EMG diagnosis of radiculopathy is based on
Abnormal “insertional activity”: positive waves and fibrillations are seen in response to needle insertion into skeletal muscles
Conduction block: compression of a nerve root may slow or block late responses through a specific nerve root level responses (Fwaves/Hwaves)
Axonal changes in muscles: damage to individual nerve axons will cause ‘denervation’ of motor units followed by reinnervation (axonal repair)
Muscle weakness or atrophy: provides clinical confirmation of EMG findings
Severity of radiculopathy is based on extent of axonal damage to muscles, degree of conduction block when present, extent of abnormal insertional activity (graded from 1+ to 4+), amplitude changes in motor response to peripheral nerve stimulation reflecting atrophy of distal muscles, and reduced voluntary recruitment.
How is acute radiculopathy differentiated from chronic radiculopathy?
In acute radiculopathy trains of positive waves followed later by fibrillation potentials are seen in response to injury to nerve roots. These are spontaneous single muscle fiber discharges that continue until either the muscle fiber is reinnervated or completely atrophies.
With acute lesions this “abnormal insertional activity” occurs in paraspinal muscles within 5-7 days after nerve root injury, in proximal extremity muscles in as little as 10-14 days, but typically may take as long as 3-6weeks before appearing in the more distal limb muscles.
As lesions become more chronic these ‘denervation’ potentials tend to gradually disappear and may be replaced by complex repetitive discharges including ‘bizarre high frequency discharges’—these groups of fibrillation potentials take time to develop, at least several months after acute injury.
A less common finding also indicative of chronic change are fasciculation potentials—these are typically localized to only a few muscles.
Fibrillations persisting for greater than three months following initial onset suggest an ongoing or progressive lesion. This is especially true if positive wave potentials are of large amplitude. Small amplitude positive waves, on the other hand, may be seen months later due to incomplete reinnervation.
In addition to progressive changes in insertional activity, chronic radiculopathy is marked by changes in configuration, firing rates, and recruitment of motor units: motor units become polyphasic with a mix of high amplitude, long duration, rapid firing motor units. Recruitment may depend on the extent of axonal repair as well as voluntary effort.
After a neuropathic lesion causes nerve root or peripheral nerve axonal loss the time lapse until abnormal findings are seen on EMG also depends on the intervening distance between the lesion and the muscle. With acute nerve root injury the only finding may be reduced recruitment of normal appearing motor units correlating with clinical weakness. The next change usually takes at least 5 days, more likely 10-14 days when fibrillation potentials and positive waves (evidence for denervation) appear in paraspinals (the muscles most proximal to the lesion if compression involves posterior rami to paraspinals as well as anterior rami divisions of nerve roots to the periphery). In another 2-3 weeks fibrillations and positive waves appear in more proximal limb muscles. It may take an additional several weeks (5-6 weeks after injury) for changes to occur in the most distal limb muscles.
During this initial injury phase motor unit morphology remains normal but with reduced recruitment. Over time as denervation is followed by reinnervation, polyphasic motor units appear as evidence of axonal repair. These will be followed later on by longer duration, higher amplitude polyphasic motor units. Within months as reinnervation becomes more successful, fibrillations diminish but large amplitude rapid firing polyphasic motor units with decreased recruitment remain.
By looking at spontaneous activity (fibrillations, positive waves), morphology of motor units, and recruitment patterns, the time course of any neuropathic lesion can be approximated. Additional data reflecting the severity of the radiculopathy include evidence for conduction block and clinical atrophy of affected muscles.
To sum up:
Fibrillations and positive waves are most consistent with a more acute lesion of less than three to six months. If these ‘denervation’ potentials are seen beyond the first few months after injury, an ongoing or progressive lesion should be suspected. If very tiny in amplitude, these potentials may persist due to incomplete axonal repair and in a chronic lesion do help to confirm a specific nerve root level of pathology.
Abnormal motor units are not seen until reinnervation has had time to take place, either axonal repair at the original site of injury or through collateral sprouting within a given muscle. The most common finding is polyphasic motor units and reduced recruitment. The degree of polyphasia and recruitment loss depends on both time and distance of the muscle away from the original site of injury.
There are some limitations to the needle EMG study of radiculopathy:
Localizing a radiculopathy to a single nerve root level may be challenging since most muscles are innervated by more than one myotome.
The EMG may be normal in the acute phase since it may take 10-14 days for evidence of nerve axonal injury to develop.
EMG may be normal if compression of the nerve root results in rare demyelination without axonal loss—requires evidence for conduction block and muscle weakness without changes in motor units
EMG will be normal if the sensory nerve root is predominantly affected and the motor nerve root is normal—somatosensory latencies may not accurately assess this either because of overlapping dermatomes
Different fascicles within a myotome may be affected while others are spared so that only one or a few muscles of a given nerve root are affected—requires careful testing of an adequate number of muscles per nerve root
Paraspinals may be normal due to more rapid reinnervation prior to testing, inadequate examiner technique, inability of patient to relax, or a sparing of the posterior primary rami of the nerve roots. Reinnervation motor units may be missed due to inexperience of the examiner or patient inability to recruit neck muscles with an EMG needle in the muscles
Paraspinals do not accurately localize nerve root level, only confirm the presence of a proximal lesion due to the overlap of myotomes in the neck or lower back although experienced electromyographers believe identification of changes in multifidi may correlate more accurately with specific nerve root levels
Abnormal changes in motor unit configuration are the same in radiculopathy as in motor neuron disease. Chronic radiculopathy looks the same as axonal neuropathy: polyphasic motor units, increases in duration and amplitude, increased firing rates, and reduced recruitment patterns. In other words, polyneuropathy may mask evidence for chronic radiculopathy in the absence of denervation potentials or paraspinal findings to confirm co-morbid disease. Sensory testing may help differentiate nerve root from plexus or peripheral nerve disease. In radiculopathy the sensory nerve is spared since the nerve root lesion is proximal to the dorsal nerve root ganglion.
A final comment regarding diagnosis of new radiculopathy in a patient with a prior history of spine surgery: For unknown reasons fibrillations may persist for several years in paraspinals following surgery in patients who otherwise are symptom free. Fibrillations may also be seen in diabetics with severe polyneuropathy and/or other neuromuscular diseases such as ALS and Guillain-Barre. In these patients the interpretation of fibrillations in paraspinals is not straightforward. The presence of fibrillations may be normal, that is, not indicative of radiculopathy. The absence of fibrillations likewise does not rule out pathology at the nerve root level. Large amplitude positive waves at a single paraspinal level in a patient with a history of spine surgery may be a more reliable indicator of acute radiculopathy.
ALL OF THE ABOVE MAY BE CONFUSING TO THE PATIENT AND EVEN SOME PHYSICIANS. THERE IS A CERTAIN LEVEL OF SOPHISTICATION BASED ON EXPERIENCE AS WELL AS MEDICAL KNOWLEDGE INVOLVED IN THE ELECTRODIAGNOSTIC EVALUATION--IT IS IMPERATIVE THAT BOTH PATIENT AND REFERRING PROVIDERS SEEK COMPETENT NEUROLOGISTS OR PHYSIATRISTS TO PERFORM AS WELL AS INTERPRET TEST RESULTS.