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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.

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.

Peer reviewed: True, Acknowledgements: Research in the senior author’s laboratory is supported by the Cambridge NIHR Brain Injury MedTech Cooperative. MRNK is supported by a NIHR Clinician Scientist Award., 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.

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.

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 2O at high (86 mmHg) spinal cord perfusion pressure versus 37 cmH2O at low (62 mmHg) spinal cord perfusion pressure (P 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.

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.

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. Electronic supplementary material The online version of this article (10.1007/s13311-019-00820-6) contains supplementary material, which is available to authorized users.

To determine the feasibility of monitoring tissue oxygen tension from the injury site (pscto2) in patients with acute, severe traumatic spinal cord injuries.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.Single-center neurosurgical and neurocritical care units.Twenty-six patients with traumatic spinal cord injuries, American spinal injury association Impairment Scale A-C. Probes were inserted within 72 hours of injury.Insertion of subarachnoid oxygen electrode (Licox; Integra LifeSciences, Sophia-Antipolis, France), pressure probe, and microdialysis catheter.pscto2 was significantly influenced by ISP (pscto2 26.7 ± 0.3 mm Hg at ISP10 mmHg vs pscto2 22.7 ± 0.8 mm Hg at ISP ≤ 10 mm Hg), SCPP (pscto2 26.8 ± 0.3 mm Hg at SCPP90 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 glucose6 mM vs 32.9 ± 0.5 mm Hg at glucose ≥ 6 mM), tissue LPR (pscto2 25.3 ± 0.4 mm Hg at LPR30 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).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.

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.

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.

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 (SCPP

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 IL1β, IL8, MCP, MIP1α, MIP1β). 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 IL1β, 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.

Background/Objectives We recently developed techniques to monitor intraspinal pressure (ISP) and spinal cord perfusion pressure (SCPP) from the injury site to compute the optimum SCPP (SCPPopt) in patients with acute traumatic spinal cord injury (TSCI). We hypothesized that ISP and SCPPopt can be predicted using clinical factors instead of ISP monitoring. Methods Sixty-four TSCI patients, grades A–C (American spinal injuries association Impairment Scale, AIS), were analyzed. For 24 h after surgery, we monitored ISP and SCPP and computed SCPPopt (SCPP that optimizes pressure reactivity). We studied how well 28 factors correlate with mean ISP or SCPPopt including 7 patient-related, 3 injury-related, 6 management-related, and 12 preoperative MRI-related factors. Results All patients underwent surgery to restore normal spinal alignment within 72 h of injury. Fifty-one percentage had U-shaped sPRx versus SCPP curves, thus allowing SCPPopt to be computed. Thirteen percentage, all AIS grade A or B, had no U-shaped sPRx versus SCPP curves. Thirty-six percentage (22/64) had U-shaped sPRx versus SCPP curves, but the SCPP did not reach the minimum of the curve, and thus, an exact SCPPopt could not be calculated. In total 5/28 factors were associated with lower ISP: older age, excess alcohol consumption, nonconus medullaris injury, expansion duroplasty, and less intraoperative bleeding. In a multivariate logistic regression model, these 5 factors predicted ISP as normal or high with 73% accuracy. Only 2/28 factors correlated with lower SCPPopt: higher mean ISP and conus medullaris injury. In an ordinal multivariate logistic regression model, these 2 factors predicted SCPPopt as low, medium–low, medium–high, or high with only 42% accuracy. No MRI factors correlated with ISP or SCPPopt. Conclusions Elevated ISP can be predicted by clinical factors. Modifiable factors that may lower ISP are: reducing surgical bleeding and performing expansion duroplasty. No factors accurately predict SCPPopt; thus, invasive monitoring remains the only way to estimate SCPPopt. Electronic supplementary material The online version of this article (10.1007/s12028-018-0616-7) contains supplementary material, which is available to authorized users.

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.

The optimum spinal cord perfusion pressure (SCPP) after traumatic spinal cord injury (TSCI) is unknown. Here, we describe techniques to compute and display the optimum SCPP in real-time. We recruited adults within 72 hours of severe TSCI (ASIA grades A-C). A pressure probe and a microdialysis catheter were placed on the injured cord. SCPP was computed as mean arterial pressure (MAP) minus intraspinal pressure (ISP), spinal pressure reactivity index (sPRx) as the running ISP/MAP correlation coefficient and continuous optimum SCPP (cSCPPopt) as the SCPP that minimizes sPRx in a moving four-hour window. In 45 patients, we monitored ISP and blood pressure. In 14 patients, we also monitored injury site metabolism. cSCPPopt could be computed 45 % of the time. Mean cSCPPopt varied by up to 60 mmHg between patients and each patient's cSCPPopt varied with time (standard deviation 10-20 mmHg). Color-coded maps showing the sPRx/SCPP curve evolution enhanced visualization of cSCPPopt. Periods when SCPP ≈ cSCPPopt were associated with low injury site glucose, high pyruvate and high lactate. Mean SCPP deviation from cSCPPopt inversely correlated with neurological outcome at 9-12 months: ASIA grade improved in 30 % patients with 15 mmHg deviation. We conclude that real-time computation and visualization of cSCPPopt after TSCI are feasible. cSCPPopt appears to enhance glucose utilization at the injury site and varies widely between and within patients. Our data suggest that targeting cSCPPopt after TSCI might improve neurological outcome.

Neuromyelitis optica (NMO) is an autoimmune disease of the central nervous system, also known as Devic’s syndrome, that typically manifests with optic neuritis and transverse myelitis and, like other antibody-mediated autoimmune diseases, primarily affects women. Most NMO cases are caused by a circulating autoantibody termed NMO-IgG or AQP4-IgG that targets the astrocytic water channel protein aquaporin-4 (AQP4). Some NMO cases are caused by a circulating autoantibody against the myelin oligodendrocyte glycoprotein termed MOG-IgG. A small proportion of NMO cases, termed seronegative NMO, are not associated with an autoantibody. AQP4-IgG binds extracellular conformational epitopes on AQP4, activates complement, which in turn causes inflammatory cell infiltration, demyelination and pan-necrosis. Acute NMO exacerbations are treated with methylprednisolone or plasmapheresis. Some drugs used to treat multiple sclerosis, such as interferon beta and natalizumab, exacerbate NMO. Maintenance treatment options include prednisolone, mycophenylate, mitoxantrone, cyclophosphamide, azathioprine, rituximab, tocilizumab and eculizumab. The discoveries of AQP4-IgG and MOG-IgG have shown that NMO is a distinct entity from multiple sclerosis with fundamentally different pathophysiology and treatment.

The management of patients having traumatic spinal cord injury (TSCI) would benefit from understanding and monitoring of spinal cord metabolic states. We hypothesized that the metabolism of the injured spinal cord could be visualized using Kohonen self-organizing maps. Sixteen patients with acute, severe spinal cord injuries were studied. Starting within 72 hours of the injury, and for up to a week, we monitored the injury site hourly for tissue glucose, lactate, pyruvate, glutamate and glycerol using microdialysis as well as intraspinal pressure and spinal cord perfusion pressure. A hexagonal Kohonen map, which is an unsupervised, self-organizing topology-preserving neural network, was used to analyze 3,366 hours of monitoring data. We first visualized the different spinal cord metabolic states. Our data show that the injured cord assumes one or more of four metabolic states. Based on their metabolite profiles, we termed these states near-normal, ischemic, hypermetabolic and distal. We then visualized how patients' intraspinal pressure and spinal cord perfusion pressure affect spinal cord metabolism. This revealed that for more than 60 % of the time, spinal cord metabolism is patient-specific; periods of high intraspinal pressure or low perfusion pressure are not associated with specific spinal cord metabolic patterns. Finally, we determined relationships between spinal cord metabolism and neurological status. Patients with complete deficits have shorter periods of near-normal spinal cord metabolic states (7±4% versus 58±12%, P

OBJECTIVE: There is lack of monitoring from the injury site to guide management of patients with acute traumatic spinal cord injury. Here we describe a bedside microdialysis monitoring technique for optimizing spinal cord perfusion and drug delivery at the injury site. METHODS: 14 patients were recruited within 72 hours of severe spinal cord injury. We inserted intradurally at the injury site a pressure probe, to monitor continuously spinal cord perfusion pressure, and a microdialysis catheter, to monitor hourly glycerol, glutamate, glucose, lactate and pyruvate. The pressure probe and microdialysis catheter were placed on the surface of the injured cord. RESULTS: Microdialysis monitoring did not cause serious complications. Spinal cord perfusion pressure 90 - 100 mmHg and tissue glucose >4.5 mM minimized metabolic derangement at the injury site. Increasing spinal cord perfusion pressure by ∼10 mmHg, increased the entry of intravenously administered dexamethasone at the injury site three-fold. INTERPRETATION: This study determined the optimum spinal cord perfusion pressure and optimum tissue glucose concentration at the injury site. We also identified spinal cord perfusion pressure as a key determinant of drug entry into the injured spinal cord. Our findings challenge current guidelines, which recommend maintaining mean arterial pressure at 85 - 90 mmHg for a week after spinal cord injury. We propose that future drug trials for spinal cord injury include pressure and microdialysis monitoring to optimize spinal cord perfusion and maximize drug delivery at the injury site. This article is protected by copyright. All rights reserved.

Patients often report sounds in the head after craniotomy. We aim to characterize the prevalence and nature of these sounds, and identify any patient, pathology, or technical factors related to them. These data may be used to inform patients of this sometimes unpleasant, but harmless effect of cranial surgery. Prospective observational study of patients undergoing cranial surgery with dural opening. Eligible patients completed a questionnaire preoperatively and daily after surgery until discharge. Subjects were followed up at 14 days with a telephone consultation. One hundred fifty-one patients with various pathologies were included. Of these, 47 (31 %) reported hearing sounds in their head, lasting an average 4–6 days (median, 4 days, mean, 6 days, range, 1–14 days). The peak onset was the first postoperative day and the most commonly used descriptors were ‘clicking’ [20/47 (43 %)] and ‘fluid moving’ in the head [9/47 (19 %)]. A significant proportion (42 %, 32/77) without a wound drain experienced intracranial sounds compared to those with a drain (20 %, 15/74, p

Study design Laboratory and human study. Objective To test the Codman Microsensor Transducer (CMT) in a cervical gel phantom. To test the CMT inserted to monitor intraspinal pressure in a patient with spinal cord injury. Summary of background data We recently introduced the technique of intraspinal pressure monitoring using the CMT to guide management of traumatic spinal cord injury [Werndle et al. Crit Care Med 2014;42:646]. This is analogous to intracranial pressure monitoring to guide management of patients with traumatic brain injury. It is unclear whether magnetic resonance imaging (MRI) of patients with spinal cord injury is safe with the intraspinal pressure CMT in situ. Methods We measured the heating produced by the CMT placed in a gel phantom in various configurations. A 3-T MRI system was used with the body transmit coil and the spine array receive coil. A CMT was then inserted subdurally at the injury site in a patient who had traumatic spinal cord injury and MRI was performed at 1.5 T. Results In the gel phantom, heating of up to 5°C occurred with the transducer wire placed straight through the magnet bore. The heating was abolished when the CMT wire was coiled and passed away from the bore. We then tested the CMT in a patient with an American Spinal Injuries Association grade C cervical cord injury. The CMT wire was placed in the configuration that abolished heating in the gel phantom. Good-quality T1 and T2 images of the cord were obtained without neurological deterioration. The transducer remained functional after the MRI. Conclusion Our data suggest that the CMT is MR conditional when used in the spinal configuration in humans. Data from a large patient group are required to confirm these findings. Level of evidence N/A.

OBJECT In contrast to intracranial pressure (ICP) in traumatic brain injury (TBI), intraspinal pressure (ISP) after traumatic spinal cord injury (TSCI) has not received the same attention in terms of waveform analysis. Based on a recently introduced technique for continuous monitoring of ISP, here the morphological characteristics of ISP are observationally described. It was hypothesized that the waveform analysis method used to assess ICP could be similarly applied to ISP. METHODS Data included continuous recordings of ISP and arterial blood pressure (ABP) in 18 patients with severe TSCI. RESULTS The morphology of the ISP pulse waveform resembled the ICP waveform shape and was composed of 3 peaks representing percussion, tidal, and dicrotic waves. Spectral analysis demonstrated the presence of slow, respiratory, and pulse waves at different frequencies. The pulse amplitude of ISP was proportional to the mean ISP, suggesting a similar exponential pressure-volume relationship as in the intracerebral space. The interaction between the slow waves of ISP and ABP is capable of characterizing the spinal autoregulatory capacity. CONCLUSIONS This preliminary observational study confirms morphological and spectral similarities between ISP in TSCI and ICP. Therefore, the known methods used for ICP waveform analysis could be transferred to ISP analysis and, upon verification, potentially used for monitoring TSCI patients.

The effect of traumatic spinal cord injury (TSCI) on spinal cord blood flow (SCBF) in humans is unknown. Whether intervention to achieve the recommended mean arterial pressure (MAP) guideline of 85-90 mm Hg improves SCBF is also unclear. Here, we use laser speckle contrast imaging intraoperatively to visualize blood flow at the injury site in 22 patients with acute, severe spinal cord injuries (American Spinal Injuries Association Impairment Scale, grades A-C). In 17 of 22 patients, injury-site metabolism was also monitored with a microdialysis catheter placed intradurally on the surface of the injured cord. We observed three different SCBF patterns, characterized by distinct injury-site metabolic signatures, which we term necrosis-penumbra, hyperperfusion, and patchy-perfusion. The necrosis-penumbra pattern, only observed in thoracic injuries, had a core of low blood flow (necrosis) with regions of intermediate blood flow on either side (penumbra). The hyperperfusion pattern, only observed in cervical injuries, had very high blood flow throughout the injury site. The patchy-perfusion pattern, found in cervical and thoracic injuries, had irregular regions of low, intermediate, and high blood flow. Though intervention to increase MAP by 20 mm Hg increased overall blood flow at the injury site, in 5 of 22 patients, blood flow increased in some regions, but, surprisingly, decreased in other regions. We term this phenomenon blood pressure-induced local steal. In 7 of 19 patients with MAP 85-90 mm Hg, parts of the injury site were only perfused in systole, but not in diastole, which we term diastolic ischemia. We conclude that acute, severe TSCI produces three pathological blood flow patterns at the injury site. Intervention to increase blood pressure may elicit potentially detrimental SCBF responses in some patients.

The injured spinal cord is a complex system influenced by many local and systemic factors that interact over many timescales. To help guide clinical management, we developed a technique that monitors intraspinal pressure from the injury site in patients with acute, severe traumatic spinal cord injuries. Here, we hypothesize that spinal cord injury alters the complex dynamics of the intraspinal pressure signal quantified by computing hourly the detrended fluctuation exponent alpha, multiscale entropy, and maximal Lyapunov exponent lambda. 49 patients with severe traumatic spinal cord injuries were monitored within 72 h of injury for 5 days on average to produce 5,941 h of intraspinal pressure data. We computed the spinal cord perfusion pressure as mean arterial pressure minus intraspinal pressure and the vascular pressure reactivity index as the running correlation coefficient between intraspinal pressure and arterial blood pressure. Mean patient follow-up was 17 months. We show that alpha values are greater than 0.5, which indicates that the intraspinal pressure signal is fractal. As alpha increases, intraspinal pressure decreases and spinal cord perfusion pressure increases with negative correlation between the vascular pressure reactivity index vs. alpha. Thus, secondary insults to the injured cord disrupt intraspinal pressure fractality. Our analysis shows that high intraspinal pressure, low spinal cord perfusion pressure, and impaired pressure reactivity strongly correlate with reduced multi-scale entropy, supporting the notion that secondary insults to the injured cord cause de-complexification of the intraspinal pressure signal, which may render the cord less adaptable to external changes. Healthy physiological systems are characterized by edge of chaos dynamics. We found negative correlations between the percentage of hours with edge of chaos dynamics (−0.01 ≤ lambda ≤ 0.01) vs. high intraspinal pressure and vs. low spinal cord perfusion pressure; these findings suggest that secondary insults render the intraspinal pressure more regular or chaotic. In a multivariate logistic regression model, better neurological status on admission, higher intraspinal pressure multi-scale entropy and more frequent edge of chaos intraspinal pressure dynamics predict long-term functional improvement. We conclude that spinal cord injury is associated with marked changes in non-linear intraspinal pressure metrics that carry prognostic information.

To characterize the effect of fever after acute, traumatic spinal cord injury on injury site metabolism and patient outcome.Longitudinal cohort study. In 44 patients (London cohort), we determined the effect of fever on intrathecal injury site metabolism by analyzing 1,767 hours of intraspinal pressure and 759 hours of microdialysis data. We also determined the effect of fever burden, computed for the first 2 weeks in hospital, on neurologic outcome. A distinct cohort of 33 patients (Berlin cohort) was used to independently validate the effect of fever burden on outcome.ICUs in London and Berlin.Seventy-seven patients with acute, traumatic spinal cord injuries.In the London patients, a pressure probe and a microdialysis catheter were placed intradurally on the surface of the injured cord for up to a week.Fever (37.5°C) occurs frequently (37% of the time) after spinal cord injury. High-grade fever (≥ 38°C) was associated with significantly more deranged metabolite levels than normothermia (36.5-37.5°C), that is, lower tissue glucose (median 2.0 vs 3.3 mM), higher lactate (7.8 vs 5.4 mM), higher glutamate (7.8 vs 6.4 µM), and higher lactate-to-pyruvate ratio (38.9 vs 29.3). High-grade fever was particularly detrimental on injury site metabolism when the peripheral leukocyte count was high. In the London and Berlin cohorts, high fever burden correlated with less neurologic improvement.Early after spinal cord injury, fever is associated with more deranged injury site metabolism than normothermia and worse prognosis.

Brain edema following traumatic brain injury (TBI) is associated with considerable morbidity and mortality. Prior indirect evidence has suggested the involvement of astrocyte water channel aquaporin-4 (AQP4) in the pathogenesis of TBI. Here, focal TBI was produced in wild type (AQP4(+/+)) and knockout (AQP4(-/-)) mice by controlled cortical impact injury (CCI) following craniotomy with dura intact (parameters: velocity 4.5 m/sec, depth 1.7 mm, dwell time 150 msec). AQP4-deficient mice showed a small but significant reduction in injury volume in the first week after CCI, with a small improvement in neurological outcome. Mechanistic studies showed reduced intracranial pressure at 6 h after CCI in AQP4(-/-) mice, compared with AQP4(+/+) control mice (11 vs. 19 mm Hg), with reduced local brain water accumulation as assessed gravimetrically. Transmission electron microscopy showed reduced astrocyte foot-process area in AQP4(-/-) mice at 24 h after CCI, with greater capillary lumen area. Blood-brain barrier disruption assessed by Evans blue dye extravasation was similar in AQP4(+/+) and AQP4(-/-) mice. We conclude that the mildly improved outcome in AQP4(-/-) mice following CCI results from reduced cytotoxic brain water accumulation, though concurrent cytotoxic and vasogenic mechanisms in TBI make the differences small compared to those seen in disorders where cytotoxic edema predominates.

BACKGROUND: We recently described a technique for monitoring intraspinal pressure (ISP) after traumatic spinal cord injury (TSCI). This is analogous to intracranial pressure monitoring after brain injury. We showed that, after severe TSCI, ISP at the injury site is elevated as the swollen cord is compressed against the dura. METHODS: In a patient with complete thoracic TSCI, we sequentially monitored subdural ISP above the injury, at the injury site, and below the injury intraoperatively. Postoperatively, we simultaneously monitored subdural ISP and intraparenchymal ISP at the injury site and compared the two ISP signals as well as their Fast Fourier Transform spectra. RESULTS: Subdural ISP recorded from the injury site was higher than subdural ISP recorded from above or below the injury site by more than 10 mmHg. The subdural and intraparenchymal ISP signals recorded from the injury site had comparable amplitudes and Fast Fourier Transform spectra. Intraparenchymal pulse pressure was twofold larger than subdural pulse pressure. CONCLUSION: After severe TSCI, three intradural compartments form (space above injury, injury site, space below injury) with different ISPs. At the level of maximum spinal cord swelling (injury site), subdural ISP is comparable to intraparenchymal ISP.

We recently showed that, after traumatic spinal cord injury (TSCI), laminectomy does not improve intraspinal pressure (ISP), spinal cord perfusion pressure (SCPP), or the vascular pressure reactivity index (sPRx) at the injury site sufficiently because of dural compression. This is an open label, prospective trial comparing combined bony and dural decompression versus laminectomy. Twenty-one patients with acute severe TSCI had re-alignment of the fracture and surgical fixation; 11 had laminectomy alone (laminectomy group) and 10 had laminectomy and duroplasty (laminectomy+duroplasty group). Primary outcomes were magnetic resonance imaging evidence of spinal cord decompression (increase in intradural space, cerebrospinal fluid around the injured cord) and spinal cord physiology (ISP, SCPP, sPRx). The laminectomy and laminectomy+duroplasty groups were well matched. Compared with the laminectomy group, the laminectomy+duroplasty group had greater increase in intradural space at the injury site and more effective decompression of the injured cord. In the laminectomy+duroplasty group, ISP was lower, SCPP higher, and sPRx lower, (i.e., improved vascular pressure reactivity), compared with the laminectomy group. Laminectomy+duroplasty caused cerebrospinal fluid leak that settled with lumbar drain in one patient and pseudomeningocele that resolved completely in five patients. We conclude that, after TSCI, laminectomy+duroplasty improves spinal cord radiological and physiological parameters more effectively than laminectomy alone.

MR scans from 65 patients with traumatic spinal cord injury were analysed; on admission 95% had evidence of cord compression - in 26% due to the dura, and in the remaining 74% due to extradural factors. Compression due to dural factors resolved with a half-life of 8.7 days. These findings suggest that bony decompression alone may not relieve spinal cord compression in the quarter of patients in whom dural factors are significant.

In the UK, blood pressure management after acute, severe traumatic spinal cord injury (TSCI) is variable.1 The American Association of Neurological Surgeons (AANS) recommends maintaining mean arterial pressure (MAP) at 85–95 mm Hg for a week after injury, but with little supporting evidence.2 To rationalise blood pressure management, we monitored intraspinal pressure (ISP) and spinal cord perfusion pressure (SCPP=MAP−ISP) from the injury site.3 Our technique is safe4 and analogous to monitoring intracranial pressure (ICP) and cerebral perfusion pressure (CPP) in traumatic brain injury (TBI). The data indicate that, after TSCI, ISP rises and SCPP falls.3 Here we show strong correlation between high ISP or low SCPP and reduced neurological recovery. Our findings raise the possibility that interventions to reduce ISP or increase SCPP after TSCI may improve neurological outcome. ### Patient recruitment Approval for this observational cohort study was granted by the National Research Ethics Service London–St Giles Committee. Inclusion criteria are: (1) Severe TSCI defined as American spinal injuries association Impairment Scale (AIS) grade A, B or C; (2) Age 18–70 years; (3) Timing between TSCI and surgery within 72 hours. Exclusion criteria are: (1) Patients unable to consent; (2) Other major injuries or comorbidities; (3) Penetrating TSCI. Surgery and early management took place at St. George's Hospital. Consent was obtained by each patient. ### Surgery Following bony realignment and posterior fixation, the ISP probe (Codman, Depuy Synthes, Leeds, UK) was tunnelled through …

Neuromyelitis optica (NMO) is an autoimmune disease of the CNS that is characterized by inflammatory demyelinating lesions in the spinal cord and optic nerve, potentially leading to paralysis and blindness. NMO can usually be distinguished from multiple sclerosis (MS) on the basis of seropositivity for IgG antibodies against the astrocytic water channel aquaporin-4 (AQP4). Differentiation from MS is crucial, because some MS treatments can exacerbate NMO. NMO pathogenesis involves AQP4-IgG antibody binding to astrocytic AQP4, which causes complement-dependent cytotoxicity and secondary inflammation with granulocyte and macrophage infiltration, blood-brain barrier disruption and oligodendrocyte injury. Current NMO treatments include general immunosuppressive agents, B-cell depletion, and plasma exchange. Therapeutic strategies targeting complement proteins, the IL-6 receptor, neutrophils, eosinophils and CD19--all initially developed for other indications--are under clinical evaluation for repurposing for NMO. Therapies in the preclinical phase include AQP4-blocking antibodies and AQP4-IgG enzymatic inactivation. Additional, albeit currently theoretical, treatment options include reduction of AQP4 expression, disruption of AQP4 orthogonal arrays, enhancement of complement inhibitor expression, restoration of the blood-brain barrier, and induction of immune tolerance. Despite the many therapeutic options in NMO, no controlled clinical trials in patients with this condition have been conducted to date.

To develop a technique for continuously monitoring intraspinal pressure at the injury site (intraspinal pressure) after traumatic spinal cord injury.A pressure probe was placed subdurally at the injury site in 18 patients who had isolated severe traumatic spinal cord injury (American Spinal Injuries Association grades A-C). Intraspinal pressure monitoring started within 72 hours of the injury and continued for up to a week. In four patients, additional probes were inserted to simultaneously monitor subdural pressure below the injury and extradural pressure. Blood pressure was recorded from a radial artery catheter kept at the same horizontal level as the injured segment of the spinal cord. We determined the effect of various maneuvers on spinal cord perfusion pressure and spinal cord function and assessed using a limb motor score and motor-evoked potentials.Neurosurgery and neuro-ICU covering a 3 million population in London.Patients with severe traumatic spinal cord injury. Control subjects without spinal cord injury (to monitor spinal cerebrospinal fluid signal and motor evoked potentials).Insertion of subdural spinal pressure probe.There were no procedure-related complications. Intraspinal pressure at the injury site was higher than subdural pressure below the injury or extradural pressure. Average intraspinal pressure from the 18 patients with traumatic spinal cord injury was significantly higher than average intraspinal pressure from 12 subjects without traumatic spinal cord injury. Change in arterial PCO2, change in sevoflurane dose, and mannitol administration had no significant effect on intraspinal pressure or spinal cord perfusion pressure. Increase in inotrope dose significantly increased spinal cord perfusion pressure. Bony realignment and laminectomy did not effectively lower intraspinal pressure. Laminectomy was potentially detrimental by exposing the swollen spinal cord to compression forces applied to the skin. By intervening to increase spinal cord perfusion pressure, we could increase the amplitude of motor-evoked potentials recorded from below or just above the injury level in nine of nine patients with traumatic spinal cord injury. In two of two patients with American Spinal Injuries Association grade C traumatic spinal cord injury, higher spinal cord perfusion pressure correlated with increased limb motor score.Our findings provide proof-of-principle that subdural intraspinal pressure at the injury site can be measured safely after traumatic spinal cord injury.

Traumatic spinal cord injury (SCI) is a devastating neurological condition characterized by a constellation of symptoms including paralysis, paraesthesia, pain, cardiovascular, bladder, bowel and sexual dysfunction. Current treatment for SCI involves acute resuscitation, aggressive rehabilitation and symptomatic treatment for complications. Despite the progress in scientific understanding, regenerative therapies are lacking. In this review, we outline the current state and future potential of invasive and non-invasive neuromodulation strategies including deep brain stimulation (DBS), spinal cord stimulation (SCS), motor cortex stimulation (MCS), transcutaneous direct current stimulation (tDCS) and repetitive transcranial magnetic stimulation (rTMS) in the context of SCI. We consider the ability of these therapies to address pain, sensorimotor symptoms and autonomic dysregulation associated with SCI. In addition to the potential to make important contributions to SCI treatment, neuromodulation has the added ability to contribute to our understanding of spinal cord neurobiology and the pathophysiology of SCI.

Actinomycosis is caused by Gram-positive filamentous anaerobic organisms of genus Actinomyces, which are commensals of mucosal membranes of the oropharyngeal cavity, and gastrointestinal and genitourinary tracts. Central nervous system involvement is rare and may present as cerebral abscess, meningitis, meningoencephalitis, subdural empyema or epidural abscess. The radiological appearances of actinomycotic brain abscesses are not well recognized. Here, we present the characteristic imaging features of an actinomycotic brain abscess.

ObjectivesIn humans the effect of spinal cord injury (SCI) on spinal cord blood flow (SCBF) is poorly understood. We imaged SCBF intraoperatively using laser speckle contrast imaging (LSCI).MethodsWe recruited 4 patients without SCI and 22 patients with SCI. Inclusion criteria for SCI patients are: AIS A–C, 18–70 years old, surgery within 72 hour of injury. In the SCI patients, we monitored spinal cord perfusion pressure and microdialysis from the injury site for 24 hour postoperatively. Mean patient follow-up after SCI was 7 m.ResultsLSCI signal is dampened by cerebrospinal fluid, but not dura. In patients without SCI we observed intact autoregulation, as well as SCBF variation with cardiac cycle, respiratory cycle and arterial pCO2. In SCI patients three pathological SCBF patterns were seen: necrosis-penumbra, patchy-perfusion and hyper-perfusion. Increase in MAP (>20 mmHg) increased overall injury site SCBF, but in 5/22 SCI patients there was a local steal effect where SCBF increased in some regions but decreased in others. In 7 SCI patients there was diastolic ischaemia, with regions only perfused in systole, but not diastole. Low injury site SCBF correlated with low spinal cord perfusion pressure, low tissue glucose, high tissue lactate and less improvement in combined sensory AIS score at follow-up.ConclusionsLSCI can be used to visualise SCBF non-invasively with high spatial-temporal resolution. We observed pathological SCBF patterns after SCI and some unanticipated SCBF responses to blood pressure changes.

ObjectivesTo identify factors which predict intra-spinal pressure (ISP) and optimal spinal cord perfusion pressure (SCPPopt) in patients with acute, severe traumatic spinal cord injuries (TSCI) that could be used instead of invasive ISP monitoring.MethodsWe monitored ISP, mean arterial pressure (MAP) and computed spinal cord perfusion pressure (SCPP), spinal pressure reactivity index (sPRx) and SCPPopt in 64 TSCI patients, AIS grades A–C who were part of the Injured Spinal Cord Pressure Evaluation (ISCoPE) study. We recorded baseline, injury/imaging and management variables which may influence ISP/SCPPopt. Statistical analysis was used to investigate differences in ISP/SCPPopt between the variablesResults51% (34/64) had U-shaped sPRx vs. SCPP curve in the first 24 hours after surgery. Mean SCPPopt was 74 mmHg (range 48–103). Lower mean 24 hour ISP was found with: older age, alcohol excess, non-conus medullaris injury, duroplasty and less surgical bleeding. Mean ISP on day 1 after surgery correlates with mean ISP over the first week. Lower 24 hour SCPPopt was associated with: higher mean ISP and conus medullaris injury. No MRI factors predicted ISP or SCPPopt.ConclusionsSeveral factors predict ISP. Modifiable factors to reduce ISP are less surgical bleeding and expansion duroplasty. No variables predict SCPPopt. ISP monitoring remains the only way to estimate SCPPopt to help prevent secondary damage and we continue to support use of ISP monitoring to individualise management in acute, severe TSCI.

This paper challenges the current management of acute traumatic spinal cord injury based on our experience with monitoring from the injury site in the neurointensive care unit. We argue that the concept of bony decompression is inadequate. The concept of optimum spinal cord perfusion pressure, which differs between patients, is introduced. Such variability suggests individualized patient treatment. Failing to optimize spinal cord perfusion limits the entry of systemically administered drugs into the injured cord. We conclude that monitoring from the injury site helps optimize management and should be subjected to a trial to determine whether it improves outcome.

OBJECTIVE A novel technique for monitoring intraspinal pressure and spinal cord perfusion pressure in patients with traumatic spinal cord injury was recently described. This is analogous to monitoring intracranial pressure and cerebral perfusion pressure in patients with traumatic brain injury. Because intraspinal pressure monitoring is a new technique, its safety profile and impact on early patient care and long-term outcome after traumatic spinal cord injury are unknown. The object of this study is to review all patients who had intraspinal pressure monitoring to date at the authors' institution in order to define the accuracy of intraspinal pressure probe placement and the safety of the technique. METHODS At the end of surgery to fix spinal fractures, a pressure probe was inserted intradurally to monitor intraspinal pressure at the injury site. Postoperatively, CT scanning was performed within 48 hours and MRI at 2 weeks and 6 months. Neurointensive care management and complications were reviewed. The American Spinal Injury Association Impairment Scale (AIS) grade was determined on admission and at 2 to 4 weeks and 12 to 18 months postoperation. RESULTS To date, 42 patients with severe traumatic spinal cord injuries (AIS Grades A–C) had undergone intraspinal pressure monitoring. Monitoring started within 72 hours of injury and continued for up to a week. Based on postoperative CT and MRI, the probe position was acceptable in all patients, i.e., the probe was located at the site of maximum spinal cord swelling. Complications were probe displacement in 1 of 42 patients (2.4%), CSF leakage that required wound resuturing in 3 of 42 patients (7.1%), and asymptomatic pseudomeningocele that was diagnosed in 8 of 42 patients (19.0%). Pseudomeningocele was diagnosed on MRI and resolved within 6 months in all patients. Based on the MRI and neurological examination results, there were no serious probe-related complications such as meningitis, wound infection, hematoma, wound breakdown, or neurological deterioration. Within 2 weeks postoperatively, 75% of patients were extubated and 25% underwent tracheostomy. Norepinephrine was used to support blood pressure without complications. Overall, the mean intraspinal pressure was around 20 mm Hg, and the mean spinal cord perfusion pressure was around 70 mm Hg. In laminectomized patients, the intraspinal pressure was significantly higher in the supine than lateral position by up to 18 mm Hg after thoracic laminectomy and 8 mm Hg after cervical laminectomy. At 12 to 18 months, 11.4% of patients had improved by 1 AIS grade and 14.3% by at least 2 AIS grades. CONCLUSIONS These data suggest that after traumatic spinal cord injury intradural placement of the pressure probe is accurate and intraspinal pressure monitoring is safe for up to a week. In patients with spinal cord injury who had laminectomy, the supine position should be avoided in order to prevent rises in intraspinal pressure.

Low back pain is a leading cause of disability worldwide and a major source of other medical problems including depression and substance misuse. In 2011–2012, lumbar spinal stenosis was diagnosed in 22,759 people in the UK and over 15,000 operations were performed for decompression of the lumbar spine (UK Hospital Episodes Statistics).

Following a traumatic brain injury (TBI), intracranial pressure (ICP) increases, often resulting in secondary brain insults. After a spinal cord injury, here the cord may be swollen, leading to a local increase in intraspinal pressure (ISP). We hypothesised that waveform analysis methodology similar to that used for ICP after TBI may be applicable for the monitoring of patients with spinal cord injury.An initial cohort of 10 patients with spinal cord injury, as presented by the first author at a meeting in Cambridge in May 2012, were included in this observational study. The whole group (18 patients) was recently presented in the context of clinically oriented findings (Werndle et al., Crit Care Med, 42(3):646-655, 2014, PMID: 24231762). Mean pressure, pulse and respiratory waveform were analysed along slow vasogenic waves.Slow, respiratory and pulse components of ISP were characterised in the time and frequency domains. Mean ISP was 22.5 ± 5.1, mean pulse amplitude 1.57 ± 0.97, mean respiratory amplitude 0.65 ± 0.45 and mean magnitude of slow waves (a 20-s to 3-min period) was 3.97 ± 3.1 (all in millimetres of mercury). With increasing mean ISP, the pulse amplitude increased in all cases. This suggests that the ISP signal is of a similar character to ICP recorded after TBI. Therefore, the methods of ICP analysis can be helpful in ISP analysis.

This case presents the case of a posterior communicating artery (PCom) aneurysm manifesting as a pupil-sparing oculomotor nerve palsy. In addition to the clinical presentation, it reviews the role and timing of different investigative tools in the diagnosis and management of subarachnoid haemorrhage (CT, lumbar puncture, angiography, transcranial Doppler ultrasound). The case discusses the neurological sequelae of aneurysmal subarachnoid haemorrhage, paying particular attention to the diagnosis and management of delayed cerebral ischaemia. It highlights the multifaceted approach needed in managing such patients, with peri-operative medical care playing a pivotal role in preserving neurological function. It also reviews the evidence surrounding the treatment of incidental cerebral aneurysms.

Antoine-Bernard Marfan first described the skeletal manifestations of Marfan’s syndrome (MFS) in 1896. Since then, a variety of associated clinical manifestations have been identified and numerous diagnostic criterions for MFS proposed. Following the identification of FBN1 as a causal gene for MFS, more stringent diagnostic criteria were put forth, referred to as the ‘Ghent nosology’ [1]. This employed a set of ‘major’ and ‘minor’ manifestations of MFS in numerous tissues. It has been criticised as difficult to use in children, that it includes non-specific physical manifestations and has poorly validated diagnostic thresholds. To address these issues a ‘revised Ghent nosology’ was proposed [2] based on clinical characteristics of large published patient cohorts and expert opinion. These systems include systemic features relevant to neurosurgical practice, most notably the identification of dural ectasia (DE). This chapter focuses on the diagnosis and management of this condition and discusses some of the other possible spinal and cerebro-vascular sequelae of MFS relevant to neurosurgical practice.

Intracranial pressure (ICP) is routinely measured in patients with severe traumatic brain injury (TBI). We describe a novel technique that allowed us to monitor intraspinal pressure (ISP) at the injury site in 14 patients who had severe acute traumatic spinal cord injury (TSCI), analogous to monitoring ICP after brain injury. A Codman probe was inserted subdurally to measure the pressure of the injured spinal cord compressed against the surrounding dura. Our key finding is that it is feasible and safe to monitor ISP for up to a week in patients after TSCI, starting within 72 h of the injury. With practice, probe insertion and calibration take less than 10 min. The ISP signal characteristics after TSCI were similar to the ICP signal characteristics recorded after TBI. Importantly, there were no associated complications. Future studies are required to determine whether reducing ISP improves neurological outcome after severe TSCI.