Slurred speech. Progressive neurological symptoms.Additional clinical history from electronic medical records: PMH of stroke, HTN, DM2, OSA, prostate cancer (s/p radioactive seed implantation), who presents for alternate opinion of chronic progressive blurry vision, dizziness, gait imbalance. Main differential consideration is demyelinating process. Less likely considerations are ischemic neoplastic. CSF protein elevated to 85.3 on 4/29/16. The study is overall at least mildly limited by patient motion. The postcontrast images are markedly limited by motion.Multifocal T2/FLAIR hyperintensity are present in the cerebral white-matter, many new since the prior outside exam. The lesions are predominantly frontal in distribution. Similar lesions are present also in the corpus callosum anteriorly. Some of the lesions are round and relatively well-defined. Similar signal abnormality lesions are present in the midbrain, middle cerebellar peduncles, left superior cerebellar peduncle, and the cerebellum. Some of the lesions are associated with expansion, for example the lesions involving the cerebellar peduncles, especially a the small lesion involving the medial aspect of the left middle cerebellar peduncle with mass effect upon the fourth ventricle, which is new since April 2016. Many of the supratentorial and infratentorial lesions are associated with patchy, non-masslike contrast enhancement, while some of the lesions show more nodular contrast enhancement. FLAIR imaging shows increased signal along the superior vermian interfolial spaces, which may reflect leptomeningeal involvement.A few of these lesions are new compared to the prior examination of April 2016; such as the lesions involving the left cerebellum, left anterior corpus callosum, and left frontal operculum. There is also a smaller right temporal lobe lesion. These new lesions are the ones that show more intense, nodular contrast enhancement. Many of these lesions are new compared to the more remote prior examination from January 2016 and June 2015. Over the same time course, few of the lesions have shown improvement. For example, in January 2016, there was extensive involvement in the occipital lobes and the splenium of the corpus callosum, which is now partially resolved. There is no acute infarct or intracranial hemorrhage. There is mild dilatation of the lateral and third ventricles, probably from volume loss. The sulci are also mildly enlarged. There is no midline shift or brain herniation.There is no destructive skull lesion. There is mild scattered mucosal thickening in the paranasal sinuses.
1.The examination is limited by motion, especially the postcontrast images.2.Relatively extensive white-matter lesions, predominantly in frontal, corpus callosal and brainstem/cerebellar peduncle distribution. The lesions show patchy and nodular contrast enhancement and no diffusion restriction. There is also suggestion of leptomeningeal involvement. While there has been an overall progressive course, compared to the previous MRIs as remote as March 2015, few of the lesions did actually improve, reflecting the waxing and waning but overall progressive nature of the disease. This pattern would be most compatible with an inflammatory/demyelinating disorder. Vasculitis/angiitis and demyelinating disorders are the more likely differential diagnoses. A neoplastic process would have a more progressive course. Within this vascular/inflammatory/demyelinating differential, the frontal involvement can be suggestive of CADASIL, however the lack of significant anterior temporal lobe involvement would be atypical. For Susac syndrome, clinical correlation to assess for retinal artery branch involvement and sensorineural hearing loss can be helpful. 