Search

Encephalitis is a condition of inflammation of the brain parenchyma, occurs as a result of infectious or autoimmune causes, and can lead to encephalopathy, seizures, focal neurological deficits, neurological disability, and death. Viral causes account for the largest proportion, but in the last decade there has been growing recognition of anti-neuronal antibody syndromes. This Seminar focuses on the diagnosis and management of acute encephalitis in adults. Although viral and autoimmune causes are highlighted because of their prominent roles in encephalitis, other infectious pathogens are also considered. The role of cerebrospinal fluid studies, MRI, and novel diagnostic modalities (eg, next-generation sequencing) are discussed. Management approaches, including treatment of acute neurological complications and the use of immune suppressive and modulatory drugs for cases of suspected or confirmed autoimmune cause, are covered. Additionally, we discuss the remaining challenges in the diagnosis, management, and prognosis of encephalitis., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

This chapter aims to provide an up-to-date review of the science and clinical practice pertaining to neurologic injury after successful cardiopulmonary resuscitation. The past two decades have seen a major shift in the science and practice of cardiopulmonary resuscitation, with a major emphasis on postresuscitation neurologic care. This chapter provides a nuanced and thoughtful historic and bench-to-bedside overview of the neurologic aspects of cardiopulmonary resuscitation. A particular emphasis is made on the anatomy and pathophysiology of hypoxic-ischemic encephalopathy, up-to-date management of survivors of cardiopulmonary resuscitation, and a careful discussion on neurologic outcome prediction. Guidance to practice evidence-based clinical care when able and thoughtful, pragmatic suggestions for care where evidence is lacking are also provided. This chapter serves as both a useful clinical guide and an updated, thorough, and state-of-the-art reference on the topic for advanced students and experienced practitioners in the field., (© 2017 Elsevier B.V. All rights reserved.)

Purpose: Cerebral vasospasm following a transsphenoidal resection of a pituitary adenoma is a devastating occurrence that can lead to delayed cerebral ischemia and poor neurologic outcome if not diagnosed and treated in a timely manner. The etiology of this condition is not well understood but can lead to significant arterial vasospasm that causes severe ischemic insults. In this paper, we identify common presenting symptoms and essential management strategies to treat this harmful disease., Methods: A retrospective case report and literature review of presentation, treatment, and outcome of cerebral vasospasm following transsphenoidal surgery., Results: We present 1 case and review 12 known cases in the literature on vasospasm following transsphenoidal surgery. Mean age was 48 (±13.8) years. There were 46.2% male patients. Factors associated with vasospasm, such as cerebral spinal fluid leaks following surgery, were seen in 38.5% of cases, and postoperative subarachnoid hemorrhage (SAH) was seen in 84.6% of cases. Hemiparesis was the presenting symptom of delayed cerebral ischemia in 61.5% of cases. For management, maintaining at least a euvolemic volume status was used in 76.9%, induced hypertension was used in 61.5%, and nimodipine was administered in 46.2% of cases. Patients returned to their neurologic baseline in 61.5% of cases, had new permanent deficits in 7.7% of cases, and died in 30.8% of cases., Conclusion: Cerebral vasospasm following transsphenoidal surgery is a dangerous disease that can lead to a high likelihood of mortality if not identified and treated. Early postoperative events, such as peritumoral subarachnoid hemorrhage and hemiparesis, may be factors associated with post-transsphenoidal surgery vasospasm. Effective treatment options used in patients that regained complete neurologic recovery were by inducing hypertension, maintaining euvolemia, and administering nimodipine., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Objectives: To confirm the previously identified EEG characteristics for HSV encephalitis and to determine the diagnostic and predictive value of electroencephalography (EEG) features for etiology and outcome of acute encephalitis in adults. In addition, we sought to investigate their independence from possible clinical confounders., Methods: This study was performed in the Intensive Care Units of two academic tertiary care centers. From 1997 to 2011, all consecutive patients with acute encephalitis who received one or more EEGs were included. Examination of the diagnostic and predictive value of EEG patterns regarding etiology, clinical conditions, and survival was performed. The main outcome measure was in-hospital death., Results: Of 103 patients with encephalitis, EEGs were performed in 76 within a median of 1 day (inter quartile range 0.5-3) after admission. Mortality was 19.7%. Higher proportions of periodic discharges (PDs) (p=0.029) and focal slowing (p=0.017) were detected in Herpes Simplex virus (HSV) encephalitis as compared to non-HSV encephalitis, while clinical characteristics did not differ. Normal EEG remained the strongest association with a low relative risk for death in multivariable analyses (RR<0.001, p<0.001) adjusting for confounders as coma, global cerebral edema and mechanical ventilation. None of the patients with a normal EEG had a GCS of 15., Conclusions: Normal EEG predicted survival independently from possible confounders, highlighting the prognostic value of EEG in evaluating patients with encephalitis. EEG revealed higher proportions of PDs along with focal slowing in HSV encephalitis as compared to other etiologies., Significance: EEG significantly adds to clinical, diagnostic and prognostic information in patients with acute encephalitis., (Copyright © 2014 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.)

Objectives: To describe a case from 1908 of apparent brain death after operative intervention by Harvey Cushing at the Johns Hopkins Hospital., Methods: After institutional review board approval, which waived the requirement of informed consent from patients, and through the courtesy of the Alan Mason Chesney Archives, we reviewed the Johns Hopkins Hospital surgical files from 1896 to 1912., Results: We selected a single adult patient operated upon by Cushing, whose respirations ceased in the operating room and who was maintained by the use of artificial respiration via a tracheostomy during a 36-hour period, whereas further surgical interventions were performed in an attempt to improve his condition. The patient's condition remained unimproved; artificial respirations were discontinued and the "cessation of all cardiac activity" was observed., Conclusions: Brain death is a concept that presents unique challenges to the practicing physician. Although recent advances have allowed for better diagnosis of brain death, the topic remains fraught with controversy. The case described here documents Harvey Cushing's struggles with the ethics of maintaining vital organ function with artificial respiration, despite clear evidence of irreversible ischemic brain damage. This case predates the earliest descriptions of brain death by more than 50 years and illustrates the dilemmas facing clinicians at the turn of the twentieth century., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Aim of the Review: To review the epidemiology, pathophysiology, treatment and prognostication in relation to the post-cardiac arrest syndrome., Methods: Relevant articles were identified using PubMed, EMBASE and an American Heart Association EndNote master resuscitation reference library, supplemented by hand searches of key papers. Writing groups comprising international experts were assigned to each section. Drafts of the document were circulated to all authors for comment and amendment., Results: The 4 key components of post-cardiac arrest syndrome were identified as (1) post-cardiac arrest brain injury, (2) post-cardiac arrest myocardial dysfunction, (3) systemic ischaemia/reperfusion response, and (4) persistent precipitating pathology., Conclusions: A growing body of knowledge suggests that the individual components of the post-cardiac arrest syndrome are potentially treatable., (Copyright (c) 2009. Published by Elsevier Ltd.)

Aim of the Review: To review the epidemiology, pathophysiology, treatment and prognostication in relation to the post-cardiac arrest syndrome., Methods: Relevant articles were identified using PubMed, EMBASE and an American Heart Association EndNote master resuscitation reference library, supplemented by hand searches of key papers. Writing groups comprising international experts were assigned to each section. Drafts of the document were circulated to all authors for comment and amendment., Results: The 4 key components of post-cardiac arrest syndrome were identified as (1) post-cardiac arrest brain injury, (2) post-cardiac arrest myocardial dysfunction, (3) systemic ischaemia/reperfusion response, and (4) persistent precipitating pathology., Conclusions: A growing body of knowledge suggests that the individual components of the postcardiac arrest syndrome are potentially treatable.

Therapeutic hypothermia is a proven part of cardio-cerebral resuscitation after cardiac arrest as it improves neurologic outcomes after hypoxic brain injury. This article reviews the mechanisms of hypothermic neuroprotection, the clinical trials that support its use after cardiac arrest, as well as the impact of hypothermia on patient management and prognosis. In caring for patients suffering hypoxic brain injury after cardiac arrest, the role of the neurologist is no longer limited to prognosis but is now to become actively involved in clinical management which includes the use of therapeutic hypothermia.

Introduction: Intracerebral hemorrhage (ICH) associated with pregnancy commonly occurs in the postpartum period in the setting of preeclampsia/eclampsia. We describe the clinical course of two patients with ICH due to postpartum cerebral vasculopathy in the absence of toxemia., Methods: We reviewed two cases with ICH and postpartum vasculopathy in our hospital (1996-2001) and compared them with seven similar case reports from the literature., Results: Mean age of all patients is 28.7+/-5.6 years (mean+/-S.D.). Toxemia of pregnancy was absent in all cases. ICHs were cortical in eight and putaminal in one patient. Erythrocyte sedimentation rate was elevated in two. Two cases rehemorrhaged during the same admission. No cerebral infarctions were reported. All patients had diffuse vasculopathy on conventional catheter angiography, with no clinical manifestations or laboratory data supportive of extracerebral or systemic vasculitis. Eight patients were treated with corticosteroids, two with additional cytotoxic agents and one with nimodipine alone. Improvement on follow-up cerebral angiography (catheter or MRA) and transcranial Doppler ultrasonography (TCD) was noted in eight cases. One did not have follow-up cerebral imaging but had an excellent clinical outcome. All cases had good to excellent functional recovery., Conclusions: Postpartum ICH in the absence of toxemia may be associated with isolated cerebral vasculopathy. The clinical course and functional outcome is good to excellent. This entity appears to be distinct from cerebral vasculitis, which is usually associated with poor outcome.

Objective: To develop a novel quantitative EEG (qEEG) based analysis method, cepstral distance (CD) and compare it to spectral distance (SD) in detecting EEG changes related to global ischemia in rats., Methods: Adult Wistar rats were subjected to asphyxic-cardiac arrest for sham, 1, 3, 5 and 7 min (n=5 per group). The EEG signal was processed and fitted into an autoregressive (AR) model. A pre-injury baseline EEG was compared to selected data segments during asphyxia and recovery. The dissimilarities in the EEG segments were measured using CD and SD. A segment measured was considered abnormal when it exceeded 30% of baseline and its duration was used as the index of injury. A comprehensive Neurodeficit Score (NDS) at 24 h was used to assess outcome and was correlated with CD and SD measures., Results: A higher correlation was found with CD and asphyxia time (r=0.81, P<0.001) compared to SD and asphyxia time (r=0.69, P<0.001). Correlation with cardiac arrest time (MAP<10 mmHg) showed that CD was superior (r=0.71, P<0.001) to SD (r=0.52, P=0.002). CD obtained during global ischemia and 90 min into recovery correlated significantly with NDS at 24 h after injury (Spearman coefficient=-0.83, P<0.005), and was more robust than the traditional SD (Spearman coefficient=-0.63, P<0.005)., Conclusion: The novel qEEG-based injury index from CD was superior to SD in quantifying early cerebral dysfunction after cardiac arrest and in providing neurological prognosis at 24 h after global ischemia in adult rats. Studying early qEEG changes after asphyxic-cardiac arrest may provide new insights into the injury and recovery process, and present opportunities for therapy.