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January2012 Vol.49 Issue:      1 Table of Contents
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Cervical Radicular Pain Induced Neuroplasticity in Somatosensory Pathway

Seyam S. Salem1, Amira M. El-Gohary1, Nevin M. Shalaby2, Al-Shaimaa S. Khalil1

Departments of Clinical Neurophysiology Unit1, Neurology2, Cairo University; Egypt


Background: Peripheral deafferentation is known to induce neuroplastic changes in the neuronal system, but there is paucity in studies addressing pain influence on neuroplasticity. Objective: To assess the relationship between chronic pain and plasticity in somatosensory pathway. Methods: A cross sectional study including 20 Egyptian patients with unilateral cervical radicular pain. Patients were neurologically assessed and pain severity was graded. Magnetic resonance imaging of the cervical spine, and electromyography, for evidence of deafferentation, were performed. Somatosensory evoked potential studies after digital nerve stimulation of thumb, little finger on painful and non painful sides were done. Somatosensory evoked potential parameters were compared within individual patients and with those of 10 age and sex matched control subjects. Results: Pain severity was graded as II in 13 patients and III in 7. The 6th cervical root was the most involved root clinically and radiologically. There was no evidence of deafferentation in 75% of patients. Amplitudes of EP, N13, N20 and P22 after stimulation of the painful thumb were greater than those of the non-painful thumb, little finger on painful and non painful sides within patients group and those of controls. The amplitude difference of EP showed the least change relative to other waves among patients. The amplitudes correlated with pain severity and duration. Conclusion: Pain can induce neuroplastic changes within the somatosensory pathway, irrespective of presence of deafferentation, involving both peripheral and central levels but more evident centrally. Such changes are selective to the involved territory. [Egypt J Neurol Psychiat Neurosurg.  2012; 49(1): 59-66]


Key Words: cervical radicular pain, neuroplasticity, somatosensory evoked potential.


Corresponding author: Amira El Gohary. Hadika Street, No. 3; Garden City, Cairo, 11451, Egypt. Tel.: +20227957778. Email:



Cervical radiculopathy is caused by compression of a nerve root in the cervical spine. Among the various pathologies which affect the nerve root, degenerative processes of the spine are the most common1. In greater than 70% of cervical radiculopathy, pain is the primary presenting feature2.

The somatosensory system of adult humans may undergo major reorganisation as a consequence of pathological modifications of sensory input3. Pain plays a crucial role in promoting neuroplasticity by showing pain-related changes in neural activity at multiple levels of the somatosensory system4,5. Data suggest that intense noxious stimulation or tissue injury can produce dramatic changes in sensitivity to both noxious and non-noxious stimulation as well as expansion of the receptive fields of neurones of the dorsal horn6 as well as the thalamus and somatosensory   cortex 7,8.

The technique of somatosensory evoked potentials (SEPs) offers the unique opportunity to assess neural activity not only of different cortical somatosensory areas but also of dorsal horn and dorsal column-medial lemniscus systems5.


This work was designed to detect the influence of chronic cervical radicular pain on the electrical activity in the somatosensory pathways and cortical sensory area using SEP studies to document possible neuroplastic changes associated with such pain.




This is a cross sectional study carried out on 20 Egyptian patient with typical unilateral cervical radicular pain defined as pain in the neck radiating to one or more of the cervical dermatomes, with or without paresthesia and/or sensory impairment of a dermatomal distribution, of at least 6 months duration, with MRI evidence of root compression caused by a cervical disc that can explain patients' symptoms. Patients were excluded if they had local neck masses, cervical spine operations, spinal cord or brain lesions, history of systemic causes for peripheral neuropathy, or evidence of peripheral neuropathy or carpal tunnel syndrome by electromyography and nerve conduction studies. Patients were recruited from neurology, outpatient clinics of Cairo University Hospitals (Kasr Al-Aini), Egypt, over the period from April 2009 to September 2010. They were compared with 10 normal age and sex matched control subjects. All participants were right handed. Informed written consent was obtained from literate participants or their relatives if illiterate. Approval from Cairo university Hospitals Research Ethics Committee was obtained.

All participants were subjected to:

*       Clinical assessment: The Arabic version of a pain grading severity questionnaire was used9. Sensory or motor complaints of dermatomal distribution were reported. Neck movements were assessed. Superficial sensation in individual cervical dermatomes was tested using pinprick test, and individual muscles of the upper limbs as well as stretch reflexes were examined. Spurling test was done10.

*       Plain X-Ray, and MRI for the cervical spine: at the X-Ray and MRI units, radiology department, Cairo University Hospitals.

*       Nerve conduction studies: for ulnar and median nerves in upper limbs and anterior tibial and common peroneal nerves in lower limbs as a preliminary step to exclude peripheral and entrapment neuropathies.

*       Electromyography (for patients only): was done using Nihon Kohden; Neuropak MEB-9200G/K EP/EMG measuring system (Neuropak M1) – 4 channels-version 08.11, Japan. Concentric needle was used. The following muscles, in both upper limbs, were examined: deltoid or biceps muscles for 5th and 6th cervical (C5 & 6) roots; pronator teres or triceps for C6 & 7 roots; and first dorsal interosseous for C8 root.

*       Somatosensory evoked potential studies after digital nerve stimulation: for each subject the thumb and little finger on both, the painful and non painful, sides were examined. Equipment:  a Nihon Kohden; Neuropak MEB-9200G/K EP/EMG measuring system (Neuropak M1) 4 channels-version 08.11, JAPAN. Procedure: Electrode placement: active electrodes were placed on the scalp at C3' (C4')11; the second cervical spinous process; and over the brachial plexus at Erb’s point. Reference electrodes: a common reference was placed at the forehead; and a ground electrode, between the stimulator and the recording electrodes. Stimulation: the digits were stimulated with ring electrodes 4 cm apart. Settings: the monitor time was set at 200 msec; stimulus duration at 0.2 msec; stimulus rate at 2 Hz; sensitivity at 10 µV; low frequency filter at 20 Hz; high frequency filter at 2 kHz; and analysis time at 50 msec. Impedance measurements were kept under 1200 Ω. Measurements: peak latencies, measured in msec, to the first positive peak. Amplitudes, measured in µV, from peak-to-peak for the scalp response, and from peak of the negative deflection to the baseline for the cervical and shoulder responses. Waves: Erb’s potential (EP), generated just distal to the brachial plexus; N13, originating from the dorsal horn of the cervical spinal cord; N20, from area 3b in the posterior bank of the Rolandic fissure; and P22, from parietal sensory/motor cortex11,12. The amplitudes and latencies of different SEP waves were compared with each other within individual subjects, and among patients and controls.


Statistical Methods

Statistical package for social science (SPSS) version 12 was used for data management and analysis. Descriptive analyses were conducted to examine frequencies, and distribution of all variables. Tests for significance: to test the significance of difference between quantitative data between cases and controls (small group) Mann-Whitney test was used. Paired T test was used to assess difference in quantitative data in cases (painful and non painful digits) after testing for normality. Wilcoxon-signed test was used to compare quantitative data in controls (painful and non painful digits). Spearman correlation was used to assess the relation between quantitative variables. P-values <0.05 were considered significant.




Demographic data and patients̕ characteristics

The study included 20 patients; 8 males (40%) and 12 females (60%), with ages ranging from 35-65 years with a mean age of 49.5±8.86, and 10 normal control subjects; 4 males (40%) and 6 females (60%) with ages ranging from 38-60 years with a mean age of 47.1±7.29. There was no statistically significant difference between both groups regarding either age or sex (P>0.05). Five patients (25%) gave history of axial load bearing; 8 (40%) of high risk occupations (driving, sewing, maids); and 6 (30%) of a positive family history of disc prolapse.


Clinical, and Radiological Data are illustrated in Tables (1) and (2).


Electrophysiological Results

1)            Electromyography (EMG)

Only 5 patients (25%) had evidence of deafferentiation on EMG in the form of broad, polyphasic motor unit potentials with reduced interference patterns involving C5 and C6 indicating a neurogenic lesion. The other 15 patients (75%) had normal EMG.


2)      Somatosensory evoked potential studies (SEPs)

The mean amplitudes and latencies of SEPs in patients and controls are displayed in Table (3).

No statistically significant difference of SEP parameters between either upper limbs in controls was found (P>0.05).

Generally, the mean amplitudes of EP, N13, N20 and P22 waves, recorded after stimulation of the thumb on the painful side in patients, were statistically significantly higher than those recorded upon stimulation of  right thumb and little finger in control group (P<0.001) (Figure 1 A & B). However, the mean latencies of various SEPs waves did not show a statistically significant difference between the 2 groups (P>0.05).

The mean amplitudes of all SEP waves: EP, N13, N20 and P22 recorded after stimulation of the thumb on the painful side were statistically significantly higher than those recorded after stimulation of the other digits within the patients’ group. The difference in EP amplitude though statistically significant, yet the degree of significance (P<0.014; <0.010; <0.015) was less than the difference in amplitude of other spinal and cortical potentials which exhibited a higher degree of statistical significance (P<0.001). No statistically significant differences were elicited in the mean latencies of various waves recorded after stimulation of the painful thumb in comparison to other digits. No statistically significant difference was detected on comparing different SEP parameters recorded after stimulation of the little finger on the painful side to those recorded after stimulation of the  thumb and little fingers on non-painful side (P>0.05).

There was a statistically significant positive correlation between the amplitude of P22, recorded from painful thumb, and that of N13 (r=0.71, P<0.001) and that of N20 (r=0.82, P<0.001) recorded after stimulation of the painful thumb, but no significant correlation with the amplitude of EP wave was found (r=0.22, P>0.05).

There was no statistically significant difference in the mean SEP amplitudes between patients with EMG evidence of deafferentation and those with normal EMG (P>0.05), or those with and without paresthesia and/or sensory impairment (P>0.05).

A statistically significant positive correlation was noticed between the duration of pain and the amplitude of N13 and N20 upon stimulating the painful thumb (r=0.69, P=0.001; r=0.65, P=0.002 respectively). Also, the mean amplitudes of N13, N20 and P22 recorded after stimulation of the painful thumb were statistically significantly higher in pain grade 3 than grade 2, but this was not the case for EP. Such difference, also, was not found on comparing SEP parameters recorded after stimulation of the other digits on both sides (P>0.05).

Mean amplitudes of SEP waves did not statistically differ between patients with neck pain referred C4 & C5 dermatomes compared to those with a more extended pain referral to C4, C5 and C6 dermatomes (P>0.05). SEP parameters were not correlated with age, and did not differ between males and females (P>0.05).


Table 1. Clinical manifestations of patients.


Clinical Symptoms & Signs

Patients (N=20)

No. (%)

Pain Duration (m) (Mean±SD)


Neck Pain Referral


Shoulder (C4)

4 (20)

Shoulder & arm (C4,5)

1 (5)

Shoulder, arm & thumb (C4,5,6)

10 (50)

Shoulder, arm, thumb & index (C4,5,6)

5 (25)



10 (50)


10 (50)

Pain Character

Dull aching

18 (90)


2 (10)

Pain severity grading

Grade II

Grade III



Treatment modalities









4 (20)


16 (80)

Distribution (C6)

·       Thumb

·       Index

·       Thumb & index


9 (56.25)

2 (12.5)

5 (31.25)

Pinprick Test

Normal sensation

16 (80)

Impaired sensation

Distribution (C6)

·       Thumb

·       Thumb & index

4 (20)


1 (25)

3 (75)

Motor Examination

Normal Power

20 (100)

Normal DTR*

20 (100)

Spurling Test


7 (35)



* Non-steroidal anti-inflammatory drugs; Adrenocortico trophic hormone; Deep tendon reflexes.

Table 2. Cervical MRI findings in patients.


MRI Finding

Patients (N=20)

No. (%)

Level of  disc lesion

Single level

C5 & C6

10 (50)

Two levels

C4,C5 & C5, C6



C6,C7 & C5,C6

6 (30)

Three levels

C4,5 & C5,6 & C6,7

1 (5)

Compromised neural exit foramina (Unilateral)

C5 & C6

20 (100)

C4 & C5

2 (10)

C6 & C7

3 (15)

Type of disc pathology


20 (100)


6 (30)


5 (25)

Degenerative changes

                                 20 (100)

Straightened cervical curvature

                                 11 (55)



Table 3. Mean parameters of SEPs in study groups.





Finger examined





Thumb painful side

Little finger painful side

Thumb non painful side

Little finger non painful side

Rt. Thumb


Rt. Little finger

Lt. Thumb

Lt. little finger

Amplitude (μV)

Mean (SD)

Erb’s (EP)




































































Latency (msec)

Mean (SD)

Erb's (EP)






































































Figure 1. SEPs recorded after stimulation of the painful thumb in patient no. 3(A), and right thumb in

control no. 2 (B). Ep, N13, N20 amplitudes are bigger in patient than in control.





Sixty percent of patients, in this study, were females. Such female preponderance could be attributed to structural gender differences that may explain altered response to dynamic loading in women leading to increased soft tissue distortion and greater injury susceptibility rendering women more susceptible to trauma-related neck pain, commonly resulting from soft tissue cervical spine injury13.  Another observation was the relatively young age of some patients (mid-thirties) which can be explained by the involvement of those patients in high risk occupations that require mal-positioning of the neck for long periods e.g. sewing, driving, maids with heavy household duties, and heavy weight lifting above head. In addition, a positive family history for intervertebral disc prolapse was present in some cases which may hint to mesenchymal weakness with liability to disc prolapse14.

All patients had neck pain referred to the shoulder, and most reported, in addition, pain referral to the arm. Taking into consideration that two patients  only had C4-C5 neural exit foramina compromise and no paresthesia was reported in C5 distribution, such pain can be explained on the basis of muscle spasm caused by nerve root irritation rather than being a typical radicular pain15,16, also, radicular  pain from lower cervical roots is usually perceived deeply through the shoulder girdle with extension to the arm and forearm, whereas numbness and paresthesias are more commonly restricted to the peripheral part of limb17. Most of the patients reported sensory complaints involving C6 in the form of pain and/or paresthesia with or without sensory impairment, these symptoms are the result of an intervertebral disc prolapse at the level of C5 and C6 with unilateral compromise of the corresponding neural exit foramen seen in all patients. Although a few patients had a compromise of neural exit foramina between C6 and C7, yet none of them had sensory complaints involving the middle finger. The discrepancies in clinical presentation in relation to radiological findings may be explained on anatomical basis as variations of intervertebral foramina, nerve roots, spinal nerves, and plexuses occur commonly. Neuro-anatomical anomalies and musculoskeletal abnormalities account for many of the variations seen with unexpected radicular patterns18,19.


Somatosensory evoked potential findings

                 Due to the comparable values and the lack of significant difference in the parameters of SEPs recorded from both right and left sides in the control group, and since all subjects were right handed, we used SEP parameters recorded  after stimulation of right upper limb only in control subjects to be compared to patients results, so as to reduce the hassle while performing statistical work, and meanwhile examine the sensory organization in the categorical hemisphere. 

In the present study, the amplitudes of peripheral (EP), spinal (N13) and cortical (N20 and P22) SEPs in response to stimulation of the patients' painful thumb were greater than those of controls. The existence of such difference clearly indicates the presence of increased excitability of peripheral, spinal, and cortical structures conveying the pain reported by patients which can reflect underlying structural and functional changes in these areas which can be explained in terms of neuroplasticity. Even within the patients' group, there was an increased electrical activity along the somatosensory pathway recorded after stimulation of painful compared to non painful side evidenced by larger amplitudes of EP, N13, N20, and P22 indicating functional alterations in this pathway in response to pain both on the central and the peripheral levels.  However, the observation that the amplitude difference of EP was as significant as other potentials when compared with controls but showed the least change relative to those potentials among patients; points that the neuronal reorganisation is more evident in the central than in the peripheral pathway. These results are comparable to another study5, however, the latter could not elicit a significant difference on the peripheral level, represented by peripheral P9 far-field potential arising from the brachial plexus, and thus, it concluded that the increased electrical activity in the somatosensory pathway originated at a central and not a peripheral level.

Functional alterations in the somatosensory pathway seem to be selective for the painful region. This observation was drawn as the amplitudes of EP, N13, N20 and P22 after stimulation of the patients' painful thumb were greater than those in response to stimulation of the little digit in the same hand, whereas, no side-to-side difference in amplitude was observed after stimulation of the little digit in the painful and non-painful hands. Functional changes being selective for the painful skin and the adjacent territories were also observed by others5,20.

In the current study, the presence of a positive correlation between the amplitude of cortical (P22) potential and that of N20 and N13 recorded after stimulation of the painful thumb, may suggest that the cortical and the spinal changes are inter-dependent. This finding was debated by Tinazzi et al.5, who suggested that the enhancement of cortical responses is largely independent from the enhancement of spinal and brainstem components. However, they based their suggestion on the lack of a  correlation between differences of amplitude of subcortical (spinal N13 and brainstem P14) and cortical (N20, P27, and N30) potentials evoked by stimulation the painful thumb in relation to non painful thumb rather than SEP amplitudes on the painful side only as it has been done in the present study.


Pain induced enhancement of neural activity in the somatosensory pathway

In this study, higher grade of pain was associated with higher mean amplitude of N13, N20 and P22, which was consistent with several studies4,5,21. To evaluate whether it is the pain per se that induced the neuroplastic changes or it is the result of a peripheral deafferentation, we compared SEP parameters in patients with clinical manifestations denoting deafferentation as paresthesia and sensory loss on pin prick test to those without such complaints and no significant differences were found, which agrees with Tinazzi et al.5, who concluded that positive perceptual phenomena cannot account for the observed subcortical and cortical enhancement5. On the electrophysiological level, EMG evidence of deafferentation was absent in 75% of patients in this study and still they showed larger amplitudes of central SEPs. Our results are also supported by magneto-encephalography studies in amputee patients who showed a positive correlation between neuromagnetic indices of cortical reorganisation and subjective reports of the intensity of phantom pain4,21. These results suggest that the increased amplitudes of central SEPs are likely to be related to pain per se and that pain plays a crucial role in promoting cortical organization in humans.

Patients recruited in this study had pain duration of at least 6 months or more. Longer duration of illness was associated with larger amplitudes of N13 and N20 waves recorded after stimulation of the painful thumb. One study found that RMS (repetitive magnetic stimulation) peak and duration of pain were significantly positively correlated suggesting increased cortical responsiveness with increasing chronicity21. On the contrary, Tinazzi et al.5 found no correlation between duration of illness and amplitudes of SEPs, however, patients in their study had pain duration of less than 3 months5.



Pain can induce neuroplastic changes within the somatosensory pathway, which are selective to the involved territory, irrespective of the presence of deafferentation. Such changes involve both the peripheral and central levels but are more evident on the central level. Cortical and spinal changes seem to be inter-dependent.


[Disclosure: Authors report no conflict of interest]



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الملخص العربي


تقييم تغيرات المطاوعه العصبية في حالات آلام جذور الأعصاب العنقيه باستخدام الجهد المثار الحسي


هدف الدراسة: تقييم تأثير آلام جذور الأعصاب العنقيه على المطاوعه العصبية فى الممرات الحسية والمنطقة القشرية الحسية. الطريقة: تم إجراء الدراسة على 20 مريض يعانون الألم في جذور الأعصاب العنقيه فى جانب واحد تراوحت أعمارهم بين 35 و 65 عاما  تمت مقارنتهم بمجموعة ضابطة مكونة من 10 أفراد طبيعيين متامثلين فى العمر والنوع. المشاركون تم فحصهم سريريا مع تقييم درجة الألم. خضع المرضى لفحص أشعة الرنين المغناطيسى على الفقرات العنقية ورسم العضلات الكهربائى. تمت دراسة الجهد المثار الحسي بعد تحفيز الأعصاب الحسيه للإبهام والصغرى على الناحيتين المؤلمة والأخرى. قورنت دراسات الجهد المثار الحسي للمرضى بنتائج المجموعة الضابطة. النتائج: عانى كل المرضى من آلام الرقبة المحالة إلى الكتف بالإضافة إلى ألم محال لليد في بعض الحالات.كان الجذر العنقى السادس متأثرا فى كل المرضى. أتضح وجود تغيرات في المطاوعه العصبية في المسار الحسي حيث لوحظ زيادة كبيرة في مقدار موجات الجهد المثار الحسي المسجلة من الإبهام المؤلم مقارنة بالصغرى على الجانب المؤلم والإبهام والصغرى على الجانب غير المؤلم والمجموعة الضابطة. تغييرات المطاوعة العصبية ليس لها تأثير على زمن كمون أي من موجات الجهد المثار الحسي. لوحظ أن فرق المقدار في الجهد المثار للموجة (EP) اظهر أقل تغيير نسبة للموجات الأخرى بين المرضى ولكن ليس عند المقارنه مع المجموعة الضابطة حيث كان الفرق جديرا بالاعتبار مثل باقي الموجات. وهذا يشير إلى أن التغيرات في المطاوعه العصبية قد حدثت على  المستويين الطرفي والمركزي ولكن  بشكل أكثر وضوحا في المسارات المركزية عنها فى الطرفية. تبين وجود علاقة طردية واضحة بين سعة جهد الموجه القشرية (P22) ومقدار جهد الموجه الفقرية (N13) والقشرية (N20) المسجلة عند استثارة الإبهام المؤلم, ولكن لم توجد علاقة واضحة مع مقدار المسارات الطرفية, مما يوحي بأن التغيرات الفقرية والقشرية مترابطة. وجد أن علاقة مقدار الموجات الفقرية (N13) والقشرية (N20) كانت طردية مع مدة الألم. وكان أيضا مقدار الموجات الفقرية (N13) والقشرية (N20 and P22) أعلى في المرضى الذين يعانون درجة ألم أعلى. كما لم توجد فروق فى مقدار الموجات بين المرضى الذين كانوا يعانون من علامات قصور فى الأعصاب الطرفية, على المستوى الاكلينيكى والكهروفسيولوجى, مقارنة بمن لم يعانوا من ذلك مما يعطى دلالة بأن التغيرات الطارئة هى نتاج الألم المزمن نفسه. الخلاصة: الألم في حد ذاته من الممكن أن يحدث تغييرات فى المرونة العصبية متضمنة المستويات المركزية والمحيطية ولكن أكثر وضوحا في المسارات المركزية. أيضا هذه التغييرات تبدو مختصة بالمنطقة المؤلمة. نتائج هذا البحث من الممكن أن تساعد في استكشاف وفهم آليات المرونة العصبية الفسيولوجية. معرفة كهذه ممكن أن تساهم في تطوير طرق علاج جديدة تركز على تعزيز الشفاء الذاتي لضرر الجهاز العصبي خاصة الجهاز العصبي المركزي, وبالتالي تحسين نوعية حياة المرضى.

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