May 26, 2009
FINDINGS: There are multiple punctate white matter foci of hyperintesity noted supratentorially in the corona radiata and centrum semiovale which in this 28-year-old young woman with family history of MS certainly is of concern for underlying demyelinating disease. These findings, however, are not specific and this also could represent sequela of migraines, inflammatory disease or vasculitis. The corpus callosum is not directly involved. No definite lesions are noted in the posterior fossa.
No other focal abnormalities are detected throughout. No diffusion abnormalities are seen. No evidence of intracranial hemorrhage, mass effect, or midline shift noted.
The visualized portions of the paranasal sinueses are unremarkable for significant inflammatory disease throughout. The visualized flow voids about the major Circle of Willis vessels reveal a dominant left vertebral artery without definitive visualization of the right vertebral artery, favor secondary to congenitally hypoplastic. Otherwise unremarkable flow voids at the base of the brain are noted.
IMPRESSION: Multiple scattered punctate foci of abnormal hyperintensity are noted in the white matter of the corona radiata and centrum semiovale which in this young 28-year-old woman certainly raises concern for possible demyelinating disease, especially in light of family history of MS. These are nonspecific findings, however, and could also represent sequela of migraines, vasculitis, or inflammatory disease. The MRI of the brain is otherwise unremarkable.
FINDINGS: No destructive bony lesions are identified within the calvarium or base of the skull. The craniocervical junction appears unremarkable. The soft tissues of the nasopharynx demonstrate mildly prominent adenoidal tissue, but are otherwise unremarkable. The sinuses appear clear. The mastoid air cells demonstrate no abnormal signal. The ventricles are normal in size without shift of midline structures. No intracranial masses, subacute intracranial hemorrhage or abnormal extaaxial fluid collections are seen. The midbrain, pons, medulla, and cerebellum are unremarkable as are the sella and suprasellar regions. Normal signal void is present within the bilateral internal carotid arteries, basilar artery and superior sagittal sinus.
Within the deep white matter of the brain are multiple small, rounded and some irregular foci of T2 prolongation within the corona radiata and centrum semiovale. These are not pericallosal or periventricular. Significant cerebral atrophy is not identified. The diffusion-weighted images demonstrate no areas of restricted diffusion to suggest acute ischemia.
IMPRESSION: Several scattered foci of T2 prolongation in the deep white matter of the brain with nonspecific distribution. This may represent sequelae of chronic microvascular ischemic disease, such as from migraine vasculopathy, vascuilitis, accelerated arthrosclerosis, such as from hypertension or diabetes. Demyelinating disease, such as multiple sclerosis, however, is also possible.
COMPARISON: Comparison is now made with previous MRI of the brain dated 8/01/03. The multiple deep white matter lesions are for the most part unchanged compared to the previous examination with the exception of one in the right coronal radiata of the posterior frontal lobe/anterior pareital lobe, which may be slightly larger on the current exam compared to the previous. No new deep white matter lesions are identified. The differential diagnosis remains that same.
FINDINGS: Again noted are multiple white matter hyperintensities on FLAIR imaging. These are stable with the exception of one of the larger lesions in the right periventricular white matter which is slightly larger. There is also a slightly more prominent left parietal lesions which appears more prominent. These are labeled #1 and #2 on the montage. The remaining white matter lesions are relatively stable. These had a similar differential diagnosis, as described previously, and include demyelinating disease, migraine vasculopathy, vasculitis changes, among other entitites. The callosal septal interface here is fairly spared but this does not exclude demyelinating disease.
The cerebellum and brainstem are unremarkable. The pituitary gland is unremarkable. There is normal flow void in the cerebral vasculature. The orbits are unremarkable. There is minimal mucus thickening in the right maxillary sinus. The VII/VIII cranial nerve complexes are symmetric.
CONCLUSION: Multifocal white matter hyperintensities bilaterally are nonspecific. Two of these are slightly more prominent compared to the previous study but the remaining lesions are all stable. The larger lesions are labeled #1 and #2 on the montage and are located in the right periventricular white matter and left pareital white matter, respectively. Differential diagnosis would have to include demyelination although these are certainly not at the callosal septal interface. Migraine vasculopathy, among other entities, are also in the differential diagnosis.