Imaging CBF and metabolism at rest reveals the cortical deafferentation that accompanies diffuse axonal injury (DAI). These studies cannot always distinguish between loss of inputs from corticocortical damage and from afferents that ascend through cerebral white matter. Identification of metabolically affected neural networks will provide insight into the causes of attentional, memory, and other cognitive and behavioral problems of patients with TBI. Resting metabolic studies that correlate rCBF with behavioral outcomes will help determine the likelihood of recovery at a particular point in time. In addition, activation studies can be designed to assess whether or not a patient is able to learn novel information or likely to benefit from a particular rehabilitative intervention.
Positron emission tomography has revealed focal and diffuse cortical hypometabolism in areas remote from, but transsynaptically connected to subcortical regions affected by DAI. Hyperglycolysis accompanies severe TBI in the first days,85 followed by a reduction in global glucose metabolism. Metabolic rates improve by 1 month after injury regardless of initial severity of injury, but functional outcomes do not necessarily improve, at least in a group of patients that did not have serial PET studies.86 Thus, PET scans of glucose metabolism may be rather unrevealing within a month of TBI, perhaps because of a ceiling effect of the measure in relation to severity of behavioral impairments.
Single photon emission computed tomography measures of diminished CBF show some general relationships to executive dysfunction and neurobehavioral impairments in more chronic TBI.87 Low flow in the thalamus correlates with greater cognitive and neurologic impairment. Low frontal CBF occurs with dis-inhibited behavior. Improvements in neu-ropsychologic test scores during rehabilitation correlates with increases in CBF by SPECT,88 although associations between rCBF changes and impairments are not demonstrated consistently. Hypometabolism in the limbic and par-alimbic areas, when MRI showed no lesion, correlated with poorer outcome on the Glasgow Outcome Scale (see Chapter 7).89
Regional cerebral glucose metabolism at rest and scores on a range of neuropsychologic tests were compared in 13 subjects who had a severe TBI a mean of 150 days earlier.90 No subjects had focal brain lesions. At the time of testing, only two had a good recovery on the Glasgow Outcome Scale. Cognitive and behavioural disorders correlated with decreased metabolism in the prefrontal cortex and cin-gulate gyrus. Impairments in memory and executive functions occurred with hypometabo-lism in the mesial and lateral prefrontal cortex and cingulate gyrus. Behavioral deficits correlated with mesial prefrontal and cingulate hy-pometabolism. As expected, BA 9 and 10 were most involved (see Chapter 1), especially in the left hemisphere for subjects with impaired verbal memory and attention/executive impairments. The bilateral dorsolateral prefrontal cortices were most hypometabolic in the most impaired subjects. Anterior cingulate dysfunction, which is essential for executive aspects of attention and goal-directed behavior, was prominent in the most disabled subjects. The investigators found no significant correlations between neuropsychologic scores and metabolism in the temporal, parietal, and occipital cortices or in subcortical regions.
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