Publications by authors named "Daryl P Fields"

A century of research established that GABA inhibits proprioceptive inputs presynaptically to sculpt spinal neural inputs into skilled motor output. Recent results in mice challenged this theory by showing that GABA can also facilitate action potential conduction in proprioceptive afferents. Here, we tackle this controversy in monkeys, the most human-relevant animal model, and show that GABA receptors (GABARs) indeed facilitate sensory inputs to spinal motoneurons and interneurons and that this mechanism also influences sensory transmission to supraspinal centers.

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Background: Proper documentation is essential for patient care. The popularity of artificial intelligence (AI) offers the potential for improvements in neurosurgical note-writing. This study aimed to assess how AI can optimize documentation in neurosurgical procedures.

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Article Synopsis
  • Spinal cord hypoperfusion negatively impacts recovery after severe spinal cord injuries, and new guidelines advocate for cerebrospinal fluid (CSF) drainage to help mitigate this issue shortly after the injury.* -
  • The study compared two CSF drainage methods in patients with varying degrees of spinal cord injury: one that drains only when spinal cord perfusion pressure (SCPP) falls below 65 mmHg (reactive) and another that drains a small amount of CSF every hour (empiric).* -
  • Results showed that empiric CSF drainage significantly reduced the occurrence of critical hypoperfusion under 50 mmHg, suggesting a more proactive approach is beneficial for patient outcomes.*
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 Expandable transforaminal interbody fusion (TLIF) devices have been developed to introduce more segmental lordosis through a narrow operative corridor, but there are concerns about the degree of achievable correction with a small graft footprint. In this report, we describe the technical nuances associated with placing bilateral expandable cages for correction of iatrogenic deformity.  A 60-year-old female with symptomatic global sagittal malalignment and a severe lumbar kyphotic deformity after five prior lumbar surgeries presented to our institution.

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Spinal serotonin enables neuro-motor recovery (i.e., plasticity) in patients with debilitating paralysis.

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Background And Objectives: Nearly 30% of older adults presenting with isolated spine fractures will die within 1 year. Attempts to ameliorate this alarming statistic are hindered by our inability to identify relevant risk factors. The primary objective of this study was to develop a prediction model that identifies feasible targets to limit 1-year mortality.

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Article Synopsis
  • Correctly choosing the uppermost instrumented vertebra (UIV) during surgery for adult spinal deformity (ASD) significantly affects patient outcomes and quality of life.
  • Factors influencing UIV selection include preoperative spinal alignment, patient health conditions, and the surgeon's experience and available resources.
  • Research indicates that optimizing UIV selection can improve deformity correction and lower the risk of complications like proximal junctional kyphosis, although the impact on postoperative quality of life remains unclear.
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Objective: The objective was to evaluate the efficacy, outcomes, and complications of surgical intervention performed within 24 hours (≤ 24 hours) versus after 24 hours (> 24 hours) in managing acute traumatic central cord syndrome (ATCCS).

Methods: Articles pertinent to the study were retrieved from PubMed, Scopus, Web of Science, and Cochrane. The authors performed a systematic review and meta-analysis of treatment procedures and outcomes according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRIMSA) guidelines.

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Background: Preoperative symptom severity in cervical spondylotic myelopathy (CSM) can be variable. Radiomic signatures could provide an imaging biomarker for symptom severity in CSM. This study utilizes radiomic signatures of T1-weighted and T2-weighted magnetic resonance imaging images to correlate with preoperative symptom severity based on modified Japanese Orthopaedic Association (mJOA) scores for patients with CSM.

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Sensory input flow is central to voluntary movements. For almost a century, GABA was believed to modulate this flow by inhibiting sensory axons in the spinal cord to sculpt neural inputs into skilled motor output. Instead, here we show that GABA can also facilitate sensory transmission in monkeys and consequently increase spinal and cortical neural responses to sensory inputs challenging our understanding of generation and perception of movement.

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Rudimentary meningoceles of the spine with dural extension are very rare and warrant surgical excision to prevent infection and long-term neurological deficits in pediatric patients. We present the case of a 5-month-old infant with a tethered spinal cord secondary to a rudimentary meningocele. The patient presented shortly after birth with a midline cervical dimple that was evaluated for a suspected dermal sinus tract.

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Spinal cord stimulation (SCS) restores motor control after spinal cord injury (SCI) and stroke. This evidence led to the hypothesis that SCS facilitates residual supraspinal inputs to spinal motoneurons. Instead, here we show that SCS does not facilitate residual supraspinal inputs but directly triggers motoneurons action potentials.

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Background: A clinical concern exists that pediatric patients with whiplash-associated disorder (WAD) might have missed structural injuries or, alternatively, subsequently develop structural injuries over time, despite initially negative imaging findings. The primary objective of this study is to assess follow-up imaging usage for pediatric patients presenting with WAD.

Methods: A retrospective review of 444 pediatric patients presenting to a level 1 pediatric trauma hospital from January 1, 2010 to December 31, 2019 was performed.

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Introduction: Lateral anterior column release (ACR) is a minimally invasive option for the correction of sagittal plane deformity. To assemble a homogeneous picture of published research on ACR, an advanced bibliometric analysis was conducted to compile the top-ten most-cited articles on the topic of ACR.

Methods: A keyword search using the Thomson Reuters Web of Knowledge was conducted to identify articles discussing the role of lateral ACR.

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Cerebral strokes can disrupt descending commands from motor cortical areas to the spinal cord, which can result in permanent motor deficits of the arm and hand. However, below the lesion, the spinal circuits that control movement remain intact and could be targeted by neurotechnologies to restore movement. Here we report results from two participants in a first-in-human study using electrical stimulation of cervical spinal circuits to facilitate arm and hand motor control in chronic post-stroke hemiparesis ( NCT04512690 ).

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Reductions in respiratory-related synaptic inputs to inspiratory motor neurons initiate a form of plasticity that proportionally enhances inspiratory motor output, even in the absence of changing blood gases. This form of plasticity is known as inactivity-induced inspiratory motor facilitation (iMF). iMF triggered by brief, recurrent reductions in respiratory neural activity requires local retinoic acid (RA) synthesis, but receptor subtypes activated by RA are unknown.

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Acute intermittent hypoxia (AIH) elicits phrenic motor plasticity via multiple distinct cellular mechanisms. With moderate AIH, phrenic motor facilitation (pMF) requires G protein-coupled serotonin type 2 receptor activation, ERK MAP kinase activity, and new synthesis of brain-derived neurotrophic factor. In contrast, severe AIH elicits pMF by an adenosine-dependent mechanism that requires exchange protein activated by cAMP, Akt, and mammalian target of rapamycin (mTOR) activity, followed by new tyrosine receptor kinase B protein synthesis; this same pathway is also initiated by G protein-coupled serotonin 7 receptors (5-HT).

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Key Points: Intermittent reductions in respiratory neural activity, a characteristic of many ventilatory disorders, leads to inadequate ventilation and arterial hypoxia. Both intermittent reductions in respiratory neural activity and intermittent hypoxia trigger compensatory enhancements in inspiratory output when experienced separately, forms of plasticity called inactivity-induced inspiratory motor facilitation (iMF) and long-term facilitation (LTF), respectively. Reductions in respiratory neural activity that lead to moderate, but not mild, arterial hypoxia occludes plasticity expression, indicating that concurrent induction of iMF and LTF impairs plasticity through cross-talk inhibition of their respective signalling pathways.

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Background: Perioperative neurologic complication after an anterior cervical discectomy and fusion (ACDF) is uncommon but may have significant clinical consequences.

Objective: We aim to estimate the incidence of perioperative neurologic complications, identify their risk factors, and evaluate their impact on morbidity and mortality after ACDF.

Methods: ACDF cases (n = 317,789 patients) were extracted from the National Inpatient Sample between 1999 and 2011.

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Key Points: Concurrent 5-HT (Q pathway) and 5-HT (S pathway) serotonin receptor activation cancels phrenic motor facilitation due to mutual cross-talk inhibition. Spinal protein kinase Cδ (PKCδ) or protein kinase A inhibition restores phrenic motor facilitation with concurrent Q and S pathway activation, demonstrating a key role for these kinases in cross-talk inhibition. Spinal PKCδ inhibition enhances adenosine-dependent severe acute intermittent hypoxia-induced phrenic long-term facilitation (S pathway), consistent with relief of cross-talk inhibition.

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Background: Cancer cachexia is an insidious process characterized by muscle atrophy with associated motor deficits, including diaphragm weakness and respiratory insufficiency. Although neuropathology contributes to muscle wasting and motor deficits in many clinical disorders, neural involvement in cachexia-linked respiratory insufficiency has not been explored.

Methods: We first used whole-body plethysmography to assess ventilatory responses to hypoxic and hypercapnic chemoreflex activation in mice inoculated with the C26 colon adenocarcinoma cell line.

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Intermittent spinal serotonin receptor activation elicits phrenic motor facilitation (pMF), a form of spinal respiratory motor plasticity. Episodic activation of either serotonin type 2 (5-HT) or type 7 (5-HT) receptors elicits pMF, although they do so via distinct cellular mechanisms known as the Q (5-HT) and S (5-HT) pathways to pMF. When coactivated, these pathways interact via mutual cross-talk inhibition.

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Phrenic long-term facilitation (pLTF) is a form of hypoxia-induced spinal respiratory motor plasticity that requires new synthesis of brain derived neurotrophic factor (BDNF) and activation of its high-affinity receptor, tropomyosin receptor kinase B (TrkB). Since the cellular location of relevant TrkB receptors is not known, we utilized intrapleural siRNA injections to selectively knock down TrkB receptor protein within phrenic motor neurons. TrkB receptors within phrenic motor neurons are necessary for BDNF-dependent acute intermittent hypoxia-induced pLTF, demonstrating that phrenic motor neurons are a critical site of respiratory motor plasticity.

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Phrenic long-term facilitation (pLTF) is a persistent increase in phrenic nerve activity after acute intermittent hypoxia (AIH). Distinct cell-signaling cascades give rise to pLTF depending on the severity of hypoxemia within hypoxic episodes. Moderate AIH (mAIH; three 5-min episodes, PaO2 ∼35-55 mmHG) elicits pLTF by a serotonin (5-HT)-dependent mechanism that requires new synthesis of brain-derived neurotrophic factor (BDNF), activation of its high-affinity receptor (TrkB), and ERK MAPK signaling.

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Acute intermittent hypoxia (AIH) induces a form of spinal motor plasticity known as phrenic long-term facilitation (pLTF); pLTF is a prolonged increase in phrenic motor output after AIH has ended. In anesthetized rats, we demonstrate that pLTF requires activity of the novel PKC isoform, PKCθ, and that the relevant PKCθ is within phrenic motor neurons. Whereas spinal PKCθ inhibitors block pLTF, inhibitors targeting other PKC isoforms do not.

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