Ignite Creation Date:
2025-12-25 @ 3:47 AM
Ignite Modification Date:
2025-12-26 @ 2:34 AM
Study NCT ID:
NCT05150002
Status:
RECRUITING
Last Update Posted:
2024-12-06
First Post:
2021-11-15
Is NOT Gene Therapy:
False
Has Adverse Events:
False
Brief Title:
Cervical Spinal Cord Stimulation in Patients With Cerebral Vasospasm After Subarachnoid Haemorrhage: VasoStim Study
Sponsor:
Insel Gruppe AG, University Hospital Bern
Organization:
Study Overview
Official Title:
Cervical Spinal Cord Stimulation in Patients With Cerebral Vasospasm After Subarachnoid Haemorrhage: VasoStim Study
Status:
RECRUITING
Status Verified Date:
2024-12
Last Known Status:
None
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:
Cerebral vasospasm is characterized by a vasoconstriction of cerebral arteries causing a reduction of cerebral blood flow (CBF) and leading to ischemia and infarction of the brain parenchyma. Cerebral vasospasm is a serious complication of aneurysmal subarachnoid hemorrhage (SAH) with high morbidity and overall mortality of 40-50%.
Although the exact mechanisms of spinal cord stimulation (SCS) on the innervation of cerebral vessels are still unclear, several hypotheses have been formulated and studies in animals and human performed with very promising results.
This is a proof of concept study to better understand the effect and mechanisms of cervical spinal cord stimulation on cerebral vasospasm after aneurysmal SAH in human.
Although the exact mechanisms of spinal cord stimulation (SCS) on the innervation of cerebral vessels are still unclear, several hypotheses have been formulated and studies in animals and human performed with very promising results.
This is a proof of concept study to better understand the effect and mechanisms of cervical spinal cord stimulation on cerebral vasospasm after aneurysmal SAH in human.
Detailed Description:
Cerebral vasospasm is characterized by a vasoconstriction of cerebral arteries causing a reduction of cerebral blood flow (CBF) and leading to ischemia and infarction of the brain parenchyma. Cerebral vasospasm is a serious complication of aneurysmal subarachnoid hemorrhage (SAH) with high morbidity and overall mortality of 40-50%. The exact pathophysiological mechanisms underlying cerebral vasospasm are still not known in detail.
A wide range of different therapeutic options with various efficacies are available, triple-H therapy and endovascular treatment options like intra-arterial application of vasodilators e.g. Nimodipine or Papaverine or transluminal balloon angioplasty have been reported and are applied to prevent and treat cerebral vasospasm after SAH. Calcium channel blockers such as nimodipine or nicardipine improve outcome in patients after SAH and reduce the risk of secondary ischemia. The benefit of the different therapies is undoubted, but there is still potential for improvement concerning the rate of morbidity and mortality.
Although the exact mechanisms of spinal cord stimulation (SCS) on the innervation of cerebral vessels are still unclear, several hypotheses have been formulated and studies in animals and human performed with very promising results.
This is a proof of concept study to better understand the effect and mechanisms of cervical spinal cord stimulation on cerebral vasospasm after aneurysmal SAH in human.
Subjects are enrolled into the study, if radiographical vasospasms are detected in CTA, CTP, cerebral angiography or TCD.
SCS leads are implanted within 12h after study enrolment following the investigator's standard practice. SCS will be continuously delivered until day 14 after SAH. Doppler ultrasound is performed before SCS lead implantation and repeated after implantation on a daily basis and appearance of a new neurological deficit device until 24h after stopping the stimulation. Efficacy of cervical SCS is further evaluated by CTA or angiography and CTA/P performed 48h and 96h after lead implantation, as well as on day 14 after SAH before stopping the stimulation. The SCS electrode(s) are explanted on day 15. Intracerebral pressure is monitored from day 7-15. Headache, measured as NRS 0-10 and the consumption of analgesics are monitored from day 7-15, at discharge, at 3 and 6 months.
A wide range of different therapeutic options with various efficacies are available, triple-H therapy and endovascular treatment options like intra-arterial application of vasodilators e.g. Nimodipine or Papaverine or transluminal balloon angioplasty have been reported and are applied to prevent and treat cerebral vasospasm after SAH. Calcium channel blockers such as nimodipine or nicardipine improve outcome in patients after SAH and reduce the risk of secondary ischemia. The benefit of the different therapies is undoubted, but there is still potential for improvement concerning the rate of morbidity and mortality.
Although the exact mechanisms of spinal cord stimulation (SCS) on the innervation of cerebral vessels are still unclear, several hypotheses have been formulated and studies in animals and human performed with very promising results.
This is a proof of concept study to better understand the effect and mechanisms of cervical spinal cord stimulation on cerebral vasospasm after aneurysmal SAH in human.
Subjects are enrolled into the study, if radiographical vasospasms are detected in CTA, CTP, cerebral angiography or TCD.
SCS leads are implanted within 12h after study enrolment following the investigator's standard practice. SCS will be continuously delivered until day 14 after SAH. Doppler ultrasound is performed before SCS lead implantation and repeated after implantation on a daily basis and appearance of a new neurological deficit device until 24h after stopping the stimulation. Efficacy of cervical SCS is further evaluated by CTA or angiography and CTA/P performed 48h and 96h after lead implantation, as well as on day 14 after SAH before stopping the stimulation. The SCS electrode(s) are explanted on day 15. Intracerebral pressure is monitored from day 7-15. Headache, measured as NRS 0-10 and the consumption of analgesics are monitored from day 7-15, at discharge, at 3 and 6 months.
Study Oversight
Has Oversight DMC:
False
Is a FDA Regulated Drug?:
False
Is a FDA Regulated Device?:
False
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?: