Clinical Trial Details
— Status: Completed
Administrative data
| NCT number |
NCT01595802 |
| Other study ID # |
DC1B-01 |
| Secondary ID |
|
| Status |
Completed |
| Phase |
|
| First received |
|
| Last updated |
|
| Start date |
January 2012 |
| Est. completion date |
July 2015 |
Study information
| Verified date |
June 2022 |
| Source |
Jan Medical, Inc. |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Observational
|
Clinical Trial Summary
The purpose of the study is to determine the sensitivity, specificity and predictive values
of the Jan Medical NeuroWave System in detecting moderate and severe vasospasm in comparison
to Trans Cranial Doppler(TCD).
Description:
Cerebral vasospasm generally occurs due to a ruptured brain aneurysm, or (very rarely)
hemorrhage from another blood vessel abnormality such as an arteriovenous malformation (AVM).
The common factor is the abnormal presence of a substantial amount of blood on the outer
("subarachnoid" or "adventitial") surface of the blood vessel. This can particularly affect
arteries at the base of the brain, i.e., around the Circle of Willis.
Depending on the severity, this can be seen using conventional angiography. Angiographic
spasm tends to be most readily detected at about 5-7 days after the SAH, although it may be
detected as early as 3 days after the hemorrhage. It occurs in between half to two-thirds of
all aneurysm patients depending on the time at which angiography was carried out. Clinical
vasospasm occurs in approximately one-third of all patients suffering aneurysmal SAH.
The essential problem with vasospasm is that it causes an artery to reduce blood flow or
completely shut down. As a result, the part of the brain formerly supplied by that artery
effectively starves (ischemia) and may die (infarction or stroke). Overall, cerebral
vasospasm accounts for approximately 20% of the severe disability and death associated with
ruptured aneurysms.
If vasospasm is detected early, a patient can be treated with balloon angioplasty to reopen
the vessels or have infusions of a vasodilator administered (typically verapamil or
nicardipine). Alternatively, or in concert with that treatment, one can administer
intravenous drugs that raise the patient's blood pressure ("pressors") to force more blood
through the narrow arteries. Both of these treatments carry risk and therefore should not be
administered unless vasospasm is detected. Therefore, in order to prevent this form of brain
injury and enhance the likelihood that a patient will do better, one needs to detect
vasospasm before it becomes severe enough to injure the brain.
Vasospasm can be detected by the signs observed on physical examination of the patient and by
radiological methods such as cerebral angiography, and Trans-Cranial Doppler (TCD)
ultrasound. The physical exam is sensitive for vasospasm in patients who are otherwise awake
and able to participate in a neurological examination. Many patients with subarachnoid
hemorrhage are not keenly aware nor participative to make this clinical exam meaningful.
Therefore clinical examination alone lacks sensitivity.
The gold standard method for detecting vasospasm is cerebral angiography. This involves
injection of a radiopaque dye into the arterial blood stream of a patient and when the dye
reaches the brain X-rays are taken. Although this is the gold-standard for diagnosing
vasospasm it carries the risk of arterial injury or even stroke, and the expense is high. In
addition the contrast dye used in these studies carries the risk of renal failure. As a
result, this technology is generally employed once vasosapasm is suspected from a Trans
Cranial Doppler (TCD) study.
TCD is a bedside test that relies on ultrasound waves generated from a probe placed on the
skin of the head and/or neck region to detect the flow of blood in a cerebral artery. It is a
convenient, safe, and frequently effective method that can be used to rapidly confirm the
clinical findings, and is much less invasive than cerebral angiography. It has, however,
numerous technical limitations; for example, one can only detect vasospasm in the proximal
vessels of the circle of Willis and therefore lacks sensitivity. It is also quite operator
dependent and limited to patients with appropriate skull thickness and acoustic windows.
What is needed is a non-invasive, user independent, safe method to detect cerebral vasospasm
before it causes brain injury. The technology needs to be simple to use and can be done at
the bedside in an ICU environment. Such a tool will likely improve patient outcome by
initiating a chain of events that can mitigate vasospasm (cerebral angioplasty or initiation
of vasopressor therapy) and will likely shorten the length of stay within the Neuro ICU
saving hospitals money.
The Jan Medical NeuroWave is a simple, rapid, non invasive aid to the diagnosis of vasospasm
that is not operator dependent nor limited by skull structure. This study will determine the
sensitivity, specificity and predictive values of the Jan Medical NeuroWave System in
detecting moderate and severe vasospasm in comparison to Trans Cranial Doppler (TCD).
