Acetazolamide Mitigates Intracranial Pressure Spikes Without Affecting Functional Outcome After Experimental Hemorrhagic Stroke

This article provides a literature review of the past 60 years, conducted using keywords through the PubMed Internet resource, dedicated to the methods of surgical treatment of hemorrhagic stroke. The existing published results of clinical studies do not allow us to draw unambiguous conclusions about the superiority of conservative or neurosurgical treatment in relation to the functional recovery of patients. There is a statistical significance of the advantages of surgery based on the prevention of dislocation syndrome, control of intracranial hypertension, and prevention or at least reduction of the effect of blood and its degradation products on the surrounding healthy tissue. However, large randomized controlled trials have failed to demonstrate this benefit in terms of mortality or functional outcome.There are two main areas of hemorrhagic stroke surgery – open surgery and minimally invasive methods. The practice of open surgery is associated with high trauma rates, as well as with certain risks and complications. However, craniotomy is a lifesaving measure in critical situations with signs of persistent increased intracranial pressure leading to neurological impairment. The ability to control intracranial pressure provides a chance for the choice of more optimal tactics of surgical treatment.Today, the gold standard for intracranial pressure monitoring is the installation of invasive intraventricular or intraparenchymal transducers. The method is appreciated for its accuracy, however, there are a number of disadvantages in the form of the possibility of hemorrhagic and infectious complications, as well as the high cost of the sensor itself, which limits its routine use. The inability to measure intracranial pressure before surgery causes an unreasonable expansion of indications for choosing an open method of surgery, which reduces the possibility of a better functional outcome.All of these points make it urgent to search for a non-invasive method for measuring intracranial pressure, which would contribute to the timely choice of a surgical method without the danger of worsening the clinical outcome.

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Neuroprotection after Hemorrhagic Stroke Depends on Cerebral Heme Oxygenase-1

Antioxidants ◽

10.3390/antiox8100496 ◽

2019 ◽

Vol 8 (10) ◽

pp. 496 ◽

Cited By ~ 3

Author(s):

Sandra Kaiser ◽

Sibylle Frase ◽

Lisa Selzner ◽

Judith-Lisa Lieberum ◽

Jakob Wollborn ◽

...

Keyword(s):

Cell Death ◽

Cerebrospinal Fluid ◽

Functional Outcome ◽

Signaling Pathway ◽

Heme Oxygenase ◽

Hemorrhagic Stroke ◽

Mrna Level ◽

Neuronal Cell Death ◽

Neuronal Cell ◽

Heme Oxygenase 1

(1) Background: A detailed understanding of the pathophysiology of hemorrhagic stroke is still missing. We hypothesized that expression of heme oxygenase-1 (HO-1) in microglia functions as a protective signaling pathway. (2) Methods: Hippocampal HT22 neuronal cells were exposed to heme-containing blood components and cell death was determined. We evaluated HO-1-induction and cytokine release by wildtype compared to tissue-specific HO-1-deficient (LyzM-Cre.Hmox1 fl/fl) primary microglia (PMG). In a study involving 46 patients with subarachnoid hemorrhage (SAH), relative HO-1 mRNA level in the cerebrospinal fluid were correlated with hematoma size and functional outcome. (3) Results: Neuronal cell death was induced by exposure to whole blood and hemoglobin. HO-1 was induced in microglia following blood exposure. Neuronal cells were protected from cell death by microglia cell medium conditioned with blood. This was associated with a HO-1-dependent increase in monocyte chemotactic protein-1 (MCP-1) production. HO-1 mRNA level in the cerebrospinal fluid of SAH-patients correlated positively with hematoma size. High HO-1 mRNA level in relation to hematoma size were associated with improved functional outcome at hospital discharge. (4) Conclusions: Microglial HO-1 induction with endogenous CO production functions as a crucial signaling pathway in blood-induced inflammation, determining microglial MCP-1 production and the extent of neuronal cell death. These results give further insight into the pathophysiology of neuronal damage after SAH and the function of HO-1 in humans.

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POSTOPERATIVE HYDROCEPHALUS IN PATIENTS UNDERGOING DECOMPRESSIVE HEMICRANIECTOMY FOR ISCHEMIC OR HEMORRHAGIC STROKE

Neurosurgery ◽

10.1227/01.neu.0000290894.85072.37 ◽

2007 ◽

Vol 61 (3) ◽

pp. 489-494 ◽

Cited By ~ 123

Author(s):

Allen Waziri ◽

David Fusco ◽

Stephan A. Mayer ◽

Guy M. McKhann ◽

E. Sander Connolly

Keyword(s):

Intracranial Pressure ◽

Hemorrhagic Stroke ◽

Communicating Hydrocephalus ◽

Imaging Data ◽

Decompressive Hemicraniectomy ◽

Pressure Dynamics ◽

Csf Diversion ◽

Postoperative Hydrocephalus ◽

Early Cranioplasty ◽

Persistent Hydrocephalus

Abstract OBJECTIVE We have frequently observed the development of postoperative communicating hydrocephalus in patients undergoing decompressive hemicraniectomy. This condition may persist in some patients after cranioplasty and require permanent cerebrospinal fluid (CSF) diversion. To confirm an independent correlation between hemicraniectomy and the development of communicating hydrocephalus, and to detail the frequency and potential clinical factors contributing to this complication, we evaluated our series of patients undergoing hemicraniectomy for life-threatening increases in intracranial pressure secondary to ischemic or hemorrhagic stroke. METHODS A retrospective analysis was performed with a cohort of consecutive patients who underwent emergent hemicraniectomy for medically refractory elevations in intracranial pressure. Patients with known independent risk factors for the development of communicating hydrocephalus were excluded. Clinical and imaging data were reviewed to determine the incidence and type of hydrocephalus after hemicraniectomy, the persistence of hydrocephalus after cranioplasty, and the need for permanent CSF diversion. RESULTS Eighty-eight percent of the eligible patients undergoing hemicraniectomy in our cohort developed postoperative communicating hydrocephalus. Half of these patients harbored persistent hydrocephalus after cranioplasty and required placement of a ventriculoperitoneal shunt. We noted a strong correlation between prolonged time to replacement of the bone flap and persistence of hydrocephalus. CONCLUSION Communicating hydrocephalus is an almost universal finding in patients after hemicraniectomy. Delayed time to cranioplasty is linked with the development of persistent hydrocephalus, necessitating permanent CSF diversion in some patients. We propose that early cranioplasty, when possible, may restore normal intracranial pressure dynamics and prevent the need for permanent CSF diversion in patients after hemicraniectomy.

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Role of extracellular glutamate measured by cerebral microdialysis in severe traumatic brain injury

Journal of Neurosurgery ◽

10.3171/2009.12.jns09689 ◽

2010 ◽

Vol 113 (3) ◽

pp. 564-570 ◽

Cited By ~ 99

Author(s):

Roukoz Chamoun ◽

Dima Suki ◽

Shankar P. Gopinath ◽

J. Clay Goodman ◽

Claudia Robertson

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Intracranial Pressure ◽

Mortality Rate ◽

Functional Outcome ◽

Excitatory Amino Acid ◽

Demographic Data ◽

Cerebral Microdialysis ◽

Factors Affecting

Object Authors of several studies have implied a key role of glutamate, an excitatory amino acid, in the pathophysiology of traumatic brain injury (TBI). However, the place of glutamate measurement in clinical practice and its impact on the management of TBI has yet to be elucidated. The authors' objective in the present study was to evaluate glutamate levels in TBI, analyzing the factors affecting them and determining their prognostic value. Methods A prospective study of patients with severe TBI was conducted with an inclusion criterion of a Glasgow Coma Scale score ≤ 8 within 48 hours of injury. Invasive monitoring included intracranial pressure measurements, brain tissue PO2, jugular venous O2 saturation, and cerebral microdialysis. Patients received standard care including mass evacuation when indicated and treatment of elevated intracranial pressure values. Demographic data, CT findings, and outcome at 6 months of follow-up were recorded. Results One hundred sixty-five patients were included in the study. Initially high glutamate values were predictive of a poor outcome. The mortality rate was 30.3% among patients with glutamate levels > 20 μmol/L, compared with 18% among those with levels ≤ 20 μmol/L. Two general patterns were recognized: Pattern 1, glutamate levels tended to normalize over the monitoring period (120 hours); and Pattern 2, glutamate levels tended to increase with time or remain abnormally elevated. Patients showing Pattern 1 had a lower mortality rate (17.1 vs 39.6%) and a better 6-month functional outcome among survivors (41.2 vs 20.7%). Conclusions Glutamate levels measured by microdialysis appear to have an important role in TBI. Data in this study suggest that glutamate levels are correlated with the mortality rate and 6-month functional outcome.

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Severe Disability After Stroke: Outcome After Inpatient Rehabilitation

Neurorehabilitation and Neural Repair ◽

10.1177/154596839901300310 ◽

1999 ◽

Vol 13 (3) ◽

pp. 199-203 ◽

Cited By ~ 9

Author(s):

John G. Schmidt ◽

Jessie Drew-Cates ◽

Mary L. Dombovy

Keyword(s):

Functional Outcome ◽

Hemorrhagic Stroke ◽

Inpatient Rehabilitation ◽

Functional Independence ◽

Efficiency Score ◽

Poor Functional Outcome ◽

Rehabilitation Unit ◽

Home Setting ◽

Severe Stroke ◽

Acute Rehabilitation

Objective: To determine the functional outcome following acute rehabilitation of patients with severe and very severe stroke using the Functional Independence Mea sure (FIM). Background: Most patients with severe and very severe stroke are reported in the literature to have a poor functional outcome. However, there are few studies that specifically address severity and their conclusions are confounding. Methods: We retrospectively reviewed charts of 41 consecutive patients with the primary diag nosis of ischemic or hemorrhagic stroke admitted to an inpatient rehabilitation unit with a admission FIM score of <60. Outcome measures included discharge residence, length of stay, and FIM score. Results: Over 63 percent (26 patients) were discharged to home. Discharge mean FIM scores (61.24) were significantly improved over the admission mean FIM (34.12) for self-care, mobility, communication, and social cog nition. The FIM Efficiency score was 0.356/day (mean[FIMdis-FIMadm]/mean LOS) as compared with previous reports of FIM Efficiency of 0.97/day for all stroke. Con clusion: Patients with severe stroke can experience improvement during inpatient rehabilitation and be discharged to a home setting, although the rate of improvement is less than that of more moderate stroke.

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Glycated Hemoglobin as a Marker for Predicting Outcomes of Patients With Stroke (Ischemic and Hemorrhagic): A Systematic Review and Meta-Analysis

Frontiers in Neurology ◽

10.3389/fneur.2021.642899 ◽

2021 ◽

Vol 12 ◽

Author(s):

Yaya Bao ◽

Dadong Gu

Keyword(s):

Functional Outcome ◽

Hemorrhagic Stroke ◽

Glycated Hemoglobin ◽

Meta Analysis ◽

Poor Functional Outcome ◽

Risk Of Mortality ◽

Increased Risk ◽

Unit Increase ◽

Symptomatic Intracranial Hemorrhage ◽

The Relationship

Background: Glycated hemoglobin (HbA1c) has emerged as a useful biochemical marker reflecting the average glycemic control over the last 3 months, and the values are not affected by short-term transient changes in blood glucose levels. However, its prognostic value in the acute neurological conditions such as stroke is still not well-established. The present meta-analysis was conducted to assess the relationship of HbA1c with outcomes such as mortality, early neurological complications, and functional dependence in stroke patients.Methods: A systematic search was conducted for the PubMed, Scopus, and Google Scholar databases. Studies, either retrospective or prospective in design that examined the relationship between HbA1c with outcomes of interest and presented the strength of association in the form of adjusted odds ratio/hazard ratios were included in the review. Statistical analysis was done using STATA version 13.0.Results: A total of 22 studies (15 studies on acute ischemic stroke and seven studies on hemorrhagic stroke) were included in the meta-analysis. For patients with acute ischemic stroke, each unit increase in HbA1c was found to be associated with an increased risk of mortality within 1 year, increased risk of poor functional outcome at 3 months, and an increased risk of symptomatic intracranial hemorrhage (sICH) within 24 h of admission. In those with HbA1c ≥ 6.5%, there was an increased risk of mortality within 1 year of admission, increased risk of poor functional outcomes at 3 and 12 months as well as an increased risk of symptomatic intracranial hemorrhage (sICH) within 24 h of admission. In patients with hemorrhagic stroke, each unit increase in HbA1c was found to be associated with increased risk of poor functional outcome within the first 3 months from the time of admission for stroke. In those with HbA1c ≥ 6.5%, there was an increased risk of poor functional outcome at 12 months.Conclusions: The findings indicate that glycated hemoglobin (HbA1c) could serve as a useful marker to predict the outcomes in patients with stroke and aid in the implementation of adequate preventive management strategies at the earliest.

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