Health & Medical Neurological Conditions

Cerebral Perfusion Imaging in Vasospasm

´╗┐Cerebral Perfusion Imaging in Vasospasm

Abstract and Introduction

Abstract


Vasospasm following cerebral aneurysm rupture is one of the most devastating sequelae and the most common cause of delayed ischemic neurological deficit (DIND). Because vasospasm also is the most common cause of morbidity and mortality in patients who survive the initial bleeding episode, it is imperative not only to diagnose the condition but also to predict which patients are likely to become symptomatic. The exact pathophysiology of vasospasm is complex and incompletely elucidated. Early recognition of vasospasm is essential because the timely use of several therapeutic interventions can counteract this disease and prevent the occurrence of DIND. However, the prompt implementation of these therapies depends on the ability to predict impending vasospasm or to diagnose it at its early stages.

A number of techniques have been developed during the past several decades to evaluate cerebral perfusion, including positron emission tomography, xenon-enhanced computed tomography, single-photon emission computed tomography, perfusion- and diffusion-weighted magnetic resonance imaging, and perfusion computed tomography. In this article, the authors provide a general overview of the currently available perfusion imaging techniques and their applications in treating vasospasm after a patient has suffered a subarachnoid hemorrhage. The use of cerebral perfusion imaging techniques for the early detection of vasospasm is becoming more common and may provide opportunities for early therapeutic intervention to counteract vasospasm in its earliest stages and prevent the occurrence of DINDs.

Introduction


Vasospasm following cerebral aneurysm rupture is one of the most devastating sequelae and is also the most common cause of DIND. Vasospasm can be demonstrated using angiography in approximately 60 to 70% of patients with ruptured aneurysms. Clinical vasospasm resulting in DIND occurs in 20 to 30% of pa tients within 3 to 14 days after aneurysmal SAH. Given that vasospasm is the most common cause of morbidity and mortality in patients who survive the initial bleeding episode, it is imperative not only to diagnose the condition but also to predict which patients are likely to become symptomatic. The pathophys iological mechanisms of va so spasm are complex and in completely elucidated. The presence of oxyhemoglobin in the sub arachnoid cisterns seems to be a key promoter of the phenomena that ultimately cause narrowing of the arterial lumen and impaired autoregulation. The vascular changes are typically reversible: when severe, however, they may cause cerebral infarction and DIND. The amount of blood in the subarachnoid space on the initial brain CT scan, age younger than 70 years, and a history of smoking are risk factors for vasospasm, but their predictive value is limited.

The most widely used monitoring technique for the detection of vasospasm is TCD ultrasonography, which was introduced in the early 1980s by Aaslid and collea gues. A demonstration of elevated blood flow velocity and an increase in turbulent flow on TCD ultrasonography can provide an early clinical awareness of vasospasm that involves the circle of Willis. Because this method is noninvasive and can be repeated as often as necessary, it is commonly used to monitor for cerebrovascular vasospasm after SAH. However, TCD ultrasonography can fail to detect vasoconstriction if vasospasm occurs beyond in sonated arteries, such as in the distal M2 (MCA), the A2 (ACA), the P2 (posterior cerebral artery), or the vertebro basilar system. In cases of severe vasospasm, decreases in CBF can occur that lead to a drop in measurable blood vel oc ity. Also, in creased intracranial pressure or brain edemacan increase the pulsatility of the waveform, which makes interpretation of higher velocities difficult. Patient movement, suboptimal insonation windows, aberrant vessel course, and clip artifacts can further inhibit the detection of pathological signals.

The diagnosis of vasospasm after SAH is often made using a combination of patient history, physical examination, CT scanning to determine the extent of rupture, and TCD ultrasonography, along with other imaging modalities such as CT angiography, MR imaging, MR angiography, and catheter angiography. Despite multimodality an a lysis of vasospasm, the ability to predict DIND is still limited. In a recent study, investigators demonstrated that when both TCD ultrasonography and catheter angiography revealed vasospasm, the positive predictive value for the occurrence of cerebral infarction was 67%. Con ver sely, when both studies indicated an absence of vasospasm, the negative predictive value of this combination was 72%. Early recognition of vasospasm and the potential risk of DIND is essential because the rapid implementation of standard therapies such as triple-H (hypertension, hypervolemia, and hemodilution) therapy, intraarterial va so dilator application, and balloon angioplasty serves to counteract vasospasm and prevent the occurrence of DIND. However, the prompt use of these therapies depends on the ability to predict impending vasospasm or to diagnose it at its early stages.

A number of techniques to evaluate cerebral perfusion have been developed during the past several decades, beginning in the 1970s with PET and Xe-CT scanning. Dur ing the next two decades, other perfusion imaging techniques were introduced, including SPECT scanning, perfusion- and diffusion-weighted MR imaging, and perfusion CT scanning ( Table 1 ). These techniques have been used to evaluate a variety of disease states, including acute and chronic ischemia and ischemia from post-SAH vaso spasm. In this article we provide a general overview of the currently available perfusion imaging techniques and their application in patients with post-SAH vasospasm.



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