I grew up in New York City where I attended the oldest school in the Country, Collegiate, from 2nd grade to high school.  I then went to college at Harvard, receiving both a BA and MA, and Medical School at Yale.  Along the way I did graduate work in Neurobiology at Stanford.  I then returned to New York City and did an internship and neurosurgical residency at the Neurological Institute.  I was then given a wonderful opportunity to do a one year traveling Peripheral Nerve Fellowship in which I spent time at the University of Toronto in Canada and time at Louisiana State University in New Orleans.  I then joined the Department of Neurosurgery at the University of Washington in Seattle.  There between 1991 and 2011 I rose through the academic ranks eventually becoming a Professor and Director of the Peripheral Nerve Center, as well as Acting Head of the section of neurosurgery at the Puget Sound VA Health Care System.  I then moved to UCSF in 2012 where I headed up their peripheral nerve effort and established their Center for Evaluation and Surgical Management of Peripheral Nerve Disorders.  In the summer of 2014 I moved to join the Department of Neurosurgery at Northwestern University Feinberg School of Medicine as Professor and Director of the Peripheral Nerve Center.  During the past year I was asked to serve as interim Chair of the Department of Neurosurgery when the Chair, a close friend and colleague, suddenly died.  At Northwestern I continue to pursue and develop my interests in the following areas:  pushing the frontiers of peripheral nerve surgery by pioneering new imaging and surgical techniques; teaching residents and medical students; collaborating with clinical and research colleagues; and continuing my ongoing interest in biotechnology by taking ideas from their inception into the clinical arena.  I am currently working part-time in the Dept of Neurosurgery at Stanford.  I remain very interested in finding ways to use the internet as a platform to educate patients and improve their care.  I also am dedicated to improving the overall patient experience.

Clinical Focus

  • The evaluation and treatment of peripheral nerve disorders.
  • Simple and complex nerve entrapment syndromes.
  • Peripheral nerve tumors both benign (eg Schwannomas and Neurofibromas) and malignant.
  • Peripheral nerve massess such as ganglion cysts.
  • Traumatic peripheral nerve injuries.
  • Diagnostic nerve biopsies.
  • Neurological Surgery

Academic Appointments

Administrative Appointments

  • Clinical Professor & Co-Director of Peripheral Nerve Center, Stanford Department of Neurosurgery (2016 - Present)

Professional Education

  • Board Certification: Neurological Surgery, American Board of Neurological Surgery (1996)
  • Fellowship: Louisiana State University GME Office (1991) LA
  • Fellowship: University of Toronto (1990) Canada
  • Residency: Columbia University Medical Center (1990) NY
  • Residency: Columbia and New York Presbyterian General Surgery Residency (1985) NY
  • Medical Education: Yale School of Medicine (1984) CT
  • BA, Harvard College, Biology (1977)
  • MA, Harvard University, Neurobiology (1977)

All Publications

  • Peripheral nerve diffusion tensor imaging as a measure of disease progression in ALS. Journal of neurology Simon, N. G., Lagopoulos, J., Paling, S., Pfluger, C., Park, S. B., Howells, J., Gallagher, T., Kliot, M., Henderson, R. D., Vucic, S., Kiernan, M. C. 2017


    Clinical trial design in amyotrophic lateral sclerosis (ALS) remains hampered by a lack of reliable and sensitive biomarkers of disease progression. The present study evaluated peripheral nerve diffusion tensor imaging (DTI) as a surrogate marker of axonal degeneration in ALS. Longitudinal studies were undertaken in 21 ALS patients studied at 0 and 3 months, and 19 patients at 0, 3 and 6 months, with results compared to 13 age-matched controls. Imaging metrics were correlated across a range of functional assessments including amyotrophic lateral sclerosis functional rating scale revised (ALSFRS-R), lower limb muscle strength (Medical Research Council sum score, MRCSS-LL), compound muscle action potential amplitudes and motor unit number estimation (MUNE). Fractional anisotropy was reduced at baseline in ALS patients in the tibial (p < 0.05), and peroneal nerve (p < 0.05). Fractional anisotropy and axial diffusivity declined in the tibial nerve between baselines, 3- and 6-month scans (p < 0.01). From a functional perspective, ALSFRS-R correlated with fractional anisotropy values from tibial (R = 0.75, p < 0.001) and peroneal nerves (R = 0.52, p = 0.001). Similarly, peroneal nerve MUNE values correlated with fractional anisotropy values from the tibial (R = 0.48, p = 0.002) and peroneal nerve (R = 0.39, p = 0.01). There were correlations between the change in ALSFRS-R and tibial nerve axial diffusivity (R = 0.38, p = 0.02) and the change in MRCSS-LL and peroneal nerve fractional anisotropy (R = 0.44, p = 0.009). In conclusion, this study has demonstrated that some peripheral nerve DTI metrics are sensitive to axonal degeneration in ALS. Further, that DTI metrics correlated with measures of functional disability, strength and neurophysiological measures of lower motor neuron loss.

    View details for DOI 10.1007/s00415-017-8443-x

    View details for PubMedID 28265751



    Studies of albino rodents have shown that an absence of pigment in the developing optic stalk may alter the position of the first retinal fibers that grow toward the brain, thereby disrupting the gross topographic relationship of fibers in the nerve (Silver and Sapiro: J. Comp. Neurol. 202:521-538, '81). The abnormalities associated with albinism are more extensive in the Siamese cat than-in previously studied species. Therefore, any abnormalities in differentiation of the stalk and axon guidance may be more readily detected. To investigate the guidance and/or misguidance of optic axons, light and electron microscope analyses were made of serial sections through the optic stalk in normally pigmented and Siamese fetal cats. On E20, before axons enter the optic stalk, the only clear morphological distinction between Siamese and normal cats is the distribution of pigment in the stalk. Pigment is found in the dorsal stalk cells of the normal cat for 200 microns from the optic disc. Although the retinal pigment epithelium of the Siamese optic stalk. By E23 axons invade the ventral optic stalk in both strains. Concurrent with the early stages of axonal exit from the retina, there is complete separation of the stalk's dorsal and ventral tiers. As the cleavage occurs, basal lamina invaginates into the zone of separation following along the plane of the old lumen. The ventral stalk fills with axons while the dorsal tier is shed gradually. In contrast, in the Siamese cat, dorsal stalk cells are not sloughed off properly and instead are incorporated ectopically into the nerve. Basal lamina invagination is irregular. Axons do not fill the Siamese stalk symmetrically but enter the region of ectopic cells, which in turn disrupts gross fiber position. Usually, in the mutant, axons originating from the retina temporal to the optic fissure are those that invade the dorsal tier of ectopic cells. The altered position of optic axons in the mutant stalk may provide an explanation for the chiasmatic misrouting of optic axons in this species.

    View details for Web of Science ID A1988M603300008

    View details for PubMedID 3372729



    In the visual system of Siamese cats, the lateral geniculate nucleus (LGN) receives an abnormally large projection from the contralateral eye and a correspondingly reduced projection from the ipsilateral eye. In order to determine how this abnormal pattern of retinal input arises, the prenatal development of the retinogeniculate projection was studied in Siamese cats using the anterograde transport of intraocularly injected [3H]leucine and horseradish peroxidase. Labeled axons from the ipsilateral eye can be detected in the optic tract by embryonic day 30 (E30; gestation is 65 days), several days later than found in normally pigmented animals. The ipsilateral projection is not only apparently delayed but also is reduced in size as compared with normal animals, and this reduction persists throughout development, indicating that the Siamese mutation acts to misdirect growing optic axons to the contralateral side of the brain as originally proposed (Guillery, R. W. (1969) Brain Res. 14: 739-741). The effect of an altered retinal projection on the ingrowth and segregation of retinal fibers to the LGN was also examined. In Siamese fetuses, not until E41 can significant label be seen within the ipsilateral LGN as compared to E35 in normally pigmented fetuses. As in normal animals, in Siamese fetuses, also, the labeled retinogeniculate afferents from the two eyes initially overlap within regions of the LGN before segregating into layers. However, measurements of the area occupied by labeled afferents from the ipsilateral and contralateral eyes indicate that maximum overlap of the two sets of afferents, although close to normal in amount, does not occur until about E51--again several days later than in normally pigmented animals (E47). The time course of segregation is also altered in Siamese cats. The onset of segregation, as signaled by the removal of contralateral eye afferents from territory destined for the ipsilateral eye and by the restriction of ipsilateral eye afferents, does not occur until about E51 in Siamese cats as compared with E47 in normally pigmented animals. Despite this delay in onset, the final segregation of the two sets of afferents in Siamese cats reaches adult-like levels at about the normal time. Thus, the misrouting of axons at the optic chiasm in Siamese cats not only alters the final pattern of innervation from the two eyes within the LGN, but also delays the onset and shortens the total duration of segregation itself.

    View details for Web of Science ID A1985ASM4200008

    View details for PubMedID 2995604


    View details for Web of Science ID A1982PT23900047

    View details for PubMedID 7144904