To the Editor:— I read with great interest the case report by Koff et al. 1The authors rightly highlighted two important points of general interest. First, patients with multiple sclerosis may have a compromise of the peripheral nerves. Second, anesthesiologists must be aware that patients with a preexisting neurologic deficit (even if subclinical) may be more susceptible to perioperative injuries (double-crush phenomenon).
However, I would like to express some consideration about this case. The authors stated that “despite testing modalities, it may be difficult to differentiate between multiple etiologies of brachial plexus injuries.” I perfectly agree with this statement but, sometimes, useful clues about the etiologies of brachial plexus damage may be achieved by the research of the site of the initial injury. I would like to examine two possible local causes of “second crush”: the peripheral nerve block and the surgical procedure.
An injury caused by the needle or by a toxic effect of the local anesthetic mixture injected at the interscalene level should probably affect, at least at the beginning, the highest part of the plexus, with a sparing of the lowest roots (C8–T1), usually not reached by the needle or by the local anesthetic. Vice versa , a local surgical factor (e.g. , a compression by a retractor protracted for several hours)2may cause an injury at the cord level (deltopectoral approach), with a possible block of the arm from the shoulder to the fingers (including the median and the ulnar nerves) and a sparing of the nerves emerging from the roots or the trunks, like the long thoracic, the dorsal scapular, and the suprascapular nerves.
Unfortunately, the authors did not provide us with data on the function of the long thoracic, the dorsal scapular, and the suprascapular nerves. Therefore, we can only analyze the clinical and instrumental data available.
On postoperative day 1, these are the data recorded: loss of light touch sensation in C6–T1, shoulder pain exacerbated by arm movements (a normal postoperative pain?), and flaccid motor block of the entire extremity (obviously including the hand). The magnetic resonance imaging performed on postoperative day 3 demonstrated swelling and increased signal of the brachial plexus at the thoracic level (no data on the cervical part of the plexus). The electromyelogram performed on postoperative day 4 showed loss of the median and ulnar F waves. On postoperative day 11, the same procedure demonstrated active denervation of all the muscles examined and absence of median, ulnar, and radial sensory nerve action potentials. All of these clinical and instrumental data seem to indicate, in my opinion, a distal (cord) site of secondary injury.
The only fact that could indicate a proximal site of injury is the recording of visible atrophy of the proximal musculature at 8 months postoperatively. However, I do not know whether this finding might be attributable to a specific nerve lesion or to the prolonged inactivity of the whole arm.
On the basis of these data (albeit incomplete), I think that, in this patient, the most probable responsible of the “second crush” should be searched at the surgical field and that the anesthesiologic factors did not play a main role in the development of the postoperative neurologic deficit. Therefore, in my opinion, other evidences are necessary before establishing a correlation between peripheral nerve blocks and nerve damage in multiple sclerosis patients.
Moreover, this case report does not give us any further information about the usefulness of ultrasound-guided techniques in the prevention of neurologic injuries.3
Centro Traumatologico Ortopedico, Florence, Italy. email@example.com