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| ID | Type | Description | Link |
|---|---|---|---|
| 38RC20.014 | Other Identifier | Promotor |
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Severe brain injury (SBI) is one of the world's leading causes of death and disability in young adults, but its peripheral vascular consequences in humans are poorly understood.
This prospective, monocentric, pathophysiological study aims to investigate differences in vasoreactivity in the anterior aspect of the contralateral forearm at the most injured cerebral hemisphere between patients with severe head trauma and patients with severe trauma without associated brain injury matched on sex and age (+/- 5 years).
Severe brain injury (SBI) is one of the world's leading causes of death and disability in young adults.
Its impact on cerebral vascularization is well known. At the systemic level, it induces transient dysfunctions that can develop into severe failures, even in cases of isolated SBI. Studies on a mouse model of SBI show alterations in peripheral vascular reactivity that persist over time and are linked to endothelial dysfunction, the mechanism of which is a decoupling of endothelial NO synthase in a context of systemic inflammation. However, no data are available regarding the peripheral vascular consequences of SBI in humans.
The main objective of this prospective, monocentric, pathophysiological study is to determine whether the postocclusive hyperaemic response at the anterior surface of the contralateral forearm to the most injured cerebral hemisphere differs between patients with severe brain injury and patients with severe trauma without associated head injury matched on sex and age (+/- 5 years), by studying the amplitude of post-occlusive hyperaemia (maximum amplitude expressed as percentage of vasodilatation and area under the curve : AUC) as a function of the group.
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| Label | Type | Description | Intervention Names |
|---|---|---|---|
| Severe traumatic brain injury | |||
| Severe trauma without brain trauma | |||
| Healthy controls |
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| Measure | Description | Time Frame |
|---|---|---|
| Post-occlusive hyperaemia | Maximum amplitude expressed as percentage of vasodilation and area under the curve: AUC | 0-60 days |
| Measure | Description | Time Frame |
|---|---|---|
| Post-occlusive hyperaemia with local anesthesia | Maximum amplitude expressed as percentage of vasodilation and area under the curve: AUC | 0-60 days |
| Current-Induced Hyperaemia | Area under the curve expressed as a percentage of the baseline. |
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Inclusion Criteria:
Healthy volunteers :
Patients with Severe Brain Injury :
Severe traumatized patients without associated severe brain injury:
Exclusion Criteria:
Hypersensitivity to lidocaine and/or prilocaine or to amide type local anesthetics or to any of the excipients of the cream.
History of axillary lymph node dissection, trauma or axillary surgery
Prohibited treatments and procedures :
Pregnant, parturient or breastfeeding women
Subject in a period of exclusion from another study,
Person deprived of liberty by judicial or administrative decision, person subject to a legal protection measure,
Subject having exceeded the annual compensation threshold for testing
Subject cannot be contacted in case of emergency
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| Name | Role | Phone | Extension | |
|---|---|---|---|---|
| Jean-Luc Cracowski, Pr | Contact | 0476767856 | 0033 | JLCracowski@chu-grenoble.fr |
| Manon Gabin, Intern | Contact | 0476767575 | 0033 | mgabin@chu-grenoble.fr |
| Name | Affiliation | Role |
|---|---|---|
| Jean-Luc Cracowksi, Pr | University Hospital, Grenoble | Principal Investigator |
| Facility | Status | City | State | ZIP | Country | Contacts |
|---|---|---|---|---|---|---|
| University Hospital | Recruiting | Grenoble | 38700 | France |
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| ID | Term |
|---|---|
| D000070642 | Brain Injuries, Traumatic |
| D014947 | Wounds and Injuries |
| ID | Term |
|---|---|
| D001930 | Brain Injuries |
| D001927 | Brain Diseases |
| D002493 | Central Nervous System Diseases |
| D009422 | Nervous System Diseases |
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| 0-60 days |
| Current-Induced Hyperaemia with local anesthesia | Area under the curve expressed as a percentage of the baseline. | 0-60 days |
| Local thermal hyperaemia | Maximum amplitude of the initial peak expressed as a percentage of the baseline and area under the curve of the delayed plateau. | 0-60 days |
| Local thermal hyperaemia with local anesthesia | Maximum amplitude of the initial peak expressed as a percentage of the baseline and area under the curve of the delayed plateau. | 0-60 days |
| Flow amplitude after local cooling | Amplitude of initial vasoconstriction averaged over 1 min around the lowest flow value during the first 5 minutes. | 0-60 days |
| Transient venous post-compression hyperaemia | Area under the curve and percentage change from baseline. | 0-60 days |
| Study of vasoreactivity in patients with severe brain injury | Extent of post-occlusive hyperaemia, current-induced hyperaemia, thermal hyperaemia and cold response in patients with severe brain injury. | 0-60 days |
| Study of vasoreactivity in healthy subjects | Description of the magnitude of post-occlusive hyperaemia, current-induced hyperaemia, thermal hyperaemia and cold response in healthy subjects. | Study visit |
| D006259 |
| Craniocerebral Trauma |
| D020196 | Trauma, Nervous System |