform myelination of these collateral sprouts during this early reinnervation stage. Once myelination is complete, the motor unit’s branches all conduct the action potential at essentially the same speed, producing a nice, uniform “roller coaster” bump (uniform-appearing MUAP) rather than the polyphasic, serrated potential seen in unmyelinated collateral sprouts.
Myasthenia gravis EMG
Motor unit action potential amplitude variability is a characteristic abnormality observed during routine electromyography in patients with neuromuscular junction disorders. This finding is due to the variability in the total number of single muscle fibers being activated at any single time.
The sensory component of the peripheral nervous system lacks a neuromuscular junction and hence the sensory responses should be normal.
Motor amplitudes can be small, but this is usually only in severe cases. Motor conduction velocities are normal, since this study assesses the conduction along the motor fibers.
Monopolar needs
Concentric needles
Bipolar needle
Single fiber
Monopolar-larger recording area, seperate needle for reference, records more abnormal activity
Standard concentric: Unidirectional recording, smaller recording area, MUAPs have smaller amplitudes;
Bipolar concentric: active and reference wires within its lumen; BEST FOR isolating MUAP, expensive and more painful
Single fiber: NMJ disorders,
What electrodiagnostic criteria are included in the diagnosis of peripheral nerve demyelination?
The criteria require conduction velocity to be reduced in 2 or more nerves, compound muscle action potential conduction block or abnormal temporal dispersion in 1 or more nerves, prolonged distal motor latencies in 2 or more nerves, and prolonged F wave or absent F wave. Three of these four criteria must be present.
F wave is short duration, anti motor, ortho motor
Hereditary motor sensory neuropathies (Charcot-Marie-Tooth disease, type 1) EMG/NCS findings
vs AIDP/GB
usually have conduction slowing without temporal dispersion of compound muscle action potentials. Acquired demyelinating conditions such as Guillain-Barré Syndrome or acute inflammatory demyelinating polyradiculoneuropathy (AIDP) usually have conduction block and temporal dispersion on nerve conduction studies in addition to conduction slowing.
sensitivity vs specificity MRI vs EMG
MRI is more sensitive than EMG for cervical radiculopathy but not as specific.
Meds for diabetic neuropathy
- If clinically appropriate, pregabalin should be offered for the treatment of PDN (Level A evidence).
- Gabapentin, sodium valproate, amitriptyline, venlafaxine, duloxetine, dextromethorphan, morphine sulfate, tramadol, oxycodone, capsaicin, isosorbide dinitrate spray, and percutaneous electrical nerve stimulation should be considered for the treatment of PDN (Level B).
- Lidoderm patch may be considered for the treatment of PDN; venlafaxine may be added to gabapentin for a better response (Level C).
TFL
L4,5, superior gluteal nerve!!
temporal dispersion,
which is pathognomonic for demyelinating disease, and is among the diagnostic criteria for acute inflammatory demyelinating polyradiculoneuropathy (AIDP), chronic inflammatory demyelinating polyradiculoneuropathy (CIPD), multifocal motor neuropathy (MMN), multifocal acquired demyelinating sensory and motor (MADSAM) neuropathy or Lewis-Sumner syndrome, and distal acquired demyelinating symmetric (DADS).
LEMS amplitude and increment
In LEMS, single stimuli produce a reduced release of acetylcholine and a reduced endplate potential. At rest, many of the endplate potentials do not reach threshold, resulting in small amplitude CMAPs on routine motor nerve conduction studies. Slow RNS (3Hz) studies results in a decremental response similar to myasthenia gravis. However brief (10s) isometric exercise produces a marked increase in CMAP amplitude (post-exercise facilitation) due to calcium accumulation in the presynaptic nerve terminal with subsequent enhancement of the release of acetylcholine. The CMAP is often significantly larger and commonly increases in amplitude by much more than 1000%.
. More than 10 % decrement between the first and the second response, followed by return to normal after a ten second maximum isometric contraction is in favor of MG whereas a 20-200% increment favors LEMS.
Critical illness polyneuropathy is an acute, diffuse, predominantly __ ___ PN
motor axonal peripheral neuropathy.
Brachial plexopathy due to metastaic disease common at what level
Brachial plexopathy due to metastatic involvement is referred to as neoplastic brachial plexopathy most commonly associated with lung and breast carcinomas. Particularly inferior trunk and medial cord are involved, presumably due to extension from upper lung fields or lymph nodes. Motor weakness and sensory loss is in the distribution of C8-T1. Horner’s syndrome can be seen in 23% and implies epidural invasion by the tumor at T1 level.
muscle most commonly involved in c5 post decompression radic
deltoid and biceps
phrenic nerve candidate level of injury
Patients with cervical spinal cord injuries above C3 are usually good candidates for phrenic nerve pacer placement.
Positive deflection for Martin Gruber
Because these fibers do not have to go through the carpal tunnel, the action potential reaches the adductor pollicis muscle before the median fibers get to the APB muscle. Therefore, there is an initial positive (downward) deflection with stimulation of the median nerve in the antecubital fossa (this occurs because the active electrode is not over the motor point of the muscle being activated, the active electrode is over the APB muscle, not the adductor motor point).
The excessively fast median forearm conduction velocity noted with a Martin-Gruber anastomosis when carpal tunnel is present is due to the proximal stimulation of ulnar fibers (which do not have to travel through the carpal tunnel). This leads to a spuriously decreased latency with proximal stimulation compared with the increased latency of the distally stimulated median nerve.
H latency side to side difference
A side-to-side latency difference of more than 1.5 msec is usually considered significant. Temp not significant bc more proximal muscle is warm
Alcoholic neuropathy
axonal sensory motor neuropathy
CSI
Three parameters are tested: difference in the latency of the ulnar and median sensory response from digit 4 (at 14 cm), difference in the radial and median sensory response from the thumb (at 10 cm), and median and ulnar midpalm orthodromic stimulation (at 8 cm). If the added differences total more than 0.9 msec, CTS is confirmed.
Involuntary group repetitive discharge of the same motor unit action potential with a high-frequency pattern within the burst and a slow-frequency between the burst
Myokymia
Spontaneous discharge of a single motor unit potential at very high frequencies, with a notable decrementing response
Neuromyotonic discharges
Action potentials of muscle fibers firing in a prolonged fashion that wax and wane in both amplitude and frequency
Myotonic discharges
Spontaneous action potentials of single muscle fibers that are firing autonomously in a regular fashion
fibrillation potentials (Triphasic)
Myopathic motor units
In myopathies, motor units usually have low/small amplitude (less than 1 mV when using a monopolar needle), short duration, polyphasicity, and early recruitment.
H reflex muscles
In healthy adults, an H-reflex can be obtained in the flexor carpi radialis muscle and can therefore be useful in the assessment of C6/C7 radiculopathies. In the healthy adult, an H-reflex elicited in any muscle besides the gastrocnemius-soleus or the flexor carpi radialis is considered pathological and may indicate an upper motor neuron lesion.
Normal latency 28-30 msec, side to side diff of 0.5-1 msec is sig
For f wave normal latency upper limg 28 msec, lower limb 56 msec, side to side diff of 2 msec in upper limbs is sig, 4 msec in lower limbs
Chronic neuropathic motor units
In chronic neuropathies, the motor units may be of large amplitude, long duration, and polyphasic.
H reflex muscles
In healthy adults, an H-reflex can be obtained in the flexor carpi radialis muscle and can therefore be useful in the assessment of C6/C7 radiculopathies. In the healthy adult, an H-reflex elicited in any muscle besides the gastrocnemius-soleus or the flexor carpi radialis is considered pathological and may indicate an upper motor neuron lesion.
The H-reflex is a monosynaptic spinal reflex involving both motor and sensory fibers. As it is a reflex and involves the Ia fibers, very little intensity is required (hence the submaximal stimulation, unlike the F-wave test). Increasing the intensity past the H-reflex peak amplitude will result in a drop in H-reflex amplitude and an increase in M-wave amplitude. The H-reflex tests for the same fibers involved in the ankle reflex (S1) and can help in differentiating an L5 from an S1 radiculopathy. An H-reflex side-to-side difference of more than 1.5 msec is considered significant.
Gain for sensory sturdy
20 mcV/division
“you want to see 20 mcv/divison on screen, it’ll be bigger than seeing 100 mcv/division”…increasing the gain is deccreasing the number and vise versa
Posterior interosseous nerve innervates
supinator, extensor digitorum communis, extensor digiti minimi, abductor pollicis longus, extensor pollicis longus and brevis, and extensor indicis propius muscles
single fiber sens/specificity
Single fiber EMG (SFEMG) has a very high sensitivity of approximately 99%, but low specificity in the evaluation of a neuromuscular junction disorder. Thus, when negative, SFEMG is helpful to rule out a suspected neuromuscular disorder. SFEMG can demonstrate jitter and blocking in some neurogenic processes such as motor neuron disease.
jitter
Jitter is the variation in interpotential interval between paired action potentials in the SAME MOTOR UNIT. It can be measured using SFEMG.
The posterior cord divides into the
radial and axillary nerves
Nerve bx may be required in what neuropathy
Mononeuropathy multiplex involves lesions in more than one peripheral nerve that may occur simultaneously or successively. The most common cause of mononeuropathy multiplex is vasculitis, which often requires nerve biopsy for identification of the cause. Nerve biopsy is rarely required in the other patterns.
at NMJ electric impulse propagates along axon and is converted into a
chemical reaction
3 types of alpha motor neurons
alpha- extrafusal fibers, skeletal muscle
gamma- intrafusal fibers, muscle spindle
beta- intrafusal and extrafusal fibers
EMG evaluates alpha motor neurons
Henneman size principle
smaller alpha motor neuron has a LOWER threshold of excitation and will be recruited FIRST during contraction; larger alpha motor neuron has a HIGHER threshold of excitation and is recruited when more motor units are needed to generate a contraction.
Muscle fiber types
Type I, smaller cell body, thinner axon, Lower innervation ratio, slower twitch (CV slow) , aerobic, longer contractions (back,leg,glut), resistant to fatigue, strong….low intensity long duration
Type II, larger cell body, thicker axon diameter, higher innervation ratio, faster twitch fibers, white muscle, anaerobic, short contraction (arms) , easily fatigue, weak
Nerve fiber classification
Ia: largest, fastest, EMG evaluates, alpha motor neurons and sensory is muscle spindle
Ib: golgi tendon, touch, pressure
II: intra and extrafusal, sensory is muscle spindle, touch, pressure
III: Gamma motor neurons, muscle spindle, sensory is touch, pain and temp
IV (b and c): pain and temp, pre and post ganglionic autonomic fibers, slowest
To bring membrane back to resting state ** channel inactivation and ** channel activation
Na, K
safety factor depends on two parameters
quantal content- number of ach quanta released with each nerve depolarization
quantal response: ability of ach receptors to respond to ach molecules that are released
demyelination increases or decr membrane capacitance
increases
Remyelination myelin and CV
myelin is thinner with shorter internodal distances, CV improves but is usually slower than normal
axon injury types (2)
wallerian degeneration or axonal degeneration….axon degen begins in a dying back fashion and affects nerves in a length dependent manner– degeneration starts distally and ascends proximally
wallergian degen- at site of nerve lesion, the axon degenerates distally and the nerve seg proximal to the injury site is essentially intact …for ditsal motor axons degeneration complete in 7 days, for distal sensory axons the degeneration is generally complete in 11 days.
axon regrowth velocity
1 mm per day, 1 cm per week and 1 inch per month
low amplitude, long duration and polyphasic potentials that occur with reinnervation are known as *** potentials
nascent
Sunderland clasification
type 1: neuropraxia/conduction block type II: axonal injury (axontemesis) type III: type 2+ endoneurium injury type IV: type 3+ perineurium injury type V: type 4 + epineurium injury
volte divided by resistance
current
anodal block
theoretical local block that occurs when reversing the stimulator’s cathode and anode. this hyperpolarizes the nerve , thus inhibiting the production of an action potential
signal to noise ratio
square root of the number of averages performed….the averages must be incr by a factor of 4 to double the S:N
S:N = signal amplitude x sq root of # averages performed divided by Noise amplitude
elevating low freq filter
reducing high freq filter
reduces peak latency
does not change onset latency (fastest fiber is still there)
reduces amplitude
changes potentials from bi to triphasic
prolongs peak latency, reduces amp, prolongs onset latency (fastest fiber is not there anymore), creates a longer negative spike
sensory , motor, EMG
sweep speed and sensitivity
Sensory sweep speed: 5 msec
Sensory sensitivity: 10 micro volt
Motor sweep speed: 2 msec
Motor sensitivity: 5 mV
EMG ss: 10 msec
EMG sensitivity: 100 micro volt insertional activity, 1 mV recruitment pattern analysis
If you make electrodes less than 4 cm apart what happens to peak latency, amplitude, duration, rise time
Peak latency: decreased
amplitude: decreased
duration: decreased
Rise time: decreased
median motor distal latency
3.7
median sensory distal latency
3.2
ulnar motor distal latency
3.2
ulnar sensory distal latency
3.2
radial motor distal latency
2.4
superficial radial sensory distal latency
2.3
peroneal motor distal latency
4.5
tibial motor distal latency
3.4
sural sensory
3.5
superficial personal sensory distal latency
2.9
vincristine neuropathy
sensory motor…distal and symmetric
what happens to amplitude and peak latency when snap recording and reference are moved closer than 4 cm apart
amplitude decreased and peak latency decreased…..bc the reference starts to pick up signals at a similar time and subtracts out more so amplitude decreased and also same effect for peak latency
What K levels for:
Flex foot, SACH foot, SAFE foot, STEN foot
Sach is basic, inexpensive for K1 users, Safe is for K2 users on uneven surfaces and is more heavy and expensive compared to SACH…and STEN foot is for K level users as well..and Flex foot is for higher K levels for vigorous activities, and is very costly.
radial palsy with midshaft humerus fx results in what
weakness in elbow flexion (brachioradialis), supination, and wrist drop (ECRL/B/ECU)
supra max stim causes
decr conduction times, shortened latencies, altered waveform, amplitudes UNCHANGED
EMG filter settings
20Hz-10,000 Hz (10kHz), EMG sweet speed is 10 ms
Default gain for normal recruitment pattern,
Gain for Motor NCS
sensory NCS sweet speed
1 mV
Gain for motor NCS: 5 mV
2 ms
what med can cause myotonic discharges
proranolol
isaac syndrome tx phenytoin
Isaac’s syndrome stems from antibodies to the potassium channels on the motor nerve, which causes progressive muscle stiffness, and cramping. There should not be sensory deficits.
paraneoplastic syndrome results in what kind of neuropathy
sensorimotor axonal findings
HIV EMG findings
sensorimotor demyelination, mostly motor > sensory, sometimes axonal too.
disuse atrophy muscle fibers affected Type I or II?
II muscle fibers
leprosy neuropathy
motor>sensory, demyelinating
Motor unit vs Muscle fiber potentials
Muscle fiber:
Epp, Fib, PSW, Myotonic discharge, CRD, Douplet/triplet
Motor unit:
Myokymic discharge, cramp potential, neuromyotonic discharge, rest tremor
