Monitoring Brain Activity in Human Brain Injury

The recruitment status of this study is unknown because the information has not been verified recently.
Verified October 2005 by Soroka University Medical Center.
Recruitment status was  Not yet recruiting
Sponsor:
Information provided by:
Soroka University Medical Center
ClinicalTrials.gov Identifier:
NCT00258505
First received: November 22, 2005
Last updated: July 31, 2007
Last verified: October 2005
  Purpose

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 Intervention
Traumatic Brain Injury
Aneurysmal Subarachnoid Hemorrhage
Cerebral Infarction
Cerebral Hemorrhage
Procedure: Procedure: intracranial monitoring up to 9 days after injury

Study Type: Observational
Study Design: Observational Model: Defined Population
Time Perspective: Longitudinal
Official Title: Incidence, Nature and Consequences of Cortical Depolarizations in Human Brain Injury From Trauma and Ischemia: The COSBID Study

Resource links provided by NLM:


Further study details as provided by Soroka University Medical Center:

Estimated Enrollment: 100
Estimated Study Completion Date: September 2007
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.

  Eligibility

Ages Eligible for Study:   18 Years and older
Genders Eligible for Study:   Both
Accepts Healthy Volunteers:   No
Criteria

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.
  Contacts and Locations
Choosing to participate in a study is an important personal decision. Talk with your doctor and family members or friends about deciding to join a study. To learn more about this study, you or your doctor may contact the study research staff using the Contacts provided below. For general information, see Learn About Clinical Studies.

Please refer to this study by its ClinicalTrials.gov identifier: NCT00258505

Contacts
Contact: Anthony Strong, Prof. Anthony.strong@kcl.ac.uk

Locations
Germany
Charite Recruiting
Berlin, Germany
Contact: Jens Dreier, MD       jens.dreier@charite.de   
Principal Investigator: Jens Dreier, MD         
Israel
Soroka Not yet recruiting
Beer-Sheva, Israel, 84101
Contact: Alon Friedman, MD/PhD       alonf@bgu.ac.il   
Principal Investigator: Alon Friedman, MD/PhD         
Sponsors and Collaborators
Soroka University Medical Center
Investigators
Principal Investigator: Alon Friedman, MD/PhD Soroka University Medical Center
Principal Investigator: Jens Dreier, MD Charite, Berlin, Germany
  More Information

Additional Information:
Publications:
ClinicalTrials.gov Identifier: NCT00258505     History of Changes
Other Study ID Numbers: sor402605ctil
Study First Received: November 22, 2005
Last Updated: July 31, 2007
Health Authority: Israel: Ministry of Health

Keywords provided by Soroka University Medical Center:
Spreading depression
Seizures
Blood-brain barrier

Additional relevant MeSH terms:
Cerebral Infarction
Stroke
Hemorrhage
Infarction
Subarachnoid Hemorrhage
Brain Injuries
Wounds and Injuries
Cerebral Hemorrhage
Brain Infarction
Brain Ischemia
Cerebrovascular Disorders
Brain Diseases
Central Nervous System Diseases
Nervous System Diseases
Vascular Diseases
Cardiovascular Diseases
Pathologic Processes
Ischemia
Necrosis
Intracranial Hemorrhages
Craniocerebral Trauma
Trauma, Nervous System

ClinicalTrials.gov processed this record on August 20, 2014