ABSTRACT
Introduction:
A-waves are late responses following the motor response during motor nerve conduction studies (NCSs) observed in healthy people and patients with neurological disorders. The aim was to define the prevalence and clinical associations of A-waves in a cohort referred to the electrophysiology laboratory for routine NCSs.
Methods:
This is a retrospective study. We analyzed the medical and electrophysiological data of 456 patients admitted to our neurophysiology laboratory between January 2022 and December 2022, evaluated by a single examiner (A.G.), and had F-wave studies.
Results:
We included 1197 nerves from 404 patients in this cohort. The most common diagnosis was entrapment neuropathy, followed by polyneuropathy, radiculopathy, motor neuron disease, myopathy, and other diagnoses. Twenty-five patients had multiple conditions, and 185 patients had no abnormal NCSs. The A-waves were seen in 42.2% of individuals with otherwise normal NCSs. The A-waves were most commonly found in patients with polyneuropathies, followed by motor neuron disorders, radiculopathy, and myopathy. However, the majority of polyneuropathy patients had multiple A-waves. A-waves were detected in 78 of 185 normal NCSs; 7 % had multiple A-waves. Multiple and single A-waves were more commonly recorded in the tibial nerves. The A-waves were more frequently observed in older subjects.
Conclusions:
Other than multiple A-waves, A-waves were commonly seen in subjects with normal NCSs. As far as we know, this is the first study reporting the presence of A-waves in myopathy and neuromuscular junction disorders. Still, this finding should be interpreted cautiously given the limited clinical data available.
Keywords: A-waves, multiple A-waves, F-waves, nerve conduction studies
INTRODUCTION
Different kinds of late responses after compound muscle action potential (CMAP) during routine motor nerve conduction studies (NCSs) are distinguished by their latency, stability, amplitude, stimulus intensity required to elicit the response, consistency, and the possibility of disappearance by paired stimulation (1). Some late responses appear under physiological conditions, such as F-waves and H reflex. In contrast, others are generally signs of some underlying pathology, such as A-waves (1).
Highlights
A-waves occur in both healthy individuals and people with neurological disorders.
The frequency of A-waves increases with age.
A-waves can also be seen in myopathy and neuromuscular junction disorders.
Both single and multiple A-waves are most commonly recorded in the tibial nerves.
The A-waves are relatively common late responses identified after CMAP, especially during F-wave studies (1). The A-waves are generally characterized by low amplitude, fixed morphology, and an almost constant latency. Furthermore, A wave latency is often less than F wave latency, although it can be the same as or longer than F waves (2). Repeated stimulation changes its latency to less than 0.5 milliseconds (ms), but sometimes it can change up to 1.5 ms (3). Although several possible mechanisms, such as extra discharges in nerves, ephaptic conduction, or axonal branching, have been suggested (4), the exact pathophysiological mechanisms responsible for forming A-waves remain unclear. The A-waves have been widely reported in abnormal and normal nerves, with unclear patterns described so far. They are frequently found in many neurogenic disorders, including demyelinating and axonal neuropathies, radiculopathies, focal mononeuropathies, or motor neuron disorders (2,3,5,6). Still, it has been reported to be shared in healthy individuals, especially in the lower extremities (2,6). In a study within a group of healthy subjects, A-waves were found in 14% of the peroneal nerves and 25% of the tibial nerves (3). The A-wave frequency increases with age in healthy subjects (3). Puksa et al. discussed age-related degeneration in motor axons, increased muscle fiber density, and slowed motor conduction velocity, emphasizing that these changes are more pronounced in the lower extremities (3).
This retrospective study aimed to reveal the presence, frequency, and association of A-waves and abnormal F-waves in different peripheral nervous system diseases among patients referred for routine electrophysiological analysis.
METHODS
Patients
This study revealed a retrospective analysis of the medical and electrophysiological findings of all patients who were admitted for electrophysiological evaluation to our neurophysiology laboratory between January 2022 and December 2022, and evaluated by a single examiner (A.G.), and who had F-wave studies. Patients without F-waves or inconclusive findings were excluded from the study. Figure 1 shows the study flowchart.
Figure 1.
Flowchart of patient selection. A total of 456 patients were admitted to the EMGlaboratory between January 2022 and December 2022. We enrolled all examinationsperformed by a single examiner (A.G.) and included F-wave studies. Thus, we excluded 52 examinations due to either the absence of F-wave recordings or inconclusive F-wave findings. Therefore, 404 patients with valid F-wave studies were included in the final analysis.
* Patients were excluded if F-wave results were not available or not interpretable.
This research study was conducted in compliance with the Declaration of Helsinki. Since it was a retrospective study, informed consent was not obtained. The local ethical committee approved the study (Number: 27.07.2023/ E-83045809-604.01.01-742186).
Clinical evaluation: The same physicians (B.G., E.K.Ç.) had examined all patients using the same datasheet. We noted demographic data, clinical prediagnoses, and diagnoses determined after the electrophysiological analysis from these records.
Electrophysiological evaluation: According to the standard techniques, electrophysiological analyses were done using the same recording electrodes and EMG machine (Keypoint 9033A07, Alpine Biomed ApS, DK-2740, Denmark). We used bar electrodes to record motor responses and ring electrodes for sensory responses. The upper limbs’ skin temperature was kept at 32°C, while the lower limbs’ skin temperature was kept at 30°C.
Nerve conduction studies and needle electromyography (EMG): We conducted NCS and EMG using conventional methods described in the literature (7).
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Motor NCSs of the median, ulnar, peroneal, and tibial nerves were performed. The details of electrode placement were made as indicated in the literature (7). The median and ulnar nerves were stimulated in the wrist and elbow, respectively, while recordings were done from the abductor digiti minimi and the abductor pollicis brevis. The tibial nerve was stimulated from the posterior to the medial malleolus and at the popliteal fossa, and recordings were done from the abductor hallucis. The peroneal nerve was stimulated at the ankle and two sites around the knee (under the head of the fibula and above the head of the fibula), while recordings were performed from the extensor digitorum brevis muscle. Recording electrodes were placed according to the belly-tendon configuration. The sensitivity was kept at 5 mV/division. The sweep speed was kept at 5 ms for the lower and 3 ms for the upper extremity nerves. The sweep speed was adjusted as needed to capture the entire CMAP waveform.
According to the previous literature, sensory NCSs were performed antidromically in the median, ulnar, superficial peroneal, and sural nerves (8,9). Upper extremity nerves were stimulated from the wrist, and responses from the median and ulnar nerves were measured at distances of 12 cm from the second and fifth fingers, respectively (8). The sural nerve in the lower extremities was stimulated from the calf and measured about 14 cm from the outer malleolus (9). The measured parameters were peak latency and sensory nerve action potentials (SNAP) amplitude.
The incidence of positive sharp waves, fibrillation potentials, and fasciculations was noted during needle EMG analysis. A qualitative analysis of interference patterns and motor unit potentials was also conducted.
The selection of the muscle was based on the clinical examination and pre-diagnosis.
F-waves: We recorded F-waves for the median, ulnar, and tibial nerves. The recording electrodes were positioned as in motor NCSs (10). The F-wave was produced by stimulation of the median, ulnar, and tibial nerve at the wrist or ankle and had a substantially longer delay than the CMAP. We do not study peroneal nerve F-waves in routine practice since their presence is lower than those of others.
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All F-wave studies were performed using 20 random supramaximal stimuli with a duration of 0.2 ms.
An effective supramaximal antidromic activation was produced by the cathode being positioned distal to the anode, with the two poles separated by a distance of 2-3 cm (11). The sensitivity and sweep speeds were 200 µV/division and 10 ms/division, respectively. Minimal F-wave latencies were noted based on the previous literature (12).
Data analysis: The A-waves were primarily identified as responses between the CMAP and F-waves. However, A-waves mixed with or later than F-waves were also accepted. The A-waves were considered present if the response met the criteria of having stable amplitude and configuration in three or more of the 20 stimuli and varying less than 1.5 ms at the onset of latencies [5]. In accordance with previous literature [3], A-waves were categorized based on their location relative to the CMAP and F-waves as follows: (i) A-waves intermixed with the F response, (ii) A-waves in the absence of F-waves, and (iii) multiple A-waves. The persistence of the A-waves and the nerves in which they were found were noted. Three or more A-waves in one nerve were considered multiple A-waves [5]. In all of our studies, supramaximal stimulation was used.
Statistical analysis: The patients were classified according to the presence of the A-wave. The diagnoses and F-wave latencies were compared among groups. Categorical data were compared with the chi-square test. For continuous data, the t-test was used for independent groups when the distribution was homogeneous, and the Mann-Whitney U test was used when the distribution was non-homogeneous. Categorical data were presented in (%), and numerical data in mean ± SD.
All analyses were performed using SPSS 20.0. P<0.05 was considered statistically significant.
RESULTS
The recordings of 404 patients who were examined in our laboratory during the study period were included in our study. The male-to-female ratio was 0.73 (171 men, 233 women). The mean age of the whole group was 48.9±18.7 years. We examined 1197 nerves, including 295 right median nerves, 187 left median nerves, 139 right ulnar nerves, 84 left ulnar nerves, 290 right tibial nerves, and 202 left tibial nerves (Table 1).
Table 1.
Presence of A-waves according to the stimulated nerves
| Individual nerve | Presence of A-waves, n (%) | ||
|---|---|---|---|
| Total | Single A-wave | Multiple A-waves | |
| Right median nerve (n=295) | 20 (6.7%) | 20 (100%) | 0 |
| Right ulnar nerve (n=139) | 15 (10.8%) | 10 (66.6%) | 5 (33.4%) |
| Right tibial nerve (n=290) | 148 (51%) | 106 (71.6%) | 42 (28.4%) |
| Left median nerve (n=187) | 19 (10.2%) | 15 (78.9%) | 4 (21.1%) |
| Left ulnar nerve (n=84) | 12 (14.3%) | 11 (91.6%) | 1 (8.4%) |
| Left tibial nerve (n=202) | 111 (55%) | 72 (64.8%) | 39 (35.2%) |
We determined patients with entrapment neuropathy (n=62), followed by polyneuropathy (n=55), radiculopathy (n=33), motor neuron disease (n=14), myopathy (n=22), and other diagnoses. Twenty-five patients had multiple conditions, and 185 patients had no abnormal findings (Table 2).
Table 2.
The presence of A-waves according to the EMG findings
| EMG findings | No A-waves n=193 | A-waves n=211 | Single A-wave n=146 | Multiple A-waves n=65 |
|---|---|---|---|---|
| Normal (n=185) | 107 (57.8%) | 78 (42.2%) | 65 (35.2%) | 13 (7%) |
| Abnormal NCSs (total) (n=219) | 86 (39.3%) | 133 (60.7%) | 81 (37%) | 52 (23.7%) |
| Polyneuropathy (n=55) | 12 (22%) | 43 (78%) | 19 (34.5%) | 24 (43.5%) |
| Myopathy (n=22) | 10 (45.5%) | 12 (54.5%) | 9 (41%) | 3 (13.5%) |
| Radiculopathy (n=33) | 15 (45.4%) | 18(55.6%) | 13 (39.4%) | 5 (15.2%) |
| Motor neuron disease (n=14) | 4 (28.5%) | 10 (71.5%) | 9 (64.3%) | 1 (7.2%) |
| Compression neuropathy (n=62)* | 34 (55%) | 28 (45%) | 21 (33.9%) | 7 (32.1%) |
| Neuromuscular Junction disorder (n=5) | 3 (60%) | 2 (40%) | 1 (20%) | 1 (20%) |
| Brachial plexopathy (n=3) | 3 (100%) | 0 | 0 | 0 |
| PNP and others (n=19)** | 5 (27%) | 14 (73%) | 6 (31%) | 8 (42%) |
| Myopathy + others (n=6)*** | 0 | 6 (100%) | 3 (50%) | 3 (50%) |
Pnp: Polyneuropathy
Most of the compression neuropathies were carpal tunnel syndrome.
Under the title of compression neuropathy, there was carpal tunnel syndrome (n=43), ulnar neuropathy at the elbow (n=13), and peroneal neuropathy at the fibula head (n=6)
Some patients with polyneuropathy had entrapment polyneuropathy or focal radiculopathy.
Some patients with myopathy had accompanying carpal tunnel syndrome
There was an A-wave in at least one nerve in 211 (52.2%) patients (104 men, 49.3%), whereas an A-wave was not detected in 193 patients (67 men, 34.7%; p=0.003). The mean ages of these two groups were 53.3±17.5 and 43.1±18.9 years, respectively (p<0.001).
Among patients with normal NCS, the mean age of those with a positive A-wave was 52.5 ± 19.2 years, while it was 40.6 ± 18.5 years in those without an A-wave (p<0.05). In patients with abnormal NCS, the mean age was 53.8 ± 17.1 years in A-wave positive cases and 48.4 ± 18.6 years in A-wave negative cases (p<0.05).
The A-waves were most commonly present in patients with polyneuropathies, followed by motor neuron disease, radiculopathy, and myopathy.
The A-waves were detected in 42.2% (n=78) of individuals who had normal electrophysiological results (n=185), whereas 60.73% of patients with various peripheral nervous system disorders had A-waves in at least one nerve (p<0.001).
Thirteen patients (7%) with normal electrophysiological results had multiple A-waves (Table 2). However, multiple A-waves were mainly observed in patients with multiple pathologies, followed by those with polyneuropathy (Table 2). Multiple A-waves were observed in all patients diagnosed with Guillain-Barré Syndrome (GBS) (n=6) and in 2 patients with chronic inflammatory demyelinating polyneuropathy (CIDP). All GBS cases were classified as the demyelinating subtype (Acute Inflammatory Demyelinating Polyneuropathy -AIDP).
In the NCSs, A-waves were more common in abnormal nerves than normal ones (Figure 2). In general, A-waves were most commonly found in the tibial nerves (51% right side, 55% left side) and much less frequently in the ulnar nerves (10.8% right side, 14.3% left side), and they were least commonly found in the median nerves (6.7% right side, 10.2% left side). Among people with normal findings in the electrophysiological tests, A-waves were again most common in the tibial nerves (34.5% on the right side, 36% on the left side), followed by ulnar (13.3% on the right side, 25% on the left side) and median nerves (10% on the right side, 5.2% on the left side) (Figure 2). Multiple A-waves were found in the tibial and ulnar nerves. However, they were more common in the tibial nerves. A-waves were slightly more common in patients older than 60 years than in patients under 60 (67.7% vs 44.9%).
Figure 2.
A-wave percentage in normal and abnormal nerves in electrophysiological tests.
Patients with A-waves had longer F-wave latencies than those without A-waves (Table 3).
Table 3.
F-wave latencies in patients with and without A-waves.
| F-wave latency (ms) | |||
|---|---|---|---|
| No A-waves (ms) (n=872) | With A-wave (ms) (n=325) | p | |
| Right median nerve (n=295) | 25.6±4.7 | 28.1±8.6 | 0.007 |
| Right ulnar nerve (n=139) | 26.3±4.7 | 28.1±9.3 | 0.215 |
| Right tibial nerve (n=290) | 46.7±9.2 | 48±16.9 | 0.009 |
| Left median nerve (n=187) | 25.9±3.9 | 23.6±15.8 | 0.153 |
| Left ulnar nerve (n=84) | 26.9±3.1 | 27.6±10.2 | <0.001 |
| Left tibial nerve (n=202) | 49.6±8.1 | 45.8±19.1 | 0.288 |
ms: milliseconds; Mann Whitney-U Test; p<0.05
A-wave was detected in 12 patients in the pure myopathy group and two patients in the NMJ disorder group. The myopathy group included patients with myositis related to rheumatological disorders, post-COVID syndrome, steroid myopathy, and metabolic myopathies. In the neuromuscular junction disorder group, one patient had presynaptic type neuromuscular junction disorder related to non-small cell lung carcinoma, and other patients had myasthenia gravis, one of whom was triggered after vaccination for COVID-19.
DISCUSSION
The major findings of our study are as follows: (i) A-waves were recorded more frequently in subjects with abnormal NCSs (60.7%) when compared to those with normal NCSs (42%); (ii) Multiple A-waves were recorded more frequently in subjects with abnormal NCSs (23.7%) when compared to those with normal NCSs (7%); (iii) A-waves and multipl A-waves were most frequently recorded from the tibial nerve stimulation; (iv) the F-wave latencies were more prolonged if A-waves were recorded as well; and (v) aging was associated with an increased frequency of A-waves.
The A-waves are abnormal late responses that differ from F-waves by shorter duration, lower amplitude, and relatively constant shape and latency (5). The importance of A-waves was first described by Bischoff et al. in routine NCSs (2). It is thought that the A-waves indicate a neurogenic disorder, mainly demyelination. They are found in acute and chronic neuropathies with a wide variety of pathophysiologies, from nerve demyelination to regeneration (13). Several mechanisms have been reported, including possible pathophysiology of proximal excitation of the axon, myo-axonal ephapses, or transaxonal waves (14). Disorders associated with A-waves include various entrapment syndromes, diabetic neuropathy, brachial plexus lesions, hereditary motor and sensory neuropathy, facial neuropathy, motor neuron disorders, GBS, and root lesions (15). Our study supports publications in the literature indicating that A-waves can be recorded in patients with diseases such as polyneuropathies (including demyelinating (5,16) and axonal (17,18)), focal mononeuropathies (2,6), root lesions (6), and motor neuron disorders (19). The most interesting finding in our study was the higher number of A-waves in myopathies, 54.5%.
The A-waves were previously recorded in the lower extremity nerves in healthy individuals. In a study conducted by Puksa et al. (3) on healthy individuals, A-waves were observed in the tibial nerve in 25% of the cases, in the peroneal nerve in 14%, and in the upper extremity nerves in only 2%. In other studies (2,6), A-waves were found in healthy subjects in 0.7% to 3%. In the retrospective study of Zhang et al. (20), A-waves were found in 38.9% of patients without a neurological diagnosis, of which 18.4% were single, and 20.5% were multiple A-waves. The frequency related to the presence of A-waves in individuals with neurophysiologically healthy nerves in our study was slightly higher. The reported percentages of A-waves that differ between our study and those from other studies are probably due in part to the diverse study designs, the number of motor nerves that were examined, and the population that was studied—particularly the real “healthy” people. The fact that it is high in normal nerves suggests that the A-wave may be a very early indicator of various diseases, as shown in previous studies (21), since all of our patients/participants were symptomatic and suspected of peripheral nerve dysfunction. However, they had nonspecific complaints suggestive of extraneurological conditions. In addition, in some of the studies (6), the amplitude criterion of 50 microvolts was used for A-waves; we did not use the amplitude criterion in our study, and we also accepted A-waves below 50 microvolts. Therefore, the amplitude criteria may somewhat explain the high A-wave frequency in normal nerves in our study.
Consistent with the literature (20), F-wave latencies were found to be longer in individuals with A-waves compared to those without A-waves across all nerves examined, and this difference was statistically significant in most nerves.
Similar to the literature, our study found that A-waves were more common in the tibial nerves and more common in older patients than in younger patients (3,20). More frequent A-wave in the tibial nerves may be related to the number of motor units in the plantar muscles compared to the extensor digitorum brevis (22). A-wave frequency increases significantly with age, probably associated with degenerative changes in peripheral nerves (3).
Multiple A-waves in a neuropathy patient who had no prior history of peripheral nerve disease supported the clinical suspicion of GBS (23). Studies showed a positive correlation between A-waves, conduction block, and demyelination (24,25). Multiple A-waves are electrophysiological connections of multiple inflammatory foci within the axon (22). In our study, multiple A-waves were observed in all patients diagnosed with GBS. This consistent finding may reflect the presence of widespread demyelination and inflammatory involvement of peripheral nerves, as supported by previous electrophysiological studies.
As a novel finding, we showed a high number of A-waves in myopathies and neuromuscular junction disorders. A waves (n=18/28, n=2/5) and multiple A-waves (n=6/28, n=1/5) were noted in patients with myopathy and neuromuscular junction disorders, respectively. Although the number of patients was small due to not recording F waves in our routine myopathy or neuromuscular junction disorders protocols, and we can not exclude other possible co-morbidities (eg, chronic S1 radiculopathy, diabetes) which may lead to A-waves, this association of A-waves with myopathies and NMJ disorders was notable.
The myopathy group was rather heterogeneous and included patients with myositis, post-COVID syndrome, steroid myopathy, and metabolic myopathies. We may speculate that the underlying metabolic disorder or infectious etiology in these patients may also affect the peripheral nerves, causing ephaptic transmission. Ephaptic transmission is defined as the propagation of an action potential between adjacent nerve fibers through direct electrical interaction, without the involvement of synaptic connections. Under normal conditions, the myelin sheath of peripheral nerves serves as an insulator, preventing aberrant transmission. However, in our cohort of patients with myopathies and neuromuscular junction disorders, we hypothesize that the underlying pathological processes may also extend beyond the primary muscle or junctional involvement to affect peripheral nerves. Inflammatory mechanisms, metabolic disturbances, or post-infectious changes—such as those observed in post-COVID syndrome—may induce nerve irritation, compromise myelin integrity, or promote the development of ectopic excitation sites. These alterations could facilitate ephaptic transmission between neighboring nerve fibers. Consequently, repetitive, unexpected responses such as A-waves following standard nerve stimulation can be attributed to this mechanism. Therefore, the increased A-wave occurrence observed in our study may reflect subclinical peripheral nerve involvement leading to ephaptic transmission. We believe that this hypothesis warrants further investigation through detailed neurophysiological and histopathological studies. Although the presence of A-waves in patients with neuromuscular junction disorders appears higher, it may have been overestimated because the F-waves were not recorded in patients who were referred with a preliminary diagnosis of neuromuscular junction disorder.
Although A-waves were detected in patients with myopathies and MG in our series, the interpretation of this finding is limited by the lack of detailed clinical information for these cases. Specifically, this retrospective dataset did not include comprehensive neurological examinations, needle EMG results, spinal imaging (e.g., lumbar MRI), comorbid conditions, and final diagnostic confirmation. As such, we did not emphasize the presence of A-waves in these groups, and their clinical significance remains uncertain. We propose that further prospective studies with comprehensive clinical and neurophysiological evaluation are needed to confirm whether A-waves are relevant in myopathy or MG.
One limitation of our study is its retrospective nature. However, our findings contribute to a better understanding of A-waves in the literature. Considering that they are also commonly found in healthy nerves, it is challenging to consider A-waves as specific markers for neurological conditions. There is a group with additional subclinical findings, like inactive chronic radiculopathies. Although they are inactive, we did not exclude these patients because we believe there is a pathophysiological change in these patients. The major challenge was distinguishing A-waves from repeater F-waves, the stable responses with similar configurations at F-waves latencies. Veltsista et al. (26) described consistency to distinguish A-waves from repeater F-waves: if >16/40, it is an A-wave; less than 16/40, it is a repeater F-wave. Therefore, this issue may be a major limitation of our study. However, there were two arguments against its limitation. First, in the dataset we described, the patients generally had F-waves. Thus, describing A-waves in the presence of F-waves was relatively more straightforward. Second, we should emphasize that patients with fewer motor neurons were few in our study.
In conclusion, other than multiple A-waves, A-waves were commonly seen in subjects with normal NCSs. Multiple and single A-waves may be observed in different neuromuscular disorders, including polyneuropathies. Thus, they should be cautiously interpreted in the early stages of polyneuropathy, where they are traditionally accepted as a kind of biomarker since F-wave changes or A-waves may develop in cases with polyneuropathy mimickers.
Footnotes
Ethics Committee Approval: This research was conducted in accordance with the Declaration of Helsinki and approved by the Istanbul University-Cerrahpaşa Ethics Committee (E-83045809-604.01.01-742186).
Peer Review: Externally Independent.
Author Contributions: Concept - AG, TA; Design - AG, TA, NUA; Supervision - AG, TA, EKÇ, BG, NUA; Materials - EKÇ, BG, AG; Data Collection and/or Processing - EKÇ, BG, AG, TA; Analysis and/or Interpretation - AG, TA; Literature Search - AG, TA; Writing - AG, TA; Critical Review - AG, TA, EKÇ, BG, NUA.
Data Sharing Statement: The author prefers not to share data. The research data will not be shared.
Use of AI: Our article does not utilize artificial intelligence (AI) or AI-supported technologies.
Financial Disclosure: This study received no funding.
Conflict of Interest: The authors declare that they have no conflict of interest.
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