Experts' recommendations for stroke management in intensive care: Intracranial hypertension

Authors: Vahedi K, Proust F, Geeraerts T. 

(Article in French)

This article aims to describe the arguments underlying the experts' recommendations for management of stroke patients in the intensive unit, focusing on intracranial hypertension. This article describes the pathophysiology, diagnostic methods and therapeutic options for intracranial hypertension after stroke, including medical and surgical management.

A literature review of the feasibility of glial fibrillary acidic protein as a biomarker for stroke and traumatic brain injury

Authors: Schiff L, Hadker N, Weiser S, Rausch C.

Traumatic brain injuries (TBIs) are potentially lethal medical conditions, with symptoms that can overlap with symptoms of injuries outside the brain. In many cases, current diagnostic methods do not fully distinguish acute brain injury from other organ damage. In the management of stroke patients, the choice of treatment depends on whether the stroke is ischemic or hemorrhagic; however, no quick lab diagnostic tests are available to distinguish between the two types of strokes. As a result, patient triage, disposition, and patient management decisions may be delayed for patients with suspected TBI and stroke. Glial fibrillary acidic protein (GFAP), a brain-specific biomarker that is released into the blood following TBI and stroke, is being explored for potential diagnostic and prognostic value in these indications. We therefore conducted a review of MEDLINE-indexed publications from 2004 to 2011 to evaluate the current status of GFAP as a prognostic and diagnostic tool for TBI and stroke within the context of current published guidelines. Our review suggests that GFAP could provide clinically valuable information for the prognosis of TBI and stroke, but it is still at an early stage of development as a biomarker. Several TBI studies have shown elevated GFAP levels following a TBI event to be associated with greater severity of injury, poorer outcomes, and increased mortality. Clinical studies also indicate that GFAP has potential clinical utility in the differential diagnosis of various types of stroke. However, more clinical research will be required to determine the ability of GFAP levels to diagnose TBI in heterogeneous patient populations, as well as the ability of GFAP to differentiate between ischemic stroke (IS), intracerebral hemorrhage (ICH), subarachnoid hemorrhage (SAH), and non-stroke conditions in populations of patients with suspected rather than confirmed stroke. Additional clinical studies will also be required to define the temporal patterns of GFAP release in IS, ICH, SAH, and TBI, and their potential use in the differential diagnosis of these conditions. Finally, such research could demonstrate the ability of GFAP test results to provide unique clinical information that informs management decisions for TBI and stroke patients.

Therapeutic Hypothermia in Stroke and Traumatic Brain Injury

Authors: Faridar A, Bershad EM, Emiru T, Iaizzo PA, Suarez JI, Divani AA.

Therapeutic hypothermia (TH) is considered to improve survival with favorable neurological outcome in the case of global cerebral ischemia after cardiac arrest and perinatal asphyxia. The efficacy of hypothermia in acute ischemic stroke (AIS) and traumatic brain injury (TBI), however, is not well studied. Induction of TH typically requires a multimodal approach, including the use of both pharmacological agents and physical techniques. To date, clinical outcomes for patients with either AIS or TBI who received TH have yielded conflicting results; thus, no adequate therapeutic consensus has been reached. Nevertheless, it seems that by determining optimal TH parameters and also appropriate applications, cooling therapy still has the potential to become a valuable neuroprotective intervention. Among the various methods for hypothermia induction, intravascular cooling (IVC) may have the most promise in the awake patient in terms of clinical outcomes. Currently, the IVC method has the capability of more rapid target temperature attainment and more precise control of temperature. However, this technique requires expertise in endovascular surgery that can preclude its application in the field and/or in most emergency settings. It is very likely that combining neuroprotective strategies will yield better outcomes than utilizing a single approach.

Patients With Traumatic Brain Injury Population-Based Study Suggests Increased Risk of Stroke

Authors: Yi-Hua Chen, PhD; Jiunn-Horng Kang, MD; Herng-Ching Lin, PhD

Background and Purpose—Previous studies have identified an array of morbidities following traumatic brain injury (TBI), including certain neurological disorders. However, no direct evidence has been reported on the link between TBI and stroke. This population-based study was designed to estimate the risk of stroke during a period of 5 years following a TBI, compared with individuals who did not suffer TBI during the same period.

Methods—Data were obtained from the Longitudinal Health Insurance Database 2000 (LHID 2000). A total of 23 199 patients receiving ambulatory or hospitalization care with a diagnosis of TBI were included, together with 69 597 non-TBI patients as our comparison group, matched by sex, age, and year of index use of health care. Each individual was followed for 5 years to identify subsequent occurrence of stroke. Cox proportional hazard regressions were performed for analysis.

Results—During the 3-month follow-up period, 675 strokes (2.91%) occurred in TBI patients and in 207 patients (0.30%) in the non-TBI comparison cohort. A diagnosis of TBI was independently associated with a 10.21 (95% CI, 8.71–11.96), 4.61 (95% CI, 4.16–5.11), and 2.32 (95% CI, 2.17–2.47) times greater risk of stroke during 3-month, 1-year, and 5-year follow-up, respectively, after adjusting for sociodemographic characteristics and selected comorbidities. The risk of intracerebral hemorrhage was more noticeable among patients with TBI compared with those without a TBI.

Conclusions—This is the first report showing an increased risk of stroke among individuals who have sustained a TBI. We suggest a need for more intensive medical monitoring and health education following TBI, especially during the first few months and years.

Etiologic features of newly diagnosed epilepsy: Hospital-based study of 892 consecutive patients in West China

Authors: Si Y, Liu L, Hu J, Mu J, Fang JJ, An DM, Zhao LL, Tian LY, Zhou D.

PURPOSE: We evaluated data from a large cohort of newly diagnosed epilepsy patients from the biggest epilepsy center in West China. The aim was to determine the most prevalent etiologic factors in this region.

METHODS: From May 2008 to May 2010, the clinical data of patients with newly diagnosed epilepsy were consecutively, systematically and prospectively recorded in a database. The data were analyzed according to sex, age, seizure type, etiology, and other factors.

RESULTS: The present study examined 892 patients with newly diagnosed epilepsy. Among these patients, 346 (38.8%) were confirmed as symptomatic, with the largest constituent ratio among the elderly (63.2%). In this symptomatic group, central nervous system (CNS) infections and traumatic brain injuries (TBI) were the two most common etiologies. When analyzed according to age bracket, cortical dysplasia, mesial temporal sclerosis, and CNS infection were the most frequent causes among young patients (<18 years). On the other hand, CNS infection and TBI were the two most common causes in patients between 18 and 60 years. Stroke was the most common cause of newly diagnosed symptomatic epilepsy in the elderly (>60 years).

CONCLUSIONS: More than 30% of newly diagnosed epilepsy cases were shown to be symptomatic by medical history as well as careful clinical and laboratory examination. Detailed epilepsy assessments are essential to formulate a therapeutic plan and to improve prognosis. The etiology spectrum found in this large cohort forms a comparative baseline for future studies.

16(R)-hydroxyeicosatetraenoic acid, a novel cytochrome P450 product of arachidonic acid, suppresses activation of human polymorphonuclear leukocyte and reduces intracranial pressure in a rabbit model of thromboembolic stroke

Authors: Bednar MM, Gross CE, Russell SR, Fuller SP, Ahern TP, Howard DB, Falck JR, Reddy KM, Balazy M.

OBJECTIVE: Activated polymorphonuclear leukocytes (PMNs) have been suggested to contribute to the development of increased intracranial pressure (ICP). We recently demonstrated that human PMNs produce a novel cytochrome P450-derived arachidonic acid metabolite, 1 6(R)-hydroxyeicosatetraenoic acid , that modulates their function. It was thus of interest to examine this novel mediator in an acute stroke model.

METHODS: 16-HETE was assessed initially in a variety of human PMN and platelet in vitro assays and subsequently in an established rabbit model of thromboembolic stroke. A total of 50 rabbits completed a randomized, blinded, four-arm study, receiving 16(R)-HETE, tissue plasminogen activator, both, or neither. Experiments were completed 7 hours after autologous clot embolization. The primary end point for efficacy was the suppression of increased ICP.

RESULTS: In in vitro assays, 16(R)-HETE selectively inhibited human PMN adhesion and aggregation and leukotriene B4 synthesis. In the thromboembolic stroke model, animals that received 16(R)-HETE demonstrated significant suppression of increased ICP (7.7 +/- 1.2 to 13.1 +/- 2.7 mm Hg, baseline versus final 7-h time point, mean +/- standard error), compared with either the vehicle-treated group (7.7 +/- 0.9 to 15.8 +/- 2.6 mm Hg) or the tissue plasminogen activator-treated group (7.6 +/- 0.6 to 13.7 +/- 2.1 mm Hg). The group that received the combination of 16(R)-HETE plus tissue plasminogen activator demonstrated no significant change in ICP for the duration of the protocol (8.6 +/- 0.6 to 11.1 +/- 1.2 mm Hg).

CONCLUSION: 16(R)-HETE suppresses the development of increased ICP in a rabbit model of thromboembolic stroke and may serve as a novel therapeutic strategy in ischemic and inflammatory pathophysiological states.


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