|Year : 2016 | Volume
| Issue : 4 | Page : 206-210
Correlation between median nerve conduction studies and ultrasonography in cases of carpal tunnel syndrome
Hala R El-Habashy1, Reem A El-Hadidy1, Sandra M Ahmed2, Basma B El Sayed1, Aya S Ahmed1
1 Clinical Neurophysiology Unit, Kasr Al Ainy Teaching Hospitals, Cairo University, Egypt
2 Department of Neurology, Kasr Al Ainy Teaching Hospitals, Cairo University, Egypt
|Date of Submission||28-Jun-2016|
|Date of Acceptance||05-Sep-2016|
|Date of Web Publication||17-Mar-2017|
Basma B El Sayed
4 Mahmoud Samy El Baroudy Street, Al Haram, Giza - 12111
Source of Support: None, Conflict of Interest: None
Nerve conduction studies (NCS) have long been the only objective measure used to confirm the diagnosis of carpal tunnel syndrome (CTS), localize median nerve abnormalities, and exclude alternative diagnosis. Ultrasonography (US) can give information about the contents of carpal tunnel (CT) as well as aid in assessing the size of the median nerve (MN).
The aim of this study was to detect the relation between median NCS and cross-sectional area (CSA) of the MN measured using US in different grades of CTS.
Patients and methods
This study was a case–control, age-group matched, cross-sectional one. It included 60 wrists of 30 patients diagnosed with CTS and 60 wrists from 30 controls. Candidates were subjected to clinical assessment, median NCS, and measurement of CSA using US.
There was a significant positive correlation between CSA of the MN at CT inlet and both motor and sensory responses latencies (r=0.638, P<0.001 and r=0.629, P<0.001, respectively). There was a significant negative correlation of CSA of the MN with sensory and motor amplitudes (r=−0.656, P<0.001 and r=−0.657, P<0.001, respectively). Median nerve CSA at CT inlet in the patients’ group was significantly higher than that in the control group (P<0.0001). CSA at CT inlet in early CTS was 13.27±1.56 mm2; 15.13±1.97 mm2 in mild, 16.47±4.16 mm2 in moderate, and 21.43±3.96 mm2 in severe CTS.
US is highly correlated to NCS results in CTS. CSA of the MN at CT inlet measured using ultrasonography can be used as a screening tool for detection as well as discrimination of severe cases of CTS.
Keywords: carpal tunnel syndrome, cross-sectional area, nerve conduction studies
|How to cite this article:|
El-Habashy HR, El-Hadidy RA, Ahmed SM, El Sayed BB, Ahmed AS. Correlation between median nerve conduction studies and ultrasonography in cases of carpal tunnel syndrome. Egypt J Neurol Psychiatry Neurosurg 2016;53:206-10
|How to cite this URL:|
El-Habashy HR, El-Hadidy RA, Ahmed SM, El Sayed BB, Ahmed AS. Correlation between median nerve conduction studies and ultrasonography in cases of carpal tunnel syndrome. Egypt J Neurol Psychiatry Neurosurg [serial online] 2016 [cited 2018 May 26];53:206-10. Available from: http://www.ejnpn.eg.net/text.asp?2016/53/4/206/202378
| Introduction|| |
Carpal tunnel syndrome (CTS) constitutes 2.7% of hand pathologies . Its diagnosis depends on subjective symptoms and nerve conduction studies (NCS). NCS assess the function of the median nerve (MN), diagnose concomitant neurological disorders, define severity of CTS, and provide baseline before surgery . However, NCS is an expensive procedure that is not always tolerated. Ultrasound (US) provides a fast, relatively cheap, painless procedure for assessment of the MN . Treatment of CTS depends mainly on defining the severity of the disease . However, the value of cross-sectional area (CSA) of the MN in diagnosis and defining the severity of CTS is still under study .
| Aim|| |
This study aimed to detect the relation between median NCS and CSA of the MN measured using US in different grades of CTS.
| Patients and methods|| |
This is a case–control, age-group matched, and a cross-sectional study. It was conducted on 60 wrists of 30 patients with clinically and electrophysiologically defined CTS  (11 with early, 16 with mild, 18 with moderate, and 15 with severe CTS), and 60 wrists of 30 healthy controls, age and sex matched. All of them provided oral informed consent to the study. Any participant with a history of wrist surgery or fracture, with evidence of secondary CTS associated with other pathologies, or showing evidence of any other neurological disorder involving the upper limbs was excluded from the study. This study was approved by the research committee at Cairo University. The patients and controls involved in the study provided and oral informed consent.
NCS were performed for both patients and controls using Nihon Kohden Neuropak M1 MEB-9200 (Nihon Kohden Corporation, Tokyo, Japan) ENMG equipment. MN sensory and motor responses were evoked by means of electrical stimulation over the middle of the wrist between the tendons of the flexor carpi radialis and the palmaris longus muscle, recording from index finger and the abductor pollicis brevis muscle, respectively .
Median versus ulnar fourth digit sensory study was conducted by means of consecutive electrical stimulation of the MN (as previously described) and the ulnar nerve (medial wrist, adjacent to the flexor carpi ulnaris tendon) and recording from fourth digit .
Median versus radial thumb sensory comparative study was conducted with consecutive electrical stimulation of the MN (as previously described) and radial nerve stimulation (distal medial forearm over the radial bone) and recording from first digit .
The patient group was subdivided into four groups according to the severity of CTS classified using NCS following Stevens’ classification :
Early CTS: abnormal findings only in both comparative studies (≥0.5 ms difference in peak latencies).
Mild CTS: abnormal median sensory studies (peak latency ≥3.5 ms).
Moderate CTS: abnormal median sensory studies and prolonged median distal motor latency (onset latency ≥4.5 ms).
Severe CTS: any of the abovementioned abnormalities together with the evidence of axonal loss either by absent median sensory response, low amplitude, or absent median motor response (<2 μV).
CSA of the MN was assessed using a 5–17 MHz linear probe of IU22 Philips machine (Philips Ultrasound 22100 Bothell-Everett Highway; Philips Healthcare, Bothell, Washington, USA). The sonographer was blinded to clinical and other neurophysiologic studies. All wrists were examined in the neutral position with the palm up and the fingers semiextended with the hands resting on examination coach. CSA was measured at CT inlet (at the proximal margin of the flexor retinaculum between the scaphoid bone and the pisiform bone). Distal wrist crease was used as an external landmark. It was also measured at the middle one-third of the forearm (12 cm from wrist crease). CSA was measured by means of a direct tracing method using the inner margin of the hypoechoic sheath as the margin of the nerve.
All statistical analyses were performed using the Statistical Package for the Social Sciences Statistics (SPSS version 22, SPSS Inc., Chicago, Illinois, USA). Data were expressed as mean±SD. The results were analyzed statistically using Student’s t-test and the Mann–Whitney test whenever needed. Analysis of variance was used to calculate confidence intervals (95% CI). Pearson correlation coefficient (r) was used to measure correlation between quantitative variables. P less than 0.05 was considered significant.
| Results|| |
The study included 60 wrists from 30 patients diagnosed with CTS and 60 healthy wrists from 30 controls. There was no significant difference in mean age, sex, or the side examined between the two groups ([Table 1]).
|Table 1 Comparison of age, sex, and the side examined between the patient and the control group|
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Median NCS and ultrasonography results revealed a significant difference between the two groups. The patient group showed more delayed and smaller MN motor and sensory responses and much larger CSA of the MN at CT inlet when compared with the control group ([Table 2]).
|Table 2 Comparison of median nerve conduction studies and cross-sectional area in the patient and control groups|
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CSA at CT inlet showed a significant positive correlation with motor and sensory latencies (r=0.638, P<0.001 and r=0.629, P<0.001, respectively). It showed a significant negative correlation with motor and sensory amplitudes (r=−0.657, P<0.001 and r=−0.656, P<0.001, respectively).
The patient group was further subdivided into four subgroups using NCS and according to Stevens’ classification of CTS : the early CTS group included 11 patients, the mild CTS group included 16 patients, the moderate CTS group included 18 patients, and the severe CTS group included 15 patients.
There was a significant delay in motor latency in patients’ subgroups (moderate and severe CTS) compared with the control group (P<0.0001 for each). However, the severe CTS group showed a significantly lower motor amplitude compared with the control group (P<0.0001). Moreover, there was a significant delay in sensory latency in patients’ subgroups (mild, moderate, and severe CTS) compared with the control group (P<0.0001 for each).
CSA of the MN at CT inlet in all patients’ subgroups was significantly thicker compared with the control group (P<0.0001 for each). However, CSA at midforearm in the moderate CTS subgroup was significantly thinner compared with the control group (P<0.0001) ([Figure 1]).
|Figure 1 Median nerve conduction studies and cross-sectional area (CSA) in controls and carpal tunnel syndrome patients’ subgroups.|
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The CSA of the MN at CT inlet (95% CI) in the control group showed no overlap with any of the patients’ subgroups. Moreover, there was no overlap between the control group and the mild, moderate, and severe CTS subgroups in motor and sensory latencies and sensory amplitude.
The moderate and severe CTS subgroups (95% CI) showed no overlap in CSA at CT inlet, motor and sensory latencies and amplitudes. However, 95% CI of motor and sensory latencies showed no overlap between mild and moderate CTS subgroups ([Figure 2]).
|Figure 2 Confidence interval at 95% of median nerve conduction studies and cross-sectional area (CSA) in the control group and patients’ subgroups. CTS, carpal tunnel syndrome.|
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| Discussion|| |
US has an established role in the diagnosis of CTS to the extent that some authors assumed it can partially replace NCS. However, its ability in the detection of severity and grading CTS is still under debate .
NCS is considered by many authors as the main subjective test used in the diagnosis of CTS. Meanwhile, US can assess the anatomy and identify the pathology of surrounding structures that may compress the MN .
It is now proposed that US acts as the initial diagnostic test in CTS as it presents higher patient acceptability, lower cost, and additional capability to assess CT anatomy and guide treatment .
In this study, the CSA of the MN at CT inlet in the patient group was much thicker compared with the control group (P<0.0001). Previous studies reported that CSA at CT inlet is the most consistent finding in CTS .
There are many theories explaining the increase in the thickness of MN in cases of CTS. Many authors suggested that MN microcirculation injury, connective tissue compression, or synovial tissue hypertrophy were the most accepted theories .
Any injury or mild trauma to the nerve may cause changes in its microvascular structure, leading to biochemical disorders causing increased permeability of these vessels and buildup of proteins and inflammatory cells. This causes edema in the nerve, which leads to interruption of blood flow within it. The resultant hypoxia will cause further pressure and subsequently more injury to the microvasculature leading to a vicious circle .
Moreover, any condition causing stiffness of the surrounding connective tissue layers or hypertrophy in the synovial tissue may limit the movement of the nerve inside the tunnel and will eventually cause its injury ,.
The distal diffusion of fluids can also explain the significant reduction in MN thickness at midforearm in the patient group.
It is worth mentioning that the US findings showed significant correlations with NCS results. There was a significant negative correlation with median sensory and motor response amplitudes and a significant positive correlation with median sensory and motor responses latencies (P<0.0001 for each). The same relation was reported by El Miedany et al. , who found a high degree of correlation between conduction abnormalities and measurements of CSA of the MN. As NCS are the gold standard in diagnosing CTS, it can be supposed that US is a promising tool in the detection of CTS.
CSA of the MN at CT inlet is correlated with CTS severity. It can be used as complementary data to diagnose and determine the severity of CTS .
Furthermore, the CSA of the MN at CT inlet (95% CI) in different grades of CTS were higher than that in the control group. However, it could not differentiate between early and mild and between mild and moderate CTS. It could detect early and severe CTS cases. This is contradictory to previous studies, which reported the ability of US to detect various levels of disease severity with confident results for diagnosis .
US may have a role in helping the physicians to decide the most favorable way to manage CTS. It can be used as a complimentary test to NCS, as early, mild, and moderate CTS cases receive the same treatment .
In accordance, Ettema et al.  stated the advantages of US, which might reveal relevant anatomic information preoperatively that may have an influence on the management of CTS. Moreover, Atroshi et al.  suggested that an abnormal US test result could eliminate the need for electrophysiological studies in CTS suspected cases. The use of US as a complementary test for CTS concomitantly with NCS should be considered .
Small sample size of each disease grade is a limitation to this study; further studies on larger samples are recommended.
| Conclusion|| |
CSA of the MN at CT inlet measured using US can be used as a screening tool for detection of CTS as well as discriminating early and moderate from severe cases of CTS.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
British Orthopedic Association; British Society for Surgery of the Hand; and Royal College of Surgeons. Commissioning guide: treatment of painful tingling fingers. UK: BOA, BSSH, RCS; 2013.
Seror P. Electrodiagnosis of the upper limbs. In: Allieu Y, Mackinnon SE, editors. Nerve compression syndromes of the upper limb. France: CRC Press; 2002. 21–46.
Pastare D, Therimadasamy AK, Lee E, Wilder-Smith EP. Sonography versus nerve conduction studies in patients referred with a clinical diagnosis of carpal tunnel syndrome. J Clin Ultrasound 2009; 37:389–393.
Ibrahim I, Khan WS, Goddard N, Smitham P. Carpal tunnel syndrome: a review of the recent literature. Open Orthop J 2012; 6:69–76.
Aboonq MS. Pathophysiology of carpal tunnel syndrome. J Neurosci 2015; 20:4–9.
Werner RA, Andary M. Electrodiagnostic evaluation of carpal tunnel syndrome. Muscle Nerve 2011; 44:597–607.
Steven CJ. The electrodiagnosis of carpal tunnel syndrome. Muscle Nerve 1997; 20:1477–1486.
Ziswiler HR, Reichenbach S, Vogelin E, Bachmann LM, Villiger PM, Juni P. Diagnostic value of sonography in patients with suspected carpal tunnel syndrome: a prospective study. Arthritis Rheum 2005; 52:304–311.
McDonagh C, Alexander M, Kane D. The role of ultrasound in the diagnosis and management of carpal tunnel syndrome: a new paradigm. Rheumatol 2015; 54:9–19.
Cartwright MS, Hobson-Webb LD, Boon AJ, Alter KE, Hunt CH, Flores VH et al.
Evidence-based guideline: neuromuscular ultrasound for the diagnosis of carpal tunnel syndrome. Muscle Nerve 2012; 46:287–293.
Ajeena IM, Al-Saad RH, Al-Mudhafar A, Hadi NR, Al-Aridhy SH. Ultrasonic assessment of females with carpal tunnel syndrome proved by nerve conduction study. Neural Plast 2013; 2013:1–6.
Mondelli M, Filippou G, Gallo A, Frediani B. Diagnostic utility of ultrasonography versus nerve conduction studies in mild carpal tunnel syndrome. Arthritis Care Res 2008; 59:357–366.
Ozkul Y, Sabuncu T, Kocabey Y, Nazligul Y. Outcomes of carpal tunnel release in diabetic and non diabetic patients. Acta Neuol Scand 2003; 106:168–172.
MacDermid JC, Doherty T. Clinical and electroidiagnostic testing of carpal tunnel syndrome: a narrative review. J Orthop Sports Phys Ther 2004; 34:565–588.
El Miedany YM, Aty SA, Ashour S. Ultrasonography versus nerve conduction study in patients with carpal tunnel syndrome: substantive or complementary tests?. Rheumtology (Oxford) 2004; 43:887–895.
Bueno-Gracia E, Tricás-Moreno JM, Fanlo-Mazas P, Malo-Urriés M, Haddad-Garay M, Estébanez-de-Miguel E et al.
Relationship between ultrasound measurements of the median nerve and electrophysiological severity in carpal tunnel syndrome. Rev Neurol 2015; 61:441–446.
Ettema AM, Amadio PC, Zhao C, Wold LE, Ann KN. A histological and immunohistochemical study of the subsynovial connective tissue in idiopathic carpal tunnel syndrome. J bone Joint Syrg Am 2004; 86:1458–1466.
Atroshi I, Gummesson C, Johnsson R, Ornstein E, Ranstam J, Rosen I. Prevalence of carpal tunnel syndrome in a general population. JAMA 1999; 282:153–158.
Jablecki CK, Andary MT, Floeter MK, Miller RG, Quartly CA, Vennix MJ et al.
Practice parameters: electrodiagnostic studies in carpal tunnel syndrome report of the American Association of Electrodiagnostic Medicine, American Academy of Neurology, and the American Academy of physical medicine and rehabilitation. Neurol 2002; 58:1589–1592.
[Figure 1], [Figure 2]
[Table 1], [Table 2]