bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spontaneous Hyperacute Postischemic Hemorrhage Leading to Death
Authors: Smith Eric E. , Fitzsimmons April L. , Nogueira Raul G. , Singhal Aneesh B. 
Published: November 2009

ABSTRACTHyperacute, spontaneous, and severe parenchymal postischemic hemorrhage is considered rare but might be frequently misdiagnosed as primary intracerebral hemorrhage. The authors report 2 patients with catastrophic postischemic hemorrhage unrelated to anticoagulation, thrombolytics, or coagulopathy. Patient 1 was a 73‐year‐old woman with left posterior frontal lobe infarction, followed at 5.5 hours by massive postischemic hemorrhage leading to death. Patient 2 was a 52‐year‐old man with recent brain irradiation who developed left middle cerebral artery occlusion and basal ganglia infarction. Initial gradient‐echo magnetic resonance imaging (MRI) showed petechial hemorrhage within areas of infarction and widespread old microbleeds. He developed massive postischemic hemorrhage at 12 hours, leading to death. The authors conclude that early brain imaging is essential to distinguish postischemic from primary brain hemorrhage. In patients with ischemic stroke, MRI findings such as hyperacute petechial hemorrhage or chronic cerebral microbleeds might predict subsequent parenchymal hemorrhage and thus have implications for tissue plasminogen activator use.
Simple Partial Status Epilepticus Localized by Single‐Photon Emission Computed Tomography Subtraction in Chronic Cerebral Paragonimiasis
Authors: Joo Eun Yeon , Kim Jee Hyun , Tae Woo Suk , Han Sun Jung , Kim Seunghwan , Kim Myoung‐Hee , Byun Hong Sik , Hong Seung Bong 
Published: November 2009

ABSTRACTA patient with chronic cerebral paragonimiasis began to have new motor seizures of the right face manifested by clonic contractions that occurred several hundred times a day, consistent with simple partial status epilepticus. Ictal electroencephalogram discharges started from the left frontal region and then spread to the left hemisphere with left frontal maximum. But clinical seizures were limited to the right face. The frequent partial seizures were controlled by the intravenous infusion of phenytoin. Brain magnetic resonance imaging showed multiple conglomerated round nodules with encephalomalacia in the left temporal and occipital lobes. Applying the technique of ictal‐interictal single‐photo emission computed tomography subtraction, the authors were able to localize the focal ictal‐hyperperfusion on left precentral cortex adjacent to the lesions that correspond to the anatomical distribution of left face motor area.
Proton Magnetic Resonance Spectroscopy and Magnetic Resonance Imaging Findings in a Patient with Central Nervous System Paracoccidioidomycosis
Authors: Faria Andréia V. , Dabus Guilherme C. , Zanardi Verônica A. , Cendes Fernando 
Published: November 2009

ABSTRACTThe authors describe a patient with brain paracoccidioidomycosis whose magnetic resonance image (MRI) showed multiple hypointense lesions on T2‐weighted images with peripheral enhancement after gadolinium injection. Single‐voxel proton magnetic resonance spectroscopy (H‐MRS) of one of the lesions showed 2 peaks at 0.9 and 1.32 ppm, corresponding to lipid signals, indicating intense necrosis. The other characteristic peaks of H‐MRS were undifferentiated from baseline. These findings, although not specific, may help to differentiate fungal abscess from tumoral lesions and other types of abscess.
Unsuccessful Tissue Plasminogen Activator Treatment of Acute Stroke Caused by a Calcific Embolus
Authors: Halloran John I. , Bekavac Ivo 
Published: November 2009

ABSTRACTIntravenous (IV) administration of tissue plasminogen activator (tPA) given to patients during acute cerebral ischemia according to National Institute of Neurological Disorders and Stroke (NINDS) guidelines improves clinical outcome by 11% to 14%. The success of IV tPA stroke therapy is dependent on several previously reported factors. The authors suggest that the presence of calcification within an embolus may represent an additional important factor. This report describes a patient with an acute stroke secondary to a spontaneous calcific cerebral embolus who had a negative outcome despite receiving proper thrombolytic therapy.
Pathogenesis of Brain and Spinal Cord Atrophy in Multiple Sclerosis
Authors: Minagar Alireza , Toledo Eduardo Gonzalez , Alexander J. Steven , Kelley Roger E. 
Published: November 2009

ABSTRACTFor more than a century, multiple sclerosis was viewed as a disease process characterized by oligodendrocyte and myelin loss, and research into the pathogenesis of multiple sclerosis was mainly focused on the mechanisms of inflammation. However, with development of more sophisticated neuroimaging and molecular biology techniques, attention has shifted to new aspects of pathogenesis of multiple sclerosis: axonal loss and neurodegeneration. Evidence is increasing that tissue destruction, primarily axonal loss and neurodegeneration, is a key element in the pathogenesis of multiple sclerosis. In addition, it is now known that brain and spinal cord atrophy begins early in the disease process of multiple sclerosis and advances relentlessly throughout the course of the disease. Cumulative data suggest that axonal loss is the major determinant of progressive neuro logic disability in patients with multiple sclerosis. Magnetic resonance imaging and magnetic resonance spectroscopy in patients with multiple sclerosis for < 5 years indicate brain atrophy and loss of axonal integrity. Neurodegeneration and axonal loss in patients with multiple sclerosis are initially accompanied by a local response from oligodendrocyte progenitor cells and some remyelination. However, these repair mechanisms eventually fail, and patients typically develop generalized brain atrophy, cognitive decline, and permanent disability. Although the exact mechanisms underlying central nervous system atrophy in patients with multiple sclerosis are largely unknown, evidence exists that atrophy may represent an epiphenomenon related to the effects of dynamic inflammation within the central nervous system, including demyelination, axonal injury, neuronal loss, Wallerian degeneration, and possibly iron deposition. This article summarizes the potential mechanisms involved in central nervous system atrophy in patients with multiple sclerosis.
Measurement of Spinal Cord Atrophy in Multiple Sclerosis
Authors: Lin Xia , Tench Christopher R. , Evangelou Nikos , Jaspan Timothy , Constantinescu Cris S. 
Published: November 2009

ABSTRACTIn multiple sclerosis (MS), the spinal cord is a common area of involvement, and its dysfunction is likely to be responsible for much of motor disability. It has been reported that atrophy in the cervical spinal cord occurs early and is detectable in patients presenting with a clinically isolated syndrome. This finding has important implications for the early treatment of patients with MS because atrophy is thought to reflect destructive, irreversible pathology and subclinical impairment. Recent clinical trials of disease‐modifying agents have included spinal cord imaging and, in particular, the measurement of atrophy as a secondary or exploratory measure of treatment efficacy. This review summarizes the underlying pathology responsible for spinal cord atrophy and the methods available to measure it. The relationships between spinal cord atrophy, other magnetic resonance imaging parameters, and clinical disability are also discussed.
Central Nervous System Atrophy and Clinical Status in Multiple Sclerosis
Authors: Zivadinov Robert , Bakshi Rohit 
Published: November 2009

ABSTRACTIn this review, the authors focus on clinical aspects of central nervous system (CNS) atrophy in multiple sclerosis (MS), including the relationship between atrophy and disability, disease course, disease duration, quality of life, and fatigue. Crosssectional studies have demonstrated a moderate but significant correlation between brain or spinal cord atrophy and physical disability in patients with MS. Longitudinal studies ([.greaterequal] 5 years) have shown that CNS atrophy is a significant predictor of subsequent long‐term neurologic deterioration. The clinical relevance of CNS atrophy is reinforced by studies showing that atrophy accounts for more variance than conventional lesion measures in predicting disability. Impaired quality of life and both urodynamic and sexual dysfunction, but not fatigue, are associated with brain atrophy. It is likely that once the level of CNS atrophy reaches a critical threshold, patients begin to suffer clinical impairment and disease progression. Longitudinal studies suggest that CNS atrophy may occur in patients with clinically isolated demyelinating syndromes who are at high risk for developing clinically definite MS. Longitudinal natural history studies in relapsing‐remitting, secondary progressive, and primary progressive MS have suggested that patients develop CNS atrophy at a faster rate in the first few years of disease than later in the disease course. Similarly, long‐term follow‐up studies have shown a poor relationship between disease duration and the rate of brain atrophy. The authors conclude that measurement of atrophy of the CNS is emerging as a clinically relevant biomarker of the MS disease process.
Correlating Brain Atrophy With Cognitive Dysfunction, Mood Disturbances, and Personality Disorder in Multiple Sclerosis
Authors: Benedict Ralph H. B. , Carone Dominic A. , Bakshi Rohit 
Published: November 2009

ABSTRACTNeuropsychological impairment is a common feature of multiple sclerosis. Affected patients often have deficits in informationprocessing speed and memory and exhibit psychopathological states such as depression. A minority of patients have rarer affect/mood disorders such as euphoria sclerotica and pathological laughter/crying. Neuropsychological impairment is a major predictor of low quality of life, unemployment, and caregiver distress. Studies evaluating correlations between neuropsychological impairment and findings on magnetic resonance imaging show that neuropsychological dysfunction is associated with lesion burden and diffuse disease in normalappearing brain tissue. However, measures of tissue atrophy including whole‐brain and central atrophy are especially well correlated with and predictive of cognitive impairment. Moreover, recent studies have shown that conventional measures of brain atrophy explain more variance in neuropsychological dysfunction than do measures of lesion burden. In particular, neuropsychological outcomes correspond highly with linear measures of subcortical atrophy such as ventricle enlargement. Within the domain of emotional dysfunction, both lesion burden and atrophy are related to major depressive disorder. Brain atrophy also predicts euphoria and disinhibition. The preliminary data suggest that although lesion burden primarily predicts depressive disorder, both lesion burden and atrophy predict the presence of euphoria. Euphoria and disinhibition likely represent personality change associated with worsening cognition as the disease progresses. Taken together, this growing body of data on magnetic resonance imaging to neuropsychological correlations supports the clinical relevance and validity of brain atrophy as a measure of disease progression in multiple sclerosis. Continuing research focuses on the possible relationship between measures of regional brain atrophy and cognitive and emotional impairment.
Impact of Disease‐Modifying Therapies on Brain and Spinal Cord Atrophy in Multiple Sclerosis
Authors: Rudick Richard A. 
Published: November 2009

ABSTRACTBrain and spinal cord atrophy occur early in the course of multiple sclerosis (MS) and continue throughout this lifelong illness, resulting in substantial parenchymal tissue loss at later disease stages. Treatments that slow or prevent atrophy may reduce disability progression in the long term. Disease‐modifying agents (DMAs) such as interferon [.beta]‐1b (IFN[.beta]‐1b), IFN[.beta]‐1a, and glatiramer acetate inhibit inflammatory events believed to initiate and perpetuate the disease process. DMAs have been shown to inhibit aspects of MS related to brain inflammation such as relapses and gadolinium‐enhanced lesions. Because brain inflammation has been linked to irreversible brain tissue injury, DMAs should be effective in reducing the rate of brain atrophy progression. Weekly IFN[.beta]‐1a (Avonex or Rebif) has been shown to slow the rate of brain atrophy; a large study of a frequent injection regimen with IFN[.beta]‐1a (Rebif) showed continued atrophy progression despite IFN[.beta]‐1a at a rate similar to placebo‐treated patients. It is not clear why weekly treatment regimens with lower total doses of IFN[.beta]‐1a would show beneficial effects on brain atrophy compared with frequent injections with larger weekly doses. This article reviews results of clinical trials that have examined the effects of DMAs on brain and spinal cord atrophy in patients with MS. Some of these agents have demonstrated positive effects in well‐controlled studies, suggesting that anti‐inflammatory therapy can delay or prevent the emergence of irreversible central nervous system pathology.
Quantitation of Contrast TCD in Patients With and Without Atrial Septal Aneurysm
Authors: Ziai Wendy C. , Oh Sangjin , Razumovsky Alexander Y. , Wityk Robert J. 
Published: November 2009

ABSTRACT Background and Purpose. Patients with a combination of atrial septal aneurysm (ASA) and patent foramen ovale (PFO) have a substantially higher rate of recurrent ischemic events as com pared to PFO alone. One possible explanation is a greater de gree of right‐to‐left shunting with the combination. Methods. Retrospective study using contrast transcranial Doppler ultrasonography (c‐TCD) to study the degree of shunting in 46 patients with PFO with either transient ischemic attack or cryp togenic ischemic stroke. Eight patients with PFO+ASA identified on transesophageal echocardiogram were compared to 38 pa tients with PFO but without ASA. Results. The number of em bolic counts was no different with or without an ASA. Valsalva maneuver increased number of emboli, especially in patients with large PFOs. Conclusions. Patients with ASA in addition to PFO do not appear to have an increased risk of right‐to‐left shunting as measured by c‐TCD as compared to PFO alone.
Etiology of Perfusion‐Diffusion Magnetic Resonance Imaging Mismatch Patterns
Authors: Restrepo Lucas , Jacobs Michael A. , Barker Peter B. , Beauchamp Norman J. , Skolasky Richard L. , Keswani Sanjay C. , Wityk Robert J. 
Published: November 2009

ABSTRACT Background and Purpose. Diffusion‐and perfusion‐weighted magnetic resonance imaging (DWI and PWI) are useful tools for the assessment of brain ischemia. Discrepancies between the extent of DWI and PWI abnormalities are thought to depend pre dominantly on time from symptom onset to magnetic resonance imaging (MRI) examination. However, underlying ischemic stroke etiology can also be important. A mismatch may indicate the presence of tissue at risk for infarction, whereas the rele vance of other DWI/PWI patterns is uncertain. The authors therefore investigated the etiology of brain ischemia in patients with different DWI/PWI patterns. Methods. Retrospective study of 130 patients with acute brain ischemia and detailed stroke workup, including MRI within a week after symptom onset (40 ± 39 hours). Patients were divided into the following groups: mis‐match (PWI > DWI), reverse mismatch (DWI > PWI), and match (<25% difference between PWI and DWI). Results. Mismatch occurred in 49% of patients, whereas 22% had reverse mis‐match and 29% matched lesions. Time from symptom onset to MRI examination was similar between the 3 groups. Largeartery atherosclerosis increased by almost 4‐fold the odds of mismatch (odds ratio: 3.89, 95% confidence interval: 1.72–8.78; P < .001), whereas patients with reverse mismatch were likely to have cryptogenic stroke. Patients with matched lesions were similarly distributed among different stroke subtypes. Con clusions. Ischemic stroke etiology appears to influence the development of specific DWI/PWI patterns. Prospective studies are needed to confirm these observations.
Aortic Dissection Presenting as an Acute Ischemic Stroke for Thrombolysis
Authors: Uchino Ken , Estrera Anthony , Calleja Sergio , Alexandrov Andrei V. , Garami Zsolt 
Published: November 2009

ABSTRACTThrombolysis for the treatment of acute ischemic stroke requires careful selection of patients. The authors report a case of aortic dissection presenting with acute ischemic stroke for which emergent ultrasonographic evaluation was helpful in the diagnosis and subsequent treatment. The patient presented with acute middle cerebral artery ischemic stroke symptoms and complained of bilateral ear and chest pain. Chest x‐ray, cardiac enzymes, and transthoracic echocardiogram were normal, and she was considered for thrombolytic therapy. Carotid ultrasound revealed right common carotid occlusion that led to the diagnosis of aortic dissection, confirmed by chest computed tomography. An experienced sonographer with skills to perform rapid intra‐ and extracranial examinations may help to change the treatment plan for acute stroke patients.
Wyburn‐Mason Syndrome
Authors: Lester Jacobo , Ruano‐Calderón Luis Angel , González‐Olhovich Irene 
Published: November 2009

ABSTRACTWyburn‐Mason syndrome is an uncommon condition in which arteriovenous malformations coexist in the visual brain area, in the retina, and in some cases, in the face. As a consequence, it has recently been defined as a brain‐retino‐facial angiomatosis. The syndrome results from an embryonary insult in the development of the optic nerve path and the related vessels from its origin in the mesencephalon all the way to the projection to the retina where it usually causes unilateral manifestations. Here the authors present an interesting case of this ailment and a review of the literature.
Talairach‐Based Parcellation of Neonatal Brain Magnetic Resonance Imaging Data: Validation of a New Approach
Authors: Haidar Haissam , Warfield Simon K. , Soul Janet S. 
Published: November 2009

ABSTRACTBackground and Purpose. Talairach‐based parcellation (TP) of human brain magnetic resonance imaging (MRI) data has been used increasingly in clinical research to make regional measurements of brain structures in vivo. Recently, TP has been applied to pediatric research to elucidate the changes in regional brain volumes related to several neurological disorders. However, all freely available tools have been designed to parcellate adult brain MRI data. Parcellation of neonatal MRI data is very challenging owing to the lack of strong signal contrast, variability in signal intensity within tissues, and the small size and thus difficulty in identifying small structures used as landmarks for TP. Hence the authors designed and validated a new interactive tool to parcellate brain MRI data from newborns and young infants. Methods. The authors' tool was developed as part of a postprocessing pipeline, which includes registration of multichannel MR images, segmentation, and parcellation of the segmented data. The tool employs user‐friendly interactive software to visualize and assign the anatomic landmarks required for parcellation, after which the planes and parcels are generated automatically by the algorithm. The authors then performed 3 sets of validation experiments to test the precision and reliability of their tool. Results. Validation experiments of intra‐and interrater reliability on data obtained from newborn and 1‐year‐old children showed a very high sensitivity of >95% and specificity >99.9%. The authors also showed that rotating and reformatting the original MRI data results in a statistically significant difference in parcel volumes, demonstrating the importance of using a tool such as theirs that does not require realignment of the data prior to parcellation. Conclusions. To the authors' knowledge, the presented approach is the first TP method that has been developed and validated specifically for neonatal brain MRI data. Their approach would also be valuable for the analysis of brain MRI data from older children and adults.
Emergent Basilar Artery and Bilateral Posterior Cerebral Artery Angioplasty, Urokinase Thrombolysis, and Stenting for Acute Basilar Artery Occlusion Secondary to Diagnostic Cardiac Catheterization: Case Presentation
Authors: Horowitz Michael , Jovin Tudor , Levy Elad , Anderson William 
Published: November 2009

ABSTRACTThis case presentation describes the use of emergent neurointerventional procedures to revascularize a patient who developed a symptomatic stroke during coronary artery angiography. Rapid identification of a neurologic deficit in the coronary angiography suite and notification of a skilled neurointerventionalist permit for early revascularization and improved patient outcomes.
Transcranial Doppler Ultrasonographic Evaluation of Middle Cerebral Artery Hemodynamics During Mild Hypothermia
Authors: Mahmood M. Asim , Voorhees Marc E. , Parnell Mel , Zweifler Richard M. 
Published: November 2009

ABSTRACT Background and Purpose. Induced hypothermia holds promise as an effective neuroprotective strategy following cerebral ischemia. The effect of mild hypothermia on cerebral hemodynamics is not well known. The authors investigated the influence of brain temperature on middle cerebral artery (MCA) mean flow velocity (MCA FV) and pulsatility index (MCA PI) in nonintubated, healthy volunteers undergoing mild induced hypothermia. Methods. Mild hypothermia (target tympanic membrane temperature [T tym]°C) was induced in subjects using the Arctic Sun® Temperature Management System (Medivance®, Inc, Louisville, CO). MCA FV and MCA PI were recorded bilaterally with a 2 MHz pulsed probe every 30 minutes via the transtemporal window. Results. Eighteen subjects (8 males, 10 females) 32 ± 8 years of age were studied. Multivariate analysis indicated that MCA FV increased with increasing change in temperature (baseline tympanic temperature – tympanic temperature [. Ttym]) (P< .001), heart rate (HR) (P< .001), end‐tidal CO2(P= .025), arterial oxygen saturation (O2%) (P= .001), and with decreasing mean arterial blood pressure (P= .004). Multivariate analysis also indicated that ln(MCA PI) (natural logarithm of MCA PI) decreased with decreasing T tym(P< .001) and increasing HR (P< .001). Conclusions. Mild induced hypothermia is associated with an increase in MCA FV and a decrease in MCA PI. The increase in MCA FV may be partially due to microcirculatory vasodilation.