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 Table of Contents  
Year : 2021  |  Volume : 16  |  Issue : 3  |  Page : 263-268

Electrodiagnostic study in patients with fibromyalgia: Implication for central sensitization

1 Department of Neurology, Baghdad Teaching Hospital, Medical City, Baghdad, Iraq
2 Department of Neurophysiology, Marjan Teaching Hospital, Babel Health Directorate, Babel, Iraq
3 Department of Physiology, College of Medicine, Al-Nahrain University, Baghdad, Iraq

Date of Submission06-Sep-2020
Date of Acceptance26-Nov-2020
Date of Web Publication21-Sep-2021

Correspondence Address:
Dr. Farqad Bader Hamdan
Department of Physiology, College of Medicine, Al-Nahrain University, Baghdad, St. 60, Baghdad
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/injr.injr_247_20

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Background: Fibromyalgia is a syndrome characterized by chronic pain, depression, fatigue, and sleep disturbance. Different hypotheses have emerged about its pathogenesis, but central sensitization, which plays an important role in the development of neuropathic pain, is considered to be the main mechanism. We aim to compare patients with fibromyalgia and healthy controls with different electrodiagnostic testing, and if present, to corroborate whether there is any relationship between electrodiagnostic measures. Also, we sought to test the diagnostic value of some of these measures.
Methods: A case-control study of thirty-one patients with fibromyalgia with a duration of illness ranging from 5 months to 10 years were recruited for the study. Full medical history, clinical neurological examination, and electrodiagnostic tests of the upper and lower extremity including nerve conduction studies, needle electromyography, sympathetic skin response, cutaneous silent period and muscle fiber conduction velocity.
Results: Sympathetic skin response latency and cutaneous silent period latency were not different between the patients and the control group. Cutaneous silent period duration was prolonged and the muscle fiber conduction velocity is faster in the subjects with fibromyalgia. The latter measures have similar diagnostic value. Sex has no significant impact on electrodiagnostic measures and the latter not correlated with patients' age.
Conclusion: A central sensitization and concomitant deregulation of the efferent higher motor centers might be implicated in the pathogenic mechanism of fibromyalgia.

Keywords: CSP, fibromyalgia, , MFCV, SSR

How to cite this article:
Al-Mahdawi AM, Sami SI, Hamdan FB. Electrodiagnostic study in patients with fibromyalgia: Implication for central sensitization. Indian J Rheumatol 2021;16:263-8

How to cite this URL:
Al-Mahdawi AM, Sami SI, Hamdan FB. Electrodiagnostic study in patients with fibromyalgia: Implication for central sensitization. Indian J Rheumatol [serial online] 2021 [cited 2022 Aug 14];16:263-8. Available from:

  Introduction Top

Fibromyalgia (FM) is a complex chronic syndrome characterized by widespread chronic pain persisting for more than 3 months, joint stiffness, fatigue, sleep disturbance, cognitive dysfunction, and depression.[1],[2]

The etiopathogenetic mechanism of FM is still unknown and unclear.[3] Studies have reported that various factors might feature the syndrome, such as neuroendocrine and autoimmune dysfunction, and genetic predisposition.[4],[5] Central sensitization or dysregulation at a spinal level was also hypothesized as a basic pathophysiologic mechanism.[6],[7]

Although the term myalgia refers to muscle, the co-existence of neuropathic features of pain and the growing information concerned with the loss of small fiber axons has raised the question of whether this pain is neuropathic in origin.[8],[9],[10]

Although various neurophysiologic tools were used to study central sensitization in patients with FM, the results were conflicting. For example, transcranial magnetic stimulation, nociceptive flexion reflex, and cutaneous silent period (CSP),[11],[12],[13] quantitative sudomotor axon reflex testing and nerve conduction study (NCS),[14],[15] muscle fiber conduction velocity (MFCV),[16],[17] and sympathetic skin response (SSR).[18],[19]

The CSP is a valuable investigation tool for pain processing in the central and peripheral nervous systems. It is a transitory pause in muscle action potentials after robust stimulation of the cutaneous nerve while the muscle under sustained voluntary contraction.[20] Few studies have previously investigated the CSP in FM with contradictory results regarding variation in its latency and duration.[21],[22],[23]

Since the muscle fiber is a structural, mechanical, and bio-energetic entity determined by a well-adjusted bioelectrical system, the electrophysiological muscle functions are vital for an intact working muscle. Many studies dealt with the electrophysiological muscle functions in patients with FM showed either an increased MFCV in the nonpainful and nontender point-related muscles or a tendency of the patients to manifest myofascial tender points,[16],[17],[24],[25] suggesting an overall functional muscular membrane disturbance.

Therefore, we sought to compare patients with FM and healthy controls by different routine NCSs and needle electromyography (EMG), CSP, SSR, and MFCV, and if present, to corroborate whether there is any relationship between these variables. Furthermore, we sought to test the diagnostic value of CSP duration and MFCV separately and in combination.

  Subjects and Methods Top

A case–control study was conducted at the Departments of Neurophysiology/Baghdad Teaching Hospital and Al-Imamain Al-Kadhimiyain Medical City for the period from June 2017 to May 2018. The study was approved by the Iraqi Council of Medical Specialization (decision no. 1257, date March 20, 2019). A written informed consent was obtained from all the participants.


Thirty-one patients with primary FM (no concurrent rheumatologic disease) referred by a consultant neurologist when they met the 2010 ACR Preliminary Diagnostic Criteria[26] which by definition they should have a normal clinical examination, laboratory, and imaging studies. They were 23 females and eight males aged 18–62 years with a duration of illness ranging from 5 months to 10 years.

Any patient with abnormal upper and lower limb NCSs, EMG, and SSR was excluded. Besides, those with a history of distal symmetrical paresthesia or abnormal sensory examination results (pinprick and thermal sensory loss) indicative of small fiber dysfunction were excluded too. Furthermore, patients with muscle disease, neuromuscular junction disorder, or medical conditions associated with peripheral nerve dysfunction such as diabetes mellitus, alcohol abuse, metabolic disorder, malignancy, or chronic drug usage were also excluded.

Another 31 healthy subjects (22 females and nine males) with an age range from 17 to 55 years serve as the control group.


Electrodiagnostic testing was done using Keypoint (Medtronic functional Diagnostic A/S-DK-2740 Skovlunde, Denmark). The skin temperature was maintained at ≥30°C recorded at the volar wrist. The right-sided median (sensory, motor, and F-wave latency), sural (sensory), peroneal (motor), and tibial (motor and F-wave latency) were examined. The examination generally followed the protocol described by Preston and Shapiro.[27] The following measurement was conducted: distal sensory latency, distal motor latency, CV, sensory nerve action potential amplitude, and compound muscle action potential amplitude.

Electromyographic studies were with disposable concentric needle electrodes (Micromed code DIN42802) to rule out the presence of myopathy and/or neuropathy. From the upper extremity, the first dorsal interosseous and brachioradialis were tested. From the lower limb, tibialis anterior and vastus medialis were examined.[27] Twenty motor unit potentials (MUPs) were analyzed for duration and amplitude during minimal volitional effort plus the recruitment pattern.

For measurement of the SSR, active surface electrodes were attached on the palmar side, and the references were placed on the dorsum of the hand. The stimulus was given at the wrist contralateral to the recording side. A stimulus with an irregular interval of more than 1 min was preferred to prevent habituation.[28] A total of ten trials were conducted for each subject. The latency then was determined.

MFCV was measured invasively by two monopolar needle electrical stimulation (4 mm apart) and a reference surface derivation. The site of needle electrical stimulation was the most distant site from where the muscle twitched when induced by the electrical stimulation. Reproducible action potential of 20–500 mV amplitudes was ensured with the manipulation of the active electrode.[29] All latencies were measured at the positive turning points, and resulting MFCVs were calculated according to the CV = distance/latency. A total of two trials were conducted for each subject.

For CSP recordings, the stimulating electrode was placed on the index finger and the recording surface electrode was placed on the abductor pollicis brevis muscle. During steady submaximal (50% of the maximal contraction) thumb abduction, 20 consecutive painful electrical stimuli of standard 80-mA intensity and 0.5-ms duration were applied to the index finger, and responses were superimposed.[23] The trace of the responses on the screen and EMG audio signal were taken into account to provide submaximal constant contraction during voluntary contraction.

Five optimal recordings showing complete silencing of the MUP with the most prolonged duration and shortest latency obtained. CSP latency was defined as the time between the stimulation and the onset of the silent period. CSP duration was calculated as the time interval between the beginning and end of the CSP.

Statistical analysis

Microsoft Excel 2016 (Microsoft Corporation, USA) and IBM Statistical Package for the Social Sciences version 23 (IBM Corp., Armonk, New York, USAsss) were used for statistical analysis. Continuous data were presented as mean ± standard deviation, and a comparison between means of study groups was made using the unpaired student t-test. Pearson correlation coefficient (r) was used to test the relationship between different neurophysiologic tests.

Cutoff values of the CSP duration and MFCV and accordingly, the sensitivity and specificity were evaluated by using the receiver operating characteristic (ROC) curve. P value of ≤0.05 was considered statistically significant.

  Results Top

[Table 1] summarizes the data of SSR, CSP, and MFCV. In the evaluation of SSR, in patients with FM, we observed a nonsignificant difference in the latency (1.45 ± 0.22 s) as compared with (1.47 ± 0.17 s) of the control group (P = 0.661). The CSP onset latency did not differ significantly between the patient (59.8 ± 8.99 ms) and control groups (61.63 ± 8.54 ms; P = 0.416). However, CSP duration in the patient group (78.68 ± 12.19 ms) was significantly longer than those in the control group (45.15 ± 7.46 ms; P < 0.001) as shown in [Figure 1]. The MFCV was markedly higher in FM subjects than in controls (P < 0.001) as shown in [Figure 2].
Figure 1: Cutaneous silent period. (a) Of a patient with fibromyalgia; (b) Of a healthy subject

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Figure 2: Muscle fiber conduction velocity. (a) Of a patient with fibromyalgia; (b) Of a healthy subject

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Table 1: Sympathetic skin response, cutaneous silent period, and muscle fiber conduction velocity in patients with fibromyalgia and control group

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In patients with FM, CSP parameters did not correlate with other electrodiagnostic parameters and the age of patients. Likewise, MFCV did not correlate with other electrodiagnostic parameters and the age of patients. Only the SSR latency was negatively correlated with the age of the patients (r = −0.374; P = 0.038) [Table 2].
Table 2: Bivariate correlation between variables in patients with fibromyalgia

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In patients with FM, sex does not have significant impact on the SSR latency (P = 0.664), the CSP latency (P = 0.413), the CSP duration (P = 0.741), and MFCV (P = 0.183) as shown in [Table 3].
Table 3: Impact of gender difference on sympathetic skin response, cutaneous silent period latency, cutaneous silent period duration, and muscle fiber conduction velocity in patients with fibromyalgia

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The ROC curve was used to find the diagnostic value of CSP duration and MFCV in the context of discrimination between patients with FM and healthy controls. For CSP duration, the AUC was 0.988, 95% confidence interval (CI) = 0.969–1, P < 0.001. The sensitivity and specificity of the test at the cutoff value of CSP duration = 57.25 ms was 93.5%. For MFCV, the AUC was 0.970, 95% CI = 0.930–1, P < 0.001. The sensitivity and specificity of the test at the cutoff value of MFCV = 5.71 m/s were also 93.5% [Figure 3].
Figure 3: Receiver operating characteristic curve for the cutaneous silent period duration and muscle fiber conduction velocity in the context of discrimination between fibromyalgia and healthy control group

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  Discussion Top

Data of multiple studies have been published about the SSR, MFCV, and CSP in different population with controversial results [Table 4]. Considering the SSR, we did not find a significant difference between patients with FM and the control group which supports the nonexistence of small fiber involvement in the former group. Özgöçmen et al.[30] also observed no statistically significant difference in SSR distal latency between patients with FMS and controls.
Table 4: Main published studies on the sympathetic skin response, muscle fiber conduction velocity, and cutaneous silent period in patients with fibromyalgia

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Our results were in contrary to the findings of Çakir et al.[19] who found significantly lower latency values for both sides claiming diminished sympathetic activity in FM patients. Likewise, our results disagree with those reported by Ulaş et al[31] El-Sawy et al.,[32] and de Tommaso et al.[33] who demonstrate an increased sympathetic tone (significantly longer SSR latencies from both palms and soles) in subjects with FM. These conflicting results confirm the heterogeneity in FM -associated dysautonomia.

It is known that there is considerable SSR amplitude variation from one response to the next.[34] Likewise, an intraindividual variation of SSR amplitudes was high (2%–48%) in different studies versus 2%–22% of the intraindividual difference for SSR latency.[30] Accordingly, SSR latency but not the amplitude was measured in this study as the former parameter is not affected by the type of stimulation or the site of stimulation and the prolongation in SSR latency or its absence may be considered as a sign of neuropathy.[21]

With regard to the CSP, the duration but not the latency was significantly differed in patients with FM from the control group. As CSP latency prolongation was primarily attributed to the long afferent conduction time rather than to a central delay, thereby reflecting dysfunction of the A-delta fibers.[23] Our findings would suggest dysfunction of supraspinal control that has modulatory influences on spinal excitability. This notion supports the dysfunction of pain modulation mechanisms in the CNS rather than small fiber neuropathy.

A Korean study conducted by Baek et al.[23] finds also prolonged CSP duration and latency, and concludes a central sensitization as the likely pathogenesis of FM.

In contradiction to our results, Sahin et al.[21] and Umay et al.[22] showed significantly prolonged CSP latency but not its duration. They concluded that the small fiber neuropathy might be the underlying pathophysiological cause in FM. The major drawback of these studies, they did not include an electrophysiologic test for the possible presence of small fiber neuropathy as it depends only on history taking. This is in contradiction to the present study, where physical history and the SSR were evaluated in an attempt to look after the presence of a small fiber neuropathy which affects the CSP latency.

For the MFCV, an invasive method was used in this study. In their study, van der Hoeven et al.[29] made a comparison between the surface and invasive recording of the MFCV and found it both methods are reliable to measure MFCV. They stated that surface MFCV is more considerable for research purposes for many reasons, i.e., the noninvasive character and the possibility to measure MFCV at different force levels or during continuous contractions. Furthermore, the higher MFCV estimates than does the invasive method, and the generalizable tendency of MFCV to increase with age.

In contrast, the invasive method gives information, particularly about the variability of the MFCV when the fibers are measured irrespective of innervation and recruitment. Also, for the higher reproducibility and its values were not affected by age. This leads to the consideration to use invasive MFCV not only for research applications but probably also for clinical use.[29]

In our study, MFCV was higher in patients with FM patients compared to the control values. This finding was in harmony with the results of Klaver-Krol et al.,[3] Klaver-Krol et al.,[17] and Casale et al.[35]

The number of recruited motor units or changes in muscle membrane properties might be the cause of MFCV increment. Based on the size principle, the MFCV would increase with both the force load and the amount of muscle activity.[36] Thus, the large, high-threshold motor units with their fast propagating muscle fibers would be activated with higher forces. Nevertheless, our patients neither changed the force load nor their muscle activity. Accordingly, what explains the higher CV in FM could be the functional alterations (depolarization) of the muscular membrane as the low- and high-threshold motor units conduct their action potentials relatively fast along the muscle membranes.

Physiologically, conduction along the membrane depends mainly on its resting potential. After producing an action potential, the muscle membrane develops a short after-depolarization, a period during which the membrane is hyper-excitable, and the membrane conduction is increased.[37] These changes denote augmented central activation and muscle membrane reaction during the after-depolarization phase in FM.

In this study, the ROC curve showed almost similar sensitivity and specificity of the MFCV and CSP duration in FM patients. Up to our knowledge, this is the first study in FM patients that evaluate those two parameters and judge their diagnostic value.

No significant correlation was demonstrated between CSP parameters and MFCV. To the best of our knowledge, no previous study correlates between them in FM patients. The results of the present study could be explained by different mechanisms underlying their involvement in FM patients, although both of them reflecting central sensitization.

  Conclusion Top

The prolonged CSP duration in patients with FM implicates a central sensitization as a pathogenic mechanism. The MFCV is faster in patients with FM, which further suggests concomitant deregulation of the efferent higher motor centers to be involved in FM.

  Acknowledgment Top

We thank assistant professor Dr. Qasim Al-Mayah from the Research Medical Unit/College of Medicine/Al-Nahrain University for helping in statistical analysis.

Financial support and sponsorship

The study was self-funded.

Conflicts of interest

There are no conflicts of interest.

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  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2], [Table 3], [Table 4]

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