|Year : 2016 | Volume
| Issue : 2 | Page : 104-110
Motor nerve conduction velocity and function in carpal tunnel syndrome following neural mobilization: A randomized clinical trial
Manu Goyal1, Sudhir Kumar Mehta2, Namita Rana1, Rikki Singal2, Amit Mittal3, Kanu Goyal1, Sorabh Sharma1, Subhasish Chatterjee1, Monika Sharma4
1 Department of Physiotherapy, M.M. Institute of Physiotherapy and Rehabilitation, M.M. University – Mullana (Ambala), Haryana, India
2 Department of Surgery, Maharishi Markandeshwer Institute of Medical Sciences and Research, M.M. University – Mullana (Ambala), Haryana, India
3 Department of Radiodiagnosis, Maharishi Markandeshwer Institute of Medical Sciences and Research, M.M. University – Mullana (Ambala), Haryana, India
4 Department of Paed, IGMC, Shimla, Himachal Pardesh, India
|Date of Web Publication||14-Apr-2016|
Department of Surgery, Maharishi Markandeshwar Institute of Medical Sciences and Research, Mullana, Ambala, Haryana
Source of Support: None, Conflict of Interest: None
Introduction: Carpal tunnel syndrome (CTS) is the most common nerve entrapment syndrome in the upper extremity leading to the functional disability. The consequence of the entrapment is the poor health of the nerve (conduction, mobility, and blood flow). Purpose of the Study: The aim of the study is to evaluate the effect of neural mobilization on the motor nerve conduction velocity and function in the CTS patients. Methods: Thirty CTS patients (only females) were scrutinized on the basis of the inclusion and exclusion criteria. They were randomized into two groups A (n = 15) and B (n = 15) using simple random sampling. Group A patients were treated with the conventional physiotherapy regimen and Group B were provided neural mobilization. Results: The data analysis was done using SPSS version 22. The t-test reveals that there was statistically significant improvement in posttreatment values of Group B for numeric pain rating scale, symptom severity scale, function status scale, motor nerve conduction latency, and velocity at P≤ 0.05. Conclusions: Neural mobilization in the CTS patients improves the motor nerve conduction and functional status. It may be incorporated in the physiotherapy treatment protocol of CTS patients.
Keywords: Carpal tunnel, function, median nerve, motor conduction, nerve slider
|How to cite this article:|
Goyal M, Mehta SK, Rana N, Singal R, Mittal A, Goyal K, Sharma S, Chatterjee S, Sharma M. Motor nerve conduction velocity and function in carpal tunnel syndrome following neural mobilization: A randomized clinical trial. Int J Health Allied Sci 2016;5:104-10
|How to cite this URL:|
Goyal M, Mehta SK, Rana N, Singal R, Mittal A, Goyal K, Sharma S, Chatterjee S, Sharma M. Motor nerve conduction velocity and function in carpal tunnel syndrome following neural mobilization: A randomized clinical trial. Int J Health Allied Sci [serial online] 2016 [cited 2020 Apr 10];5:104-10. Available from: http://www.ijhas.in/text.asp?2016/5/2/104/180434
| Introduction|| |
Carpal tunnel syndrome (CTS) is the most common peripheral nerve entrapment syndrome and is caused by compression of median nerve in carpal tunnel. Its clinical features include nocturnal pain, sensory and motor deficit leading to the deformities in the later stages. The multifactorial etiology of CTS includes mechanical, vascular, metabolic, inflammatory, and traumatic causes, among which abnormal postures, over-activity of hand muscles, and chronic repetitive overuse were reported to be common mechanical pathogenetic factors. Prevalence rate according to the symptomatic presentation is 14.4%, clinical presentation is 3.8%, and nerve conduction studies is 4.9%.
The evaluation of CTS includes the combination of clinical, radiological, and electro-physiological investigation. The clinical examination of CTS comprises subjective complaints, joint mobility testing, intercarpal bone mobility, intrinsic and extrinsic hand muscles strength, flexibility, and endurance, special tests such as Phalen's maneuver, carpal compression, neurological examination (sensory, motor), and neurodynamic testing. The electrophysiological measures for CTS involves sensory and motor nerve conduction velocities (MNCVs) test for thenar muscles. Increased latency and decreased velocity on nerve conduction studies of median nerve confirms the diagnosis for CTS and is recommended as the gold standard diagnostic tool.
Treatment options in the management of CTS involve multidisciplinary approach that includes medical, surgical, physical, and occupational therapy. The physical therapy treatment approaches according to the stages includes rest, splinting, therapeutic ultrasound, neuromuscular electrical stimulation, grip and pinch strengthening exercises, joint mobilization, and nerve and tendon gliding exercises. Neural mobilization techniques (sliders and tensioners) are passive or active movements that focus on restoring the ability of the nervous system to tolerate the normal compressive, friction and tensile forces associated with daily and sport activities. It is hypothesized that these therapeutic movements can have a positive impact on symptoms by improving intraneural circulation, axoplasmic flow, neural connective tissue viscoelasticity, and by reducing the sensitivity of abnormal impulse-generating sites.
Sliders are neurodynamic maneuvers executed in a nonprovocative fashion that attempt to produce a sliding movement between neural structures and adjacent non-neural tissues. Tensile loading technique (are not stretches) is to restore the physical capabilities of neural tissue to tolerate movements that lengthen the corresponding nerve bed. These neurodynamic maneuvers are performed in an oscillatory fashion so as to gently engage resistance to movement that is usually associated with protective muscle activity. Neural mobilization is based on neurodynamics, which is now a more dynamic term referring to the integrated biomechanical, physiological, and morphological functions of the nervous system.
Regardless of the underlying construct, it is vital that the nervous system can adapt to mechanical loads and it must undergo distinct mechanical events such as elongation, sliding, cross-sectional change, angulations, and compression. If these dynamic protective mechanisms fail, the nervous system is vulnerable to neural edema, ischemia, fibrosis, and hypoxia, which may cause altered neurodynamics. When neural mobilization is used for the treatment of adverse neurodynamics, the primary theoretical objective is to attempt to restore the dynamic balance between the relative movement of neural tissues and surrounding mechanical interfaces, thereby allowing reduced intrinsic pressures on the neural tissues and thus promoting optimum physiologic function. The hypothesized benefits from such techniques include facilitation of nerve gliding, reduction of nerve adherence, dispersion of noxious fluids, increased neural vascularity, and improvement of axoplasmic flow.,
Neurodynamic assessment techniques are incorporated into treatment involving passive movement of the nerve relative to its environment. Such mobilizing techniques are described extensively throughout the physiotherapy and biomedical literature. Treatment avoids pain and mobilizes nerve tissue in conjunction with the surrounding tissue to avoid painful stretching which will further mechanosensitize the nervous tissue. Treatment aims to decrease pain related to movement and bodily positions and therefore restores normal movement, posture, and hence function. Effectiveness of neural mobilization techniques is reported by several researchers for the ulnar, radial, median, and sciatic nerves.,,, Literature regarding the efficacy of nerve mobility exercise has shown beneficial effects on symptoms, functional disability, and nerve conduction. However, those studies utilized tensioner techniques given in a graded manner. The study by Coppier and Butler showed that median nerve excursion was better with slider technique than to tensioner technique. The study utilizes slider technique and there is a need to evaluate the effect of the technique on motor nerve conduction in patients' with CTS.
| Methods|| |
Thirty females between the age of 35 and 65 years who had acute to subacute unilateral CTS due to hypothyroidism, idiopathic in nature were included as study participants. Females were excluded for any sensory or motor deficit for ulnar or radial nerve, previous carpal tunnel release or injection, any cervical and other upper extremity pathologies, pregnancy, systematic musculoskeletal pathology, and diabetes. The Institutional Review Board approved the study. Written informed consent was obtained prior to intervention, and the rights of participants were protected.
Participants in this randomized clinical trial were randomly allocated using sealed opaque envelope method into two groups, i.e. A (n = 15) and B (n = 15), respectively [Figure 1].
Participants' demographic information was collected regarding age, occupational status, ethnicity, and gender. The females completed the Symptom Severity Scale (SSS) Questionnaire, a validated self-report measure used to monitor symptoms for typical 24 h period and the Functional Status Scale (FSS) Questionnaire to collect data regarding disability in performing the daily activities before and after application of the intervention. Pain was evaluated using the numeric pain rating scale (NPRS) that ranged from 0 (no pain) to 10 (worst imaginable pain). The NPRS is a valid and reliable measure of pain intensity in adults.
A NCV apparatus (Allengers Scorpio – 2/4 EMG, NCS, EP system, manufactured by Allenger Global Healthcare Pvt., Ltd.,) was used to measure MNCV and latency. The preparation of the skin was done prior to testing. The silver chloride surface recording electrode, reference electrode, and ground electrode were placed on the mid of abductor pollicis longus (APL) muscle, insertion of APL, and hypothenar eminence, respectively [Figure 2]. To measure the velocity and latency, the stimulation was provided at the carpal tunnel.
|Figure 2: Mean and standard deviation of numeric pain rating scale between groups|
Click here to view
Group A participants' were given conventional physiotherapy in the form of therapeutic ultrasound with parameters of frequency 1 MHz, pulsed mode 1:4, for 5 min. Treatment was given for two sessions per week for 3 weeks.
Group B participants' received active neural mobilization (slider technique) under the supervision of a physiotherapist on the affected side. The technique consisted of two simultaneously performed active movements – loading of the median nerve distally (elbow extension) and unloading (cervical ipsilateral lateral flexion). Treatment was given for two sessions per week for 3 weeks.
The data were analyzed using statistical computer software SPSS 22 software package (RMS, Med Care System, Chandigar). The paired t-test and unpaired t-test were used. The level of significance was P < 0.05. Mean and standard deviation (SD) were used as descriptive statistics.
| Results|| |
The mean age of Group A was 46.87 years with SD of ± 7.800 and mean age of Group B was 45.47 with a SD of ± 7.415. The mean body mass index (BMI) of Group A was 22.85 with SD of ± 1.100 and mean BMI of Group B was 22.50 with SD of ± 1.615 and there was no statistically significant difference. The mean latency of the right side of wrist of Group A was 6.51 with SD of ± 0.382 and of Group B was 6.53 with SD of ± 0.427. Mean latency of the left side of wrist of Group A was 6.74 with SD of ± 0.538 and of Group B was 6.78 with SD of ± 0.384. The mean velocity of the right side of wrist of Group A was 6.58 with SD of ± 0.515 and for Group B was 6.50 with SD of ± 0.352. The mean velocity of the left side of wrist of Group A was 6.62 with SD of ± 0.124 and for Group B was 6.59 with SD of ± 0.217. The mean difference in mean age, BMI, SSS, FSS, latency, and velocity between Group A and Group B was not statistically significant [Table 1].
The pre- and post-treatment values of NPRS, SSS, FSS, MNC latency, and velocity within and between the groups [Table 2] reveal that there was statistically significant improvement in the post-treatment values of Group B for NPRS, SSS, FSS, MNC latency, and velocity at P ≤ 0.05.
The mean and SD of Group A for NPRS was 5.80 ± 0.676 at baseline and after 3 weeks, mean and SD was 3.60 ± 0.737. The mean and SD of Group B for NPRS was 5.87 ± 0.834 and after 3 weeks, mean and SD was 1.47 ± 0.516. A statistical significant difference was found in the NPRS score in Group B [Figure 3].
|Figure 3: Mean and standard deviation of symptom severity scale and functional status scale between groups|
Click here to view
The mean and SD of Group A for SSS at baseline was 3.54 ± 0.230 and after 3 weeks, mean and SD was 2.44 ± 0.362. The mean and SD of Group A for FSS at baseline was 3.21 ± 0.249 and after 3 weeks, mean and SD was 2.13 ± 0.455. The mean and SD of Group B for SSS at baseline 3.56 ± 0.393 and after 3 weeks, mean and SD was 1.27 ± 0.173. The mean and SD of Group B for FSS at baseline was 3.36 ± 0.318 and after 3 weeks, mean and SD was 1.45 ± 0.298. A statistical significant improvement was found in Group B as compared to Group A [Figure 4].
The mean and SD of Group A for latency at baseline was 6.76 ± 0.500 and after 3 weeks, mean and SD was 4.77 ± 0.649. The mean and SD of Group B for latency at baseline was 6.69 ± 0.435 and after 3 weeks, mean and SD was 3.16 ± 0.415. There was statistically significant difference between Group A and B; the Group B showed more improvement [Figure 5].
The mean and SD of Group A for velocity at baseline was 43.06 ± 3.69 and after 3 weeks, mean and SD was 49.75 ± 1.09. The mean and SD of Group B for velocity at baseline was 41.33 ± 4.37 and after 3 weeks, mean and SD was 57.36 ± 2.82. There was statistically significant difference between Group A and B; the Group B showed more improvement [Figure 6].
| Discussion|| |
The statistical analysis reveals that there is improvement in mean values of NPRS [Figure 3], SSS, FSS [Figure 4], latency [Figure 5], and velocity [Figure 6] of median nerve after treatment in both groups [Table 3]. However, statistical analysis revealed that there is more significant improvement in Group B [Table 4]. The results obtained after the data analysis did not support the null hypothesis and thus research hypothesis was accepted. Between the groups, effect size was large for all outcome measures (d > 0.9).
The concept of nerve sliding plays a major role in formulating a treatment plan for nerve mobilization. Tissue mobility, blood circulation, and axonal transport, which are necessary for the functional and structural integrity of a neuron, will be increased after neural mobilization.
Shacklock theory of neurodynamic shows the interconnection between nerve mechanics and physiology. Mechanical factors such as tension, compression, or traction of neural tissue influence physiological responses in intraneural blood flow, axonal transport, mechanosensitivity, and sympathetic evaluation. In this study, the attempt was made to measure the effect of nerve mechanics following a technique theorized to affect the nerve physiology as measured by the latency and velocity of median nerve.
This comes in agreement with Cleland et al. who mentioned that when the nerve root was compressed, microcirculation was compromised and the pressure received by the nerve will affect the edema and demyelination. Neural mobilization was sufficient to disperse the edema, thus alleviating the hypoxia and reducing the associated symptoms and increases the nerve conduction. Our result bolsters this premise and shows a significant reduction in latency and increase in conduction velocity of the median nerve after nerve sliding technique. Upper limb nerve mobilization (ULNM) is a widely used treatment method for dysfunctions of the upper limbs. Butler reported that ULNM suppresses spasm and facilitates muscular tension and the overall recovery of patients with upper limb dysfunctions due to brain damage.
Another author performed median nerve mobilization for CTS patients and reported that it reduces pressure in carpal tunnel, improves NCV, grip strength, and alleviated pain. Our result supports this and shows the improved nerve conduction velocity. In nerve mobilization, tension is placed upon the nervous system, which contracts the cross-sectional area of the nerve, closing small blood vessels that cross the nerve epineurium and thus increasing blood flow to the neurofibers. In this process, the axonal transport system increases the flexibility of the contracted median nerve and structures around the joints accelerating NCV. Therefore, nerve mobilization is an effective treatment method for patients with peripheral neuropathy. O'Connor et al. concluded no significant effect of nerve sliding for the treatment of CTS which supports the null hypothesis of the present study.
The participants in the study demonstrated significant improvement in the measures of clinical pain intensity and upper extremity disability, and these findings are consistent with prior studies of neurodynamic technique in the treatment of CTS. Similar to the findings for pressure pain sensitivity and immediate within-session changes in clinical pain intensity, regardless of the clinical pain and disability observed in the current study, 3-week improvements occurred. Threats of external validity were also reduced by a set of strict inclusion criteria, and all the participants in both the groups showed same demographic and baseline characteristics.
The two groups had equal number of subjects with unilateral involvement and there were no significant differences with respect to their BMI, age, and side involved, which could have altered the results of the study when enhanced the internal validity of the result findings by reducing the between-group heterogeneity of confounding variables.
| Conclusions|| |
On the basis of findings of statistical analysis and discussion, the present study concludes that nerve slider technique can be implicated in patients with CTS due to its statistically significant improvement in the experimental group. Therefore, both nerve slider technique and conventional treatment are effective in reduction of pain and improving the functional status of patient suffering from CTS.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Werner RA, Andary M. Carpal tunnel syndrome: Pathophysiology and clinical neurophysiology. Clin Neurophysiol 2002;113:1373-81.
Atroshi I, Gummesson C, Johnsson R, Ornstein E, Ranstam J, Rosén I. Prevalence of carpal tunnel syndrome in a general population. JAMA 1999;282:153-8.
Werner RA, Andary M. Electrodiagnostic evaluation of carpal tunnel syndrome. Muscle Nerve 2011;44:597-607.
Bialosky JE, Bishop MD, Price DD, Robinson ME, Vincent KR, George SZ. A randomized sham-controlled trial of a neurodynamic technique in the treatment of carpal tunnel syndrome. J Orthop Sports Phys Ther 2009;39:709-23.
Shacklock MO. Neurodynamics. Physiotherapy 1995;81:9-16.
Butler DS, Jones MA. Mobilization of the Nervous System. London, UK: Churchill Livingstone; 1991.
Gifford L, Pitt-Brooke J, Reid H, Lockwood J, Kerr K. Neurodynamics. Rehabilitation of Movement. London, UK: WB Saunders Company Ltd.; 1998. p. 159-95.
Coppieters MW, Stappaerts KH, Wouters LL, Janssens K. The immediate effects of a cervical lateral glide treatment technique in patients with neurogenic cervicobrachial pain. J Orthop Sports Phys Ther 2003;33:369-78.
Rozmaryn LM, Dovelle S, Rothman ER, Gorman K, Olvey KM, Bartko JJ. Nerve and tendon gliding exercises and the conservative management of carpal tunnel syndrome. J Hand Ther 1998;11:171-9.
Scrimshaw SV, Maher CG. Randomized controlled trial of neural mobilization after spinal surgery. Spine (Phila Pa 1976) 2001;26:2647-52.
Kostopoulos D. Treatment of carpal tunnel syndrome: A review of non-surgical approaches with emphasis in neural mobilization. J Bodyw Mov Ther 2004;8:2-8.
Coppieters MW, Stappaerts KH, Staes FF, Everaert DG. Shoulder girdle elevation during neurodynamic testing: An assessable sign? Man Ther 2001;6:88-96.
Sweeney J, Harms A. Persistent mechanical allodynia following injury of the hand. Treatment through mobilization of the nervous system. J Hand Ther 1996;9:328-38.
Totten PA, Hunter JM. Therapeutic techniques to enhance nerve gliding in thoracic outlet syndrome and carpal tunnel syndrome. Hand Clin 1991;7:505-20.
Oskay D, Meriç A, Kirdi N, Firat T, Ayhan C, Leblebicioglu G. Neurodynamic mobilization in the conservative treatment of cubital tunnel syndrome: Long-term follow-up of 7 cases. J Manipulative Physiol Ther 2010;33:156-63.
Shacklock MO. Clinical Neurodynamics: A New System of Neuromusculoskeletal Treatment. London, UK: Elsevier Butterworth Heinemann; 2005a. p. 2-29, 154-8.
Cleland JA, Childs JD, Palmer JA, Eberhart S. Slump stretching in the management of non-radicular low back pain: A pilot clinical trial. Man Ther 2006;11:279-86.
Ha M, Son Y, Han D. Effect of median nerve mobilization and median nerve self-mobilization on median motor nerve conduction velocity. J Phys Ther Sci2012;24:801-4.
O'Connor D, Marshall S, Massy-Westropp N. Non-surgical treatment (other than steroid injection) for carpal tunnel syndrome. Cochrane Database Syst Rev 2003;1:CD003219.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
[Table 1], [Table 2], [Table 3], [Table 4]