Localization & Practice Cases
Localization & Practice Cases
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Localization in space
Localization in space
Nerve conduction studies can be used to localize a lesion to pre-ganglionic vs post-ganglionic. The ganglion in question is the dorsal root ganglion.
Figure 9.1: Top: normal SNAP and CMAP in nerve conduction without any lesions. Middle: reduced CMAP (in red) but normal SNAP indicative of pre-ganglionic lesion. Bottom: reduced CMAP and SNAP (both in red) indicative of post-ganglionic lesion.
Localization in time
Localization in time
It is primarily EMG (not the nerve conduction portion) that helps determine whether axonal nerve injury is acute or chronic. This is an extremely important concept to help understand why we often don't see abnormalities on EMG in the acute phase of injury and schedule EMG studies a few weeks after patients' symptom onset.
MUAP morphology changes over time in axonal neuropathy
MUAP morphology changes over time in axonal neuropathy
Acute denervation: In the acute phase of Wallerian degeneration the distal axon remains electrically excitable. Usually, MUAP morphology remains normal, but you can sometimes see reduced/low amplitude and duration of MUAPs (due to nascent motor units during early reinnervation). We also see reduced recruitment due to loss of motor units.
Subacute: Surviving terminal axons sprout collateral branches to reinnervate muscle fibers that previously lost their parent axons. As a result, surviving motor units become enlarged by innervating a greater number of muscle fibers. These newly formed axon sprouts are unmyelinated or thinly myelinated and therefore conduct more slowly. This results in MUAPs that are long duration (more total muscle fibers) and polyphasic (asynchronous firing of old and newly innervated fibers). MUAPs may also demonstrate instability (“jiggle”) as a result of immature endplates of the newly innervated fibers.
Chronic denervation with reinnervation: As the reinnervated units mature, there are fewer total motor units (reduced recruitment) but the surviving individual motor units are larger and produce MUAPs with increased amplitude, prolonged duration, and polyphasia.
Abnormal spontaneous activity over time
Abnormal spontaneous activity over time
The earliest abnormal needle EMG findings following axonal nerve injury are positive sharp waves (PSWs) and fibrillation potentials. Due to the process of Wallerian degeneration, it takes between 1 and 4 weeks after a nerve injury before they appear on EMG.
Early after their appearance, fibrillation potentials and PSWs often have relatively large amplitudes. Over time, their amplitudes generally decrease as reinnervation and muscle fiber atrophy occur.
In general, larger-amplitude fibrillation potentials and PSWs suggest more recent denervation, whereas smaller amplitudes are more consistent with a more chronic process. However, amplitude alone cannot precisely date the timing of injury.
Common Patterns in EMG/NCS
Common Patterns in EMG/NCS
Neuropathies
Neuropathies
Axonal lesions
NCS: Reduced amplitudes (CMAP or SNAP). There can be mild increased latency and decreased conduction velocity if there is loss of the faster conducting axons. However, distal latency is generally not increased more than 130% the upper limit of normal and conduction velocity is not decreased below 75% the lower limit of normal in axonal lesions.
EMG: Findings are dependent on the time course of the injury. See section above about localization in time.
Demyelinating lesions
NCS: Increased distal latency (prolonged >130% of ULN) and/or decreased conduction velocity (slower than 75% of LLN). SNAP amplitudes may appear reduced because demyelinating slowing exaggerates temporal dispersion and phase cancellation. Similarly, CMAP amplitude and area may be reduced with prolonged CMAP duration. According to Preston and Shapiro, ≤20% proximal-to-distal CMAP reduction is normal, 20–49% is abnormal but indeterminate, and ≥50% with minimal duration change defines conduction block. Late response (F-wave and H-reflex) latencies are significantly prolonged.
EMG: Typically normal with the exception of reduced recruitment in the presence of significant conduction block.
Radiculopathies
Radiculopathies
NCS: Sensory studies are normal, because the lesion is proximal to the dorsal root ganglion. Motor nerve conduction studies are often also normal in mild radiculopathies, as each muscle receives innervation from multiple nerve roots. In turn, the affected motor fibers may not innervate or may only minimally contribute to the muscle being tested. In severe chronic radiculopathies, axonal degeneration results in reduced CMAP amplitudes, while distal latency and conduction velocity are generally preserved. F waves may be prolonged or absent.
EMG: May show signs of active denervation with abnormal spontaneous activity (fibrillations and positive sharp waves), or reinnervation with a chronic neurogenic pattern (large-amplitude, polyphasic motor unit potentials with reduced recruitment). Changes typically appear first in proximal muscles closest to the affected nerve root (i.e. the paraspinal muscles).
Abnormalities must be present in ≥2 muscles innervated by the same nerve root but different peripheral nerves. Note that the electrodiagnostic criteria for radiculopathy are specific but have limited sensitivity for the reasons discussed above.
Plexopathies
Plexopathies
NCS: Decreased CMAP and SNAP amplitudes can be seen if there is axonal loss affecting both motor and post-ganglionic sensory fibers. Late response latencies may be prolonged. We often study less commonly tested sensory nerves when we are doing a plexus study in order to more precisly localize the lesion. For example, we include testing of the lateral and medial antebrachial cutaneous nerves in upper extremity studies, and the saphenous nerve in lower extremity studies.
EMG: Findings are dependent on the time course of the injury and may show signs of either active (fibrillations and positive sharp waves) or chronic (large amplitude, polyphasic motor unit potentials with reduced recruitment) denervation in affected muscles. Unlike radiculopathies, paraspinal muscles are typically normal, as the lesion is distal to the nerve root.
Abnormalities must be present in at least two peripheral nerves innervated by different nerve roots to meet electrodiagnostic criteria.
Myopathies
Myopathies
NCS: Sensory studies are normal. Motor nerve conduction studies of proximal muscles are typically normal. However, if distal muscles are affected, CMAP amplitudes may be reduced while distal latencies and conduction velocities remain normal. CMAP duration is also generally preserved, except in critical illness myopathy where it is classically prolonged.
EMG: Low-amplitude, short-duration, polyphasic MUAPs with early recruitment.
Practice cases
Practice cases
A useful resource on a stepwise approach to performing and summarizing EMG/NCS findings is outlined in
"How to Interpret a Nerve Conduction Study" by Zelikovich et al, 2025 (PMID 41244751). Try to use this as you go through practice cases.
If you would like additional practice, a great resource is "emgwhiz.com" created by Dr. Zachary London, MD.
Case 1
Case 1
Patient is a 68 year old left handed female who presents for numbness in her hands, especially when driving. Symptoms are minimal in the right hand and prominent in the left hand. She needs to "shake it out" to get feeling back in her hands. What is her diagnosis based on the EMG/NCS results below?
Reference values Median nerve at APB: amp ≥4, latency ≤4, CV ≥50Ulnar nerve at ADM: amp ≥6, latency ≤3, CV ≥50
F wave latency: median nerve ≤31, ulnar nerve ≤32
F wave latency: median nerve ≤31, ulnar nerve ≤32
Reference values Median nerve at digit 2: amp ≥20, peak latency ≤3, CV ≥50Ulnar nerve at digit 5: amp ≥17, peak latency ≤3, CV ≥50Radial nerve at anatomical snuff box: amp ≥15, peak latency ≤3, CV ≥50
Case 1 Answer
Case 1 Answer
Bilateral median neuropathy at the wrists, moderate in the left and mild on the right.
Case 2
Case 2
Patient is a 54 year old male presenting for numbness and weakness in the right leg for a few years. It has been worse in the last six months, and he experiences pain radiating from his lower back down his leg. Examination reveals atrophy of the right calf muscle and difficulty with toe walking in the right leg. What is his diagnosis based on the EMG/NCS results below?
Reference values Peroneal at EDB: amp ≥2, latency ≤6 CV ≥40Peroneal at tibialis anterior: amp ≥3, latency ≤6 CV ≥40
Tibial at abductor hallucis brevis: amp ≥4, latency ≤6 CV ≥40
F wave latency: peroneal nerve ≤56, tibial nerve ≤56
Tibial at abductor hallucis brevis: amp ≥4, latency ≤6 CV ≥40
F wave latency: peroneal nerve ≤56, tibial nerve ≤56
Reference values Sural nerve at posterior ankle: amp ≥6, peak latency ≤4, CV ≥40Superficial peroneal at lateral ankle: amp ≥6, peak latency ≤4, CV ≥40
Case 2 Answer
Case 2 Answer
Right S1 radiculopathy.
Motor nerve conduction studies show that there is no response to stimulation at the right tibial nerve, and that CMAP amplitude is significantly diminished in the left tibial nerve. Note that the SNAPs are normal as we would expect in radiculopathy.
Case 3
Case 3
The patient is a 73 year old female presenting with a few years of gait imbalance and falls. Examination reveals mildly decreased distal sensation, positive Romberg sign, and wide-based, ataxic-appearing gait. What is your impression based on the EMG/NCS results below?
Reference values Median nerve at APB: amp ≥4, latency ≤4, CV ≥50Ulnar nerve at ADM: amp ≥6, latency ≤3, CV ≥50
Peroneal at EDB: amp ≥2, latency ≤6 CV ≥40Peroneal at tibialis anterior: amp ≥3, latency ≤6 CV ≥40
Tibial at abductor hallucis brevis: amp ≥4, latency ≤6 CV ≥40Tibial at abductor digiti quinti: amp ≥3, latency ≤6 CV ≥40
Peroneal at EDB: amp ≥2, latency ≤6 CV ≥40Peroneal at tibialis anterior: amp ≥3, latency ≤6 CV ≥40
Tibial at abductor hallucis brevis: amp ≥4, latency ≤6 CV ≥40Tibial at abductor digiti quinti: amp ≥3, latency ≤6 CV ≥40
Reference values Median nerve at digit 2: amp ≥20, peak latency ≤3, CV ≥50Ulnar nerve at digit 5: amp ≥17, peak latency ≤3, CV ≥50 Radial nerve at anatomical snuff box: amp ≥15, peak latency ≤3, CV ≥50
Sural nerve at posterior ankle: amp ≥6, peak latency ≤4, CV ≥40Superficial peroneal at lateral ankle: amp ≥6, peak latency ≤4, CV ≥40
Case 3 Answer
Case 3 Answer
Sensory neuronopathy, also known as ganglionopathy.
There is complete loss of sensory responses with relative sparing of motor nerves, and no evidence of denervation on EMG.
Case 4
Case 4
The patient is a 62 year old male who presents for weakness and numbness in the right hand. He describes awakening a few weeks ago with horrible pain in the right scapula radiating into the right arm. Within 1-2 days he began to experience weakness and numbness in the right hand. EMG/NCS studies and imaging reports are below.
Reference values Median nerve at APB: amp ≥4, latency ≤4, CV ≥50Ulnar nerve at ADM: amp ≥6, latency ≤3, CV ≥50
F wave latency: median nerve ≤31, ulnar nerve ≤32
F wave latency: median nerve ≤31, ulnar nerve ≤32
Reference values Median nerve at digit 2: amp ≥20, peak latency ≤3.5, CV ≥50Ulnar nerve at digit 5: amp ≥17, peak latency ≤3.1, CV ≥50 Radial nerve at anatomical snuff box: amp ≥15, peak latency ≤2.9, CV ≥50
Lateral antebrachial cutaneous at lateral forearm: amp ≥10, peak latency ≤3.0, CV ≥55Medial antebrachial cutaneous at medial forearm: amp ≥5, peak latency ≤3.2, CV ≥50
Lateral antebrachial cutaneous at lateral forearm: amp ≥10, peak latency ≤3.0, CV ≥55Medial antebrachial cutaneous at medial forearm: amp ≥5, peak latency ≤3.2, CV ≥50
MRI of the brachial plexus
MRI of the brachial plexus
Ultrasound of the brachial plexus
Ultrasound of the brachial plexus
Case 4 Answer
Case 4 Answer
Right brachial plexopathy, lower trunk vs medial cord.
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