Background and Purpose-We conducted this study to determine, through use of multivariate analyses, the independent predictors of hematoma enlargement occurring after hospital admission in patients with spontaneous intracerebral hemorrhage (ICH). Methods-We reviewed 627 patients with ICH admitted within 24 hours of onset. The first CT was performed at admission and the second within 24 hours of admission, and a blood sample was taken for laboratory examinations. Univariate and multivariate analyses were performed to assess the relationships between hematoma enlargement and time from onset, consciousness level, CT findings, amount of alcohol consumption, systolic blood pressure at and after admission, clinical outcome, and hematologic parameters. Hematoma enlargement was an independent factor increasing the mortality rate in the ICH patients (OR, 1.57; PϽ0.001). Conclusions-A particularly high likelihood of hematoma enlargement was observed in patients who (in order of importance) were admitted shortly after onset, who were heavy drinkers; who had an irregularly shaped hematoma, whose consciousness was disturbed, and who had a low level of fibrinogen.

In order to evaluate the incidence and risk factors of hematoma enlargement in spontaneous intracerebral hemorrhage (ICH), 419 cases of ICH were reviewed. The first computerized tomography (CT) scan was performed within 24 hours of onset and the second within 24 hours of admission; a blood sample was taken for laboratory examination within 1 hour of admission. In 60 patients (14.3%) the second CT scan showed an enlarged hematoma. The incidence of enlargement significantly decreased with time (p < 0.05) and significantly increased with the severity of liver dysfunction and the volume of the hematoma on the first CT scan. Patients with an irregularly shaped hematoma had a higher risk of hematoma growth than those with a round hematoma. In addition, patients with hematoma enlargement were more likely to have coagulation abnormalities (low platelet counts and low levels of fibrinogen, alpha 2-antiplasmin activity and platelet aggregation). Moreover, hematoma growth was associated with a poor clinical outcome. It is concluded that patients admitted to a hospital within 6 hours of onset of ICH, especially those admitted within 2 hours, and patients with liver dysfunction or irregularly shaped large hematomas should be closely observed for at least 6 hours after onset in preparation for emergency surgery, since the risk of hematoma growth in these circumstances is high.

To determine the incidence of, and risk factors for, the occurrence of rebleeding between admission and early operation (ultra-early rebleeding) in patients with spontaneous subarachnoid hemorrhage (SAH), the authors reviewed the cases of 179 patients admitted within 24 hours after their last attack of SAH. Thirty-one (17.3%) of these patients had ultra-early rebleeding despite scheduling of early operation (within 24 hours after admission). The incidence of rebleeding significantly decreased as the time interval between the last attack and admission increased. Patients with rebleeding before admission, high systolic blood pressure, intracerebral or intraventricular hematoma, those in poor neurological condition on admission, and those who underwent angiography within 6 hours of the last SAH were significantly more likely to have ultra-early rebleeding than those without these factors. The incidence of rebleeding also significantly increased as levels of enhancement of platelet sensitivity and thrombin-antithrombin complex increased. Multivariate analysis revealed that the following three factors were independently associated with ultra-early rebleeding: the level of enhancement of platelet sensitivity; the time interval between the last attack and admission; and the level of thrombin-antithrombin complex. On the basis of these findings, the authors suggest that many of the risk factors for ultra-early rebleeding are interrelated. A particularly high risk of ultra-early rebleeding was observed in those patients 1) who had platelet hypoaggregability; 2) who were admitted shortly after their last SAH; and 3) whose thrombin-antithrombin complex levels were extremely high and were thus in severe clinical condition.

SummaryBackgroundIntracerebral haemorrhage growth is associated with poor clinical outcome and is a therapeutic target for improving outcome. We aimed to determine the absolute risk and predictors of intracerebral haemorrhage growth, develop and validate prediction models, and evaluate the added value of CT angiography.MethodsIn a systematic review of OVID MEDLINE—with additional hand-searching of relevant studies' bibliographies— from Jan 1, 1970, to Dec 31, 2015, we identified observational cohorts and randomised trials with repeat scanning protocols that included at least ten patients with acute intracerebral haemorrhage. We sought individual patient-level data from corresponding authors for patients aged 18 years or older with data available from brain imaging initially done 0·5–24 h and repeated fewer than 6 days after symptom onset, who had baseline intracerebral haemorrhage volume of less than 150 mL, and did not undergo acute treatment that might reduce intracerebral haemorrhage volume. We estimated the absolute risk and predictors of the primary outcome of intracerebral haemorrhage growth (defined as >6 mL increase in intracerebral haemorrhage volume on repeat imaging) using multivariable logistic regression models in development and validation cohorts in four subgroups of patients, using a hierarchical approach: patients not taking anticoagulant therapy at intracerebral haemorrhage onset (who constituted the largest subgroup), patients taking anticoagulant therapy at intracerebral haemorrhage onset, patients from cohorts that included at least some patients taking anticoagulant therapy at intracerebral haemorrhage onset, and patients for whom both information about anticoagulant therapy at intracerebral haemorrhage onset and spot sign on acute CT angiography were known.FindingsOf 4191 studies identified, 77 were eligible for inclusion. Overall, 36 (47%) cohorts provided data on 5435 eligible patients. 5076 of these patients were not taking anticoagulant therapy at symptom onset (median age 67 years, IQR 56–76), of whom 1009 (20%) had intracerebral haemorrhage growth. Multivariable models of patients with data on antiplatelet therapy use, data on anticoagulant therapy use, and assessment of CT angiography spot sign at symptom onset showed that time from symptom onset to baseline imaging (odds ratio 0·50, 95% CI 0·36–0·70; p<0·0001), intracerebral haemorrhage volume on baseline imaging (7·18, 4·46–11·60; p<0·0001), antiplatelet use (1·68, 1·06–2·66; p=0·026), and anticoagulant use (3·48, 1·96–6·16; p<0·0001) were independent predictors of intracerebral haemorrhage growth (C-index 0·78, 95% CI 0·75–0·82). Addition of CT angiography spot sign (odds ratio 4·46, 95% CI 2·95–6·75; p<0·0001) to the model increased the C-index by 0·05 (95% CI 0·03–0·07).InterpretationIn this large patient-level meta-analysis, models using four or five predictors had acceptable to good discrimination. These models could inform the location and frequency of observations on patients in clinical practice, explain treatment effects i...

SummaryNeuronal growth cones are essential for nerve growth and regeneration, as well as for the formation and rearrangement of the neural network. To elucidate phosphorylation-dependent signaling pathways and establish useful molecular markers for axon growth and regeneration, we performed a phosphoproteomics study of mammalian growth cones, which identified >30,000 phosphopeptides of ∼1,200 proteins. The phosphorylation sites were highly proline directed and primarily MAPK dependent, owing to the activation of JNK, suggesting that proteins that undergo proline-directed phosphorylation mediate nerve growth in the mammalian brain. Bioinformatics analysis revealed that phosphoproteins were enriched in microtubules and the cortical cytoskeleton. The most frequently phosphorylated site was S96 of GAP-43 (growth-associated protein 43-kDa), a vertebrate-specific protein involved in axon growth. This previously uncharacterized phosphorylation site was JNK dependent. S96 phosphorylation was specifically detected in growing and regenerating axons as the most frequent target of JNK signaling; thus it represents a promising new molecular marker for mammalian axonal growth and regeneration.

The aim of this study was to assess the growth of incidental meningiomas, to establish a strategy for dealing with these tumours. The cases of 37 patients with a meningioma revealed incidentally by computerized tomography or magnetic resonance imaging, who were followed at least once by an additional imaging study, were reviewed. The tumour volume was calculated, to estimate the annual growth rate of the incidental meningiomas. Nine of the 37 patients (24.3%) showed a considerable increase (the annual growth rate > 1 cu cm/year) in their tumour volume (tumour growth). There was no significant difference in the follow-up period, age, or the volume of tumour between the patients with and without tumour growth. However, a multivariate analysis revealed that the likelihood of tumour growth independently and significantly increased according to a decrease in the age of the patients (Odds ratio 0.18 for one-standard-deviation change (ISD) 12.6 years, p = 0.042) and according to an increase in the volume of the tumour (Odds ratio 3.64 for ISD 4.46 cu cm, p = 0.042). The majority of patients with incidental meningioma can be apparently observed without any surgical intervention, because their annual growth rates are generally less than 1 cu cm/year. However, clinical and radiological observations would be advisable for these patients (especially young patients and patients with a large tumour), in view of the presence of rapidly growing tumours in some of the patients.

Intraoperative FNMEP monitoring can be useful for predicting facial nerve function after skull base surgery. This new method is a valuable adjunct to conventional facial nerve monitoring.

Although the precise mechanisms leading to the higher susceptibility rendering SP-like pathology observable within the cortical mantle are not totally understood, the study unambiguously demonstrated that MR microscopy is capable of directly visualizing cortical pathology in AD patients in vivo.