ORIGINAL ARTICLE
Sympathetic Dysfunction in Patients With Chronic Low Back Pain and Failed Back Surgery Syndrome Mohja A. El-Badawy, MD and Dalia M.E. El Mikkawy, MD
Background: Chronic low back pain (CLBP) is defined as pain that persists longer than 12 weeks and is often attributed to degenerative or traumatic conditions of the spine. Failed back surgery syndrome is a condition in which chronic pain persists after spinal surgery. Electrodiagnostic studies can be used to confirm the diagnosis of lumbosacral radiculopathy, but other diagnostic methods are often needed to assess sympathetic nervous system dysfunction. Objectives: The aim of this study was to investigate the affection of sympathetic skin response (SSR) in cases of chronic low back pain (LBP) and failed back surgery syndrome (FBSS) and to assess the association of SSR abnormalities with perceived functional disability and pain among these patients. Methodology: Twenty patients with CLBP and 10 patients with failed FBSS who fulfilled the inclusion criteria were recruited to the present study. All cases had back, leg, or back and leg pain of at least 3-month duration or following spinal surgery. The control group consists of 10 healthy participants matched in age and sex. Electrophysiologic nerve conduction studies and SSR recording were applied on the symptomatic and normal side in study cases and on both sides in the control group. Pain intensity was analyzed by the visual analogue scale (VAS) and perceived functional disability was assessed with the Oswestry disability index (ODI). Conclusions: It was concluded that the sympathetic nervous system is affected in CLBP and FBSS patients with abnormalities in SSR and that the dysfunction of sympathetic nervous system may contribute to the intensity and chronicity of pain in these groups of patients. Moreover, a strong association was found between SSR and functional disabilities in these patients. Key Words: chronic pain, low back pain (LBP), failed back surgery syndrome (FBSS), sympathetic skin response (SSR), Oswestry disability index (ODI)
(Clin J Pain 2016;32:226–231)
C
hronic low back pain (CLBP), including failed back surgery syndrome (FBSS), is very difficult to manage for both the patient and practitioner.1 Patients with CLBP and/or failed back surgery syndrome endured considerable disabling pain and a significant decrease in their quality of life. Their pain is often resistant to conventional medical therapies and management strategies.2 Received for publication January 9, 2015; revised May 20, 2015; accepted April 21, 2015. From the Physical Medicine & Rheumatology Department. Physical Medicine, Rheumatology & Rehabilitation Department, Ain Shams University, Cairo, Egypt The authors declare no conflict of interest. Reprints: Mohja A. El-Badawy, MD, 211 Abdel- Hamid Keshk Street. Hadaeq EL-Qubba. Cairo, Egypt. 4th floor, Department 8, Postal code 11646 (e-mail: [email protected]). Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved. DOI: 10.1097/AJP.0000000000000250
Failed back surgery syndrome (FBSS) is a term embracing a constellation of conditions that describes persistent or recurring low back pain (LBP), with or without sciatica following Z1 spine surgeries. Most patients with failed spine surgery have a “peripheral” mechanical structural lesion as a source of nociception. Because of the iatrogenic changes associated with surgical intervention, identifying the source of symptoms is difficult. Occult lesions are expected to be more frequent in these patients than in those not previously operated on and may explain the failure of surgery. A systematic approach is necessary to evaluate the various factors in both central and peripheral nervous systems that contribute to the patients experience of pain.3 Research reports state that the major cause for FBSS is lateral spine stenosis and has a prevalence of 29% to 58%, whereas recurring distal hernia, arachnoid-its, central stenosis, epidural fibrosis, instability, pseudoarteriosis, discitis, and psychological factors have frequencies of 12% to 17%, 1.1% to 16%, 7% to 29%, 6% to 9%,5%, 14.8%, 0.15 to 3%, and 3%, respectively.4–6 Varied and complicated etiology of LBP radiates distally at the extremities is still causing disagreement and controversies over the issue of its diagnosis and treatment. A combination of nociceptive and neuropathic pain-generating mechanism is thought to be involved, which established the term mixed pain syndrome.7 It is indicated that neuropathic pain can occur via mechanical nerve root compression (mechanical neuropathic root pain), lesions of nociceptive sprouts within the degenerated disk (local neuropathic root pain), or by the action of inflammatory mediators such as chemokines and cytokines, which can originate from the degenerative disk even without any mechanical stress (inflammatory neuropathic root pain).8 Some studies have shown poor correlation between radiologic imaging and clinical symptoms.9 During magnetic resonance imaging (MRI) evaluation, one should consider that in the majority of patients with pathology within disk area, a strong correlation with pain in the lower limb is visible,10 but sometimes it is possible to observe improvement with no change concerning the disk,11 or no improvement occurs despite removing the disk protrusion or other reasons of nerve compression.12 Takahashi et al12 claimed that compression itself caused only loss of function rather than pain. Therefore, it is suggested that processes other than compression are engaged with the development of sciatica and the leading role of inflammation in causing the feeling of strong pain along the sciatic nerve is underlined.13,14 Neurophysiological examination to support a proximal nerve root lesion includes the distal motor latency and the F-wave latency of nerve, which receives those fibers from the affected root. This examination will show just
226 | www.clinicalpain.com Clin J Pain Volume 32, Number 3, March 2016 Copyright r 2016 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Pain
Volume 32, Number 3, March 2016
abnormalities if motor fibers are involved in the damage. Furthermore, proximal lesions to the dorsal root ganglion can give norm of sensory conduction as the traditional electrophysiological techniques assess atmost, the function of myelinated peripheral axonal system.15 The early detection of sympathetic failure using conventional electrodiagnostic procedures has been poorly documented.16,17 The SSR has been proposed as a reliable and simple test and is commonly used in the evaluation of the functional impairment of nonmyelinated postganglionic sudomotor sympathetic fibers in polyneuropathies and dysautonomic disorders.17,18 It measures transient changes in the electric potential across the skin both spontaneously and by various internal and external stimuli.19 Regarding CLBP, including FBSS as a chronic pain state and the contribution of autonomic nervous system in the evolution and maintenance of chronic pain, we have aimed to investigate whether sympathetic nervous system is affected in cases of CLBP.
MATERIALS AND METHODS The study group consists of 35 cases, 20 cases with CLBP and 15 cases with FBSS that referred to the outpatient clinic of physical Medicine, Rheumatology, and Rehabilitation Department, Ain Shams University Hospitals. The control group comprised 10 ages, sex, and body mass index (BMI)–matched healthy volunteers (with normal findings on neurologic examination). None of the participants within the control group had a history of significant back pain or any previous history of sciatica or neuropathy and all submitted to Nerve Conduction Study (NCS) and SSR evaluation. We received the approval of the ethical committee of Ain Shams University and each participant (both case and control groups) gave verbal and written consent before participation in the study. The inclusion criteria were: LBP (with or without radiation to the leg), pain duration of at least 3 months or following spinal surgery, ages between 24 and 50 years, and being able to participate in the study during their working day. The exclusion criteria were: weakened general condition, malignancies, severe osteoporosis, severe osteoarthritis, ankylosing spondylitis, progressive neurological diseases, hemophilia, spinal infection, vertebral fracture during the previous 6 months, and severe sciatica with straight leg raising positive below 35 degrees. Patients with marked over weight (BMI > 32) were also excluded from the study. Patients were excluded if comorbidities were present that could interfere with evaluation of Autonomic Nervous System function (eg, diabetes mellitus, renal failure, polyneuropathy, liver failure, collagen disease). The patient basic data were shown in Table 1. The study group was also examined for lumbar range of motion (ROM), muscle strength, muscular atrophy of the affected extremity, and sensory integrity. Pain at rest, in motion and at night was also recorded on a 1 to 10 mm VAS.20 The perceived disability was evaluated using the Oswestry Low Back Pain Disability Index (ODI).21 The ODI was designed to assess limitations of various activities of daily living. Each of the 10 sections contains 6 statements. The scores of all sections were added together and expressed in a percentage. The patients were classified as having minimal perceived disability (< 20%) or moderate disability (20% to 40%). Copyright
r
Sympathetic Dysfunction in Chronic Low Back Pain
TABLE 1. Patient Characteristics Characteristics Patients (n) Sex ratio (M:F) Age, years [mean ± SD] Occupation (n [%]) Physically light work Physically moderate or heavy work Pain duration (y) (mean ± SD) Pain frequency (n [%]) Daily Weekly Monthly
35 2:3 49.44 ± 7.09 21 (60) 14 (40) 3.12 ± 0.95 22 (62.9) 11 (31.4) 2 (5.7)
Electrophysiological Studies The electrophysiological tests were performed with (NEC multisystem LCD 175 VXM) electrophysiological instrument in a quiet, ventilated room 231C. Motor nerve conduction studies of tibial and peroneal nerves were done with recording of distal motor latencies, amplitudes, and conduction velocities from abductor hallucis and extensor digitorum brevis muscles. Sensory nerve conduction was recorded from the sural nerve. Tibial, peroneal, and sural nerves were electromyographically (EMG) tested and L3-S1 innervated muscles of both legs of the study group were also tested by needle EMG. Plantar SSR of both tibial nerves was recorded. For SSR recording, tibial nerve was stimulated by a supramaximal stimulus (0.5 to 1/h). Standard surface electrodes were used for recording by applying active electrode on the plantar and reference electrode on the dorsal side of the foot. Stimulus was given with intervals longer than 1 minute. Basal duration was 5 seconds, and amplifier filter was set at 2 Hz for low frequency and at 200 Hz for high frequency with a sensitivity of 200 mv/div. Ten stimuli were administered at random intervals of >60 seconds in the absence of distraction to avoid habituation. Only reproducible responses that are consistent were selected for analysis. Patients with no response to 3 maximal stimuli recording with 50 mv/div voltage sensitivity were accepted as nonresponders. SSR latency was measured from the start of the stimulus artifact to the first deflection of the trace from baseline. The amplitude was measured from the peak of the first deflection to the peak of the next one (peak to peak).22 SSR was recorded at lower extremities of both the study and control groups, and recordings were compared. SSR has a form of biphasic or triphasic wave exposing the interindividual variation of the shape, latency, and amplitude by repetitive stimulation. On the lower extremity, it is usually biphasic. Two types of responses were recorded according to polarity of the waveform with maximal amplitude: P-type with maximum positive deflection and N-type with maximum negative deflection. In healthy controls, the P-type of SSR is more frequent.22
Statistical Analysis Data was analyzed using SPSS version 10. The means for age and neurophysiology’s parameters established through neurophysiological study were compared between participants and control groups using an independent sample’s t test taking into account the similarity between variances verified by Levine’s test. The frequencies of clinical variables (categorical) were compared between
2015 Wolters Kluwer Health, Inc. All rights reserved.
www.clinicalpain.com |
Copyright r 2016 Wolters Kluwer Health, Inc. All rights reserved.
227
Clin J Pain
El-Badawy and El Mikkawy
participants using the Pearson w2 test. P values r5% were considered to be significant.
The study group consists of 14 males and 21 females with a mean age of 49.44 ± 7.09 years, and the control group consisted of 5 males and 5 females with a mean age of 48.30 ± 7.33 years. There was no statistical difference with regard to age, sex, and BMI between the groups (P > 0.05) (Table 2). The cases had pain radiating from the back to the right leg (n = 20) and to the left leg (n = 15) and 70% of them had sensory deficits on physical examination. The VAS scores were 7.58 ± 0.79 in motion, 6.67 ± 0.69 at rest, and 5.97 ± 0.67 at night. The distal motor and F-wave minimum (F-min) latencies were longer, and the CMAP amplitudes and conduction velocities (CVs) of both the tibial and peroneal nerves were lower in the patient group than in the control group. The H-wave latency (H-latency) was longer in the patient group than in the control group. These differences were statistically significant. The sural nerve electrophysiological parameters did not differ significantly between the patient and control groups (Table 3). Needle EMG studies on the LBP cases demonstrated that 16 patients had had 1 root compression on both sides, 10 patients had 2 nerve root compressions on the symptomatic side, 6 patients had 2 nerve root compressions on both sides, and 3 patients had multiple root compressions on both sides. Four patients had no SSR. There was a statistically significant longer duration of SSR latency of painful leg in LBP cases compared with 20 lower extremity values of normal controls (P = 0.000). There were also significant longer SSR latencies between nonsymptomatic extremities of LBP cases and controls (P = 0.002), although a nonsignificant difference was found for SSR amplitude on both lower extremities between patients and controls (P > 0.05) (Table 4). The ODI was on average (27.11 ± 5.74), that for men (27.97 ± 5.70) not differing from that for women (26.53 ± 5.83), P = 0.476. Twenty-eight patients had a score >20% (21 to 40; moderate disability) and 7 patients had a score
Sympathetic Dysfunction in Patients With Chronic Low Back Pain and Failed Back Surgery Syndrome Mohja A. El-Badawy, MD and Dalia M.E. El Mikkawy, MD
Background: Chronic low back pain (CLBP) is defined as pain that persists longer than 12 weeks and is often attributed to degenerative or traumatic conditions of the spine. Failed back surgery syndrome is a condition in which chronic pain persists after spinal surgery. Electrodiagnostic studies can be used to confirm the diagnosis of lumbosacral radiculopathy, but other diagnostic methods are often needed to assess sympathetic nervous system dysfunction. Objectives: The aim of this study was to investigate the affection of sympathetic skin response (SSR) in cases of chronic low back pain (LBP) and failed back surgery syndrome (FBSS) and to assess the association of SSR abnormalities with perceived functional disability and pain among these patients. Methodology: Twenty patients with CLBP and 10 patients with failed FBSS who fulfilled the inclusion criteria were recruited to the present study. All cases had back, leg, or back and leg pain of at least 3-month duration or following spinal surgery. The control group consists of 10 healthy participants matched in age and sex. Electrophysiologic nerve conduction studies and SSR recording were applied on the symptomatic and normal side in study cases and on both sides in the control group. Pain intensity was analyzed by the visual analogue scale (VAS) and perceived functional disability was assessed with the Oswestry disability index (ODI). Conclusions: It was concluded that the sympathetic nervous system is affected in CLBP and FBSS patients with abnormalities in SSR and that the dysfunction of sympathetic nervous system may contribute to the intensity and chronicity of pain in these groups of patients. Moreover, a strong association was found between SSR and functional disabilities in these patients. Key Words: chronic pain, low back pain (LBP), failed back surgery syndrome (FBSS), sympathetic skin response (SSR), Oswestry disability index (ODI)
(Clin J Pain 2016;32:226–231)
C
hronic low back pain (CLBP), including failed back surgery syndrome (FBSS), is very difficult to manage for both the patient and practitioner.1 Patients with CLBP and/or failed back surgery syndrome endured considerable disabling pain and a significant decrease in their quality of life. Their pain is often resistant to conventional medical therapies and management strategies.2 Received for publication January 9, 2015; revised May 20, 2015; accepted April 21, 2015. From the Physical Medicine & Rheumatology Department. Physical Medicine, Rheumatology & Rehabilitation Department, Ain Shams University, Cairo, Egypt The authors declare no conflict of interest. Reprints: Mohja A. El-Badawy, MD, 211 Abdel- Hamid Keshk Street. Hadaeq EL-Qubba. Cairo, Egypt. 4th floor, Department 8, Postal code 11646 (e-mail: [email protected]). Copyright r 2015 Wolters Kluwer Health, Inc. All rights reserved. DOI: 10.1097/AJP.0000000000000250
Failed back surgery syndrome (FBSS) is a term embracing a constellation of conditions that describes persistent or recurring low back pain (LBP), with or without sciatica following Z1 spine surgeries. Most patients with failed spine surgery have a “peripheral” mechanical structural lesion as a source of nociception. Because of the iatrogenic changes associated with surgical intervention, identifying the source of symptoms is difficult. Occult lesions are expected to be more frequent in these patients than in those not previously operated on and may explain the failure of surgery. A systematic approach is necessary to evaluate the various factors in both central and peripheral nervous systems that contribute to the patients experience of pain.3 Research reports state that the major cause for FBSS is lateral spine stenosis and has a prevalence of 29% to 58%, whereas recurring distal hernia, arachnoid-its, central stenosis, epidural fibrosis, instability, pseudoarteriosis, discitis, and psychological factors have frequencies of 12% to 17%, 1.1% to 16%, 7% to 29%, 6% to 9%,5%, 14.8%, 0.15 to 3%, and 3%, respectively.4–6 Varied and complicated etiology of LBP radiates distally at the extremities is still causing disagreement and controversies over the issue of its diagnosis and treatment. A combination of nociceptive and neuropathic pain-generating mechanism is thought to be involved, which established the term mixed pain syndrome.7 It is indicated that neuropathic pain can occur via mechanical nerve root compression (mechanical neuropathic root pain), lesions of nociceptive sprouts within the degenerated disk (local neuropathic root pain), or by the action of inflammatory mediators such as chemokines and cytokines, which can originate from the degenerative disk even without any mechanical stress (inflammatory neuropathic root pain).8 Some studies have shown poor correlation between radiologic imaging and clinical symptoms.9 During magnetic resonance imaging (MRI) evaluation, one should consider that in the majority of patients with pathology within disk area, a strong correlation with pain in the lower limb is visible,10 but sometimes it is possible to observe improvement with no change concerning the disk,11 or no improvement occurs despite removing the disk protrusion or other reasons of nerve compression.12 Takahashi et al12 claimed that compression itself caused only loss of function rather than pain. Therefore, it is suggested that processes other than compression are engaged with the development of sciatica and the leading role of inflammation in causing the feeling of strong pain along the sciatic nerve is underlined.13,14 Neurophysiological examination to support a proximal nerve root lesion includes the distal motor latency and the F-wave latency of nerve, which receives those fibers from the affected root. This examination will show just
226 | www.clinicalpain.com Clin J Pain Volume 32, Number 3, March 2016 Copyright r 2016 Wolters Kluwer Health, Inc. All rights reserved.
Clin J Pain
Volume 32, Number 3, March 2016
abnormalities if motor fibers are involved in the damage. Furthermore, proximal lesions to the dorsal root ganglion can give norm of sensory conduction as the traditional electrophysiological techniques assess atmost, the function of myelinated peripheral axonal system.15 The early detection of sympathetic failure using conventional electrodiagnostic procedures has been poorly documented.16,17 The SSR has been proposed as a reliable and simple test and is commonly used in the evaluation of the functional impairment of nonmyelinated postganglionic sudomotor sympathetic fibers in polyneuropathies and dysautonomic disorders.17,18 It measures transient changes in the electric potential across the skin both spontaneously and by various internal and external stimuli.19 Regarding CLBP, including FBSS as a chronic pain state and the contribution of autonomic nervous system in the evolution and maintenance of chronic pain, we have aimed to investigate whether sympathetic nervous system is affected in cases of CLBP.
MATERIALS AND METHODS The study group consists of 35 cases, 20 cases with CLBP and 15 cases with FBSS that referred to the outpatient clinic of physical Medicine, Rheumatology, and Rehabilitation Department, Ain Shams University Hospitals. The control group comprised 10 ages, sex, and body mass index (BMI)–matched healthy volunteers (with normal findings on neurologic examination). None of the participants within the control group had a history of significant back pain or any previous history of sciatica or neuropathy and all submitted to Nerve Conduction Study (NCS) and SSR evaluation. We received the approval of the ethical committee of Ain Shams University and each participant (both case and control groups) gave verbal and written consent before participation in the study. The inclusion criteria were: LBP (with or without radiation to the leg), pain duration of at least 3 months or following spinal surgery, ages between 24 and 50 years, and being able to participate in the study during their working day. The exclusion criteria were: weakened general condition, malignancies, severe osteoporosis, severe osteoarthritis, ankylosing spondylitis, progressive neurological diseases, hemophilia, spinal infection, vertebral fracture during the previous 6 months, and severe sciatica with straight leg raising positive below 35 degrees. Patients with marked over weight (BMI > 32) were also excluded from the study. Patients were excluded if comorbidities were present that could interfere with evaluation of Autonomic Nervous System function (eg, diabetes mellitus, renal failure, polyneuropathy, liver failure, collagen disease). The patient basic data were shown in Table 1. The study group was also examined for lumbar range of motion (ROM), muscle strength, muscular atrophy of the affected extremity, and sensory integrity. Pain at rest, in motion and at night was also recorded on a 1 to 10 mm VAS.20 The perceived disability was evaluated using the Oswestry Low Back Pain Disability Index (ODI).21 The ODI was designed to assess limitations of various activities of daily living. Each of the 10 sections contains 6 statements. The scores of all sections were added together and expressed in a percentage. The patients were classified as having minimal perceived disability (< 20%) or moderate disability (20% to 40%). Copyright
r
Sympathetic Dysfunction in Chronic Low Back Pain
TABLE 1. Patient Characteristics Characteristics Patients (n) Sex ratio (M:F) Age, years [mean ± SD] Occupation (n [%]) Physically light work Physically moderate or heavy work Pain duration (y) (mean ± SD) Pain frequency (n [%]) Daily Weekly Monthly
35 2:3 49.44 ± 7.09 21 (60) 14 (40) 3.12 ± 0.95 22 (62.9) 11 (31.4) 2 (5.7)
Electrophysiological Studies The electrophysiological tests were performed with (NEC multisystem LCD 175 VXM) electrophysiological instrument in a quiet, ventilated room 231C. Motor nerve conduction studies of tibial and peroneal nerves were done with recording of distal motor latencies, amplitudes, and conduction velocities from abductor hallucis and extensor digitorum brevis muscles. Sensory nerve conduction was recorded from the sural nerve. Tibial, peroneal, and sural nerves were electromyographically (EMG) tested and L3-S1 innervated muscles of both legs of the study group were also tested by needle EMG. Plantar SSR of both tibial nerves was recorded. For SSR recording, tibial nerve was stimulated by a supramaximal stimulus (0.5 to 1/h). Standard surface electrodes were used for recording by applying active electrode on the plantar and reference electrode on the dorsal side of the foot. Stimulus was given with intervals longer than 1 minute. Basal duration was 5 seconds, and amplifier filter was set at 2 Hz for low frequency and at 200 Hz for high frequency with a sensitivity of 200 mv/div. Ten stimuli were administered at random intervals of >60 seconds in the absence of distraction to avoid habituation. Only reproducible responses that are consistent were selected for analysis. Patients with no response to 3 maximal stimuli recording with 50 mv/div voltage sensitivity were accepted as nonresponders. SSR latency was measured from the start of the stimulus artifact to the first deflection of the trace from baseline. The amplitude was measured from the peak of the first deflection to the peak of the next one (peak to peak).22 SSR was recorded at lower extremities of both the study and control groups, and recordings were compared. SSR has a form of biphasic or triphasic wave exposing the interindividual variation of the shape, latency, and amplitude by repetitive stimulation. On the lower extremity, it is usually biphasic. Two types of responses were recorded according to polarity of the waveform with maximal amplitude: P-type with maximum positive deflection and N-type with maximum negative deflection. In healthy controls, the P-type of SSR is more frequent.22
Statistical Analysis Data was analyzed using SPSS version 10. The means for age and neurophysiology’s parameters established through neurophysiological study were compared between participants and control groups using an independent sample’s t test taking into account the similarity between variances verified by Levine’s test. The frequencies of clinical variables (categorical) were compared between
2015 Wolters Kluwer Health, Inc. All rights reserved.
www.clinicalpain.com |
Copyright r 2016 Wolters Kluwer Health, Inc. All rights reserved.
227
Clin J Pain
El-Badawy and El Mikkawy
participants using the Pearson w2 test. P values r5% were considered to be significant.
The study group consists of 14 males and 21 females with a mean age of 49.44 ± 7.09 years, and the control group consisted of 5 males and 5 females with a mean age of 48.30 ± 7.33 years. There was no statistical difference with regard to age, sex, and BMI between the groups (P > 0.05) (Table 2). The cases had pain radiating from the back to the right leg (n = 20) and to the left leg (n = 15) and 70% of them had sensory deficits on physical examination. The VAS scores were 7.58 ± 0.79 in motion, 6.67 ± 0.69 at rest, and 5.97 ± 0.67 at night. The distal motor and F-wave minimum (F-min) latencies were longer, and the CMAP amplitudes and conduction velocities (CVs) of both the tibial and peroneal nerves were lower in the patient group than in the control group. The H-wave latency (H-latency) was longer in the patient group than in the control group. These differences were statistically significant. The sural nerve electrophysiological parameters did not differ significantly between the patient and control groups (Table 3). Needle EMG studies on the LBP cases demonstrated that 16 patients had had 1 root compression on both sides, 10 patients had 2 nerve root compressions on the symptomatic side, 6 patients had 2 nerve root compressions on both sides, and 3 patients had multiple root compressions on both sides. Four patients had no SSR. There was a statistically significant longer duration of SSR latency of painful leg in LBP cases compared with 20 lower extremity values of normal controls (P = 0.000). There were also significant longer SSR latencies between nonsymptomatic extremities of LBP cases and controls (P = 0.002), although a nonsignificant difference was found for SSR amplitude on both lower extremities between patients and controls (P > 0.05) (Table 4). The ODI was on average (27.11 ± 5.74), that for men (27.97 ± 5.70) not differing from that for women (26.53 ± 5.83), P = 0.476. Twenty-eight patients had a score >20% (21 to 40; moderate disability) and 7 patients had a score
