8.3 A Waves and the Blink Reflex

8.3 A Waves and the Blink Reflex

Quick Answer: A waves are axon reflexes: intermediate between M and F, stable in latency and shape, often from sprouting or ephaptic transmission. The blink reflex uses a trigeminal (V) afferent and a facial (VII) efferent. R1 is ipsilateral and oligosynaptic (pons); R2 is bilateral and polysynaptic (medulla/pons).

Domain IV finishes with two late responses that look nothing like each other on the screen and everything like each other on a content outline: a small motor extra spike that tricks people into a false Fmin, and a cranial-nerve reflex that maps pons and medulla. OpenExamPrep teaches both here as independent study material for nerve-conduction technologists.

IV.C A waves (axon reflexes)

What an A wave is

An A wave, also called an axon reflex, is a muscle potential whose latency usually sits between the M wave and the F wave. Unlike the F wave, it is stereotyped: the same shape and nearly the same latency on sweep after sweep. If F waves are a handful of different motor neurons backfiring, A waves look as if the same extra pathway is being taken every time.

That stability is the identification rule. F varies; A is stereotyped. If you are marking Fmin on a bump that is identical in 15 of 16 traces and sits earlier than the variable F cloud, you are probably marking an A wave.

How A waves are generated

Two related mechanisms dominate teaching:

1. Axonal sprouting / branching after injury. A motor axon that has sprouted a proximal branch can be stimulated along one limb. The impulse travels proximally to the branch point, then down the other limb to the muscle. The extra time to the branch point and back down the sister branch places the potential after the M but usually before the true F round trip to the cord.
2. Ephaptic transmission. In demyelinated or tightly packed injured nerve, an action potential on one axon can jump to a neighbor through an ephapse (nonsynaptic electrical crosstalk). The neighbor then fires the muscle with a fixed extra delay.

Both mechanisms become more common after axonal injury with reinnervation and in demyelinating neuropathy. Multiple A waves in several nerves are a recognized clue in inflammatory demyelinating polyneuropathies. A single A wave after an old focal injury is less dramatic but still a technical trap if it is labeled as Fmin.

A waves are not reflexes in the Ia sense. They do not require a spindle afferent or a spinal synapse. They are axon-pathway extras. That is why they can appear in purely motor recordings and why they survive as stereotyped late spikes when you are in the F-wave intensity range.

How to tell A from F, M, and H

Practical rules:

• If it is glued to the end of the M and changes when you move the recording electrode, think late M or satellite, not A.
• If it sits between M and F and does not jitter, think A.
• If it jitters in the true F window at supramaximal intensity, think F.
• If it exists only at low intensity and dies as M grows, think H (especially soleus after popliteal stimulation).

Do not include A-wave latency in the Fmin calculation. Doing so falsely shortens proximal motor time and can hide the very proximal slowing you were trying to detect.

Clinical context for A waves

Expect A waves when the history includes prior nerve injury, entrapment with sprouting, radiculopathy with reinnervation, or demyelinating neuropathy such as Guillain-Barré or CIDP. They are a finding to recognize and not mis-measure, not a stand-alone diagnosis. A tracing full of extra stereotyped spikes should prompt you to slow down, raise gain, and separate the A series from the F series before anyone types a number into the report.

IV.D Blink reflex

Origin: trigeminal in, facial out

The blink reflex is a brainstem reflex recorded from orbicularis oculi. The routine laboratory version stimulates the supraorbital nerve (a trigeminal, cranial nerve V1, cutaneous branch) and records from orbicularis oculi on both sides. The afferent limb is trigeminal. The efferent limb is the facial nerve (VII) to orbicularis oculi.

Two components matter:

• R1 is ipsilateral only. It is oligosynaptic and generated in the pons (trigeminal principal sensory connections onto the ipsilateral facial nucleus). Latency is short, typically on the order of about 10–13 ms in many published adult series. It is relatively stable and less dependent on attention than R2.
• R2 is bilateral. It is polysynaptic and travels through the spinal trigeminal nucleus in the medulla and internuncial neurons that then drive both facial nuclei in the pons. Latency is longer, typically in a roughly 30–44 ms teaching window, with the contralateral R2 often a little later than the ipsilateral R2. Laboratories apply their own reference values; learn the pattern, not a fake universal cutoff from this page.

There should not be a contralateral R1 in a standard supraorbital blink study. A contralateral R1 usually means swapped channels, extreme volume conduction, or a setup error.

Technique

• Stimulate the supraorbital nerve at the supraorbital notch, cathode over the notch, anode more proximal or lateral on the forehead depending on laboratory method.
• Record orbicularis oculi bilaterally. Active electrodes sit on the inferior orbicularis oculi; references are commonly at the lateral canthus or temple. Ground on the chin or forehead.
• Intensity is enough to produce a stable R1, not a limb-motor supramaximal hunt. Excess current spreads to the facial nerve and produces a very early direct M wave (about 3–4 ms) that is not R1. R1 lives near 10–13 ms. If you see a 3 ms blob, turn the stimulator down and check cathode position.
• Rate should be slow enough that R2 does not habituate into invisibility. R2 is polysynaptic and is easily suppressed by fast trains, drowsiness, or inattention.
• Always stimulate each side and display four traces conceptually: ipsilateral R1, ipsilateral R2, contralateral R2, and the same trio from the other stimulus. In practice you inspect both channels for each stimulus side.

Direct facial CMAPs (stimulating near the stylomastoid foramen or over facial branches) still matter for distal facial axonal loss. The blink reflex adds proximal facial nerve, trigeminal afferent, and brainstem internuncial information that a distal facial CMAP cannot provide.

Pathway table

Interpretation: delayed or absent R1 versus R2

Read blink studies as a pattern, never as a single latency. Stimulate one side, then the other, and ask which limb of the arc failed.

Ipsilateral facial (VII) neuropathy (for example, Bell palsy on the left):

• Stimulate the affected side: R1 and ipsilateral R2 delayed or absent; contralateral R2 preserved (afferent V is intact; the opposite face can still blink).
• Stimulate the unaffected side: R1 and ipsilateral R2 normal; contralateral R2 delayed or absent because that contralateral R2 must use the sick facial nerve.

Trigeminal (V) lesion on one side:

• Stimulate the affected side: R1, ipsilateral R2, and contralateral R2 all delayed or absent, because the afferent volley never enters the brainstem well.
• Stimulate the unaffected side: all responses normal, including contralateral R2 to the affected face, if VII on that side still works.

Brainstem internuncial / pontomedullary pattern:

• R1 relatively spared (oligosynaptic pons still working) with R2 delayed or absent on both sides. This pattern is the internuncial signature and is the one that shows up in brainstem and some coma discussions: R2, being polysynaptic and more caudal, is more vulnerable than R1.

Mixed lesions occur. A large cerebellopontine-angle or skull-base process can hit V and VII together. Report the pattern you recorded rather than forcing a single-nerve story onto mixed data.

Clinical applications

Facial neuropathy. Blink testing evaluates facial nerve function through a more proximal and trans-synaptic route than a distal nasalis or orbicularis oris CMAP. Together with a direct facial CMAP, it helps describe conduction along VII, but it does not by itself grade every axon that a needle study or CMAP amplitude would address.

Trigeminal lesions. Unilateral loss of all responses from one stimulus side, with a normal contralateral stimulus, is the afferent pattern. Compare it with the clinical sensory examination; the blink reflex is not a facial-pain diagnosis by itself.

Guillain-Barré. Facial weakness is common. Blink latencies can prolong from facial motor involvement, and in demyelinating disease the internuncial R2 can also suffer. Use the same R1/R2 laterality logic; do not invent a unique Guillain-Barré-only waveform.

Coma and brainstem context. In selected intensive-care and brainstem examinations, preserved R1 with degraded R2, or loss of both, is interpreted in clinical context with imaging, other cranial-nerve findings, and the examiner's purpose. This is not a standalone coma score for a technologist to assign. It is a pathway test whose R2 component is more sensitive to internuncial and arousal-related suppression.

Technical traps unique to blink studies

• Facial-nerve spread: early 3–4 ms M wave mistaken for R1.
• Channel swap: apparent contralateral R1 or a facial-lesion pattern that flips when you restick the electrodes.
• Habituation: R2 called absent because the stimulator was clicking too fast.
• Drowsy patient: R2 melts; R1 remains. Do not over-call internuncial disease in a sleeping outpatient without repeating the run.
• Unilateral recording: you cannot interpret contralateral R2 if you only wired one eye.

A waves keep you honest about motor late-component labeling. The blink reflex keeps you honest about which cranial-nerve limb and which brainstem loop failed. Together they close Domain IV: F waves for proximal somatic motor round trips, H reflexes for Ia monosynaptic arcs, A waves for stereotyped axonal extras, and the blink reflex for V–VII brainstem circuitry.