André Feil (1884–1955) was a French physician best recognized for his description, coauthored with Maurice Klippel, of patients with congenital fusion of cervical vertebrae, a condition currently known as Klippel-Feil syndrome. However, little is known about his background aside from the fact that he was a student of Klippel and a physician who took a keen interest in describing congenital anomalies. Despite the relative lack of information on Feil, his contributions to the fields of spinal disease and teratology extended far beyond science to play an integral role in changing the misguided perception shrouding patients with disfigurements, defects, deformities, and so-called monstrous births. In particular, Feil's 1919 medical school thesis on cervical abnormalities was a critical publication in defying long-held theory and opinion that human “monstrosities,” anomalies, developmental abnormalities, and altered congenital physicality were a consequence of sinful behavior or a reversion to a primitive state. Indeed, his thesis on a spinal deformity centering on his patient, L. Joseph, was at the vanguard for a new view of a patient as nothing less than fully human, no matter his or her physicality or appearance.
Evgenii Belykh, Kashif Malik, Isabelle Simoneau, Kaan Yagmurlu, Ting Lei, Daniel D. Cavalcanti, Vadim A. Byvaltsev, Nicholas Theodore and Mark C. Preul
Sam Safavi-Abbasi, Adrian J. Maurer, Jacob B. Archer, Ricardo A. Hanel, Michael E. Sughrue, Nicholas Theodore and Mark C. Preul
During his lifetime and a career spanning 42 years, James Watson Kernohan made numerous contributions to neuropathology, neurology, and neurosurgery. One of these, the phenomenon of ipsilateral, false localizing signs caused by compression of the contralateral cerebral peduncle against the tentorial edge, has widely become known as “Kernohan's notch” and continues to bear his name. The other is a grading system for gliomas from a neurosurgical viewpoint that continues to be relevant for grading of glial tumors 60 years after its introduction. In this paper, the authors analyze these two major contributions in detail within the context of Kernohan's career and explore how they contributed to the development of neurosurgical procedures.
Abstracts of the 2013 Annual Meeting of the AANS/CNS Section on Disorders of the Spine and Peripheral Nerves
Phoenix, Arizona • March 6–9, 2013
Rachid Assina, Tejas Sankar, Nicholas Theodore, Sam P. Javedan, Alan R. Gibson, Kris M. Horn, Michael Berens, Volker K. H. Sonntag and Mark C. Preul
Axonal regeneration may be hindered following spinal cord injury (SCI) by a limited immune response and insufficient macrophage recruitment. This limitation has been partially surmounted in small-mammal models of SCI by implanting activated autologous macrophages (AAMs). The authors sought to replicate these results in a canine model of partial SCI.
Six dogs underwent left T-13 spinal cord hemisection. The AAMs were implanted at both ends of the lesion in 4 dogs, and 2 other dogs received sham implantations of cell media. Cortical motor evoked potentials (MEPs) were used to assess electrophysiological recovery. Functional motor recovery was assessed with a modified Tarlov Scale. After 9 months, animals were injected with wheat germ agglutinin–horseradish peroxidase at L-2 and killed for histological assessment.
Three of the 4 dogs that received AAM implants and 1 of the 2 negative control dogs showed clear recovery of MEP response. Behavioral assessment showed no difference in motor function between the AAM-treated and control groups. Histological investigation with an axonal retrograde tracer showed neither local fiber crossing nor significant uptake in the contralateral red nucleus in both implanted and negative control groups.
In a large-animal model of partial SCI treated with implanted AAMs, the authors saw no morphological or histological evidence of axonal regeneration. Although they observed partial electrophysiological and functional motor recovery in all dogs, this recovery was not enhanced in animals treated with implanted AAMs. Furthermore, there was no morphological or histological evidence of axonal regeneration in animals with implants that accounted for the observed recovery. The explanation for this finding is probably multifactorial, but the authors believe that the AAM implantation does not produce axonal regeneration, and therefore is a technology that requires further investigation before it can be clinically relied on to ameliorate SCI.
Eric M. Horn, Nicholas Theodore, Rachid Assina, Robert F. Spetzler, Volker K. H. Sonntag and Mark C. Preul
Venous stasis and intrathecal hypertension are believed to play a significant role in the hypoperfusion present in the spinal cord following injury. Lowering the intrathecal pressure via cerebrospinal fluid (CSF) drainage has been effective in treating spinal cord ischemia during aorta surgery. The purpose of the present study was to determine whether CSF drainage increases spinal cord perfusion and improves outcome after spinal injury in an animal model.
Anesthetized adult rabbits were subjected to a severe contusion spinal cord injury (SCI). Cerebrospinal fluid was then drained via a catheter to lower the intrathecal pressure by 10 mm Hg. Tissue perfusion was assessed at the site of injury, and values obtained before and after CSF drainage were compared. Two other cohorts of animals were subjected to SCI: 1 group subsequently underwent CSF drainage and the other did not. Results of histological analysis, motor evoked potential and motor function testing were compared between the 2 cohorts at 4 weeks postinjury.
Cerebrospinal fluid drainage led to no significant improvement in spinal cord tissue perfusion. Four weeks after injury, the animals that underwent CSF drainage demonstrated significantly smaller areas of tissue damage at the injury site. There were no differences in motor evoked potentials or motor score outcomes at 4 weeks postinjury.
Cerebrospinal fluid drainage effectively lowers intrathecal pressure and decreases the amount of tissue damage in an animal model of spinal cord injury. Further studies are needed to determine whether different draining regimens can improve motor or electrophysiological outcomes.
Nicholas C. Bambakidis, John Butler, Eric M. Horn, Xukui Wang, Mark C. Preul, Nicholas Theodore, Robert F. Spetzler and Volker K. H. Sonntag
✓ The development of an acute traumatic spinal cord injury (SCI) inevitably leads to a complex cascade of ischemia and inflammation that results in significant scar tissue formation. The development of such scar tissue provides a severe impediment to neural regeneration and healing with restoration of function. A multimodal approach to treatment is required because SCIs occur with differing levels of severity and over different lengths of time. To achieve significant breakthroughs in outcomes, such approaches must combine both neuroprotective and neuroregenerative treatments. Novel techniques modulating endogenous stem cells demonstrate great promise in promoting neuroregeneration and restoring function.
Sam Safavi-Abbasi, Leonardo B. C. Brasiliense, Ryan K. Workman, Melanie C. Talley, Iman Feiz-Erfan, Nicholas Theodore, Robert F. Spetzler and Mark C. Preul
✓In 25 years, the Mongolian army of Genghis Khan conquered more of the known world than the Roman Empire accomplished in 400 years of conquest. The recent revised view is that Genghis Khan and his descendants brought about “pax Mongolica” by securing trade routes across Eurasia. After the initial shock of destruction by an unknown barbaric tribe, almost every country conquered by the Mongols was transformed by a rise in cultural communication, expanded trade, and advances in civilization. Medicine, including techniques related to surgery and neurological surgery, became one of the many areas of life and culture that the Mongolian Empire influenced.
Implications of his work for the understanding of cerebrovascular pathology and stroke
Sam Safavi-Abbasi, Cassius Reis, Melanie C. Talley, Nicholas Theodore, Peter Nakaji, Robert F. Spetzler and Mark C. Preul
✓ The history of apoplexy and descriptions of stroke symptoms date back to ancient times. It was not until the mid-nineteenth century, however, that the contributions of Rudolf Ludwig Karl Virchow, including his descriptions of the phenomena he called “embolism” and “thrombosis” as well as the origins of ischemia, changed the understanding of stroke. He suggested three main factors that conduce to venous thrombosis, which are now known as the Virchow triad. He also showed that portions of what he called a “thrombus” could detach and form an “embolus.” Thus, Virchow coined these terms to describe the pathogenesis of the disorder. It was also not until 1863 that Virchow recognized and differentiated almost all of the common types of intracranial malformations: telangiectatic venous malformations, arterial malformations, arteriovenous malformations, cystic angiomas (possibly what are now called hemangioblastomas), and transitional types of these lesions. This article is a review of the contributions of Rudolf Virchow to the current understanding of cerebrovascular pathology, and a summary of the life of this extraordinary personality in his many roles as physician, pathologist, anthropologist, ethnologist, and politician.
Nicholas C. Bambakidis, Nicholas Theodore, Peter Nakaji, Adrian Harvey, Volker K. H. Sonntag, Mark C. Preul and Robert H. Miller
The continuous regeneration of glial cells arising from endogenous stem cell populations in the central nervous system (CNS) occurs throughout life in mammals. In the ongoing research to apply stem cell therapy to neurological diseases, the capacity to harness the multipotential ability of endogenous stem cell populations has become apparent. Such cell populations proliferate in response to a variety of injury states in the CNS, but in the absence of a supportive microenvironment they contribute little to any significant behavioral recovery. In the authors' laboratory and elsewhere, recent research on the regenerative potential of these stem cells in disease states such as spinal cord injury has demonstrated that the cells' proliferative potential may be greatly upregulated in response to appropriate growth signals and exogenously applied trophic factors. Further understanding of the potential of such multipotent cells and the mechanisms responsible for creating a favorable microenvironment for them may lead to additional therapeutic alternatives in the setting of neurological diseases. These therapies would require no exogenous stem cell sources and thus would avoid the ethical and moral considerations regarding their use. In this review the authors provide a brief overview of the enhancement of endogenous stem cell proliferation following neurological insult.