Search

Few studies have examined the consequences of alcohol and drug abuse on TBI though they commonly co-occur. Both TBI and substance abuse independently result in neuropathological changes in the brain such as ventricular enlargement and cortical atrophy, thus it is reasonable to hypothesize that the combination of the two would result in more significant cerebral damage. In this study, 3 groups of patients—traumatically brain injured (TBI) with substance abuse (N = 19), TBI without substance abuse (N = 19), and substance abuse with no TBI (N = 16)—were compared with normal controls (N = 20) on several quantitative MRI (QMRI) measures. Since TBI most frequently occurs in older adolescents and young men, we examined only male participants between 16 and 30 years of age. Comparing young substance abusers to controls resulted in no QMRI differences. When controlling for head injury severity, the effects of substance abuse in combination with TBI resulted in greater atrophic changes than seen in any other group. TBI and substance abuse patients' neuropsychological test performances also were examined, and no differences were found among patient groups on any measures. These findings have implications for the deleterious interaction of substance abuse combining with TBI to result in greater neuropathological changes that can be detected by QMRI techniques. (JINS, 1999, 5, 593–608.)

This study quantified lesion volume in relation to damage location and executive functioning in traumatic brain-injured (TBI) patients. Magnetic resonance (MR) scans of 68 TBI patients were analyzed by taking volumetric measures of lesion sites. Patients were grouped according to the presence/absence of frontal lobe lesions. Measures of frontal lesion volume were studied as predictors for outcome on designated tests of executive functioning (Halstead Category Test and Wisconsin Card Sorting Test). Results showed no significant differences in level of deficit between groups. In addition, no significant differences were found between groups on other tests of neuropsychological functioning (Trail Making Test, Parts A and B, and Wechsler Adult Intelligence Scale-Revised). These results suggest that tests that are traditionally used to detect "frontal lobe" damage may not be adequate for distinguishing specific frontal lobe dysfunction, and do not add anything unique about frontal lobe integrity and neuropsychological functioning in TBI patients.

The possibility of a 'subcortical' syndrome differentially affecting memory in traumatic brain injury (TBI) subjects was examined. Magnetic resonance imaging scans of 46 traumatic brain injured male patients were compared with those of 34 male control subjects. Surface area measurements of the corpus striatum were calculated for both groups. Results demonstrated no significant differences in corpus striatum surface area measurements. Additionally, TBI patients were grouped according to severity of injury, as well as degree of corpus striatum atrophy, and neuropsychological outcome was examined. There were modest (r = 0.35) but significant correlations between corpus striatum degeneration and the delayed recall trial and total score of the Rey Auditory Verbal Learning Test, but no other correlations between neuropsychological and corpus striatal surface area were significant. Because subcortical pathology may have a differential effect on memory, recognition and recall memory were further analysed, but no significant differences were found. TBI subjects with the smallest corpus striatum values did not test significantly different from TBI patients with normal corpus striatum values or differences in cortical atrophy, as determined by a ventricle-to-brain ratio. These findings suggest that there is not a unique pattern of subcortical pathology involving the corpus striatum in TBI.

Magnetic resonance (MR) scans of 63 traumatic brain injury (TBI) patients were analyzed to examine the relationship between injury severity, lesion volume (nonthalamic cortical/subcortical lesions), ventricle-to-brain ratio (VBR), and thalamic volume. For comparison, 33 normal control subjects were used. Patients with visible nonthalamic structural lesions showed significantly smaller thalamic volumes than patients without visible lesions or control subjects. Results also indicated that patients with visible lesions had significantly more severe injuries than patients without lesions. Patients with moderate-severe injuries had significantly smaller thalamic volumes and greater VBRs than patients with mild-moderate injuries. Although several variables related to thalamic volume, the presence of nonthalamic lesions was sufficient to result in smaller thalamic volume. Decreased thalamic volume following head injury suggests that subcortical brain structures may be susceptible to transneuronal degeneration following cortical lesions, and that this can be detected by in vivo MR-based volumetric analysis.

Without controversy, magnetic resonance (MR) imaging achieves exquisite approximation of gross anatomy. This has been appreciated from the onset of the se of MR technology to image the brain. However, what has been clinically lacking in the first decade of MR use is a rapid yet automated means to quantify various neuroanatomic structures. As such, much of the interpretation of MR imaging has been based primarily on a qualitative rather than quantitative analysis (see Osborn, 1994).

Significant anoxia may cause a variety of neuropathologic changes as well as cognitive deficits. We have recently seen 3 patients who have suffered severe anoxic episodes all with initial Glasgow Coma Scores (GCS) of 3 with sustained coma for 10–14 d. All 3 patients had extended hospitalizations and rehabilitation therapy. A neuropsychological test battery was administered and volumetric analyses of MRI scans were carried out in each case at least 6 mo postinjury. Two of the patients display distinct residual cognitive and neuropathologic changes while 1 patient made a remarkable recovery without evidence of significant morphological abnormality. These three cases demonstrate, that even with similar admission GCS, the outcome is variable and the degree of neuropsychological impairment appears to match the degree of morphologic abnormalities demonstrated by quantitative MR image analysis. An important finding of this study is that even though subjects with an anoxic insult exhibit severe cognitive and memory impairments along with concomitant morphologic changes, their attention/concentration abilities appear to be preserved. MR morphometry provides an excellent means by which neural structural changes can be quantified and compared to neuropsychological and behavioral outcomes. (JINS, 1995, I, 501–509.)

Day-of-injury computed tomographic scans were compared with postinjury magnetic resonance imaging of 38 patients with traumatic brain injury. Ventricles and several white and gray matter structures were measured. Results demonstrated significant changes in ventricular sizes and all measures of white matter. Changes in gray matter were nonsignificant, except in the putamen/globus pallidus. Patients were grouped according to ventricular change, and neuropsychological outcome was examined. The group with the highest ventricular change had significantly lower memory scores but did not show significant differences on tests of intellectual functioning. A three-dimensional image analysis was performed to enhance visualization of the injured brain.

Day-of-injury computerized tomography (CT) scans were compared to post-injury (at least 6 weeks) magnetic resonance (MR) imaging of 30 traumatic brain-injured (TBI) patients. Scans were matched as closely as possible at the head of the caudate nucleus (CN), a grey matter structure, and the anterior horns (AH) of the lateral ventricle. The CN and AH surface areas and width of the corpus callosum (CC), a white-matter structure, were measured. Results demonstrated a non-significant change in CN surface area, while AH showed a significant increase. CC showed a significant decrease in width. Lack of significant change in the CN, combined with a significant decrease in CC width, suggests that AH dilation is probably due to surrounding white as opposed to grey-matter atrophy.