Male, 64 years old, with GBM, findings on recent prior exam concerning for stroke and for disease progression, but post contrast images were technically inadequate. Repeat post contrast imaging is requested along with further evaluation of suspected stroke and tumoral changes. Again seen is evidence of left anterior temporal tumor resection. Enhancing tissue immediately surrounding the resection cavity has not significantly changed from the immediate prior examination. However, it is more nodular when compared to prior examinations, particularly along the roof of the resection cavity where ill-defined enhancement tracts along and may even encase the left MCA. More posteriorly along the left temporal lobe, nodular cortically based or extra-axial enhancement has increased in size now measuring up to 18 mm in length, previously 8 mm. In addition, there is a band of thickened and faintly enhancing white matter along the lateral aspect of the left temporal horn which has progressed from the prior examination. Also noted is a new 6 mm focus of enhancement at the posterior aspect of the left gyrus rectus.rCBV mapping demonstrates elevated blood volume which correlates with the progressive nodular enhancement along the left lateral temporal lobe. Elevated blood volume is also seen in the thickened tissue along the lateral aspect of the left temporal horn.Single voxel spectroscopic assessment of the enhancing nodule demonstrates significant reduction of NAA and a modest elevation of the choline peak. More convincing, however, is the multi voxel assessment of the entire region which demonstrates reduced NAA and moderately elevated choline in the white matter surrounding the enhancing nodule.Signal abnormality correlating to the suspected infarct involving the left basal ganglia and overlying white matter is again seen. No part of this lesion demonstrates true enhancement. The apex of the lesion again shows intrinsic T1 hyperintensity.MRA images are degraded by motion artifact. Nevertheless, it does appear that the left MCA is narrowed through most of its M1 segment as it passes along the roof of the resection cavity. This is the same area that appears to be encased by enhancing tissue, and stenosis in this segment correlates with the patients lenticulostriate stroke. The visualized left MCA distal branches are also of somewhat smaller caliber than the right. There may be some narrowing of the supraclinoid right ICA, but the right MCA vessels are free of significant stenosis. The posterior circulation is also free of significant stenosis.On perfusion imaging, the area of left basal ganglia and periventricular infarct demonstrates expected matched deficits of cerebral blood volume and cerebral blood flow. In addition, however, mean transit time and time to peak are significantly elevated through a large portion of the left MCA territory which corroborates the MRI and MRA findings of left M1 stenosis.
Since the prior examinations, an enhancing nodule which may be cortically based or leptomeningeal along the left posterolateral temporal lobe has increased in size. In addition, there is progressive ill-defined thickening and enhancement in the adjacent white matter tracking along the lateral surface of the left temporal horn. There is also a new small focus of enhancement along the left gyrus rectus. The enhancing nodule and the surrounding abnormal white matter both demonstrate spectroscopic and rCBV evidence of tumor, and as such these findings are favored to represent progressive disease over treatment effect.Ill-defined somewhat nodular enhancement along the roof of the left anterior temporal resection cavity is stable when compared to the immediate prior examination, but progressed when compared to older exams. This enhancing tissue tracks along and appears to encase the left M1 MCA.MRA imaging demonstrates narrowing of the left M1 MCA as it passes along the roof of the resection cavity. The possibility is raised that the enhancing tissue which surrounds the vessel in this area may represent tumor which is either extrinsically compressing or possibly invading the vessel. In corroboration, there are perfusion findings which indicate vascular compromise in the left MCA distribution. As such, the patient may be at risk for additional ischemic events.