F Wave

F waves were named in reference to “foot” since they were originally recorded in small foot muscles, though they may be generated by the stimulation of any motor or mixed nerve. A supramaximal stimulus applied at any point along the course of a motor nerve elicits an F wave in a distal muscle that follows the CMAP (M response). The impulse travels antidromically to the spinal cord and the F wave is produced by backfiring of motor neurons. An average of 5–10% of the motor neurons available in the motor neuron pool backfire after each stimulus. The afferent and efferent loops of the F wave are motor with no intervening synapse. Hence, the F waves test the integrity of the entire motor axons, including the ventral roots.

The F waves are low-amplitude and ubiquitous responses that are typically variable in latency, amplitude, and morphology (Figure 3-1A and B). Their variability is explained by differing groups of motor neurons generating the recurring discharge with each individual group of neurons having different number of motor neurons and conducting properties. Several parameters may be analyzed, but the minimal F wave latency is the most reliable and useful measurement since it represents conduction of the largest and fastest motor fibers. Since F wave latencies vary from one stimulus to the next, an adequate study requires that about 10 F waves be clearly identified. The minimal F wave latency is also dependent on the length of motor axons which correlates with the patient’s height and limb length. The most sensitive criterion of abnormality in a unilateral disorder is a latency difference between the two sides, or between two similar nerves in the same limb. Absolute latencies are most useful only for sequential reassessment of the same nerve. F wave persistence is a measure of the number of F waves obtained for the number of stimulations. This varies between individuals and is inhibited by muscle activity while it is enhanced by relaxation or the use of Jendrasik maneuver. It is usually above 50% except when stimulating the peroneal nerve while recording the extensor digitorum brevis. F wave chronodispersion is the degree of scatter among consecutive F waves and is determined by the difference between the minimal and maximal F wave latencies. It indicates the range of motor conduction velocities between the smallest and largest myelinated motor axon in the nerve. The F wave conduction velocity may be calculated after distal and proximal supramaximal stimulations and provides a better comparison between proximal and distal (forearm or leg) segments.

F wave latencies are prolonged in most polyneuropathies, particularly the demyelinating type, including Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) (Figure 3-1C and D). F wave latencies in radiculopathies have a limited use. They may be normal despite partial motor axonal loss because the surviving axons conduct normally, and in single radiculopathies since most muscles have multiple root innervation. Finally, focal slowing at the root level may get diluted by the relatively long motor axon.

A Wave

The A wave (axonal wave) is a potential that is seen occasionally during recording of F waves at supramaximal stimulation. The A wave follows the CMAP and often precedes, but occasionally follows, the F wave. The A wave may be mistakenly considered for an F response but its constant latency and morphology in at least 10 out of 20 stimulations differentiates it from the highly variable morphology and latency of the F wave (Table 3-1).

Table 3-1 Comparisons Between the Common Late Responses Recorded in Limb Muscles

The A wave may be seen in up to 5% of asymptomatic individuals, particularly while studying the tibial nerve (Figure 3-2A and B). In contrast, recording multiple or complex A waves from several nerves is often associated with acquired or inherited demyelinating polyneuropathies (Figure 3-3). A waves are sometimes seen in axon-loss polyneuropathies, motor neuron disease, and radiculopathies. The exact pathway of the A wave is unknown but it may be generated as a result of ephaptic transmission between two axons with the action potential conducting back down the nerve fiber to the muscle. The A wave may also appear following sprouting and reinnervation along the examined nerve. The constant morphology and latency of the A wave is best explained by the fixed point of a collateral sprout or ephapse. When the A wave follows rather than precedes the F response, it suggests that the regenerating collateral fibers are conducting very slowly.

Figure 3-2 Tibial A wave, stimulating the tibial nerve at the ankle while recording the abductor hallucis muscle. (A) Waveforms shown in a raster mode. (B) Waveforms superimposed. Note that the response has a constant morphology and latency, which results in perfect superimposition.

Figure 3-3 Complex A wave stimulating the median nerve at the wrist while recording abductor pollicis brevis in a patient with Guillian-Barré syndrome shown in a raster form. Note that the complex response has a constant morphology and latency.

H Reflex

The H reflex, named after Hoffmann for his original description, is an electrical counterpart of the stretch reflex which is elicited by a mechanical tap. Group 1A sensory fibers constitute the afferent arc which monosynaptically or oligosynaptically activate the alpha motor neurons that in turn generate the efferent arc of the reflex through their motor axons. The H reflex amplitude may be occasionally as high as the M amplitude but it is often lower with the H/M amplitude ratio usually not exceeding 0.75.

The H reflex and F wave can be distinguished by increasing stimulus intensity (see Table 3-1). The H reflex is best elicited by a long-duration stimulus which is submaximal to produce an M response, whereas the F wave requires supramaximal stimulus Also, the F wave can be elicited from any limb muscle while the H reflex is most reproducible with stimulating the tibial nerve while recording the soleus muscle which assess the integrity of the S1 arc reflex and is equivalent to the Achilles reflex (Figure 3-4). Finally, the H reflex latency (and often amplitude) is constant when elicited by the same stimulus intensity, since it reflects activation of the same motor neuron pool.

Figure 3-4 H reflex stimulating the tibial nerve at the popliteal fossa while recording the soleus/gastrocnemius muscles. (A) Waveforms in a raster form. (B) Waveforms superimposed. Note that the response appears with submaximal stimulations and disappears with supramaximal stimulations.

The H reflex is most useful as an adjunct study in the diagnosis of peripheral polyneuropathy or S1 radiculopathy. The H reflex latency and amplitude is the most sensitive, yet nonspecific, among the nerve conduction studies in the early phases of Guillain-Barré syndrome. The H reflex may be absent in healthy elderly subjects and isolated abnormalities of the H reflex are nondiagnostic since they may reflect pathology anywhere along the reflex arc.

Blink Reflex

The blink reflex generally assesses the facial and trigeminal nerves and their connections within the pons and medulla. It has an afferent limb, mediated by sensory fibers of the supraorbital branch of the ophthalmic division of the trigeminal nerve, and an efferent limb mediated by motor fibers of the facial nerve and its superior motor branches.

The supraorbital nerve is stimulated over the suprarorbital notch and the blink responses are recorded from the orbicularis oculi bilaterally using a two channel recording setting. The blink reflex has two components, an early R1 and a late R2 response. The R1 response is present only ipsilateral to the stimulation and is usually a simple triphasic waveform with a di-synaptic pathway between the main trigeminal sensory nucleus in the midpons and the ipsilateral facial nucleus in the lower pontine tegmentum. The R2 response is a complex waveform and is the electrical counterpart of the corneal reflex. It is typically present bilaterally with an oligosynaptic pathway between the nucleus of the trigeminal spinal tract in the ipsilateral pons and medulla, and interneurons forming connections to the ipsilateral and contralateral facial nuclei.

The blink reflex is most useful in unilateral lesions such as facial palsy, trigeminal neuropathy, or lower brainstem lesion. With facial nerve lesions, the R1 and R2 potentials are absent or delayed with supraorbital stimulation ipsilateral to the lesion, while the R2 response on the contralateral side is normal. With trigeminal nerve lesions, the ipsilateral R1 and R2, contralateral R2 are absent or delayed with ipsilateral stimulation while all responses are normal with contralateral stimulation. With a midpontine lesion involving the main sensory trigeminal nucleus or the pontine interneurons to the ipsilateral facial nerve nucleus or both, supraorbital stimulation on the side of the lesion results in an absent or delayed R1, but an intact ipsilateral and contralateral R2. Finally, with a medullary lesion involving the spinal tract and trigeminal nucleus or the medullary interneurons to the ipsilateral facial nerve nucleus or both, supraorbital stimulation on the affected side results in a normal R1 and contralateral R2, but an absent or delayed ipsilateral R2. In demyelinating polyneuropathies such as the Guillain-Barré syndrome or Charcot-Marie-Tooth disease type 1, the R1 and R2 responses may be markedly delayed, reflecting slowing of motor fibers, sensory fibers, or both.