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The Electrodiagnostic evaluation is considered to be an extension of the neurological examination of the peripheral nervous system. At times it can reveal some dysfunction of the nerves and muscles, which was not detected in the physical exam.1It is commonly used to diagnose entrapment neuropthies, plexopathies, radiculopathies, neuromuscular junction disorders, myopathies, anterior horn cell disease and can prognosticate functional recovery. It has a role in localization of the site of the lesion, and identifying the pathology2

The velocity of conduction of the action potential depends on the diameter of the axon and the presence of myelin. In unmyelinated fibers e.g. autonomic and pain fibers the conduction velocity is between 5-15m/sec, while in myelinated fibers the conduction velocity rises to 40-70m/sec. 2,3

Nerve conduction (NCS):

When a nerve is electrically stimulated the action potential can be recorded through surface electrodes and is termed compound nerve action potential (CNAP). CNAPs measure the potentials of large myelinated fibers 2,3. The nerve, the side tested, the site of stimulation and recording, the distances between stimulation and recording site, and the temperature should be documented in the report.4

Sensory nerve conduction (SNCS):

Sensory nerve action potentials (SNAP) are recorded after the stimulation of a sensory nerve. If it was propagated in a physiologic direction it is termed orthodromic.Antidromic impulses are recorded an unphysiologic direction.2

Reporting SNCS should mention whether the test was performed orthodromically or antidromically, whether peak or onset latency was used, and the amplitude (peak to peak or baseline to peak) of the SNAP.4,5 Onset latency reflects the arrival of the impulse in the fastest conducting fibers, but can be difficult to measure. Peak latency is easier to record and therefore more commonly used.2

Motor nerve conduction (MNCS):

MNCS measure the compound muscle action (CMAP) potential .The distal latency of the CMAP includes the conduction of the impulse in the nerve, across the neuromuscular junction, and in the muscle fibers. To measure the conduction velocity it is necessary to stimulate the nerve at two sites, and the distance between the two sites is divided by the difference in latencies. This eliminates the conduction time across the neuromuscular junction, and the muscle fiber. 2

Reporting MNCS should include comment on distal latency, amplitude (baseline to negative peak) and conduction velocity along the different nerve segments. 4,5 Duration of the negative phase and overall area under the curve are helpful as well.

Late responses:

H reflexes (Hoffman) result from the activation of the lowest threshold Ia fibers of a mixed nerve. An afferent voley reaches the motor neurons of the corresponding nerve and a late response is recorded from the muscle. Clinically the H reflexes can be recorded from the soleus (S1) and the flexor carpi radialis(C6/C7) in adults. Usually only the the H reflex latency is noted .H reflexes are most useful in detection of S1 radiculopathies.2,5

F waves result from the supramaximal antidromic stimulation of a motor nerve. This results in the activation of a subpopulation of anterior horn cells (2-5%) of the corresponding motor nerve and the generation of an orthodromic action potential that is recorded on the distal muscle. This potential has a small amplitude (100-200µV) and a prolonged latency.2,5

When recording F-waves, indication of the nerve tested, muscle tested and the minimal F wave latency are recommended. Other parameters e.g. F wave persistence and chronodispersion can be measured but require more responses to be recorded.4,5

F wave latency measurement is most useful in detecting multifocal or diffuse demyelinating proximal lesions, particularly in the early stages. It is not useful in root lesions, as muscles are supplied by multiple roots. Root lesions typically spare the fastest conducting fibers which are mainly measured by the F wave latency.5

Blink reflexes are done to evaluate patients with suspected facial nerve, trigeminal nerve or brainstem lesions and sometimes in evaluation of patients with polyneuropathy.6

Repetitive nerve stimulation (RNS):

This is performed to assess the neuromuscular junction (NMJ) . NMJ disorders are classified into post synaptic disorders e.g. Myasthenia Gravis (MG), presynaptic disorders e.g. Eaton Lambert Syndrome, and combined pre- and post synaptic disorders e.g. aminoglycoside induced myasthenic syndrome. 7 It is first necessary to perform routine motor , sensory nerve conduction studies, and electromyography to rule out a neuropathic or a myopathic disorders.5

Supramaximal stimulation is used in RNS with the recording electrodes firmly attached in a belly tendon fashion; similarly the stimulating electrodes should be firmly attached to minimize movement. The limb should be immobilized and warm.7

  1. RNS should be performed at rest at 3HZ for 5-10 impulses, and repeated 3 times 1 minute apart. A consistently observed decrement between the 1st and the 5thresponse of 10% or greater is considered abnormal 3
  2. If a significant decrement is observed then the patient should perform maximumvoluntary activity for 10 seconds and immediately the RNS is repeated to demonstrate a repair of the decrement.3
  3. If no significant decrement is observed in the initial RNS the patient should perform maximal voluntary exercise for 1 minute and RNS at 3 HZ should be repeated every 1 minute for 4 minutes to demonstrate post exercise exhaustion.3
  4. If a significant decrement is then observed demonstration of repair after 10 seconds of maximal voluntary exercise is necessary.
  5. RNS should be performed in one distal, and one proximal muscle, and if necessary in a facial muscle.3

Indication of the nerve stimulated, the side, the muscle used for recording, if the muscle was at rest or if the test was done after exercise, the duration of the exercise and the time interval after the exercise is necessary. The rate of stimulation and the number of stimuli used should be mentioned4.

EMG testing:

Theoretically the electrophysiologic signal resulting from the voluntary firing of a MU is the summation of the firing of all the muscle fibers (MF) within the motor unit (MUAP). Generally MUAPs have a simple triphasic configuration. The increasing phases or turns (complexity) is a sensitive nonspecific marker of abnormality. The recruitment pattern reflects the graded activation of MUAPs, on voluntary contraction, while the interference pattern reflects full activation5.

Insertional activity results from the movement of the needle in the muscle. Spontaneous activity are waves seen in the absence of needle movement or voluntary muscle contraction2Fibrillation potentials(fibs), positive sharp waves (PSW), complex repetitive discharges, and myotonic discharges are abnormal discharges from a single muscle fiber. Fasciculations, myokymic discharges, cramps and neuromyotonic discharges emerge from the motor unit

It is important to sample an adequate number of muscles and to start with the muscles most likely to be affected in case the patient does not tolerate further testing. Reporting should include the muscles tested, the side, the presence or absence of abnormal insertional activity or spontaneous activity at rest. Reporting muscle activity on volition should include comment on size, amplitude, duration and phases of the MUAPs, motor unit recruitment, and the interference pattern.4,5.



Electrodiagnostic testing can differentiate between demyelination and axonal loss in a nerve.

  1. In demyelinating lesions the compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) are large distal to the lesion, and demonstrate slowing, potential conduction block and temporal dispersion when stimulated proximal to the lesion. In pure demyelinating lesions there should not be findings of axonal loss on EMG.
  2. In axonal loss the CMAP and SNAP amplitudes are reduced with stimulation of the nerve proximal and distal to the lesion as compared with the contralateral side with relatively preserved latencies and conduction velocities. EMG of the muscles supplied by the affected nerve show decreased recruitment followed by the appearance of denervation potentials. In the chronic stages reinervation follows with enlargement of the motor unit size, increased number of phases and duration.2,3


  1. Electrodiagnosis is useful in localization of the site of the nerve lesion whether it involves the root, plexus or peripheral nerve. The presence of a normal SNAP in an area of sensory loss is indicative of a lesion proximal to the dorsal root ganglion, or in a central sensory pathway. Focal conduction slowing or block on nerve conduction studies can localize a site of entrapment. The distribution of the abnormalities in the muscles tested can also clarify the site of the lesion.2,5
  2. EMG can be helpful in identifying neuromuscular junction disorders, myopathic and neuropathic disorders through the MUAP size, configuration and stability.


  1. Identifying whether a neuropathy is predominantly sensory or motor, length dependent, and primarily axonal or demyelinating process can also guide the classification and workup.5
  2. EMG can predict the activity of some myopathic disorders. The presence of fibs and PSW in association with short duration MUAPs indicates active disease in inflammatory myopathy. They disappear with treatment.7
  3. In ongoing denervation fibs, PSWs, decreased recruitment and polyphasic motor units are present. In chronic denervation fibs and PSWs are minimal and small in amplitude with large sized polyphasic MUAPS.

Measurement and prediction of outcome:

  1. NCS can be an indicator of the severity of a lesion. The larger amplitude of the nerve action potential distal to the lesion the better prognosis for recovery.5
  2. EMG can be a measure of the severity of a lesion. Abnormal spontaneous activity indicates axon loss, the quantity of which is unrelated to the severity of the lesion. The absence of motor unit action potentials in the muscles supplied by a nerve indicates no action potentials traversing the lesion due to either axon loss or conduction block.


  1. There is an increasing role for ultrasound examination of the nerves and muscles as a complementary technique to the electrodiagnostic examination. It can guide needle placement in electromyography thus improving safety and accuracy. It may also help localize nerves that are challenging to find to perform NCS.
  2. Motor unit number estimation is a technique that can be used to determine the approximate number of motor units in a nerve. It can measure motor unit loss, change in the motor unit size, and collateral reinnervation. It is been used to study amyotrophic lateral sclerosis, poliomyelitis, spinal muscular atrophy, aging and a neuropathies in the reseach setting.9
  3. Electrical impedance myography is a new non-invasive technique for the evaluation of neuromuscular disease that relies upon the application and measurement of high-frequency, low-intensity electrical current. It can detect pathologic changes in muscles e.g. myocyte atrophy, reinnervation, edema, deposition of connective tissue and fat, and grade the severity of neuromuscular diseases.10


  1. In electrodiagnostic studies axonotemeis and neurotemesis cannot usually be distinguished, as the primary difference between the two is the supporting structure integrity.2
  2. Patients with small fiber neuropathies may show normal electrodiagnostic studies as they do not involve the larger fibers, which are studied in electrodiagnostic testing.5
  3. EMG of the MUAP can measure only physiologic changes that affect the electrical signal of the muscle fiber, and is unable to detect some pathologic changes (e.g., abnormal accumulation of storage products like glycogen).5
  4. Many findings in electrodiagnostic testing are sensitive indicators of abnormality, but are not specific for a disease. An example is that fibrillation potentials and positive sharp are present in both neuropathic and myopathic disorders, and sometimes even in neuromuscular disorders.5


  1. Podnar S. Critical reappraisal of referrals to electromyography and nerve conduction studies. European J Neurol 2005;12:150-5.
  2. Robinson LR. Role of neurophysiologic evaluation in diagnosis.Journal of the American Academy of Orthopedic Surgeons. May/June 2000: Vol 8, No 3:190-199.
  3. Preston DC, Shapiro BE. Electromyography and Neuromuscular Disorders. Clinical –Electrophysiologic Correlations.1998. Butterworth- Heinemann.
  4. Jablecki CK, Busis NA, Brandstater MA, Krivickas LS, Miller RG, Robinton JE. Reporting the results of needle EMG and nerve conduction studies: An educational report. Muscle Nerve 2005:1-4.
  5. Barboi AC, Barkhaus PE. Electrodiagnostic testing in neuromuscular disorders. Neurol Clin 2004;4:619-41.
  6. Katriji B. The clinical electromyography examination. An overview. Neurol Clin N Am 2002;20:291-303.
  7. Shin J Oh. Principles of Clinical Electromyography, Case Studies. 1998. Williams& Wilkins.
  8. Boon A. Ultrasonography and electrodiagnosis: are they complimentary techniques? PM&R 2013;Suppl 1 S100-106
  9. 9- Gooch CL, Doherty TJ, Chan KM, Bromberg MB, Lewis RA, Stashuk DW, Berger MJ, Andary MT, Daube JR. Motor unit number estimation: a technology and literature review. Muscle Nerve. 2014;50(6):884.
  10. Seward B. Rutkove. Electrical Impedance Myography: Background, Current State, and Future Directions. Muscle Nerve. 2009 Dec; 40(6): 936–946.

Author Disclosure

Eathar A. Saad, MD
Nothing to Disclose

Abir Naguib, MD
Nothing to Disclose