Spinal alignment shift between supine and prone CT imaging occurs frequently and regardless of the anatomic region, risk factors, or pathology

Computer-assisted spine surgery based on preoperative CT imaging may be hampered by sagittal alignment shifts due to an intraoperative switch from supine to prone. In the present study, we systematically analyzed the occurrence and pattern of sagittal spinal alignment shift between corresponding preoperative (supine) and intraoperative (prone) CT imaging in patients that underwent navigated posterior instrumentation between 2014 and 2017. Sagittal alignment across the levels of instrumentation was determined according to the C2 fracture gap (C2-F) and C2 translation (C2-T) in odontoid type 2 fractures, next to the modified Cobb angle (CA), plumbline (PL), and translation (T) in subaxial pathologies. One-hundred and twenty-one patients (C1/C2: n = 17; C3-S1: n = 104) with degenerative (39/121; 32%), oncologic (35/121; 29%), traumatic (34/121; 28%), or infectious (13/121; 11%) pathologies were identified. In the subaxial spine, significant shift occurred in 104/104 (100%) cases (CA: *p = .044; T: *p = .021) compared to only 10/17 (59%) cases that exhibited shift at the C1/C2 level (C2-F: **p = .002; C2-T: *p 5 segments (" increment PL > 5 segments": 4.5 +/- 1.8 mm; " increment PL <= 5 segments": 2 +/- 0.6 mm; *p = .013) or in revision surgery with pre-existing instrumentation (" increment PL presence": 5 +/- 2.6 mm; " increment PL absence": 2.4 +/- 0.7 mm; **p = .007). Interestingly, typical morphological instability risk factors did not influence the degree of shift. In conclusion, intraoperative spinal alignment shift due to a change in patient position should be considered as a cause for inaccuracy during computer-assisted spine surgery and when correcting spinal alignment according to parameters that were planned in other patient positions

Clinical management and outcome of adult patients with extracorporeal life support device–associated intracerebral hemorrhage—a neurocritical perspective and grading

Intracerebral hemorrhage (ICH) is a devastating complication in patients treated with extracorporeal membrane oxygenation (ECMO) due to respiratory or cardiac issues. Neurosurgical evaluation and management of such cases has only insufficiently been studied. We conducted a retrospective, cohort study of adult patients treated with ECMO between January 2007 and January 2017 in a tertiary healthcare center. Demographics, clinical data, coagulation status, ICH characteristics, and treatment modalities were analyzed. The primary outcome parameter was defined as mortality caused by ICH during ECMO. 525 patients with ECMO therapy were eligible for analysis. An overall incidence for any type of intracranial bleeding of 12.3% was found. Small hemorrhages accounted for 6.4% and acute subdural and epidural hematoma for 1.2%. Twenty-four (4.6%) patients developed ICH, and 11 patients (46%) died due to the ICH. Mortality was significantly higher in patients with larger ICH volumes (86.8 +/- 34.8 ml vs 9.9 +/- 20.3 ml, p < 0.001), intraventricular hemorrhage (83% vs 8%, p = 0.01), and a fluid level inside the ICH (75% vs 31%, p = 0.04). All patients were classified according to the bleeding pattern on the initial CT scan into 3 types. Patients with type 1 bleeding were statistically more likely to die (p < 0.001). In 15 out of 24 patients (63%), correction of the coagulation status was possible within 12 h after ICH onset. Seven out of 9 patients (78%) without early coagulation correction died compared to 2 out of 15 patients (13%), in whom early coagulation correction was successful (p = 0.01). This is the first study evaluating the course and management of patients experiencing an ICH under ECMO therapy and establishing an ICH classification based on the bleeding patterns. Early correction of the coagulation is of paramount importance in the treatment of these patients

Perfusion‐Dependent Cerebral Autoregulation Impairment in Hemispheric Stroke

Objective: Loss of cerebral autoregulation (CA) plays a key role in secondary neurologic injury. However, the regional distribution of CA impairment after acute cerebral injury remains unclear because, in clinical practice, CA is only assessed within a limited compartment. Here, we performed large-scale regional mapping of cortical perfusion and CA in patients undergoing decompressive surgery for malignant hemispheric stroke. Methods: In 24 patients, autoregulation over the affected hemisphere was calculated based on direct, 15 to 20-minute cortical perfusion measurement with intraoperative laser speckle imaging and mean arterial blood pressure (MAP) recording. Cortical perfusion was normalized against noninfarcted tissue and 6 perfusion categories from 0% to >100% were defined. The interaction between cortical perfusion and MAP was estimated using a linear random slope model and Pearson correlation. Results: Cortical perfusion and CA impairment were heterogeneously distributed across the entire hemisphere. The degree of CA impairment was significantly greater in areas with critical hypoperfusion (40-60%: 0.42% per mmHg and 60-80%: 0.46% per mmHg) than in noninfarcted (> 100%: 0.22% per mmHg) or infarcted (0-20%: 0.29% per mmHg) areas (*p 100% (r = 0.36; *p < 0.05). Tissue integrity had no impact on the degree of CA impairment. Interpretation: In hemispheric stroke, CA is impaired across the entire hemisphere to a variable extent. Autoregulation impairment was greatest in hypoperfused and potentially viable tissue, suggesting that precise localization of such regions is essential for effective tailoring of perfusion pressure-based treatment strategies. ANN NEUROL 202

Migraine Aura, Transient Ischemic Attacks, Stroke, and Dying of the Brain Share the Same Key Pathophysiological Process in Neurons Driven by Gibbs–Donnan Forces, Namely Spreading Depolarization

Neuronal cytotoxic edema is the morphological correlate of the near-complete neuronal battery breakdown called spreading depolarization, or conversely, spreading depolarization is the electrophysiological correlate of the initial, still reversible phase of neuronal cytotoxic edema. Cytotoxic edema and spreading depolarization are thus different modalities of the same process, which represents a metastable universal reference state in the gray matter of the brain close to Gibbs-Donnan equilibrium. Different but merging sections of the spreading-depolarization continuum from short duration waves to intermediate duration waves to terminal waves occur in a plethora of clinical conditions, including migraine aura, ischemic stroke, traumatic brain injury, aneurysmal subarachnoid hemorrhage (aSAH) and delayed cerebral ischemia (DCI), spontaneous intracerebral hemorrhage, subdural hematoma, development of brain death, and the dying process during cardio circulatory arrest. Thus, spreading depolarization represents a prime and simultaneously the most neglected pathophysiological process in acute neurology. Aristides Leao postulated as early as the 1940s that the pathophysiological process in neurons underlying migraine aura is of the same nature as the pathophysiological process in neurons that occurs in response to cerebral circulatory arrest, because he assumed that spreading depolarization occurs in both conditions. With this in mind, it is not surprising that patients with migraine with aura have about a twofold increased risk of stroke, as some spreading depolarizations leading to the patient percept of migraine aura could be caused by cerebral ischemia. However, it is in the nature of spreading depolarization that it can have different etiologies and not all spreading depolarizations arise because of ischemia. Spreading depolarization is observed as a negative direct current (DC) shift and associated with different changes in spontaneous brain activity in the alternating current (AC) band of the electrocorticogram. These are non-spreading depression and spreading activity depression and epileptiform activity. The same spreading depolarization wave may be associated with different activity changes in adjacent brain regions. Here, we review the basal mechanism underlying spreading depolarization and the associated activity changes. Using original recordings in animals and patients, we illustrate that the associated changes in spontaneous activity are by no means trivial, but pose unsolved mechanistic puzzles and require proper scientific analysis

Age-dependent microstructural changes of the intervertebral disc: a validation of proteoglycan-sensitive spectral CT

Objective: To analyze the two major components of the intervertebral disc (IVD) in an ex vivo phantom, as well as age-related changes in patients. Methods: Collagen and chondroitin sulfate were imaged at different concentrations in agar solution. Age-related changes in disc density were retrospectively analyzed in normal-appearing discs in dual-energy computed tomography (DECT) images from a patient cohort with various spinal pathologies (n = 136). All computed tomography (CT) scans were acquired using single-source DECT at 80 and 135 kVp with automatic exposure calculation. In 136 patients, the attenuation of normal-appearing discs on collagen/chondroitin maps (cMaps) correlated with the patients' age with Pearson's r using standardized regions of interest in the anterior anulus fibrosus (AAF) and nucleus pulposus (NP). Results: DECT collagen mapping revealed concentration-dependent Hounsfield units (HU) of IVD components. For collagen, we found Pearson's r = 0.9610 (95% CI 0.6789-0.9959), p = 0.0023 at 120 kVe, and r = 0.8824 (95% CI 0.2495-0.9871), p = 0.0199 in cMap. For chondroitin sulfate, Pearson's r was 0.9583 (95% CI 0.6603-0.9956), p = 0.0026 at 120 kVp, and r = 0.9646 (95% CI 0.7044-0.9963), p = 0.0019 in cMap. Analysis of normal-appearing IVDs revealed an inverse correlation of density with age in the AAF: Pearson's r = - 0.2294 at 135 kVp (95% CI - 0.4012 to - 0.04203; p=0.0141) and r = - 0.09341 in cMap (95% CI - 0.2777 to 0.09754; p = 0.0003). In the NP, age and density did not correlate significantly at 135 kVp (p = 0.9228) and in cMap (p = 0.3229). Conclusions: DECT-based collagen mapping allows microstructural analysis of the two main intervertebral disc components-collagen and chondroitin sulfate. IVD density declines with age, presumably due to a reduction in collagen and chondroitin sulfate content. Age-related alterations of disc microstructure appear most pronounced in the AAF

Reduction in wound healing complications and infection rate by lumbar CSF drainage after decompressive hemicraniectomy

Objective: Wound healing disorders and surgical site infections are the most frequently encountered complications after decompressive hemicraniectomy (DHC). Subgaleal CSF accumulation causes additional tension of the scalp flap and increases the risk of wound dehiscence, CSF fistula, and infection. Lumbar CSF drainage might relieve subgaleal CSF accumulation and is often used when a CSF fistula through the surgical wound appears. The aim of this study was to investigate if early prophylactic lumbar drainage might reduce the rate of postoperative wound revisions and infections after DHC. Methods: The authors retrospectively analyzed 104 consecutive patients who underwent DHC from January 2019 to May 2021. Before January 2020, patients did not receive lumbar drainage, whereas after January 2020, patients received lumbar drainage within 3 days after DHC for a median total of 4 (IQR 2-5) days if the first postoperative CT scan confirmed open basal cisterns. The primary endpoint was the rate of severe wound healing complications requiring surgical revision. Secondary endpoints were the rate of subgaleal CSF accumulations and hygromas as well as the rate of purulent wound infections and subdural empyema. Results: A total of 31 patients died during the acute phase; 34 patients with and 39 patients without lumbar drainage were included for the analysis of endpoints. The predominant underlying pathology was malignant hemispheric stroke (58.8% vs 66.7%) followed by traumatic brain injury (20.6% vs 23.1%). The rate of surgical wound revisions was significantly lower in the lumbar drainage group (5 [14.7%] vs 14 [35.9%], p = 0.04). A stepwise linear regression analysis was used to identify potential covariates associated with wound healing disorder and reduced them to lumbar drainage and BMI. One patient was subject to paradoxical herniation. However, the patient's symptoms rapidly resolved after lumbar drainage was discontinued, and he survived with only moderate deficits related to the primary disease. There was no significant difference in the rate of radiological herniation signs. The median lengths of stay in the ICU were similar, with 12 (IQR 9-23) days in the drainage group compared with 13 (IQR 11-23) days in the control group (p = 0.21). Conclusions: In patients after DHC and open basal cisterns on postoperative CT, lumbar drainage appears to be safe and reduces the rate of surgical wound revisions and intracranial infection after DHC while the risk for provoking paradoxical herniation is low early after surgery

Balanced single-vector co-delivery of VEGF/PDGF-BB improves functional collateralization in chronic cerebral ischemia

The myoblast-mediated delivery of angiogenic genes represents a cell-based approach for targeted induction of therapeutic collateralization. Here, we tested the superiority of myoblast-mediated co-delivery of vascular endothelial growth factor-A (VEGF) together with platelet-derived growth factor-BB (PDGF-BB) on transpial collateralization of an indirect encephalomyosynangiosis (EMS) in a model of chronic cerebral ischemia. Mouse myoblasts expressing a reporter gene alone (empty vector), VEGF, PDGF-BB or VEGF and PDGF-BB through a single bi-cistronic vector (VIP) were implanted into the temporalis muscle of an EMS following permanent ipsilateral internal carotid artery occlusion in adult, male C57BL/6N mice. Over 84 days, myoblast engraftment and gene product expression, hemodynamic impairment, transpial collateralization, angiogenesis, pericyte recruitment and post-ischemic neuroprotection were assessed. By day 42, animals that received PDGF-BB in combination with VEGF (VIP) showed superior hemodynamic recovery, EMS collateralization and ischemic protection with improved pericyte recruitment around the parenchymal vessels and EMS collaterals. Also, supplementation of PDGF-BB resulted in a striking astrocytic activation with intrinsic VEGF mobilization in the cortex below the EMS. Our findings suggest that EMS surgery together with myoblast-mediated co-delivery of VEGF/PDGF-BB may have the potential to serve as a novel treatment strategy for augmentation of collateral flow in the chronically hypoperfused brain

Correlates of Spreading Depolarization, Spreading Depression, and Negative Ultraslow Potential in Epidural Versus Subdural Electrocorticography

Spreading depolarizations (SDs) are characterized by near-complete breakdown of the transmembrane ion gradients, neuronal oedema and activity loss (=depression). The SD extreme in ischemic tissue, termed 'terminal SD,' shows prolonged depolarization, in addition to a slow baseline variation called 'negative ultraslow potential' (NUP). The NUP is the largest bioelectrical signal ever recorded from the human brain and is thought to reflect the progressive recruitment of neurons into death in the wake of SD. However, it is unclear whether the NUP is a field potential or results from contaminating sensitivities of platinum electrodes. In contrast to Ag/AgCl-based electrodes in animals, platinum/iridium electrodes are the gold standard for intracranial direct current (DC) recordings in humans. Here, we investigated the full continuum including short-lasting SDs under normoxia, long-lasting SDs under systemic hypoxia, and terminal SD under severe global ischemia using platinum/iridium electrodes in rats to better understand their recording characteristics. Sensitivities for detecting SDs or NUPs were 100% for both electrode types. Nonetheless, the platinum/iridium-recorded NUP was 10 times smaller in rats than humans. The SD continuum was then further investigated by comparing subdural platinum/iridium and epidural titanium peg electrodes in patients. In seven patients with either aneurysmal subarachnoid hemorrhage or malignant hemispheric stroke, two epidural peg electrodes were placed 10 mm from a subdural strip. We found that 31/67 SDs (46%) on the subdural strip were also detected epidurally. SDs that had longer negative DC shifts and spread more widely across the subdural strip were more likely to be observed in epidural recordings. One patient displayed an SD-initiated NUP while undergoing brain death despite continued circulatory function. The NUP's amplitude was -150 mV subdurally and -67 mV epidurally. This suggests that the human NUP is a bioelectrical field potential rather than an artifact of electrode sensitivity to other factors, since the dura separates the epidural from the subdural compartment and the epidural microenvironment was unlikely changed, given that ventilation, arterial pressure and peripheral oxygen saturation remained constant during the NUP. Our data provide further evidence for the clinical value of invasive electrocorticographic monitoring, highlighting important possibilities as well as limitations of less invasive recording techniques