About Vasospasm

Cerebral vasospasm generally occurs due to a ruptured brain aneurysm. 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.

Cerebral vasospasm is a term that refers to physical narrowing of the central lumen of a brain blood vessel due to over-contraction of the vessel wall. In the worst-case scenario, a vasospastic brain artery no longer permits blood flow, a state that can be likened to a tightly clenched fist. Vasospasm is generally thought to occur only in arteries and not in smaller arterioles, capillaries or veins.

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, 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.

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 subarachnoid hemorrhage (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.

Vasospasm is currently diagnosed and managed with a combination of technologies and tests, each with significant deficiencies.

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 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. Vasospastic arteries on a cerebral angiogram appear to have abnormally thin columns of blood in their lumens, almost string-like in their width or no blood flow at all when the spasm closes the artery entirely. Although this is the standard method used for diagnosing vasospasm, it carries the risk of arterial injury or even stroke, and the expense is high.

It is safer to perform a brain CT scan in a patient with suspected vasospasm as it may show new strokes in the distribution of the vasospastic artery or arteries. However, this only documents the problem after the fact, and the goal of therapy is to detect vasospasm before it gets sufficiently severe to cause brain injury. In addition the contrast dye used in these studies carries the risk of renal failure.

An MRI of the brain, especially in its Diffusion Weighted Image, DWI and FLAIR sequences, may more precisely show the extent of brain tissue damaged (infarcted) by vasospasm, but this too is after the fact.

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. It is significantly less invasive than cerebral angiography. However, it has numerous technical limitations. For example, you can only detect vasospasm in the proximal vessels of the circle of Willis and therefore lacks sensitivity. It is also operator dependent and not enough technologists are available in the United States to perform these studies.

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 able to perform at the bedside in an ICU environment. The BrainPulse device has been designed with these needs in mind. Such a tool will likely improve patient outcome by initiating a chain of events that can mitigate vasospasm (cerebral angioplasty or initiation of vasospressor therapy) and will likely shorten the length of stay within the neuro ICU, ultimately saving hospitals money.