LAUSR

Ulnar neuropathy at the elbow (UNE) is the second most common mechanical mononeuropathy after carpal tunnel syndrome (CTS). Despite the frequency with which it is seen in the neurophysiology clinic, UNE still poses clinical and diagnostic challenges. The clinical diagnosis of ulnar neuropathy is generally easy to determine, but UNE may be difficult to localize on nerve conduction studies. Diagnostic localization is improved when the ulnar nerve is examined by ultrasound (Simon et al., 2015) and best with magnetic resonance neurography (Keen et al., 2012). UNE is often automatically referred to as an entrapment neuropathy. It is important to consider whether this is indeed true. Nerve entrapment requires that the nerve is caught or trapped by an aberrant, anomalous or normal anatomic structure causing compression of the nerve at that site. However, ultrasound studies in UNE do not identify features indicative of nerve entrapment in the majority of cases (Omejec and Podnar, 2015; 2016). Compression of the nerve through extrinsic pressure or traction of the nerve around the elbow related to habitual and occupational limb positioning are more common mechanisms of nerve injury. For these reasons, the term entrapment neuropathy should be avoided when discussing mechanistically undifferentiated UNE. The above conjecture is borne out in the neurophysiology clinic. Occasionally, UNE may be identified in manual workers complaining of relatively rapidly progressive sensory and motor ulnar nerve symptoms in the dominant hand, likely caused by true entrapment of the nerve by thickened Osborne’s fascia at the entry to the cubital tunnel. There are more frequent examples of office-based workers presenting with fluctuating, predominantly sensory symptoms in the non-dominant hand, probably caused by chronic repeated trauma to the ulnar nerve in the retroepicondylar groove from extrinsic pressure or traction of the nerve around the medial epicondyle or both. The proliferation of smart phone and tablet devices has led to an epidemic of elbows being held for a prolonged period in a maximum flexion position causing transient ulnar nerve ischemia or in some instances fixed neuropathy. The most troubling aspect of this common peripheral nerve syndrome is that there are still no management guidelines to assist choice of treatment in patients with UNE, which largely stems from a lack of appropriately conducted clinical trials. In this issue of Clinical Neurophysiology, Drs. Omejec and Podnar provide an analysis of the outcomes of treatment in patients with UNE, where treatment decisions (surgical decompression or non-operative treatment) were largely based on morphological nerve abnormalities identified on ultrasound (Omejec and Podnar, 2018). Based on their earlier work, the authors’ hypothesized that UNE with focal constriction and maximal morphological abnormalities just proximal to the cubital tunnel is caused by nerve entrapment while UNE with morphological changes proximal to the medial epicondyle without focal constriction is not caused by nerve entrapment. They used these parameters to select the former group for surgery and the latter group for non-surgical treatment irrespective of neuropathy severity. With respect to treatment for UNE, the guidance from the existing literature is disappointingly sparse. There is evidence that education about avoiding aggravating activities with or without elbow splinting and nerve gliding exercises reduces discomfort in patients with mild to moderate ulnar neuropathy (Svernlov et al., 2009). Targeted corticosteroid injections do not improve symptoms in UNE (vanVeen et al., 2015). The failure of UNE to respond to corticosteroid injection around the elbow is particularly interesting when compared with the excellent results seen in CTS, which is almost always caused by nerve entrapment. This suggests that the mechanisms of UNE and CTS are different. The evidence base regarding surgical treatment is particularly disappointing. There are no randomized controlled trials comparing surgical intervention with non-surgical intervention. The only trials available compare different surgical techniques and indicate that UNE symptoms often improve following surgery irrespective of the technique used (Caliandro et al., 2016). While some may argue that this supports surgery as a treatment of UNE, there is no data to support the superiority of decompression surgery over any other treatment, and ignores the natural history of mild and moderate UNE, which includes fluctuating symptoms and spontaneous improvement in some cases. In addition, surgical decompression should only be effective if there is compression or entrapment of the nerve caused by intrinsic surgically-modifiable structures, and would not necessarily be effective for patients with extrinsic compression or nerve traction. In total, we already know that ulnar neuropathy improves with either surgical or non-surgical treatment. The concepts proposed by Drs. Omejec and Podnar invite clinicians to think about the possible mechanism of nerve injury before selecting the appropriate treatment, and this approach is supported by recent imaging data. However, despite this new contribution to the literature on UNE treatment, there is still no guidance available on when to choose surgical intervention. This question will only be resolved with a surgical treatment trial of UNE with an appropriate non-surgical