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April2015 Vol.52 Issue:      2 Table of Contents
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Fibromyalgia: Clinical Evaluation, Electrophysiological Assessment and Serum Serotonin Level Measurement

Nihal Z. El Shazly1, Shereen F. Sheir2, Shaheera M. Moustfa1, Shereen H. Debala3

Departments of Neurophysiology1, Neurology2, Cairo University; Rheumatology3, Police Hospital; Egypt


Fibromyalgia (FM) is a chronic pain illness. The causes of FM are not fully understood. Biochemical, metabolic and disturbed immune-regulatory abnormalities were suggested as possible causes of FM. Objective: The study aims at the evaluation of serum serotonin in FM and its correlation with the pain and the possible electrophysiological abnormalities. Methods: Thirty patients suffering from FM (diagnosed according American College of Rheumatology for classification of FM ) ,  not under any medical treatment  had  i) An evaluation of  serum serotonin ii) quantitative electromyography (qEMG) iii) Sympathetic skin response test (SSR). Results: Serum Serotonin (SSL) level was significantly lower in FM patients compared to control group. A SSL 400 ng/L was found to be a cut off point for existence of the disease. SSR latency as well tends to be longer in FM patients. The qEMG showed motor unit potential de-synchronization, temporal dispersion and increased size. Conclusion: FM is a disease of low serotonin levels. Determination of SSL is a sensitive and selective test to assist in the diagnosis and follow up of FM patients. The value of SSR latency and qEMG tests still need to be verified however, they can be used to follow up the effects of the pharmacological and non-pharmacological treatments of FM. [Egypt J Neurol Psychiat Neurosurg.  2015; 52(2): 101-110]

 Key Words: fibromyalgia, quantitative EMG, serum serotonin, sympathetic skin response.

Correspondence to Nihal El Shazly, Assistant Professor of Clinical Neurophysiology; Cairo University, Egypt. Email:



Fibromyalgia is a syndrome that is characterized by widespread muscle aches, point tenderness and general fatigue. The most common sites of pain include the neck, back and shoulders, however any part of the body can be involved.1, 2 FM was found to be 4-7 times more common in women. Symptoms of fibromyalgia were reported to start in the age range of 20-55 years 3

What really starts the sequence of events that underlie FM is so far unknown. The widespread body pain and tenderness may originate from a centrally mediated process resulting in augmentation of pain sensation. It is possibly mediated by the neuro-transmitters of pain 4. The lower levels of serotonin and  increased levels of substance P (a pain neurotransmitter) to point a probable hypersensitivity to pain due to abnormal central processing of nociceptive inputs5. Abnormalities in the brain’s regional blood flow as well as endocrinal and autonomic disturbances could all result from alterations or otherwise imbalance in the relative levels of central neurochemicals.

Conventional electromyography showed minor non-specific abnormalities in FM hence some researchers concluded that there is no significant loss

of motor units and no conspicuous muscle fiber degeneration in FM. Factors as muscle tension may be responsible for maintaining the pain in FM6.

Recently automatic methods of EMG motor unit potentials (MUP’s) and interference pattern analysis (IPA) became powerful tools for diagnostic purposes. Quantitative MUP analysis (qEMG) reflects pathophysiological changes in single MUP’s that are recruited at low muscle activation on the other hand the IPA describes the changes in motor units recruited from weaker to stronger efforts. One method of the IPA is the Turns Amplitude analysis (TAA). It reflects the number of turning points of the IP that are separated from the preceding and following turning points by an amplitude difference greater than a 100 µV 7.

The aim of this study is the evaluation of the possible inter-play between the serum serotonin level, activity of the sympathetic nervous system (reflected by the sympathetic skin response test) and functional muscle abnormalities.(reflected by qEMG and IPA) all of which could be involved in the pathophysiology underlying fibro-myalgia.




The study was carried out in the Neurology Department of Kasr Al-Aini Hospital, Cairo University. Thirty patients suffering from FM selected among patients attending the Neurology outpatient clinic (1 male and 29 females). They were diagnosed as having FM according to American College of Rheumatology for classification of FM.8 Thirty normal subjects were selected from Kasr Al-Aini Hospital staff served as a control group.

All participants were subjected to: (1) Thorough history taking, (2) Clinical assessment with special emphasis on neurological and musculoskeletal examination. (3) Assessment of tender points of FM (4) Severity of pain using Visual analog scale (VAS) 9 translated to Arabic by the examining physician. (Figure 1)  (5) Routine Laboratory investigations (complete blood picture, blood glucose levels, liver and kidney function tests, thyroid function test, serum uric acid, (6) Autoimmune profile including erythrocyte sedimentation rate and C reactive protein titer. (7) MRI for the cervical and lumbar spine. (8) EMG for proximal limb muscles as well as Motor and sensory nerve conduction studies for the median, ulnar, tibial and common peroneal nerves.


Excluded from the study were cases:

·          Suffering from any medical or psychiatric illnesses other than the fibromyalgia.

·          Who presented by secondary fibromyalgia due to underlying disease (particularly auto-immune disease to avoid any bias to results of EMG or serum serotonin level

·          Cases presented by radiculopathy verified by EMG and/or MRI, peripheral neuropathies, entrapment neuropathies (verified by nerve conduction studies) or any other neurologic diseases whether central or peripheral.

·          Who receive any kind of treatment either pharmacological or non - pharmacological (particularly anti-depressants or mood modulating drugs) for fear of modification of serum serotonin levels.


Serum serotonin level (SSL):

SSL was determined by enzyme-linked immuno-sorbent assay (ELISA): A Blood sample was collected from the antecubital vein and then centrifuged. SSL was then calculated using a standard curve.


 Neurophysiology Techniques:

All Neurophysiology examinations were carried out on a digital MEB-9100 Version 0.3-0.6 Neuropack µ (Nihon Kohden, Japan).  

I.             qEMG:

qEMG of the supraspinatus , trapezius and deltoid muscles was carried out using concentric needle electrodes The band pass was 5 Hz - 10 kHz. The sweep speed was 10 ms/div and the gain was 0.2 mV/div. The needle electrode was inserted into the middle part of the muscle and EMG was recorded during minimal volition (≈ 10% of muscle power). The computer program extracted 1 to 5 MUPs each time. At least 10 different needle positions and different depths were studied. The recruited MUP were of a sharp contour and short rise time. MUP that appeared to have originated from the same motor unit were excluded. Necessary manual cursor adjustments were made for amplitude or duration. Parameters automatically measured were peak-to-peak amplitude, duration, area, phases and turns, firing rate and MUP rise-time. 

II.           Interference pattern analysis:

The patient was then asked to contract the examined muscle to the maximum possible extent and 10 different epochs of 100 ms duration were sampled by changing the position of the tip of the needle for each epoch. Filter settings were maintained the same as for qEMG, sensitivity was 0.5 mV/ div. Sweep speed was 100ms/div. The mean data were then entered for statistical analysis. The analyzed parameters for the IP analysis were turns/s and turns/amplitudes (T/A),

III.          Sympathetic Skin Response:

SSR was recorded using surface disc electrodes, 6 mm in diameter, the active and reference electrodes were placed on the palmar and dorsal surface of one hand respectively. The ground electrode was placed on the ipsilateral wrist. The contralateral median nerve was stimulated at the wrist. Stimulations were of randomized intervals. The duration of the stimulus was between 0.1 ms and 0.5 ms the stimulus intensity 20 - 60 mA. Sensitivity was set at 0.5mV/div and sweep at 5ms/div. Band pass was 0.2-500 Hz. At least 3 responses from both hands were recorded after stimulation and were superimposed. Latencies were measured from onset of the first deflection from baseline (L1) and amplitudes were measured from peak to peak.


Statistical Methods:

IBM SPSS statistics (V. 21.0, IBM Corp., USA, 2012 was used for data analysis .Chi-square test was used to compare qualitative variables. Unpaired student's t- test was used to compare two groups as ranged quantitative variables. Correlation co-efficient r- test was used to rank different variables against each other directly or indirectly. The probability of error at 0.05 was considered significant, while at 0.01 and 0.001 are highly significant.




Patient and control groups’ demographic characteristics, clinical, SSL and SSR (L1) are summarized in Table (1).

All the patients (100%) complained of maximum pain and tender points involving the shoulder , front of the arm and neck areas  and to a lesser extent other sites (side of the arm , lower scapular region and front of the leg below the knee. The mean pain severity by VAS is shown in Table (1).

Automated analysis of the MUP obtained from the supraspinatus, biceps and trapezius muscles is shown in Tables (2) and (3).

SSL showed significantly lower mean levels in the patients compared to the control group (p<0.001), Table (4), Figure (2).

ROC curve between both groups showed that a SSL of 400 ng/L is a cutoff point. At or below this point patients’ group existed .Two patients had a SSL slightly above this cutoff point (Figure 3).

The negative predictive value of serotonin level 95.5% and the sensitivity was 96.7% (Table 5 and Figure 4).

There was a significant inverse correlation between SSL and the pain severity by VAS (r= - 0.604, p= 0.0001)

There was a tendency  towards a delay of the   SSR latency (L1) in the patients compared to control (1.2± 1.7 versus 1.2±1.9) however it did not reach statistical significance (p=0,085)

Compared to the control group the

(i)            qEMG in the patient group showed (Table 2):

A.     De-synchronization and temporal dispersion as indicated by the:

1.      Significantly higher polyphasia in all the  examined muscles p=0.001

2.      Increased number of turns in 2 of the examined muscles (p=0.01)

B.     Increased motor unit size as indicated by the:

1.      Significantly higher MUP area (p = 0.001, 0.005) in two of the examined muscles.

2.      Significantly higher MUP amplitude (p = 0.001, 0.03 respectively)

3.      There was a significant higher MUP duration in the one of the examined muscle (p=0.02).


(ii)           IP analysis in the patient group showed:

1.      Significantly higher number of turns / sec. in two of the examined muscle.  (p = 0.001, 0.014)

2.      Significantly higher turn / amplitude in two of the examined muscle (p = 0.01, 0.002). 


Correlation SSR L1, SSL & pain by VAS are summarized in Table (6).

There was no significant correlation between the SSL and the mean MUP parameters in any of the examined muscles.





Figure 1.  Visual analogue scale (English).



Figure 2. Serum serotonin level in patient and control groups.





Figure 3. Roc curve  serum serotonin level in the patients (Group I) and control (Group II) patients



Figure 4. Sensitivity and specificity of serum serotonin level test.



Table 1. Demographic characteristics, clinical, laboratory (serum serotonin level) and Sympathetic skin responses in patients and control groups.



Group I

Group II

Mean Age ±SD/


37.1±12.1  years

28-45 years

31.1± 5.6 years

24 -42 years





96.67% (n=29)

3.33% (n=1)


66.67% (n=20)



Housewives  53.3% (n=16)

Office jobs 26.7 (n=8)

Students 20% (n=6)

Office jobs 100 % (n=30)


Duration of symptoms

42.2 ±39.2 months (6-168)


Pain severity by VAS

mean ±SD



8.5± 1.26



Serum serotonin level

Mean ± SD



134.6 ± 113.2 ng/ L

22 – 500


430.2 ±202.5 ng/L

94 - 200

Sympathetic skin response

Mean ± SD



1.5 ± 0.1 msec

1.2 - 1.7


1.6 ± 0.2 msec

1.2 - 1.9

Group I : patients ; Group II : control


Table 2. qEMG of muscles in the patients (Group I) and controls (Group II)


MUP parameters

Biceps Brachii









Phases I







Phases II











Turns I




Turns II








Area  I







Area II











Amplitude I







Amplitude II











Duration I

6.1 - 10.0

7.8 ± 0.9

6.1 - 11.9

8.5 ± 1.7

6.0 -10.0

7.2 ± 0.9

Duration II

7.0 - 8.9

8.1 ± 0.6

7.1 - 8.3

7.7 ± 0.4

0.8 - 8.5

7.7  ± 1.3





*Significant at P<0.05 **Significant at P<0.01


Table 3. Interference pattern analysis in the patients (Group I) and controls (Group II)


MUP parameters

Biceps Brachii









Turn/second I







Turn/second II











Turn/ Amplitude I







turn /Amplitude II











*Significant at P<0.01


Table 4. Comparison of Serum Serotonin level in patients and control groups



Serotonin .serotonin

Mann-Whitney Test







Group I









Group II









Table 5. Sensitivity and specificity of Serum serotonin in patient and control groups.















Table 6. Correlation between SSRL1, SSL and pain by VAS.








SSR L1 &  Pain VAS

- 0.386 **


*Significant at P<0.05 **Significant at P<0.01





The exact pathogenesis of FM is still not well understood.  It is believed to be due to the interaction of multiple factors involving the processing of pain by the central nervous system. Disturbance in the levels of neurotransmitters particularly serotonin and norepinephrine may lead to a whole body hypersensitivity to pain10. Experimental studies have shown that serotonin and norepinephrine agonists given intrathecal can block pain-related behaviors. 11   Preclinical data suggest that neuropathic pain may be inhibited by enhancement of central norepinephrine and serotonin transmission and those deficiencies in one or both of them may contribute to hyperactive pain processing12

In accordance with previous studies 7, 13, 14 the SSL was significantly lower among our patients in comparison to the control group (P=0.001). Roc curve of the SSL, showed that 400 ng /L is a cutoff point at or below which our FM patients existed. Only two of our patients had an SSL higher than 400 ng/L, probably their SSL is relatively lower than their premorbid values. Some studies showed that it is not the absolute reduction of blood serotonin level per se that is the cause of FM but rather pathological serotonin receptors or anti-5 HT receptor antibodies that account for FM.15 Reduced receptor activity or numbers can cause accumulation of serotonin in blood hence increased serum level in spite of existence of the disease. 

Jaschko et al, 200716 found lower concentration of serotonin in the sera of rheumatoid arthritis (RA) patients as well as FM patients. The level of the serotonin exhibited a tendency to be lower in the FM group, compared to the RA group, but because of the wide variation of serotonin level in his disease group, he concluded that serotonin is not useful as a single test for diagnosis of FM. Our criticism is that a secondary fibromyalgia in the RA could be the cause of the lower serotonin level since the presence of secondary FM in several rheumatic diseases has been reported as much as 11-30 % 17-20. One study showed that 6.6% of the Turkish patients having RA had concomitant FM.21

In our study the SSL measurement had a diagnostic sensitivity for FM of 96.7% and specificity of 70% with 76.3%  PPV and 95.5% NPP which makes the determination of SSL a reliable confirmatory test for the existence of FM  in a patient who fulfils the clinical criteria and the guidelines of the ACR  

Autonomic dysfunction in FM was suggested by many researchers. Lower levels of plasma neuropeptide Y was found in FM patients.21. Previous studies of the SSR in FM patients showed delayed latencies from palms and soles or reduced amplitudes or both22,23, while other studies showed no significant difference in the SSR in patients compared to controls24. In our study, although the latencies of the SSR tended to be longer yet it was statistically non-significant (0.085). SSL had a direct relation to SSR latency (p=0.01) and an inverse relation to pain severity (p=0.0001). Since FM is a process of centralized pain10,25, and Serotonin is a neurotransmitter that reduces the amount and intensity of pain signals sent to the brain, thus, reduced SSL can reduce the pain threshold, and cause a whole-body hypersensitivity to pain.14,26,27. Faulty perception of minor noxious stimuli may elicit an exaggerated sympathetic body response28 and reduce sympathetic threshold hence account for the tendency towards shorter SSR latencies detected in the study. 

Previous investigators proposed that the amplitude of the MUP is dependent on the density of the muscle fibers attached to that one motor neuron and that a MUP amplitude and area are accurate discriminators of MUP size. Increase of both parameters may indicate an increased MUP thickness29. In this study qEMG of the muscle tender points showed that the MUP area and amplitude were significantly  higher compared to the controls and that there was an incomplete asynchronous motor unit activation as  expressed by a significantly higher polyphasia. The number of phases and turns reflect the temporal dispersion of the action potentials within the motor unit. It results from the loss and regeneration of muscle fibers or variation in muscle fiber diameter30. In view of that we may suggest that in FM the there is a probable increase in the MU thickness  and disorganization of  MUP synchronization that may have resulted from a continuous process of wear and tear  within the muscle in FM. This process could be either the cause or the consequence of pain.

Previous studies reported increased number of T/S second with decreased mean T/A in myopathic muscle disorders31, while neuropathic muscle lesions show increase in mean T/A associated with normal T/S.32 In our study the pattern of IP changes was somehow unique . It is neither a complete myopathic nor a complete neuropathic pattern. There was a significantly higher T/S associated with a significantly increased T/A. It cannot either be explained by my muscle fatigue since fatigue causes decreased T/S while the T/A increases33. Previous studies of chronic muscle pain in headache, orofacial pain and myofascial trigger points34 showed higher average amplitude (root mean square) of the needle EMG at rest in muscles of humans compared to healthy controls but to the best of our knowledge there was no direct study of the qEMG or IP analysis in FM patients. We suggest that such abnormalities in the electro-physiologic muscle behavior revealed by unique combination of the previously mentioned  abnormal MUP parameters and IP analysis could be a consequence of the a series of pathophysiological mechanisms accompanying FM. The Lower concentrations of hydroxyproline and collagen and a higher level of atrophied muscle fibrils may lower the threshold for muscle micro-injury and thereby result altered pain threshold and non-specific signs of muscle pathology35.  Defective sympathetic control may result in disturbed microcirculation, muscle ischemia and nociceptor excitation36.

In conclusion We can  suggest that  in addition to the clinical criteria serum serotonin concentration less than 400nm/ml and qEMG that shows  a relative increase of MUP areas , amplitudes and polyphasia  as well as increased IP T/s and T/A are useful confirmatory investigations  in patients suspected to have FM. In addition to the above; Detection of shorted SSR latencies in FM patients may indicate the existence of a sympathetic over drive and an exaggerated pain perception.


[Disclosure: Authors report no conflict of interest]




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الملخص العربي


تقييم معدل  السيروتونين بالدم والفحص السريري  والفحص العصبي الكهربي في مرض ألم العضلات الليفي  


ألم العضلات الليفي هو مرض الآلام المزمنة. يختص هذا المرض بنطاق واسع من الآلام المزمنة في العضلات والعظام مع تعب عام واضطرابات في النوم. تعد الرقبة والكتفين والحوض واليدين من أكثر اماكن شيوع الألم.

 مازالت الاسباب المؤدية الى المرض غير معروفة وقد اظهرت بعض الدراسات السابقة وجود اضطرابات حيوية كيمائية والمناعة التنظيمية المصاحبة للمرض.

تتمثل التغيرات الحيوية في انخفاض مستويات السيروتونين في الدم وزيادة عامل نمو الأعصاب اربعة اضعاف مما يؤدى الى فرط حساسية الجسم للألم.

اجريت هذه الدراسة على مدى عامين على ثلاثين مريض بمرض مرض العضلات الليفي وثلاثون شخص صحيح (كمجموعة ضابطة) بهدف تقييم مستوى السيروتونين وتحليل رسم العضلات الكمي مع تقييم استجابة الجال السمباتوية في محاولة لرصد اسباب ونتائج الاضطرابات الفسيولوجية والمرضية المصاحبة للمرض.

كشفت الدراسة انخفاضا في مستوى السيروتونين في الدم مقارنة بالأصحاء ووفقا للدراسات الاحصائية فان معدل السيروتونين اقل من 400 نانوجرام/ليتر يعد نقطة قاطعة في تحديد وجود هذا المرض من عدمه في الرضى الذين يعانون من الام عضلية في غياب أي اسباب اخرى للأعراض. كشفت الدراسة ايضا عن وجود تأخير في استجابة الجلد السمباتوية كما اظهر التحليل الكمي لجهد الوحدة الحركية اضطرابات متمثلة في زيادة في ومنطقة وعدد مراحل جهد الوحدة العضلية بالإضافة الى زيادة نسبة السعة / الدورة وعدد اللفات / الدورة

الخلاصة ان قياس مستوى السيروتونين في الدم يعد اختبارا شديد الحساسية للمساعدة في تشخيص ومتابعة المرض. التحليل الكمي لجهد الوحدة الحركية يمكن ان يكون اختبار بسيط لمتابعة تأثير العلاج الدوائي


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