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Paul M. Foreman, Christoph J. Griessenauer, Michelle Chua, Mark N. Hadley and Mark R. Harrigan

OBJECT

Approximately 10% of patients with blunt traumatic extracranial cerebrovascular injury have a complete occlusion of the vertebral artery (VA). Ischemic stroke due to embolization of thrombus from an occluded VA following cervical spine surgery has been observed. The risk of ischemic stroke with cervical spine surgery in the presence of an occluded VA, however, has never been determined.

METHODS

A retrospective chart review of 52 patients with a VA occlusion following a blunt trauma was performed. Clinical and radiographic characteristics were collected and analyzed.

RESULTS

Ten patients (19.2%) suffered an ischemic stroke attributable to a traumatic VA occlusion. Univariate analysis demonstrated that patients with ischemic stroke were significantly older (p = 0.042) and had a lower rate of cervical spine surgery (p < 0.005). Multivariate analysis found cervical spine surgery to be protective against ischemic stroke (OR 0.049 [95% CI 0.014–0.167], p = 0.014); increasing age and bilateral VA injury (bilateral occlusion or unilateral occlusion with contralateral dissection) were risk factors for ischemic stroke (OR 1.05 [95% CI1.02–1.07], p = 0.065 and OR 13.2 [95% CI 2.98–58.9], p = 0.084, respectively).

CONCLUSIONS

Traumatic VA occlusion is associated with a risk of ischemic stroke and mortality. Corrective cervical spine surgery potentially decreases the risk of ischemic stroke by stabilizing the spine and thereby reducing motion across the occluded segment of the VA and preventing embolization of thrombus. While a high stoke risk may be inherent to the disease, novel therapies should be investigated.

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Jan-Karl Burkhardt, Michelle H. Chua, Ethan A. Winkler, W. Caleb Rutledge and Michael T. Lawton

OBJECTIVE

During the microsurgical clipping of known aneurysms, angiographically occult (AO) aneurysms are sometimes found and treated simultaneously to prevent their growth and protect the patient from future rupture or reoperation. The authors analyzed the incidence, treatment, and outcomes associated with AO aneurysms to determine whether limited surgical exploration around the known aneurysm was safe and justified given the known limitations of diagnostic angiography.

METHODS

An AO aneurysm was defined as a saccular aneurysm detected using the operative microscope during dissection of a known aneurysm, and not detected on preoperative catheter angiography. A prospective database was retrospectively reviewed to identify patients with AO aneurysms treated microsurgically over a 20-year period.

RESULTS

One hundred fifteen AO aneurysms (4.0%) were identified during 2867 distinct craniotomies for aneurysm clipping. The most common locations for AO aneurysms were the middle cerebral artery (60 aneurysms, 54.1%) and the anterior cerebral artery (20 aneurysms, 18.0%). Fifty-six AO aneurysms (50.5%) were located on the same artery as the known saccular aneurysm. Most AO aneurysms (95.5%) were clipped and there was no attributed morbidity. The most common causes of failed angiographic detection were superimposition of a large aneurysm (type 1, 30.6%), a small aneurysm (type 2, 18.9%), or an adjacent normal artery (type 3, 36.9%). Multivariate analysis identified multiple known aneurysms (odds ratio [OR] 3.45, 95% confidence interval [CI] 2.16–5.49, p < 0.0001) and young age (OR 0.981, 95% CI 0.965–0.997, p = 0.0226) as independent predictors of AO aneurysms.

CONCLUSIONS

Meticulous inspection of common aneurysm sites within the surgical field will identify AO aneurysms during microsurgical dissection of another known aneurysm. Simultaneous identification and treatment of these additional undiagnosed aneurysms can spare patients later rupture or reoperation, particularly in those with multiple known aneurysms and a history of subarachnoid hemorrhage. Limited microsurgical exploration around a known aneurysm can be performed safely without additional morbidity.

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Paul M. Foreman, Michelle H. Chua, Mark R. Harrigan, Winfield S. Fisher III, R. Shane Tubbs, Mohammadali M. Shoja and Christoph J. Griessenauer

OBJECTIVE

Delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH) occurs in approximately 30% of patients. The Practical Risk Chart was developed to predict DCI based on admission characteristics; the authors seek to externally validate and critically appraise this prediction tool.

METHODS

A prospective cohort of aSAH patients was used to externally validate the previously published Practical Risk Chart. The model consists of 4 variables: clinical condition on admission, amount of cisternal and intraventricular blood on CT, and age. External validity was assessed using logistic regression. Model discrimination was evaluated using the area under the receiver operating characteristic curve (AUC).

RESULTS

In a cohort of 125 patients with aSAH, the Practical Risk Chart adequately predicted DCI, with an AUC of 0.66 (95% CI 0.55–0.77). Clinical grade on admission and amount of intracranial blood on CT were the strongest predictors of DCI and clinical vasospasm. The best-fit model used a combination of the Hunt and Hess grade and the modified Fisher scale to yield an AUC of 0.76 (95% CI 0.675–0.85) and 0.70 (95% CI 0.602–0.8) for the prediction of DCI and clinical vasospasm, respectively.

CONCLUSIONS

The Practical Risk Chart adequately predicts the risk of DCI following aSAH. However, the best-fit model represents a simpler stratification scheme, using only the Hunt and Hess grade and the modified Fisher scale, and produces a comparable AUC.

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Paul M. Foreman, Michelle Chua, Mark R. Harrigan, Winfield S. Fisher III, Nilesh A. Vyas, Robert H. Lipsky, Beverly C. Walters, R. Shane Tubbs, Mohammadali M. Shoja and Christoph J. Griessenauer

OBJECTIVE

Delayed cerebral ischemia (DCI) is a recognized complication of aneurysmal subarachnoid hemorrhage (aSAH) that contributes to poor outcome. This study seeks to determine the effect of nosocomial infection on the incidence of DCI and patient outcome.

METHODS

An exploratory analysis was performed on 156 patients with aSAH enrolled in the Cerebral Aneurysm Renin Angiotensin System study. Clinical and radiographic data were analyzed with univariate analysis to detect risk factors for the development of DCI and poor outcome. Multivariate logistic regression was performed to identify independent predictors of DCI.

RESULTS

One hundred fifty-three patients with aSAH were included. DCI was identified in 32 patients (20.9%). Nosocomial infection (odds ratio [OR] 3.5, 95% confidence interval [CI] 1.09–11.2, p = 0.04), ventriculitis (OR 25.3, 95% CI 1.39–458.7, p = 0.03), aneurysm re-rupture (OR 7.55, 95% CI 1.02–55.7, p = 0.05), and clinical vasospasm (OR 43.4, 95% CI 13.1–143.4, p < 0.01) were independently associated with the development of DCI. Diagnosis of nosocomial infection preceded the diagnosis of DCI in 15 (71.4%) of 21 patients. Patients diagnosed with nosocomial infection experienced significantly worse outcomes as measured by the modified Rankin Scale score at discharge and 1 year (p < 0.01 and p = 0.03, respectively).

CONCLUSIONS

Nosocomial infection is independently associated with DCI. This association is hypothesized to be partly causative through the exacerbation of systemic inflammation leading to thrombosis and subsequent ischemia.

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Christoph J. Griessenauer, Jeffrey D. Lebensburger, Michelle H. Chua, Winfield S. Fisher III, Lee Hilliard, Christina J. Bemrich-Stolz, Thomas H. Howard and James M. Johnston

OBJECT

Pediatric patients with sickle cell disease (SCD) and moyamoya syndrome (MMS) are at significant risk for cerebrovascular accidents despite chronic transfusion therapy. Encephaloduroarteriosynangiosis (EDAS) and encephalomyoarteriosynangiosis (EMAS) are additional therapeutic options for these patients. To date, the incidence of complications after and efficacy of EDAS and EMAS in stroke prevention in this population have been described in several institutional case series reports, but no randomized prospective trials have been reported.

METHODS

The authors retrospectively reviewed the cases of all pediatric patients at the University of Alabama at Birmingham with a history of homozygous hemoglobin S (HbS) and sickle cell/β-thalassemia (SB0 thalassemia) and on chronic transfusion therapy, including 14 patients with MMS who underwent EDAS or EMAS.

RESULTS

Sixty-two patients with SCD and on chronic transfusion therapy were identified. After exclusion of patients on chronic transfusion therapy for indications other than stroke prevention, 48 patients (77.4%) remained. Of those patients, 14 (29.1%) underwent EDAS or EMAS. Nine (18.8%) and 25 (52.1%) patients were on chronic transfusion therapy for primary or secondary stroke prevention, respectively, but did not undergo EDAS or EMAS. The 14 patients with SCD and radiological evidence of MMS and on chronic transfusion therapy for primary or secondary stroke prevention underwent 21 EDAS or EMAS procedures for progressive vascular disease (92.9% of patients), stroke (71.4%), and/or seizure (7.1%). The mean (± SD) time from initiation of chronic transfusion therapy to EDAS or EMAS was 76.8 ± 58.8 months. Complications included 1 perioperative stroke, 1 symptomatic subdural hygroma, 1 postoperative seizure, and 1 case of intraoperative cerebral edema that required subsequent cranioplasty. Before EDAS or EMAS, the stroke rate was calculated to be 1 stroke per 7.8 patient-years. One additional stroke occurred during the follow-up period (mean follow-up time 33.7 ± 19.6 months), resulting in a post-EDAS/EMAS stroke rate of 1 stroke per 39.3 patient-years, a 5-fold reduction compared with that in the pre-EDAS/EMAS period. The patients’ mean pre-EDAS/EMAS HbS level of 29.5% ± 6.4% was comparable to the mean post-EDAS/EMAS HbS level of 25.5% ± 6.1% (p = 0.104).

CONCLUSIONS

The results of this retrospective case series in a large cohort of pediatric patients with SCD and MMS suggest that EDAS/EMAS provides a stroke-prevention benefit with an acceptably low morbidity rate. Given the combined experience with EDAS and EMAS for this indication at this and other institutions, a prospective clinical trial to assess their efficacy compared with that of chronic transfusion therapy alone is warranted.

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Christoph J. Griessenauer, Christopher S. Ogilvy, Paul M. Foreman, Michelle H. Chua, Mark R. Harrigan, Christopher J. Stapleton, Aman B. Patel, Lucy He, Matthew R. Fusco, J Mocco, Peter A. Winkler, Apar S. Patel and Ajith J. Thomas

OBJECTIVE

Contemporary treatment for paraophthalmic artery aneurysms includes flow diversion utilizing the Pipeline Embolization Device (PED). Little is known, however, about the potential implications of the anatomical relationship of the ophthalmic artery (OA) origin and aneurysm, especially in smaller aneurysms.

METHODS

Four major academic institutions in the United States provided data on small paraophthalmic aneurysms (≤ 7 mm) that were treated with PED between 2009 and 2015. The anatomical relationship of OA origin and aneurysm, radiographic outcomes of aneurysm occlusion, and patency of the OA were assessed using digital subtraction angiography. OA origin was classified as follows: Type 1, OA separate from the aneurysm; Type 2, OA from the aneurysm neck; and Type 3, OA from the aneurysm dome. Clinical outcome was assessed using the modified Rankin Scale, and visual deficits were categorized as transient or permanent.

RESULTS

The cumulative number of small paraophthalmic aneurysms treated with PED between 2009 and 2015 at the 4 participating institutions was 69 in 52 patients (54.1 ± 13.7 years of age) with a male-to-female ratio of 1:12. The distribution of OA origin was 72.5% for Type 1, 17.4% for Type 2, and 10.1% for Type 3. Radiographic outcome at the last follow-up (median 11.5 months) was available for 54 aneurysms (78.3%) with complete, near-complete, and incomplete occlusion rates of 81.5%, 5.6%, and 12.9%, respectively. Two aneurysms (3%) resulted in transient visual deficits, and no patient experienced a permanent visual deficit. At the last follow-up, the OA was patent in 96.8% of treated aneurysms. Type 3 OA origin was associated with a lower rate of complete aneurysm occlusion (p = 0.0297), demonstrating a trend toward visual deficits (p = 0.0797) and a lower rate of OA patency (p = 0.0783).

CONCLUSIONS

Pipeline embolization treatment of small paraophthalmic aneurysms is safe and effective. An aneurysm where the OA arises from the aneurysm dome may be associated with lower rates of aneurysm occlusion, OA patency, and higher rates of transient visual deficits.

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Christoph J. Griessenauer, R. Shane Tubbs, Paul M. Foreman, Michelle H. Chua, Nilesh A. Vyas, Robert H. Lipsky, Mingkuan Lin, Ramaswamy Iyer, Rishikesh Haridas, Beverly C. Walters, Salman Chaudry, Aisana Malieva, Samantha Wilkins, Mark R. Harrigan, Winfield S. Fisher III and Mohammadali M. Shoja

OBJECTIVE

Renin-angiotensin system (RAS) genetic polymorphisms are thought to play a role in cerebral aneurysm formation and rupture. The Cerebral Aneurysm Renin Angiotensin System (CARAS) study prospectively evaluated associations of common RAS polymorphisms and clinical course after aneurysmal subarachnoid hemorrhage (aSAH).

METHODS

The CARAS study prospectively enrolled aSAH patients at 2 academic centers in the United States. A blood sample was obtained from all patients for genetic evaluation and measurement of plasma angiotensin converting enzyme (ACE) concentration. Common RAS polymorphisms were detected using 5′exonuclease genotyping assays and pyrosequencing. Analysis of associations of RAS polymorphisms and clinical course after aSAH were performed.

RESULTS

A total of 166 patients were screened, and 149 aSAH patients were included for analysis. A recessive effect of allele I (insertion) of the ACE I/D (insertion/deletion) polymorphism was identified for Hunt and Hess grade in all patients (OR 2.76, 95% CI 1.17–6.50; p = 0.0206) with subsequent poor functional outcome. There was a similar effect on delayed cerebral ischemia (DCI) in patients 55 years or younger (OR 3.63, 95% CI 1.04–12.7; p = 0.0439). In patients older than 55 years, there was a recessive effect of allele A of the angiotensin II receptor Type 2 (AT2) A/C single nucleotide polymorphism (SNP) on DCI (OR 4.70, 95% CI 1.43–15.4; p = 0.0111).

CONCLUSIONS

Both the ACE I/D polymorphism and the AT2 A/C single nucleotide polymorphism were associated with an age-dependent risk of delayed cerebral ischemia, whereas only the ACE I/D polymorphism was associated with poor clinical grade at presentation. Further studies are required to elucidate the relevant pathophysiology and its potential implication in the treatment of patients with aSAH.

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Christoph J. Griessenauer, R. Shane Tubbs, Paul M. Foreman, Michelle H. Chua, Nilesh A. Vyas, Robert H. Lipsky, Mingkuan Lin, Ramaswamy Iyer, Rishikesh Haridas, Beverly C. Walters, Salman Chaudry, Aisana Malieva, Samantha Wilkins, Mark R. Harrigan, Winfield S. Fisher III and Mohammadali M. Shoja

OBJECTIVE

Renin-angiotensin system (RAS) genetic polymorphisms are thought to play a role in cerebral aneurysm formation and rupture. The Cerebral Aneurysm Renin-Angiotensin System (CARAS) study prospectively evaluated common RAS polymorphisms and their relation to aneurysmal subarachnoid hemorrhage (aSAH).

METHODS

The CARAS study prospectively enrolled aSAH patients and controls at 2 academic centers in the United States. A blood sample was obtained from all patients for genetic evaluation and measurement of plasma angiotensin-converting enzyme (ACE) concentration. Common RAS polymorphisms were detected using 5′ exonuclease (TaqMan) genotyping assays and restriction fragment length polymorphism analysis.

RESULTS

Two hundred forty-eight patients were screened, and 149 aSAH patients and 50 controls were available for analysis. There was a recessive effect of the C allele of the angiotensinogen (AGT) C/T single-nucleotide polymorphism (SNP) (OR 1.94, 95% CI 0.912–4.12, p = 0.0853) and a dominant effect of the G allele of the angiotensin II receptor Type 2 (AT2) G/A SNP (OR 2.11, 95% CI 0.972–4.57, p = 0.0590) on aSAH that did not reach statistical significance after adjustment for potential confounders. The ACE level was significantly lower in aSAH patients with the II genotype (17.6 ± 8.0 U/L) as compared with the ID (22.5 ± 12.1 U/L) and DD genotypes (26.6 ± 14.2 U/L) (p = 0.0195).

CONCLUSIONS

The AGT C/T and AT2 G/A polymorphisms were not significantly associated with aSAH after controlling for potential confounders. However, a strong trend was identified for a dominant effect of the G allele of the AT2 G/A SNP. Downregulation of the local RAS may contribute to the formation of cerebral aneurysms and subsequent presentation with aSAH. Further studies are required to elucidate the relevant pathophysiology and its potential implication in treatment of patients with aSAH.