Female, 84 years old, with altered mental status. Assess for leptomeningeal disease and brain metastases. Please note that this examination consists of primarily pre- and post contrast T1-weighted images as complete pre-contrast imaging was obtained for the brain and C spine recently, and due to patient request to terminate the exam early.Brain:A 2 mm focus of enhancement is seen within the right middle frontal gyrus which previously measured 3 mm. A very ill-defined 2-mm focus of enhancement within the left basal ganglia is also decreased size and conspicuity.Other small enhancing lesions noted on prior examinations are either undetectable or significantly reduced in conspicuity on the present study.No new enhancing lesions are detected. No mass-effect or parenchyma edema is suspected. No evidence of pathologic leptomeningeal or cranial nerve enhancement is seen.C-spine:Postcontrast images are significantly degraded by motion artifact. Within this limitation, no obvious spinal cord or leptomeningeal enhancement is seen. Bone marrow signal characteristics remain heterogeneous on T1-weighted images but without obvious pathologic enhancement. Multilevel cervical spondylosis is better assessed on prior imaging.T-spine:Postcontrast images are degraded by motion artifact as well as susceptibility in the upper thoracic region on the sagittal sequence. No obvious spinal cord or leptomeningeal enhancement is seen.The thoracic kyphosis is exaggerated. Vertebral body marrow signal characteristics are heterogeneous. No aggressive or worrisome areas of pathologic marrow enhancement are seen. Scattered small foci of enhancement within the upper thoracic vertebral bodies and within T8 are nonspecific. Mild scattered degenerative disk disease is seen without significant spinal canal or neuroforaminal stenosis.A right hilar mass is evident along with scattered additional areas of lung parenchymal nodularity and a small right pleural effusion.L-spine:Based on the number of rib bearing vertebral bodies, there appear to be 6 lumbar type vertebral bodies.The visualized spinal cord, conus and cauda equina are free of pathologic enhancement. No intraspinal masses are identified.T2 hyperintensity involving the marrow adjacent to the L5-6 (labeled L4-5 previously) endplates is again seen, particularly affecting the left aspect of L5 and the left L5 pedicle. Corresponding pathologic enhancement is also seen. The extent of this process is stable or at most mildly progressed relative to the prior examination from 1/1/15. As before, no evidence of pathologic epidural soft tissue or enhancement is seen. Mild inflammatory signal and enhancement is seen along the facets of the lower lumbar spine similar to prior. Mild enhancement seen along the L4 inferior endplate previously has resolved.Spondylosis is redemonstrated with disk bulging at every level. Disk degeneration is particularly severe at L5-6 where there is complete loss of disk height. Also noted is marked facet hypertrophy at lower lumbar levels. No significant interval change in the degenerative findings is seen in comparison with the prior examination.Resulting spinal canal stenosis at L4-5, and to a lesser degree at L5-6, does not appear to have significantly changed. Likewise marked foraminal narrowing at L3-4 on the right, L4-5 bilaterally, and L5-S1 on the left is also unchanged.Multiple renal cystic lesions are identified.
1.Interval resolution or reduction in size of several previously seen enhancing brain parenchymal lesions. No new lesions are detected, and there is no evidence to suggest intracranial leptomeningeal disease.2.Within the limitations of a significantly degraded examination, no clear evidence of leptomeningeal disease is seen in the spine, though image quality is not adequate to detect subtle abnormalities.3.Marked marrow signal abnormality and enhancement affecting the L5 and to a lesser degree L6 vertebral bodies (previously labeled as L4-5) is stable to most mildly progressed. Given the lack of any epidural or paraspinal soft tissue mass, the significant disk degeneration at this level, and the lack of convincing interval progression, findings are favored to represent reactive inflammation secondary to degeneration. Other etiologies including infection and metastatic disease, although not eliminated, are probably less likely.