1.COMPUTED TOMOGRAPHY (CT) : While severe and moderate traumatic head and brain injuries often mandate head CT, several clinical scales require specific criteria in determining the need for neuroimaging after a mild TBI. These include the New Orleans Criteria (NOC) and the Canadian CT Head Rule (CCHR).(45) Both are relatively straight forward and use seven criteria readily obtained in the setting and evaluation of mild TBI. A head-to-head comparison of the two found that they had equivalent sensitivity in determining the need for neurosurgical intervention, but the Canadian CT Head Rules had a far superior specificity (76.3% versus 12.1%).(47) Because the incidence of TBI is highest in age groups 0 to 4 and 15 to 24, there are often many more years of life expectance at stake.2 Therefore, the threshold …show more content…
to get immediate neuroimaging is low. A cost effectiveness study conducted by Stein and associates showed that the costs of not using head CT in mild TBI patients paled in comparison to the consequences of a delayed intracranial hemorrhage diagnosis.(49) Serial neurologic examinations can also show changes in patient presentation after the initial post-TBI presentation. Such a change also warrants a prompt head CT.9(50)Some recent literature points to CT potentially causing an increased cancer incidence; however, these studies have intrinsic flaws including how they compare forms of radiation exposure, and brain CT scans are typically of relatively low radiation dose.(51) It is also self-evident that there is much more to lose by deferring imaging in the setting of TBI on several levels, including economic. Computed tomography has several advantages in the acute TBI setting, including speed and general lack of patient contraindications (for noncontrast studies), as well as sensitivity and specificity for several conditions that are often suspected in traumatic head injuries, including skull fractures (Fig. 1), brain herniation, and intracranial bleeding (Fig. 2). Imaging findings in brain contusions tend to vary as the lesion evolves. Initial CT typically demonstrates isodense lesions that become more evident on follow-up CT. Contusion near the zone of impact usually appear as hyperdensities within brain tissue in area . CT progression over time in the size and number of contusions and the amount of hemorrhage in the contusions. Subdural hematomas typically appear as crescentic extra-axial collections on CT. Epidural hematomas appear on CT as a biconvex lesion, limited by calvarial suture lines. The reader is referred to a separate article in this journal volume on the neuroimaging features of intracranial hemorrhage. Despite its strengths of speed and sensitivity for fracture and bleed detection following a TBI, CT is limited in predicting the long-term neuropsychological and cognitive outcomes of such injuries.(53) The IMPACT study published in 2007 demonstrated a strong correlation between CT classification in presenting TBI patients and Glasgow Outcome Scale assessed 6 months after the injury.(54) However, the Glasgow Outcome Scale is nonspecific, and other neuroimaging modalities should be sought to most accurately assess the TBI patient after acute clinical management and patient stabilization.
2.MAGNETIC RESONANCE IMAGING (MRI) : Magnetic resonance imaging represents another imaging modality that is exceptional at visualizing TBI.
Advances in MRI techniques, both structural and functional, continue to occur at a rapid pace. Although MRI scanners are readily available in most United States Hospitals, arranging acute MRI for a patient can be challenging. This is because equipment is expensive, and image acquisition and interpretation are both time-consuming. Thus, it is relatively unavailable for acute imaging. However, as previously discussed, MRI is optimal in the acute setting. Magnetic resonance imaging of TBI in the subacute time frame can greatly assist in optimal patient management. Early comparative studies showed that brain CT failed to detect 10 to 20% of brain abnormalities visualized by MRI after mild TBI.(56) However, 48 to 72 hours after injury, MRI is superior to CT in detection of swelling, bleeding, brain contusions, and axonal injury. Magnetic resonance imaging is also more sensitive and specific for brainstem, basal ganglia, and thalamic imaging than
CT.(56,67) Conventional gradient-echo MR sequences (e.g., T2*) are widely available on the vast majority of clinical MR scanners. Fluid-attenuated inversion recovery (FLAIR) is a special MR technique (Fig. 3) that was pioneered in the early 1990s and is rapidly becoming universally available with most commercial MRI scanners. (56,59)Fluid-attenuated inversion recovery imaging uses a long signal inversion time (T1) to suppress the high signal from cerebrospinal fluid (CSF).16–18 Because of this ability, FLAIR imaging is often used in the setting of stroke.(60,61) Its utility in TBI neuroimaging is gaining momentum as more is learned about its sensitivity and specificity to detect TBI brain lesions. Fluidattenuated inversion recovery imaging has been correlated with prognosis of the severe TBI patient.(62,65) No discussion of TBI would be complete without inclusion of diffuse axonal injury (DAI). Diffuse axonal injury is characterized by generalized damage to brain white matter and occurs in over half of all TBI patients.(65,67) Computed tomography, at best, can indirectly detect DAI by quantifying cerebral atrophy.(65,68) Magnetic resonance imaging, in comparison, is superior at defining the gray-white matter boundaries and is a better choice for volumetric comparisons. Magnetic resonance FLAIR imaging has shown great promise in predicting TBI DAI outcome.(63-64) Diffusion tensor imaging (DTI) is another rapidly developing MRI technique that has shown impressive potential in detecting subtle structural white matter pathologies in many neurologic diseases, including multiple sclerosis, Alzheimer’s disease, epilepsy, motor neuron disease, and TBI.(65,69–75) Diffusion tensor imaging is able to visualize the diffusion of water along white matter fiber bundles. Abnormal white matter has an increased radial diffusion in water away from fiber bundles.(65,69,76) Loss of white matter axonal bundle integrity is precisely the basis for DAI.26 Extensive damage to brain white matter, usually caused by rapid accelerations and decelerations, is the hallmark of DAI.(77) Grading of DAI can be done using histology.(78) Diffusion tensor imaging techniques are still in their infancy and require extensive computing resources and imaging time. Therefore, DTI is not usually available at most hospitals. In addition to the aforementioned MRI structural techniques, there are two prominent MRI methods for demonstrating function: magnetic resonance spectroscopy (MRS) and functional MRI (fMRI). Both have been applied to TBI with varied levels of success. Functional MRI was first used by neuroscientists to demonstrate cortical activity using a visual stimulus.(79) Since that time, fMRI using the same blood oxygenation level-dependent (BOLD) technique has been used to map the different senses, pain, motor function, memory, learning, plasticity, and emotion.(80–86) The basis of fMRI is in the oxygenation status of the hemoglobin molecule by the red blood cell.(87–89) When a brain region requires more oxygen because it is metabolically active, local red blood cells become deoxygenated. Deoxygenated hemoglobin, unlike oxygenated hemoglobin, has a magnetic dipole. Therefore, if enough molecules become deoxygenated within a brain region, a lack of magnetic homogeneity can be detected, using statistical analysis, within the very homogenous magnetic field of an MRI scanner.(87) The strength of the fMRI signal changes are proportional to the strength of the magnetic field of the MRI scanner (e.g., a 3T MRI machine has a more sensitive fMRI detection threshold than 1.5T).(88,89) This also translates into the fact that the more subtle the change in deoxy/oxygenated hemoglobin ratio or the smaller the area in which a change occurs, the more likely such change can be detected by a stronger MRI magnet. This technique has been utilized in the setting of TBI primarily to test changes in working memory and learning.(90–96) Such neurocognitive effects constitute many of the disabilities seen over time in the TBI patient. However, fMRI can be especially problematic for these patients. Functional MRI, like MRS, does not require contrast or IV access. However, the subject or patient needs to focus on a specific task. Maintaining attention in a very foreign and intimidating environment can be challenging for even those very familiar with its workings, let alone a TBI patient with a cognitive deficit. For example, such tasks may include: asking a patient to direct his or her focus to listening to a phrase or music, finding an object within his or her visual field at certain times, remembering the sequence of newly learned events, or imagining the smell of flowers. Each of these ‘‘stimulation’’ tasks must then be compared with another state. Such a change (and often several task periods are used for each study) can also be challenging. Additionally, such tasks are difficult to standardize between patients and, especially, between institutions. Even so, neuroscientists and clinicians have so far been relatively successful. Like the other aforementioned imaging techniques and modalities, the clinician needs to understand the individual limit of each when ordering a particular study. Functional MRI is no exception. At its most basic level, MRI works at the nuclear level, on individual protons.46 Magnetic resonance spectroscopy uses the same general principles as MRI but takes them a step further by determining changes in the number of protons at a spatial location, and thus an estimation of the relative change in representation of a particular molecule. Magnetic resonance spectroscopy has the ability to detect the biochemical signatures of several molecules including choline, creatine, glucose, N-acetylaspartate (NAA), alanine, and lactate.(96) Unlike fMRI, MRS does not require the patient to perform a particular task; rather, data can be obtained at rest. In the context of TBI, MRS has been used to measure choline, NAA, glutamine, and glutamate at various times after the injury occurred.56–60 Specifically, identification of lactate 1 to 2 weeks after injury has been shown to be a predictor of poor outcome.(102–104) Whether they are due to the brain’s need for a nonglucose-based source of energy or a buildup of by-product of anaerobic metabolism, the reason for increased lactate levels observed after TBI remains unknown.(105) Early NAA levels have predicted the Glasgow Outcome Scale 6 months after TBI.(98) Because there are no known adverse long-term Consequences of MRI, MRS has been extensively used in the setting of pediatric TBI.(70,102,106–108) However, at 2 cm_2 cm within a 5-cm thick slice, MRS’s spatial resolution is suboptimal, especially since many brain lesions and structures are much smaller. Finally, it is important to note that MRS—like fMRI—is not an absolute measurement. Rather, MRS detects the presence of a particular compound or changes in the ratios between certain molecules. Therefore, no absolute comparisons can be made between patients and conditions.