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"H" stands for Hoffman, after the investigator who first recorded the late response in 1918. The H-reflex is often said to be the NCS parallel of the clinical ankle tendon reflex, but the two tests are probably not evaluating the exact same group of nerve fibers. The tibial nerve is stimulated in the popliteal fossa, with the cathode proximal to the anode, and the response is recorded with the active electrode overlying the belly of the soleus muscle and the reference electrode placed at the calcaneal tendon. As with F-waves, the "reversed" cathode-anode orientation avoids the possibility of anodal block. The nerve is stimulated with a long-duration (1 ms) pulse rather than the short-duration pulse commonly used in routine NCS (0.05-0.2 ms) because the longer pulse is more effective at selectively stimulating the type 1A sensory fibers from muscle spindle organs that initiate the response.

In clinical practice, the H-reflex in adults is generally mostly recorded from the soleus; however, it is also readily obtainable form flexor carpi radialis with medial nerve stimulation, but is generally not performed because it provides little additional information over conventional EMG. However, in children and in diseased states, H-reflexes may also be elicitable from many other nerves and muscles.

The H-reflex is best studied by generating a recruitment curve, accomplished by gradually increasing stimulus intensities such that the variability of the H-reflex can be measured (Fig. 4). At very low stimulus intensities, no response can be elicited. At slightly higher intensity, a small H-reflex can be seen without the M-wave. This occurs because the type 1A fibers are being stimulated without direct depolarization of the adjacent alpha motor neurons. The 1A fibers conduct the stimulus to the spinal cord, where a monosynaptic reflex occurs, as it does with the clinical ankle jerk, where the afferent volley is initiated by the Golgi tendon organs. From the spinal cord, the response travels orthodromically down the motor neuron to the soleus, where the triphasic H-wave is recorded. With further increasing stimulation, the H-reflex continues to grow in amplitude as more and more 1A afferents are stimulated. Then, as motor fibers are directly depolarized, an M-wave begins to appear. The H-reflex then begins to decline in amplitude with increasing stimulus intensity caused by collision with the

L TIBIAL

L TIBIAL

Fig. 4. H-reflex recruitment. Note how the potential comes in initially before the M-wave, maximizes just as the M-wave appears, and then gradually decreases in size as the M-wave becomes supramaximal. Once the M-wave is supramaximal, the only recorded late responses will be the F-waves. The bottom tracing shows the superimposed data.

Fig. 4. H-reflex recruitment. Note how the potential comes in initially before the M-wave, maximizes just as the M-wave appears, and then gradually decreases in size as the M-wave becomes supramaximal. Once the M-wave is supramaximal, the only recorded late responses will be the F-waves. The bottom tracing shows the superimposed data.

antidromic impulse being conducted along the motor neurons. Eventually, the H-reflex is completely abolished, as a supramaximal motor response is elicited and antidromic motor responses collide with all the descending motor input arriving via the sensory pathways. At this point, any late responses recorded will be F-waves only.

The minimum onset latency (usually 25-34 ms) is the only routinely measured aspect of the H-reflex and, similar to the F-wave, is dependent on the height of the subject and the integrity of the nerves. Comparing the affected and unaffected leg reflexes is more useful than analysis of a unilateral response, and most laboratories consider up to a 1.5 ms difference as normal. Also, comparing bilateral H-reflex amplitudes can be informative, as can comparing the ratio of the H-reflex amplitude with the M-wave amplitude. The ratio may reflect the degree of AHC excitability. The ratio usually increases in upper motor neuron lesions and can be used to evaluate spasticity. Amplitude can be measured as long as care is taken to move the recording electrodes to ensure optimum positioning.

The H-reflex suffers from a lack of specificity for similar reasons as outlined for F-waves. The absolute latency is increased in polyneuropathies (axonal and demyelinating), or the reflex may be absent. Comparison of the healthy and diseased legs may be useful for diagnosing S1 radiculopathies.

The A-wave (Fig. 5) is another late response; however, it is only prominent in pathological states. It can be distinguished from F-waves by its invariable latency and morphology with each stimulus. The A-wave latency is typically shorter than the F-wave but can be longer. A-waves can be seen in the setting of any neuropathic process, but are quite common in polyneuropathies and radiculopathies.

Fig. 5. An example of A-wave (arrow), obtained while evaluating ulnar F-waves.

A number of potential explanations have been suggested for the occurrence of A-waves. One possibility is that an abnormal axon may give off a branch proximally. Stimulation of the nerve may result in antidromic excitation of the branch, leading to a descending orthodromic depolarization. This would essentially represent a so-called "axon reflex." Another possibility is that ephaptic transmission is occurring between the axons proximally because of abnormal (crosstalk) demyelination. An impulse can then travel antidromically up one neuron and orthodromically down another, exciting the muscle at a constant latency.

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