Publications by authors named "John Arena"

Article Synopsis
  • The diagnosis of mTBI primarily relies on clinical symptoms and neuroimaging, but predicting poor recovery outcomes remains difficult due to a lack of early objective testing.
  • Recent research suggests that measuring the neurofilament light (NfL) protein in the serum may serve as a promising biomarker for assessing mTBI and that disruptions in the blood-brain barrier may play a key role in NfL dynamics.
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Objective: Fractures of the atlas are typically considered stable or unstable based on the integrity of the transverse ligament. Whereas stable Jefferson burst fractures can be treated nonoperatively, unstable fractures with disruption of the transverse ligament often require surgical intervention. Atlas osteosynthesis has been proposed as a motion-preserving alternative to atlantoaxial fusion.

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Objective: Surgical correction of adult spinal deformity (ASD) is associated with a high rate of hardware complication that can be challenging to predict. Hardware integrity and alignment after surgery are typically followed with standing radiography, where pedicle screw loosening may be incidentally identified but the clinical significance of which is often unclear. This study aimed to identify the incidence and implications of pedicle screw loosening at the upper instrumented vertebra (UIV) after surgical correction of ASD.

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Purpose: This study aimed to investigate the relationship of preoperative hemoglobin levels as an independent prognostic factor for hospital and intensive care unit (ICU) length of stay (LOS) in patients undergoing surgery for adult spinal deformity (ASD), with the intent of determining whether there exists a correlation and enhancing patient preoperative optimization protocols.

Methods: The authors reviewed consecutive patients who underwent elective thoracolumbosacral posterior spinal fusion (PSF) involving six or more vertebrae for ASD from January 1, 2013, to December 13, 2021, with a minimum follow-up period of two years. This study primarily investigated the association of preoperative hemoglobin levels with hospital and ICU LOS.

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Traumatic brain injury (TBI) often results in persistent learning and memory deficits, likely due to disrupted hippocampal circuitry underlying these processes. Precise temporal control of hippocampal neuronal activity is important for memory encoding and retrieval and is supported by oscillations that dynamically organize single unit firing. Using high-density laminar electrophysiology, we discovered a loss of oscillatory power across CA1 lamina, with a profound, layer-specific reduction in theta-gamma phase amplitude coupling in injured rats.

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Traumatic brain injury (TBI) remains a pervasive clinical problem associated with significant morbidity and mortality. However, TBI remains clinically and biophysically ill-defined, and prognosis remains difficult even with the standardization of clinical guidelines and advent of multimodality monitoring. Here we leverage a unique data set from TBI patients implanted with either intracranial strip electrodes during craniotomy or quad-lumen intracranial bolts with depth electrodes as part of routine clinical practice.

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Background: Ewing's sarcoma is an uncommon, aggressive malignancy that typically presents as an osseous lesion, most commonly in children and adolescents. Very rarely Ewing's sarcoma can present as an intradural extramedullary mass mimicking more common tumors.

Observations: A 32-year-old female had a left L3 nerve root-associated lesion identified in the setting of recent-onset radiculopathy.

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Objective: Augmented reality (AR) is an emerging technology that may accelerate skill acquisition and improve accuracy of thoracolumbar pedicle screw placements. We aimed to quantify the relative assistance of AR compared with freehand (FH) pedicle screw accuracy across different surgical experience levels.

Methods: A spine fellowship-trained and board-certified attending neurosurgeon, postgraduate year 4 neurosurgery resident, and second-year medical student placed 32 FH and 32 AR-assisted thoracolumbar pedicle screws in 3 cadavers.

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Background: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the CNS with a variety of clinical manifestations, including cerebral edema.

Case Summary: A 7-year-old boy presented with headaches, nausea, and somnolence. He was found to have cerebral edema that progressed to brainstem herniation.

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Lymphomatoid granulomatosis is an Epstein-Barr virus-associated lymphoproliferative B-cell neoplasm that typically involves multiple organ systems. This disease is exceedingly rare when confined to the central nervous system (CNS), usually presenting as a mass lesion or diffuse disease, with no existing standard of care. We present the case of a 67-year-old patient who had a unique and insidious course of isolated CNS lymphomatoid granulomatosis.

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Objectives: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an immune-mediated neuroinflammatory disorder leading to demyelination of the CNS. Interleukin (IL)-6 receptor blockade is under study in relapsing MOGAD as a preventative strategy, but little is known about the role of such treatment for acute MOGAD attacks.

Methods: We discuss the cases of a 7-year-old boy and a 15-year-old adolescent boy with severe acute CNS demyelination and malignant cerebral edema with early brain herniation associated with clearly positive serum titers of MOG-IgG, whose symptoms were incompletely responsive to standard acute therapies (high-dose steroids, IV immunoglobulins (IVIGs), and therapeutic plasma exchange).

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Background: The optimal time to restart direct oral anticoagulants (DOACs) for nonvalvular atrial fibrillation (NVAF) after traumatic intracranial hemorrhage (tICH) is unknown. Physicians must weigh the risk of recurrent hemorrhage against ischemic stroke. We investigated rates of stroke while holding anticoagulation, hemorrhage after anticoagulation resumption, and factors associated with the decision to restart anticoagulation.

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Damage to the microtubule lattice, which serves as a rigid cytoskeletal backbone for the axon, is a hallmark mechanical initiator of pathophysiology after concussion. Understanding the mechanical stress transfer from the brain tissue to the axonal cytoskeleton is essential to determine the microtubule lattice's vulnerability to mechanical injury. Here, we develop an ultrastructural model of the axon's cytoskeletal architecture to identify the components involved in the dynamic load transfer during injury.

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Tentorial margin arteriovenous malformations (AVMs) at the cerebello-mesencephalic fissure are deep lesions, which can be safely resected via a lateral supracerebellar infratentorial approach. This video illustrates the case of a patient who presented with hemorrhage from a tentorial AVM. He was managed in the hybrid neurovascular operating room with Onyx (Medtronic) embolization of a superior cerebellar artery feeder followed by resection of the AVM, which included cerebellar relaxation from lumbar cerebrospinal fluid (CSF) drainage and lateral positioning.

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Article Synopsis
  • Regeneration after spinal cord injury (SCI) is hindered by glial scars and inhibitory signals, but tissue engineering with micro-tissue engineered neural networks (micro-TENNs) shows potential for promoting nerve repair.
  • In a study involving 43 female rats, micro-TENNs containing sensory neurons were implanted across the injury site after a minimally invasive SCI model was created, demonstrating the survival of graft neurons and axonal growth.
  • The positive findings, including minimal trauma and scar formation, suggest that micro-TENNs could serve as a living bridge to enhance recovery following SCI, laying the groundwork for further research.
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Current diagnostic criteria for the neuropathological evaluation of the traumatic brain injury-associated neurodegeneration, chronic traumatic encephalopathy, define the pathognomonic lesion as hyperphosphorylated tau-immunoreactive neuronal and astroglial profiles in a patchy cortical distribution, clustered around small vessels and showing preferential localization to the depths of sulci. However, despite adoption into diagnostic criteria, there has been no formal assessment of the cortical distribution of the specific cellular components defining chronic traumatic encephalopathy neuropathologic change. To address this, we performed comprehensive mapping of hyperphosphorylated tau-immunoreactive neurofibrillary tangles and thorn-shaped astrocytes contributing to chronic traumatic encephalopathy neuropathologic change.

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Objective: We studied the risk of associated spinal and nonspinal injuries (NSIs) in the setting of observed thoracolumbar transverse process fracture (TPF) and examined the clinical management of TPF.

Methods: Patients treated at a Level I trauma center over a 5-year period were screened for thoracolumbar TPF. Prevalence of associated spinal fractures and NSIs as well as relationship to level of TPF was explored.

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While hippocampal-dependent learning and memory are particularly vulnerable to traumatic brain injury (TBI), the functional status of individual hippocampal neurons and their interactions with oscillations are unknown following injury. Using the most common rodent TBI model and laminar recordings in CA1, we found a significant reduction in oscillatory input into the radiatum layer of CA1 after TBI. Surprisingly, CA1 neurons maintained normal firing rates despite attenuated input, but did not maintain appropriate synchronization with this oscillatory input or with local high-frequency oscillations.

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Traumatic brain injury (TBI) is a risk factor for neurodegenerative disease, including chronic traumatic encephalopathy (CTE). Preliminary consensus criteria define the pathognomonic lesion of CTE as patchy tau pathology within neurons and astrocytes at the depths of cortical sulci. However, the specific tau isoform composition and post-translational modifications in CTE remain largely unexplored.

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Diffuse axonal injury (DAI) is an important consequence of traumatic brain injury (TBI). At the moment of trauma, axons rarely disconnect, but undergo cytoskeletal disruption and transport interruption leading to protein accumulation within swellings. The amyloid precursor protein (APP) accumulates rapidly and the standard histological evaluation of axonal pathology relies upon its detection.

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Although millions of individuals suffer a traumatic brain injury (TBI) worldwide each year, it is only recently that TBI has been recognized as a major public health problem. Beyond the acute clinical manifestations, there is growing recognition that a single severe TBI (sTBI) or repeated mild TBIs (rTBI) can also induce insidious neurodegenerative processes, which may be associated with early dementia, in particular chronic traumatic encephalopathy (CTE). Identified at autopsy examination in individuals with histories of exposure to sTBI or rTBI, CTE is recognized as a complex pathology featuring both macroscopic and microscopic abnormalities.

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Chronic traumatic encephalopathy (CTE) is associated with repetitive mild traumatic brain injury (mTBI) in the context of contact and collision sports, but not all exposed individuals develop this condition. In addition, experiments in animal models in several laboratories have shown that non-transgenic mice do not develop tauopathy after exposure to repetitive mTBI schedules. It is thus reasonable to assume that genetic factors may play an etiological role in the development of CTE.

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Repetitive mild traumatic brain injury (mTBI) is implicated in chronic neurological illness. The development of animal models of repetitive mTBI in mice is essential for exploring mechanisms of these chronic diseases, including genetic vulnerability by using transgenic backgrounds. In this study, the rat model of impact acceleration (IA) was redesigned for the mouse cranium and used in two clinically relevant repetitive mTBI paradigms.

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