18 Neuroimaging

18.1 Introduction

Neuroimaging plays an essential role in the diagnosis and management of critical neurological disease. Advances in the fields of neurology and neurosurgery have directly paralleled advances in neuroimaging, for which their inventors have won numerous Nobel Prizes since Röntgen developed X-rays.¹ An in-depth discussion of the physics of neuroimaging, interpretation of neuroradiography, and clinical application thereof are beyond the scope of this chapter. The following should serve as a brief introduction to commonly used imaging modalities in the neurocritical care patient.

18.2 Types of Imaging

18.2.1 Brain Imaging

18.2.2 Spine Imaging

As with brain imaging, CT and MRI form the core of modern neuroimaging for spinal disorders. They form a direct complement to one another, with CT most useful for imaging bony elements, and MRI most adept at demonstrating neural elements or soft-tissue pathology. The exception to this is CT myelography (CT-M), which uses lumbar puncture to inject iodinated contrast to image the intra-thecal contents. Unlike brain imaging, plain X-rays are used extensively in management of spine disease, particularly in order to demonstrate dynamic changes in spinal alignment to motion or weight-bearing.

18.3 Advantages and Limitations (▶ Table 18.1)

18.3.1 Brain Imaging

The X-rays are absorbed by tissues depending on density, which is translated to different intensities on a grey scale. The scale of absorption is referred to in terms of Hounsfield units (HU) and ranges from + 1,000 (bone) to −1,000 (air) (▶ Table 18.2). The higher the number the brighter it is on imaging and likewise the lower the number the darker it is.¹⁷

Table 18.2 Hounsfield units

CT has significant advantages that often make it the initial study for patients with suspected intracranial pathology. The ease of acquisition makes it the ideal study for emergent or repeat brain imaging in the acute inpatient setting.² Routine head CT imaging (HCT) produces 5 mm thick axial sections, although multi-detector scanners can now generate submillimeter thickness images which accommodate MPR with minimal interpolation artifact. Routine HCT is full of clinically relevant information, such as the presence of brain edema or herniation, ventricular configuration, ischemia, and osseous imaging of the skull and sinuses (▶ Fig. 18.1). Generally speaking, it is the study of choice for intracranial hemorrhage for several reasons. First, the speed of acquisition allows interventional decisions to be made rapidly. Also, the evolution of blood products from the acute to subacute to chronic phase is much more straightforward than on MRI. Finally, the advent of portable CT scanners has meant that all but the most extremely unstable critical care patients can undergo HCT imaging as clinically indicated.³

However, CT does have several limitations. As with all X-ray-based imaging technologies, CT requires exposure to ionizing radiation, which is of particular concern with pediatric patients. HCT is also significantly limited in its ability to demonstrate parenchymal changes. Contrast-enhanced HCT can help improve tissue contrast for certain disease states, but does require iodinated contrast administration, with its attendant renal and allergic risks. The major classes of image artifacts encountered in CT imaging include motion (though less so than MRI), streak artifact from metal in the image field, and beam hardening artifact (which limits the utility of HCT in imaging the posterior fossa).⁴

Fig. 18.1 Noncontrast head computed tomography (CT) demonstrating right thalamic intraparenchymal hemorrhage with intraventricular extension and nonspecific white matter changes. The mnemonic “Blood Can Be Very Bad” may aid in systematic review of intracranial structures for the novice (B: Blood, C: Cisterns, B: Brain, V: Ventricles, B: Bone) to avoid missing key findings.

CT angiography (CTA) has become one of three core imaging techniques for imaging cervical and intracranial vascular disease (see below). High-resolution acquisition can be reconstructed in multiple planes, and can be rendered in three dimensions. In combination with CT perfusion (CTP), CTA is an essential component of neuroimaging in acute brain ischemia when considering endovascular thrombectomy.⁵ Acute thrombus is identified as an abrupt cutoff in a vascular tree. CTA approaches the sensitivity and specificity of digital subtraction angiography (DSA) for detection of cerebral aneurysms and other intra-cranial vascular lesions, although without the benefit of dynamic imaging of cerebral blood flow. The presence of vascular intervention devices, such as aneurysm clips, coils, or stents, results in significant streak artifact that can limit the utility of CTA for long-term follow-up.⁶ Poor bolus timing (as with cardiomyopathy) can result in poor arterial opacification or venous contamination.

CT Venography

CT venography (CTV) is a useful and rapid imaging technique used to diagnose cerebral venous thrombosis. The CTV is reported to have 95% sensitivity with multi-planar reformatting compared to traditional DSA.¹⁹ It can provide detailed anatomy of intracranial venous system, both the deep and superficial veins. That being said, it is common to have normal variants of the venous system and should not be mistaken for pathologic event.¹⁸ It carries the same limitation as any study that requires contrast and should be used with caution in pregnancy.

CT Perfusion

Described first by Axel in 1980,²² perfusion imaging of the brain has taken on a core role in the acute management of ischemic stroke. At a basic level, perfusion imaging relies on dynamic imaging of a contrast bolus through a volume of tissue. Parenchymal blood flow parameters can be mapped on a voxel-by-voxel basis, and reconstruction of perfusion maps allows for identification of cerebral blood flow (CBF), mean transit time (MTT), and cerebral blood volume (CBV), which are related by the equation:

Clinical application of this imaging technique allows for delineation of ischemic/oligemic versus infarcted cerebral tissue. Regions of ischemia significant enough to produce cell death (less than 8–10 mL/100 cc tissue/minute) will have matched regions of decreased CBF and CBV (▶ Table 18.3). However, intermediate ranges of ischemia or oligemia can result in impaired neuronal function without cell death, resulting in potentially reversible clinical symptoms. This is seen as regions of decreased CBF but with preserved CBV, which receive enough collateral flow to preserve neuronal integrity for a period of time, known as the ischemic penumbra, which can potentially be salvaged with thrombolytic or mechanical thrombectomy therapies (▶ Fig. 18.2).⁷ CT-based perfusion imaging is, generally speaking, more reliable than MR perfusion (MRP) due to the fixed relationship between iodinated contrast concentration and density, unlike the nonlinear relationship between Gd-contrast and the T2* signal which forms the basis for MRP.

Fig. 18.2 Imaging studies in an acute stroke patient. Computed tomography (CT) perfusion imaging shows elevated mean transit time (a) in the territory of the right middle cerebral artery. Cerebral blood volume in the same region (b) was preserved, suggesting salvageable penumbra. CT angiography (CTA) demonstrated distal right M1 cutoff (c, black arrow). This finding correlated during emergent cerebral angiography (d, white arrow), with subsequent reperfusion following mechanical thrombectomy (e), and postoperative magnetic resonance imaging (MRI) demonstrating minimal ischemic changes on diffusion-weighted imaging (DWI) (f).

While brain MRI is the imaging modality of choice for evaluation of intracranial pathology, contrast-enhanced head CT still has some utility. Most commonly, it is utilized for patients with non-MRI compatible metallic or implantable hardware. Additionally, in some cases, contrast imaging is preferred or required. Patients with renal failure are unable to receive gadolinium (Gd)-based contrast due to the risk of development of nephrogenic systemic fibrosis (NSF) and CT contrast is iodinated which can be dialyzed.

MRI is based on the principle in physics of nuclear magnetic resonance.⁸ It uses interactions of hydrogen nuclei, radiofrequency energy, and a magnetic field. The majority of images are created from the magnetic properties of the hydrogen nuclei contained with water molecules within tissue, of which the human body is abundant. The exact physics behind the individual sequences are beyond the scope of this chapter.

MRI has far greater brain tissue contrast compared to CT. This is particularly true for new higher field strength magnets (3 Tesla or greater), although with notable limitations for certain types of artifacts.⁹ MR-based imaging is also capable of a wide array of advanced imaging techniques such as diffusion imaging or spectroscopy, and does not use ionizing radiation. Conversely, MRI is significantly more susceptible to motion artifact than CT, requires longer image acquisition times, is significantly more expensive to install and maintain, and requires safety protocols for patients and equipment in the magnetic environment. In comparison to CT, findings are referred to in terms of intensity: hypointense, hyperintense, and isointense. There are various sequences that are completed with routine MRI which are noted within ▶ Table 18.4.

Diffusion

Diffusion-weighted imaging (DWI) is currently the imaging modality of choice for the evaluation of cerebral infarction. DWI utilizes motion of water molecules for tissue contrast. Normal brain tissue has relatively low diffusion restriction, as the majority of water is contained in the interstitial space. However, in the setting of stroke, Na² +/K⁺ pump failure results in loss of cellular homeostasis, sodium influx, and net inflow of water into the intracellular space. This results in an extremely conspicuous hyperintense signal in the region of infarction referred to as diffusion restriction. A similar effect is seen with cerebral abscesses and epidermoid cysts, both of which show diffusion restriction on MRI. Due to short acquisition times, DWI can be performed quickly and is relatively resistant to motion artifact. However, DWI can be significantly limited by susceptibility artifact, particularly near the skull base due to air–tissue interface, in the region of blood/blood products or from metal-containing hardware. Diffusion imaging can also be complicated by the presence of underlying edema, which independently shows up hyperintense on DWI with the absence of true diffusion restriction. This is called T2 shine-through which refers to a hyperintense signal on DWI image without restricted diffusion but due to a high T2 signal which “shines through.”¹⁰ Use of apparent diffusion coefficient (ADC) maps can help delineate the difference between true diffusion restriction and T2 shine-through, with dark regions on ADC correlating with diffusion restriction. ADC changes also are the earliest identifiable features on MRI in the setting of acute stroke.

Table 18.4 MRI sequences

Perfusion

MRP imaging is used to demonstrate similar measures of cerebral blood flow and perfusion as CTP. As noted above, computational challenges exist for contrast-based MRP methods due to the nonlinear dose-dependent enhancement. However, acquisition time can limit its utility for acute stroke by delaying intervention relative to CTP.¹¹ At our institution, MRP is most commonly used as an adjunct to anatomic MRI and MR spectroscopy in the determination of recurrent tumor versus radiation necrosis in the glioma patient population.

T1-weighted

The sequence is good in identification of anatomy. It is best for viewing post-contrast images. Hyperintense signal can be caused by fat, methemoglobin, Gd contrast, or other paramagnetic contrast, melanin.

T2-weighted FLAIR and GRE

T2-weighted fluid-attenuated inversion recovery (FLAIR) imaging is a particularly useful sequence in the evaluation of cerebral pathology. Due to magnetic differences in the local environment, CSF signal can be nulled while accentuating intraparenchymal edema (▶ Fig. 18.3). As a result, FLAIR imaging is particularly useful for identifying regions of periventricular edema (such as trans-ependymal flow in hydrocephalus or periventricular white matter lesions in multiple sclerosis). Furthermore, FLAIR imaging (along with T₂*-gradient recalled echo [GRE] imaging) is considered the single most sensitive test for the identification of subarachnoid hemorrhage (SAH), and calls into question the utility of lumbar puncture in the evaluation of thunderclap headache.

Structures have different appearance when looking at T1 and T2 images (▶ Table 18.5). Blood and blood products in particular have varying signal characteristics which make it useful in determining the age of a hemorrhage at the time of MRI (▶ Table 18.6).

Role of Contrast

Gd-based contrast agents are utilized for intravenous contrast enhancement due to their paramagnetic properties at room temperature. A full accounting of contrast-enhancing lesions is beyond the scope of this text, but contrast should be administered during MRI evaluation of any nonischemic focal lesion of the parenchyma. Compared to iodinated contrast, Gd agents have a significantly improved safety profile. Although Gd can cause mild renal injury, causation of overt renal failure is very rare, and allergy is extremely rare. The feared complication of Gd-contrast administration is NSF, in which large fibrosing plaques developing on the skin and internal organs, resulting in severe flexion contractures and pain. NSF is an extremely rarely reported disease, which has been nearly uniformly identified in patients on chronic hemodialysis (though a few cases in patients with a history of peritoneal or pre-dialysis patients have been reported in the literature).¹²

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