Assessment of Neuropathology

The assessment of neuropathology after pediatric TBI involves a variety of neurological and neurora-diological procedures. Neurological examinations are often conducted during the acute stage of recovery to document changes in level of consciousness (i.e., changes in Glasgow Coma Scale scores) and focal neurological signs (Miller 1991; Vincent and

Table 27-2. Glasgow Coma Scale




Eye opening



Not attributable to ocular swelling

To pain


Pain stimulus applied to chest or limbs

To speech


Nonspecific response to speech or shout



Eyes open; does not imply intact awareness

Motor response

No response





Decerebrate posturing

Abnormal flexion


Decorticate posturing



Normal flexor response; withdraws from pain stimulus

Localizes pain


Pain stimulus applied to supraocular region or fingertip; limb attempts to remove it

Obeys command


Follows simple commands

Verbal response

No response


No vocalization



Vocalizes but not recognizable words



Intelligible speech but no sustained or coherent conversation; may be shouting or swearing



Responds to questions but is disoriented



Normal orientation to time, person, place

Note. Glasgow Coma Scale = eye opening score + motor response score +verbal response score. Source. Adapted from Teasdale and Jennet 1974.

Berre 2005). Computed tomography (CT) is the preferred method of neuroimaging during the acute phase of TBI because it is rapidly and widely available, relatively inexpensive, and sensitive to lesions such as epidural hematoma that may necessitate neurosurgical intervention (Bigler 1999; Poussaint and Moeller 2002). CT is used to detect hemorrhage, pneumocephalus, hydrocephalus, midline shift, mass effect, ischemia, and herniation. Magnetic resonance imaging (MRI) is superior to CT in documenting most pathology associated with TBI because it possesses superior sensitivity and specificity to abnormalities in brain structure and function (Poussaint and Moeller 2002). MRI is superior to CT in documenting both focal lesions and diffuse axonal injury and particularly the subacute and chronic changes that can occur across time (Bigler 1999; Sigmund et al. 2007).

Numerous advanced imaging procedures have been developed to assess neuropathology in TBI. An extensive review of these methods is beyond the scope of this chapter but can be found in the literature (see Ashwal et al. 2006; Bigler 1999, 2005; Munson et al. 2006). Techniques such as functional MRI, proton magnetic resonance spectroscopy, positron emission tomography, and single-photon emission CT allow the correlation of neuropsycho-logical functions with imaging results in order to assist with documenting neuropathology and predicting outcomes (Munson et al. 2006). Diffusion-weighted magnetic resonance images hold potential for the early detection of ischemic injury (Ashwal et al. 2006) and generally may be more sensitive to pathology than standard MRI (Bigler 1999). Diffusion tensor imaging is a specific form of diffusion-weighted MRI and is an emerging technology that documents white matter tracts (Ashwal et al. 2006). Magnetic resonance spectroscopy measures metabolic information, potentially providing TBI bio-markers (Ashwal et al. 2006; Bigler 1999).

Diagnostic procedures are also available to document cerebral electrophysiology following TBI.

Standard electroencephalography is relatively limited in detecting changes after TBI (Arciniegas et al. 2005). In contrast, evoked potentials, particularly somatosensory evoked potentials, have been found to be a predictor of TBI outcomes (Carter and Butt 2001). In one study, brain stem auditory evoked potentials were found to add significant prognostic value when used in addition to Glasgow Coma Scale scores and standard electroencephalography in predicting coma outcome following severe pediatric TBI (Liesiene et al. 2008).

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