Debate continues as to which treatment provides optimal results in patients with cubital tunnel syndrome. In cases in which a surgical procedure is recommended, there has been a recent increase in the number of in situ decompressions performed, with a concomitant decrease in ulnar nerve transpositions1. Proponents of in situ decompression of the ulnar nerve cite the faster recovery2 and lack of clinical studies demonstrating a difference in clinical outcomes between the 2 procedures3. Advocates for anterior transposition of the ulnar nerve have described the need to address the incipient cause of the neuropathy4 (compression by the overlying fascia, traction against the medial epicondyle, and the relative vulnerability of the ulnar nerve to repetitive trauma in its in situ location) as well as the poorer clinical outcomes that follow a revision surgical procedure (patients who have persistent symptoms after an in situ decompression and then proceed to transposition5). Ultimately, the decision hinges on the surgeon’s experience and patient characteristics (such as stability of the ulnar nerve within the cubital tunnel, patient comorbidities, and preferences and expectations for postoperative recovery).
What has been lacking (and what may ultimately influence clinical decision-making) is the ability to determine the severity of disease within the ulnar nerve. Clinical examination, including manual muscle testing, presence of atrophy, and sensory assessments, is a relatively blunt tool, as detectable changes do not occur until relatively advanced stages of the disease. The traditionally used electrodiagnostic measure of nerve conduction velocity across the elbow also does not accurately reflect the severity of disease, as the test detects the portions of the ulnar nerve that are functioning well and may be falsely interpreted as normal or mild. Signs of denervation within ulnar-innervated muscles on electromyography are prone to the same pitfall as the clinical examination; by the time these are detected, it may already be too late.
In their investigation, Power et al. analyzed electrodiagnostic studies to determine whether motor amplitude from the nerve conduction study can predict the severity of ulnar neuropathy. Unlike nerve conduction velocity, which measures only the fastest fibers of the nerve, the motor amplitude assesses the number of functioning axons. A higher motor amplitude reflects a greater number of functioning axons. Changes in motor amplitude would not be expected in early-stage cubital tunnel syndrome (dynamic ischemia of the nerve provoked by elbow flexion, analogous to a demyelinating injury), but they would be expected in long-standing chronic compressive neuropathy in which the nerve has undergone fibrosis of the epineurium and perineurium, analogous to an axonotmetic injury. Of note, changes in the motor amplitude would also be expected in cases of cervical radiculopathy or nerve injury. After adjusting for age, sex, laterality, symptom duration, a prior surgical procedure, and body mass index, Power et al. demonstrated that the motor amplitude of the first dorsal interosseous muscle predicted weakness in preoperative grip and key pinch. Nerve conduction velocity did not predict these changes. It should be noted that the findings are reflective of a single surgeon’s practice and that electrodiagnostic studies are prone to inter-performer variability. Furthermore, only preoperative electrodiagnostic studies were assessed and postoperative changes in motor amplitude were not assessed.
Although further prospective study is needed to clarify these findings, it is conceivable that a threshold of motor amplitude may exist upon which surgeons can determine whether an in situ decompression will provide an adequate opportunity for axonal regeneration, or whether the compressive neuropathy is too advanced and ulnar nerve transposition is warranted. Furthermore, it is possible that the motor amplitude could be used as an objective measure to determine the appropriateness of a distal, reverse, end-to-side nerve transfer in the most severe cases of ulnar neuropathy. Power et al. should be congratulated for advancing the scientific understanding of cubital tunnel syndrome.
1. Soltani AM, Best MJ, Francis CS, Allan BJ, Panthaki ZJ. Trends in the surgical treatment of cubital tunnel syndrome: an analysis of the national survey of ambulatory surgery database. J Hand Surg Am. 2013 Aug;38(8):1551-6. Epub 2013 Jul 3.
2. Staples R, London DA, Dardas AZ, Goldfarb CA, Calfee RP. Comparative morbidity of cubital tunnel surgeries: a prospective cohort study. J Hand Surg Am. 2018 Mar;43(3):207-13. Epub 2017 Dec 6.
3. Staples JR, Calfee R. Cubital tunnel syndrome: current concepts. J Am Acad Orthop Surg. 2017 Oct;25(10):e215-24.
4. Gelberman RH, Yamaguchi K, Hollstien SB, Winn SS, Heidenreich FP Jr, Bindra RR, Hsieh P, Silva MJ. Changes in interstitial pressure and cross-sectional area of the cubital tunnel and of the ulnar nerve with flexion of the elbow. An experimental study in human cadavera. J Bone Joint Surg Am. 1998 Apr;80(4):492-501.
5. Aleem AW, Krogue JD, Calfee RP. Outcomes of revision surgery for cubital tunnel syndrome. J Hand Surg Am. 2014 Nov;39(11):2141-9. Epub 2014 Aug 29.