Ignite Creation Date:
2024-05-05 @ 12:07 PM
Last Modification Date:
2024-10-26 @ 9:21 AM
Study NCT ID:
NCT00258505
Status:
UNKNOWN
Last Update Posted:
2007-08-01
First Post:
2005-11-22
Brief Title:
Monitoring Brain Activity in Human Brain Injury
Sponsor:
Soroka University Medical Center
Organization:
Soroka University Medical Center
Study Overview
Official Title:
Incidence Nature and Consequences of Cortical Depolarizations in Human Brain Injury From Trauma and Ischemia The COSBID Study
Status:
UNKNOWN
Status Verified Date:
2005-10
Last Known Status:
NOT_YET_RECRUITING
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
False
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
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
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 1992Chen Q et al 1993Busch 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 CSDPID 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 PIDCSD in brain regions adjacent to the primary injury
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 1992Chen Q et al 1993Busch 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 CSDPID 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 PIDCSD in brain regions adjacent to the primary injury
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None