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Haitham Dababneh, V. Shushrutha Hedna, Jenna Ford, Ziad Taimeh, Keith Peters, J Mocco and Michael F. Waters

The overall incidence of neurological complications due to infective endocarditis is as high as 40%, with embolic infarcts more common than hemorrhagic strokes. The standard of care for typical strokes does not apply to infective endocarditis because there is a substantial risk of hemorrhage with thrombolysis. In the last decade there have been multiple case reports of intravenous and intraarterial thrombolysis with successful outcomes for acute strokes with related infective endocarditis, but successful endovascular interventions for acute strokes associated with infective endocarditis are rarely reported. To the authors' knowledge, this report is the first case in the literature to use a mechanical retrieval device in successful vegetation retrieval in an infective endocarditis acute stroke. Although an interventional approach for treatment of acute stroke related to infective endocarditis is a promising option, it is controversial and a cautious clinical decision should be made on a case-by-case basis. The authors conclude that this approach can be tested in a case series with matched controls, because this condition is rare and a randomized clinical trial is not a realistic option.

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Vishnumurthy Shushrutha Hedna, Abhay Kumar, Bayard Miller, Sharathchandra Bidari, Arash Salardini, Michael F. Waters, Maria Hella, Edward Valenstein and Stephan Eisenschenk

Intracranial hypotension (IH) has been a known entity in neurocritical care since 1938. Even though many cases are spontaneous, the incidence of intracranial hypotension in the neurocritical care setting is increasing by virtue of the increased number of neurosurgical interventions. Whether spontaneous or secondary in etiology, diagnosis of IH usually requires the presence of orthostatic symptoms, including headaches and nausea with low opening CSF pressure. However, typical clinical features in the appropriate clinical context and imaging, even with normal CSF pressure, can indicate IH. In the neurocritical care setting, challenges for accurate semiology include altered sensorium and reduced levels of responsiveness for which many etiologies may exist, including metabolic dysfunction, traumatic brain injury, IH, or nonconvulsive status epilepticus (NCSE). The authors describe 3 patients whose clinical picture and electroencephalography (EEG) findings initially suggested NCSE but who did not respond to treatment with antiepileptic drugs alone. Neuroimaging suggested IH, and subsequent treatment of IH successfully improved the patient's clinical status. To the authors' knowledge this paper is the first in the literature that reports a correlation of IH with electrographic findings similar to NCSE as cause and effect. The authors' hypothesis is that thalamocortical dysfunction causes EEG findings that appear to be similar to those in NCSE but that these conditions do not coexist. The EEG activity is not epileptogenic, and IH results in blocking network pathways producing thalamocortical dysfunction. The authors discuss the hypothesis and pathophysiology of these epileptiform changes in relation to IH.

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Kyle M. Fargen, Brian L. Hoh, Gregory L. Fautheree, Walter R. Morgan, Gregory J. Velat, Michael F. Waters and J Mocco

Stroke patients whose condition does not improve after intravenous administration of tissue plasminogen activator (tPA) may be candidates for endovascular intervention. Patients with new intracerebral hemorrhage noted during such interventions pose a difficult challenge to neurointerventionists and are often sequestered as treatment failures and deemed inappropriate for intraarterial recanalization efforts. The authors present a case in which aggressive intervention was performed despite evidence of contrast extravasation on preintervention angiography. This 37-year-old woman presented with an occlusion of the M1 segment of the left middle cerebral artery and a National Institutes of Health Stroke Scale score of 24. She received intravenous tPA without improvement. Angiography revealed M1 thrombus as well as active contrast extravasation without arterial displacement. Thromboaspiration was performed in light of her known hemorrhage with excellent recanalization. Immediate postprocedure imaging demonstrated a large insular hematoma and emergent craniectomy and hematoma evacuation were performed. At 4 months' follow-up, the patient was living at home, was ambulating, and had excellent comprehension with mild expressive aphasia. There is little peer-reviewed data in the literature to aid in the decision-making process when contrast extravasation is recognized at the time of preinterevention angiography. Continuation of mechanical endovascular stroke intervention, in light of active contrast extravasation, may be warranted in young patients with major deficits and absence of arterial displacement or delayed global filling. Further thrombolytics are not advised. In select stroke patients, continuation of a planned attempt at mechanical recanalization without the further use of thrombolytics may be warranted in light of known intracerebral hemorrhage.

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Brian L. Hoh, Yan Gong, Caitrin W. McDonough, Michael F. Waters, Adrienne J. Royster, Tiffany O. Sheehan, Ben Burkley, Taimour Y. Langaee, J Mocco, Scott L. Zuckerman, Nishit Mummareddy, Marcus L. Stephens II, Christie Ingram, Christian M. Shaffer, Joshua C. Denny, Murray H. Brilliant, Terrie E. Kitchner, James G. Linneman, Dan M. Roden and Julie A. Johnson


Symptomatic intracranial atherosclerotic disease (ICAD) has a high risk of recurrent stroke. Genetic polymorphisms in CYP2C19 and CES1 are associated with adverse outcomes in cardiovascular patients, but have not been studied in ICAD. The authors studied CYP2C19 and CES1 single-nucleotide polymorphisms (SNPs) in symptomatic ICAD patients.


Genotype testing for CYP2C19*2, *3, *8, *17 and CES1 G143E was performed on 188 adult symptomatic ICAD patients from 3 medical centers who were medically managed with clopidogrel and aspirin. Testing was performed prospectively at 1 center, and retrospectively from a DNA sample biorepository at 2 centers. Multiple logistic regression and Cox regression analysis were performed to assess the association of these SNPs with the primary endpoint, which was a composite of transient ischemic attack (TIA), stroke, myocardial infarction, or death within 12 months.


The primary endpoint occurred in 14.9% of the 188 cases. In multiple logistic regression analysis, the presence of the CYP2C19 loss of function (LOF) alleles *2, *3, and *8 in the medically managed patients was associated with lower odds of primary endpoint compared with wild-type homozygotes (odds ratio [OR] 0.13, 95% CI 0.03–0.62, p = 0.0101). Cox regression analysis demonstrated the CYP2C19 LOF carriers had a lower risk for the primary endpoint, with hazard ratio (HR) of 0.27 (95% CI 0.08–0.95), p = 0.041. A sensitivity analysis of a secondary composite endpoint of TIA, stroke, or death demonstrated a significant trend in multiple logistic regression analysis of CYP2C19 variants, with lower odds of secondary endpoint in patients carrying at least 1 LOF allele (*2, *3, *8) than in wild-type homozygotes (OR 0.27, 95% CI 0.06–1.16, p = 0.078). Cox regression analysis demonstrated that the carriers of CYP2C19 LOF alleles had a lower risk forthe secondary composite endpoint (HR 0.22, 95% CI 0.05–1.04, p = 0.056).


This is the first study examining genetic variants and their effects in symptomatic ICAD. Variant alleles of CYP2C19 (*2, *3, *8) were associated with lower odds of the primary and secondary composite endpoints. However, the direction of the association was opposite of what is expected based on this SNP. This may reflect an incomplete understanding of this genetic variation and its effect in symptomatic ICAD and warrants further investigations.