in Figure 5–14. The implications of such refined image anal-yses are obvious in studying the integrity and effects of TBI on motor, sensory, and language systems that have a known anatomical basis. It is likely that the use of such technology will make possible more refined image analysis of subtle per-turbations associated with TBI. Although these applications are a bit futuristic, DTI has current application in TBI, as il-lustrated in Figure 5–15, which depicts a patient who sus-tained TBI 20 years before DTI. Using what is called frac-tional anisotropy (FA), FA maps of the brain can be created in which brighter voxels represent greater anisotropy and thus greater integrity, directionality, or coherence. As clearly seen in Figure 5–15, through the use of the DTI technique there is a general loss of integrity throughout the brain in severe TBI, particularly in frontal regions.
Last, there is a host of functional imaging methods, dis-cussed in Chapter 6, Functional Imaging, that will be inte-grated with structural imaging in the future for the detec-tion of objective abnormalities that can be related to the neuropsychiatric state of the patient after a brain injury.
Clinical Rating of Scans
alized cerebral atrophy (note the ventricular dilatation and corpus callosum atrophy). Neuropsychologically, the patient manifested significant deficits in memory and ex-ecutive function.
Examples of the susceptibility of WM pathology in TBI have been demonstrated throughout this chapter as well as
elsewhere (Goetz et al. 2004; Graham et al. 2002). When MR imaging detects WM pathology, characteristic signal differences are present depending on the image sequence used (see Table 5–2). WM pathology, regardless of its etiol-ogy, is the basis of a wide variety of neuropsychiatric disor-ders (Filley 2001; Litcher and Cummings 2001). Simple rat-F I G U R E 5 – 1 6 . Clinical rating of cerebral atrophy.
In these images, left is on left. This patient sustained a severe TBI caused by a fall from a roof. As shown in A, the day-of-injury (DOI) computed tomography (CT) bone window clearly shows the location of a linear skull fracture (arrow) just beneath where major extracranial trauma occurred (note swelling in both A and B) as a result of blunt impact associated with the fall. On admission, the patient had a Glasgow Coma Scale score of 5. B: The clinical DOI CT scan showing the location of an epidural hematoma (bottom arrow) and massive swelling about the head (top arrow). Parts D (fluid-attenuated inversion recovery image) and E (T1 image) show the chronic effects of this injury manifested by ventricular dilatation as well as other pathology. As shown in B, the left aspect of the lateral ventricle is effaced by expanding pressure over the left hemisphere because of the hematoma and lateralized intraparenchymal edema. Nonetheless, even though the ventricle is distorted and some cerebrospinal fluid is displaced to the right lateral ventricle, the original size of the lateral ventricle can still be assessed in this DOI scan. Comparing ventricular size in the DOI scan in B with that shown in D and E, the follow-up magnetic resonance imaging clearly shows ventricular dilatation. E clearly shows the asymmetry of the lateral ventricle on the left, which represents some degree of hydrocephalus ex vacuo affected by volume loss of the major frontal lesion, shown in both D and E. Part F depicts the three-dimensional dorsal view of the lateral ventricle, which clearly shows general dilatation of the ventricular system. Note that the ventricle is nonspecifically expanded in F, a reflection of global volume loss seen in TBI. Also, note in C that temporal horns of the lateral ventricle are not visualized. This is common in moderate to severe TBI because of bilateral temporal lobe edema. In F, the temporal horns (arrows) are visible and dilated, an indication of temporal lobe atrophy that occurred over time from the DOI scan. Last, note that in D–F the ventricle is slightly asymmetric in its enlargement, reflective of the more lateralized damage to the left hemisphere.
ing methods for WM pathology were first used in aging and dementia (Victoroff et al. 1994) as well as in disorders such as multiple sclerosis and anoxic brain damage (Parkinson et al. 2002) that more selectively damage WM. More recently, these methods have been applied to TBI (Hopkins et al.
2003). When WM abnormalities are identified, they are rated on a four-point scale (same categories as the atrophy ratings given in the preceding paragraph) on the basis of their location and size. Much of the WM literature shows that damage to the periventricular region tends to be more disruptive of neurobehavioral and neurocognitive function by interrupting long coursing tracts that participate in inte-gration of function and speed of processing. Lesions more in the region of the centrum-semiovale may be more locally disruptive of function than productive of more global defi-cits (Bigler et al. 2002b, 2003). Figure 5–18 demonstrates a case of WM pathology and its rating and relationship to neuropsychological outcome in an older adolescent who sustained severe TBI in a head-on motor vehicle collision.
The last point to make is that in TBI, damage can oc-cur anywhere in the brain and be manifested in numerous
ways on neuroimaging studies. As a quick guide to the cli-nician, one should first view the brain for any differences in normal symmetry or obvious abnormalities or devia-tions from normal. Next, viewing the midsagittal view of the corpus callosum provides a quick reference regarding general WM integrity. Figure 5–5 provides a nice refer-ence of how normal symmetry should look, and Figure 5–8 shows an atrophic corpus callosum contrasted with a normal-appearing one. Next, viewing the ventricular sys-tem and cortical sulcal widths offers a quick reference of the degree of generalized atrophy. The third ventricle is particularly susceptible to enlargement in TBI, and clini-cal rating methods for such enlargement have been pub-lished by Groswasser et al. (Groswasser et al. 2002; Re-ider-Groswasser et al. 2002). Temporal horn dilation is often not only a sign of temporal lobe atrophy but also of atrophy of the hippocampus and amygdala (Bigler et al.
2002a). By reviewing the location and degree of the struc-tural imaging abnormality, the clinician may use that in-formation in the neuropsychiatric assessment, care, and treatment of the patient with TBI.
F I G U R E 5 – 1 7 . Temporal and frontal lobe clinical rating.
These ratings are based on Victoroff et al.’s (1994) method of lobular rating, again using a 4-point scale (0 = no atrophy, 0.5 = mild, 1.0
= moderate, and 2.0 = severe). These are all T1 images obtained approximately 3 years postinjury. Part A represents an axial view in which the red line shows the plane of the coronal cut, which is also reflected in D (vertical red line). The coronal plane is used for rating temporal lobe atrophy, as shown in B. The temporal lobe region rated is highlighted in C. There is marked temporal horn dilation, increased cerebrospinal fluid signal, and volume reduction noted in the temporal lobe rated (temporal atrophy rating = 2). Frontal atrophy is rated in the axial plane as shown in E, focusing on the anterior region of the frontal lobe as highlighted in F. The horizontal line shown in D shows the level of the axial cut in E and F. Attention is directed to the width of the frontal gyri and prominence of the interhemispheric fissure. The frontal atrophy rating is 2. Increased ratings of frontal or temporal atrophy are associated with deficits in cognitive ability, particularly short-term memory, attention/concentration, and executive function (see Bergeson et al. 2004).
F I G U R E 5 – 1 8 . White matter (WM) abnormalities and traumatic brain injury (TBI).
In these images, left is on left. As shown in the figures that are part of Table 5–3, different MR imaging sequences are sensitive to different aspects of WM damage. For clinical rating, the Victoroff et al. (1994) method is again used but is adapted to include fluid-attenuated inversion recovery image (FLAIR) and gradient recalled echo sequences. Lesions are “quantified” by their size and loca-tion. No lesion is rated as 0, small as 0.5, medium as 1.0, and large as 2.0. More explicit details for rating can be found in Parkinson et al. (2002). In the Victoroff et al. (1994) study, the WM lesions were hyperintense, or white, because they used T2- and proton density–weighted MR images. This is also true on the FLAIR sequence, but often these WM shear lesions are also associated with hemosiderin deposits, which classify oppositely as hypointense, or black. As shown in this illustration, the images at the top depict the boundaries for lesions within the periventricular (PV) area, defined by Victoroff et al. (1994) as hyperintensities hugging the ventricle. The image used (see A in the FLAIR sequence and B in the T2 sequence) is typically at the body of the lateral ventricle where the dorsal aspect of the head and body of the caudate nucleus can be visualized (partly identified by the white box). The centrum semiovale (CS) region is taken at a similar level to that for the lateral ventricle but is defined as residing outside the WM adjacent to the ventricle, which defines the PV region. The TBI patient in C (FLAIR) and D (T2) shows extensive white matter lesions in the CS region. Because the WM pathology seen in TBI may be more widely distributed than that observed in some other disorders, this rating method can be applied to any region of the brain or could be done lobe by lobe. The clinician using these rating methods should refer back to Victoroff et al.’s (1994) original for the standard comparisons as referenced for rating pathology. The Victoroff et al. (1994) method for rating WM hyperintensities can be adapted for use in rating WM pathology in TBI (Hopkins et al. 2003).
The patient shown in A and B is an adolescent female (the same FLAIR and T2 scans appear in Table 5–3) who sustained a severe TBI in a high-speed rollover motor vehicle accident. There is an obvious large residual hemorrhagic cortical contusion in the frontal region (arrow) that represents a mixture of gliotic tissue, old blood (hemosiderin), and cerebrospinal fluid (CSF). Note the ventricular asymmetry, particularly the expansion toward the lesion. In rating PV lesions, the signal intensity involving the WM that “hugs” the ventricle is rated. The signal intensity is abnormal in the box on the left that highlights the anterior aspect of the lateral ventricle in comparison with the box on the right. Note that the FLAIR sequence better defines the abnormality than the T2 image of this subject.
The WM rating abnormality is 1.0. The patient whose images are shown in C (FLAIR) and D (T2) also sustained a severe TBI after being ejected from a vehicle after impact. Extensive CS WM lesions are present that are rated as 2.0. A third patient is depicted in F–H who sustained a severe TBI as a consequence of a head-on collision. Initial CT imaging demonstrated numerous bilateral frontal petechial hemorrhages, the largest one located where the residual focal shear lesion is identified (arrow) in the T1 image (E). The FLAIR sequence (G) shows both PV and CS WM abnormalities, which can also be seen in the T2 image, although they are not always prominent there. The shear lesion has left a cavitation within the WM that has filled with CSF. The clinical rating in this patient is 1.0 for both PV and CS regions.
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