Spinal Cord Blood Flow Research Articles

Therapeutic efficacy of adrenergic agents on systemic and spinal hemodynamics in an acute cervical spinal cord injury rodent model

BACKGROUNDCervical spinal cord injury usually results in cardiorespiratory dysfunctions due to interruptions of the bulbospinal pathways innervating the cervical phrenic motoneurons and thoracic sympathetic preganglionic neurons. PURPOSEThe present study aimed to evaluate the therapeutic effects of adrenergic agents on systemic and spinal hemodynamics during acute cervical spinal cord injury. STUDY DESIGNIn vivo animal study. METHODSThe cardiorespiratory function and spinal cord blood flow and oxygenation level were monitored in response to cervical spinal cord contusion and intravenous infusion of three types of adrenergic agents (phenylephrine, dobutamine, and norepinephrine). RESULTSCervical spinal cord contusion resulted in immediate reduction of respiratory airflow, arterial blood pressure, and spinal cord blood flow. The arterial blood pressure and spinal cord blood flow remained lower than the preinjury value in contused animals infused with saline at 60 min postinjury. Infusion of phenylephrine (500, 1000, and 2000 μg/kg) and norepinephrine (125, 250, and 500 μg/kg) significantly increased the arterial blood pressure, while only norepinephrine augmented the spinal cord blood flow. Conversely, dobutamine (1000 and 2000 μg/kg) reduced both arterial blood pressure and spinal cord blood flow. Notably, administration of adrenergic agents tended to increase spinal cord hemorrhage in contused animals. CONCLUSIONSInfusion of norepinephrine can effectively maintain the blood pressure and improve spinal cord blood flow during acute spinal cord injury. CLINICAL SIGNIFICANCENorepinephrine may be a superior medicine for hemodynamic management; however, the potential hemorrhage should be considered when utilizing the vasopressor to regulate systemic and spinal hemodynamics at the acute injured stage.

Application of super-resolution and ultrafast ultrasound to reveal the characteristics of vascular blood flow changes after rat spinal cord injury at different segments

Objective: To investigate the changes of spinal vascular blood flow in SD rats after cervical, thoracic and lumbar spinal cord injury (SCI) using super-resolution ultrafast ultrasound technology. Methods: A total of 9 SD rats were used to construct SCI models at different segments using a 50 g aneurysm clip. Super-resolution ultrafast ultrasound technology was used to perform vascular blood flow imaging on the spinal cord of rats before and after injury at 6 hours, obtaining quantitative information such as spinal cord vascular density and blood flow velocity. Results: Ultrasound imaging showed that after SCI, the vascular density in the thoracic segment decreased (18.16%±1.04%) more than in the cervical segment (11.42%±1.39%) and lumbar segment (13.88%±1.43%, both P<0.05). The length of the spinal cord with decreased vascular density in the thoracic segment [(4.80±0.34)mm] was longer than that in the cervical segment [(2.80±0.57)mm] and lumbar segment [(3.10±0.36)mm, both P<0.05]. After injury, the decrease of blood flow in the thoracic segment [(8.87±0.85)ml/min] was higher than that in the cervical segment [(4.88±0.56)ml/min] and lumbar segment [(6.19±0.71)ml/min, both P<0.05]. HE staining and Nissl staining showed that the proportion of cavity area after thoracic SCI (11.53%±0.93%) was higher than that in the cervical segment (4.90%±1.72%) and lumbar segment (7.64%±0.84%, both P<0.05). The number of Nissl bodies in the thoracic segment (18.0±5.3) was also lower than that in the cervical segment (32.3±5.1) and lumbar segment (37.0±5.6) (both P<0.05). Conclusions: There are different changes in vascular blood flow after SCI in different segments of rats. The same injury causes the most severe damage to blood vessels in the thoracic spinal cord, followed by the lumbar spinal cord, and the cervical spinal cord has the least damage.

Enhancing Workplace Neuro Health and Productivity: The Synergy of Wearable Technology with Biophilic and Oxygenation Strategies

In the contemporary workplace, where a staggering 62% of employees reported experiencing burnout in 2023 according to a Medium article, the integration of wearable technology with biophilic and oxygenation strategies emerges as a vital Neurohemal initiative. This approach is particularly relevant for supporting neurodivergent individuals, as well as those recovering from stroke and long-COVID, in the context of return-to-office mandates. The article underscores the significance of research on increased hydrostatic pressure in circulation, particularly its impact on spinal and spinal cord blood flow during water immersion. This insight lays the groundwork for innovations like non-wet water massage devices, which could significantly aid in neurological recovery, thereby facilitating smoother reintegration into the workplace. Moreover, the fusion of biometrics with medical technology in wearables is explored, with a focus on enhancing interoception and proprioception. This technological synergy is key in activating the parasympathetic nervous system (PSNS), inducing a relaxed state conducive to effective digestion and oxygenation, crucial in mitigating workplace stress. The concept of ‘Interoceptive in Water’ is examined for its potential to improve blood flow and overall bodily function. In addition, the article advocates for the introduction of oxygenation bars in office spaces. These bars would offer a dedicated environment for enhanced oxygen intake, vital for cognitive function and stress alleviation, benefitting neurodivergent individuals, stroke survivors, and long-COVID patients. Wearables capable of detecting and correcting low oxygen or circulation issues are highlighted as essential tools for fostering a more inclusive, productive, and healthier workplace, thereby contributing to the overarching goal of NeuroHealth in the professional sphere.

Non-contrast ultrasound image analysis for spatial and temporal distribution of blood flow after spinal cord injury

Ultrasound technology can provide high-resolution imaging of blood flow following spinal cord injury (SCI). Blood flow imaging may improve critical care management of SCI, yet its duration is limited clinically by the amount of contrast agent injection required for high-resolution, continuous monitoring. In this study, we aim to establish non-contrast ultrasound as a clinically translatable imaging technique for spinal cord blood flow via comparison to contrast-based methods and by measuring the spatial distribution of blood flow after SCI. A rodent model of contusion SCI at the T12 spinal level was carried out using three different impact forces. We compared images of spinal cord blood flow taken using both non-contrast and contrast-enhanced ultrasound. Subsequently, we processed the images as a function of distance from injury, yielding the distribution of blood flow through space after SCI, and found the following. (1) Both non-contrast and contrast-enhanced imaging methods resulted in similar blood flow distributions (Spearman’s ρ = 0.55, p < 0.0001). (2) We found an area of decreased flow at the injury epicenter, or umbra (p < 0.0001). Unexpectedly, we found increased flow at the periphery, or penumbra (rostral, p < 0.05; caudal, p < 0.01), following SCI. However, distal flow remained unchanged, in what is presumably unaffected tissue. (3) Finally, tracking blood flow in the injury zones over time revealed interesting dynamic changes. After an initial decrease, blood flow in the penumbra increased during the first 10 min after injury, while blood flow in the umbra and distal tissue remained constant over time. These results demonstrate the viability of non-contrast ultrasound as a clinical monitoring tool. Furthermore, our surprising observations of increased flow in the injury periphery pose interesting new questions about how the spinal cord vasculature reacts to SCI, with potentially increased significance of the penumbra.

Spinal cord protection for thoracoabdominal aortic aneurysm repair: from bench to bedside.

This keynote lecture and corresponding presentation discuss the anatomy and pathophysiology surrounding spinal cord injury in aortic surgery. This article will discuss risk factors and mechanisms for spinal cord injury, including loss of direct and collateral spinal cord perfusion and ischemia-reperfusion injury. This review will examine these elements in both the laboratory and clinical setting, in addition to other neuroprotective strategies applied in clinical practice. Addressing spinal cord injury requires an integrated and considerate approach to simultaneously optimize spinal cord blood flow, promote collateralization and improve ischemic tolerance. Given the catastrophic clinical consequences for both the patient and their caregivers, continuing to investigate and examine spinal cord injury is of the utmost importance.

Meglumine cyclic adenylate improves cardiovascular hemodynamics and motor-function in a rat model of acute T4 thoracic spinal cord injury.

Animal experimental study. Spinal cord injury (SCI) at or above the T6 level causes cardiovascular dysfunction. Maintaining cAMP levels with cAMP analogs can facilitate neurological recovery. In the present study, the effects of meglumine cyclic adenylate (MCA), a cAMP analog and approved cardiovascular drug, on cardiovascular and neurological recovery in acute T4-SCI in rats were investigated. Hospital in Kunming, China. Eighty rats were randomly allocated to five groups, and groups A-D received SCI: (A) a group administered MCA at 2 mg/kg/d iv qd, (B) a group administered dopamine at 2.5 to 5 μg/kg/min iv to maintain mean arterial pressure above 85 mm Hg, (C) a group administered atropine at 1 mg/kg iv bid, (D) a group receiving an equal volume of saline iv qd for 3 weeks after SCI and (E) a group undergoing laminectomy only. The cardiovascular and behavioral parameters of the rats were examined, and spinal cord tissues were processed for hematoxylin and eosin staining, Nissl staining, electron microscopy, and analysis of cAMP levels. Compared with dopamine or atropine, MCA significantly reversed the decrease in cAMP levels in both myocardial cells and the injured spinal cord; improved hypotension, bradycardia and behavioral parameters at 6 weeks; and improved spinal cord blood flow and histological structure at 7 days post-SCI. The regression analysis suggested spinal cord motor-function improved as decreased heart rate and mean arterial pressure were stopped post-SCI. MCA may be an effective treatment for acute SCI by sustaining cAMP-dependent reparative processes and improving post-SCI cardiovascular dysfunction. N/A.

Increased blood flow of spinal cord lesion after decompression improves neurological recovery of degenerative cervical myelopathy: an intraoperative ultrasonography-based prospective cohort study.

Surgical decompression is a highly effective therapy for degenerative cervical myelopathy (DCM), but the mechanisms of neurological recovery following decompression remain unclear. This study aimed to evaluate the spinal cord blood flow status after sufficient decompression by intraoperative contrast-enhanced ultrasonography (CEUS) and to analyze the correlation between neurological recovery and postdecompressive spinal cord blood perfusion in DCM. Patients with multilevel DCM were treated by ultrasound-guided modified French-door laminoplasty using a self-developed rongeur. Neurological function was evaluated using the modified Japanese Orthopaedic Association (mJOA) score preoperatively and at 12 months postoperatively. Spinal cord compression and cervical canal enlargement before and after surgery were assessed by magnetic resonance imaging and computerized tomography. The decompression status was evaluated in real time by intraoperative ultrasonography, while the spinal cord blood flow after sufficient decompression was assessed by CEUS. Patients were categorized as favourable (≥50%) or unfavourable (<50%) recovery according to the recovery rate of the mJOA score at 12 months postoperatively. Twenty-nine patients were included in the study. The mJOA scores were significantly improved in all patients from 11.2±2.1 preoperatively to 15.0±1.1 at 12 months postoperatively, with an average recovery rate of 64.9±16.2%. Computerized tomography and intraoperative ultrasonography confirmed adequate enlargement of the cervical canal and sufficient decompression of the spinal cord, respectively. CEUS revealed that patients with favourable neurological recovery had a greater increased blood flow signal in the compressive spinal cord segment after decompression. In DCM, intraoperative CEUS can clearly reflect spinal cord blood flow. Patients with increased blood perfusion of the spinal cord lesion immediately after surgical decompression tended to achieve greater neurological recovery.

Mechanism of Increased Spinal Cord Blood Flow due to Noradrenaline Administration Using Vascular Resistance: An Experimental Study Using a Canine Model

During thoracoabdominal aortic surgery, the spinal cord is placed under ischemic conditions. Elevation of systemic blood pressure is thus recommended as a method of increasing the blood supply from collateral networks. This study examined the mechanisms by which noradrenaline administration increases spinal cord blood flow (SCBF) by elevating systemic blood pressure. In beagles (n = 7), the thoracoabdominal aorta and L2-L7 spinal cord segmental arteries (SAs) were exposed and a distal perfusion bypass was created to simulate clinical practice. SCBF was measured by laser flowmetry at the L5 dura mater and spinal cord perfusion pressure (SCPP) was measured inside the clamped aorta. The six pairs of SAs from L2 to L7 were clamped, and mean systemic blood pressure (mSBP), SCBF, and SCPP were measured before and after clamping and after starting continuous infusion of noradrenaline at 0.5 µg/kg/min. Rates of change in systemic vascular resistance (SVR) and spinal cord vascular resistance (SCVR) were calculated from the measured values. With no SA clamping (control), the rate of increase in SCVR was 0.74 times the rate of increase in SVR (y = 0.2 + 0.74x, r = 0.889, r2 = 0.789; P < 0.01). When all six pairs of SAs were clamped, a weak correlation was evident between rate of change in SCVR and rate of change in SVR, and the rate of increase in SCVR was lower than the rate of increase in SVR (y = 0.39 + 0.07x, r = 0.209, r2 = 0.039; P < 0.01). When all six pairs of SAs were clamped in the absence of distal perfusion, a weak correlation was also evident between rate of change in SCVR and rate of change in SVR, and the rate of increase in SCVR was lower than the rate of increase in SVR (y = 0.19 + 0.08x, r = 0.379, r2 = 0.144; P < 0.01). The rate of increase in SCVR induced by noradrenaline administration was lower than the rate of increase in SVR in the control group with no spinal cord SA clamping and in both experimental groups with clamped SAs (with and without distal perfusion), creating an environment conducive to spinal cord flow distribution.

Comparison and optimization of pCASL and VSASL for rat thoracolumbar spinal cord MRI at 9.4T.

To evaluate pseudo-continuous arterial spin labeling (pCASL) and velocity-selective arterial spin labeling (VSASL) for quantification of spinal cord blood flow (SCBF) in the rat thoracolumbar spinal cord. Labeling efficiency (LE) was compared between pCASL and three VSASL variants in simulations and both phantom and in vivo experiments at 9.4T. For pCASL, the effects of label plane position and shimming were systematically evaluated. For VSASL, the effects of composite pulses and phase cycling were evaluated to reduce artifacts. Additionally, vessel suppression, respiratory, and cardiac gating were evaluated to reduce motion artifacts. pCASL and VSASL maps of spinal cord blood flow were acquired with the optimized protocols. LE of the descending aorta was larger in pCASL compared to VSASL variants. In pCASL, LE off-isocenter was improved by local shimming positioned at the label plane and the anatomical level of labeling for the thoracic cord was only viable at the level of the T10 vertebra. Cardiac gating was essential to reduce motion artifacts. Both pCASL and VSASL successfully demonstrated comparable SCBF values in the thoracolumbar cord. pCASL demonstrated high and consistent LE in the thoracic aorta, and VSASL was also feasible, but with reduced efficiency. A combination of cardiac gating and recording of actual post-label delays was important for accurate SCBF quantification. These results highlight the challenges and solutions to achieve sufficient ASL labeling and contrast at high field in organs prone to motion.

Differential Trajectory of Diffusion and Perfusion Magnetic Resonance Imaging of Rat Spinal Cord Injury.

Traumatic spinal cord injury causes rapid neuronal and vascular injury, and predictive biomarkers are needed to facilitate acute patient management. This study examined the progression of magnetic resonance imaging (MRI) biomarkers after spinal cord injury and their ability to predict long-term neurological outcomes in a rodent model, with an emphasis on diffusion-weighted imaging (DWI) markers of axonal injury and perfusion-weighted imaging of spinal cord blood flow (SCBF). Adult Sprague-Dawley rats received a cervical contusion injury of varying severity (injured = 30, sham = 9). MRI at 4 h, 48-h, and 12-weeks post-injury included T1, T2, perfusion, and DWI. Locomotor outcome was assessed up to 12 weeks post-injury. At 4 h, the deficit in SCBF was larger than the DWI lesion, and although SCBF partially recovered by 48 h, the DWI lesion expanded. At 4 h, the volume of the SCBF deficit (R2 = 0.56, padj < 0.01) was significantly correlated with 12-week locomotor outcome, whereas DWI (R2 = 0.30, padj < 0.01) was less predictive of outcome. At 48 h, SCBF (R2 = 0.41, padj < 0.01) became less associated with outcome, and DWI (R2 = 0.38, padj < 0.01) lesion volume became more closely related to outcome. Spinal cord perfusion has unique spatiotemporal dynamics compared with diffusion measures of axonal damage and highlights the importance of acute perfusion abnormalities. Perfusion and diffusion offer complementary and clinically relevant insight into physiological and structural abnormalities following spinal cord injury beyond those afforded by T1 or T2 contrasts.

Spinal neurovascular coupling is preserved despite time-dependent alterations of spinal cord blood flow responses in a rat model of chronic back pain: implications for functional spinal cord imaging.

Functional magnetic resonance imaging has been used to investigate nociceptive processes in patients with chronic pain. However, the results may be confounded with changes in neurovascular coupling induced by chronic pain. The objective of this study was to examine spinal neurovascular coupling in a rat model of chronic back pain induced by muscle inflammation. Rats received 150 µL intramuscular injections of either complete Freund adjuvant (CFA: n = 18) or saline (control [CTL]: n = 18) in L5-L6 paravertebral muscles. Under 1.2% isoflurane anesthesia, spinal cord blood flow (SCBF) and local field potentials evoked by electrical stimulation of the sciatic nerve were recorded simultaneously in the lumbar enlargement of the spinal cord, 14 or 28 days after the injections. Mechanical hypersensitivity was observed in CFA rats compared with CTL rats for the back ( P < 0.001) and hind paws ( P < 0.01). Spinal cord blood flow response amplitude and local field potential amplitude were not significantly different between groups (day 14: P > 0.5; day 28: P > 0.6). However, the time course of SCBF responses was different between groups on day 14 ( P < 0.001) and day 28 ( P < 0.001). Nevertheless, neurovascular coupling was comparable between groups on days 14 and 28, whether neurovascular coupling was calculated with the amplitude or the area under the curve of SCBF responses (all P > 0.2). These results indicate that spinal hemodynamic changes reflect neuronal activity in this animal model, although the time course of SCBF responses is affected by chronic inflammatory back pain. This warrants a careful use of spinal functional magnetic resonance imaging in animal models and patients with chronic back pain.

Protective Effect of Extended Laminectomy on Spinal Cord Injury Induced by Spinal Shortening.

This study investigates the effect of extended laminectomy (EL) on spinal cord injury (SCI) caused by spinal shortening, and further, the timing and the optimal length of removal. Dogs received spinal column shortening at T13 segment, following which the control group underwent regular laminectomy while other groups underwent laminectomy with an additional 1-lamina length removed 6h after shortening ("1-lamina EL 6 h"), an extra 1.5-lamina length resected at 6 h or 12 h after shortening ("1.5-lamina EL 6 h" and "1.5-lamina EL 12 h"), and an extra 2-lamina length removed at 6 or 12 h after shortening ("2-lamina EL 6 h" and 2-lamina EL 12 h"), respectively. Somatosensory evoked potential (SSEP) and neurological function were recorded periodically; spinal cord blood flow (SCBF) and nerve cell apoptosis were detected. The results showed that resection of an additional 1-lamina length appeared inadequate to relieve the sharp kinking of the spinal cord, whereas the kinking disappeared with an additional 2-lamina length resection. The "1-lamina EL 6 h" and "1.5-lamina EL 12 h" groups showed no significant differences from the control in latency of SSEP, SCBF, hindlimb function and apoptosis. By contrast, significant recovery of SSEP, SCBF and hindlimb function as well as reduction of apoptosis were presented in other three groups. The "2-lamina EL 6 h" group, in particular, showed the most prominent recovery. In conclusion, an additional resection of two laminae at 6 h after shortening showed the best effect in alleviating SCI. Timely and adequately extended laminectomy could be a potential therapeutic strategy for SCI attributable to spinal shortening.

Spinal Cord Parenchyma Vascular Redistribution Underlies Hemodynamic and Neurophysiological Changes at Dynamic Neck Positions in Cervical Spondylotic Myelopathy.

Cervical spondylotic myelopathy (CSM) is a degenerative condition of the spine that caused by static and dynamic compression of the spinal cord. However, the mechanisms of motor and somatosensory conduction, as well as pathophysiological changes at dynamic neck positions remain unclear. This study aims to investigate the interplay between neurophysiological and hemodynamic responses at dynamic neck positions in the CSM condition, and the pathological basis behind. We first demonstrated that CSM patients had more severe dynamic motor evoked potentials (DMEPs) deteriorations upon neck flexion than upon extension, while their dynamic somatosensory evoked potentials (DSSEPs) deteriorated to a similar degree upon extension and flexion. We therefore generated a CSM rat model which developed similar neurophysiological characteristics within a 4-week compression period. At 4 weeks-post-injury, these rats presented decreased spinal cord blood flow (SCBF) and oxygen saturation (SO2) at the compression site, especially upon cervical flexion. The dynamic change of DMEPs was significantly correlated with the change in SCBF from neutral to flexion, suggesting they were more sensitive to ischemia compared to DSSEPs. We further demonstrated significant vascular redistribution in the spinal cord parenchyma, caused by angiogenesis mainly concentrated in the anterior part of the compressed site. In addition, the comparative ratio of vascular densities at the anterior and posterior parts of the cord was significantly correlated with the perfusion decrease at neck flexion. This exploratory study revealed that the motor and somatosensory conductive functions of the cervical cord changed differently at dynamic neck positions in CSM conditions. Compared with somatosensory conduction, the motor conductive function of the cervical cord suffered more severe deteriorations upon cervical flexion, which could partly be attributed to its higher susceptibility to spinal cord ischemia. The uneven angiogenesis and vascular distribution in the spinal cord parenchyma might underlie the transient ischemia of the cord at flexion.

P.187 Evaluating congruency between intramedullary and subdural pressure in a porcine model of acute spinal cord injury

Background: Clinical guidelines recommend MAP maintenance at 85-90 mmHg to optimize spinal cord perfusion post-SCI. Recently, there has been increased interest in spinal cord perfusion pressure as a surrogate marker for spinal cord blood flow. The study aims to determine the congruency of subdural and intramedullary spinal cord pressure measurements at the site of SCI, both rostral and caudal to the epicenter of injury. Methods: Seven Yucatan pigs underwent a T5 to L1 laminectomy with intramedullary (IM) and subdural (SD) pressure sensors placed 2 mm rostral and 2 mm caudal to the epicenter of SCI. A T10 contusion SCI was performed followed by an 8-hour period of monitoring. Axial ultrasound images were captured at the epicenter of injury pre-SCI, post-SCI, and hourly thereafter. Results: Pigs with pre-SCI cord to dural sac ratio (CDSR) of &gt;0.8 exhibited greater occlusion of the subdural space post-SCI with a positive correlation between IM and SD pressure rostral to the injury and a negative correlation caudal to the epicenter. Pigs with pre-SCI CDSR &lt;0.8 exhibited no correlation between IM and SD pressure. Conclusions: Congruency of IM and SD pressure is dependent on compartmentalization of the spinal cord occurring secondary to swelling that occludes the subdural space.

Delayed Post-Traumatic Spinal Cord Infarction with Quadriplegia: A Case Report

Traumatic spinal cord infarction is a rare condition that causes serious paralysis. The regulation of spinal cord blood flow in injured spinal cords remains unknown. Spinal cord infarction or ischemia has been reported after cardiovascular interventions, scoliosis correction, or profound hypotension. In this case, a 52-year-old man revisited the emergency center with motor and sensory abnormalities in all four extremities 56 hours after a motor vehicle collision. Despite the clinical presentation and imaging examination, there were no specific findings on the patient’s first visit to the trauma center. Cervical spine computed tomography angiography showed a narrow vertebral artery, and diffusion-weighted imaging revealed spinal cord infarction from C3 to C5 with high signal intensity. It should be kept in mind that delayed-onset spinal cord infarction may occur in minor or major trauma patients as a result of head and neck injuries.

Postdecompressive spinal cord blood flow increments in a cervical chronic myelopathy model in rats.

In cervical spondylotic myelopathy (CSM), compromise of blood flow to the compressed spinal cord has been postulated to contribute to the development of myelopathy. Although decompressive surgery has been considered to improve spinal cord blood flow, evidence to support this notion is scarce. To determine whether blood flow improves after decompressive surgery for CSM, regional blood flow was measured in a model of chronic cervical compression in rats by using a fluorescent microsphere technique. Thin polyurethane sheets, measuring precisely 3 × 5 × 0.7 mm, were implanted under the C5-6 laminae in 24 rats to induce continuous compression on the cervical spinal cord. These sheets expand gradually by absorbing tissue fluid. This animal model has been demonstrated to reproduce the clinical features and histological changes of CSM, including progressive motor weakness with delayed onset and insidious tissue damage prior to symptom onset. Twenty-four rats that underwent sham operation were allocated to a control group. To confirm the development of cervical myelopathy, motor functions were measured weekly over the study period. Nine weeks after implantation of the sublaminar expanding sheets, histological studies and C5-6 decompressive surgery were conducted. Regional blood flow in the brainstem and cervical spinal cord was measured sequentially until 120 minutes after decompression. In the CSM group, bilateral forepaw grip strength deteriorated progressively from 5 weeks after implantation. In the compressed C5-6 segment of the spinal cord, significant flattening of the cord, a decreased number of motor neurons, and vacuolations of gray matter were demonstrated. In the control group, blood flow in the brainstem and cervical spinal cord was unchanged by the decompressive surgery. In the CSM group, however, diminished blood flow and continuous blood flow increments for 120 minutes after decompression were demonstrated in the compressed C5-6 spinal cord segment. Chronic mechanical compression induced regional spinal cord blood flow insufficiency concomitant with progressive neuronal loss and motor dysfunction in a chronic compression model in rats. Decompressive surgery increased spinal cord blood flow. These findings suggest that blood flow recovery may contribute to postoperative neurological improvement.

Contribution of astrocytes to neurovascular coupling in the spinal cord of the rat

Functional magnetic resonance imaging (fMRI) of the spinal cord relies on the integrity of neurovascular coupling (NVC) to infer neuronal activity from hemodynamic changes. Astrocytes are a key component of cerebral NVC, but their role in spinal NVC is unclear. The objective of this study was to examine whether inhibition of astrocyte metabolism by fluorocitrate alters spinal NVC. In 14 rats, local field potential (LFP) and spinal cord blood flow (SCBF) were recorded simultaneously in the lumbosacral enlargement during noxious stimulation of the sciatic nerve before and after a local administration of fluorocitrate (N = 7) or saline (N = 7). Fluorocitrate significantly reduced SCBF responses (p < 0.001) but not LFP amplitude (p = 0.22) compared with saline. Accordingly, NVC was altered by fluorocitrate compared with saline (p < 0.01). These results support the role of astrocytes in spinal NVC and have implications for spinal cord imaging with fMRI for conditions in which astrocyte metabolism may be altered.

Towards rapid intraoperative axial localization of spinal cord ischemia with epidural diffuse correlation monitoring.

Spinal cord ischemia leads to iatrogenic injury in multiple surgical fields, and the ability to immediately identify onset and anatomic origin of ischemia is critical to its management. Current clinical monitoring, however, does not directly measure spinal cord blood flow, resulting in poor sensitivity/specificity, delayed alerts, and delayed intervention. We have developed an epidural device employing diffuse correlation spectroscopy (DCS) to monitor spinal cord ischemia continuously at multiple positions. We investigate the ability of this device to localize spinal cord ischemia in a porcine model and validate DCS versus Laser Doppler Flowmetry (LDF). Specifically, we demonstrate continuous (>0.1Hz) spatially resolved (3 locations) monitoring of spinal cord blood flow in a purely ischemic model with an epidural DCS probe. Changes in blood flow measured by DCS and LDF were highly correlated (r = 0.83). Spinal cord blood flow measured by DCS caudal to aortic occlusion decreased 62%. This monitor demonstrated a sensitivity of 0.87 and specificity of 0.91 for detection of a 25% decrease in flow. This technology may enable early identification and critically important localization of spinal cord ischemia.

Selective Angiography to Detect Anterior Spinal Artery Stenosis in Thoracic Ossification of the Posterior Longitudinal Ligament.

Study DesignSingle-center prospective study.PurposeTo investigate anterior spinal artery (ASA) status using preoperative selective angiography in patients undergoing surgery for thoracic ossification of the posterior longitudinal ligament (T-OPLL).Overview of LiteratureSurgery for T-OPLL has a high risk of neurological complications, which might be associated with insufficient spinal cord blood flow.MethodsThis study prospectively examined nine T-OPLL patients who underwent posterior thoracic decompression with kyphosis correction and instrumented fusion at Hamamatsu University School of Medicine between 2017 and 2019. All underwent preoperative selective angiography to detect and evaluate the Adamkiewicz artery and ASA. Intraoperative neuromonitoring and Doppler ultrasonography were performed to analyze neurological complications and spinal cord blood flow.ResultsAll nine patients showed ASA stenosis in the area of T-OPLL. In all patients, the Adamkiewicz artery was located between T7 and L2 and the area of ASA stenosis corresponded to the level of T-OPLL and greatest spinal cord compression; intraoperative Doppler ultrasonography confirmed the ASA defect at the same spinal level. The number of spinal levels from the Adamkiewicz artery to the most compressive OPLL lesion was greater in the two patients who developed postoperative neurological deficit compared to those who did not (5.5 vs. 2.3, p=0.014).ConclusionsThis is the first study to report detection of ASA stenosis in patients with T-OPLL. Maintaining spinal cord blood flow is important in these patients to avoid neurological deterioration.

Effect of cerebrospinal fluid pressure elevation on spinal cord perfusion during aortic cross-clamping with distal aortic perfusion.

Distal aortic perfusion (DaP) is a widely accepted protective adjunct facilitating early reinstitution of visceral perfusion during extended thoracic and thoraco-abdominal aortic repair. DaP has also been suggested to secure distal inflow to the paraspinal collateral network via the hypogastric arteries and thereby reduce the risk of spinal cord ischaemia. However, an increase in cerebrospinal fluid (CSF) pressure is frequently observed during thoracoabdominal aortic aneurysm repair. The aim of this study was to evaluate the effects of DaP on regional spinal cord blood flow (SCBF) during descending aortic cross-clamping and iatrogenic elevation of cerebrospinal fluid pressure. Eight juvenile pigs underwent central cannulation for cardiopulmonary bypass according to our established experimental protocol followed by aortic cross-clamping of the descending thoracic and abdominal aorta-mimicking sequential aortic clamping-with the initiation of DaP. Thereafter, CSF pressure elevation was induced by the infusion of blood plasma until baseline CSF pressure was tripled. At each time-point, microspheres of different colours were injected allowing for regional SCBF analysis. DaP led to a pronounced hyperperfusion of the distal spinal cord [SCBF up to 480%, standard deviation (SD): 313%, compared to baseline]. However, DaP provided no or only limited additional flow to the upper and middle segments of the spinal cord (C1-Th7: 5% of baseline, SD: 5%; Th8-L2: 24%, SD: 39%), which was compensated by proximal flow only at C1-Th7 level. Furthermore, DaP could not counteract an experimental CSF pressure elevation, which led to a further decrease in regional SCBF most pronounced in the mid-thoracic spinal cord segment. Protective DaP during thoraco-abdominal aortic repair may be associated with inadequate spinal protection particularly at the mid-thoracic spinal cord level ('watershed area') and result in the adverse effect of a potentially dangerous hyperperfusion of the distal spinal cord segments.