Dynamic Intracranial Pressure Waveform Morphology Predicts Ventriculitis.

BACKGROUND: Intracranial pressure waveform morphology reflects compliance, which can be decreased by ventriculitis. We investigated whether morphologic analysis of intracranial pressure dynamics predicts the onset of ventriculitis. METHODS: Ventriculitis was defined as culture or Gram stain positive cerebrospinal fluid, warranting treatment. We developed a pipeline to automatically isolate segments of intracranial pressure waveforms from extraventricular catheters, extract dominant pulses, and obtain morphologically similar groupings. We used a previously validated clinician-supervised active learning paradigm to identify metaclusters of triphasic, single-peak, or artifactual peaks. Metacluster distributions were concatenated with temperature and routine blood laboratory values to create feature vectors. A L2-regularized logistic regression classifier was trained to distinguish patients with ventriculitis from matched controls, and the discriminative performance using area under receiver operating characteristic curve with bootstrapping cross-validation was reported. RESULTS: Fifty-eight patients were included for analysis. Twenty-seven patients with ventriculitis from two centers were identified. Thirty-one patients with catheters but without ventriculitis were selected as matched controls based on age, sex, and primary diagnosis. There were 1590 h of segmented data, including 396,130 dominant pulses in patients with ventriculitis and 557,435 pulses in patients without ventriculitis. There were significant differences in metacluster distribution comparing before culture-positivity versus during culture-positivity (p < 0.001) and after culture-positivity (p < 0.001). The classifier demonstrated good discrimination with median area under receiver operating characteristic 0.70 (interquartile range 0.55-0.80). There were 1.5 true alerts (ventriculitis detected) for every false alert. CONCLUSIONS: Intracranial pressure waveform morphology analysis can classify ventriculitis without cerebrospinal fluid sampling.

SDF1-a facilitates Lin-/Sca1+ cell homing following murine experimental cerebral ischemia.

BACKGROUND: Hematopoietic stem cells mobilize to the peripheral circulation in response to stroke. However, the mechanism by which the brain initiates this mobilization is uncharacterized. METHODS: Animals underwent a murine intraluminal filament model of focal cerebral ischemia and the SDF1-A pathway was evaluated in a blinded manner via serum and brain SDF1-A level assessment, Lin-/Sca1+ cell mobilization quantification, and exogenous cell migration confirmation; all with or without SDF1-A blockade. RESULTS: Bone marrow demonstrated a significant increase in Lin-/Sca1+ cell counts at 24 hrs (272 ± 60%; P<0.05 vs sham). Mobilization of Lin-/Sca1+ cells to blood was significantly elevated at 24 hrs (607 ± 159%; P<0.05). Serum SDF1-A levels were significant at 24 hrs (Sham (103 ± 14), 4 hrs (94 ± 20%, p = NS) and 24 hrs (130 ± 17; p<0.05)). Brain SDF1-A levels were significantly elevated at both 4 hrs and 24 hrs (113 ± 7 pg/ml and 112 ± 10 pg/ml, respectively; p<0.05 versus sham 76 ± 11 pg/ml). Following administration of an SDF1-A antibody, Lin-/Sca1+ cells failed to mobilize to peripheral blood following stroke, despite continued up regulation in bone marrow (stroke bone marrow cell count: 536 ± 65, blood cell count: 127 ± 24; p<0.05 versus placebo). Exogenously administered Lin-/Sca1+ cells resulted in a significant reduction in infarct volume: 42 ± 5% (stroke alone), versus 21 ± 15% (Stroke+Lin-/Sca1+ cells), and administration of an SDF1-A antibody concomitant to exogenous administration of the Lin-/Sca1+ cells prevented this reduction. Following stroke, exogenously administered Lin-/Sca1+ FISH positive cells were significantly reduced when administered concomitant to an SDF1-A antibody as compared to without SDF1-A antibody (10 ± 4 vs 0.7 ± 1, p<0.05). CONCLUSIONS: SDF1-A appears to play a critical role in modulating Lin-/Sca1+ cell migration to ischemic brain.

Effect of rebleeding on the course and incidence of vasospasm after subarachnoid hemorrhage.

OBJECTIVE: Rebleeding of an aneurysm is a leading cause of morbidity and mortality after subarachnoid hemorrhage (SAH). Whereas numerous studies have demonstrated the risk factors associated with rebleeding, few data on complications of rebleeding, including its effect on the development of delayed cerebral ischemia (DCI), are available. METHODS: A nested case-control study was performed on patients with rebleeding and control subjects matched for modified Fisher scale, Hunt-Hess grade, age, and sex previously entered into a prospective database. Rebleeding was defined as new hemorrhage apparent on repeat CT with or without new symptoms. Incidence and time course of DCI and hospital complications were compared. A secondary analysis of DCI and hospital complications was also performed on subjects surviving to postbleed day 7. RESULTS: We identified 120 patients with rebleeding and 359 control subjects from 1996 to 2011. The rebleeding rate was 8.6%. In both the primary and secondary analyses, there was no difference in the incidence of DCI or its time course (29% vs. 27%, p = 0.6; 7 ± 5 vs. 7 ± 6 days, p = 0.9 for primary analysis; 39% vs. 31%, p = 0.1, 7 ± 5 vs. 7 ± 6 days, p = 0.6 for the secondary analysis). In a multivariate logistic regression model, rebleeding was associated with the complications of hyponatremia, respiratory failure, and hydrocephalus. Patients with rebleeding had higher rates of mortality, brain death, and poor outcomes. CONCLUSIONS: Rebleeding after SAH is associated with multiple medical and neurologic complications, resulting in higher morbidity and mortality, but is not associated with change of incidence or timing of DCI.

Revised and updated recommendations for the establishment of primary stroke centers: a summary statement from the brain attack coalition.

BACKGROUND AND PURPOSE: The formation and certification of Primary Stroke Centers has progressed rapidly since the Brain Attack Coalition's original recommendations in 2000. The purpose of this article is to revise and update our recommendations for Primary Stroke Centers to reflect the latest data and experience. METHODS: We conducted a literature review using MEDLINE and PubMed from March 2000 to January 2011. The review focused on studies that were relevant for acute stroke diagnosis, treatment, and care. Original references as well as meta-analyses and other care guidelines were also reviewed and included if found to be valid and relevant. Levels of evidence were added to reflect current guideline development practices. RESULTS: Based on the literature review and experience at Primary Stroke Centers, the importance of some elements has been further strengthened, and several new areas have been added. These include (1) the importance of acute stroke teams; (2) the importance of Stroke Units with telemetry monitoring; (3) performance of brain imaging with MRI and diffusion-weighted sequences; (4) assessment of cerebral vasculature with MR angiography or CT angiography; (5) cardiac imaging; (6) early initiation of rehabilitation therapies; and (7) certification by an independent body, including a site visit and disease performance measures. CONCLUSIONS: Based on the evidence, several elements of Primary Stroke Centers are particularly important for improving the care of patients with an acute stroke. Additional elements focus on imaging of the brain, the cerebral vasculature, and the heart. These new elements may improve the care and outcomes for patients with stroke cared for at a Primary Stroke Center.

Rebleeding after aneurysmal subarachnoid hemorrhage.

Rebleeding after initial aneurysmal subarachnoid hemorrhage (SAH) can have substantial impact on overall patient outcome. While older studies have suggested rebleeding occurs in about 4% of patients during the first day after initial aneurysmal bleed, these studies may have failed to capture very early rebleeds and, consequently, underestimated the impact of rebleeding. An electronic literature search was performed to identify English-language articles published or available for review from February 1975 through October 2010. A total of 43 articles (40 original research and 3 review articles) focused on rebleeding after initial aneurysmal SAH in humans were selected for review. Although most studies supported an incidence of rebleeding ≤4%, studies investigating ultra-early rebleeding reported bleeding within the first 24 h following aneurysmal SAH in as many as 9-17% of patients, with most cases occurring within 6 h of initial hemorrhage. Overall, studies investigating antifibrinolytic therapy to reduce rebleeding have failed to clearly demonstrate overall therapeutic benefit. Short-course antifibrinolytic therapy may have a role prior to initial aneurysm repair, although insufficient data are currently available.

Brain interstitial fluid TNF-alpha after subarachnoid hemorrhage.

OBJECTIVE: TNF-alpha is an inflammatory cytokine that plays a central role in promoting the cascade of events leading to an inflammatory response. Recent studies have suggested that TNF-alpha may play a key role in the formation and rupture of cerebral aneurysms, and that the underlying cerebral inflammatory response is a major determinate of outcome following subrarachnoid hemorrhage (SAH). METHODS: We studied 14 comatose SAH patients who underwent multimodality neuromonitoring with intracranial pressure (ICP) and cerebral microdialysis as part of their clinical care. Continuous physiological variables were time-locked every 8h and recorded at the same point that brain interstitial fluid TNF-alpha was measured in brain microdialysis samples. Significant associations were determined using generalized estimation equations. RESULTS: Each patient had a mean of 9 brain tissue TNF-alpha measurements obtained over an average of 72h of monitoring. TNF-alpha levels rose progressively over time. Predictors of elevated brain interstitial TNF-alpha included higher brain interstitial fluid glucose levels (beta=0.066, p<0.02), intraventricular hemorrhage (beta=0.085, p<0.021), and aneurysm size >6mm (beta=0.14, p<0.001). There was no relationship between TNF-alpha levels and the burden of cisternal SAH; concurrent measurements of serum glucose, or lactate-pyruvate ratio. INTERPRETATION: Brain interstitial TNF-alpha levels are elevated after SAH, and are associated with large aneurysm size, the burden of intraventricular blood, and elevation brain interstitial glucose levels.

Correlation of cerebral metabolites with functional outcome in experimental primate stroke using in vivo 1H-magnetic resonance spectroscopy.

BACKGROUND AND PURPOSE: Ensuring the translatability of primate stroke models is critical for preclinical testing of cerebroprotective strategies, and such models would benefit from further characterization of the experimental ischemic tissue. Our purpose was to examine the cerebral metabolic response to stroke in baboons with MR spectroscopy and to correlate metabolite levels with functional neurologic outcomes. METHODS: Seven baboons underwent 1 hour of middle cerebral artery occlusion. At 3 and 10 days, each animal was imaged with traditional MR imaging and multivoxel proton (1)H-MR spectroscopy, and a neurologic examination was performed. Spectra obtained from the infarcted hemisphere of each animal were compared with the contralateral hemisphere, and metabolite levels were correlated with neurologic outcome scores. RESULTS: Spectra obtained at 3 days postischemia revealed prominent lactate (LAC) resonances and attenuated N-acetylaspartate (NAA) peaks in infarcted hemispheres. Ten-day spectra showed persistence of these findings in animals with large strokes (>30% of the hemisphere), with partial normalization of the spectra in animals with small strokes (<30% of the hemisphere). Mean area under the curve from LAC spectra had a negative correlation with functional outcome by 2 different scoring systems (r(2) = 0.72 and 0.73), whereas NAA showed a positive correlation (r(2) = 0.79 and 0.62). CONCLUSIONS: The metabolic alterations observed in our primate model of reperfused ischemia by (1)H-MR spectroscopy recapitulate those seen in clinical stroke. Furthermore, correlations between LAC and NAA peaks with functional outcome further suggest that MR spectroscopy may play a role in outcome prediction following cerebral infarction in higher primates.

Predictors of hemorrhage in patients with untreated brain arteriovenous malformation.

BACKGROUND: Intracranial hemorrhage is a serious possible complication in patients with brain arteriovenous malformation (AVM). Several morphologic factors associated with hemorrhagic AVM presentation have been established, but their relevance for the risk of subsequent AVM hemorrhage remains unclear. METHODS: The authors analyzed follow-up data on 622 consecutive patients from the prospective Columbia AVM database, limited to the period between initial AVM diagnosis and the start of treatment (i.e., any endovascular, surgical, or radiation therapy). Univariate and multivariate logistic regression and Cox proportional hazard models were applied to analyze the effect of patient age, gender, AVM size, anatomic location, venous drainage pattern, and associated arterial aneurysms on the risk of intracranial hemorrhage at initial presentation and during follow-up. RESULTS: The mean pretreatment follow-up was 829 days (median: 102 days), during which 39 (6%) patients experienced AVM hemorrhage. Increasing age (hazard ratio [HR] 1.05, 95% CI 1.03 to 1.08), initial hemorrhagic AVM presentation (HR 5.38, 95% CI 2.64 to 10.96), deep brain location (HR 3.25, 95% CI 1.30 to 8.16), and exclusive deep venous drainage (HR 3.25, 95% CI 1.01 to 5.67) were independent predictors of subsequent hemorrhage. Annual hemorrhage rates on follow-up ranged from 0.9% for patients without hemorrhagic AVM presentation, deep AVM location, or deep venous drainage to as high as 34.4% for those harboring all three risk factors. CONCLUSIONS: Hemorrhagic arteriovenous malformation (AVM) presentation, increasing age, deep brain location, and exclusive deep venous drainage appear to be independent predictors for AVM hemorrhage during natural history follow-up. The risk of spontaneous hemorrhage may be low in AVMs without these risk factors.

Shunt failure in idiopathic intracranial hypertension presenting with spontaneous cerebrospinal fluid leak.

A case of spontaneous cerebrospinal (CSF) fluid leak after ventriculoperitoneal shunt (VPS) failure in a patient with idiopathic intracranial hypertension (IIH) is reported. This is the first report of spontaneous CSF leak in an IIH patient without a history of trauma, sinus surgery, or intracranial surgery. The diagnosis was confirmed using thin-sliced post-contrast computed tomography, which revealed a micro-dehiscence of the cribiform plate at the superior aspect of the ethmoid sinus. The patient underwent VPS revision without complication, resulting in complete amelioration of symptoms and cessation of CSF rhinorrhoea at 1 year follow up.

APOE-epsilon4 predisposes to cognitive dysfunction following uncomplicated carotid endarterectomy.

BACKGROUND: Between 9% and 23% of patients undergoing otherwise uncomplicated carotid endarterectomy (CEA) develop subtle cognitive decline 1 month postoperatively. The APOE-epsilon4 allele has been associated with worse outcome following stroke. OBJECTIVE: To investigate the ability of APOE-epsilon4 to predict post-CEA neurocognitive dysfunction. METHODS: Seventy-five patients with CEA undergoing elective CEA were prospectively recruited in this nested cohort study and demographic variables were recorded. Patients were evaluated before and 1 month after surgery with a standard battery of five neuropsychological tests. APOE genotyping was performed by restriction fragment length polymorphism analysis in all patients. Neuropsychological deficits were identified by comparing changes (before to 1 month post-operation) in individual performance on the test battery. Logistic regression was performed for APOE-epsilon4 and previously identified risk factors. RESULTS: Twelve of 75 (16%) CEA patients possessed the APOE-epsilon4 allele. Eight of 75 (11%) patients experienced neurocognitive dysfunction on postoperative day 30. One month post-CEA, APOE-epsilon4-positive patients were more likely to be cognitively injured (42%) than APOE-epsilon4-negative patients (5%) (p = 0.002). In multivariate analysis, the presence of the APOE-epsilon4 allele increased the risk of neurocognitive dysfunction at 1 month 62-fold (62.28, 3.15 to 1229, p = 0.007). Diabetes (51.42, 1.94 to 1363, p = 0.02), and obesity (24.43, 1.41 to 422.9, p = 0.03) also predisposed to injury. CONCLUSION: The APOE-epsilon4 allele is a robust independent predictor of neurocognitive decline 1 month following CEA.

Anti-adhesion molecule strategies as potential neuroprotective agents in cerebral ischemia: a critical review of the literature.

Despite recent advances in the understanding of the pathophysiology of cerebral ischemia, current approaches attempting to prevent ischemic brain damage after an acute stroke remain quite inadequate. Today, ischemic stroke remains the third leading cause of death in industrialized nations, and the leading cause of disability requiring long term institutional care in the U.S and other industrialized nations. While one treatment, tissue plasminogen activator, has shown efficacy in clinical trials, safety concerns limit its role in clinical practice to a narrow time window of use. Acute cerebral ischemia has been shown to evoke a profound and deleterious upregulation of the inflammatory response, initiated within the cerebral microvasculature. Recently, research efforts have focused on targeting individual components of the inflammatory cascade, such as leukocyte activation and adhesion, in an attempt to develop potential neuroprotective agents. While these strategies have shown promise preclinically, clinical trials have yet to show clear benefit. Here, we review the current understanding of the pathophysiologic consequences of acute cerebral ischemic injury. Additionally, we discuss the role of the inflammatory cascade, with specific attention given to the deleterious role played by leukocyte activation and adhesion in stroke. Finally, relevant efforts to translate these basic science observations into clinical efficacy in acute stroke trials are critically reviewed.

Laser Doppler flowmetry in non-human primate stroke studies: model refinement for pre-clinical development of cerebroprotective strategies.

BACKGROUND: Safety, feasibility, and efficacy trials in non-human primate stroke models are essential to the evaluation of experimental therapies and their translation to humans. Although Laser Doppler Flowmetry has been successfully employed in rodent stroke to continuously monitor cerebral blood flow, it has not been applied in primate studies. This investigation examined the utility of Laser Doppler Flowmetry in refining an existing baboon model of cerebral ischemia/reperfusion. METHOD: Continuous Laser Doppler Flowmetry monitoring was used, in non-human primates, to document local cerebral blood flow before, during, and after middle cerebral artery territory occlusion. In each baboon (n = 7) a single Doppler probe was placed into the left frontal cortex through a precoronal burr hole. Correlations between Laser Doppler Flowmetry values and latencies to Motor Evoked Potential dropout were compared using a linear regression model. FINDINGS: Placement of the Laser Doppler probe was easily accomplished in all animals. Laser Doppler Flowmetry tracings accurately documented blood flow changes that occurred with each technical manipulation during the procedure. Laser Doppler confirmed decreased perfusion that coincided both regionally and temporally with vessel occlusion. Depth of ischemia as measured by Laser Doppler Flowmetry was associated with Motor Evoked Potential dropout latencies for individual animals. CONCLUSIONS: Continuous, single probe Laser Doppler Flowmetry is a reliable method of documenting perfusion changes following middle cerebral artery territory occlusion in a baboon model of reperfused stroke. This advanced intraoperative monitoring technique may lead to more accurate evaluation of acute stroke therapies in pre-clinical trials.

Predictors and clinical impact of epilepsy after subarachnoid hemorrhage.

OBJECTIVE: To determine the frequency, predictors, and impact on outcome of epilepsy developing during the first year after subarachnoid hemorrhage (SAH). METHODS: The authors prospectively analyzed 247 of 431 patients with SAH treated over a period of 5 years who were alive with follow-up at 12 months. Epilepsy was defined as two or more unprovoked seizures after hospital discharge. RESULTS: New-onset epilepsy occurred in 7% (n = 17) of patients; an additional 4% (n = 10) had only one seizure after discharge. Independent predictors of epilepsy included subdural hematoma (OR 9.9, 95% CI 1.9 to 52.8) and cerebral infarction (OR 3.9, 95% CI 1.4 to 11.3). Unlike those without seizures, patients who developed epilepsy failed to experience functional recovery on the modified Rankin Scale (mRS) between 3 and 12 months after SAH. At 12 months epilepsy was independently associated with severe disability (score >/= 3) on the mRS (OR 10.3, 95% CI 2.5 to 42.0), increased instrumental disability on the Lawton Instrumental Activities of Daily Living scale (OR 4.9; 95% CI 1.1 to 22.2), reduced quality of life on the Sickness Impact Profile (OR 4.5; 95% CI 1.1 to 18.0), and increased state anxiety on the Spielberger Anxiety Inventory (OR 4.8; 95% CI 1.1 to 20.4). Epilepsy was not associated with cognitive impairment, depression, or subjective life satisfaction. CONCLUSION: Epilepsy occurred in 7% of patients with SAH, was predicted by subdural hematoma and cerebral infarction, and was associated with poor functional recovery and quality of life. Our findings indicate that focal pathology, rather than diffuse injury from hemorrhage, is the principal cause of epilepsy after SAH.

Global and domain-specific cognitive impairment and outcome after subarachnoid hemorrhage.

BACKGROUND: Cognitive dysfunction is the most common form of neurologic impairment after subarachnoid hemorrhage (SAH). OBJECTIVE: To evaluate the impact of global and domain-specific cognitive impairment on functional recovery and quality of life (QOL) after SAH. METHODS: One hundred thirteen patients (mean age 49 years; 68% women) were evaluated 3 months after SAH. Three simple tests of global mental status and neuropsychological tests to assess seven specific cognitive domains were administered. Four aspects of outcome (global handicap, disability, emotional status, and QOL) were compared between cognitively impaired and unimpaired patients with analysis-of-covariance models controlling for age, race/ethnicity, and education. Multiple linear regression was used to evaluate the relative contribution of global and domain-specific cognitive status for predicting concurrent modified Rankin Scale (mRS) and Sickness Impact Profile (SIP) scores. RESULTS: Impairment of global mental status on the Telephone Interview of Cognitive Status (TICS) was associated with poor performance in all seven cognitive domains (all p < 0.0005) and was the only cognitive measure associated with poor recovery in all four aspects of outcome (all p < or = 0.005). Cognitive impairment in four specific domains was also associated with functional disability or reduced QOL. After accounting for global cognitive impairment with the TICS, however, neuropsychological testing did not contribute additional predictive value for concurrent mRS or SIP total scores. CONCLUSIONS: Cognitive impairment impacts broadly on functional status, emotional health, and QOL after SAH. The TICS may be a useful alternative to more detailed neuropsychological testing for detecting clinically relevant global cognitive impairment after SAH.

Dysplastic vessels after surgery for brain arteriovenous malformations.

BACKGROUND AND PURPOSE: The cause and clinical significance of residual dysplastic vessels after surgery for brain arteriovenous malformations (AVM) are unclear. We studied predictors and frequency of residual dysplastic vessels on cerebral angiography after AVM surgery. METHODS: The 240 prospectively enrolled surgical patients from the New York AVM Databank underwent 269 AVM-related surgical procedures. Reported postoperative brain angiographic findings were classified post hoc as showing (1) persistent dysplastic vessels, (2) a residual AVM, (3) focal hyperemia in the surgical bed, (4) other changes, or (5) a normal angiogram. Univariate and multivariate models were applied to test for an association between residual dysplastic vessels and patient age, sex, preoperative AVM size, anatomic AVM location, number of embolization procedures before surgery, and the time interval between AVM surgery and the postoperative angiogram. RESULTS: Of the 224 documented postoperative angiograms, 78 (35%) showed dysplastic vessels, 24 (11%) had evidence for a residual AVM, 16 (7%) showed focal hyperemia, 6 (2%) revealed other findings, and 100 (45%) were normal. The number of cases showing angiographic evidence for dysplastic vessels was significantly associated with increasing size of the AVM (in millimeter increments; P=0.0001); the mean diameter of AVMs in patients showing dysplastic vessels after surgery was significantly larger (41 mm, SD +/-14) than in those without residual dysplastic vessels (27 mm, SD +/-13; P<0.001). Symptomatic postoperative intracerebral hemorrhage occurred in 4 patients (1%), in 2 of whom dysplastic vessels were seen on the postoperative angiogram. CONCLUSIONS: The findings suggest that persistent dysplastic vessels may be found in approximately one third of angiograms after AVM surgery. Preoperative AVM size was found to be an independent predictor for the occurrence of dysplastic vessels on the postoperative angiogram.

The baboon (Papio anubis) extracranial carotid artery: an anatomical guide for endovascular experimentation.

BACKGROUND: As novel endovascular strategies are developed for treating neurological disease, there is an increasing need to evaluate these techniques in relevant preclinical models. The use of non-human primates is especially critical given their structural and physiological homology with humans. In order to conduct primate endovascular studies, a comprehensive understanding of the carotid anatomy is necessary. We therefore performed a detailed examination of the vessel lengths, lumen diameters and angles of origin of the baboon extracranial carotid system. METHODS: We characterized the extracranial carotid system often male baboons (Papio anubis, range 15.1-28.4 kg) by early post-mortem dissection. Photographic documentation of vessel lengths, lumen diameters, and angles of origin were measured for each segment of the carotid bilaterally. RESULTS: The common carotid arteries averaged 94.7 +/- 1.7 mm (left) and 87.1 +/- 1.6 mm (right) in length. The average minimal common carotid lumen diameters were 3.0 +/- 0.3 mm (left) and 2.9 +/- 0.2 mm (right). Each animal had a common brachiocephalic artery arising from the aorta which bifurcated into the left common carotid artery and right braciocephalic artery after 21.5 +/- 1.6 mm. The vascular anatomy was found to be consistent among animals despite a wide range of animal weights. CONCLUSIONS: The consistency in the Papio anubis extracranial carotid system may promote the use of this species in the preclinical investigation of neuro-interventional therapies.

Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after subarachnoid hemorrhage: the Fisher scale revisited.

BACKGROUND AND PURPOSE: Thick cisternal clot on CT is a well-recognized risk factor for delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH). Whether intraventricular hemorrhage (IVH) or intracerebral hemorrhage (ICH) predisposes to DCI is unclear. The Fisher CT grading scale identifies thick SAH but does not separately account for IVH or ICH. METHODS: We studied 276 consecutively admitted patients with an available admission CT scan performed within 72 hours of onset. Demographic, clinical, laboratory, and neuroimaging data were recorded, and the amount and location of SAH, IVH, and ICH on admission CT scans were quantified. The relationship between these variables and DCI was analyzed separately and in combination with multiple logistic regression. RESULTS: DCI developed in 20% of patients (54 of 276). Among SAH variables, thick clot completely filling any cistern or fissure was the best predictor of DCI (P=0.008), and among IVH variables, blood in both lateral ventricles was most predictive (P=0.001). These variables had independent predictive value for DCI in a multivariate analysis of CT findings, and both were included in a final multivariate model when evaluated in conjunction with other clinical risk factors: IVH (OR 4.1, 95% CI 1.7 to 9.8), SAH (OR 2.3, 95% CI 1.5 to 9.5), mean arterial pressure >112 mm Hg (OR 4.9, 95% CI 2.1 to 11.4), and transcranial Doppler mean velocity >140 cm/s within 5 days of hemorrhage (OR 3.8, 95% CI 1.5 to 9.5). Similar results were obtained in a repeat analysis with infarction due to vasospasm as the dependent variable. CONCLUSIONS: SAH completely filling any cistern or fissure and IVH in the lateral ventricles are both risk factors for DCI, and their risk is additive. We propose a new SAH rating scale that accounts for the independent predictive value of subarachnoid and ventricular blood for DCI.