Role of Sulfonylurea Receptor 1 and Glibenclamide in Traumatic Brain Injury: A Review of the Evidence

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Abstract

Cerebral edema and contusion expansion are major determinants of morbidity and mortality after TBI. Current treatment options are reactive, suboptimal and associated with significant side effects. First discovered in models of focal cerebral ischemia, there is increasing evidence that the sulfonylurea receptor 1 (SUR1)—Transient receptor potential melastatin 4 (TRPM4) channel plays a key role in these critical secondary injury processes after TBI. Targeted SUR1-TRPM4 channel inhibition with glibenclamide has been shown to reduce edema and progression of hemorrhage, particularly in preclinical models of contusional TBI. Results from small clinical trials evaluating glibenclamide in TBI have been encouraging. A Phase-2 study evaluating the safety and efficacy of intravenous glibenclamide (BIIB093) in brain contusion is actively enrolling subjects. In this comprehensive narrative review, we summarize the molecular basis of SUR1-TRPM4 related pathology and discuss TBI-specific expression patterns, biomarker potential, genetic variation, preclinical experiments, and clinical studies evaluating the utility of treatment with glibenclamide in this disease.

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Most cited references 114

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Decompressive craniectomy in diffuse traumatic brain injury.

D James Cooper, Jeffrey Rosenfeld, Lynnette Murray … (2011)

It is unclear whether decompressive craniectomy improves the functional outcome in patients with severe traumatic brain injury and refractory raised intracranial pressure. From December 2002 through April 2010, we randomly assigned 155 adults with severe diffuse traumatic brain injury and intracranial hypertension that was refractory to first-tier therapies to undergo either bifrontotemporoparietal decompressive craniectomy or standard care. The original primary outcome was an unfavorable outcome (a composite of death, vegetative state, or severe disability), as evaluated on the Extended Glasgow Outcome Scale 6 months after the injury. The final primary outcome was the score on the Extended Glasgow Outcome Scale at 6 months. Patients in the craniectomy group, as compared with those in the standard-care group, had less time with intracranial pressures above the treatment threshold (P<0.001), fewer interventions for increased intracranial pressure (P<0.02 for all comparisons), and fewer days in the intensive care unit (ICU) (P<0.001). However, patients undergoing craniectomy had worse scores on the Extended Glasgow Outcome Scale than those receiving standard care (odds ratio for a worse score in the craniectomy group, 1.84; 95% confidence interval [CI], 1.05 to 3.24; P=0.03) and a greater risk of an unfavorable outcome (odds ratio, 2.21; 95% CI, 1.14 to 4.26; P=0.02). Rates of death at 6 months were similar in the craniectomy group (19%) and the standard-care group (18%). In adults with severe diffuse traumatic brain injury and refractory intracranial hypertension, early bifrontotemporoparietal decompressive craniectomy decreased intracranial pressure and the length of stay in the ICU but was associated with more unfavorable outcomes. (Funded by the National Health and Medical Research Council of Australia and others; DECRA Australian Clinical Trials Registry number, ACTRN012605000009617.).

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Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension.

Peter J. Hutchinson, Angelos G. Kolias, Ivan Timofeev … (2016)

Background The effect of decompressive craniectomy on clinical outcomes in patients with refractory traumatic intracranial hypertension remains unclear. Methods From 2004 through 2014, we randomly assigned 408 patients, 10 to 65 years of age, with traumatic brain injury and refractory elevated intracranial pressure (>25 mm Hg) to undergo decompressive craniectomy or receive ongoing medical care. The primary outcome was the rating on the Extended Glasgow Outcome Scale (GOS-E) (an 8-point scale, ranging from death to "upper good recovery" [no injury-related problems]) at 6 months. The primary-outcome measure was analyzed with an ordinal method based on the proportional-odds model. If the model was rejected, that would indicate a significant difference in the GOS-E distribution, and results would be reported descriptively. Results The GOS-E distribution differed between the two groups (P<0.001). The proportional-odds assumption was rejected, and therefore results are reported descriptively. At 6 months, the GOS-E distributions were as follows: death, 26.9% among 201 patients in the surgical group versus 48.9% among 188 patients in the medical group; vegetative state, 8.5% versus 2.1%; lower severe disability (dependent on others for care), 21.9% versus 14.4%; upper severe disability (independent at home), 15.4% versus 8.0%; moderate disability, 23.4% versus 19.7%; and good recovery, 4.0% versus 6.9%. At 12 months, the GOS-E distributions were as follows: death, 30.4% among 194 surgical patients versus 52.0% among 179 medical patients; vegetative state, 6.2% versus 1.7%; lower severe disability, 18.0% versus 14.0%; upper severe disability, 13.4% versus 3.9%; moderate disability, 22.2% versus 20.1%; and good recovery, 9.8% versus 8.4%. Surgical patients had fewer hours than medical patients with intracranial pressure above 25 mm Hg after randomization (median, 5.0 vs. 17.0 hours; P<0.001) but had a higher rate of adverse events (16.3% vs. 9.2%, P=0.03). Conclusions At 6 months, decompressive craniectomy in patients with traumatic brain injury and refractory intracranial hypertension resulted in lower mortality and higher rates of vegetative state, lower severe disability, and upper severe disability than medical care. The rates of moderate disability and good recovery were similar in the two groups. (Funded by the Medical Research Council and others; RESCUEicp Current Controlled Trials number, ISRCTN66202560 .).

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THE ROLE OF SECONDARY BRAIN INJURY IN DETERMINING OUTCOME FROM SEVERE HEAD INJURY

Randall Chesnut, Lawrence Marshall, Melville R Klauber … (1993)

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Journal ID (nlm-ta): Int J Mol Sci

Journal ID (iso-abbrev): Int J Mol Sci

Journal ID (publisher-id): ijms

Title: International Journal of Molecular Sciences

Publisher: MDPI

ISSN (Electronic): 1422-0067

Publication date (Electronic): 09 January 2020

Publication date Collection: January 2020

Volume: 21

Issue: 2

Electronic Location Identifier: 409

Affiliations

[1 ]Departments of Critical Care Medicine, Neurology, Neurological Surgery, Clinical and Translational Science Institute, University of Pittsburgh, Pittsburgh, PA 15201, USA

[2 ]Biogen, Cambridge, MA 02142, USA; josh.bell@ 123456biogen.com

[3 ]School of Medicine and Surgery, University of Milan-Bicocca, 20121 Milan, Italy; giuseppe.citerio@ 123456unimib.it

[4 ]Anaesthesia and Intensive Care, San Gerardo and Desio Hospitals, ASST-Monza, 20900 Monza, Italy

[5 ]Department of Neurology, University of California, San Francisco, CA 94110, USA; claude.hemphill@ 123456ucsf.edu

[6 ]Division of Neurocritical Care and Center for Genomic Medicine, Department of Neurology, Massachusetts General Hospital, Boston, MA 02108, USA; WTKIMBERLY@ 123456mgh.harvard.edu

[7 ]Department of Neurosurgery, North Shore University Hospital, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Manhasset, NY 11030, USA; RNarayan@ 123456northwell.edu

[8 ]Neurotrauma and Neurosurgery Research Unit (UNINN), Vall d′Hebron Research Institute (VHIR), 08001 Barcelona, Spain; sahuquillo.juan@ 123456gmail.com

[9 ]Department of Neurosurgery, Universitat Autònoma de Barcelona (UAB), 08001 Barcelona, Spain

[10 ]Department of Neurosurgery, Vall d′Hebron University Hospital, 08001 Barcelona, Spain

[11 ]Division of Neurocritical Care and Emergency Neurology, Department of Neurology, Yale University School of Medicine, New Haven, CT 06501, USA; kevin.sheth@ 123456yale.edu

[12 ]Department of Neurosurgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA

Author notes

[* ]Correspondence: ruchirajha@ 123456gmail.com (R.M.J.); MSimard@ 123456som.umaryland.edu (J.M.S.)

Author information

Ruchira M. Jha https://orcid.org/0000-0002-3047-7649

Giuseppe Citerio https://orcid.org/0000-0002-5374-3161

J. Marc Simard https://orcid.org/0000-0002-5373-1988

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Publisher ID: ijms-21-00409

DOI: 10.3390/ijms21020409

PMC ID: 7013742

PubMed ID: 31936452

SO-VID: 7f922cbe-a703-4f07-9bd9-156380c44d99

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Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Role of Sulfonylurea Receptor 1 and Glibenclamide in Traumatic Brain Injury: A Review of the Evidence

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Higher order chromatin architecture

Most cited references 114

Decompressive craniectomy in diffuse traumatic brain injury.

Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension.

THE ROLE OF SECONDARY BRAIN INJURY IN DETERMINING OUTCOME FROM SEVERE HEAD INJURY

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