7 9
an excellent clinical tool in determining the presence of treatable lesions, such as subdural hematoma (see Figure 5–1), and providing baseline information concerning the location and nature of pathological conditions such as cortical contusion, intraparenchymal hemorrhage, pete-chial hemorrhage, and localized or generalized edema.
CT is also excellent in detecting skull fractures and asso-ciated pneumocephalus, which may require surgical intervention. There is a direct relationship between CT imaging findings and the acute clinical status of the TBI patient, based on the Glasgow Coma Scale (GCS) score and other characteristics such as pupillary abnormalities, loss of consciousness (LOC), and posttraumatic amne-sia. There are also several CT rating scales available, but probably the most common is the Trauma Coma
Data-bank as outlined by Marshall et al. (1991) and presented in Table 5–1. What is important about this rating scale is that it provides a basis for evaluating the severity of injury during the acute stage. It also can provide a base-line for future monitoring of change over time (Vos et al. 2001), as is discussed in the section Relationship of Acute Computed Tomography Abnormalities to Reha-bilitation Outcome. Additionally, this scale overviews the common injuries observed in CT imaging of the acute TBI patient.
Relationship of Acute Computed Tomography Findings to Severity of Injury
The most clinically important aspect of acute CT imaging is the initial management, monitoring, and surgical intervention for any treatable lesion(s). Additionally, acute CT imaging of the TBI patient often provides more clinical information than what comes from the physical examination of the acutely injured patient, par-ticularly the patient with altered mental status. For example, the comatose patient may have no visible abnormalities on CT imaging, whereas the patient with only mild disorientation may be found to have signifi-cant CT abnormalities, some requiring emergent inter-vention. This is shown in Figure 5–2, which illustrates that the frequency of CT abnormalities, using the rat-ings outlined in Table 5–1, was associated with the GCS score (highest within 24 hours of injury) and LOC in 240 consecutively admitted rehabilitation patients (Big-ler et al. 2004). As can be seen, the entire gamut of CT abnormalities was observed in this large sample of TBI patients who had injuries sufficient to require hospital-ization, but the most common was a level II injury (see Table 5–1)—some mild edema; the presence of small, mostly petechial hemorrhages or contusions; and no mass effect. As for LOC, similar observations are made in Figure 5–2, which demonstrates that LOC of any duration was most likely to be related with a level II injury as well.
Relationship of Acute Computed Tomography Abnormalities to Rehabilitation Outcome
Despite the accuracy of CT in identifying gross structural pathology during the acute stage, such findings often do not relate well to the neurobehavioral outcome at the time of discharge from rehabilitation, which makes the accurate prediction of outcome from acute CT findings alone diffi-cult (Dikmen et al. 2001; Temkin et al. 2003). The excep-tion occurs with patients who have brainstem lesions, because the presence of brainstem pathology typically relates to poor outcome. Using both the Disability Rating F I G U R E 5 – 1 . The axial section of a computed
to-mography scan of the head at the level of the lateral ventricles.
Obtained without the addition of contrast medium, this scan re-vealed four types of acute posttraumatic intracranial hemorrhages (left is on the reader’s right side): an epidural hematoma (thick white arrow) and a squamous temporal fracture (not shown) on the left side, a laminate subdural hematoma (thick black arrow) on the right side, right-sided periventricular and frontal lobe contu-sions containing an intraparenchymal hematoma (thin white ar-row), and a subarachnoid hemorrhage (thin black arrow) in the right frontal region. These injuries were sustained in a fall.
Source. Reproduced from Mattiello JA, Munz M: “Four Types of Acute Post-Traumatic Intracranial Hemorrhage.”
New England Journal of Medicine 344:580, 2001. Used with per-mission. Copyright 2001, Massachusetts Medical Society. All rights reserved.
Scale (DRS)1 and Functional Independence Measure (FIM)2 discharge scores, Bigler et al. (2004) demonstrated that the 240 TBI patients with CT ratings from no visible abnormality to discernible major abnormalities had similar rehabilitation outcomes (i.e., diffuse injury category I to category IV; see Table 5–1). This means that outcome is poorly predicted by just the acute injury characteristics seen on CT imaging performed on the day of injury (DOI).
This finding should come as no surprise, because it may take days to weeks to track the evolution of a lesion and months before stable degenerative patterns are established by neuroimaging findings ([Blatter et al. 1997; Shiozaki et al. 2001; Vos et al. 2001]; see section Relationship of Mag-netic Resonance Imaging Findings to Outcome for better predictors of rehabilitation outcome). As is shown later in
this chapter, the better predictor of long-term outcome comes from quantitative analysis of MR imaging done after 3–6 months postinjury, and these relationships are often enhanced by tracking changes in neuroimaging using the DOI CT scan. Accordingly, instead of using CT as an absolute predictor of outcome, it is often better to consider CT as a tool for establishing the baseline at the acute stage of injury and then tracking the injury with either CT or MR imaging at follow-up intervals.
Day of Injury as Baseline
Because the DOI scan is typically one of the first diagnostic tests run on the acutely injured TBI patient, it is performed early in the injury process. Because the morphological con-sequences from trauma take time to evolve, the DOI scan T A B L E 5 – 1 . Diagnostic categories of abnormalities visualized on computed tomography (CT) scan
Category Definition
1: Diffuse injury I (no visible pathology) No visible intracranial pathology seen on CT scan 2: Diffuse injury II Cisterns present with midline shift 0–5 mm and/or:
Lesion densities present
No high- or mixed-density lesion >25 cc May include bone fragments and foreign bodies
3: Diffuse injury III (swelling) Cisterns compressed or absent with midline shifts 0–5 mm, no high- or mixed-density lesion >25 cc
4: Diffuse injury IV (shift) Midline shift >5 mm, no high- or mixed-density lesion >25 cc 5: Evacuated mass lesion V Any lesion surgically evacuated
6: Nonevacuated mass lesion VI High- or mixed-density lesion >25 cc, not surgically evacuated 7: Brainstem injury VII Focal brainstem lesion, no other lesion present
Source. Adapted from Marshall LF, Marshall SB, Klauber MR, et al: “A New Classification of Head Injury Based on Computerized Tomography.”
Journal of Neurosurgery 75:514–520, 1991.
1Disability Rating Scale (DRS). The DRS consists of the following eight items and range of scores (0 = no disability): 1) eye opening, 0–3; 2) verbal response, 0–4; 3) motor response, 0–4; 4) cognitive ability in feeding, 0–3; 5) cognitive ability in toileting, 0–3; 6) cog-nitive ability in grooming, 0–3; 7) dependence on others, 0–5; and 8) employability, 0–3. A total DRS score is calculated by adding the scores for each of the eight items (see Rappaport et al. 1982). Hall et al. (1993) offered the following distinctions in considering the DRS score: 0 = no disability, 1 = mild disability; 2–3 = partial disability; 4–6 = moderate disability; 7–11 = moderately severe dis-ability; 12–16 = severe disdis-ability; 17–21 = extremely severe disdis-ability; 22–24 = vegetative state; 25–29 = extreme vegetative state; and 30 = death. For the purposes of comparing DRS admission and discharge findings by ventricle to brain ratio outcome, DRS scores were combined as follows: 0 = no disability; 1–3 = mild disability; 4–11 = moderate disability; 12–21 = moderately severe disability;
and 22+ = extremely severe-vegetative (see Figure 5–11).
2Functional Independence Measure (FIM). The FIM (State University of New York at Buffalo Department of Rehabilitation Medicine 1990) is an 18-item, 7-level ordinal scale that can be used to assess level of function at time of admission to and discharge from a rehabilitation unit. It is a general tool for all types of rehabilitation patients and has been successfully used in TBI (Hamilton et al.
1987). The version used in this study was the 3.1 version. By virtue of its ordinal scale, the lowest score is 7 and the highest is 126.
often provides important baseline information. This is dem-onstrated in Figure 5–3, which depicts a 3-year-old restrained passenger involved in a high-speed motor vehi-cle accident. The DOI scan demonstrates a right intra-parenchymal hemorrhage in the region of the internal capsule-putamen. The anterior horns of the lateral ventricu-lar system can be identified on the DOI scan, but cortical sulci are not well visualized, which can be a sign of general-ized edema. By 2 days postinjury, there is definite generalgeneral-ized cerebral edema with obliteration of the ventricular system—
a clear sign of massive cerebral edema. One year later, there is global atrophy manifested by generalized ventricular dila-tation, prominent cortical sulci, and a large cavitation in the right basal ganglia area—–a consequence of the focal hemor-rhage. The hemorrhage likely resulted from shearing forces disrupting the deep vascular supply to the basal ganglia.
Limitations
The problem with all contemporary imaging methods is that they provide only a gross inspection of the macroscopi-cally visible brain, whereas most of the critical functioning is at the microscopic (neuronal and synaptic) level. For struc-tural imaging using CT or MR, detection of an abnormality is based on resolution measured in millimeters, whereas at the microscopic level the resolution of clinically significant abnormalities is measured at the micron level (Bain et al.
2001; Ding et al. 2001). Simply stated, a “normal” scan merely indicates that no visible macroscopic pathology was detected that reached a threshold of 1 mm or more. CT, or any other neuroimaging method, simply cannot answer the question of brain pathology below its level of detection. This circumstance is nicely demonstrated in Figure 5–4. The scan F I G U R E 5 – 2 . Computed tomography (CT)
over-view of 240 patients with traumatic brain injury (TBI).
The charts presented in this figure overview the acute CT of 240 TBI patients admitted to an inpatient rehabilitation facility by av-erage Glasgow Coma Scale (GCS) (A) and GCS frequency by CT classification (B), demonstrating that the most frequent CT abnor-mality was a diffuse injury II, which occurred with a near-similar frequency across all levels of severity; and loss of consciousness (LOC) by CT abnormality classification (C), demonstrating again that diffuse injury II was the most common classification wherein the majority of TBI patients experienced some LOC. Acute CT classification abnormalities are given in Table 5–1.
Source. Bigler ED, Ryser DK, Ghandi P, et al: “Day-of-Injury Computerized Tomography, Rehabilitation Status, and Long-Term Outcome as They Relate to Magnetic Resonance Imaging Findings After Traumatic Brain Injury.” Brain Impairment 5:S122–123, 2004.
A
B
C
represented in the middle of the figure is the acute DOI CT, interpreted as within normal limits, taken approximately 2 hours after injury (brief LOC, GCS score of 14 at the scene of a severe head-on high-speed motor vehicle accident; GCS score of 15 on hospital admission). The patient was also found to have a cervical fracture that was neurosurgically repaired, along with a large frontal scalp laceration. He was hospitalized for 4 days. He developed the typical constella-tion of postconcussive symptoms, including headache,
fatigue, irritability, some depression, and mild cognitive problems, which gradually but not completely abated over the next several months. He was able to return to work on a part-time basis, but he complained of problems of mental inefficiency and feeling “dull.” He was in excellent general health, but he unexpectedly experienced a spontaneous car-diac arrest while exercising and died 7 months postinjury, at which time a full brain autopsy was performed. Gross brain anatomy was normal, as shown Figure 5–4A, but histolog-F I G U R E 5 – 3 . Computed tomography scans from a 3-year-old male traumatic brain injury patient injured in a high-speed motor vehicle accident.
Right is on the reader’s left side. Day of injury (A). Note the right intraparenchymal hemorrhage and blood in the right Sylvian fissure.
However, in addition to these acute injury factors, note the size of the anterior horns of the lateral ventricle, which offer a baseline from which to monitor atrophic changes over time. By 2 days postinjury (B), there is severe cerebral edema, manifested by obliteration of cortical sulcal patterns, loss of definition between gray and white matter, and delineation of the anterior aspect of the interhemispheric fissure, along with collapse of the ventricular system. By 7 months postinjury (C), there is extensive atrophy noted by generalized ventricular dilatation, prominent cortical sulci, and the right Sylvian fissure. Also note the large cavitation left by the intraparenchymal hemorrhage. By viewing these different scans, an excellent picture of how the brain changes over time after an injury can be objectively established.
F I G U R E 5 – 4 . Findings in mild traumatic brain injury (TBI).
This patient sustained a mild TBI (admission Glasgow Coma Scale, 14) 7 months before an unexpected death from cardiac arrest. The ventral view of the intact brain at autopsy showed no cortical contusions or other gross abnormalities (A). Likewise, the computed tomog-raphy (CT) scan performed on the day of injury shows no abnormalities (B), again supporting the clinical view of no gross brain abnormal-ities. However, on microscopic examination, scattered hemosiderin (white arrow) deposits were observed, as shown in the histological section (C). These were most prominent in the white matter. This demonstrates microscopic abnormalities as a consequence of brain injury, even mild TBI, that are below detection by direct visual inspection of the brain using neuroimaging techniques (see Bigler et al. 2004).
B C
A
B C
A
ical examination demonstrated hemosiderin (a blood by-product)-laden macrophages and lymphocytes in the white matter (WM). Obviously, this finding suggests perturbation of brain microvasculature and WM injury that was well below the detection of the “normal” CT. Such microscopic lesions are undoubtedly the basis of many neurobehavioral sequelae associated with brain injury when imaging is “nor-mal.” This is further supported by the work of Gorrie et al.
(2001) who examined 32 children at postmortem who suc-cumbed to road accidents. With direct visual inspection, 17 of these TBI cases demonstrated no macroscopic abnormal-ities of the type that would be detected by CT imaging.
However, when viewed at ×100 magnification, all cases readily demonstrated microscopic injury.