August 24, 2007
Muscle Atrophy at Diagnosis of Carpal and Cubital Tunnel Syndrome
By Mallette, Paige Zhao, Meijuan; Zurakowski, David; Ring, David
Purpose: This study was designed to test the hypothesis that patients with an initial diagnosis of cubital tunnel syndrome are more likely to present with muscle atrophy than patients with an initial diagnosis of carpal tunnel syndrome. Methods: A list of patients presenting to the office of a single hand surgeon from January 2000 to June 2005 with an initial diagnosis of isolated, idiopathic carpal tunnel syndrome or cubital tunnel syndrome was generated from billing records. The medical records of 58 patients with cubital tunnel syndrome and 370 patients with carpal tunnel syndrome were reviewed for age, gender, diabetes, and presence of atrophy.Results: Twenty-three of 58 patients with an initial diagnosis of cubital tunnel syndrome had atrophy compared with only 62 out 370 patients with an initial diagnosis of carpal tunnel syndrome. Multiple logistic regression revealed that age (odds ratio, 1.06; 95% Cl, 1.041.08) and diagnosis (cubital tunnel patients were more likely than carpal tunnel patients to present with atrophy; odds ratio, 4.5; 95% Cl, 2.7-8.6) were factors significantly associated with atrophy at presentation.
Conclusions: Patients with carpal tunnel syndrome present earlier in the course of their disease than patients with cubital tunnel syndrome. Patients with cubital tunnel syndrome are more likely to present with muscle atrophy, reflecting advanced nerve damage that may not respond to surgery. (J Hand Surg 2007;32A:855-858. Copyright (c) 2007 by the American Society for Surgery of the Hand.)
Type of study/level of evidence: Prognostic IV.
Key words: Atrophy, carpal tunnel syndrome, cubital tunnel syndrome.
Cubital tunnel syndrome-idiopathic compression of the ulnar nerve at the elbow-is second only to carpal tunnel syndrome among common compressive neuropathies of the upper extremity in adults.1,2 Patients with either disease present with complaints of numbness. Night-time numbness or numbness upon waking are characteristic. Signs of advanced nerve damage include persistent numbness, muscle atrophy, and weakness.
Whereas surgical intervention is effective at reducing or eliminating intermittent symptoms, advanced nerve damage is less likely to improve after operative treatment.3-8 We hypothesize that patients with cubital tunnel syndrome are more likely than patients with carpal tunnel syndrome to have muscle atrophy at the time of initial diagnosis.9,10 This hypothesis was tested by reviewing the medical records of patients that presented to a single hand surgeon with an initial diagnosis of an isolated and idiopathic carpal or cubital tunnel syndrome.
Materials and Methods
A list of patients presenting to the office of a single hand surgeon from January 2000 through June 2005 was generated from billing records. Inclusion criteria included (1) patients with an initial diagnosis of carpal tunnel or cubital tunnel syndrome; (2) the compressive neuropathy was idiopathic; (3) this was the only diagnosis made-it was an isolated problem (eg, no cervical radiculopathy, elbow arthrosis, etc.).
Fifty-eight patients with cubital tunnel syndrome and 370 patients with carpal tunnel syndrome satis- fied the inclusion criteria (Table 1). The average age of patients with cubital tunnel syndrome was 54 years (range, 22-90 years), and the average age of carpal tunnel patients was 56 years (range, 26-84 years). Patients with carpal tunnel syndrome were significantly more likely to be female: 255 (69%) of the carpal tunnel patients and 24 (41%) of the cubital tunnel patients were female (p
Table 1. Univariate Analysis of Carpal and Cubital Tunnel Syndrome Groups
The diagnosis of cubital or carpal tunnel syndrome was based on complaints of numbness. Painful numbness was included, but patients with complaints of pain only were not given these diagnoses. A specific diagnosis was applied only when the complaints and examination findings were consistent and characteristic of one of these diagnoses. In general, there had to be a complaint of intermittent or persistent numbness in the distribution of the involved nerve that could either be reproduced with the appropriate provocative test (Durkan's or Phalen's for carpal tunnel syndrome and an elbow flexion test for cubital tunnel syndrome) or was associated with objective signs of advanced nerve damage (weakness or atrophy). The following data points were recorded anonymously from individual medical records and placed into a database: age, gender, diabetes, and finding of atrophy (visible loss of muscle mass) on physical examination.
Data from electrophysiologic data were available in 30 of 58 (52%) patients with cubital tunnel syndrome and 231 of 370 (62%) patients with carpal tunnel syndrome. Electrophysiologic testing was ordered for all patients requesting surgery and in a few patients in whom the diagnosis was in some doubt. Several patients had testing prior to referral. Patients that did not have electrophysiologic testing had a presumptive diagnosis of carpal tunnel syndrome or cubital tunnel syndrome based on clinical and physiologic examination and were either not offered or declined operative intervention. The electrophysiologic testing confirmed the suspected diagnosis in all 261 patients in whom it was obtained. One neurophysiologist interpreted all the electrophysiologic studies and assigned categorical ratings: mild, moderate, or severe. Intrinsic hand muscle atrophy was diagnosed on physical examination: atrophy of the first dorsal interosseous for cubital tunnel and atrophy of the thenar eminence in carpal tunnel syndrome.
A chi-square analysis was used to evaluate the association between diagnosis and atrophy. Logistic regression modeling was also applied to determine (1) the relative odds of atrophy between patients with carpal versus cubital tunnel syndrome after adjustment for covariates including age, gender, and diabetes; (2) the factors associated with atrophy in carpal tunnel syndrome and cubital tunnel syndrome adding neurophysiologic testing parameters (distal motor and sensory latencies and the neurologist's overall rating [mild, moderate, severe] for carpal tunnel syndrome, and the neurologist's overall rating for cubital tunnel syndrome) to the other covariates. A backward selection procedure was used to identify significant variables, and 95% confidence intervals were constructed. Model fit was assessed using R-square, and maximum likelihood estimation was used to derive the probability of muscle atrophy based on diagnosis and other variables.12 All 2-tailed values of p
In univariate analysis, age, diabetes, and diagnosis (carpal tunnel vs cubital tunnel syndrome) were significantly associated with atrophy and gender showed a non-significant trend for association with atrophy (Table 2). Twenty-three of 58 (40%) patients with cubital tunnel syndrome and 62 of 370 (17%) patients with carpal tunnel syndrome presented with muscle atrophy (p
Table 2. Univariate Analysis of Candidate Predictors or Risk Factors of Atrophy
Multivariate logistic regression revealed that older age (odds ratio, 1.06; 95% CI, 1.04-1.08) and diagnosis (cubital tunnel patients were more likely than carpal tunnel patients to present with muscle atrophy; odds ratio, 4.5; 95% CI, 2.3-8.6) were independently associated with atrophy at presentation (Table 3; Fig. 1) Determinants of atrophy among patients with carpal tunnel syndrome and electrophysiologic (EMG) data were age (odds ratio, 1.06; 95% CI, 1.03-1.10) and neurologist's rating (odds ratio, 3.8; 95% CI, 1.8-7.8), but not distal motor or sensory latency. Neurologist's rating was associated with atrophy among patients with cubital tunnel syndrome and EMG data, although this association only reached a trend (p = .09).
Table I. Multivariate Results for Significant Independent Predictors of Atrophy
Figure 1. Curves depict the age-based probability of atrophy for patients with carpal tunnel syndrome and cubital tunnel syndrome independent of gender and diabetes. Age and diagnosis were both associated with atrophy in multivariate analysis (p
This study is limited by the fact that it represents a single surgeon's practice and practice style, and electrophysiologic testing was not used routinely to confirm the diagnosis. Use of the neurophysiologist's overall rating, although practical in a retrospective study, is also somewhat subjective. It is possible that the patients presenting to this surgeon and the diagnostic criteria used by this surgeon and neurophysiologist cannot be generalized to the average practice. An additional limitation of the study is that intrinsic muscle atrophy was determined by the judgment of the examiner, without objective testing. On the other hand, the diagnostic criteria are fairly well established, and routine objective neurophysiologic testing is not justified. Furthermore, muscle atrophy was only diagnosed when it was obvious and therefore might be considered as severe muscle atrophy. It could be argued that a case-control design would be better for determining risk factors for atrophy. We used a retrospective cohort design (1 ) because of the relatively low number of patients with ulnar neuropathy and (2) because our intention was to describe descriptive statistics of the overall consecutive cohort of patients presenting with carpal or cubital tunnel syndrome. In this manner, our study is able to report the prevalence of atrophy in one surgeon's practice as well as factors associated with atrophy. In the final analysis, this study simply recognizes that patients with cubital tunnel present at a more advanced stage, and either study design demonstrates this.
Very few scientific investigations have addressed the initial clinical diagnosis of cubital tunnel syndrome, and we are not aware of any prior work addressing the prevalence of atrophy in patients with an initial diagnosis. Buschbacher studied weakness in patients referred for electrodiagnostic evaluation of numbness and made observations similar to those in our study.10 He identified weakness in 61 of 74 (82%) patients with electrophysiologic evidence of cubital tunnel syndrome compared with only 11 of 69 (16%) patients with electrophysiologic evidence of carpal tunnel syndrome.
If our data regarding atrophy can be reproduced by others, then it suggests some differences between these otherwise relatively similar diseases. One can only speculate as to why patients with carpal tunnel syndrome present with less advanced disease, prior to the development of intrinsic muscle atrophy or weakness. Perhaps it is easier to provoke the symptoms in a way that disturbs sleep. Perhaps the involvement of the median nerve aspect of the hand is more notable, more bothersome, or more worrisome to patients than involvement of the ulnar nerve aspect.
In any case, the findings are both interesting and useful for counseling patients. The observation of a higher prevalence of muscle atrophy at presentation in cubital tunnel than in carpal tunnel patients remains even after adjusting for age, gender, and diabetes. The greater prevalence of atrophy upon presentation would seem to reflect that cubital tunnel syndrome presents at a more advanced stage than carpal tunnel syndrome. Given that the damage associated with compressive peripheral neuropathies is incompletely reversible,3-8 patients and surgeons may be less satisfied with the results of surgery for ulnar nerve compression than they are for carpal tunnel syndrome if they are expecting complete recovery. Operations for carpal tunnel syndrome - where symptoms are annoying and even disabling and advanced nerve dysfunction relatively uncommon - may be perceived as curative and of having a major impact on quality of life. Based on evaluation of symptoms and signs, carpal tunnel release can often be assessed as having cured the problem although neurophysiologic testing usually remains somewhat abnormal except in very mild cases. In contrast, patients with cubital tunnel syndrome may be less likely to notice an effect from surgery and more likely to be left with residual symptomatic nerve dysfunction.
1. Latinovic R, Gulliford MC, Hughes RA. Incidence of common compressive neuropathies in primary care. J Neurol Neurosurg Psychiatry 2006;77:263-265.
2. Mondelli M, Giannini F, Ballerini M, Ginanneschi F, Martorelli E. Incidence of ulnar neuropathy at the elbow in the province of Siena (Italy). J Neurol Sei 2005;234:5-10.
3. Gelberman RH, Pfeffer GB, Galbraith RT, Szabo RM, Rydevik B, Dimick M. Results of treatment of severe carpal-tunnel syndrome without internal neurolysis of the median nerve. J Bone Joint Surg 1987;69A:896-903.
4. Lett ME, Weiser RW, Tomaino MM. Patient-reported outcome after carpal tunnel release for advanced disease: a prospective and longitudinal assessment in patients older than age 70. J Hand Surg 2004;29A:379-383.
5. Matsuzaki H, Yoshizu T, Maki Y, Tsubokawa N, Yamamoto Y, Toishi S. Long-term clinical and neurologic recovery in the hand after surgery for severe cubital tunnel syndrome. J Hand Surg 2004;29A:373-378.
6. Mondelli M, Reale F, Padua R, Aprile I, Padua L. Clinical and neurophysiological outcome of surgery in extreme carpal tunnel syndrome. Clin Neurophysiol 2001;1 12:1237-1242.
7. Mowlavi A, Andrews K, Lille S, Verhulst S, Zook EG, Milner S. The management of cubital tunnel syndrome: a meta-analysis of clinical studies. Plast Reconstr Surg 2000; 106:327-334.
8. Rhoades CE, Mowery CA, Gelberman RH. Results of internal neurolysis of the median nerve for severe carpal-tunnel syndrome. J Bone Joint Surg 1985;67A:253-256.
9. Clark CB. Cubital tunnel syndrome. JAMA 1979;241:801802.
10. Buschbacher R. Side-to-side confrontational strength-testing for weakness of the intrinsic muscles of the hand. J Bone Joint Surg 1997;79A:401-405.
11. Browner W, Newman T, Cummings S, Hulley S. Estimating sample size and power: the nitty-gritty. In: Hulley S, Cummings S, Browner W, Grady D, Hearst N, Newman T, eds. Designing clinical research. 2nd ed. Philadelphia: Lippincott Williams & Wilkins, 2001:65-91.
12. Hosmer DW, Lemeshow S. Applied logistic regression. 2nd ed. New York: John Wiley; 2000:92-128.
Paige Mallette, BA, Meijuan Zhao, MD, David Zurakowski, PhD, David Ring, MD
From the Hand and Upper Extremity Service, Department of Orthopaedic Surgery, Massachusetts General Hospital, Boston, MA; Orthopaedic Hand and Upper Extremity Service, Massachusetts General Hospital, Boston, MA; Harvard Medical School, Boston, MA; Children's Hospital Boston, Boston, MA.
The authors would like to acknowledge the expert and generous assistance of David Zurakowski, PhD. with the statistical analysis.
Received for publication September 2, 2006; accepted in revised form March 16, 2007.
Supported by unrestricted research grants from AO Foundation, Wright Medical, Joint Active Systems, Smith and Nephew Richards, and Small Bone Innovations.
Corresponding author: David Ring, MD, Orthopaedic Hand and Upper Extremity Service, Massachusetts General Hospital, Yawkey Center Suite 2100, 55 Fruit Street, Boston, MA 02114; e-mail: dring(R) partners.org
Copyright (c) 2007 by the American Society for Surgery of the Hand
Copyright Churchill Livingstone Inc., Medical Publishers Jul/Aug 2007
(c) 2007 Journal of Hand Surgery, The. Provided by ProQuest Information and Learning. All rights Reserved.