Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension.

BACKGROUND: The effect of decompressive craniectomy on clinical outcomes in patients with refractory traumatic intracranial hypertension remains unclear. METHODS: From 2004 through 2014, we randomly assigned 408 patients, 10 to 65 years of age, with traumatic brain injury and refractory elevated intracranial pressure (>25 mm Hg) to undergo decompressive craniectomy or receive ongoing medical care. The primary outcome was the rating on the Extended Glasgow Outcome Scale (GOS-E) (an 8-point scale, ranging from death to "upper good recovery" [no injury-related problems]) at 6 months. The primary-outcome measure was analyzed with an ordinal method based on the proportional-odds model. If the model was rejected, that would indicate a significant difference in the GOS-E distribution, and results would be reported descriptively. RESULTS: The GOS-E distribution differed between the two groups (P<0.001). The proportional-odds assumption was rejected, and therefore results are reported descriptively. At 6 months, the GOS-E distributions were as follows: death, 26.9% among 201 patients in the surgical group versus 48.9% among 188 patients in the medical group; vegetative state, 8.5% versus 2.1%; lower severe disability (dependent on others for care), 21.9% versus 14.4%; upper severe disability (independent at home), 15.4% versus 8.0%; moderate disability, 23.4% versus 19.7%; and good recovery, 4.0% versus 6.9%. At 12 months, the GOS-E distributions were as follows: death, 30.4% among 194 surgical patients versus 52.0% among 179 medical patients; vegetative state, 6.2% versus 1.7%; lower severe disability, 18.0% versus 14.0%; upper severe disability, 13.4% versus 3.9%; moderate disability, 22.2% versus 20.1%; and good recovery, 9.8% versus 8.4%. Surgical patients had fewer hours than medical patients with intracranial pressure above 25 mm Hg after randomization (median, 5.0 vs. 17.0 hours; P<0.001) but had a higher rate of adverse events (16.3% vs. 9.2%, P=0.03). CONCLUSIONS: At 6 months, decompressive craniectomy in patients with traumatic brain injury and refractory intracranial hypertension resulted in lower mortality and higher rates of vegetative state, lower severe disability, and upper severe disability than medical care. The rates of moderate disability and good recovery were similar in the two groups. (Funded by the Medical Research Council and others; RESCUEicp Current Controlled Trials number, ISRCTN66202560 .).

Monitoring Cerebral Autoregulation After Subarachnoid Hemorrhage.

INTRODUCTION: Delayed cerebral ischemia (DCI) is a major contributor to morbidity and mortality after subarachnoid hemorrhage (SAH). Data challenge vasospasm being the sole cause of ischemia and suggest other factors. We tested the hypothesis that early autoregulatory failure might predict DCI. METHODS: This is a prospective observational study of cerebral autoregulation following SAH in which the primary end point was DCI at 21 days. Cox proportional hazards and multivariate models were used and the benefit of using multiple indices was analyzed. RESULTS: Ninety-eight patients were included in the study. There was an increased risk of DCI with early dysautoregulation (odds ratio [OR]: 7.46, 95% confidence interval [CI]: 3.03-18.40 and OR: 4.52, 95 % CI: 1.84-11.07 for the transcranial Doppler index of autoregulation [Sxa] and near-infrared spectroscopy index of autoregulation [TOxa], respectively), but not vasospasm (OR: 1.36, 95 % CI: 0.56-3.33). Sxa and TOxa remained independent predictors of DCI in the multivariate model (OR: 12.66, 95 % CI: 2.97-54.07 and OR: 5.34, 95 % CI: 1.25-22.84 for Sxa and TOxa, respectively). There was good agreement between different indices. All 13 patients with impaired autoregulation in all three methods developed DCI. CONCLUSIONS: Disturbed autoregulation in the first 5 days after SAH is predictive of DCI. Although colinearities exist between the methods assessed, multimodal monitoring of cerebral autoregulation can aid the prediction of DCI.

Decompressive craniectomy following traumatic brain injury: developing the evidence base.

In the context of traumatic brain injury (TBI), decompressive craniectomy (DC) is used as part of tiered therapeutic protocols for patients with intracranial hypertension (secondary or protocol-driven DC). In addition, the bone flap can be left out when evacuating a mass lesion, usually an acute subdural haematoma (ASDH), in the acute phase (primary DC). Even though, the principle of "opening the skull" in order to control brain oedema and raised intracranial pressure has been practised since the beginning of the 20th century, the last 20 years have been marked by efforts to develop the evidence base with the conduct of randomised trials. This article discusses the merits and challenges of this approach and provides an overview of randomised trials of DC following TBI. An update on the RESCUEicp study, a randomised trial of DC versus advanced medical management (including barbiturates) for severe and refractory post-traumatic intracranial hypertension is provided. In addition, the rationale for the RESCUE-ASDH study, the first randomised trial of primary DC versus craniotomy for adult head-injured patients with an ASDH, is presented.

Regional brain monitoring in the neurocritical care unit.

Regional multimodality monitoring has evolved over the last several years as a tool to understand the mechanisms of brain injury and brain function at the cellular level. Multimodality monitoring offers an important augmentation to the clinical exam and is especially useful in comatose neurocritical care patients. Cerebral microdialysis, brain tissue oxygen monitoring, and cerebral blood flow monitoring all offer insight into permutations in brain chemistry and function that occur in the context of brain injury. These tools may allow for development of individual therapeutic strategies that are mechanistically driven and goal-directed. We present a summary of the discussions that took place during the Second Neurocritical Care Research Conference regarding regional brain monitoring.

Bilateral failure of cerebral autoregulation is related to unfavorable outcome after subarachnoid hemorrhage.

BACKROUND: The extent of hemodynamic disturbances following subarachnoid hemorrhage (SAH) varies. We aim to determine the prognostic implications of unilateral and bilateral autoregulatory failure on delayed cerebral ischemia (DCI) and outcome. METHODS: Ninety-eight patients with aneurysmal SAH were recruited. Autoregulation was assessed using systolic flow index-Sxa. Interhemispheric difference in autoregulation was calculated to assess the spatial distribution and symmetry of autoregulatory changes. Assessment of interhemispheric difference in autoregulation in combination with overall autoregulation was used to measure the extent of autoregulatory impairment. Patients were dichotomized by the presence of DCI and 3-month mRS. RESULTS: Higher flow velocity and worse autoregulation (p < 0.0000001, 95 % CI 10.7-21.3 and p = 0.00001, 95 % CI 0.03-0.07 for difference in FV and Sxa, respectively) were found ipsilateral to the ischemic hemisphere or location of aneurysm (if no ischemia detected). DCI group had a higher interhemispheric difference of autoregulation than non-DCI group (p = 0.035, 95 % CI 0.003-0.08). 16/18 patients with unfavorable outcome vs. 17/72 with favorable outcome had overall poor autoregulation with low interhemispheric differences (p = 0.0013, χ (2)). Unilateral autoregulatory failure was seen on a median day 3, bilateral on day 4, and vasospasm was detected on day 6. CONCLUSIONS: Unilateral autoregulation failure was seen in patients who developed DCI (worse ipsilateral to the ischemic hemisphere). Bilateral autoregulation failure was seen more frequently in patients with unfavorable outcome. Analysis of the temporal profile showed unilateral dysautoregulation as the primary event predisposing to DCI, which in selected cases led to bilateral failure and unfavorable outcomes.

Multidisciplinary consensus on assessment of unruptured intracranial aneurysms: proposal of an international research group.

BACKGROUND AND PURPOSE: To address the increasing need to counsel patients about treatment indications for unruptured intracranial aneurysms (UIA), we endeavored to develop a consensus on assessment of UIAs among a group of specialists from diverse fields involved in research and treatment of UIAs. METHODS: After composition of the research group, a Delphi consensus was initiated to identify and rate all features, which may be relevant to assess UIAs and their treatment by using ranking scales and analysis of inter-rater agreement (IRA) for each factor. IRA was categorized as very high, high, moderate, or low. RESULTS: Ultimately, 39 specialists from 4 specialties agreed (high or very high IRAs) on the following key factors for or against UIA treatment decisions: (1) patient age, life expectancy, and comorbid diseases; (2) previous subarachnoid hemorrhage from a different aneurysm, family history for UIA or subarachnoid hemorrhage, nicotine use; (3) UIA size, location, and lobulation; (4) UIA growth or de novo formation on serial imaging; (5) clinical symptoms (cranial nerve deficit, mass effect, and thromboembolic events from UIAs); and (6) risk factors for UIA treatment (patient age and life expectancy, UIA size, and estimated risk of treatment). However, IRAs for features rated with low relevance were also generally low, which underlined the existing controversy about the natural history of UIAs. CONCLUSIONS: Our results highlight that neurovascular specialists currently consider many features as important when evaluating UIAs but also highlight that the appreciation of natural history of UIAs remains uncertain, even within a group of highly informed individuals.

The pathophysiology and treatment of delayed cerebral ischaemia following subarachnoid haemorrhage.

Cerebral vasospasm has traditionally been regarded as an important cause of delayed cerebral ischaemia (DCI) which occurs after aneurysmal subarachnoid haemorrhage, and often leads to cerebral infarction and poor neurological outcome. However, data from recent studies argue against a pure focus on vasospasm as the cause of delayed ischaemic complications. Findings that marked reduction in the incidence of vasospasm does not translate to a reduction in DCI, or better outcomes has intensified research into other possible mechanisms which may promote ischaemic complications. Early brain injury and cell death, blood-brain barrier disruption and initiation of an inflammatory cascade, microvascular spasm, microthrombosis, cortical spreading depolarisations and failure of cerebral autoregulation, have all been implicated in the pathophysiology of DCI. This review summarises the current knowledge about the mechanisms underlying the development of DCI. Furthermore, it aims to describe and categorise the known pharmacological treatment options with respect to the presumed mechanism of action and its role in DCI.

Recovery of oculomotor nerve palsy secondary to posterior communicating artery aneurysms.

BACKGROUND: Recent studies suggest more favourable recovery of oculomotor nerve palsy (ONP) caused by posterior communicating artery (PComA) aneurysms with microsurgical clipping compared to endovascular coiling. We describe a consecutive series of patients with ONP from PComA aneurysms treated by microsurgical clipping or endovascular coiling. METHODS: We retrospectively reviewed medical records of all patients from 2005 to 2009 with complete or partial ONP from PComA aneurysms. RESULTS: Twenty patients were identified, three with unruptured aneurysms. Two patients with ruptured aneurysms were unfit for treatment and therefore excluded. Of the 18 patients included (15 female), 9 underwent microsurgical clipping and 9 received endovascular coiling. Patients treated by surgical clipping were significantly younger compared to those treated by endovascular coiling (mean 52.3 vs. 67.9 years; p = 0.039). Five patients had incomplete ONP (3 clipped, 2 coiled) and thirteen had complete ONP. At 6 months, six of nine patients treated with clipping and five of nine patients treated with coiling had complete resolution of their ONP (p = 1.0); the remainder had partial improvement. There was no significant difference in duration of pre-treatment ONP, age, sex or status of aneurysm (ruptured or unruptured) between patients in the two groups or between those with full or partial recovery. However, all 5 patients with incomplete ONP at presentation recovered fully, compared with 6 of 13 patients who presented with complete ONP. CONCLUSIONS: We found no significant difference between clipping and coiling in the recovery of ONP due to PComA aneurysms. Patient who present with incomplete ONP are more likely to have a full recovery of ONP following either treatment modality than those who present with complete ONP.

The phase coherence of the neurovascular unit is reduced in Huntington's disease.

Huntington's disease is a neurodegenerative disorder in which neuronal death leads to chorea and cognitive decline. Individuals with ≥40 cytosine-adenine-guanine repeats on the interesting transcript 15 gene develop Huntington's disease due to a mutated huntingtin protein. While the associated structural and molecular changes are well characterized, the alterations in neurovascular function that lead to the symptoms are not yet fully understood. Recently, the neurovascular unit has gained attention as a key player in neurodegenerative diseases. The mutant huntingtin protein is known to be present in the major parts of the neurovascular unit in individuals with Huntington's disease. However, a non-invasive assessment of neurovascular unit function in Huntington's disease has not yet been performed. Here, we investigate neurovascular interactions in presymptomatic (N = 13) and symptomatic (N = 15) Huntington's disease participants compared to healthy controls (N = 36). To assess the dynamics of oxygen transport to the brain, functional near-infrared spectroscopy, ECG and respiration effort were recorded. Simultaneously, neuronal activity was assessed using EEG. The resultant time series were analysed using methods for discerning time-resolved multiscale dynamics, such as wavelet transform power and wavelet phase coherence. Neurovascular phase coherence in the interval around 0.1 Hz is significantly reduced in both Huntington's disease groups. The presymptomatic Huntington's disease group has a lower power of oxygenation oscillations compared to controls. The spatial coherence of the oxygenation oscillations is lower in the symptomatic Huntington's disease group compared to the controls. The EEG phase coherence, especially in the α band, is reduced in both Huntington's disease groups and, to a significantly greater extent, in the symptomatic group. Our results show a reduced efficiency of the neurovascular unit in Huntington's disease both in the presymptomatic and symptomatic stages of the disease. The vasculature is already significantly impaired in the presymptomatic stage of the disease, resulting in reduced cerebral blood flow control. The results indicate vascular remodelling, which is most likely a compensatory mechanism. In contrast, the declines in α and γ coherence indicate a gradual deterioration of neuronal activity. The results raise the question of whether functional changes in the vasculature precede the functional changes in neuronal activity, which requires further investigation. The observation of altered dynamics paves the way for a simple method to monitor the progression of Huntington's disease non-invasively and evaluate the efficacy of treatments.

Stenting venous outflow gives symptomatic improvement in a patient with an inoperable brainstem arteriovenous malformation.

The extent to which arterial steal or venous hypertension contributes to symptoms in patients with high flow brain arteriovenous malformations (AVMs) is not always clear. We describe a patient with an inoperable AVM of the pons, presenting with headache and neurological deficit where improving venous outflow by stenting produced substantial clinical benefit.

Results of Surgical Treatment of Aneurysmal Subarachnoid Hemorrhage in a Single Institution Over 12 Years.

OBJECTIVE: For patients with aneurysmal subarachnoid hemorrhage (aSAH) in whom endovascular treatment is not the optimal treatment strategy, microsurgical clipping remains a viable option. We examined changes in morbidity and outcome over time in patients treated surgically and in relation to surgeon volume and experience. METHODS: All patients who underwent microsurgery for aSAH from 2007 to 2019 at our institution were included. We compared technical complication rates and surgical outcomes between experienced (≥50 independent cases) and inexperienced (<50 independent cases) surgeons and between high-volume (≥20 cases/year) and low-volume (<20 cases/year) surgeons. RESULTS: Most of the 1,003 aneurysms (970 patients, median age 56 years) were in the middle cerebral (41.4%), anterior communicating (27.6%), and posterior communicating (17.5%) arteries; 46.5% were <7 mm. The technical complication rate was 7%, resulting in postoperative infarct in 4.9% of patients. Nineteen patients (2%) died within 30 days of admission. There were no significant changes in rates of technical complication, postoperative infarct, or mortality over the study period. There were no differences in postoperative infarction and technical complication rates between experienced and inexperienced surgeons (P = 0.28 and P = 0.05, respectively), but there were differences when comparing high-volume and low-volume surgeons (P = 0.03 and P < 0.001, respectively). The independent predictors of postoperative infarctions were aneurysm size (P = 0.001), intraoperative large-vessel injury (P < 0.001), and low surgeon volume (P = 0.03). CONCLUSIONS: We present real-world data on surgical morbidity and outcomes after aSAH. We demonstrated a relationship between surgeon volume and outcome for surgical treatment of aSAH, which supports the benefit of subspecialization in cerebrovascular surgery.

Impairment of cerebral autoregulation predicts delayed cerebral ischemia after subarachnoid hemorrhage: a prospective observational study.

BACKGROUND AND PURPOSE: Delayed cerebral ischemia (DCI) is a recognized contributor to unfavorable outcome after subarachnoid hemorrhage (SAH). Recent data challenge the concept of vasospasm as the sole cause of ischemia and suggest a multifactorial process with dysfunctional cerebral autoregulation as a component. We tested the hypothesis that early autoregulatory failure, detected using near-infrared spectroscopy-based index, TOxa and transcranial Doppler-based index, Sxa, can predict DCI. METHODS: In this prospective observational study we enrolled consecutive patients with aneurysmal SAH that occurred <5 days from admission. The primary end point was the occurrence of DCI within 21 days of ictus. The predictive value of autoregulatory disturbances detected in the first 5 days was assessed using univarate proportional hazards model and a multivariate model. RESULTS: Ninety-eight patients were included. Univariate analysis demonstrated increased odds of developing DCI when early autoregulation failure was detected (odds ratio [OR], 7.46; 95% confidence interval [CI], 3.03-18.40 and OR, 4.52; 95% CI, 1.84-11.07 for Sxa and TOxa, respectively) but not TCD-vasospasm (OR, 1.36; 95% CI, 0.56-3.33). In a multivariate model Sxa and TOxa remained independent predictors of DCI (OR, 12.66; 95% CI, 2.97-54.07 and OR, 5.34; 95% CI, 1.25-22.84 for Sxa and TOxa, respectively). CONCLUSIONS: Disturbed autoregulation in the first 5 days after SAH significantly increases the risk of DCI. Autoregulatory disturbances can be detected using near-infrared spectroscopy and transcranial Doppler technologies.

Cerebral extracellular chemistry and outcome following traumatic brain injury: a microdialysis study of 223 patients.

Secondary insults can adversely influence outcome following severe traumatic brain injury. Monitoring of cerebral extracellular chemistry with microdialysis has the potential for early detection of metabolic derangements associated with such events. The objective of this study was to determine the relationship between the fundamental biochemical markers and neurological outcome in a large cohort of patients with traumatic brain injury. Prospectively collected observational neuromonitoring data from 223 patients were analysed. Monitoring modalities included digitally recorded intracranial pressure, cerebral perfusion pressure, cerebrovascular pressure reactivity index and microdialysis markers glucose, lactate, pyruvate, glutamate, glycerol and the lactate/pyruvate ratio. Outcome was assessed using the Glasgow Outcome Scale at 6 months post-injury. Patient-averaged values of parameters were used in statistical analysis, which included univariate non-parametric methods and multivariate logistic regression. Monitoring with microdialysis commenced on median (interquartile range) Day 1 (1-2) from injury and median (interquartile range) duration of monitoring was 4 (2-7) days. Averaged over the total monitoring period levels of glutamate (P = 0.048), lactate/pyruvate ratio (P = 0.044), intracranial pressure (P = 0.006) and cerebrovascular pressure reactivity index (P = 0.01) were significantly higher in patients who died. During the initial 72 h of monitoring, median glycerol levels were also higher in the mortality group (P = 0.014) and median lactate/pyruvate ratio (P = 0.026) and lactate (P = 0.033) levels were significantly lower in patients with favourable outcome. In a multivariate logistic regression model (P < 0.0001), which employed data averaged over the whole monitoring period, significant independent positive predictors of mortality were glucose (P = 0.024), lactate/pyruvate ratio (P = 0.016), intracranial pressure (P = 0.029), cerebrovascular pressure reactivity index (P = 0.036) and age (P = 0.003), while pyruvate was a significant independent negative predictor of mortality (P = 0.004). The results of this study suggest that extracellular metabolic markers are independently associated with outcome following traumatic brain injury. Whether treatment-related improvement in biochemistry translates into better outcome remains to be established.

Fixed, dilated pupils following traumatic brain injury: historical perspectives, causes and ophthalmological sequelae.

Pupillary abnormalities are commonly seen in patients presenting with severe traumatic brain injury (TBI). The objectives of this study were to determine the underlying condition responsible, the natural history of recovery of third nerve palsy and the ultimate clinical outcome in 60 patients admitted to a regional neurosurgical centre with a diagnosis of TBI and unilateral or bilateral fixed, dilated pupils (FDP). In approximately three-quarters of cases, some form of road traffic incident was the mechanism of injury. In patients presenting with a unilateral FDP, the CT-defined condition was most commonly diffuse brain injury (49%) with no obvious lateralising condition. In 34% of cases CT demonstrated a lateralising condition ipsilateral to the side of the FDP and in 9% cases the FDP was contralateral to the side of the CT abnormality. Of those patients who survived an FDP, 72% were left with some form of ophthalmological deficit. Most patients with bilateral FDP did not survive (88%); however, of those who did survive, none was left in a persistent vegetative state or with any ophthalmological sequelae. A FDP is a grave prognostic sign following TBI commonly resulting in long term ophthalmological sequelae; however, a favourable outcome is still attainable.

Time constant of the cerebral arterial bed.

We have defined a novel cerebral hemodynamic index, a time constant of the cerebral arterial bed (τ), the product of arterial compliance (C(a)) and cerebrovascular resistance (CVR). C(a) and CVR were calculated based on the relationship between pulsatile arterial blood pressure (ABP) and transcranial Doppler cerebral blood flow velocity. This new parameter theoretically estimates how fast the cerebral arterial bed is filled by blood volume after a sudden change in ABP during one cardiac cycle. We have explored this concept in 11 volunteers and in 25 patients with severe stenosis of the internal carotid artery (ICA). An additional group of 15 subjects with non-vascular dementia was studied to assess potential age dependency of τ. The τ was shorter (p = 0.011) in ICA stenosis, both unilateral (τ = 0.18 ± 0.04 s) and bilateral (τ = 0.16 ± 0.03 s), than in controls (τ = 0.22 ± 0.0 s). The τ correlated with the degree of stenosis (R = -0.62, p = 0.001). In controls, τ was independent of age. Further study during cerebrovascular reactivity tests is needed to establish the usefulness of τ for quantitative estimation of haemodynamics in cerebrovascular disease.

Outcome following evacuation of acute subdural haematomas: a comparison of craniotomy with decompressive craniectomy.

BACKGROUND: Acute subdural haematomas (ASDH) occur commonly following traumatic brain injury and may be evacuated by either craniotomy (CR) or decompressive craniectomy (DC). We reviewed a series of consecutive patients undergoing evacuation of a traumatic ASDH at a regional centre, comparing observed clinical outcomes (assessed by Glasgow Outcome Scale at six months) with those predicted by the CRASH-CT prognostic model. METHODS: Retrospective review of prospectively collected data. RESULTS: Ninety-one patients were identified (51 DC and 40 CR ). Eighty-five had available admission data sets from which predicted outcome could be calculated. The DC group were younger than the CR group (p = 0.015). The DC group also had a greater proportion of patients whose pre-intubation GCS was ≤8 (p = 0.001), with significant extracranial injuries (p = 0.001) and obliterated basal cisterns (p = 0.001) on their pre-operative CT scan. Bone flaps in the DC group (n = 45) were longer (mean 11.6 cm; 95 % CI: 11.1-12.1) in comparison to bone flaps in the CR (n = 34) group [(mean 10.2 cm; 95 % CI: 9.35 - 10.9); p = 0.0024] The mean CRASH-CT predicted risk of 14-day mortality and of unfavourable outcome at six months was significantly higher in the DC group compared with the CR group. Eighty-eight patients had available 6-month Glasgow Outcome Scale scores. Favourable outcomes were observed in 42 % of DC versus 45 % of CR (p = 0.83). The overall mortality rate was 38 % in DC versus 32 % in CR (p = 0.65). The standardised morbidity ratio (observed/expected unfavourable outcomes) was 0.75 (95 % CI: 0.51-1.07) for DC and 0.90 (95 % CI: 0.57-1.35) for CR. CONCLUSIONS: CR and DC for traumatic ASDH are both commonly used for primary evacuation of ASDH. Primary DC may be more effective than CR for selected patients with ASDH. Class I evidence is required in order to refine the indications for DC following evacuation of ASDH.

Monitoring cerebral autoregulation after head injury. Which component of transcranial Doppler flow velocity is optimal?

BACKGROUND: Cerebral autoregulation assessed using transcranial Doppler (TCD) mean flow velocity (FV) in response to various physiological challenges is predictive of outcome after traumatic brain injury (TBI). Systolic and diastolic FV have been explored in other diseases. This study aims to evaluate the systolic, mean and diastolic FV for monitoring autoregulation and predicting outcome after TBI. METHODS: 300 head-injured patients with blood pressure (ABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), and FV recordings were studied. Autoregulation was calculated as a correlation of slow changes in diastolic, mean and systolic components of FV with CPP (Dx, Mx, Sx, respectively) and ABP (Dxa, Mxa, Sxa, respectively) from 30 consecutive 10 s averaged values. The relationship with age, severity of injury, and dichotomized 6 months outcome was examined. RESULTS: Association with outcome was significant for Mx and Sx. For favorable/unfavorable and death/survival outcomes Sx showed the strongest association (F = 20.11; P = 0.00001 and F = 13.10; P = 0.0003, respectively). Similarly, indices derived from ABP demonstrated the highest discriminatory value when systolic FV was used (F = 12.49; P = 0.0005 and F = 5.32; P = 0.02, respectively). Indices derived from diastolic FV demonstrated significant differences (when calculated using CPP) only when comparing between fatal and non-fatal outcome. CONCLUSIONS: Systolic flow indices (Sx and Sxa) demonstrated a stronger association with outcome than the mean flow indices (Mx and Mxa), irrespective of whether CPP or ABP was used for calculation.

Vasospasm shortens cerebral arterial time constant.

BACKGROUND: Cerebrovascular time constant (τ) estimates how fast cerebral blood arrives in cerebral arterial bed after each heart stroke. We investigate the pattern of changes in τ following subarachnoid hemorrhage (SAH), with specific emphasis on the temporal profile of changes in relation to the development of cerebral vasospasm. METHODS: Simultaneous recordings of arterial blood pressure (ABP) and transcranial Doppler (TCD) blood flow velocity (CBFV) in MCA were performed daily in patients after SAH. In 22 patients (10 males and 12 females; median age: 48 years, range: 34-84 years) recordings done before spasm were compared to those done during spasm. Vasospasm was confirmed with TCD (mean CBFV in MCA > 120 cm/s and Lindegaard ratio > 3). τ was estimated as a product of compliance of cerebral arteries (C (a)) and cerebrovascular resistance (CVR). C (a) and CVR were estimated using mathematical transformations of ABP and CBFV waveforms. RESULTS: Vasospasm caused shortening of τ on both the spastic (before: 0.20 ± 0.05 s vs. spasm: 0.14 ± 0.04 s, P < 0.0008) and contralateral side (before: 0.22 ± 0.05 s vs. spasm: 0.16 ± 0.04 s, P < 0.0008). Before TCD signs of vasospasm were detected, τ demonstrated asymmetry with lower values on ipsilateral side to aneurysm, in comparison to contralateral side (P < 0.009), CONCLUSIONS: Cerebral vasospasm causes shortening of τ. Shorter τ at the side of aneurysm can be observed before formal TCD signs of vasospasm are observed, therefore, potentially reducing time to escalation of treatment.

Coiling of a residual internal carotid artery aneurysm via an extracranial-intracranial bypass graft following parent vessel occlusion.

We report the case of a ruptured internal carotid artery (ICA) aneurysm that demonstrated significant persistent filling despite management with a common carotid to middle cerebral artery saphenous vein extracranial-intracranial bypass and subsequent permanent ICA balloon occlusion. The residual aneurysm was successfully embolised with detachable coils using a novel endovascular approach via the bypass graft.

Evaluation of Outcomes Among Patients With Traumatic Intracranial Hypertension Treated With Decompressive Craniectomy vs Standard Medical Care at 24 Months: A Secondary Analysis of the RESCUEicp Randomized Clinical Trial.

Importance: Trials often assess primary outcomes of traumatic brain injury at 6 months. Longer-term data are needed to assess outcomes for patients receiving surgical vs medical treatment for traumatic intracranial hypertension. Objective: To evaluate 24-month outcomes for patients with traumatic intracranial hypertension treated with decompressive craniectomy or standard medical care. Design, Setting, and Participants: Prespecified secondary analysis of the Randomized Evaluation of Surgery With Craniectomy for Uncontrollable Elevation of Intracranial Pressure (RESCUEicp) randomized clinical trial data was performed for patients with traumatic intracranial hypertension (>25 mm Hg) from 52 centers in 20 countries. Enrollment occurred between January 2004 and March 2014. Data were analyzed between 2018 and 2021. Eligibility criteria were age 10 to 65 years, traumatic brain injury (confirmed via computed tomography), intracranial pressure monitoring, and sustained and refractory elevated intracranial pressure for 1 to 12 hours despite pressure-controlling measures. Exclusion criteria were bilateral fixed and dilated pupils, bleeding diathesis, or unsurvivable injury. Interventions: Patients were randomly assigned 1:1 to receive a decompressive craniectomy with standard care (surgical group) or to ongoing medical treatment with the option to add barbiturate infusion (medical group). Main Outcomes and Measures: The primary outcome was measured with the 8-point Extended Glasgow Outcome Scale (1 indicates death and 8 denotes upper good recovery), and the 6- to 24-month outcome trajectory was examined. Results: This study enrolled 408 patients: 206 in the surgical group and 202 in the medical group. The mean (SD) age was 32.3 (13.2) and 34.8 (13.7) years, respectively, and the study population was predominantly male (165 [81.7%] and 156 [80.0%], respectively). At 24 months, patients in the surgical group had reduced mortality (61 [33.5%] vs 94 [54.0%]; absolute difference, -20.5 [95% CI, -30.8 to -10.2]) and higher rates of vegetative state (absolute difference, 4.3 [95% CI, 0.0 to 8.6]), lower or upper moderate disability (4.7 [-0.9 to 10.3] vs 2.8 [-4.2 to 9.8]), and lower or upper severe disability (2.2 [-5.4 to 9.8] vs 6.5 [1.8 to 11.2]; χ27 = 24.20, P = .001). For every 100 individuals treated surgically, 21 additional patients survived at 24 months; 4 were in a vegetative state, 2 had lower and 7 had upper severe disability, and 5 had lower and 3 had upper moderate disability, respectively. Rates of lower and upper good recovery were similar for the surgical and medical groups (20 [11.0%] vs 19 [10.9%]), and significant differences in net improvement (≥1 grade) were observed between 6 and 24 months (55 [30.0%] vs 25 [14.0%]; χ22 = 13.27, P = .001). Conclusions and Relevance: At 24 months, patients with surgically treated posttraumatic refractory intracranial hypertension had a sustained reduction in mortality and higher rates of vegetative state, severe disability, and moderate disability. Patients in the surgical group were more likely to improve over time vs patients in the medical group. Trial Registration: ISRCTN Identifier: 66202560.