An electrodiagnostic report arrives as two tables and a paragraph. The tables carry numbers that mean very little without knowing what each column is measuring, and the paragraph tells you what the person who performed the study concluded.
This guide explains what each value represents and how the pattern — not any single number — produces a diagnosis.
The three numbers on the nerve conduction table
Latency is time, measured in milliseconds, from the electrical stimulus to the start of the recorded response. Jim Lewis R. NCS.T, CNCT describes it simply: “From the time of the stimulus to the onset of the waveform, that tells me time. How long did it take for that signal to travel down the nerve?”
Latency is meaningless without a distance, which is why the distance is fixed by protocol rather than measured on each patient. As Lewis explains, “whether I'm measuring a seven-foot-two individual or a five-foot-one individual, that distance remains the same. And that way I can compare this latency with my normal values.” The standard sensory recording distance is 14 centimetres. If a laboratory uses a different convention it must use it consistently, or the reference ranges stop applying.
Amplitude is the height of the response, in microvolts for sensory studies and millivolts for motor. It is a rough count of working nerve fibres — “amplitude, in a very general sense, is the number of axons.” It may fall slightly as recordings move proximally, but it should not collapse.
Conduction velocity is speed in metres per second, calculated from latency and distance. It reflects the quality of the myelin insulating the nerve.
The pattern that turns numbers into a diagnosis
The single most useful line in the whole subject is Lewis's summary of what each measure is telling you: “Myelin's got more to do with speed. The number of axons has more to do with the number of axons.”
From that, two patterns follow:
- Slow conduction with preserved amplitude points to a demyelinating problem — the insulation is damaged, the wiring is intact. Compression neuropathies such as carpal tunnel typically begin here.
- Reduced amplitude with relatively preserved speed points to axon loss — fewer fibres are conducting. This carries a different prognosis, because axons recover slowly and sometimes incompletely.
Real patients frequently show both, which is why the report is read as a pattern rather than judged on one abnormal value. Lewis's caution applies throughout: “this is neurology, this is the nervous system. And for every rule, there's a hundred exceptions to the rule.”
Why “normal” is not one number
Reference ranges are population-derived and age-dependent. Lewis puts it plainly: “Our nerves work differently when we're in our twenties than they do when we're in our eighties.” A velocity that is unremarkable at seventy may be genuinely abnormal at twenty-five.
Height, limb length and the individual laboratory's technique all move the numbers too, which is why a value should be read against the reference range printed on that report rather than against one remembered from elsewhere.
And before any of it: check the limb temperature. Cold slows conduction and mimics demyelination. Lewis calls temperature “the number one thing,” warms every patient to at least 32 degrees in the upper limb, and flags the counterintuitive case — a Florida patient who has spent fifteen minutes in an air-conditioned waiting room may be cooler than a Minnesota patient who has been indoors for an hour. A report that does not state temperature has omitted the variable most likely to explain a borderline result.
Comparison values, and when they fail
Comparing the symptomatic limb against the asymptomatic one is powerful when a condition is one-sided. Lewis gives brachial plexopathy as the model: “because it's a single-sided abnormality, we can always compare the values on the other side. Gives us an idea of how much axon loss there is, how slow it is.”
It fails where the background condition is bilateral: “that doesn't work in all conditions, especially when we have underlying conditions like a diabetic peripheral neuropathy, because then the side-to-side comparison may not be quite as useful.” Two abnormal sides provide no internal control.
Within-limb comparisons help here. The palmar orthodromic comparison study sets the median nerve against the ulnar across the same wrist — useful, as Lewis notes, specifically for carpal tunnel rather than as a general tool.
Reading the needle EMG section
The needle table is usually organised by muscle, with columns for insertional activity, spontaneous activity, motor unit morphology and recruitment. Each is examined in sequence.
Spontaneous activity is what the muscle does at rest. A healthy muscle goes quiet. Where the nerve supply is injured, fibrillations and positive sharp waves appear — involuntary discharges that Lewis describes as arising when “a nerve is injured and it's making an inappropriate connection to the muscle.” He notes these are identified as much by sound as by sight: “it's better to hear it than to see it.”
Motor unit morphology is assessed during light contraction — duration, amplitude and the number of phases. Long-duration, high-amplitude, polyphasic units suggest chronic reinnervation after nerve injury. Short-duration, low-amplitude units point toward muscle disease.
Recruitment describes how motor units are called into action as effort increases. Reduced recruitment means few units firing very fast — in Lewis's words, “even though I'm contracting as full as I can, I'm not producing a lot of motor units.” A full interference pattern at low amplitude points instead toward myopathy.
How muscle selection localises the problem
Muscle choice is not arbitrary, and understanding it explains why the report lists the muscles it does.
Each muscle is supplied by a specific nerve, travelling from a specific nerve root through a specific part of the plexus. Comparing muscles that share a root but differ in their route localises the lesion. Lewis gives the worked example: “if we stick the needle in the deltoid muscle, we're looking at the axillary nerve, and we're looking at C5. Well, then if I move down to the biceps, I'm also looking at the C5 nerve root, but it's a different place through the brachial plexus. It goes through the lateral cord.”
The aim is maximum coverage from minimum sampling — “we pick them carefully to cover as many anatomical positions, nerve roots, brachial plexus and nerves as we can with the fewest number of needle insertions as we can.”
What the report cannot tell you
Electrodiagnostic testing assesses large myelinated fibres. Small-fibre neuropathy can produce a normal study in a genuinely symptomatic patient. It does not image structures, so it cannot see a disc, and it will not explain pain arising from a joint or tendon. Needle findings take weeks to develop after an injury, so a study performed too early may be normal.
A normal report narrows the differential. It does not close it.
Questions worth asking about your report
- What was the limb temperature? If it is not recorded, ask.
- Which nerves and muscles were examined, and was the other side studied for comparison?
- Is the pattern demyelinating, axonal, or mixed?
- Does the finding match my symptoms, and if not, what explains the difference?
- Does this change the treatment plan, and when would repeating it be useful?
Learn blocks with your hands, not from a page
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