Carissa Pineda

Perfusion-CT Assessment of Infarct Core and Penumbra: Receiver Operating Characteristic Curve Analysis in 130 Patients Suspected of Acute Hemispheric Stroke

Background and Purpose— Different definitions have been proposed to define the ischemic penumbra from perfusion-CT (PCT) data, based on parameters and thresholds tested only in small pilot studies. The purpose of this study was to perform a systematic evaluation of all PCT parameters (cerebral blood flow, volume [CBV], mean transit time [MTT], time-to-peak) in a large series of acute stroke patients, to determine which (combination of) parameters most accurately predicts infarct and penumbra. Methods— One hundred and thirty patients with symptoms suggesting hemispheric stroke ≤12 hours from onset were enrolled in a prospective multicenter trial. They all underwent admission PCT and follow-up diffusion-weighted imaging/fluid-attenuated inversion recovery (DWI/FLAIR); 25 patients also underwent admission DWI/FLAIR. PCT maps were assessed for absolute and relative reduced CBV, reduced cerebral blood flow, increased MTT, and increased time-to-peak. Receiver-operating characteristic curve analysis was performed to determine the most accurate PCT parameter, and the optimal threshold for each parameter, using DWI/FLAIR as the gold standard. Results— The PCT parameter that most accurately describes the tissue at risk of infarction in case of persistent arterial occlusion is the relative MTT (area under the curve=0.962), with an optimal threshold of 145%. The PCT parameter that most accurately describes the infarct core on admission is the absolute CBV (area under the curve=0.927), with an optimal threshold at 2.0 ml×100 g−1. Conclusion— In a large series of 130 patients, the optimal approach to define the infarct and the penumbra is a combined approach using 2 PCT parameters: relative MTT and absolute CBV, with dedicated thresholds.

Light therapy for seasonal affective disorder with blue narrow-band light-emitting diodes (LEDs).

BACKGROUND While light has proven an effective treatment for Seasonal Affective Disorder (SAD), an optimal wavelength combination has not been determined. Short wavelength light (blue) has demonstrated potency as a stimulus for acute melatonin suppression and circadian phase shifting. METHODS This study tested the efficacy of short wavelength light therapy for SAD. Blue light emitting diode (LED) units produced 468 nm light at 607 microW/cm2 (27 nm half-peak bandwidth); dim red LED units provided 654 nm at 34 microW/cm2 (21 nm half-peak bandwidth). Patients with major depression with a seasonal pattern, a score of > or =20 on the Structured Interview Guide for the Hamilton Depression Rating Scale-SAD version (SIGH-SAD) and normal sleeping patterns (routine bedtimes between 10:00 pm and midnight) received 45 minutes of morning light treatment daily for 3 weeks. Twenty-four patients completed treatment following random assignment of condition (blue vs. red light). The SIGH-SAD was administered weekly. RESULTS Mixed-effects analyses of covariance determined that the short wavelength light treatment decreased SIGH-SAD scores significantly more than the dimmer red light condition (F = 6.45, p = .019 for average over the post-treatment times). CONCLUSIONS Narrow bandwidth blue light at 607 microW/cm2 outperforms dimmer red light in reversing symptoms of major depression with a seasonal pattern.

Association between hyperoxia and mortality after stroke: a multicenter cohort study.

Objective:To test the hypothesis that hyperoxia was associated with higher in-hospital mortality in ventilated stroke patients admitted to the ICU. Design:Retrospective multicenter cohort study. Setting:Primary admissions of ventilated stroke patients with acute ischemic stroke, subarachnoid hemorrhage, and intracerebral hemorrhage who had arterial blood gases within 24 hours of admission to the ICU at 84 U.S. ICUs between 2003 and 2008. Patients were divided into three exposure groups: hyperoxia was defined as PaO2 ≥300 mm Hg (39.99 kPa), hypoxia as any PaO2<60 mm Hg (7.99 kPa) or PaO2/FiO2 ratio ⩽300, and normoxia, not defined as hyperoxia or hypoxia. The primary outcome was in-hospital mortality. Participants:Two thousand eight hundred ninety-four patients. Methods:Patients were divided into three exposure groups: hyperoxia was defined as PaO2 more than or equal to 300 mm Hg (39.99 kPa), hypoxia as any PaO2 less than 60 mm Hg (7.99 kPa) or PaO2/FIO2 ratio less than or equal to 300, and normoxia, not defined as hyperoxia or hypoxia. The primary outcome was in-hospital mortality. Interventions:Exposure to hyperoxia. Results:Over the 5-year period, we identified 554 ventilated patients with acute ischemic stroke (19%), 936 ventilated patients with subarachnoid hemorrhage (32%), and 1,404 ventilated patients with intracerebral hemorrhage (49%) of whom 1,084 (38%) were normoxic, 1,316 (46%) were hypoxic, and 450 (16%) were hyperoxic. Mortality was higher in the hyperoxia group as compared with normoxia (crude odds ratio 1.7 [95% CI 1.3-2.1]; p < 0.0001) and hypoxia groups (crude odds ratio, 1.3 [95% CI, 1.1–1.7]; p < 0.01). In a multivariable analysis adjusted for admission diagnosis, other potential confounders, the probability of being exposed to hyperoxia, and hospital-specific effects, exposure to hyperoxia was independently associated with in-hospital mortality (adjusted odds ratio, 1.2 [95% CI, 1.04–1.5]). Conclusion:In ventilated stroke patients admitted to the ICU, arterial hyperoxia was independently associated with in-hospital death as compared with either normoxia or hypoxia. These data underscore the need for studies of controlled reoxygenation in ventilated critically ill stroke populations. In the absence of results from clinical trials, unnecessary oxygen delivery should be avoided in ventilated stroke patients.

Beyond intravenous thrombolysis

The National Institute of Neurological Disorders and Stroke trial of recombinant tissue plasminogen activator has been considered a landmark study in the acute treatment of ischemic stroke. Unfortunately, only a small percentage of all ischemic stroke patients presents to the hospital in time to receive the drug. Moreover, the recannalization rate of a major artery occlusion, such as the proximal middle cerebral artery or top of the internal carotid artery occlusion, after intravenous (IV) thrombolytic therapy has been disappointingly low. Since the Food and Drug Administrations approval of IV plasminogen activator, there have been numerous randomized clinical trials investigating the safety and efficacy of different thrombolytics administered in various time frames. In addition to the IV administration, efforts have been made in order to study the radiographic as well as clinical effects of intra-arterial (IA) thrombolysis. The combination of IV and IA thrombolysis has been studied. For patients who do not qualify for receiving chemical thrombolysis, new devices have been developed for mechanical thrombectomy. Angioplasty and stenting procedures are being performed more frequently than in the past as one of the treatment modalities for acute ischemic stroke patients. Relentless research effort is being made internationally in order to fight the devastating disease which now goes beyond the conventional IV thrombolysis.

Fluid levels in the bleeding brain: a marker for coagulopathy and hematoma expansion

A 72-year-old man with baseline vascular dementia was admitted for 3 days of confusion, unintelligible speech, and incontinence. His past medical history was notable for a right middle cerebral artery territory infarction 4 years prior, coronary artery disease treated with angioplasty and stenting, hypertension, and diabetes. Upon evaluation in our emergency department, his examination was notable for expressive aphasia and confusion. He was moving all extremities spontaneously against gravity. A noncontrast head CT was performed that showed a subacute infarct in the left frontal lobe, subsequently confirmed on MRI (panel A). Since he was outside the window for thrombolysis and intervention, he was given one full-dose aspirin (325 mg tablet), and admitted to our hospital for a stroke evaluation. During the course of his stroke work-up, he was found to have an apical left ventricular thrombus, presumably the etiology of his subacute left frontal lobe infarct. Given his increased risk of further ischemic strokes, he was started on anticoagulation 7 days after his stroke using intravenous heparin and then switched to an oral vitamin K antagonist (warfarin). While awaiting transfer to a rehabilitation facility on post-stroke day 14, he was found in a stuporous state. He was not following commands, and was only minimally arousable to noxious stimuli. An emergent head CT was performed, which showed hemorrhagic conversion of the left frontal lobe infarct with fluid levels (panel B). A radial arterial line was placed for blood pressure monitoring, and he was started on a nicardipine drip. Four units of fresh frozen plasma and intravenous vitamin K were administered enroute to the intensive care unit (ICU). While in the ICU, he was intubated and started on hypertonic saline for cerebral edema. On a repeat CT scan 6 h later, there was interval expansion of his left temporal hematoma (panel B). After a family discussion, he was made comfort measures only, and no aggressive measures were pursued (Fig. 1).