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Low-intensity focused ultrasound (LIFU) uses ultrasonic pulsations at lower intensities than ultrasound and is being tested as a reversible and precise neuromodulatory technology. Although LIFU-mediated blood-brain barrier (BBB) opening has been explored in detail, no standardized technique for blood-spinal cord barrier (BSCB) opening has been established to date. Therefore, this protocol presents a method for successful BSCB disruption using LIFU sonication in a rat model, including descriptions of animal preparation, microbubble administration, target selection and localization, as well as BSCB disruption visualization and confirmation. The approach reported here is particularly useful for researchers who need a fast and cost-effective method to test and confirm target localization and precise BSCB disruption in a small animal model with a focused ultrasound transducer, evaluate the BSCB efficacy of sonication parameters, or explore applications for LIFU at the spinal cord, such as drug delivery, immunomodulation, and neuromodulation. Optimizing this protocol for individual use is recommended, especially for advancing future preclinical, clinical, and translational work.

Tethered cord syndrome (TCS) occurs as a constellation of neurologic signs and symptoms resulting from longitudinal traction on the spinal cord between fixed points. This condition involves a tug-of-war between ascent and inhibition of ascent of intrathecal nervous tissue within the vertebral canal during growth. Causes include thickened filum terminale, myelomeningocele, split cord malformation, and previous intradural surgery. Patients report low back, lower extremity, and perineal pain; lower extremity sensory and motor deficits; urinary and bowel incontinence; and sexual dysfunction. When not treated early or adequately, TCS can lead to neurologic devastation.

OBJECT The arterial basket of the conus medullaris (ABCM) consists of 1 or 2 arteries arising from the anterior spinal artery (ASA) and circumferentially connecting the ASA and the posterior spinal arteries (PSAs). The arterial basket can be involved in arteriovenous fistulas and arteriovenous malformations of the conus. In this article, the authors describe the microsurgical anatomy of the ABCM with emphasis on its morphometric parameters and important role in the intrinsic blood supply of the conus medullaris. METHODS The authors performed microsurgical dissections on 16 formalin-fixed human spinal cords harvested within 24 hours of death. The course, diameter, and branching angles of the arteries comprising the ABCM were then identified and measured. In addition, histological sections were obtained to identify perforating vessels arising from the ABCM. RESULTS The ASA tapers as it nears the conus medullaris (mean preconus diameter 0.7 ± 0.12 mm vs mean conus diameter 0.38 ± 0.08 mm). The ASA forms an anastomotic basket with the posterior spinal artery (PSA) via anastomotic branches. In most of the specimens (n= 13, 81.3%), bilateral arteries formed connections between the ASA and PSA. However, in the remaining specimens (n= 3, 18.7%), a unilateral right-sided anastomotic artery was identified. The mean diameter of the right ABCM branch was 0.49 ± 0.13 mm, and the mean diameter of the left branch was 0.53 ± 0.14 mm. The mean branching angles of the arteries forming the anastomotic basket were 95.9° ± 36.6° and 90° ± 34.3° for the right- and left-sided arteries, respectively. In cases of bilateral arterial anastomoses between the ASA and PSA, the mean distance between the origins of the arteries was 4.5 ± 3.3 mm. Histological analysis revealed numerous perforating vessels supplying tissue of the conus medullaris. CONCLUSIONS The ABCM is a critical anastomotic connection between the ASA and PSA, which play an important role in the intrinsic blood supply of the conus medullaris. The ABCM provides an important compensatory function in the blood supply of the spinal cord. Its involvement in conus medullaris vascular malformations makes it a critical anatomical structure.

Background: Acute spinal cord injury (SCI) is commonly treated by elevating the mean arterial pressure (MAP). Other potential interventions include cerebrospinal fluid drainage (CSFD)., Objective: To determine the efficacy of aggressive MAP elevation combined with intrathecal pressure (ITP) reduction; our primary objective was to improve spinal cord blood flow (SCBF) after SCI., Methods: All 15 pigs underwent laminectomy. Study groups included control (n = 3); SCI only (n = 3); SCI combined with MAP elevation (SCI + MAP) (n = 3); SCI combined with CSFD (SCI + CSFD) (n = 3); and SCI combined with both MAP elevation and CSFD (SCI + MAP + CSFD) (n = 3). SCBF was measured with laser Doppler flowmetry., Results: In the SCI group, SCBF decreased by 56% after SCI. MAP elevation after SCI resulted in a 34% decrease in SCBF, whereas CSFD resulted in a 59% decrease in SCBF. The combination of CSFD and MAP elevation resulted in a 24% increase in SCBF. The SCI + MAP group had an average ITP increase of 5.45 mm Hg after MAP elevation 1 hour after SCI and remained at that level throughout the experiment., Conclusion: Both MAP elevation alone and CSFD alone led to only short-term improvement of SCBF. The combination of MAP elevation and CSFD significantly and sustainably improved SCBF and spinal cord perfusion pressure. Although laser Doppler flowmetry can provide flow measurements to a tissue depth of only 1.5 mm, these results may represent pattern of blood flow changes in the entire spinal cord after injury.

Spinal cord injury is a highly prevalent condition associated with significant morbidity and mortality. The pathophysiology underlying it is extraordinarily complex and still not completely understood. We performed a comprehensive literature review of the pathophysiologic processes underlying spinal cord injury. The mechanisms underlying primary and secondary spinal cord injury are distinguished based on a number of factors and include the initial mechanical injury force, the vascular supply of the spinal cord which is associated with spinal cord perfusion, spinal cord autoregulation, and post-traumatic ischemia, and a complex inflammatory cascade involving local and infiltrating immunomodulating cells. This review illustrates the current literature regarding the pathophysiology behind spinal cord injury and outlines potential therapeutic options for reversing these mechanisms., (© 2014 Wiley Periodicals, Inc.)

The authors present a review of spinal cord blood supply, discussing the anatomy of the vascular system and physiological aspects of blood flow regulation in normal and injured spinal cords. Unique anatomical functional properties of vessels and blood supply determine the susceptibility of the spinal cord to damage, especially ischemia. Spinal cord injury (SCI), for example, complicating thoracoabdominal aortic aneurysm repair is associated with ischemic trauma. The rate of this devastating complication has been decreased significantly by instituting physiological methods of protection. Traumatic SCI causes complex changes in spinal cord blood flow, which are closely related to the severity of injury. Manipulating physiological parameters such as mean arterial blood pressure and intrathecal pressure may be beneficial for patients with an SCI. Studying the physiopathological processes of the spinal cord under vascular compromise remains challenging because of its central role in almost all of the body's hemodynamic and neurofunctional processes.

Object: The definition of tethered cord syndrome (TCS) relies mainly on radiological criteria and clinical picture. The presence of a thickened filum terminale and a low-lying conus medullaris in symptomatic patients is indicative of TCS. The radiological definition of TCS does not take into account cases that involve a normal-lying conus medullaris exhibiting symptoms of the disease., Methods: The authors performed a MEDLINE search using the terms "tethered cord" and "pathophysiology." The search returned a total of 134 studies. The studies were further filtered to identify mostly basic research studies in animal models or studies related to the biomechanics of the filum terminale and spinal cord., Results: Spinal cord traction and the loss of filum terminale elasticity are the triggers that start a cascade of events occurring at the metabolic and vascular levels leading to symptoms of the disease. Traction on the caudal cord results in decreased blood flow causing metabolic derangements that culminate in motor, sensory, and urinary neurological deficits. The untethering operation restores blood flow and reverses the clinical picture in most symptomatic cases., Conclusions: Although classically defined as a disease of a low-lying conus medullaris, the pathophysiology of TCS is much more complex and is dependent on a structural abnormality, with concomitant altered metabolic and vascular sequelae. Given the complex mechanisms underlying TCS, it is not surprising that the radiological criteria do not adequately address all presentations of the disease.

The secondary phase of spinal cord injury (SCI) is characterized by ischemic injury. Spinal cord perfusion pressure (SCPP), calculated as the difference between mean arterial pressure (MAP) and intrathecal pressure (ITP), has arisen as a therapeutic target for improving outcomes. Cerebrospinal fluid drainage (CSFD) may reduce ITP and thereby increase SCPP. Randomized controlled trial to evaluate the safety and feasibility of CSFD to improve SCPP and outcomes after acute SCI. Inclusion criteria included acute cervical SCI within 24 hours of presentation. All patients received lumbar drain placement and appropriate decompressive surgery. Patients randomized to the control group received MAP elevation only. Patients in the experimental group received MAP elevation and CSFD to achieve ITP <10 mmHg for 5 days. ITP and MAP were recorded hourly. Adverse events were documented and patients underwent functional assessments at enrollment, 72 hours, 90 days, and 180 days post-injury. Eleven patients were enrolled; 4 were randomized to receive CSFD. CSFD patients had a mean ITP of 5.3 ± 2.5 mmHg versus. 15 ± 3.0 mmHg in the control group. SCPP improved significantly, from 77 ± 4.5 mmHg in the control group to 101 ± 6.3 mmHg in the CSFD group (P < 0.01). Total motor scores improved by 15 ± 8.4 and 57 ± 24 points in the control and CSFD groups, respectively, over 180 days. No adverse events were attributable to CSFD. CSFD is a safe, effective mechanism for reducing ITP and improving SCPP in the acute period post-SCI. The favorable safety profile and preliminary efficacy should help drive recruitment in future studies. [ABSTRACT FROM AUTHOR]

Objective Since the first resections of intradural extramedullary neoplasms, neurosurgeons have tended to preserve as much of the integrity of the spine as possible while ensuring a safe corridor to resect these lesions. A dimensional analysis of intradural lesions superimposed on a dimensional analysis of the thoracic canal would provide the anatomic basis for a minimal access approach. The authors report the results of such an analysis on a series of patients with intradural extramedullary lesions. Methods A retrospective analysis was undertaken of 26 thoracic intradural extramedullary lesions managed with open or minimally invasive resection. The size of each lesion was measured in the rostrocaudal, lateral, and anteroposterior dimensions and then averaged and compared with reported dimensions of the thoracic spinal canal. Results The mean (range) dimensions of the surgically resected thoracic lesions were 18.6 mm (10–25 mm) for rostrocaudal, 13.0 mm (7–18 mm) for lateral, and 13.6 mm (9–17 mm) for anteroposterior. No patient had any evidence of thoracic canal remodeling. Conclusions Thoracic intradural extramedullary lesions become symptomatic as they approach the limits of the thoracic canal, resulting in an inherent dimensional limitation in the rostrocaudal, lateral, and anteroposterior dimensions. Displacement of the spinal cord by the lesion to one side further favors a minimally invasive unilateral approach. A paraspinal unilateral hemilaminectomy approach with a 35 × 20 mm exposure centered over the lesion offers a safe surgical corridor for resection while preserving the posterior tension band, facet complexes, and paraspinal musculature. [ABSTRACT FROM AUTHOR]

Spinal cord stimulation has been shown to be an effective treatment for some patients diagnosed with chronic pain and failed back syndrome. However, lead migration from the implantation site is a potential complication that may reduce treatment efficacy, produce unintended symptoms, and require invasive and costly surgical replacement or removal. A 71-year-old woman presented to the emergency department with diffuse headache and burning left-sided facial pain consistent with trigeminal neuralgia. She had a history of chronic regional pain syndrome that had been successfully treated for 8 years with a percutaneous spinal cord stimulator, and 2 weeks before presentation she had had the cervical lead replaced. Computed tomography demonstrated intradural and intracranial migration of the cervical lead, which had traversed along the left lateral aspect of the medulla and terminated at the pontomedullary junction. The migrated cervical lead was removed surgically. At follow-up, her trigeminal pain had resolved. Although spinal cord stimulation has demonstrated effectiveness as a treatment for chronic pain, care must be taken to ensure that the spinal cord stimulator leads are properly placed within the epidural space and are firmly anchored to avoid migration. Intracranial migration of a spinal cord stimulator lead poses significant risks for injury to adjacent cortical structures and may produce pain syndromes including trigeminal neuralgia. [ABSTRACT FROM AUTHOR]

Prompt surgical decompression after traumatic spinal cord injury (TSCI) may be associated with improved sensorimotor outcomes. Delays in presentation may prevent timely decompression after TSCI. To systematically review existing studies investigating delays in presentation after TSCI in low- and middle-income countries (LMICs) and high-income countries (HICs). A systematic review was conducted and studies featuring quantitative or qualitative data on prehospital delays in TSCI presentation were included. Studies lacking quantitative or qualitative data on prehospital delays in TSCI presentation, case reports or series with <5 patients, review articles, or animal studies were excluded from our analysis. After exclusion criteria were applied, 24 studies were retained, most of which were retrospective. Eleven studies were from LMICs and 13 were from HICs. Patients with TSCI in LMICs were younger than those in HICs, and most patients were male in both groups. A greater proportion of patients with TSCI in studies from LMICs presented >24 hours after injury (HIC average proportion, 12.0%; LMIC average proportion, 49.9%; P = 0.01). Financial barriers, lack of patient awareness and education, and prehospital transportation barriers were more often cited as reasons for delays in LMICs than in HICs, with prehospital transportation barriers cited as a reason for delay by every LMIC study included in this review. Disparities in prehospital infrastructure between HICs and LMICs subject more patients in LMICs to increased delays in presentation to care. [ABSTRACT FROM AUTHOR]

Spinal cord injury (SCI) is a devastating condition that affects about 17,000 individuals every year in the United States, with approximately 294,000 people living with the ramifications of the initial injury. After the initial primary injury, SCI has a secondary phase during which the spinal cord sustains further injury due to ischemia, excitotoxicity, immune-mediated damage, mitochondrial dysfunction, apoptosis, and oxidative stress. The multifaceted injury progression process requires a sophisticated injury-monitoring technique for an accurate assessment of SCI patients. In this narrative review, we discuss SCI monitoring modalities, including pressure probes and catheters, micro dialysis, electrophysiologic measures, biomarkers, and imaging studies. The optimal next-generation injury monitoring setup should include multiple modalities and should integrate the data to produce a final simplified assessment of the injury and determine markers of intervention to improve patient outcomes. [ABSTRACT FROM AUTHOR]

Background Context: Cervical spondylosis may lead to spinal cord compression, poor vascular perfusion, and ultimately, cervical myelopathy. Studies suggest a neuroprotective effect of renin-angiotensin system (RAS) inhibitors in the brain, but limited data exist regarding their impact on the spinal cord.Purpose: To investigate whether RAS blockers and other antihypertensive drugs are correlated with preoperative functional status and imaging markers of cord compression in patients with symptomatic cervical spondylosis.Study Design: Retrospective observational study.Patient Sample: Individuals with symptomatic degenerative cervical stenosis who underwent surgery.Outcome Measures: Imaging features of spinal cord compression and functional status (modified Japanese Orthopedic Association [mJOA] and Nurick grading scales).Methods: Two hundred sixty-six operative patients with symptomatic degenerative cervical stenosis were included. Demographic data, comorbidities, antihypertensive medications, and functional status (including mJOA and Nurick grading scales) were collected. We evaluated canal compromise, cord compromise, surface area of T2 signal cord change, and pixel intensity of signal cord change compared with normal cord on T2-weighted magnetic resonance imaging sequences.Results: Of 266 patients, 41.7% were women, 58.3% were men; median age was 57.2 years; 20.6% smoked tobacco; 24.7% had diabetes mellitus. One hundred forty-nine patients (55.8%) had hypertension, 142 (95.3%) of these were taking antihypertensive medications (37 angiotensin-II receptor blockers [ARBs], 44 angiotensin-converting enzyme inhibitors, and 61 other medications). Patients treated with ARBs displayed a higher signal intensity ratio (ie, less signal intensity change in the compressed cord area) compared with untreated patients without hypertension (p=.004). Patients with hypertension had worse preoperative mJOA and Nurick scores than those without (p<.001). In the multivariate analysis, ARBs remained an independent beneficial factor for lower signal intensity change (p=.04), whereas hypertension remained a risk factor for worse preoperative neurological status (p<.01).Conclusions: In our study, patients with hypertension who were treated with RAS inhibitors had decreased T2-weighted signal intensity change than untreated patients without hypertension. Patients with hypertension also had worse preoperative functional status. Prospective case-control studies may deepen understanding of RAS modulators in the imaging and functional status of chronic spinal cord compression. [ABSTRACT FROM AUTHOR]

Background: Of the more than 30,000 posterior cervical spine fusions performed annually, 7%-12% will be complicated by postoperative C5 palsy, a condition characterized by new-onset deltoid weakness with or without C5 dermatomal findings and biceps weakness. Posterior translation of the cervical spinal cord has been proposed as a risk factor for this complication.Purpose: To evaluate if C5 palsy can be predicted by spinal cord float back.Study Design/setting: Retrospective cohort.Patient Sample: Patients ≥18 years of age undergoing posterior cervical decompression between 2002 and 2017 for degenerative cervical spine pathologies.Outcome Measures: Occurrence of C5 palsy as evaluated by manual motor testing (MMT).Methods: We recorded baseline neurological status, operative notes, details of postoperative course, and both pre- and postoperative magnetic resonance imaging images. Float back was defined by the change in the distance between the spinal cord and posterior face of the C4/5 annulus from preoperative to postoperative imaging. C5 palsy was defined by new-onset deltoid weakness on MMT.Results: We identified 242 patients with a mean age of 62.4 years and mean follow-up of 27.9 months. Forty-two (17.4%) experienced postoperative C5 palsy. On univariable analysis, significant predictors of postoperative C5 palsy were mean C4/5 foraminal diameter (2.8 vs. 3.2 mm; p<.001), anterior projection of the C5 superior articular process (4.12 vs. 3.70 mm; p=.04), cord float back (0.35 vs. 0.28 cm; p=.02), undergoing laminectomy of the C5 (p=.02) or C4 and C5 levels (p=.02), and undergoing instrumented fusion extending one level above and below the C4/5 level. Foraminotomy of the C4/5 level was not predictive of postoperative palsy. On multivariable analysis mean C4/5 foraminal diameter (odds ratio=0.38 per mm; p<.01) predicted C5 palsy; cord float back at the C4/5 level was not predictive of C5 palsy.Conclusions: Spinal cord float back was not an independent predictor of C5 palsy on multivariable analysis. Only smaller foraminal diameter was independently predictive of postoperative C5 palsy. This suggests that chronic preoperative compression of the C5 roots, not postdecompression float back may be the biggest contributor to the etiology of postoperative C5 palsy. [ABSTRACT FROM AUTHOR]

Postoperative C5 palsy affects 8% of patients undergoing posterior cervical decompression. It is associated with a period functional disability that may exceed 12 months and increase direct care costs > $2000. All patients undergoing posterior cervical decompression at a single tertiary-care facility for degenerative conditions were evaluated for preoperative imaging, clinical presentation, surgical operation, and postoperative course. We sought to identify those variables predictive of postoperative C5 palsy. Of 221 included patients (mean age, 63 years; 54% male), 12.2% experienced C5 palsy. On univariate analysis, C5 palsy was associated with foraminal diameter (P = 0.0005), spinal cord cross-sectional area (P = 0.11), number of levels undergoing laminectomy (P = 0.14), and clinical presentation of dropping objects (P = 0.07), hand clumsiness (P = 0.13), or paresthesias in the upper extremities (P = 0.08). Foraminal diameter (odds ratio, 0.31 per mm increase; 95% confidence interval, 0.16–0.60; P < 0.001) and patient report of gait disturbance (odds ratio, 0.53; 95% confidence interval, 0.33–0.85; P = 0.008) were the only significant predictors on multivariate analysis. A foraminal diameter <2 mm had 2-fold greater odds of postoperative C5 palsy. A receiver operating curve for the multivariate logistic model had an associated C -statistic of 0.7818. The absolute error of this model was 9.3% on internal validation. Foraminal stenosis most strongly predicted postoperative C5 palsy. A proof-of-concept model incorporating foramen size, as well as clinical complaints of paresthesias, hand clumsiness, and gait abnormality, successfully predicts the occurrence of postoperative palsy with an overall accuracy of 78%. [ABSTRACT FROM AUTHOR]