Monitoring Brain Activity in Human Brain Injury

Traumatic Brain Injury Clinical Trial

Official title:

Incidence, Nature and Consequences of Cortical Depolarizations in Human Brain Injury From Trauma and Ischemia: The COSBID Study

Clinical Trial Details — Status: Not yet recruiting

Administrative data

• NCT number: NCT00258505
• Other study ID #: sor402605ctil
• Status: Not yet recruiting
• Phase: N/A
• First received: November 22, 2005
• Last updated: July 31, 2007
• Est. completion date: September 2007

Study information

• Verified date: October 2005
• Source: Soroka University Medical Center
• Contact: Anthony Strong, Prof.
• Email: Anthony.strong[@]kcl.ac.uk
• Is FDA regulated: No
• Health authority: Israel: Ministry of Health
• Study type: Observational

Clinical Trial 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.

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.

Recruitment information / eligibility

• Status: Not yet recruiting
• Enrollment: 100
• Est. completion date: September 2007
• Accepts healthy volunteers: No
• Gender: Both
• Age group: 18 Years and older

Eligibility

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.

Study Design

Observational Model: Defined Population, Time Perspective: Longitudinal

Related Conditions & MeSH terms

• Aneurysmal Subarachnoid Hemorrhage
• Brain Injuries
• Cerebral Hemorrhage
• Cerebral Infarction
• Hemorrhage
• Subarachnoid Hemorrhage
• Traumatic Brain Injury

Intervention

Procedure:
• Procedure: intracranial monitoring up to 9 days after injury

Locations

Country	Name	City	State
Germany	Charite	Berlin
Israel	Soroka	Beer-Sheva

Sponsors (1)

Lead Sponsor	Collaborator
Soroka University Medical Center

Countries where clinical trial is conducted

Germany,  Israel, 

References & Publications (1)

Strong AJ, Fabricius M, Boutelle MG, Hibbins SJ, Hopwood SE, Jones R, Parkin MC, Lauritzen M. Spreading and synchronous depressions of cortical activity in acutely injured human brain. Stroke. 2002 Dec;33(12):2738-43. — View Citation