Little background i went to my neuro for a 6 month checkup left eye was not tracking correctly as it was before so she ordered MRI to be done as precautionary. She called with these results on wednesday morning and is scheduling a lumbar puncture under sedation ASAP. she has told me to call her office immediately if i have any vision changes. I have advised her i get frequent pressure headaches, nothing severe but i know they are there type of thing. more annoying than anything else. eyes hurt when tired. i guess i am at a loss as to what is happening now. any one with any ideas? i know i will most likely need a neurosurgeon to follow now and possible surgery but i am just worried. I am currently a T6 incomplete para also.
MRI Brain with & without Contrast ***Final Report***
DATE OF EXAM: Dec 3 2019
MRI BRAIN W and W/O CON (Acc#:7412465):
EXAMINATION: Brain MRI without and with
HISTORY: New left cranial nerve VI palsy. Comment. Past medical history
with a question of multiple sclerosis in the past (never definitively
diagnosed). Question of spinal cord infarct with resulting paraplegia.
Baseline right eccentric osteopenia now with the left lateral rectus
palsy without signs of optic neuritis.
TECHNIQUE: An MS protocol MRI of the brain and internal auditory canals
was performed both before and after the administration of intravenous
contrast, as per the standard department protocol.
Contrast: 10 mL of Gadavist
COMPARISON: Head MRI dated May 14, 2015.
FINDINGS:
BRAIN MRI:
There are few nonspecific FLAIR hyperintensities within the left corona
radiata again noted.
The ventricles, sulci and cisterns are age-appropriate. There is no
mass-effect, midline shift, or space-occupying lesion. There is no
abnormal enhancement.
There is no hemorrhage or extra-axial fluid collection. There are
scattered susceptibility foci again noted noted within the right frontal,
left temporal, and right parietal lobes.
There is no decreased diffusion to indicate an acute infarct.
The principal intracranial flow voids are present.
There is a partially empty sella again noted.
There is mild prominence of the CSF space surrounding the optic nerves.
The orbits are otherwise unremarkable. The left eye is deviated medially
and compatible with history of left lateral rectus muscle palsy. There
are bilateral staphylomas.
The visualized paranasal sinuses and mastoid air cells are clear.
IAC MRI:
There is no abnormal signal within the brainstem specifically at the
pontomedullary junction. There is no abnormal enhancement along the
expected course of cranial nerve VI. The cavernous sinuses are normal in
appearance.
Cerebellopontine angles, internal auditory canals and inner ear
structures are unremarkable.
IMPRESSION:
Medial deviation of the left eye compatible with the history of left
lateral rectus palsy. No abnormal enhancement identified along the
expected course of cranial nerve VI bilaterally. Also, there is no signal
abnormality within the brainstem identified.
No acute/subacute infarct, hemorrhage, mass effect or abnormal
enhancement.
Redemonstration of a partially empty sella as well as mild prominence of
the CSF surrounding the optic nerves. Findings could reflect idiopathic
intracranial hypertension in the appropriate clinical setting.
Unchanged few scattered non-specific FLAIR hyperintensities in the left
corona radiata. Differential is broad and would include sequela of prior
infection/inflammation, sequela of chronic microangiopathy, or
vasculitis, amongst many others. Pattern not typical for demyelinating
disease.
Redemonstration of multiple susceptibility foci as detailed above likely
reflecting chronic microbleeds.
MRI Brain with & without Contrast ***Final Report***
DATE OF EXAM: Dec 3 2019
MRI BRAIN W and W/O CON (Acc#:7412465):
EXAMINATION: Brain MRI without and with
HISTORY: New left cranial nerve VI palsy. Comment. Past medical history
with a question of multiple sclerosis in the past (never definitively
diagnosed). Question of spinal cord infarct with resulting paraplegia.
Baseline right eccentric osteopenia now with the left lateral rectus
palsy without signs of optic neuritis.
TECHNIQUE: An MS protocol MRI of the brain and internal auditory canals
was performed both before and after the administration of intravenous
contrast, as per the standard department protocol.
Contrast: 10 mL of Gadavist
COMPARISON: Head MRI dated May 14, 2015.
FINDINGS:
BRAIN MRI:
There are few nonspecific FLAIR hyperintensities within the left corona
radiata again noted.
The ventricles, sulci and cisterns are age-appropriate. There is no
mass-effect, midline shift, or space-occupying lesion. There is no
abnormal enhancement.
There is no hemorrhage or extra-axial fluid collection. There are
scattered susceptibility foci again noted noted within the right frontal,
left temporal, and right parietal lobes.
There is no decreased diffusion to indicate an acute infarct.
The principal intracranial flow voids are present.
There is a partially empty sella again noted.
There is mild prominence of the CSF space surrounding the optic nerves.
The orbits are otherwise unremarkable. The left eye is deviated medially
and compatible with history of left lateral rectus muscle palsy. There
are bilateral staphylomas.
The visualized paranasal sinuses and mastoid air cells are clear.
IAC MRI:
There is no abnormal signal within the brainstem specifically at the
pontomedullary junction. There is no abnormal enhancement along the
expected course of cranial nerve VI. The cavernous sinuses are normal in
appearance.
Cerebellopontine angles, internal auditory canals and inner ear
structures are unremarkable.
IMPRESSION:
Medial deviation of the left eye compatible with the history of left
lateral rectus palsy. No abnormal enhancement identified along the
expected course of cranial nerve VI bilaterally. Also, there is no signal
abnormality within the brainstem identified.
No acute/subacute infarct, hemorrhage, mass effect or abnormal
enhancement.
Redemonstration of a partially empty sella as well as mild prominence of
the CSF surrounding the optic nerves. Findings could reflect idiopathic
intracranial hypertension in the appropriate clinical setting.
Unchanged few scattered non-specific FLAIR hyperintensities in the left
corona radiata. Differential is broad and would include sequela of prior
infection/inflammation, sequela of chronic microangiopathy, or
vasculitis, amongst many others. Pattern not typical for demyelinating
disease.
Redemonstration of multiple susceptibility foci as detailed above likely
reflecting chronic microbleeds.
Comment