Attitudes and opinions of US neurosurgical residents toward research and scholarship: a national survey.

OBJECTIVE: The analysis of resident research productivity in neurosurgery has gained significant recent interest. Resident scholarly output affects departmental productivity, recruitment of future residents, and likelihood of future research careers. To maintain and improve opportunities for resident research, the authors evaluated factors that affect resident attitudes toward neurosurgical research on a national level. METHODS: An online survey was distributed to all US neurosurgical residents. Questions assessed interest in research, perceived departmental support of research, and resident-perceived limitations in pursuing research. Residents were stratified based on number of publications above the median (AM; ≥ 14) or below the median (BM; < 14) for evaluation of factors influencing productivity. RESULTS: A total of 278 resident responses from 82 US residency programs in 30 states were included (a 20% overall response rate). Residents predominantly desired future academic positions (53.2%), followed by private practice with some research (40.3%). Residents reported a mean ± SD of 11 ± 14 publications, which increased with postgraduate year level. The most common type of research involved retrospective cohort studies (24%) followed by laboratory/benchtop (19%) and case reports (18%). Residents as a group spent on average 14.1 ± 18.5 hours (median 7.0 hours) a week on research. Most residents (53.6%) had ≥ 12 months of protected research time. Mentorship (92.4%), research exposure (89.9%), and early interest in science (78.4%) had the greatest impact on interest in research while the most limiting factors were time (91.0%), call scheduling (47.1%), and funding/grants (37.1%). AM residents cited research exposure (p = 0.003), neurosurgery conference exposure (p = 0.02), formal research training prior to residency (p = 0.03), internal funding sources (p = 0.05), and software support (p = 0.02) as most important for their productivity. Moreover, more productive residents applied and received a higher number of < $10,000 and ≥ $10,000 grants (p < 0.05). A majority of residents (82.4%) agreed or strongly agreed with pursuing research throughout their professional careers. Overall, about half of residents (49.6%) were encouraged toward continued neurosurgical research, while the rest were neutral (36.7%) or discouraged (13.7%). Free-text responses helped to identify solutions on a departmental, regional, and national level that could increase interest in neurosurgical research. CONCLUSIONS: This survey evaluates various factors affecting resident views toward research, which may also be seen in other specialties. Residents remain enthusiastic about neurosurgical research and offer several solutions to the ever-scarce commodities of time and funding within academic medicine.

Increased chondroitin sulfate proteoglycan expression in denervated brainstem targets following spinal cord injury creates a barrier to axonal regeneration overcome by chondroitinase ABC and neurotrophin-3.

Increased chondroitin sulfate proteoglycan (CSPG) expression in the vicinity of a spinal cord injury (SCI) is a primary participant in axonal regeneration failure. However, the presence of similar increases of CSPG expression in denervated synaptic targets well away from the primary lesion and the subsequent impact on regenerating axons attempting to approach deafferented neurons have not been studied. Constitutively expressed CSPGs within the extracellular matrix and perineuronal nets of the adult rat dorsal column nuclei (DCN) were characterized using real-time PCR, Western blot analysis and immunohistochemistry. We show for the first time that by 2 days and through 3 weeks following SCI, the levels of NG2, neurocan and brevican associated with reactive glia throughout the DCN were dramatically increased throughout the DCN despite being well beyond areas of trauma-induced blood brain barrier breakdown. Importantly, regenerating axons from adult sensory neurons microtransplanted 2 weeks following SCI between the injury site and the DCN were able to regenerate rapidly within white matter (as shown previously by Davies et al. [Davies, S.J., Goucher, D.R., Doller, C., Silver, J., 1999. Robust regeneration of adult sensory axons in degenerating white matter of the adult rat spinal cord. J. Neurosci. 19, 5810-5822]) but were unable to enter the denervated DCN. Application of chondroitinase ABC or neurotrophin-3-expressing lentivirus in the DCN partially overcame this inhibition. When the treatments were combined, entrance by regenerating axons into the DCN was significantly augmented. These results demonstrate both an additional challenge and potential treatment strategy for successful functional pathway reconstruction after SCI.

Chondroitinase ABC digestion of the perineuronal net promotes functional collateral sprouting in the cuneate nucleus after cervical spinal cord injury.

Upregulation of extracellular chondroitin sulfate proteoglycans (CSPGs) after CNS injuries contributes to the impediment of functional recovery by restricting both axonal regeneration and synaptic plasticity. In the present study, the effect of degrading CSPGs with the application of the bacterial enzyme chondroitinase ABC (chABC) into the cuneate nucleus of rats partially denervated of forepaw dorsal column axons was examined. A dorsal column transection between the C6-C7 dorsal root entry zones was followed immediately by an ipsilateral brainstem injection of either chABC or a bacterial-derived control enzyme [penicillinase (P-ase)] and then subsequently (1 week later) followed with a second brainstem enzyme injection and cholera toxin B subunit (CTB) tracer injection into the ipsilateral forepaw digits and pads. After 1 additional week, the rats underwent electrophysiological receptive field mapping of the cuneate nucleus and/or anatomical evaluation. Examination of the brainstems of rats from each group revealed that CSPGs had been reduced after chABC treatment. Importantly, in the chABC-treated rats (but not in the P-ase controls), a significantly greater area of the cuneate nucleus was occupied by physiologically active CTB traced forepaw afferents that had been spared by the initial cord lesion. These results demonstrate, for the first time, a functional change directly linked to anatomical evidence of sprouting by spinal cord afferents after chABC treatment.