Abstract & Commentary
Source: Stewart JD. Peripheral nerve fascicles: Anatomy and clinical relevance. Muscle Nerve. 2003;28:525-541.
How does one physiologically explain ulnar neuropathies at the elbow that clinically localize to the wrist? Why do proximal sciatic neuropathies sometimes masquerade clinically as peroneal neuropathies at the knee? In this lucid, well-articulated review, Stewart thoroughly and evenhandedly comments on the literature going back to 1913, convincingly arguing that nerve fibers do not randomly intertwine as they progress distally in nerve bundles. Evidence indicates that specific axons remain grouped together, particularly through their distal course, as they travel cable-like toward their destination. Adjacent muscles and, similarly, adjacent sensory dermatomes, are innervated by nerve fascicles that remain together within the nerve bundle. At the plexus and root level this has yet to be demonstrated, but once the peripheral nerve has formed, somatotopic clustering reigns. Clinical conundrums now make anatomic sense.
Nerve fibers within the ulnar nerve are grouped such that those to forearm muscles are separate from those innervating the intrinsic hand muscles, which are separate yet again from the dorsal ulnar cutaneous nerve. Ulnar neuropathy at the elbow may preferentially compress the nerve fascicle to distal hand muscles while sparing the sensory branches, as well as the motor fascicle to the more proximal flexor carpi ulnaris and flexor digitorum profundus. Clinically, this would mimic a Guyon’s canal ulnar neuropathy when the lesion is, in fact, at the elbow. Careful electrodiagnostic studies would, hopefully, correctly localize the abnormality. Differential involvement of radial nerve fascicles along the spiral groove in "Saturday night palsy" might also explain the variable presence of brachioradialis weakness or sensory impairment, either of which may be absent. Proximal median neuropathy can impersonate anterior interosseous neuropathy (AIN), particularly with supracondylar humeral fractures, because the AIN fascicle lies posteriorly at the elbow and thus, is most prone to injury by the fracture. Such fascicular phenomena could also explain how proximal peroneal neuropathy can present as a deep peroneal neuropathy and how sciatic nerve injury may at times appear as a tibial or peroneal injury. Proximity to bone, less protective connective tissue sleeves, or uneven vaso nervorum ischemia are various mechanisms by which these observations may occur. There is indeed order in the morass.
Rules are made to be broken, and nerves are no exception. To neurosurgeons, the vestibular nerve traditionally has a superior and an inferior component, with schwannomas, for instance, arising from one or the other. Yet, careful examination of 20 vestibulocochlear nerves, obtained from 16 cadavers, failed to bear out a superior/inferior or any fascicular pattern.1 Following mastoidectomy to fully expose the cerebellopontine angle, the nerves were carefully removed and the superior and posterior aspects dyed different colors to permit identification after sectioning. Cross sections of the nerve varied in appearance along the course of the same nerve, and no cleavage plane could be appreciated to distinguish nerve divisions. Not surprisingly, the vestibular component remained distinct from the cochlear, although the spatial relationship between them varied along their course. For the most part, anatomically distinct divisions of the vestibular nerve do not exist despite arising from different nuclei. Fascicular phenomena exist and explain much. Curiously, they may not be present in all nerves. Michael Rubin
Dr. Rubin, Professor of Clinical Neurology, New York Presbyterian Hospital-Cornell Campus is Assistant Editor of Neurology Alert.
1. Terasaka S, et al. Neurosurgery. 2000;47:162-168.