Evolving trends in the surgical, anaesthetic, and intensive care management of acute spinal cord injuries in the UK.

PURPOSE: We surveyed the treatment of acute spinal cord injuries in the UK and compared current practices with 10 years ago. METHODS: A questionnaire survey was conducted amongst neurosurgeons, neuroanaesthetists, and neurointensivists that manage patients with acute spinal cord injuries. The survey gave two scenarios (complete and incomplete cervical spinal cord injuries). We obtained opinions on the speed of transfer, timing and aim of surgery, choice of anaesthetic, intraoperative monitoring, targets for physiological parameters, and drug treatments. RESULTS: We received responses from 78.6% of UK units that manage acute spinal cord injuries (33 neurosurgeons, 56 neuroanaesthetists/neurointensivists). Most neurosurgeons operate within 12 h for incomplete (82%) and complete (64%) injuries. There is a significant shift from 10 years ago, when only 61% (incomplete) and 30% (complete) of neurosurgeons operated within 12 h. The preferred anaesthetic technique in 2022 is total intravenous anaesthesia (TIVA), used by 69% of neuroanaesthetists. Significantly more intraoperative monitoring is now used at least sometimes, including bispectral index (91%), non-invasive cardiac output (62%), and neurophysiology (73-77%). Methylprednisolone is no longer used by surgeons. Achieving at least 80 mmHg mean arterial blood pressure is recommended by 70% neurosurgeons, 62% neuroanaesthetists, and 75% neurointensivists. CONCLUSIONS: Between 2012 and 2022, there was a paradigm shift in managing acute spinal cord injuries in the UK with earlier surgery and more intraoperative monitoring. Variability in practice persists due to lack of high-quality evidence and consensus guidelines.

Spinal cord perfusion pressure correlates with breathing function in patients with acute, cervical traumatic spinal cord injuries: an observational study.

OBJECTIVE: This study aims to determine the relationship between spinal cord perfusion pressure (SCPP) and breathing function in patients with acute cervical traumatic spinal cord injuries. METHODS: We included 8 participants without cervical TSCI plus 13 patients with cervical traumatic spinal cord injuries, American Spinal Injury Association Impairment Scale grades A-C. In the TSCI patients, we monitored intraspinal pressure from the injury site for up to a week and computed the SCPP as mean arterial pressure minus intraspinal pressure. Breathing function was quantified by diaphragmatic electromyography using an EDI (electrical activity of the diaphragm) nasogastric tube as well as by ultrasound of the diaphragm and the intercostal muscles performed when sitting at 20°-30°. RESULTS: We analysed 106 ultrasound examinations (total 1370 images/videos) and 198 EDI recordings in the patients with cervical traumatic spinal cord injuries. During quiet breathing, low SCPP (< 60 mmHg) was associated with reduced EDI-peak (measure of inspiratory effort) and EDI-min (measure of the tonic activity of the diaphragm), which increased and then plateaued at SCPP 60-100 mmHg. During quiet and deep breathing, the diaphragmatic thickening fraction (force of diaphragmatic contraction) plotted versus SCPP had an inverted-U relationship, with a peak at SCPP 80-90 mmHg. Diaphragmatic excursion (up and down movement of the diaphragm) during quiet breathing did not correlate with SCPP, but diaphragmatic excursion during deep breathing plotted versus SCPP had an inverse-U relationship with a peak at SCPP 80-90 mmHg. The thickening fraction of the intercostal muscles plotted versus SCPP also had inverted-U relationship, with normal intercostal function at SCPP 80-100 mmHg, but failure of the upper and middle intercostals to contract during inspiration (i.e. abdominal breathing) at SCPP < 80 or > 100 mmHg. CONCLUSIONS: After acute, cervical traumatic spinal cord injuries, breathing function depends on the SCPP. SCPP 80-90 mmHg correlates with optimum diaphragmatic and intercostal muscle function. Our findings raise the possibility that intervention to maintain SCPP in this range may accelerate ventilator liberation which may reduce stay in the neuro-intensive care unit.

Feasibility of comparing medical management and surgery (with neurosurgery or stereotactic radiosurgery) with medical management alone in people with symptomatic brain cavernoma - protocol for the Cavernomas: A Randomised Effectiveness (CARE) pilot trial.

INTRODUCTION: The top research priority for cavernoma, identified by a James Lind Alliance Priority setting partnership was 'Does treatment (with neurosurgery or stereotactic radiosurgery) or no treatment improve outcome for people diagnosed with a cavernoma?' This pilot randomised controlled trial (RCT) aims to determine the feasibility of answering this question in a main phase RCT. METHODS AND ANALYSIS: We will perform a pilot phase, parallel group, pragmatic RCT involving approximately 60 children or adults with mental capacity, resident in the UK or Ireland, with an unresected symptomatic brain cavernoma. Participants will be randomised by web-based randomisation 1:1 to treatment with medical management and with surgery (neurosurgery or stereotactic radiosurgery) versus medical management alone, stratified by prerandomisation preference for type of surgery. In addition to 13 feasibility outcomes, the primary clinical outcome is symptomatic intracranial haemorrhage or new persistent/progressive focal neurological deficit measured at 6 monthly intervals. An integrated QuinteT Recruitment Intervention (QRI) evaluates screening logs, audio recordings of recruitment discussions, and interviews with recruiters and patients/parents/carers to identify and address barriers to participation. A Patient Advisory Group has codesigned the study and will oversee its progress. ETHICS AND DISSEMINATION: This study was approved by the Yorkshire and The Humber-Leeds East Research Ethics Committee (21/YH/0046). We will submit manuscripts to peer-reviewed journals, describing the findings of the QRI and the Cavernomas: A Randomised Evaluation (CARE) pilot trial. We will present at national specialty meetings. We will disseminate a plain English summary of the findings of the CARE pilot trial to participants and public audiences with input from, and acknowledgement of, the Patient Advisory Group. TRIAL REGISTRATION NUMBER: ISRCTN41647111.

Duroplasty for injured cervical spinal cord with uncontrolled swelling: protocol of the DISCUS randomized controlled trial.

BACKGROUND: Cervical traumatic spinal cord injury is a devastating condition. Current management (bony decompression) may be inadequate as after acute severe TSCI, the swollen spinal cord may become compressed against the surrounding tough membrane, the dura. DISCUS will test the hypothesis that, after acute, severe traumatic cervical spinal cord injury, the addition of dural decompression to bony decompression improves muscle strength in the limbs at 6 months, compared with bony decompression alone. METHODS: This is a prospective, phase III, multicenter, randomized controlled superiority trial. We aim to recruit 222 adults with acute, severe, traumatic cervical spinal cord injury with an American Spinal Injury Association Impairment Scale grade A, B, or C who will be randomized 1:1 to undergo bony decompression alone or bony decompression with duroplasty. Patients and outcome assessors are blinded to study arm. The primary outcome is change in the motor score at 6 months vs. admission; secondary outcomes assess function (grasp, walking, urinary + anal sphincters), quality of life, complications, need for further surgery, and mortality, at 6 months and 12 months from randomization. A subgroup of at least 50 patients (25/arm) also has observational monitoring from the injury site using a pressure probe (intraspinal pressure, spinal cord perfusion pressure) and/or microdialysis catheter (cord metabolism: tissue glucose, lactate, pyruvate, lactate to pyruvate ratio, glutamate, glycerol; cord inflammation: tissue chemokines/cytokines). Patients are recruited from the UK and internationally, with UK recruitment supported by an integrated QuinteT recruitment intervention to optimize recruitment and informed consent processes. Estimated study duration is 72 months (6 months set-up, 48 months recruitment, 12 months to complete follow-up, 6 months data analysis and reporting results). DISCUSSION: We anticipate that the addition of duroplasty to standard of care will improve muscle strength; this has benefits for patients and carers, as well as substantial gains for health services and society including economic implications. If the addition of duroplasty to standard treatment is beneficial, it is anticipated that duroplasty will become standard of care. TRIAL REGISTRATION: IRAS: 292031 (England, Wales, Northern Ireland) - Registration date: 24 May 2021, 296518 (Scotland), ISRCTN: 25573423 (Registration date: 2 June 2021); ClinicalTrials.gov number : NCT04936620 (Registration date: 21 June 2021); NIHR CRN 48627 (Registration date: 24 May 2021).

Adverse Effect of Neurogenic, Infective, and Inflammatory Fever on Acutely Injured Human Spinal Cord.

This study aims to determine the effect of neurogenic, inflammatory, and infective fevers on acutely injured human spinal cord. In 86 patients with acute, severe traumatic spinal cord injuries (TSCIs; American Spinal Injury Association Impairment Scale (AIS), grades A-C) we monitored (starting within 72 h of injury, for up to 1 week) axillary temperature as well as injury site cord pressure, microdialysis (MD), and oxygen. High fever (temperature ≥38°C) was classified as neurogenic, infective, or inflammatory. The effect of these three fever types on injury-site physiology, metabolism, and inflammation was studied by analyzing 2864 h of intraspinal pressure (ISP), 1887 h of MD, and 840 h of tissue oxygen data. High fever occurred in 76.7% of the patients. The data show that temperature was higher in neurogenic than non-neurogenic fever. Neurogenic fever only occurred with injuries rostral to vertebral level T4. Compared with normothermia, fever was associated with reduced tissue glucose (all fevers), increased tissue lactate to pyruvate ratio (all fevers), reduced tissue oxygen (neurogenic + infective fevers), and elevated levels of pro-inflammatory cytokines/chemokines (infective fever). Spinal cord metabolic derangement preceded the onset of infective but not neurogenic or inflammatory fever. By considering five clinical characteristics (level of injury, axillary temperature, leukocyte count, C-reactive protein [CRP], and serum procalcitonin [PCT]), it was possible to confidently distinguish neurogenic from non-neurogenic high fever in 59.3% of cases. We conclude that neurogenic, infective, and inflammatory fevers occur commonly after acute, severe TSCI and are detrimental to the injured spinal cord with infective fever being the most injurious. Further studies are required to determine whether treating fever improves outcome. Accurately diagnosing neurogenic fever, as described, may reduce unnecessary septic screens and overuse of antibiotics in these patients.

Targeting patient recovery priorities in degenerative cervical myelopathy: design and rationale for the RECEDE-Myelopathy trial-study protocol.

INTRODUCTION: Degenerative cervical myelopathy (DCM) is a common and disabling condition of symptomatic cervical spinal cord compression secondary to degenerative changes in spinal structures leading to a mechanical stress injury of the spinal cord. RECEDE-Myelopathy aims to test the disease-modulating activity of the phosphodiesterase 3/phosphodiesterase 4 inhibitor Ibudilast as an adjuvant to surgical decompression in DCM. METHODS AND ANALYSIS: RECEDE-Myelopathy is a multicentre, double-blind, randomised, placebo-controlled trial. Participants will be randomised to receive either 60-100 mg Ibudilast or placebo starting within 10 weeks prior to surgery and continuing for 24 weeks after surgery for a maximum of 34 weeks. Adults with DCM, who have a modified Japanese Orthopaedic Association (mJOA) score 8-14 inclusive and are scheduled for their first decompressive surgery are eligible for inclusion. The coprimary endpoints are pain measured on a visual analogue scale and physical function measured by the mJOA score at 6 months after surgery. Clinical assessments will be undertaken preoperatively, postoperatively and 3, 6 and 12 months after surgery. We hypothesise that adjuvant therapy with Ibudilast leads to a meaningful and additional improvement in either pain or function, as compared with standard routine care. STUDY DESIGN: Clinical trial protocol V.2.2 October 2020. ETHICS AND DISSEMINATION: Ethical approval has been obtained from HRA-Wales.The results will be presented at an international and national scientific conferences and in a peer-reviewed journals. TRIAL REGISTRATION NUMBER: ISRCTN Number: ISRCTN16682024.

Removal or retention of minimally invasive screws in thoracolumbar fractures? Systematic review and case-control study.

BACKGROUND: There is uncertainty regarding delayed removal versus retention of minimally invasive screws following percutaneous fixation for thoracolumbar fractures. We conducted a systematic review and case-control study to test the hypothesis that delayed metalwork removal following percutaneous fixation for thoracolumbar fractures improves outcome. METHODS: A systematic review was performed in accordance with the PRISMA guidelines. Our case-control study retrospectively evaluated 55 consecutive patients with thoracolumbar fractures who underwent percutaneous fixation in a single unit: 19 with metalwork retained (controls) and 36 with metalwork removed. Outcomes were the Oswestry Disability Index (ODI), a supplemental questionnaire, and complications. RESULTS: The systematic review evaluated nine articles. Back pain was reduced in most patients after metalwork removal. One study found no difference in the ODI after versus before metalwork removal, whereas three studies reported significant improvement. Six studies noted no significant alterations in radiological markers of stability after metalwork removal. Mean complication rate was 1.7% (0-6.7). Complications were superficial wound infection, screw breakage at the time of removal, pull-out screw, and a broken rod. In the case-control study, both groups were well matched. For metalwork removal, mean operative time was 69.5 min (range 30-120) and length of stay was 1.3 days (0-4). After metalwork removal, 24 (68.6%) patients felt better, 10 (28.6%) the same and one felt worse. Two patients had superficial hematomas, one had a superficial wound infection, and none required re-operation. Metalwork removal was a significant predictor of return to work or baseline household duties (odds ratio 5.0 [1.4-18.9]). The ODI was not different between groups. CONCLUSIONS: The findings of both the systematic review and our case-control study suggest that removal of metalwork following percutaneous fixation of thoracolumbar fractures is safe and is associated with improved outcome in most patients.

Chronic relapsing ascending myelopathy: a treatable progressive neurological syndrome following traumatic spinal cord injury.

BACKGROUND: We describe a novel progressive neurological syndrome complicating traumatic spinal cord injury (TSCI). Based on clinical and radiological features, we propose the term 'Chronic Relapsing Ascending Myelopathy' (CRAM). We distinguish between the previously described sub-acute progressive ascending myelopathy (SPAM) and post-traumatic syringomyelia (PTS), which may lie on a spectrum with CRAM. CASE REPORT: A 60-year-old man sustained a T4 ASIA-A complete TSCI. Four months post-injury, he developed a rapidly progressive ascending sensory level to C4. Clinical and radiological evaluation revealed ascending myelopathy with progressive T2 hyper-intense cord signal change. He underwent cord detethering and expansion duroplasty. Following an initial dramatic resolution of symptoms, the patient sustained two relapses, each 1-month post-discharge characterised by recurrence of disabling ascending sensory changes, each correlating with the radiological recurrence of cord signal change. Symptoms and radiological signal change permanently resolved with more extensive detethering and expansion duroplasty. There is radiological and clinical resolution at 1-year follow-up. CONCLUSION: Acute neurological deterioration post-TSCI may be due to SPAM or may occur after years due to PTS. We propose CRAM as a previously unrecognised phenomenon. The radiological characteristics overlap with SPAM. However, CRAM presents later and, clinically, behaves like PTS, but without cord cystic change. Cord detethering with expansion duroplasty are an effective treatment.

Monitoring Spinal Cord Tissue Oxygen in Patients With Acute, Severe Traumatic Spinal Cord Injuries.

OBJECTIVES: To determine the feasibility of monitoring tissue oxygen tension from the injury site (pscto2) in patients with acute, severe traumatic spinal cord injuries. DESIGN: We inserted at the injury site a pressure probe, a microdialysis catheter, and an oxygen electrode to monitor for up to a week intraspinal pressure (ISP), spinal cord perfusion pressure (SCPP), tissue glucose, lactate/pyruvate ratio (LPR), and pscto2. We analyzed 2,213 hours of such data. Follow-up was 6-28 months postinjury. SETTING: Single-center neurosurgical and neurocritical care units. SUBJECTS: Twenty-six patients with traumatic spinal cord injuries, American spinal injury association Impairment Scale A-C. Probes were inserted within 72 hours of injury. INTERVENTIONS: Insertion of subarachnoid oxygen electrode (Licox; Integra LifeSciences, Sophia-Antipolis, France), pressure probe, and microdialysis catheter. MEASUREMENTS AND MAIN RESULTS: pscto2 was significantly influenced by ISP (pscto2 26.7 ± 0.3 mm Hg at ISP > 10 mmHg vs pscto2 22.7 ± 0.8 mm Hg at ISP ≤ 10 mm Hg), SCPP (pscto2 26.8 ± 0.3 mm Hg at SCPP < 90 mm Hg vs pscto2 32.1 ± 0.7 mm Hg at SCPP ≥ 90 mm Hg), tissue glucose (pscto2 26.8 ± 0.4 mm Hg at glucose < 6 mM vs 32.9 ± 0.5 mm Hg at glucose ≥ 6 mM), tissue LPR (pscto2 25.3 ± 0.4 mm Hg at LPR > 30 vs pscto2 31.3 ± 0.3 mm Hg at LPR ≤ 30), and fever (pscto2 28.8 ± 0.5 mm Hg at cord temperature 37-38°C vs pscto2 28.7 ± 0.8 mm Hg at cord temperature ≥ 39°C). Tissue hypoxia also occurred independent of these factors. Increasing the Fio2 by 0.48 increases pscto2 by 71.8% above baseline within 8.4 minutes. In patients with motor-incomplete injuries, fluctuations in pscto2 correlated with fluctuations in limb motor score. The injured cord spent 11% (39%) hours at pscto2 less than 5 mm Hg (< 20 mm Hg) in patients with motor-complete outcomes, compared with 1% (30%) hours at pscto2 less than 5 mm Hg (< 20 mm Hg) in patients with motor-incomplete outcomes. Complications were cerebrospinal fluid leak (5/26) and wound infection (1/26). CONCLUSIONS: This study lays the foundation for measuring and altering spinal cord oxygen at the injury site. Future studies are required to investigate whether this is an effective new therapy.

Acute, severe traumatic spinal cord injury: improving urinary bladder function by optimizing spinal cord perfusion.

OBJECTIVE: The authors sought to investigate the effect of acute, severe traumatic spinal cord injury on the urinary bladder and the hypothesis that increasing the spinal cord perfusion pressure improves bladder function. METHODS: In 13 adults with traumatic spinal cord injury (American Spinal Injury Association Impairment Scale grades A-C), a pressure probe and a microdialysis catheter were placed intradurally at the injury site. We varied the spinal cord perfusion pressure and performed filling cystometry. Patients were followed up for 12 months on average. RESULTS: The 13 patients had 63 fill cycles; 38 cycles had unfavorable urodynamics, i.e., dangerously low compliance (< 20 mL/cmH2O), detrusor overactivity, or dangerously high end-fill pressure (> 40 cmH2O). Unfavorable urodynamics correlated with periods of injury site hypoperfusion (spinal cord perfusion pressure < 60 mm Hg), hyperperfusion (spinal cord perfusion pressure > 100 mm Hg), tissue glucose < 3 mM, and tissue lactate to pyruvate ratio > 30. Increasing spinal cord perfusion pressure from 67.0 ± 2.3 mm Hg (average ± SE) to 92.1 ± 3.0 mm Hg significantly reduced, from 534 to 365 mL, the median bladder volume at which the desire to void was first experienced. All patients with dangerously low average initial bladder compliance (< 20 mL/cmH2O) maintained low compliance at follow-up, whereas all patients with high average initial bladder compliance (> 100 mL/cmH2O) maintained high compliance at follow-up. CONCLUSIONS: We conclude that unfavorable urodynamics develop within days of traumatic spinal cord injury, thus challenging the prevailing notion that the detrusor is initially acontractile. Urodynamic studies performed acutely identify patients with dangerously low bladder compliance likely to benefit from early intervention. At this early stage, bladder function is dynamic and is influenced by fluctuations in the physiology and metabolism at the injury site; therefore, optimizing spinal cord perfusion is likely to improve urological outcome in patients with acute severe traumatic spinal cord injury.

Spinal Cord Perfusion Pressure Correlates with Anal Sphincter Function in a Cohort of Patients with Acute, Severe Traumatic Spinal Cord Injuries.

BACKGROUND: Acute, severe traumatic spinal cord injury often causes fecal incontinence. Currently, there are no treatments to improve anal function after traumatic spinal cord injury. Our study aims to determine whether, after traumatic spinal cord injury, anal function can be improved by interventions in the neuro-intensive care unit to alter the spinal cord perfusion pressure at the injury site. METHODS: We recruited a cohort of patients with acute, severe traumatic spinal cord injuries (American Spinal Injury Association Impairment Scale grades A-C). They underwent surgical fixation within 72 h of the injury and insertion of an intrathecal pressure probe at the injury site to monitor intraspinal pressure and compute spinal cord perfusion pressure as mean arterial pressure minus intraspinal pressure. Injury-site monitoring was performed at the neuro-intensive care unit for up to a week after injury. During monitoring, anorectal manometry was also conducted over a range of spinal cord perfusion pressures. RESULTS: Data were collected from 14 patients with consecutive traumatic spinal cord injury aged 22-67 years. The mean resting anal pressure was 44 cmH2O, which is considerably lower than the average for healthy patients, previously reported at 99 cmH2O. Mean resting anal pressure versus spinal cord perfusion pressure had an inverted U-shaped relation (Ȓ2 = 0.82), with the highest resting anal pressures being at a spinal cord perfusion pressure of approximately 100 mmHg. The recto-anal inhibitory reflex (transient relaxation of the internal anal sphincter during rectal distension), which is important for maintaining fecal continence, was present in 90% of attempts at high (90 mmHg) spinal cord perfusion pressure versus 70% of attempts at low (60 mmHg) spinal cord perfusion pressure (P < 0.05). During cough, the rise in anal pressure from baseline was 51 cmH2O at high (86 mmHg) spinal cord perfusion pressure versus 37 cmH2O at low (62 mmHg) spinal cord perfusion pressure (P < 0.0001). During anal squeeze, higher spinal cord perfusion pressure was associated with longer endurance time and spinal cord perfusion pressure of 70-90 mmHg was associated with stronger squeeze. There were no complications associated with anorectal manometry. CONCLUSIONS: Our data indicate that spinal cord injury causes severe disruption of anal sphincter function. Several key components of anal continence (resting anal pressure, recto-anal inhibitory reflex, and anal pressure during cough and squeeze) markedly improve at higher spinal cord perfusion pressure. Maintaining too high of spinal cord perfusion pressure may worsen anal continence.

Acute, Severe Traumatic Spinal Cord Injury: Monitoring from the Injury Site and Expansion Duraplasty.

We discuss 2 evolving management options for acute spinal cord injury that hold promise to further improve outcome: pressure monitoring from the injured cord and expansion duraplasty. Probes surgically implanted at the injury site can transduce intraspinal pressure, spinal cord perfusion pressure, and cord metabolism. Intraspinal pressure is not adequately reduced by bony decompression alone because the swollen, injured cord is compressed against the dura. Expansion duraplasty may be necessary to effectively decompress the injured cord. A randomized controlled trial called DISCUS is investigating expansion duraplasty as a novel treatment for acute, severe traumatic cervical spinal cord injury.

Acute Spinal Cord Injury: Correlations and Causal Relations Between Intraspinal Pressure, Spinal Cord Perfusion Pressure, Lactate-to-Pyruvate Ratio, and Limb Power.

BACKGROUND/OBJECTIVE: We have recently developed monitoring from the injury site in patients with acute, severe traumatic spinal cord injuries to facilitate their management in the intensive care unit. This is analogous to monitoring from the brain in patients with traumatic brain injuries. This study aims to determine whether, after traumatic spinal cord injury, fluctuations in the monitored physiological, and metabolic parameters at the injury site are causally linked to changes in limb power. METHODS: This is an observational study of a cohort of adult patients with motor-incomplete spinal cord injuries, i.e., grade C American spinal injuries association Impairment Scale. A pressure probe and a microdialysis catheter were placed intradurally at the injury site. For up to a week after surgery, we monitored limb power, intraspinal pressure, spinal cord perfusion pressure, and tissue lactate-to-pyruvate ratio. We established correlations between these variables and performed Granger causality analysis. RESULTS: Nineteen patients, aged 22-70 years, were recruited. Motor score versus intraspinal pressure had exponential decay relation (intraspinal pressure rise to 20 mmHg was associated with drop of 11 motor points, but little drop in motor points as intraspinal pressure rose further, R2 = 0.98). Motor score versus spinal cord perfusion pressure (up to 110 mmHg) had linear relation (1.4 motor point rise/10 mmHg rise in spinal cord perfusion pressure, R2 = 0.96). Motor score versus lactate-to-pyruvate ratio (greater than 20) also had linear relation (0.8 motor score drop/10-point rise in lactate-to-pyruvate ratio, R2 = 0.92). Increased intraspinal pressure Granger-caused increase in lactate-to-pyruvate ratio, decrease in spinal cord perfusion, and decrease in motor score. Increased spinal cord perfusion Granger-caused decrease in lactate-to-pyruvate ratio and increase in motor score. Increased lactate-to-pyruvate ratio Granger-caused increase in intraspinal pressure, decrease in spinal cord perfusion, and decrease in motor score. Causality analysis also revealed multiple vicious cycles that amplify insults to the cord thus exacerbating cord damage. CONCLUSION: Monitoring intraspinal pressure, spinal cord perfusion pressure, lactate-to-pyruvate ratio, and intervening to normalize these parameters are likely to improve limb power.

Effects of local hypothermia-rewarming on physiology, metabolism and inflammation of acutely injured human spinal cord.

In five patients with acute, severe thoracic traumatic spinal cord injuries (TSCIs), American spinal injuries association Impairment Scale (AIS) grades A-C, we induced cord hypothermia (33 °C) then rewarming (37 °C). A pressure probe and a microdialysis catheter were placed intradurally at the injury site to monitor intraspinal pressure (ISP), spinal cord perfusion pressure (SCPP), tissue metabolism and inflammation. Cord hypothermia-rewarming, applied to awake patients, did not cause discomfort or neurological deterioration. Cooling did not affect cord physiology (ISP, SCPP), but markedly altered cord metabolism (increased glucose, lactate, lactate/pyruvate ratio (LPR), glutamate; decreased glycerol) and markedly reduced cord inflammation (reduced IL1ß, IL8, MCP, MIP1α, MIP1ß). Compared with pre-cooling baseline, rewarming was associated with significantly worse cord physiology (increased ICP, decreased SCPP), cord metabolism (increased lactate, LPR; decreased glucose, glycerol) and cord inflammation (increased IL1ß, IL8, IL4, IL10, MCP, MIP1α). The study was terminated because three patients developed delayed wound infections. At 18-months, two patients improved and three stayed the same. We conclude that, after TSCI, hypothermia is potentially beneficial by reducing cord inflammation, though after rewarming these benefits are lost due to increases in cord swelling, ischemia and inflammation. We thus urge caution when using hypothermia-rewarming therapeutically in TSCI.

Acute Spinal Cord Injury: Monitoring Lumbar Cerebrospinal Fluid Provides Limited Information about the Injury Site.

In some centers, monitoring lumbar cerebrospinal fluid (CSF) is used to guide management of patients with acute traumatic spinal cord injuries (TSCI) and draining lumbar CSF to improve spinal cord perfusion. Here, we investigate whether the lumbar CSF provides accurate information about the injury site and the effect of draining lumbar CSF on injury site perfusion. In 13 TSCI patients, we simultaneously monitored lumbar CSF pressure (CSFP) and intraspinal pressure (ISP) from the injury site. Using CSFP or ISP, we computed spinal cord perfusion pressure (SCPP), vascular pressure reactivity index (sPRx) and optimum SCPP (SCPPopt). We also assessed the effect on ISP of draining 10 mL CSF. Metabolites at the injury site were compared with metabolites in the lumbar CSF. We found that ISP was pulsatile, but CSFP had low pulse pressure and was non-pulsatile 21% of the time. There was weak or no correlation between CSFP versus ISP (R = -0.11), SCPP(csf) versus SCPP(ISP) (R = 0.39), and sPRx(csf) versus sPRx(ISP) (R = 0.45). CSF drainage caused no significant change in ISP in 7/12 patients and a significant drop of <5 mm Hg in 4/12 patients and of ∼8 mm Hg in 1/12 patients. Metabolite concentrations in the CSF versus the injury site did not correlate for lactate (R = 0.00), pyruvate (R = -0.12) or lactate-to-pyruvate ratio (R = -0.05) with weak correlations noted for glucose (R = 0.31), glutamate (R = 0.61), and glycerol (R = 0.56). We conclude that, after a severe TSCI, monitoring from the lumbar CSF provides only limited information about the injury site and that lumbar CSF drainage does not effectively reduce ISP in most patients.

Targeted Perfusion Therapy in Spinal Cord Trauma.

We review state-of-the-art monitoring techniques for acute, severe traumatic spinal cord injury (TSCI) to facilitate targeted perfusion of the injured cord rather than applying universal mean arterial pressure targets. Key concepts are discussed such as intraspinal pressure and spinal cord perfusion pressure (SCPP) at the injury site, respectively, analogous to intracranial pressure and cerebral perfusion pressure for traumatic brain injury. The concept of spinal cord autoregulation is introduced and quantified using spinal pressure reactivity index (sPRx), which is analogous to pressure reactivity index for traumatic brain injury. The U-shaped relationship between sPRx and SCPP defines the optimum SCPP as the SCPP that minimizes sPRx (i.e., maximizes autoregulation), and suggests that not only ischemia but also hyperemia at the injury site may be detrimental. The observation that optimum SCPP varies between patients and temporally in each patient supports individualized management. We discuss multimodality monitoring, which revealed strong correlations between SCPP and injury site metabolism (tissue glucose, lactate, pyruvate, glutamate, glycerol), monitored by surface microdialysis. Evidence is presented that the dura is a major, but unappreciated, cause of spinal cord compression after TSCI; we thus propose expansion duroplasty as a novel treatment. Monitoring spinal cord blood flow at the injury site has revealed novel phenomena, e.g., 3 distinct blood flow patterns, local steal, and diastolic ischemia. We conclude that monitoring from the injured spinal cord in the intensive care unit is a safe technique that appears to enable optimized and individualized spinal cord perfusion.

Heterogeneous effect of increasing spinal cord perfusion pressure on sensory evoked potentials recorded from acutely injured human spinal cord.

PURPOSE: To investigate the effect of increasing spinal cord perfusion pressure (SCPP) on sensory evoked potentials (SEPs) and injury site metabolism in patients with severe traumatic spinal cord injury TSCI. MATERIALS AND METHODS: In 12 TSCI patients we placed a pressure probe, a microdialysis catheter and a strip electrode with 8 contacts on the surface of the injured cord. We monitored SCPP, lactate-to-pyruvate ratio (LPR) and SEPs (after median or posterior tibial nerve stimulation). RESULTS: Increase in SCPP by ~20 mmHg produced a heterogeneous response in SEPs and injury site metabolism. In some patients, SEP amplitudes increased and the LPR decreased indicating improved tissue metab olism. In others, SEP amplitudes decreased and the LPR increased indicating more impaired metabolism. Compared with patients who did not improve at follow-up, those who improved had significantly more electrode contacts with SEP amplitude increase in response to increasing SCPP. CONCLUSIONS: Increasing SCPP after acute, severe TSCI may be beneficial (if associated with increase in SEP amplitude) or detrimental (if associated with decrease in SEP amplitude). Our findings support individualized management of patients with acute, severe TSCI guided by monitoring from the injury site rather than applying universal blood pressure targets as is current clinical practice.

Contralateral lumbosacral plexopathy following lumbar microdiscectomy.

We describe the unique case of a 51-year-old lady who developed a contralateral lumbosacral plexopathy two days after a lumbar microdiscectomy. This is the first report to date of this complication occurring following this procedure. We review the literature regarding lumbosacral plexopathy and discuss the evidence base behind investigating and managing this condition and the potential pathophysiological mechanisms which underlie its development. We draw comparisons with the more widely recognised post-operative brachial neuritis, characterised by delayed onset brachial plexopathy developing after cervical decompression, and propose an immune-mediated inflammatory mechanism linking the two conditions.