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Clinical History:  Neurofibromatosis 1.  Follow up study.

Technique:  MRI of the brain is performed on the 1.5 Tesla scan utilizing sagittal T1, axial TSE T2, axial FLAIR, axial MT, axial diffusion and post-contrast axial T1 images of the brain.  In addition, thin-section images through the orbits were obtained with axial T1, axial and coronal TSE T2, and post-contrast axial and coronal T1 sequences.

Comparison:  MRI brain and orbits 8/26/04

Findings:  compared to the prior study there is a change in the appearance of the large hypothalamic/chiasmatic mass lesion.

There remains a large mass in the region of the hypothalamus and optic chiasm which demonstrates heterogeneous signal.  There is an increase in the size of the nonenhancing cystic/semisolid components within the mass especially posteriorly and along the right lateral margin.  There has been a change in the enhancement pattern also.  Some of the thick, nodular enhancing areas which were noted on the prior study are not visualized on the current study.  The largest AP dimension of this mass is approximately 4.7 cm.  The largest cranio-caudad dimension of this mass is approximately 3.4 cm.  The largest transverse dimension of this mass is approximately 3.3 cm vs 3 cm on the previous study.  There is mild interval increase in the transverse dimension of the mass.  However the overall size of the mass in the AP and craniocaudal dimensions remains almost unchanged.

The large hypothalamic/chiasmatic mass is seen again to displace the carotid arteries slightly laterally and anteriorly, to deviate the A1 segments of the anterior cerebral arteries anteriorly, to widen the interpeduncular cistern, and to push upward on the third ventricle and downward on the pituitary gland.  The chiasm itself cannot be distinguished from this mass.  This mass demonstrates heterogeneous but avid contrast enhancement, including ring enhancement around the central portions (low on T1 and high on T2) of the mass

Stable scattered foci of T2 hyperintensity are noted in the bilateral medial temporal lobes, glovi pallidus and thalami, in keeping with spongiform dysplasia of neurofibromatosis.  There is mild asymmetry noted in the hippocampi with a larger right hippocampus demonstrating mild T2/flair hyperintensity.  The prominent extaaxial CSF spaces/arachnoid cysts seen anterior to the temporal remain unchanged.

There remains moderate expansion of the pons, greater on the left than the right, with increased T2 and decreased T1 weighted signal and extension into the cerebellar and cerebral peduncles bilaterally.  The signal abnormality also extends into the cerebellar hemispheric white matter (more so on the left than on the right), and inferiorly into the medulla.  No significant enhancement is seen in this region.

The lateral ventricles are normal in size and configuration.  As noted, there is mass effect upon the third ventricle, although the aqueduct and fourth ventricle appear normal.  There is no extraaxial fluid collections.  There is no intracranial hemorrhage.

There remains marked expansion and tortuosity of the intraorbital optic nerves, greater on the left than the right.  The left optic nerve demonstrates stable enhancement following gadolinium administration.  There is minimal interval increase in the thickness of the intraorbital portion of the right optic nerve.  

The major intracranial vessels are patent.  New left maxillary sinus mucosal thickening is noted.  The remainder of the paranasal sinuses and mastoid air cells are grossly unremarkable.  

Impression:    Interval increase in size of the large hypothalamic/chiasmatic mass, especially in the transverse dimension, and change in the morphology and enhancement patter, as detailed. Spongiform changes of neurofibromatosis are seen within the bilateral medial temporal lobes, globi pallidus, thalami, midbrain, pons and the cerebellum, stable.  The pons remains prominently asymmetric and therefore closer follow-up is recommended to exclude the possibility of a low grade glioma. Minimal interval increase in the thickness of the intraorbital portion of the right optic nerve.  Stable change of NF 1 in the left optic nerve.


Clinical History:   NF-1 with hypothalamic and optic nerve gliomas.  Follow-up examination.

Technique:  ORBITS:  Thin sagittal and axial T1, thin axial and coronal turbo spin echo T2 with fat saturation, and after uneventful intravenous contrast administration, axial and coronal thin post gadolinium T1 weighted images with fat saturation.  BRAIN:  Axial magnetization transfer, axial turbo spin echo T2, axial flair with fat saturation, axial post gadolinium T1weighted images using magnetization transfer and fat saturation, and echo planar diffusion weighted imaging with additional ADC maps obtained.

Comparison:  MRI 11/9/04

Findings: 

Since the prior MRI examination there has been no significant change in the overall size of the heterogeneously enhancing mixed solid and cystic hypothalamic glioma.  This glioma exerts stable mass effect on the surrounding structures with stable splaying of the supraclinoid internal carotid arteries and cerebral peduncles.

Following gadolinium administration, however, the components of the tumor that enhance have decreased in size both anteriorly and posteriorly.

We note progressive asymmetry of the pons, the left side being larger than the right side, increased since the prior examination.  No enhancement is identified in this region.

Stable spongiform changes are again noted.

There is stable tortuosity of the intraorbital optic nerves with stable enhancement noted on the left anteriorly.

The ventricular system remains stable with no evidence of hydrocephalus.  There is no evidence of an acute infarction or extraaxial collection.

The intracranial flow voids are normal.

Minimal bilateral ethmoid air cell mucosal thickening is noted.  Minimal left mastoid air cell opacification is identified.

Impression:   

No change in the overall size of the hypothalamic glioma with interval decrease size of the enhancing anterior and posterior components of the tumor.

Increased prominence of the pontine glioma on the left.

Stable optic nerve gliomas.


Clinical History:   NF-1 with hypothalamic and optic nerve gliomas.  Follow-up examination.

Technique: 

ORBITS:  Thin sagittal and axial T1, thin axial and coronal turbo spin echo T2 with fat saturation, and after uneventful intravenous contrast administration, axial and coronal thin post gadolinium T1 weighted images with fat saturation. 

BRAIN:  Axial magnetization transfer, axial turbo spin echo T2, axial FLAIR with fat saturation, axial post gadolinium T1weighted images using magnetization transfer and fat saturation, and echo planar diffusion weighted imaging with additional ADC maps obtained.

Comparison:  MRI 1/11/05

Findings: 

Since the prior MRI examination there has been no significant change in the overall size of the heterogeneously enhancing mixed solid and cystic hypothalamic glioma.  This glioma exerts stable mass effect on the surrounding structures with stable splaying of the supraclinoid internal carotid arteries and cerebral peduncles.

Following gadolinium administration the component of the tumor that enhances appears to have minimally decreased in size posteriorly.

We note progressive asymmetry of the pons, the left side being larger than the right side, not significantly changed since the prior examination.  No enhancement is identified in this region.

Stable spongiform changes are again noted.

There is stable tortuosity of the intraorbital optic nerves, with nodular enhancement noted on the left anteriorly.

The ventricular system remains stable with no evidence of hydrocephalus.  There is no evidence of an acute infarction or extraaxial collection.

The intracranial flow voids are normal.

Minimal bilateral ethmoid air cell mucosal thickening is unchanged.

Impression:   

1. Stable overall size of the hypothalamic glioma, with probable minimal decrease in size of the posterior cystic component.

2. Stable pontine glioma on the left, without contrast enhancement.

3. Stable optic nerve glioma.

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