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Erdheim-Chester disease (ECD) is a rare and elusive hematopoietic malignancy that may involve the nervous system in various ways. Cerebrovascular ECD involves the perivascular infiltration and compromise of any cervicocranial vessel by transformed proliferating histiocytes. Presented is the novel case of a patient with pathologically proven perivascular microangiopathy, manifesting in multifaceted fashion with ischemia, hemorrhage, mass lesions, and edema. [ABSTRACT FROM AUTHOR]

Background: Two recent cerebrovascular studies, Clopidogrel (Clo) in High-risk patients with Acute Nondisabling Cerebrovascular Events (CHANCE) and Platelet-Oriented Inhibition in New TIA and minor ischemic stroke (POINT), have purportedly demonstrated the superiority of early dual antiplatelet therapy (DAPT), using aspirin (ASA) plus Clo, in comparison to ASA alone following the occurrence of acute minor cerebral infarction or transient ischemic attack. However, limitations to these trials exist that may not have been adequately explored and presented in the literature, and which may impact the overall efficacy and benefit of DAPT in these situations. Herein we provide a detailed and extensive critique of these 2 trials and of a combined analysis, with particular attention to study data and analyses pertaining to hemorrhagic complications. Summary: DAPT may be superior to ASA alone in preventing recurrent cerebral ischemic events, but exclusively during the first 7–10 days of treatment, and probably only in the presence of acute infarction on cerebral imaging. The impact of minor hemorrhages, which are often clinically consequential and which frequently lead to permanent DAPT discontinuation, has not been adequately considered in the available analyses. Based on data from the trials, DAPT use causes more major and minor hemorrhages than ASA use alone or Clo alone, and Clo use results in fewer hemorrhages than the use of ASA alone. Analyses that include hemorrhage data from the period of Clo alone use as part of the DAPT data may provide inaccurate and erroneous conclusions regarding the relative safety and overall net benefit of DAPT use over ASA alone. [ABSTRACT FROM AUTHOR]

Purpose To evaluate the relationship between anterior cerebral artery (ACA) velocities (and ancillary parameters) and ACA infarction following aneurysmal subarachnoid hemorrhage (aSAH), and to examine the factors that influence velocities. Methods Retrospective investigation of 500 consecutive aSAH patients. ACA mean velocities (Vm) were evaluated by daily transcranial ultrasound during the early (days 1–4) and late (days 5–20) periods posthemorrhage. Presence and timing of acute ACA infarctions were identified by serial retrospective review of cerebral computerized tomography (CT) scans. Predictors of ACA velocities were identified and compared to predictors of vasospasm and infarction from the literature. Results Decreased velocities on the day of infarction were observed in infarct-positive vessels when compared to infarct-negative vessels. ACA velocity increases, ipsilateral/contralateral ACA velocity ratios, and ACA velocity ranges, were inaccurate in anticipating infarction. Decreased ACA index velocities were moderately accurate in anticipating ACA infarction during the early [Vm < 60 cms/s], late [Vm < 70 cms/s] and overall [Vm < 70 cms/s] time periods. Decreased index velocities also independently predicted infarction during all time periods. ACA velocities were most consistently predicted by age, race, hemorrhage quantity on CT, and ACA/ACom (anterior communicating artery) aneurysm location. Conclusions ACA velocity increases and ancillary parameters do not relate to the development of infarction, whereas velocity decreases are moderately accurate in anticipating infarction. Predictors of velocity increases generally coincide with those of vasospasm, whereas predictors of velocity decreases coincide more with those of infarction following aSAH. [ABSTRACT FROM AUTHOR]

Introduction: Sympathetic activation promotes hemostasis, and subarachnoid hemorrhage (SAH) is associated with pronounced sympathetic activation. This investigation will assess whether catecholaminergic activity relates to venous thrombotic events in patients with acute SAH. Methods: Observational study of consecutive SAH grade 3-5 patients requiring ventriculostomy insertion who did not undergo open surgical treatment of cerebral aneurysm. Cerebrospinal fluid (CSF) samples were obtained within 48 h of hemorrhage for assay of catecholamines, which were related to occurrence of deep venous thrombosis (DVT) and pulmonary embolization (PE). Results: Of the 92 subjects, mean age was 57 years, 76 % were female, and 57 % Caucasian; 11 % experienced lower extremity (LE) DVT, 12 % developed upper extremity (UE) or LE DVT, and 23 % developed any DVT/PE. Mean time to occurrence of UE/LE DVT was 7.8 days (+/−5.9 days), and mean time to development of PE was 8.8 days (+/−5.4 days). In hazards analysis models, independent predictors of LE DVT included neurogenic cardiomyopathy (NC) [HR 4.97 (95%CI 1.32-18.7)], norepinephrine/3,4-dihydroxyphenylglycol ratio (NE/DHPG) [3.81 (2.04-7.14)], NE [5.91 (2.14-16.3)], and dopamine (DA) [2.27 (1.38-3.72)]. Predictors of UE/LE DVT included NC [5.78 (1.70-19.7)], cerebral infarction [4.01 (1.18-13.7)], NE [3.58 (1.40-9.19)], NE/DHPG [3.38 (1.80-6.33)] and DA [2.01 (1.20-3.35)]. Predictors of DVT/PE included Hunt-Hess grade (H/H) [3.02 (1.19-7.66)], NE [2.56 (1.23-5.37)] and 3,4-dihydroxyphenylalanine (DOPA) [3.49 (1.01-12.0)]. Conclusions: In severe SAH, central sympathetic activity and clinical manifestations of (nor)adrenergic activity relate to the development of venous thromboemboli. Catecholamine activation may promote hemostasis, or may represent a biomarker for venous thromboses. [ABSTRACT FROM AUTHOR]

Anterior cerebral artery (ACA) ischemia may be underdiagnosed following subarachnoid hemorrhage (SAH). The purpose of this study is to characterize the prevalence, timing, and risk factors for ACA infarction, following primary spontaneous SAH. This was a retrospective study of consecutive SAH patients. Final admission CT scans were reviewed for the presence of ACA infarction, and prior scans serially reviewed to determine timing of infarct. Infarctions were categorized as any, early (days 0-3), late (days 4-15), or perioperative (2 days after aneurysm treatment). Demographic and clinical variables were statistically interrogated to identify predictors of infarct types. Of the 474 study patients, ACA infarctions occurred in 8 % of patients, with 42 % occurring during the early period. Multivariate logistic regression identified H/H grade 4/5 ( p < 0.001), ACA/ACom aneurysm location ( p < 0.001), and surgical clipping ( p = 0.011) as independent predictors of any ACA infarct. In Cox hazards analysis, H/H grade 4/5 ( p < 0.001), CT score 3/4 ( p = 0.042), ACA/ACom aneurysm location ( p < 0.001), and surgical clipping ( p = 0.012) independently predicted any ACA infarct. Bivariate logistic regression identified non-Caucasian race ( p = 0.032), H/H grade 3/4 ( p < 0.001), CT score 3/4 ( p = 0.006), IVH ( p = 0.027), and ACA/ACom aneurysm ( p = 0.001) as predictors of early infarct (EI). Late infarct (LI) was predicted by H/H grade 4/5 ( p = 0.040), ACA/ACom aneurysm ( p < 0.001), and vasospasm ( p = 0.027), while postoperative infarct (PI) was predicted by surgical clipping ( p = 0.044). Log-rank analyses confirmed non-Caucasian race ( p = 0.024), H/H grade 3/4 ( p < 0.001), CT score 3/4 ( p = 0.003), IVH ( p = 0.010), and ACA/ACom aneurysm ( p < 0.001) as predictors of EI. LI was predicted by ACA/ACom aneurysm ( p < 0.001) while surgical clipping ( p = 0.046) again predicted PI. Clinical severity/grade and ACA/ACom aneurysm location are the most consistent predictors of ACA infarctions. Vasospastic and non-vasospastic processes may concurrently contribute to ACA infarcts. [ABSTRACT FROM AUTHOR]

Background: Subarachnoid hemorrhage (SAH) has been associated with pronounced acute sympathetic activation. The purpose of this investigation is to identify demographic, clinical, radiological, and anatomical features of SAH that relate to sympathetic activation. Methods: Observational study of consecutive Grades 3-5 SAH patients requiring ventriculostomy and undergoing endovascular aneurysmal obliteration. All patients underwent cerebrospinal fluid (CSF) sampling within 48 h of SAH onset, and samples were assayed for various catecholamine compounds and metabolites. Univariate analyses were performed to identify variables associated with catecholamine levels, and to correlate linearity among catecholamine compounds and metabolites. Variables demonstrating a possible association and variables of interest were entered into linear regression models to determine predictors of catecholamine elevations. Results: Of the 102 patients, mean age was 58 years and 74% were female; 42% were Hunt-Hess (H/H) grade 4/5, 61% had a computed tomography (CT) score of 3/4, 57% had anterior cerebral or communicating artery (ACA/ACom) aneursysms, and 23% had aneurysms in the posterior circulation. In the univariate analysis, age, gender, H/H grade, CT score, and aneurysm location demonstrated various associations with catecholamine levels, and substantial positive correlations existed between the various catecholamine compounds and metabolites. Linear regression analyses revealed H/H grade to be an independent predictor of elevated CSF epinephrine (EPI), 3,4-dihydroxyphenylalanine (DOPA) and 3,4-dihydroxyphenyl acetic acid (DOPAC) levels, and of the norepinephrine/3,4-dihydroxyphenylglycol (NE/DHPG) ratio ( p < 0.05 for all analyses). Female gender independently predicted increased dopamine (DA) and DOPAC levels ( p < 0.05 for two analyses), as well as possibly DOPA levels ( p < 0.1). Age, CT score and aneurysm location demonstrated only inconsistent associations and trends. Conclusions: Central sympathetic activation relates to clinical severity and female gender. No definitive associations were found for age, hemorrhage amount, or aneurysm location. [ABSTRACT FROM AUTHOR]

Objective: Subarachnoid hemorrhage (SAH) is associated with marked sympathetic activation at the time of ictus. The purpose of this study is to determine whether early central catecholamine levels measured from cerebrospinal fluid (CSF) relate to outcome in patients with SAH. Methods: Observational study of consecutive SAH grade 3-5 patients who underwent ventriculostomy placement, but did not undergo open craniotomy for aneurysm obliteration. CSF samples were obtained during the first 48 h following symptom onset and assayed for catecholamine levels. Statistical analyses were performed to determine whether the levels predicted mortality by day 15 or mortality/disability by day 30. Results: For the 102 patients included, mean age was 58, and 73% were female - 21% experienced day-15 mortality, and 32% experienced mortality/disability by day 30. Early mortality was related to Hunt-Hess (H/H) grade (p < 0.001), neurogenic cardiomyopathy (NC) (p = 0.003), cerebral infarction (p = 0.001), elevated intracranial pressure (ICP) (p = 0.029), epinephrine (EPI) level (p = 0.002) and norepinephrine/3,4-dihydroxyphenylglycol (NE/DHPG) ratio (p = 0.003). Mortality/disability was related to H/H grade (p < 0.001), NC (p = 0.018), infarction (p < 0.001), elevated ICP (p = 0.002), EPI (p = 0.004) and NE/DHPG (p = 0.014). Logistic regression identified age [OR 1.09 (95% CI 1.01-1.17)], H/H grade [9.52 (1.19-77)], infarction [10.87 (1.22-100)], ICP elevation [32.26 (2-500)], EPI [1.06 (1.01-1.10)], and (inversely) DHPG [0.99 (0.99-1.00)] as independent predictors of early mortality. For mortality/disability, H/H grade [OR 21.74 (95% CI 5.62-83)], ICP elevation [18.52 (1.93-166)], and EPI [1.05 (1.02-1.09)] emerged as independent predictors. Proportional-hazards analysis revealed age [HR 1.041 (95% CI 1.003-1.08)], H/H grade [6.9 (1.54-31.25)], NC [4.31 (1.5-12.35)], and EPI [1.032 (1.009-1.054)] independently predicted early mortality. Conclusions: CSF catecholamine levels are elevated in SAH patients who experience early mortality or disability. EPI may potentially serve as useful index of outcome in this population of patients with SAH. Copyright © 2012 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Patients experiencing apoplectic intracranial processes may develop neurogenic cardiomyopathy (NC). The purpose of this research is to determine whether cerebrospinal fluid (CSF) catecholamine levels are elevated in subarachnoid hemorrhage (SAH) patients with NC when compared to those without NC. Methods: Observational study of consecutive grades 3-5 SAH patients requiring ventriculostomy. All patients underwent CSF sampling for catecholamine levels, and transthoracic echocardiography (TTE) to assess for NC, within 48 h of SAH onset. Univariate analyses were performed to identify clinical and laboratory variables associated with NC. Clinical variables associated with NC in the univaritate analysis were entered into logistic regression models along with the candidate catecholamine variables to identify predictors of NC. Results: The study group contained 100 patients-mean age of study subjects was 58 years, 73% were female, and 15% developed NC. NC patients were more likely to have a worse clinical grade than patients without NC (80 vs. 34%, P = 0.001). NC patients possessed greater DOPA levels (5.83 vs. 4.60 nmol/l, P = 0.044), and a trend toward greater noradrenergic activity as determined by NE/DHPG ratio (0.3799 vs. 0.2519, P = 0.073). Multivariate analysis identified worse clinical grade (OR 7.09, P = 0.005) and possibly NE levels (OR 1.005, P = 0.057) as independent predictors of NC. Bivariate analysis reinforced the findings for NE (OR 1.006, P = 0.022), and also identified DOPA levels (OR 1.001, P = 0.034) and NE/DHPG (OR 22.18, P = 0.019) as predictors of NC. Conclusions: SAH patients with NC tend to have greater CSF catecholamine levels than those without NC. However, the development of NC may also be related to factors not evaluated by our study. [ABSTRACT FROM AUTHOR]

Background: The purpose of this study is to determine whether intraventricular hemorrhage (IVH) exerts a 'decompressive' effect that limits intracerebral hemorrhage (ICH) enlargement. Methods: Retrospective review of patients with spontaneous supratentorial ICH diagnosed within 6 h of onset, who underwent follow-up head CT approximately 48 h later. Digital imaging analysis of CT scans was performed to compare hematoma volume changes between patients with and without IVH. Hemorrhage locations were classified as paraventricular (PV) or non-PV. Regression analyses were employed to identify predictors of IVH, hematoma expansion, and mortality. Results: Of the 70 patients included 57% developed IVH, 85% of which occurred before initial CT. 71% of PV hemorrhages developed IVH, all before initial CT, and 48% of non-PV hemorrhages developed IVH, 29% of which occurred after initial CT. IVH was associated with PV location ( P = 0.04), and among IVH patients PV location was associated with early IVH ( P = 0.003). Predictors of mortality included age ( P = 0.037), initial hematoma volume ( P < 0.04), absolute volume change ( P = 0.01), and final hematoma volume ( P < 0.001). Variables predicting IVH included PV location ( P < 0.0001), larger initial hematoma volume ( P = 0.002), and greater absolute volume increase ( P = 0.01). Hematoma expansion was greatest for non-PV with IVH ( P = 0.08), and graphic inspection suggested that ICH volume tended to decrease with PV location and increase with IVH. Final hematoma volume was associated with initial volume ( P < 0.0001), non-PV location ( P = 0.02), and IVH ( P = 0.04). Conclusions: IVH was not associated with less hematoma volume expansion, and for non-PV hemorrhages IVH was linked to greater volume increase. [ABSTRACT FROM AUTHOR]

Presents information on a case study on anterograde amnesia resulting from bilateral anterior fornix infarction. Medical history of a 61-year-old male admitted to the hospital after awakening with confusion; Findings of cerebral imaging performed on the patient; Results of the neuropsychological test conducted.

Combination antiplatelet agents with multiple mechanisms of action are being used with increasing frequency for vascular disorders, including cerehrovascular disease. Limited data exist regarding the efficacy of combination antiplatelet therapy in the primary or secondary prevention of cerebral ischemia, and combination therapies are often used without adequate evidence of efficacy. However, over the last few years, several cerebrovascular and cardiovascular trials have provided some preliminary information on the effectiveness of various combination therapies in preventing cerebral ischemic disease. This article reviews recently completed cerebrovascular and cardiovascular trials that tested a combination antiplatelet regimen against aspirin alone, and that assessed cerebral ischemia as an outcome measure. Controversies pertaining to these trials and to the use of the various combination antiplatelet regimens are discussed. Based on cardiovascular studies, clopidogrel in combination with aspirin has not been proven superior to aspirin alone for the primary prevention of cerebral ischemia. No data exists regarding the combination of clopidogrel and aspirin for the secondary prevention of cerebrovascular disease. The combination of aspirin plus extended-release dipyridamole (xrDP) appears to be superior to aspirin alone in the secondary prevention of cerebral ischemia, but may compromise cardiovascular protection in patients with coexisting coronary artery disease. Combination therapy with aspirin and clopidogrel seems to increase the risk of major hemorrhages, whereas aspirin plus xrDP does not. Ongoing trials are expected to clarify the role of various combination antiplatelet regimens. [ABSTRACT FROM AUTHOR]

Purpose. A case of resistance to rocuronium and cisatracurium in a patient with a spinal injury who developed acute respiratory distress syndrome (ARDS) is reported. Summary. A 34-year-old, 88-kg Caucasian man with a history of polysubstance abuse fell from a bridge approximately 30-ft high, landing head first in about 2-3 ft of water. The patient sustained anterior subluxation at cervical spine levels C5-C6 and severe spinal canal compromise with cord compression and edema from C5 to C7, resulting in quadriplegia. The patient developed aspiration pneumonia for which he was given vancomycin and piperacillin- tazobactam. His pneumonia progressed to ARDS, and drug-induced paralysis was attempted to reduce barotrauma and improve ventilation. Rocuronium was initiated, but the patient did not adequately respond to this treatment. Cisatracurium was then initiated, but the patient did not Kristina Riley, Pharm.D., is Pharmacist, Capital Health Medical Center, Hopewell, NJ; at the time of writing she was Postgraduate Year 1 Pharmacy Resident, Capital Health Regional Medical Center, Trenton, NJ. Natalie Yampolsky, Pharm.D., BCPS, is Clinical Pharmacist, Neurosurgery/Critical Care, Capital Health Regional Health Center. Zakaria Hakma, M.D., is Neurosurgeon; and Michael Moussouttas, M.D., is Neurointensivist, Capital Institute for Neurosciences, Trenton. Address correspondence to Dr. Yampolsky (nyampolsky@capitalhealth. org). The authors have declared no potential conflicts of interest. Copyright © 2015, American Society of Health-System Pharmacists, Inc. All rights reserved. 1079-2082/15/0402-0632. DOI 10.2146/ajhp140343 respond. The decision was made to discontinue the cisatracurium infusion at that time and manage the patient's ARDS without a neuromuscular blocking agent (NMBA). After several attempts to manage the patient's ARDS by adjusting ventilatory values, the patient required the reinitiation of an NMBA. The decision was made to try cisatracurium again. Cisatracurium was again unsuccessful and therefore discontinued. As a last attempt to improve oxygenation, the patient received nitric oxide and sedation with propofol. The patient died due to his complicated hospital course that included quadriplegia, ARDS, cardiac arrest, and sepsis secondary to a gastric perforation. Conclusion. Inadequate paralysis was achieved with rocuronium and cisatracurium in a patient who sustained a significant trauma resulting in quadriplegia. [ABSTRACT FROM AUTHOR]

Objectives: To determine the association between myocardial infarction (AMI) and clinical outcome in patients with primary admissions diagnosis of acute cerebral ischemia (ACI) in the US. Methods: Data from Nationwide Inpatient Sample (NIS) was queried from 2002–2011 for inpatient admissions of patients with a primary diagnosis of ACI with and without AMI using International Classification of Diseases, Ninth Revision, Clinical Modification coding (ICD-9). A multivariate stepwise regression analysis was performed to assess the correlation between identifiable risk factors and clinical outcomes. Results: During 10 years the NIS recorded 886,094 ACI admissions with 17,526 diagnoses of AMI (1.98%). The overall cumulative mortality of cohort was 5.65%. In-hospital mortality was associated with AMI (aOR 3.68; 95% CI 3.49–3.88, p≤0.0001), rTPA administration (aOR 2.39 CI, 2.11–2.71, p<0.0001), older age (aOR 1.03, 95% CI, 1.03–1.03, P<0.0001) and women (aOR 1.06, 95% CI 1.03–1.08, P<0.0001). Overall, mortality risk declined over the course of study; from 20.46% in 2002 to 11.8% in 2011 (OR 0.96, 95% CI 0.95–0.96, P<0.0001). Survival analysis demonstrated divergence between the AMI and non-AMI sub-groups over the course of study (log-rank p<0.0001). Conclusion: Our study demonstrates that although the prevalence of AMI in patients hospitalized with primary diagnosis of ACI is low, it negatively impacts survival. Considering the high clinical burden of AMI on mortality of ACI patients, a high quality monitoring in the event of cardiac events should be maintained in this patient cohort. Whether prompt diagnosis and treatment of associated cardiovascular diseases may improve outcome, deserves further study. [ABSTRACT FROM AUTHOR]

Background and Purpose: Red blood cell transfusion (RBCT) may increase the risk of thrombotic events (TE) in patients with subarachnoid hemorrhage (SAH) through changes induced by storage coupled with SAH-related hypercoagulability. We sought to investigate the association between RBCT and the risk of TE in patients with SAH. Methods: 205 consecutive patients with acute, aneurysmal SAH admitted to the neurovascular intensive care unit of a tertiary care, academic medical center between 3/2008 and 7/2009 were enrolled in a retrospective, observational cohort study. TE were defined as the composite of venous thromboembolism (VTE), myocardial infarction (MI), and cerebral infarction noted on brain CT scan. Secondary endpoints included the risk of VTE, poor outcome (modified Rankin score 3-6 at discharge), and in-hospital mortality. Results: 86/205 (42 %) received RBCT. Eighty-eight (43 %) had a thrombotic complication. Forty (34 %) of 119 non-transfused and 48/86 (56 %) transfused patients had a TE ( p = 0.002). In multivariate analysis, RBCT was associated with more TE by [OR 2.4; 95 % CI (1.2, 4.6); p = 0.01], VTE [OR 2.3; 95 % CI (1.0, 5.2); p = 0.04], and poor outcome [OR 5.0; 95 % CI (1.9, 12.8); p < 0.01]. The risk of TE increased by 55 % per unit transfused when controlling for univariate variables. Neither mean nor maximum age of blood was significantly associated with thrombotic risk. Conclusions: RBCT is associated with an increased risk of TE and VTE in SAH patients. A dose-dependent relationship exists between number of units transfused and thrombosis. Age of blood does not appear to play a role. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To determine the prevalence of status epilepticus, associated factors, and relationship with in-hospital mortality in primary admissions of septic patients in the United States. DESIGN: Cross-sectional study. SETTING: Primary admissions of adult patients more than 18 years old with a diagnosis of sepsis and status epilepticus from 1988 to 2008 identified through the Nationwide Inpatient Sample. PARTICIPANTS: A total of 7,669,125 primary admissions of patients with sepsis. INTERVENTIONS: None. RESULTS: During the 21-year study period, the prevalence of status epilepticus in primary admissions of septic patients increased from 0.1% in 1988 to 0.2% in 2008 (p < 0.001). Status epilepticus was also more common among later years, younger admissions, female gender, Black race, rural hospital admissions, and in those patients with organ dysfunctions. Mortality of primary sepsis admissions decreased from 20% in 1988 to 18% in 2008 (p < 0.001). Mortality in status epilepticus during sepsis decreased from 43% in 1988 to 28% in 2008. In-hospital mortality after admissions for sepsis was associated with status epilepticus, older age, and Black and Native American/Eskimo race; patients admitted to a rural or urban private hospitals; and patients with organ dysfunctions. CONCLUSION: Our analysis demonstrates that status epilepticus after admission for sepsis in the United States was rare. Despite an overall significant reduction in mortality after admission for sepsis, status epilepticus carried a higher risk of death. More aggressive electrophysiological monitoring and a high level of suspicion for the diagnosis of status epilepticus may be indicated in those patients with central nervous system organ dysfunction after sepsis. [ABSTRACT FROM AUTHOR]

Objective: To determine the prevalence of status epilepticus, associated factors, and relationship with in-hospital mortality in primary admissions of septic patients in the United States. Design: Cross-sectional study. Setting: Primary admissions of adult patients more than 18 years old with a diagnosis of sepsis anc status epilepticus from 1988 to 2008 identified through the Nationwide Inpatient Sample. Participants: A total of 7,669,125 primary admissions of patients with sepsis. Interventions: None. Results: During the 21-year study period, the prevalence of status epilepticus in primary admissions of septic patients increased from 0.1% in 1988 to 0.2% in 2008 (p < 0.001). Status epilepticus was also more common among later years, younger admissions, female gender, Black race, rural hospital admissions, and in those patients with organ dysfunctions. Mortality of primary sepsis admissions decreased from 20% in 1988 to 1 8% in 2008 (p < 0.001). Mortality iii status epilepticus during sepsis decreased from 43% in 1988 to 28% in 2008. In-hospital mortality after admissions for sepsis was associated with status epilepticus, older age, and Black and Native American/Eskimo race; patients admitted to a rura or urban private hospitals; and patients with organ dysfunctions. Conclusion: Our analysis demo.istrates that status epilepticus after admission for sepsis in the United States was rare. Despite an overall significant reduction in mortality after admission for sepsis, status epilepticus carried a higher risk of death. More aggressive electrophysiological monitorng and a high level of suspicion for the diagnosis of status epilepticus may be indicated in those patients with central nervous system organ dysfunction after sepsis. [ABSTRACT FROM AUTHOR]

Opsoclonus-myoclonus may be caused by various neurological conditions and toxic-metabolic states, but typically occurs as a parainfectious or paraneoplastic manifestation. The development of opsoclonus-myoclonus has been variably attributed to lesions in the pons or cerebellum. Herein the authors describe a case of opsoclonus-myoclonus due to posterior reversible encephalopathy syndrome in which magnetic resonance imaging revealed lesions in the region of the cerebellar dentate nuclei. Clinical and radiological resolution of the opsoclonus-myoclonus and of the posterior reversible encephalopathy syndrome followed antihypertensive therapy. [ABSTRACT FROM AUTHOR]

Background: The risk of perioperative stroke following cardiac and carotid artery surgery is well documented. There is an apparent lack of recognition and appreciation of this complication after total joint arthroplasty. The present study was designed to determine the prevalence of, and outcome after, perioperative stroke following total joint arthroplasty. In addition, risk factors for the development of this complication were evaluated in an attempt to identify a strategy that could minimize the prevalence of this complication.Methods: We performed an observational study of 18,745 consecutive patients undergoing primary or revision total hip or total knee arthroplasty from 2000 to 2007 at our institution. The institutional perioperative stroke rate was 0.2% (thirty-six of 18,745). The thirty-six patients who had a stroke included seventeen men and nineteen women with a mean age of 68.2 years (range, forty-five to eighty-seven years). The average duration of follow-up for all patients and controls in the present study was sixty-two months (range, zero to 124.9 months). In a predictive model, different patient-related and surgery-related factors that could predispose patients to this complication and/or affect outcome were evaluated.Results: The first-year mortality among stroke patients was 25% (nine of thirty-six), and four of these nine patients died in the hospital following total joint arthroplasty. Of three patients who received emergency intra-arterial thrombolysis, two had complete neurologic recovery and one died in the hospital. The final regression model showed that a history of noncoronary heart disease, urgent (versus elective) surgery, general (versus regional) anesthesia, and an intraoperative arrhythmia or other alterations in the heart rate during surgery are significant predictors of perioperative stroke.Conclusions: Perioperative stroke is a rare but potentially devastating complication of total joint arthroplasty, with a high rate of morbidity and mortality. Vigilant attention to prevent, detect, and treat this complication in a timely manner may alter the course of the disease. [ABSTRACT FROM AUTHOR]

Background: The risk of perioperative stroke following cardiac and carotid artery surgery is well documented. There is an apparent lack of recognition and appreciation of this complication after total joint arthroplasty. The present study was designed to determine the prevalence of, and outcome after, perioperative stroke following total joint arthroplasty. In addition, risk factors for the development of this complication were evaluated in an attempt to identify a strategy that could minimize the prevalence of this complication. Methods: We performed an observational study of 18,745 consecutive patients undergoing primary or revision total hip or total knee arthroplasty from 2000 to 2007 at our institution. The institutional perioperative stroke rate was 0.2% (thirty-six of 18,745). The thirty-six patients who had a stroke included seventeen men and nineteen women with a mean age of 68.2 years (range, forty-five to eighty-seven years). The average duration of follow-up for all patients and controls in the present study was sixty-two months (range, zero to 124.9 months). In a predictive model, different patient-related and surgery-related factors that could predispose patients to this complication and/or affect outcome were evaluated. Results: The first-year mortality among stroke patients was 25% (nine of thirty-six), and four of these nine patients died in the hospital following total joint arthroplasty. Of three patients who received emergency intra-arterial thrombolysis, two had complete neurologic recovery and one died in the hospital. The final regression model showed that a history of noncoronary heart disease, urgent (versus elective) surgery, general (versus regional) anesthesia, and an intraoperative arrhythmia or other alterations in the heart rate during surgery are significant predictors of perioperative stroke. Conclusions: Perioperative stroke is a rare but potentially devastating complication of total joint arthroplasty, with a high rate of morbidity and mortality, Vigilant attention to prevent, detect, and treat this complication in a timely manner may alter the course of the disease. Level of Evidence: Prognostic Level II. See Instructions to Authors for a complete description of levels of evidence. [ABSTRACT FROM AUTHOR]

Background: Oral anticoagulants have been associated with greater hematoma expansion in patients with intracerebral hemorrhage (ICH). The purpose of this study was to determine whether the reported use of antiplatelet agents also results in greater hematoma expansion.Methods: Retrospective review of patients with spontaneous supratentorial ICH diagnosed within 6 h of onset, who underwent follow-up head CT approximately 48 h later. Digital imaging analysis of initial and second CT scans was performed for comparison of hematoma volume changes between patients reporting and those not reporting antecedent antiplatelet use. Statistical analyses to determine predictors of ICH volume change and in-hospital mortality were also performed via multivariate regression models.Results: Of the 70 patients included, 17 were documented as taking antiplatelet agents. Groups were comparable regarding baseline demographic, clinical and laboratory characteristics, and the timing of CT scans was similar. Patients reporting antiplatelet use experienced greater absolute increase (7.7 ml vs. 5.5 ml) and proportional increase (110% vs. 21%) in ICH volume than those not reporting antiplatelet use, but these differences were not statistically significant (P = 0.94 and 0.61 respectively; Wilcoxon test). Baseline hematoma volume tended to correlate with percentage volume increase (P < 0.1), whereas IVH was inversely associated with percent volume increase (P < 0.05). Age (P < 0.05), absolute volume increase (P < 0.005), and final volume (P < 0.001) were associated with in-hospital mortality, the rates of which were similar between the two study groups (18% vs. 17%).Conclusions: Patients reporting antiplatelet use experienced similar degrees of hematoma expansion compared to patients not reporting antiplatelet use. [ABSTRACT FROM AUTHOR]