Cardiac Troponin-I: A Predictor of Prognosis in Subarachnoid Hemorrhage

Background  Release of cardiac biomarkers is reported in patients with subarachnoid hemorrhage (SAH). Data addressing the impact of cardiac injury on outcome in these patients is sparse. This study was conducted to ascertain the association of elevation of serum cardiac Troponin-I (cTnI) with mortality and neurological outcome in patients with SAH. Methods  Medical records of all patients admitted with a diagnosis of SAH and at least one measured cTnI were reviewed. Demographic and clinical variables including admission neurological status were collected. Conservative and non-parametric statistics were used to assess association between cTnI and death or neurological outcome at discharge. Results  The study group comprised of 83 patients with a mean age of 59 years. There was a female (60%) and African-American (60%) preponderance. At admission, the median Glasgow Coma Scale (GCS) was 9, and 47% had a severe Hunt–Hess grade (HHG) of ≥4. Elevation of cTnI was found in 31 (37%) patients and was associated with worse baseline Fisher grade (p=0.01) and neurological status: GCS score (p=0.006) and HHG (p=0.007). Patients with abnormal cTnI were more likely to die (55% vs.27%; odds ratio 1.3–8.4, p = 0.01) and had a worse GCS score (p = 0.008) and HHG (p = 0.004) on discharge. On multivariate analysis, peak cTnI (p = 0.04) and admission GCS score of <12 (p = 0.02) were independent predictors of death at discharge. Conclusion  Patients with subarachnoid hemorrhage and elevated cTnI are found to have worse neurological status at admission. These patients have a worse neurological outcome and in-hospital mortality.     

Cerebral inflammatory response and predictors of admission clinical grade after aneurysmal subarachnoid hemorrhage

Poor admission clinical grade is the most important determinant of outcome after aneurysmal subarachnoid hemorrhage (aSAH); however, little attention has been focused on independent predictors of poor admission clinical grade. We hypothesized that the cerebral inflammatory response initiated at the time of aneurysm rupture contributes to ultra-early brain injury and poor admission clinical grade. We sought to identify factors known to contribute to cerebral inflammation as well as markers of cerebral dysfunction that were associated with poor admission clinical grade. Between 1997 and 2008, 850 consecutive SAH patients were enrolled in our prospective database. Demographic data, physiological parameters, and location and volume of blood were recorded. After univariate analysis, significant variables were entered into a logistic regression model to identify significant associations with poor admission clinical grade (Hunt–Hess grade 4–5). Independent predictors of poor admission grade included a SAH sum score >15/30 (odds ratio [OR] 2.3, 95% confidence interval [CI] 1.5–3.6), an intraventricular hemorrhage sum score >1/12 (OR 3.1, 95% CI 2.1–4.8), aneurysm size >10 mm (OR 1.7, 95% CI 1.1–2.6), body temperature ?38.3 °C (OR 2.5, 95% CI 1.1–5.4), and hyperglycemia >200 mg/dL (OR 2.7, 95% CI 1.6–4.5). In a large, consecutive series of prospectively enrolled patients with SAH, the inflammatory response at the time of aneurysm rupture, as reflected by the volume and location of the hemoglobin burden, hyperthermia, and perturbed glucose metabolism, independently predicts poor admission Hunt–Hess grade. Strategies for mitigating the inflammatory response to aneurysmal rupture in the hyper-acute setting may improve the admission clinical grade, which may in turn improve outcomes.     

Pupillary Reactivity Upon Hospital Admission Predicts Long-term Outcome in Poor Grade Aneurysmal Subarachnoid Hemorrhage Patients

Background  Historically, the prognosis for poor grade subarachnoid hemorrhage patients has been considered dismal. As a result, many hospitals have chosen conservative management over aggressive therapy. This guarded approach, however, is based on studies that do not take into account newer, more effective, management protocols and more recent long-term evidence that significant neurological recovery occurs in the months to years following discharge. More accurate and predictive methods are needed to decide when aggressive therapy is warranted. Methods  Two hundred and twenty-six grade aneurysmal subarachnoid hemorrhage (aSAH) patients of grades IV and V were admitted to Columbia University Medical Center and enrolled in our study. Demographics, clinical information (e.g. pupillary reactivity on admission), and treatment course (operative versus non-operative) were recorded. Rankin scores at 14 days, 3 months, and 1 year were also recorded. A favorable Rankin score was defined as 0–3. Unfavorable was defined as 4–6. Results  Among all poor grade patients who received operative therapy, pupillary reactivity at admission was not predictive of a favorable Rankin score at day 14 (odds ratio = 3.3, P = 0.129). Pupillary reactivity, however, was predictive of Rankin score at 3 months (odds ratio = 4.57, P = 0.05) and 12 months (odds ratio = 6.44, P = 0.008). After constructing a Kaplan–Meiers survival curve, pupillary reactivity was a better predictor of survival at 12 months than H&H grade [Hazard ratio 3.342 (1.596–7.000) P = 0.001 versus 1.964 (1.016–3.798) P = 0.045]. Conclusions  This study demonstrates that significant recovery occurs in the weeks to months after poor grade aSAH. Pupillary reactivity on admission can be used as a predictor of survival and recovery at intermediate and long-term time points, more so than Hunt and Hess grade.     

Cardiovascular predictors of in-patient mortality after subarachnoid hemorrhage

Background and Purpose

Whether cardiac dysfunction contributes to morbidity and mortality after subarachnoid hemorrhage (SAH) remains controversial. The objective of this study was to test the hypothesis that cardiovascular abnormalities are independently related to in-patient mortality after SAH.

Methods

This was a prospective cohort study of patients with aneurysmal SAH. Heart rate and blood pressure were measured, a blood sample was obtained, and echocardiography was performed on three study days, starting as soon after admission as possible. The cardiovascular predictor variables were heart rate, systolic blood pressure (SBP), cardiac troponin I (cTi) level, B-type natriuretic peptide (BNP) level, and left ventricular ejection fraction. The primary outcome measure was in-patient mortality. The association between each predictor variable and mortality was quantified by multivariate logistic regression, including relevant covariates and reporting odds ratios (OR) and 95% confidence intervals (CI).

Results

The study included 300 patients. An initial BNP level greater than 600 pg/mL was markedly associated with death (OR 37.7, p<0.001). On the third study day (9.1±4.1 days after SAH symptom onset), a cTi level greater than 0.3 mg/L (OR 7.6, p=0.002), a heart rate of 100 bpm or greater (OR 4.9, p=0.009), and a SBP less than 130 mmHg (OR 6.7, p=0.007) were significantly associated with death.

Conclusions

Cardiovascular abnormalities are independent predictors of in-patient mortality after SAH. Though these effects may be explained by a reduction in cerebral perfusion pressure or other mechanisms, further research is required to determine whether or not they are causal in nature.     

Roller coaster-associated subarachnoid hemorrhage--report of 2 cases

The most common neurological injuries associated with roller coaster rides are subdural hematoma and cervical artery dissection. We report two cases of roller-coaster associated subarachnoid hemorrhage (SAH). A 40-year-old healthy man developed a strong, holocephalic headache during a roller coaster ride. SAH Hunt & Hess grade II and Fisher grade 3 was diagnosed. An underlying aneurysm of the anterior communicating artery was successfully treated with coil embolization. A 41-year-old female (smoker, otherwise healthy) experienced a sudden, strong headache and diplopia during a roller coaster ride. A perimesencephalic SAH (Hunt & Hess grade II, Fisher grade 3) was disclosed by a CT scan. No aneurysm was detected on angiography. Both patients were discharged without neurological disability. In conclusion, SAH is a rare but relevant differential diagnosis in cases of acute headache during roller coaster rides. Both aneurysmal and non-aneurysmal perimesencephalic SAH can occur. A combination of mechanical factors and excessive blood pressure rises in vulnerable persons is discussed.     

Evaluation of a revised Glasgow Coma Score scale in predicting long-term outcome of poor grade aneurysmal subarachnoid hemorrhage patients

Although many scales attempt to predict outcome following aneurysmal subarachnoid hemorrhage (aSAH), none have achieved universal acceptance, and most scales in common use are not statistically derived. We propose a statistically validated scale for poor grade aSAH patients that combines the Hunt and Hess grades and the Glasgow Coma Scale (GCS) scores; we refer to this as the Poor Grade GCS (PGS).The GCS scores of 160 poor grade aSAH patients (Hunt and Hess Grades 4 and 5) were recorded throughout their hospital stay. Outcomes were assessed by the modified Rankin scale (mRS). Analysis of variance and the Chi-square test were used to guide an analysis of GCS breakpoints according to outcomes. Multivariable logistic regression analysis was used to assess the ability of the Hunt and Hess, GCS, World Federation of Neurological Surgeons Grading Scale, and the PGS to predict long-term outcome.Outcome analysis revealed significant breakpoints in admission GCS scores: PGS-A (GCS 10–12); PGS-B (GCS 8–9); PGS-C (GCS 5–7); PGS-D (GCS 3–4) (p < 0.001). In surgical patients, 95.2% of PGS-A, 58.1% of PGS-B, 35.4% of PGS-C, and 28.6% of PGS-D had a favorable one-year outcome. When controlling for age, sex, and operation status, PGS was the only scale predictive of long-term outcome. The odds ratios (OR) for unfavorable outcome according to PGS admission scores (with PGS-A as the reference) were: PGS-B, OR = 14.2 (95% CI 1.5–140.5); PGS-C, OR = 38.5 (95% CI 4.2–340.0); and PGS-D, OR = 63.4 (95% CI 5.6–707.1). In addition to PGS admission scores, an age of 70 or greater was a significant predictor of poor outcome with an OR of 7.5 (95% CI 1.8–30.7). No patients with a PGS-C or PGS-D over the age of 70 had a favorable long-term outcome.Therefore, elements of the Hunt and Hess and GCS can be combined into the PGS to predict long-term outcome in poor grade aSAH patients. However, patients with PGS-C and PGS-D over the age of 70 should be assessed carefully prior to definitive treatment.     

Acute Ischemic Injury on Diffusion-Weighted Magnetic Resonance Imaging after Poor Grade Subarachnoid Hemorrhage

Background

Poor clinical condition is the most important predictor of neurological outcome and mortality after subarachnoid hemorrhage (SAH). Rupture of an intracranial aneurysm was shown to be associated with acute ischemic brain injury in poor grade patients in autopsy studies and small magnetic resonance imaging series.

Methods

We performed diffusion-weighted magnetic resonance imaging (DWI) within 96 h of onset in 21 SAH patients with Hunt–Hess grade 4 or 5 enrolled in the Columbia University SAH Outcomes Project between July 2004 and February 2007. We analyzed demographic, radiological, clinical data, and 3 months outcome.

Results

Of the 21 patients 13 were Hunt–Hess grade 5, and eight were grade 4. Eighteen patients (86%) displayed bilateral and symmetric abnormalities on DWI, but not on computed tomography (CT). Involved regions included both anterior cerebral artery territories (16 patients), and less often the thalamus and basal ganglia (4 patients), middle (6 patients) or posterior cerebral artery territories (2 patients), or cerebellum (2 patients). At 1-year, 15 patients were dead (life support had been withdrawn in 6), 2 were moderately to severely disabled (modified Rankin Scale [mRS] = 4–5), and 4 had moderate-to-no disability (mRS = 1–3).

Conclusions

Admission DWI demonstrates multifocal areas of acute ischemic injury in poor grade SAH patients. These ischemic lesions may be related to transient intracranial circulatory arrest, acute vasoconstriction, microcirculatory disturbances, or decreased cerebral perfusion from neurogenic cardiac dysfunction. Ischemic brain injury in poor grade SAH may be a feasible target for acute resuscitation strategies.     

Statins in the Management of Patients with Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-analysis

Background: Delayed ischemic neurological deficits (DINDs) contribute to morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). Based on promising preliminary reports, some clinicians routinely administer statins to prevent DINDs. Methods: Without language restriction, we searched MEDLINE, EMBASE, the Cochrane Central Register, references of review articles, proceedings of the International Stroke Conference, and gray literature sources. Studies were selected if they compared outcomes between statin-treated and untreated patients during the 2 weeks following SAH. Data were extracted and appraised independently and in duplicate, using standardized forms. Fixed or random effects models, as appropriate based on the degree of study heterogeneity, were applied to calculate summary measures. Results: Four RCTs, two “pseudo” RCTs, five cohort studies, and one case–control study met eligibility criteria. In the RCTs, which enrolled a total of 309 patients, statins were found to significantly reduce the occurrence of DINDs [OR 0.38 (0.23–0.65); P < 0.001], but not mortality [OR 0.51 (0.25–1.02); P = 0.06] or poor neurological recovery [OR 0.81 (0.49–1.32); P = 0.39]. Observational studies assessed 1,542 patients, of whom 385 received statins. Statin-use was not associated with any reduction in DINDs [OR 0.96 (0.71–1.31); P = 0.80], mortality [OR 1.16 (0.78–1.73); P = 0.47] or poor neurological recovery [OR 1.20 (0.84–1.72); P = 0.31]. When the results of all studies were combined, statins had no statistically significant effect. Conclusions: Existing RCTs suggest that statins reduce DINDs, with a possible trend toward lower mortality. These findings are not supported by observational research. Although not assessed in all studies, current data do not indicate that statins improve neurological outcomes.     

Clipping or coiling of ruptured cerebral aneurysms and shunt-dependent hydrocephalus

Background  Hydrocephalus may develop either early in the course of aneurysmal subarachnoid hemorrhage (SAH) or after the first 2 weeks. Because the amount of SAH is a predictor of hydrocephalus, the two available aneurysmal treatments, clipping or coiling, may lead to differences in the need for cerebrospinal fluid (CSF) diversion, as only surgery permits clot removal. Methods  Hospital and University Hospitals Consortium (UHC) databases were used to retrieve data on all patients admitted to our hospital with aneurysmal SAH during the last 4 years. The incidence of permanent ventricular shunt (VS) according to treatment modality used was evaluated. Results  One hundred eighty-eight patients were admitted with aneurysmal SAH. Coiling was performed on 48 (26%) and clipping on 135 (73.8%) patients. Fifty-six (31%) patients required CSF diversion. External ventricular drain was placed in 30 (22.2%) clipped and 13 (27.1%) coiled patients (p=0.5), and VS in 6 patients of the two treatment groups (4.4 versus 12.5%, respectively; p=0.08). Patients requiring VS had longer UHC-expected hospital length of stay (LOS), as well as observed ICU and hospital LOS, compared to patients with temporary or no CSF diversion (24±14 versus 15±8, 20.5±9 versus 11±7, and 30±13 versus 16±11 days, respectively; p≤0.01). In a logistic regression model, VS was independently associated with rebleeding, external ventricular drain placement, coiling, and UHC-expected LOS (odds ratios, 95% confidence interval 12.1, 2.3–62.6, 6.9, 1.6–30, 6.25, 1.3–29, and 1.1, 1.02–1.14, respectively). Conclusions  One-third of patients admitted with aneurysmal SAH require temporary or permanent CSF diversion. Permanent shunting was found to be associated with coiling in our patient population.     

Calcium Homeostasis During Magnesium Treatment in Aneurysmal Subarachnoid Hemorrhage

Objective  Magnesium treatment in patients with subarachnoid hemorrhage (SAH) can result in hypocalcemia; this hypocalcemia increases the risk of delayed cerebral ischemia (DCI) and poor outcome. We assessed whether low serum levels of total calcium in patients with SAH treated with magnesium is mediated by parathyroid hormone (PTH) or calcitriol, and whether increased PTH or low serum levels of ionized calcium are associated with an increased risk of DCI and poor outcome. Patients and Methods  We studied 167 patients included in a randomized, placebo controlled trial on magnesium in SAH. Mean serum magnesium during treatment was related to mean serum levels of ionized calcium, PTH and calcitriol with linear regression. Hypocalcemia (Ca²⁺) and high serum PTH were related to the occurrence of DCI by means of the Cox proportional hazards model and to poor outcome by logistic regression. Results  Serum magnesium was inversely related to ionized calcium (B = −0.1; 95% CI −0.12 to −0.06), but not to PTH or calcitriol. Neither hypocalcemia nor high serum PTH was related to DCI. Hypocalcemia did not increased the risk for poor outcome (OR 1.2; 95% CI 0.6–2.3). In the subgroup of patients with known PTH (n = 67), high serum PTH increased the risk for poor outcome (OR 5.4; 1.6–18.9). Conclusions  Magnesium treatment in patients with SAH leads to hypocalcemia without effect on outcome. PTH is related to poor outcome, but this is independent of magnesium therapy.     

Acute brain MRI–DWI patterns and stroke recurrence after mild-moderate stroke

Brain ischemic lesions identified by diffusion-weighted imaging (DWI) have been shown to predict high risk of early future ischemic events in patients with transient ischemic attacks and minor stroke. The aim of this study is to analyze different brain MRI–DWI patterns in patients with mild-moderate stroke to define acute patterns related with a higher risk of stroke recurrence in long-term follow-up (from 6 to 36 months). Retrospective review of case series from a prospective stroke record including 253 patients with mild-moderate stroke (NIHSS from 1 to 7) and acute MRI–DWI lesions. MRI–DWI lesions were analyzed to determine clinically relevant lesions, based on the number, location, age and affected arterial territories. We defined three patterns: (1) multiple versus single lesions; (2) single deep versus single cortical lesions; and (3) single lesions versus multiple lesions affecting different arterial territories and/or of different age. The impact of these patterns on recurrence was analyzed by Cox regression analysis. 38 patients (15.0%) suffered a recurrence. Univariate analysis showed the risk of recurrence for each pattern. Pattern 1: patients with multiple lesions had greater risk of recurrence than those with single lesions (28.2 vs. 9.9%; OR: 3.75 (95% CI: 1.76–7.27), p < 0.0001). Pattern 2: patients with single cortical lesions had higher risk than those with deep lesions (14.3 vs. 6.7% OR: 2.33 (95% CI: 0.86–6.33), p < 0.089). Pattern 3: patients with multiple DWI in different territories or different age had the highest recurrence rate (30.6%), OR: 4.01 (95% CI: 1.70–9.47), p < 0.001, compared to patients with single lesions. Cox regression analysis adjusted by possible confounders, showed that for pattern 1 the OR for recurrence was 2.49 (95% CI: 1.27–4.89), p = 0.008; for pattern 2, OR:1.99 (95% CI: 0.74–5.37), p = 0.17; for pattern 3, OR: 2.85 (95% CI: 1.31–6.15), p = 0.008. Brain MRI–DWI patterns assessed in the acute phase of mild-moderate stroke are useful to identify those patients at high risk of recurrence.     

Migraine and delayed ischaemic neurological deficit after subarachnoid haemorrhage in women: a case–control study

The aim of the present case–control study was to investigate the role of migraine as a potential risk factor for a delayed ischaemic neurological deficit (DIND) after subarachnoid haemorrhage (SAH). A telephone interview was performed in patients or their relatives to determine the prevalence of migraine. Thirty-six women aged <60 years had SAH with Hunt & Hess grade I–III and DIND (group A). This group was compared with an age-matched group of 36 female SAH patients, Hunt & Hess grade I–III without DIND (group B). The two populations were also characterized regarding hypertension, smoking, diabetes mellitus and alcohol use. A significant difference was only found for the prevalence of migraine with 47% in group A and 25% in group B ( P  < 0.05; odds ratio: 2.68, confidence interval: 0.99–7.29). Migraineurs revealed similar prevalences of risk factors independently of the presence of DINDs. This retrospective study suggests that women with migraine have a higher risk to develop a DIND than women without migraine.     

An exploratory study of serum urate levels in patients with amyotrophic lateral sclerosis

Urate is a natural antioxidant, and high serum urate levels could be protective against the development of amyotrophic lateral sclerosis (ALS). To determine if serum urate concentrations were lower in ALS patients than in healthy controls, we compared serum urate levels in 132 ALS patients and 337 age/sex-matched controls. Median urate levels were lower in ALS patients compared to controls (4.2mgl/dL [range:1.4–8.2], vs. 4.7 [1.7–13.1]; p = 0.04). In univariate analysis, high urate levels were less likely to be associated with ALS (odds ratio [OR]: 0.53; 95% CI: 0.29–0.97; p = 0.04), but after adjusting for age, sex and kidney function, the association was not statistically significant (OR: 0.63; 95% CI: 0.32–1.24; p = 0.18). Urate levels were lower in bulbar-onset ALS (3.9 mg/dL), compared to limb-onset ALS (4.3; p = 0.001), and in cases with longer disease duration compared to controls (4.1 mg/dL, vs. 4.7; p = 0.01). In this cross-sectional study, lower levels of serum urate were evident in ALS cases with bulbar-onset and longer disease duration, but were likely to be related to the malnutrition induced by ALS.     

Ventricular Arrhythmia Risk After Subarachnoid Hemorrhage

Introduction  Cardiac morbidity and mortality after aneurysmal subarachnoid hemorrhage (SAH) are attributable to myocardial injury, decreased ventricular function, and ventricular arrhythmia (VA). Our objective was to test the relationships between QTc prolongation, VA, and survival after SAH. Methods  In 200 subjects with acute aneurysmal SAH, electrocardiograms, echocardiograms, and telemetry were evaluated. Serum electrolytes and troponin were also evaluated. Results  Initial QTc (mean 460 ± 45 ms) was prolonged (≥470 ms) in 38% of subjects and decreased on follow-up (469 ± 49 initial vs. 435 ± 31 ms follow-up; N = 89; P < 0.0001). VA was present in 14% of subjects, 52% of subjects with VA had QTc ≥ 470 ms, and initial QTc trended toward longer duration in subjects with VA (474 ± 61 vs. 457 ± 42 ms; P = 0.084). Multivariate analysis demonstrated significant predictors of VA after SAH were increasing age (OR 1.3/5 years; P = 0.025), increasing stroke severity (OR 1.8; P = 0.009), decreasing heart rate (OR 0.5/10 beats/min; P= 0.006), and the absence of angiotensin converting enzyme inhibitor or angiotensin II receptor antagonist use at SAH onset (OR 0.10; P = 0.027). All-cause mortality was 19% (25/135) at 3 months and subjects with VA had significantly higher mortality than those without VA (37% vs. 16%; P = 0.027). Conclusions  These data demonstrate that QTc prolongation and arrhythmias are frequently noted after SAH, but arrhythmias are often not associated with QTc prolongation. In addition, the presence of VA identified subjects at greater risk of mortality following their SAH.     

Terson’s syndrome – Pathophysiologic considerations of an underestimated concomitant disease in aneurysmal subarachnoid hemorrhage

Terson syndrome (TS) is a common and underestimated concomitant disease in patients suffering from subarachnoid hemorrhage (SAH). Aim of this study was to evaluate the influence of an initial unconsciousness and raised intracranial pressure (ICP) on the development of TS. We performed a retrospective analysis of 213 prospective collected SAH patients screened for TS to investigate the impact of an initial unconsciousness and raised ICP on the development of TS. A univariate analysis followed by a multivariate logistic regression model was performed to identify risk factors that are associated with TS. The findings are all discussed and correlated with the present pathophysiologic considerations of TS. The rate of TS in this study was 23.9%. A higher risk of TS in the univariate analysis was associated with a Glasgow Coma scale ⩽ 7 (p = 0.001), higher Hunt and Hess grade (p = 0.001), Fisher grade IV (p = 0.002), intracerebral hemorrhage (p = 0.011), initial unconsciousness (p = 0.013) and an ICP of ⩾25 mmHg (p < 0.001). An ICP of ⩾25 mmHg was the only independent predictor for TS in the multivariate analysis (p = 0.007). TS patients had a higher mortality (p = 0.012) and a higher risk for a worse long-term outcome (p = 0.002). Notable that 5 of 51 TS patients (9.8%) in this study developed TS with no raised ICP or initial unconsciousness. Terson syndrome is a common concomitant disease in SAH patients. The pathomechanism leading to TS is not exclusively related to raised ICP levels and/or unconsciousness. However, these factors may be associated with a high percentage of TS.     

Clinical outcome of spontaneous non-aneurysmal subarachnoid hemorrhage in 108 patients

Background: The cause of spontaneous subarachnoid hemorrhage (SAH) is unknown in 15% of cases; idiopathic SAH has a better prognosis than aneurysmal SAH. When bleeding is confined to the perimesencephalic cisterns, SAH has an especially benign course. Methods: We retrospectively studied 108 patients admitted for spontaneous non‐aneurysmal SAH between 1991 and 2004. We divided patients into two groups according to the bleeding pattern at cranial CT: perimesencephalic pattern (n = 60) and aneurysmal pattern (n = 48). We included only patients in whom no source of bleeding was detected at angiography; patients with aneurysmal pattern underwent at least two angiographic examinations. Mean follow‐up was 5.5 years; follow‐up consisted of telephone interview in 84.7% of patients. Results: All but one patient with perimesencephalic pattern were classified as grade I or II on the Hunt and Hess scale; the exception was the only patient in this group with a complication (hydrocephalus), who was classified as grade IV. Three‐quarters of the patients with aneurysmal pattern were classified as grade I or II on the Hunt and Hess scale; 5 patients presented with hydrocephalus that required drainage and 2 with vasospasms without repercussions. No rebleeding or long‐term complications were observed in either group. Conclusions: Non‐aneurysmal SAH with a perimesencephalic pattern of bleeding has a benign course and excellent short‐term and long‐term prognosis. Patients with non‐aneurysmal SAH with an aneurysmal pattern of bleeding have more complications, and the initial clinical situation has a significant impact on their prognosis.     

Plasma brain natriuretic peptide level on admission predicts long-term outcome in patients with non-traumatic subarachnoid hemorrhage

IntroductionNon-traumatic subarachnoid hemorrhage (SAH) is a type of stroke that still has a high mortality rate. Some patients with SAH have electrocardiography (ECG) abnormalities or asymptomatic left ventricular apical ballooning, and requires intervention by cardiologists. However, the impact of cardiac abnormalities after SAH onset remains unclear. We investigated whether ECG abnormalities, myocardial damage, sympathetic nervous activity or echocardiographic left ventricular wall motion abnormalities (WMA) could provide additional risk stratification in patients with SAH.MethodsWe studied 118 SAH patients (78 women, age 63 ± 15) without a history of heart disease. Neurological grade (Hunt and Kosnik Grade) and clinical factors were evaluated. A standard 12-lead ECG, echocardiography and blood samples were obtained within 48 h after SAH onset. ECG abnormalities were defined as abnormal Q wave, ST elevation, giant T-wave inversion or QT prolongation.ResultsTwenty of 118 patients (17%) died during the follow-up (35 ± 31 months). Death was significantly associated with higher age (p < 0.0001), neurological grade (p < 0.0001), elevated BNP level (p < 0.0001), increased plasma norepinephrine levels (p < 0.0001) and WMA (p = 0.0070), while ECG abnormalities were not significantly associated. Neurological grade (p < 0.0001), age (p = 0.0047) and BNP (p = 0.0014, hazard ratio 1.0255 for each 1 pg/mL increase in BNP, 95%CI 1.0088 to 1.0499) were independently associated with death. Patients with BNP ≥ 96.6 had a higher risk of death (log- rank p < 0.0001).ConclusionPlasma BNP might provide an additional risk stratification in patients with non-traumatic SAH that requires intervention by cardiologists for both its prevention management after onset.     

Depressive symptoms and quality of life after thrombolysis in stroke: the TEMPiS study

Intravenous thrombolysis leads to a reduction of post-stroke disability. No data exist about whether depression and poor quality of life (QoL) remain relevant problems in patients with good functional outcome. We assessed mood and QoL at 3 and 6 months after stroke in consecutive patients who received intravenous thrombolysis in stroke centers and telemedicine hospitals within the TEMPiS network. The Beck Depression Inventory (BDI) was used with BDI ≥18 indicating clinically relevant depressive symptoms. Stroke specific quality of life (SSQOL) was used for QoL assessment with the definition of SSQOL total score <60% for poor QoL. Associations of BDI and SSQOL with baseline parameters and modified Rankin scale (mRS) in follow-up were analyzed. In patients with known mRS 0–4 at 3 months (N = 213), BDI was available in 74% and SSQOL in 77%. At 3 and 6 months, 23 and 18% of patients had clinically relevant depressive symptoms; 25 and 24% reported a poor QoL. The mRS at 3 months correlated with BDI (r = 0.43, p < 0.01) and SSQOL (r = −0.75, p < 0.01). BDI ≥18 was observed in 11% of patients with mRS 0–1 and 16% in mRS 0–2. Severe stroke (NIHSS ≥12) at admission (OR 1.23, 0.57–2.66; p = 0.57) was not predictive for depressive symptoms but for poor QoL (OR 2.77, 95%CI 1.34–5.74). Depressive symptoms and impaired QoL are observed in a substantial proportion of stroke patients at 3 months after intravenous thrombolysis. Health professionals should be aware that thrombolysed patients may have relevant mood disorders despite good functional outcome.     

Lower initial red blood cell count in cerebrospinal fluid predicts good functional outcome in patients with spontaneous subarachnoid haemorrhage

Background and purpose

Red blood cell (RBC) degradation after subarachnoid haemorrhage (SAH) negatively affects functional outcome. Although the detection of RBCs in the cerebrospinal fluid (CSF) is a widely available part of neurological routine diagnostics, the prognostic value as a biomarker remains unclear. This study was undertaken to investigate whether CSF RBC count correlates with established radiological markers of SAH volume and whether the CSF RBC count can predict functional outcome in SAH patients.

Methods

A total of 121 consecutive spontaneous SAH patients were retrospectively analyzed. CSF was collected from external ventricular drain as part of routine diagnostic procedures. We used multivariable binary logistic regression to investigate associations between CSF RBC counts and functional outcome 3 months after SAH or hospital survival. Good functional outcome was defined as modified Rankin Scale ≤ 2.

Results

Patients' age was 60 ± 14 years, and the median admission Hunt & Hess grade (H&H) was 4. CSF samples were collected 2 days after intensive care unit admission. High CSF RBC counts positively correlated with radiological measurements for SAH volume, for example, modified Fisher score (p = 0.002) and Hijdra ventricle score (p = 0.016). Multivariable regression analysis adjusted for age, H&H grade, modified Fisher and Hijdra scores showed that low CSF RBC counts predicted hospital survival (per 100,000 CSF RBCs: adjusted odds ratio [adjOR] = 0.74, 95% confidence interval [CI] = 0.61–0.89, p = 0.001) and good functional outcome after 3 months (per 100,000 CSF RBC: adjOR = 0.76, 95% CI = 0.60–0.96, p = 0.020).

Conclusions

CSF RBC counts correlate with radiographic scores quantifying SAH volume and may serve as an early independent biomarker for hospital survival and good functional 3-month outcome in patients requiring ventriculostomy after SAH.     

Relation between intracranial artery calcifications and aortic atherosclerosis in ischemic stroke patients

We previously demonstrated a strong relation between carotid atherosclerosis (defined as carotid artery stenosis ≥50%) and intracranial artery calcification (IAC) in ischemic stroke patients. The purpose of this study was to evaluate the relation between aortic atherosclerosis and IAC. Four hundred fifty-four patients with ischemic stroke were included. Complex aortic plaques (CAP) were assessed by transesophageal echocardiography (TEE) and defined as plaques ≥4 mm thick or with mobile components in the proximal aorta. IAC were assessed in the seven major cerebral arteries and a semiquantitative score system was applied, ranging from 0 (no calcification) to 7. Forty-two patients (9.3%) had CAP. Patients with CAP were older compared with patients without CAP (73.6 vs. 63.6 years, p < 0.001), had more vascular risk factors, more significant carotid artery atherosclerosis (p < 0.001), more chronic kidney disease (p < 0.001), and a higher IAC score (3.0 vs. 1.8; p < 0.001). Stepwise logistic regression selected the following independent factors for CAP: previous stroke or TIA (OR 3.3; 95%CI 1.5–7.0; p = 0.002), carotid artery stenosis ≥50% (OR 3.7; 95%CI 1.7–8.0; p = 0.001), chronic kidney disease (OR 3.8; 95%CI 1.9–7.8; p < 0.001), and IAC score (OR 1.5; 95%CI 1.2–1.9; p = 0.002). IAC was present in 100% of patients with CAP. Moreover, IAC had a high sensitivity (100%) and negative predictive value (100%) for the presence of CAP. In ischemic stroke patients, the absence of IAC strongly points to the lack of CAP. However, these results warrant confirmation in prospective studies before concluding the non-utility of the use of TEE to exclude CAP as a potential source of cerebral embolism in patients without IAC.