Faculty Bibliography

BACKGROUND:Public awareness of concussion has grown significantly over the past 2 decades, driven largely by media coverage of sports-related injuries. This has paralleled a rise in traumatic brain injury (TBI)-related emergency department visits, underscoring the need for specialized concussion care centers. Despite this, most existing programs focus on sports or pediatric populations, leaving critical care gaps. RECENT FINDINGS/RESULTS:The NYU Langone Concussion Center was established in 2013 to address these gaps by providing interdisciplinary care for both sports-related and non-sports-related concussions. Approximately 60% of cases seen at the center are not sports related. This article outlines the center's inception, operational model, patient demographics, and evolution over the past decade. IMPLICATIONS FOR PRACTICE/CONCLUSIONS:Lessons learned from the NYU Langone model offer valuable guidance for developing comprehensive concussion programs that can serve diverse urban populations. Key strategies include cross-specialty collaboration, flexible infrastructure, and systems-level integration to address heterogeneous mechanisms of injury and outcomes.

Diabetic neuropathy is a debilitating disorder characterized by spontaneous and mechanical pain. The role of skin mechanoreceptors in the development of mechanical pain (allodynia) is unclear. We discovered that mice with diabetic neuropathy had decreased sirtuin 1 (SIRT1) deacetylase activity in foot skin, leading to reduced expression of brain-derived neurotrophic factor (BDNF) and subsequent loss of innervation in Meissner corpuscles, a mechanoreceptor expressing the BDNF receptor TrkB. When SIRT1 was depleted from skin, the mechanical allodynia worsened in diabetic neuropathy mice, likely due to retrograde degeneration of the Meissner-corpuscle innervating Aβ axons and aberrant formation of Meissner corpuscles which may have increased the mechanosensitivity. The same phenomenon was also noted in skin BDNF knockout mice. Furthermore, overexpression of SIRT1 in skin induced Meissner corpuscle reinnervation and regeneration, resulting in significant improvement of diabetic mechanical allodynia. Overall, the findings suggested that skin-derived SIRT1 and BDNF function in the same pathway in skin sensory apparatus regeneration and highlighted the potential of developing topical SIRT1-activating compounds as a novel treatment for diabetic mechanical allodynia.

Diabetic neuropathy is a debilitating disorder characterized by spontaneous and mechanical allodynia. The role of skin mechanoreceptors in the development of mechanical allodynia is unclear. We discovered that mice with diabetic neuropathy had decreased sirtuin 1 (SIRT1) deacetylase activity in foot skin, leading to reduced expression of brain-derived neurotrophic factor (BDNF) and subsequent loss of innervation in Meissner corpuscles, a mechanoreceptor expressing the BDNF receptor TrkB. When SIRT1 was depleted from skin, the mechanical allodynia worsened in diabetic neuropathy mice, likely due to retrograde degeneration of the Meissner-corpuscle innervating Aβ axons and aberrant formation of Meissner corpuscles which may have increased the mechanosensitivity. The same phenomenon was also noted in skin-keratinocyte specific BDNF knockout mice. Furthermore, overexpression of SIRT1 in skin induced Meissner corpuscle reinnervation and regeneration, resulting in significant improvement of diabetic mechanical allodynia. Overall, the findings suggested that skin-derived SIRT1 and BDNF function in the same pathway in skin sensory apparatus regeneration and highlighted the potential of developing topical SIRT1-activating compounds as a novel treatment for diabetic mechanical allodynia.

PURPOSE:The purpose of this case report is to present the cases of 2 boys with benign paroxysmal positional vertigo (BPPV). KEY POINTS:Patient A (11 years old) and Patient B (9 years old) had complaints of vertigo with position changes. Both exhibited left torsion upbeating nystagmus in the left Dix-Hallpike (DH) test and complaints of vertigo with reproduction of their symptoms, indicating BPPV. Both were treated with a left canalith repositioning maneuver and reported decreased incidence of positional vertigo upon reevaluation. Scores on the Dizziness Handicap Inventory and the Visual Analog Scale for Dizziness decreased after treatment for 1 of the boys. CONCLUSION:Benign paroxysmal positional vertigo is considered rare in children. Migraines may also cause vertigo. Differential diagnosis in these cases was made by performing the DH test. RECOMMENDATIONS FOR CLINICAL PRACTICE:Children with vertigo should be screened for BPPV through use of history taking, and the DH test.