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Monitoring Brain Activity in Human Brain Injury

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. Identifier: NCT00258505
Recruitment Status : Unknown
Verified October 2005 by Soroka University Medical Center.
Recruitment status was:  Not yet recruiting
First Posted : November 24, 2005
Last Update Posted : August 1, 2007
Information provided by:
Soroka University Medical Center

Brief Summary:
The outcome of brain injury (physical or stroke) may be related to a brain electrical phenomenon known as Cortical Spreading Depression (CSD). This is a brief cessation of function in a local region of brain tissue. It has been hypothesized that CSD may occur after brain injury and may expand the damage to adjacent brain areas. Our aim is to detect CSD by means of intracranial electrodes in patients with brain injuries and asses how these events alter the outcome of the patients.

Condition or disease Intervention/treatment
Traumatic Brain Injury Aneurysmal Subarachnoid Hemorrhage Cerebral Infarction Cerebral Hemorrhage Procedure: Procedure: intracranial monitoring up to 9 days after injury

Detailed Description:

Cortical spreading depression (CSD) is a wave of mass neuronal firing and neuronal and glial depolarisation which propagates through grey matter in the central nervous system in response to a pathologic stimulus, at a rate of between 1 and 5 mm per minute. First described by Leão in 1944 as a sudden depression of ECoG amplitude spreading across the cortex of the rabbit (Leao, A. A. P. 1944), CSD can be elicited in experimental animals by chemical, electrical, and mechanical stimuli, with varying degrees of ease. CSD provoked in healthy, normally perfused neural tissue does not induce persistent metabolic stress or cellular damage, and indeed such induction of CSD in animal experiments may confer protection against the adverse effects of a subsequent ischaemic insult (Kobayashi, S. et al. 1995).

In animal models of focal cerebral ischaemia, usually induced by occlusion of the middle cerebral artery, a spontaneous phenomenon occurs around the periphery of the core territory, with electrophysiological features essentially identical with CSD, and similar capacity to propagate across cerebral cortex. Designated "peri-infarct depolarisation" (PID), this event is associated with infarct expansion, or recruitment of at-risk cortical territory into the expanding core, and has been shown capable of causing this expansion, in the absence of therapeutic intervention. Indeed it has been hypothesized that glutamate release may be involved in PID generation, and that excitotoxicity may accomplish detrimental effects via this route (Hossmann, K. A. 1994), (Obrenovitch, T. P. and Urenjak, J. 1997). Some experimental neuroprotection treatments for stroke act to decrease the incidence of PID (Iijima, T. et al. 1992;Chen, Q. et al. 1993;Busch, E. et al. 1996).

In traumatic and ischaemic (especially in middle cerebral artery occlusion and aneurysmal subarachnoid haemorrhage) brain injury in humans, a phase of delayed deterioration often associated with severe and refractory brain swelling develops between 2 and 5 days after the initial ictus, and is associated with poor or fatal outcome. The cause and mechanism of this deterioration remain poorly understood, and the possibility exists that CSD/PID events might contribute to deterioration.

To date, CSD or PID have been reported in only ten human subjects in two papers (Mayevsky, A. et al. 1996; Strong, A. J. et al. 2002). Strong et al. reported that transient ECoG suppressions suggestive of depolarisations are common - but by no means universal - after brain injury in humans. Sub-dural ECoG electrode strips were placed in 14 patients who had undergone craniotomy for trauma or intracranial hemorrhage; monitoring was for up to 60 h following the injury. Five of these patients (36%) showed patterns of ECoG depression consistent with PID/CSD in brain regions adjacent to the primary injury.

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Study Type : Observational
Estimated Enrollment : 100 participants
Observational Model: Defined Population
Observational Model: Natural History
Time Perspective: Longitudinal
Time Perspective: Prospective
Official Title: Incidence, Nature and Consequences of Cortical Depolarizations in Human Brain Injury From Trauma and Ischemia: The COSBID Study
Study Completion Date : September 2007

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Ages Eligible for Study:   18 Years and older   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   No

Inclusion Criteria:

Immediately following:

  • traumatic brain injury
  • aneurysmal subarachnoid haemorrhage or
  • spontaneous intracerebral haematoma or
  • stroke involving cerebral cortex

Exclusion Criteria:

  • GCS = 3
  • Bilateral fixed & dilated pupils or other evidence of massive irreversible brain injury
  • more than 5 days post Injury/ictus.

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its identifier (NCT number): NCT00258505

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Contact: Anthony Strong, Prof.

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Berlin, Germany
Contact: Jens Dreier, MD   
Principal Investigator: Jens Dreier, MD         
Beer-Sheva, Israel, 84101
Contact: Alon Friedman, MD/PhD   
Principal Investigator: Alon Friedman, MD/PhD         
Sponsors and Collaborators
Soroka University Medical Center
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Principal Investigator: Alon Friedman, MD/PhD Soroka University Medical Center
Principal Investigator: Jens Dreier, MD Charite, Berlin, Germany

Additional Information:
Layout table for additonal information Identifier: NCT00258505    
Other Study ID Numbers: sor402605ctil
First Posted: November 24, 2005    Key Record Dates
Last Update Posted: August 1, 2007
Last Verified: October 2005
Keywords provided by Soroka University Medical Center:
Spreading depression
Blood-brain barrier
Additional relevant MeSH terms:
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Brain Injuries
Brain Injuries, Traumatic
Subarachnoid Hemorrhage
Cerebral Infarction
Cerebral Hemorrhage
Wounds and Injuries
Pathologic Processes
Brain Diseases
Central Nervous System Diseases
Nervous System Diseases
Craniocerebral Trauma
Trauma, Nervous System
Intracranial Hemorrhages
Cerebrovascular Disorders
Vascular Diseases
Cardiovascular Diseases
Brain Infarction
Brain Ischemia