Louise D McCullough

University of Connecticut, Сторс, Connecticut, United States

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Publications (152)646.07 Total impact

  • Robert J Brown · Abhay Kumar · Louise D McCullough · Karyn Butler
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    ABSTRACT: Materials and methods: An 18-question survey was distributed to physicians and advanced practitioner members of the Neurocritical Care Society. Respondents were asked which BP parameter they manipulated and what their thresholds were in different clinical scenarios. They were also asked whether they were influenced by the presence of incidental aneurysms. Answers were analyzed for differences in training background and treatment setting. Results: There were 128 responses. The majority were neurointensivists (47 neurology and 37 non-neurology) and treated patients in dedicated neurointensive care units (n = 98). Systolic BP (SBP) was preferred over mean arterial pressure (MAP). Prior to aneurysm treatment, SBP limits ranged from 140 to 180 mm Hg. After aneurysm treatment, SBP limits ranged from 160 to 240 mm Hg. The maximum and minimum MAPs varied by as much as 50%. Nearly two-thirds of the respondents were influenced by the presence of incidental aneurysms. Training background influenced tolerance to BP limits with neurology-trained neurointensivists accepting higher BP limits when treating delayed ischemia ( p = .018). They were also more likely to follow SBP ( p = .018) and have a limit of 140 mm Hg prior to aneurysm treatment ( p = .001). Conclusions: There is large practice variability in BP management following aSAH. There is also uncertainty over the importance of incidental aneurysms. Further research could evaluate whether this variability has clinical significance.
    No preview · Article · Jan 2016 · The International journal of neuroscience
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    ABSTRACT: Females experience poorer recovery after ischemic stroke compared to males, even after controlling for age and stroke severity. IL-10 is an anti-inflammatory cytokine produced by T regulatory cells and Th2 CD4+ helper T cells. In ischemic stroke, an excessive IL-10 response contributes to post-stroke immunosuppression, which worsens outcomes. However, it is unknown if sex differences exist in IL-10 levels after ischemic stroke. In this study, we found that higher levels of IL-10 were associated with poor acute and long-term outcomes after ischemic stroke in female patients but not in males. After controlling for confounders, IL-10 was not an independent predictor of functional outcomes. This suggests that higher serum IL-10 levels may reflect factors that interact with sex such as age and stroke severity.
    Full-text · Article · Dec 2015 · Biology of Sex Differences
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    ABSTRACT: Background Natriuresis with polyuria is common after aneurysmal subarachnoid hemorrhage (aSAH). Previous studies have shown an increased risk of symptomatic cerebral vasospasm or delayed cerebral ischemia (DCI) in patients with hyponatremia and/or the cerebral salt wasting syndrome (CSW). However, natriuresis may occur in the absence of hyponatremia or hypovolemia and it is not known whether the increase in DCI in patients with CSW is secondary to a concomitant hypovolemia or because the physiology that predisposes to natriuretic peptide release also predisposes to cerebral vasospasm. Therefore, we investigated whether polyuria per se was associated with vasospasm and whether a temporal relationship existed. Methods A retrospective review of patients with aSAH was performed. Exclusion criteria were admission more than 48 h after aneurysmal rupture, death within 5 days, and the development of diabetes insipidus or acute renal failure. Polyuria was defined as >6 liters of urine in a 24 h period. Vasospasm was defined as a mean velocity > 120 m/s on Transcranial Doppler Ultrasonography (TCDs) or by evidence of vasospasm on computerized tomography (CT) or catheter angiography. Multivariable logistic regression was performed to assess the relationship between polyuria and vasospasm. Results 95 patients were included in the study. 51 had cerebral vasospasm and 63 met the definition of polyuria. Patients with polyuria were significantly more likely to have vasospasm (OR 4.301, 95 % CI 1.378–13.419) in multivariate analysis. Polyuria was more common in younger patients (52 vs 68, p <.001) but did not impact mortality after controlling for age and disease severity. The timing of the development of polyuria was clustered around the diagnosis of vasospasm and patients with polyuria developed vasospasm faster than those without polyuria. Conclusions Polyuria is common after aSAH and is significantly associated with cerebral vasospasm. The development of polyuria may be temporally related to the development of vasospasm. An increase in urine volume may be a useful clinical predictor of patients at risk for vasospasm.
    Preview · Article · Dec 2015 · BMC Neurology
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    Mehwish A Mirza · Rodney Ritzel · Yan Xu · Louise D McCullough · Fudong Liu
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    ABSTRACT: Neonatal hypoxic-ischemic encephalopathy (HIE) is an important cause of motor and cognitive impairment in children. Clinically, male infants are more vulnerable to ischemic insults and suffer more long-term deficits than females; however, the mechanisms underlying this sex difference remain elusive. Inflammatory processes initiated by microglial activation are fundamental in the pathophysiology of ischemia. Recent studies report a sexual dimorphism in microglia numbers and expression of activation markers in the neonatal brain under normal conditions. How these basal sex differences in microglia affect HIE remains largely unexplored. This study investigated sex differences in ischemic outcomes and inflammation triggered by HIE. We hypothesize that ischemia induces sex-specific brain injury in male and female neonates and that microglial activation and inflammatory responses play an important role in this sexual dimorphism. Male and female C57BL6 mice were subjected to 60-min Rice-Vanucci modeling (RVM) at post-natal day 10 (P10) to induce HIE. Stroke outcomes were measured 1, 3, 7, and 30 days after stroke. Microglial activation and inflammatory responses were evaluated by flow cytometry and cytokine analysis. On day 1 of HIE, no difference in infarct volumes or seizure scores was seen between male and female neonates. However, female neonates exhibited significantly smaller infarct size and fewer seizures compared to males 3 days after HIE. Females also had less brain tissue loss and behavioral deficits compared to males at the chronic stage of HIE. Male animals demonstrated increased microglial activation and up-regulated inflammatory response compared to females at day 3. HIE leads to an equivalent primary brain injury in male and female neonates at the acute stage that develops into sexually dimorphic outcomes at later time points. An innate immune response secondary to the primary injury may contribute to sexual dimorphism in HIE.
    Preview · Article · Dec 2015 · Journal of Neuroinflammation
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    ABSTRACT: The use and effectiveness of current stroke reperfusion therapies are limited by the complications of reperfusion injury, which include increased cerebrovascular permeability and haemorrhagic transformation. Sphingosine-1-phosphate (S1P) is emerging as a potent modulator of vascular integrity via its receptors (S1PR). By using genetic approaches and a S1PR2 antagonist (JTE013), here we show that S1PR2 plays a critical role in the induction of cerebrovascular permeability, development of intracerebral haemorrhage and neurovascular injury in experimental stroke. In addition, inhibition of S1PR2 results in decreased matrix metalloproteinase (MMP)-9 activity in vivo and lower gelatinase activity in cerebral microvessels. S1PR2 immunopositivity is detected only in the ischemic microvessels of wild-type mice and in the cerebrovascular endothelium of human brain autopsy samples. In vitro, S1PR2 potently regulates the responses of the brain endothelium to ischaemic and inflammatory injury. Therapeutic targeting of this novel pathway could have important translational relevance to stroke patients.
    Full-text · Article · Aug 2015 · Nature Communications
  • Matthew D. Howe · Louise D. McCullough
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    ABSTRACT: Stroke is one of the leading causes of death and disability worldwide. The limited utility of current treatments, the increasing rates of stroke survivorship and subsequent long-term disability necessitate novel approaches to improve functional recovery after injury. The underlying immune mechanisms mediating inflammation and subsequent repair beyond the acute phase of injury remain understudied. The relative balance of injury and repair is dependent in part on the polarization state of microglia, the resident tissue macrophage of the central nervous system. Microglia can be classically activated to a pro-inflammatory phenotype, or alternatively activated to an immunomodulatory, tissue repair phenotype depending on the balance of local environmental cues. Once activated, they orchestrate a complex symphony of inflammation and repair, interacting with both the peripheral immune system and local cells such as astrocytes and neural stem cells to coordinate the resolution of inflammation and repair of damaged tissues. Furthermore, neural stem cells and astrocytes themselves appear to have intrinsic immunomodulatory properties which could be used in the development of future therapies. Enhancing these “reparative” functions with pharmacologic agents could open up exciting new avenues to improve long-term functional recovery in stroke patients.
    No preview · Article · Aug 2015 · Current Immunology Reviews
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    ABSTRACT: Stroke is the fifth leading cause of death and the primary cause of long-term adult disability in the United States. Increasing evidence suggests that low T3 levels immediately following acute ischemic stroke are associated with greater stroke severity, higher mortality rates, and poorer functional outcomes. Prognosis is also poor in critically ill hospitalized patients who have non-thyroidal illness syndrome (NTIS), where T3 levels are low, but TSH is normal. However, data regarding the association between TSH levels and functional outcomes are contradictory. Thus, this study investigated the role of TSH on stroke outcomes, concomitantly with T3 and T4. In this work, blood was collected from patients with radiologically confirmed acute ischemic stroke at 24±6 hours post-symptom onset and serum levels of TSH, free T3, and free T4 were measured. Stroke outcomes were measured at discharge, 3 and 12 months using the modified Rankin scale and modified Barthel Index as markers of disability. Though we found that lower levels of free T3 were associated with worse prognosis at hospital discharge, and at 3 and 12 months post-stroke, none of these outcomes held after multivariate analysis. Thus, it is likely that thyroid hormones are associated with other factors that impact stroke outcomes, such as sex, age and stroke etiology. This study found that lower levels of free T3 were associated with poorer outcomes at hospital discharge, and at 3 and 12 months post stroke, however, these associations diminished after correction for other known predictors of stroke outcome. Thyroid hormones have a complex relationship with ischemic stroke and stroke recovery, which merits further larger investigations.
    Preview · Article · Jul 2015 · Thyroid Research
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    ABSTRACT: Memory deficits are common among stroke survivors. Identifying neuroprotective agents that can prevent memory impairment or improve memory recovery is a vital area of research. Glycogen synthase kinase-3β (GSK-3β) is involved in several essential intracellular signaling pathways. Unlike many other kinases, GSK-3β is active only when dephosphorylated and activation promotes inflammation and apoptosis. In contrast, increased phosphorylation leads to reduced GSK-3β (pGSK-3β) activity. GSK-3β inhibition has beneficial effects on memory in other disease models. GSK-3β regulates both the 5'AMP-activated kinase (AMPK) and transforming growth factor-β-activated kinase (TAK1) pathways. In this work, we examined the effect of GSK-3β inhibition, both independently, in conjunction with a TAK inhibitor, and in AMPK-α2 deficient mice, after stroke to investigate mechanistic interactions between these pathways. GSK-3β inhibition was neuroprotective and ameliorated stroke-induced cognitive impairments. This was independent of AMPK signaling as the protective effects of GSK-3β inhibition were seen in AMPK deficient mice. However, GSK-3β inhibition provided no additive protection in mice treated with a TAK inhibitor suggesting that TAK1 is an upstream regulator of GSK-3β. Targeting GSK-3β could be a novel therapeutic strategy for post-stroke cognitive deficits. © 2015 Venna et al.; Published by Cold Spring Harbor Laboratory Press.
    No preview · Article · Jun 2015 · Learning & memory (Cold Spring Harbor, N.Y.)
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    ABSTRACT: Patients with acute ischemic stroke have improved outcomes when cared for in designated stroke centers (SC), in part due to enhanced thrombolytic use. Whether patients with intracerebral hemorrhage (ICH) also benefit from SC care is unknown. In this study, we compared the clinical characteristics and outcomes of ICH patients who underwent interhospital transfer (IHT) to a Joint Commission (JC) designated SC, to ICH patients who presented directly to the SC's emergency department (ED). Patients with ICH admitted between 2006 and 2013 were evaluated. The primary outcome measure was in-hospital death or hospice. Among 760 consecutive admissions for ICH, 321 (42.2%) were IHTs. There has been a 30% annual increase in IHT of ICH patients since 2006. The IHT group was younger (70.26 vs 72.28; P =.055), had lower ICH scores (P = .007), a higher Glasgow Coma Scale (GCS) (P = .037), and lower systolic blood pressure (SBP) (P = .003) than those arriving directly to the ED. Female sex was a predictor of in-hospital mortality (OR = 2.26). IHT is increasingly common for patients with ICH. The benefit of transfer remains unclear, as younger, healthier patients were the most likely to be transferred. Comprehensive stroke registries are needed to determine if outcomes differ for ICH patients based on transfer or SC care.
    No preview · Article · Jun 2015 · Connecticut medicine
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    ABSTRACT: The brain's initial innate response to stroke is primarily mediated by microglia, the resident macrophage of the CNS. However, as early as 4 h after stroke, the blood-brain barrier is compromised and monocyte infiltration occurs. The lack of discriminating markers between these two myeloid populations has led many studies to generate conclusions based on the grouping of these two populations. A growing body of evidence now supports the distinct roles played by microglia and monocytes in many disease models. Using a flow cytometry approach, combined with ex-vivo functional assays, we were able to distinguish microglia from monocytes using the relative expression of CD45 and assess the function of each cell type following stroke over the course of 7 days. We found that at 72 h after a 90-min middle cerebral artery occlusion (MCAO), microglia populations decrease whereas monocytes significantly increase in the stroke brain compared to sham. After stroke, BRDU incorporation into monocytes in the bone marrow increased. After recruitment to the ischemic brain, these monocytes accounted for nearly all BRDU-positive macrophages. Inflammatory activity peaked at 72 h. Microglia produced relatively higher reactive oxygen species and TNF, whereas monocytes were the predominant IL-1β producer. Although microglia showed enhanced phagocytic activity after stroke, monocytes had significantly higher phagocytic capacity at 72 h. Interestingly, we found a positive correlation between TNF expression levels and phagocytic activity of microglia after stroke. In summary, the resident microglia population is vulnerable to the effects of severe ischemia, show compromised cell cycle progression, and adopt a largely pro-inflammatory phenotype after stroke. Infiltrating monocytes are primarily involved with early debris clearance of dying cells. These findings suggest that the early wave of infiltrating monocytes may be beneficial to stroke repair and future therapies aimed at mitigating microglia cell death may prove more effective than attempting to elicit targeted anti-inflammatory responses from damaged cells.
    Preview · Article · May 2015 · Journal of Neuroinflammation
  • Matthew D Howe · Louise D McCullough
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    ABSTRACT: Stroke is the leading cause of acquired disability and the third leading cause of death in women worldwide. Sex differences in risk factors, treatment response and quality of life after stroke complicate stroke management in women. Women have an increased lifetime incidence of stroke compared to men, largely due to a sharp increase in stroke risk in older postmenopausal women. Women also have an increased lifetime prevalence of stroke risk factors, including hypertension and atrial fibrillation in postmenopausal women, as well as abdominal obesity and metabolic syndrome in middle-aged women. Controversy continues over the risks of oral contraceptives, hormone therapy and surgical intervention for carotid stenosis in women. Pregnancy and the postpartum period represent a time of increased risk, presenting challenges to stroke management. Recognition of these issues is critical to improving acute care and functional recovery after stroke in women.
    No preview · Article · Mar 2015 · Expert Review of Cardiovascular Therapy
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    ABSTRACT: Inflammation in the central nervous system (CNS) is primarily regulated by microglia. No longer considered a homogenous population, microglia display a high degree of heterogeneity, immunological diversity and regional variability in function. Given their low rate of self-renewal, the microenvironment in which microglia reside may play an important role in microglial senescence. This study examines age-related changes in microglia in the brain and spinal cord. Using ex-vivo flow cytometry analyses, functional assays were performed to assess changes in microglial morphology, oxidative stress, cytokine production, and phagocytic activity with age in both the brain and spinal cord. The regional CNS environment had a significant effect on microglial activity with age. Blood-CNS barrier permeability was greater in the aging spinal cord compared with aging brain; this was associated with increased tissue cytokine levels. Aged microglia had deficits in phagocytosis at baseline and after stimulus-induced activation. The identification of age-specific, high scatter microglia together with the use of ex-vivo functional analyses provides the first functional characterization of senescent microglia. Age and regional-specificity of CNS disease should be taken into consideration when developing immune-modulatory treatments. Copyright © 2015 Elsevier Inc. All rights reserved.
    No preview · Article · Feb 2015 · Neurobiology of aging
  • Mehwish A. Mirza · Yan Xu · Louise D. McCullough · Fudong Liu

    No preview · Conference Paper · Feb 2015
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    ABSTRACT: Speech impairments affect one in four stroke survivors. However, animal models of post-ischemic vocalization deficits are limited. Male mice vocalize at ultrasonic frequencies when exposed to an estrous female mouse. In this study we assessed vocalization patterns and quantity in male mice after cerebral ischemia. FOXP2, a gene associated with verbal dyspraxia in humans, with known roles in neurogenesis and synaptic plasticity, was also examined after injury. Using a transient middle cerebral artery occlusion (MCAO) model, we assessed correlates of vocal impairment at several time-points after stroke. Further, to identify possible lateralization of vocalization deficits induced by left and right hemispheric strokes were compared. Significant differences in vocalization quantity were observed between stroke and sham animals that persisted for a month after injury. Injury to the left hemisphere reduced early vocalizations more profoundly than those to the right hemisphere. Nuclear expression of Foxp2 was elevated early after stroke (at 6hours), but significantly decreased 24hours after injury in both the nucleus and the cytoplasm. Neuronal Foxp2 expression increased in stroke mice compared to sham animals 4 weeks after injury. This study demonstrates that quantifiable deficits in ultrasonic vocalizations (USVs) are seen after stroke. USV may be a useful tool to assess chronic behavioral recovery in murine models of stroke. Copyright © 2015 Elsevier B.V. All rights reserved.
    No preview · Article · Jan 2015 · Behavioural Brain Research
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    Sherry-Ann Brown · Louise D McCullough · Leslie M Loew
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    ABSTRACT: Hereditary ataxia, or motor incoordination, affects approximately 150,000 Americans and hundreds of thousands of individuals worldwide with onset from as early as mid-childhood. Affected individuals exhibit dysarthria, dysmetria, action tremor, and diadochokinesia. In this review, we consider an array of computational studies derived from experimental observations relevant to human neuropathology. A survey of related studies illustrates the impact of integrating clinical evidence with data from mouse models and computational simulations. Results from these studies may help explain findings in mice, and after extensive laboratory study, may ultimately be translated to ataxic individuals. This inquiry lays a foundation for using computation to understand neurobiochemical and electrophysiological pathophysiology of spinocerebellar ataxias and may contribute to development of therapeutics. The interdisciplinary analysis suggests that computational neurobiology can be an important tool for translational neurology.
    Full-text · Article · Jan 2015 · Frontiers in Neuroscience
  • Violiza Inoa · Louise D McCullough
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    ABSTRACT: Movement disorders have been reported as rare complications of stroke. The basal ganglia have been implicated in the pathophysiology of most post-stroke dyskinesias. We outline different types of post-stroke myoclonus and their possible pathophysiology. A middle-aged man developed generalized myoclonus after an ischemic stroke in the superior midbrain and subthalamic nuclei. Spontaneous resolution was seen by 72 hours. A lesion to the subthalamic nuclei disrupted the normal thalamic inhibition, which likely led to the involuntary movements seen in our patient. In this case, myoclonus was generalized, which, to the best of our knowledge, has not been reported in the literature as a direct consequence of focal stroke.
    No preview · Article · Jan 2015
  • Brett Friedler · Joshua Crapser · Louise McCullough
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    ABSTRACT: The deleterious effects of chronic social isolation (SI) have been recognized for several decades. Isolation is a major source of psychosocial stress and is associated with an increased prevalence of vascular and neurological diseases. In addition, isolation exacerbates morbidity and mortality following acute injuries such as stroke or myocardial infarction. In contrast, affiliative social interactions can improve organismal function and health. The molecular mechanisms underlying these effects are unknown. Recently, results from large epidemiological trials and pre-clinical studies have revealed several potential mediators of the detrimental effects of isolation. At least three major biological systems have been implicated: the neuroendocrine (HPA) axis, the immune system, and the autonomic nervous system. This review summarizes studies examining the relationship between isolation and mortality and the pathophysiological mechanisms underlying SI. Cardiovascular, cerebrovascular, and neurological diseases including atherosclerosis, myocardial infarction, ischemic stroke and Alzheimer's disease are given special emphasis in the context of SI. Sex differences are highlighted and studies are separated into clinical and basic science for clarity.
    No preview · Article · Dec 2014 · Acta Neuropathologica
  • Abraham W Aron · Ilene Staff · Gilbert Fortunato · Louise D McCullough
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    ABSTRACT: Substantial evidence from both experimental and clinical studies has demonstrated that social isolation can increase stroke incidence and impair recovery. Social isolation leads to higher rates of recurrent stroke but is often not reported as a risk factor. We examined prospectively collected stroke center database variables, which included prestroke living situation, to determine if social isolation could be determined from existing data using living arrangement as a proxy. Patients were categorized into 4 groups hypothesized to represent increasing levels of social isolation: living with spouse, living with family, living alone with visiting services, and living alone. Initial stroke severity and recovery were measured using the National Institutes of Health Stroke Scale and Barthel Index, respectively. A multivariate model was used to determine the relationship among prestroke living situation, stroke severity, and functional outcome. Patients living alone had less severe strokes on admission and better recovery at 3 months compared with the other cohorts. Patients living alone or those who lived with a spouse had less severe strokes on presentation and better recovery at both 3 and 12 months after stroke compared with the other cohorts. However, on detailed examination, it was found that these patients also had significantly higher prestroke function. Pre-existing depression was significantly higher in women, and depressed patients had poorer outcomes 3 months after stroke. Information regarding isolation is notably absent from most large stroke databases. A more comprehensive evaluation of social interaction should be obtained to more accurately measure social isolation. Copyright © 2014 National Stroke Association. Published by Elsevier Inc. All rights reserved.
    No preview · Article · Dec 2014 · Journal of stroke and cerebrovascular diseases: the official journal of National Stroke Association
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    ABSTRACT: Epidemiologic studies have shown sex differences in ischemic stroke. The four core genotype (FCG) mouse model, in which the testes determining gene, Sry, has been moved from Y chromosome to an autosome, was used to dissociate the effects of sex hormones from sex chromosome in ischemic stroke outcome. Middle cerebral artery occlusion (MCAO) in gonad intact FCG mice revealed that gonadal males (XXM and XYM) had significantly higher infarct volumes as compared with gonadal females (XXF and XYF). Serum testosterone levels were equivalent in adult XXM and XYM, as was serum estrogen in XXF and XYF mice. To remove the effects of gonadal hormones, gonadectomized FCG mice were subjected to MCAO. Gonadectomy significantly increased infarct volumes in females, while no change was seen in gonadectomized males, indicating that estrogen loss increases ischemic sensitivity. Estradiol supplementation in gonadectomized FCG mice rescued this phenotype. Interestingly, FCG male mice were less sensitive to effects of hormones. This may be due to enhanced expression of the transgene Sry in brains of FCG male mice. Sex differences in ischemic stroke sensitivity appear to be shaped by organizational and activational effects of sex hormones, rather than sex chromosomal complement.Journal of Cerebral Blood Flow & Metabolism advance online publication, 12 November 2014; doi:10.1038/jcbfm.2014.186.
    No preview · Article · Nov 2014 · Journal of Cerebral Blood Flow & Metabolism
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    ABSTRACT: Neurogenic stress cardiomyopathy (NCM) has been associated with poor outcomes in the setting of aneurysmal subarachnoid hemorrhage (aSAH). Much less is known regarding recovery of cardiac function. The aim of this prospective cohort study was to study the rate of early cardiac recovery after NCM and the potential effect of NCM on short term functional recovery. A secondary aim sought to determine whether certain biomarkers may be associated with the development of NCM.Methods Patients with confirmed aSAH between November 2012 and October 2013 were prospectively enrolled and received echocardiograms within 48 h of admission. Ejection fraction (%) and regional wall motion abnormality score index (RWMI) were noted. All patients with confirmed aSAH had a troponin and BNP level drawn on admission. Patients with confirmed NCM received a follow up echocardiogram 7–21 days after the initial echocardiogram. Clinical follow up at 3 months evaluated mortality, mRS and mBI scores.Results63 patients with confirmed aSAH were enrolled. In this cohort 11 (17%) patients were confirmed to have NCM. The NCM group had higher in-hospital mortality [n = 4(36.4%)] compared to the non-NCM group [n = 5(9.6%)] (p = .021). At 3 months the development of NCM was associated with an unfavorable mRS (p = 0.042) and mBI (p = 0.005). Both an elevated BNP (>100 pg/mL) and elevated troponin (>0.3 mg/dL) were associated with the development of NCM. Follow-up echocardiograms were performed within 21 days of admission on 8 patients with NCM. An abnormal RWMI of 1.5 or higher was present in 5(71%) patients.ConclusionNCM is a frequent complication associated with aSAH. The onset of the disease occurs early in the course of aSAH and an elevated BNP and troponin may be associated with the onset of NCM. Cardiac function often remains impaired during the acute recovery phase potentially impeding resuscitation during this period. The routine use of short term follow-up echocardiography may be recommended.
    No preview · Article · Nov 2014 · Clinical Neurology and Neurosurgery

Publication Stats

4k Citations
646.07 Total Impact Points


  • 2007-2015
    • University of Connecticut
      Сторс, Connecticut, United States
  • 2005-2015
    • Hartford Hospital
      • • Department of Neurology
      • • Stroke Center
      Hartford, Connecticut, United States
  • 2011
    • UConn Health Center
      Фармингтон, Connecticut, United States
    • Saint Francis Hospital And Medical Center, Hartford, Ct
      Hartford, Connecticut, United States
  • 2004-2007
    • Oregon Health and Science University
      • Department of Anesthesiology & Perioperative Medicine
      Portland, Oregon, United States
  • 2001-2007
    • Johns Hopkins University
      • Department of Anesthesiology and Critical Care Medicine
      Baltimore, Maryland, United States
  • 2001-2005
    • Johns Hopkins Medicine
      • • Department of Neurology
      • • Department of Anesthesiology and Critical Care Medicine
      Baltimore, MD, United States