Katharina M. Busl

Aspirin and recurrent intracerebral hemorrhage in cerebral amyloid angiopathy.

Objective: To identify and compare clinical and neuroimaging predictors of primary lobar intracerebral hemorrhage (ICH) recurrence, assessing their relative contributions to recurrent ICH. Methods: Subjects were consecutive survivors of primary ICH drawn from a single-center prospective cohort study. Baseline clinical, imaging, and laboratory data were collected. Survivors were followed prospectively for recurrent ICH and intercurrent aspirin and warfarin use, including duration of exposure. Cox proportional hazards models were used to identify predictors of recurrence stratified by ICH location, with aspirin and warfarin exposures as time-dependent variables adjusting for potential confounders. Results: A total of 104 primary lobar ICH survivors were enrolled. Recurrence of lobar ICH was associated with previous ICH before index event (hazard ratio [HR] 7.7, 95% confidence interval [CI] 1.4–15.7), number of lobar microbleeds (HR 2.93 with 2–4 microbleeds present, 95% CI 1.3–4.0; HR = 4.12 when ≥5 microbleeds present, 95% CI 1.6–9.3), and presence of CT-defined white matter hypodensity in the posterior region (HR 4.11, 95% CI 1.01–12.2). Although aspirin after ICH was not associated with lobar ICH recurrence in univariate analyses, in multivariate analyses adjusting for baseline clinical predictors, it independently increased the risk of ICH recurrence (HR 3.95, 95% CI 1.6–8.3, p = 0.021). Conclusions: Recurrence of lobar ICH is associated with previous microbleeds or macrobleeds and posterior CT white matter hypodensity, which may be markers of severity for underlying cerebral amyloid angiopathy. Use of an antiplatelet agent following lobar ICH may also increase recurrence risk.

Hypoxic-ischemic brain injury: pathophysiology, neuropathology and mechanisms.

Hypoxic-ischemic brain injury is a well known consequence of cardiac arrest. Variable injuries can occur with purely hypoxic or histotoxic insults such as asphyxiation and carbon monoxide poisoning. The injury may happen at the time of the insult, but there may also be continued damage after circulation and oxygenation are reestablished. The nature and extent of the damage appears to depend on the severity, time course and duration of the oxygen deprivation and lack of blood supply, as well as on the underlying mechanism. This review describes the pathophysiological and molecular basis of hypoxic ischemic brain injury, and differentiates between the mechanisms of injury by cardiac arrest, pure respiratory arrest, and arrest secondary to cytotoxicity (e.g. carbon monoxide poisoning).

Pitfalls in the diagnosis of brain death.

Since the establishment of the concept of declaring death by brain criteria, a large extent of variability in the determination of brain death has been reported. There are no standardized practical guidelines, and major differences exist in the requirements for the declaration of brain death throughout the USA and internationally. The American Academy of Neurology published evidence-based practice parameters for the determination of brain death in adults in 1995, requiring the irreversible absence of clinical brain function with the cardinal features of coma, absent brainstem reflexes, and apnea, as well as the exclusion of reversible confounders. Ancillary tests are recommended in cases of uncertainty of the clinical diagnosis. Every step in the determination of brain death bears potential pitfalls which can lead to errors in the diagnosis of brain death. These pitfalls are presented here, and possible solutions identified. Suggestions are made for improvement in the standardization of the declaration of brain death.

Neurogenic Pulmonary Edema.

Objective:Neurogenic pulmonary edema is an underrecognized and underdiagnosed form of pulmonary compromise that complicates acute neurologic illness and is not explained by cardiovascular or pulmonary pathology. This review aims to provide a concise overview on pathophysiology, epidemiology, clinical characteristics, impact on outcome and treatment of neurogenic pulmonary edema, and considerations for organ donation. Data Sources:Database searches and a review of the relevant medical literature. Study Selection:Selected studies included English-language articles concerning neurogenic pulmonary edema using the search terms “neurogenic” with “pulmonary oedema” or “pulmonary edema,” “experimental neurogenic pulmonary edema,” “donor brain death,” and “donor lung injury.” Data Extraction:Selected studies were reviewed by both authors, and data extracted based on author consensus regarding relevance for this review. Data Synthesis:Existing evidence is organized to address: 1) pathophysiology, 2) epidemiology and association with different neurologic diseases, 3) clinical presentation, 4) impact on outcome, 5) treatment, and 6) implications for organ donation after brain death. Conclusions:Neurogenic pulmonary edema occurs as a complication of acute neurologic illness and may mimic acute lung injury of other etiology. Its presence is important to recognize in patients due to its impact on clinical course, prognosis, and treatment strategies.

Predictors of mortality in nontraumatic subdural hematoma

OBJECT Subdural hematoma (SDH) is a common diagnosis in neurosurgical and neurocritical practice. Comprehensive outcome data are lacking for nontraumatic SDH. The authors determined which factors are associated with in-hospital mortality in a large sample of patients with nontraumatic SDH. METHODS Using the Nationwide Inpatient Sample, the authors selected adults who had been hospitalized in the US between 2007 and 2009 and in whom a primary diagnosis of nontraumatic SDH (ICD-9-CM code 432.1) had been made. Demographics, comorbidities, surgical treatment, and discharge outcomes were identified. Univariate and multivariate analyses were performed to identify predictors of in-hospital mortality. RESULTS Among 14,093 patients with acute nontraumatic SDH, the mean age was 71.4 ± 14.8 (mean ± standard deviation). In addition, 22.2% of the patients were admitted during the weekend. Surgical evacuation was performed in 51.4% of the patients, and 11.8% of all patients died during hospitalization. In multivariate analyses, patient age (adjusted OR 1.02, 95% CI 1.012-1.022), congestive heart failure (adjusted OR 1.42, 95% CI 1.19-1.71), warfarin use (adjusted OR 1.41, 95% CI 1.17-1.70), coagulopathy (adjusted OR 2.14, 95% CI 1.75-2.61), mechanical ventilation (adjusted OR 16.85, 95% CI 14.29-19.86), and weekend admission (adjusted OR 1.19, 95% CI 1.02-1.38) were independent predictors of in-hospital mortality. Race (Hispanic: adjusted OR 0.65, 95% CI 0.51-0.83; black: adjusted OR 0.78, 95% CI 0.63-0.96), urban hospital location (adjusted OR 0.69, 95% CI 0.54-0.89), and surgical SDH evacuation (adjusted OR 0.52, 95% CI 0.45-0.60) were strong independent predictors for decreased mortality. CONCLUSIONS One in 9 patients with nontraumatic SDH dies during hospitalization. Among the several predictors of in-hospital mortality, the weekend effect and treatment with surgical evacuation are potentially modifiable factors. Further investigation may lead to improvements in management and outcomes.

Bacterial Infections of the Central Nervous System

Bacterial CNS infections comprise a wide spectrum of diseases, which may be acquired outside or inside the hospital, affect immunocompetent or immunocompromised patients, and be associated with trauma or procedures, as well as other exposures.

Treatment of Neuroterrorism

Bioterrorism is defined as the intentional use of biological, chemical, nuclear, or radiological agents to cause disease, death, or environmental damage. Early recognition of a bioterrorist attack is of utmost importance to minimize casualties and initiate appropriate therapy. The range of agents that could potentially be used as weapons is wide, however, only a few of these agents have all the characteristics making them ideal for that purpose. Many of the chemical and biological weapons can cause neurological symptoms and damage the nervous system in varying degrees. Therefore, preparedness among neurologists is important. The main challenge is to be cognizant of the clinical syndromes and to be able to differentiate diseases caused by bioterrorism from naturally occurring disorders. This review provides an overview of the biological and chemical warfare agents, with a focus on neurological manifestation and an approach to treatment from a perspective of neurological critical care.

Three-Month Outcomes Are Poor in Stroke Patients with Cancer Despite Acute Stroke Treatment

INTRODUCTION Stroke risk is increased in cancer patients. Prognosis in these patients is poor, with higher in-hospital mortality and increased subsequent mortality. However, data on stroke in cancer patients are limited, specifically regarding acute stroke treatment and functional outcomes. We aim to determine the functional outcomes of cancer patients admitted with acute stroke. MATERIALS AND METHODS We retrospectively reviewed patients carrying a diagnosis of cancer who were admitted with acute ischemic stroke between March 2013 and February 2016. Demographics, cerebrovascular risk factors, stroke characteristics including acute treatment, and characteristics of their cancer history and treatment were abstracted. The primary outcome measures included in-hospital mortality and 3-month functional outcome (as assessed by the modified Rankin Scale [mRS] score, with mRS scores of 3-6 considered poor functional outcome). Further outcome measures included length of stay and discharge destination. FINDINGS Forty-nine patients met the inclusion criteria, with a median admission National Institutes of Health Stroke Scale score of 8. Twelve patients (24.4%) underwent acute stroke treatment. The most common stroke etiology was hypercoagulability of malignancy (21, 42.9%). The three-month mortality was 46.9%; half of survivors had poor functional outcome. Functional outcomes did not differ by cancer type, stage, or year since diagnosis; on multivariate analysis only high admission NIHSS score was associated with poor functional outcome (P = .002). CONCLUSION Nearly half of patients with cancer and stroke die within 3 months, and functional outcome is poor for 50% of 3-month survivors despite consideration of acute stroke treatment. Future research should address the role of hypercoagulability in the outcome prediction of stroke patients with cancer.

Neuroimaging in subclavian steal syndrome

We present two cases of subclavian steel syndrome to give an impression of the wide spectrum of possible symptoms and of the commonly used imaging modalities in subclavian steal syndrome. Case one is a 49-year-old female with periodic numbness in her left arm, followed by dizziness and nausea, occurring only while hanging laundry. MRI with angiography (fig 1A) and conventional angiography revealed a moderate proximal left subclavian artery stenosis (fig 2A–C), while Duplex ultrasound demonstrated the functional haemodynamic consequences (fig 1B–D) and the stenosis was eventually treated with a stenting procedure (fig 2D). Figure 1 (A) Contrast-enhanced MRI/angiography of the supra-aortal arteries showing moderate left subclavian artery stenosis and unremarkable finding on time-of-flight MR-angiography of the intracranial vessels. (B) Doppler and duplex Doppler sonography showing …

Seizures and Epileptiform Discharges in Patients with Acute Subdural Hematoma.

Purpose: Subdural hematomas (SDH) are associated with seizures and epileptiform discharges, but little is known about the prevalence and impact of seizures, status epilepticus (SE), and epileptiform discharges on outcomes in patients with isolated acute SDH (aSDH). Methods: Continuous EEG reports from 76 adult patients admitted to Rush University Medical Center with aSDH between January 2009 and March 2012 were reviewed. Clinical and radiographic findings, comorbidities, treatment, and outcome parameters, such as mortality, discharge destination, need for tracheostomy/percutaneous endoscopic gastrostomy placement, and length of stay (LOS), were assessed. Univariate and multivariate analyses were performed to assess the impact of clinical seizures, SE, and epileptiform EEG on outcomes. Results: Of 76 patients with aSDH who underwent EEG monitoring, 74 (97.4%) received antiseizure prophylaxis. Thirty-two (41.1%) patients had seizures, most of which were clinical seizures. Twenty-four (32%) patients had epileptiform EEG findings. Clinical or nonconvulsive SE was diagnosed in 12 (16%) patients. Clinical seizures were not associated with outcome parameters. Epileptiform EEG findings were independently associated with longer hospital LOS (13 vs. 8 days, P = 0.04) and intensive care unit LOS (10 vs. 4 days, P = 0.002). The SE also predicted longer intensive care unit LOS (10 vs. 4 days, P = 0.002). Neither epileptiform EEG nor SE was significantly related to mortality, discharge destination, or need for tracheostomy/percutaneous endoscopic gastrostomy placement. Conclusions: Seizures and epileptiform EEG findings are very common in patients with aSDH despite antiseizure prophylaxis. While clinical seizures did not affect outcomes, the presence of epileptiform EEG findings and SE was independently associated with longer intensive care unit LOS and hospital LOS.