Aa
MS questions and help please
Long post and sorry for that.
A. sypmtoms first appeared around eight months ago. Blurred vision, headache, numb left hand and right leg, difficulty walking.
Family DR sent me for MRI, MRI findings were
Technique: Multiplanar and multiple spin-echo T1- and T2-weighted images were
performed through the brain. Postcontrast images and diffusion-weighted images were
also obtained.
Findings: There is no restricted diffusion to suggest an acute infarct. There are a
few foci of abnormal high signal in the subcortical white matter, predominantly of the
frontal lobe. A total of eight foci are present. There is no signal abnormality of
the deep white matter of the brain. The pattern and distribution of these are
nonspecific.
There are no intra- or extra-axial collections. There is no hydrocephalus or midline
shift. The major intracranial vascular flow voids are present. The midline
craniocervical junction structures are normal. The pituitary gland is within
acceptable limits.
There is no abnormal enhancement. There is no susceptibility artifact in the brain.
High resolution FLAIR images were also obtained. There is a punctate area of high
signal within the corpus callosum. This measures only 2 mm. Additionally there is
some very mild signal hyperintensity along the periventricular white matter of the
frontal horns bilaterally. This is nonspecific. These findings were not appreciated
on the axial FLAIR sequence.
IMPRESSION:
1. Mild amount of signal abnormality in the brain seen only on the FLAIR sequences.
The differential diagnoses include the sequela of migraines, the sequela of prior
injury. A demyelinating process cannot be excluded. Clinical correlation is
recommended.
2. No abnormal enhancement to suggest an active process.
3. There is no restricted diffusion to suggest an acute infarct.
I never got headaches before this. then the Family DR sent me to Nueroligist.
Nueroligist order second MRI brain, MRI c & T Spine, VEP and EEP EEG. and Lumbar Puncture.
VEP came back normal, EEG normal, VEP done on ankles able to get 61 of 200 on left leg and 0 of 200 on right leg. So no reading on right leg. Lumbar punture came back normal.
Second MRI Brain :
EXAM: MRI BRAIN W/WO CONTRAST
REASON FOR EXAM: 35-YEAR-OLD WITH DIZZINESS, LOSS OF SHORT-TERM MEMORY, LACK OF
COORDINATION
BRAIN MRI
Technique: Multiplanar and multiple spin-echo T1- and T2-weighted images were
performed through the brain. Postcontrast images and diffusion-weighted images were
also obtained.
Findings: There are a few small areas of abnormal signal intensity within the brain.
There are foci of abnormal high signal in the subcortical white matter of each frontal
lobe. Additionally, there is a mild amount of signal hyperintensity adjacent to the
frontal horns of the lateral ventricles. A total of 11 to 12 foci of abnormal high
signal are present. There is no discrete signal abnormality of the corpus callosum.
No signal abnormality radiates outward from the corpus callosum. There is no abnormal
enhancement present.
The brain volume is normal. There is no hydrocephalus, midline shift or mass effect.
There are no intra- or extra- axial collections. As mentioned, there is no abnormal
enhancement.
There is a tiny area of signal abnormality adjacent to the frontal horn of the left
lateral ventricle best seen on the T2-weighted images. This is seen on image 13. This
suppresses on the FLAIR sequence. This is compatible with a tiny periventricular
cyst. This measures only 2 mm. This is of doubtful clinical significance.
The paranasal sinuses are normally aerated. The major intracranial vascular flow
voids are present.
IMPRESSION
1. Mild amount of signal abnormality involving predominantly the subcortical white
matter of both frontal lobes, but also the deeper white matter. The pattern and
distribution is nonspecific. The differential diagnosis includes a demyelinating
process, the sequela of prior injury, the sequela of migraines and less likely
early chronic small vessel ischemic changes given the patient's age. Clinical
correlation is recommended to determine if the patient has a history of
hypertension. A follow-up brain MRI in three to six months is recommended.
2. No abnormal enhancement to suggest an active process.
JOB:639753 0803-0106 D:08/03/10 1136 T:08/03/10 1205 BY:KKF
T & C Spine MRI didn't show anything remarkable but Neuroligist has ordered the radioligist to look at them again.
Third MRI 6 months later of the brain:
EXAM: MRI BRAIN W/WO CONTRAST
REASON FOR EXAM: HEADACHES, DIZZINESS, NUMBNESS, POSSIBLE MS.
MR BRAIN WITHOUT AND WITH CONTRAST
Technique: Multiplanar and multispin-echo including pre- and postgadolinium MR images
of the brain were obtained.
Comparison: 8/3/2010
Findings: The diffusion-weighted images appear unremarkable without foci of increased
signal seen. The apparent diffusion coefficient maps do not demonstrate any areas of
restricted diffusion.
On the standard FLAIR images, the previously identified multiple bilateral
predominantly deep cerebral white matter foci of high T2 signal as well as some
increased periventricular white matter high T2 signal near the frontal horns have not
progressed appreciably in the interim. 3D sagittal FLAIR images were obtained as part
of the study. These demonstrate over nine supratentorial white matter lesions. The
majority of the deep white matter lesions are somewhat punctate in appearance and
measure less than 6 mm in maximal size.
There is a single small punctate focus of increased subependymal corpus callosal T2
signal measuring approximately 2 mm involving the anterior corpus callosum body noted.
The remainder of the corpus callosum appears unremarkable. The infratentorial white
matter structures appear unremarkable.
There is mild bilateral ethmoid, sphenoid and maxillary sinus mucosal thickening.
Small subependymal cyst left caudothalamic groove region measuring 2 mm once again
identified, unchanged.
The craniocervical junction appears unremarkable without evidence of cerebellar
tonsillar ectopia. The imaged portions of the cervical cord on the sagittal FLAIR
images also appear unremarkable.
There are no foci of abnormal intracranial enhancement seen.
There is no abnormal meningeal enhancement. The major dural venous sinuses appear to
be patent.
IMPRESSION
1. Unchanged MR appearance of the brain.
2. Stable appearance of the previously identified nonspecific cerebral white matter lesions without any foci of enhancement noted. Differential is as per previous but given the interval stability, there is no definitive MR evidence of active white matter disease.
Now the Neuroligist has ordered EMG and Nerve conductivity study as well as radioligist to review all MRI's. My left hand is numb, left side of face is numb, right foot is numb, lower back pain, chest often feels like it is being squeezed hard. very little control of bladder, headache. They currently have me on anexity meds, gabapentin and vicodin. There was aprox over month between attacks and during that time i was able to play softball and everything like before all this. Now it is difficult for me to get around. Neuroligist does not think MS but wont rule it out. Any ideas what can do this to someone so quickly?
A. sypmtoms first appeared around eight months ago. Blurred vision, headache, numb left hand and right leg, difficulty walking.
Family DR sent me for MRI, MRI findings were
Technique: Multiplanar and multiple spin-echo T1- and T2-weighted images were
performed through the brain. Postcontrast images and diffusion-weighted images were
also obtained.
Findings: There is no restricted diffusion to suggest an acute infarct. There are a
few foci of abnormal high signal in the subcortical white matter, predominantly of the
frontal lobe. A total of eight foci are present. There is no signal abnormality of
the deep white matter of the brain. The pattern and distribution of these are
nonspecific.
There are no intra- or extra-axial collections. There is no hydrocephalus or midline
shift. The major intracranial vascular flow voids are present. The midline
craniocervical junction structures are normal. The pituitary gland is within
acceptable limits.
There is no abnormal enhancement. There is no susceptibility artifact in the brain.
High resolution FLAIR images were also obtained. There is a punctate area of high
signal within the corpus callosum. This measures only 2 mm. Additionally there is
some very mild signal hyperintensity along the periventricular white matter of the
frontal horns bilaterally. This is nonspecific. These findings were not appreciated
on the axial FLAIR sequence.
IMPRESSION:
1. Mild amount of signal abnormality in the brain seen only on the FLAIR sequences.
The differential diagnoses include the sequela of migraines, the sequela of prior
injury. A demyelinating process cannot be excluded. Clinical correlation is
recommended.
2. No abnormal enhancement to suggest an active process.
3. There is no restricted diffusion to suggest an acute infarct.
I never got headaches before this. then the Family DR sent me to Nueroligist.
Nueroligist order second MRI brain, MRI c & T Spine, VEP and EEP EEG. and Lumbar Puncture.
VEP came back normal, EEG normal, VEP done on ankles able to get 61 of 200 on left leg and 0 of 200 on right leg. So no reading on right leg. Lumbar punture came back normal.
Second MRI Brain :
EXAM: MRI BRAIN W/WO CONTRAST
REASON FOR EXAM: 35-YEAR-OLD WITH DIZZINESS, LOSS OF SHORT-TERM MEMORY, LACK OF
COORDINATION
BRAIN MRI
Technique: Multiplanar and multiple spin-echo T1- and T2-weighted images were
performed through the brain. Postcontrast images and diffusion-weighted images were
also obtained.
Findings: There are a few small areas of abnormal signal intensity within the brain.
There are foci of abnormal high signal in the subcortical white matter of each frontal
lobe. Additionally, there is a mild amount of signal hyperintensity adjacent to the
frontal horns of the lateral ventricles. A total of 11 to 12 foci of abnormal high
signal are present. There is no discrete signal abnormality of the corpus callosum.
No signal abnormality radiates outward from the corpus callosum. There is no abnormal
enhancement present.
The brain volume is normal. There is no hydrocephalus, midline shift or mass effect.
There are no intra- or extra- axial collections. As mentioned, there is no abnormal
enhancement.
There is a tiny area of signal abnormality adjacent to the frontal horn of the left
lateral ventricle best seen on the T2-weighted images. This is seen on image 13. This
suppresses on the FLAIR sequence. This is compatible with a tiny periventricular
cyst. This measures only 2 mm. This is of doubtful clinical significance.
The paranasal sinuses are normally aerated. The major intracranial vascular flow
voids are present.
IMPRESSION
1. Mild amount of signal abnormality involving predominantly the subcortical white
matter of both frontal lobes, but also the deeper white matter. The pattern and
distribution is nonspecific. The differential diagnosis includes a demyelinating
process, the sequela of prior injury, the sequela of migraines and less likely
early chronic small vessel ischemic changes given the patient's age. Clinical
correlation is recommended to determine if the patient has a history of
hypertension. A follow-up brain MRI in three to six months is recommended.
2. No abnormal enhancement to suggest an active process.
JOB:639753 0803-0106 D:08/03/10 1136 T:08/03/10 1205 BY:KKF
T & C Spine MRI didn't show anything remarkable but Neuroligist has ordered the radioligist to look at them again.
Third MRI 6 months later of the brain:
EXAM: MRI BRAIN W/WO CONTRAST
REASON FOR EXAM: HEADACHES, DIZZINESS, NUMBNESS, POSSIBLE MS.
MR BRAIN WITHOUT AND WITH CONTRAST
Technique: Multiplanar and multispin-echo including pre- and postgadolinium MR images
of the brain were obtained.
Comparison: 8/3/2010
Findings: The diffusion-weighted images appear unremarkable without foci of increased
signal seen. The apparent diffusion coefficient maps do not demonstrate any areas of
restricted diffusion.
On the standard FLAIR images, the previously identified multiple bilateral
predominantly deep cerebral white matter foci of high T2 signal as well as some
increased periventricular white matter high T2 signal near the frontal horns have not
progressed appreciably in the interim. 3D sagittal FLAIR images were obtained as part
of the study. These demonstrate over nine supratentorial white matter lesions. The
majority of the deep white matter lesions are somewhat punctate in appearance and
measure less than 6 mm in maximal size.
There is a single small punctate focus of increased subependymal corpus callosal T2
signal measuring approximately 2 mm involving the anterior corpus callosum body noted.
The remainder of the corpus callosum appears unremarkable. The infratentorial white
matter structures appear unremarkable.
There is mild bilateral ethmoid, sphenoid and maxillary sinus mucosal thickening.
Small subependymal cyst left caudothalamic groove region measuring 2 mm once again
identified, unchanged.
The craniocervical junction appears unremarkable without evidence of cerebellar
tonsillar ectopia. The imaged portions of the cervical cord on the sagittal FLAIR
images also appear unremarkable.
There are no foci of abnormal intracranial enhancement seen.
There is no abnormal meningeal enhancement. The major dural venous sinuses appear to
be patent.
IMPRESSION
1. Unchanged MR appearance of the brain.
2. Stable appearance of the previously identified nonspecific cerebral white matter lesions without any foci of enhancement noted. Differential is as per previous but given the interval stability, there is no definitive MR evidence of active white matter disease.
Now the Neuroligist has ordered EMG and Nerve conductivity study as well as radioligist to review all MRI's. My left hand is numb, left side of face is numb, right foot is numb, lower back pain, chest often feels like it is being squeezed hard. very little control of bladder, headache. They currently have me on anexity meds, gabapentin and vicodin. There was aprox over month between attacks and during that time i was able to play softball and everything like before all this. Now it is difficult for me to get around. Neuroligist does not think MS but wont rule it out. Any ideas what can do this to someone so quickly?
Other Findings: Numerous foci of abnormal signal predominantly around
the margin of the corpus callosum and extending up the around the
ventricular margins across the centrum semiovale to the subcortical
region. some involvement of the corpus callosum. Some of the
larger lesions measure up to about 12 x 12 x 21 mm and 21 x 10 x 15
mm. None demonstrate mass effect. The pons appears to be relatively
spared. None of the lesions appear to enhance with gadolinium.
the margin of the corpus callosum and extending up the around the
ventricular margins across the centrum semiovale to the subcortical
region. some involvement of the corpus callosum. Some of the
larger lesions measure up to about 12 x 12 x 21 mm and 21 x 10 x 15
mm. None demonstrate mass effect. The pons appears to be relatively
spared. None of the lesions appear to enhance with gadolinium.
thanks for your reply, I am a push over to much. its nice to hear someone else say i need to be more assertive with this. Thanks again.
Obviously, these doctors can't agree on your condition, so the real matter should be treating your symptoms, which in my opinion do seem to be MS like. You are on some medications that can help with nerve pain and numbness, but I think it's time you demands some MS treatments despite the fact that they can't quite figure it out yet. They have been putting you through all of these tests for long enough.
I do hope, however, and I do think that the NCV and the EMG helps convince the doctors of your condition and the need to begin acting more aggressively. Although it's the other more intense testing that usually helps Neurologists to build a case of MS. Also, nerve distress from the brain will not appear from an NCV or a EMG, so it's strange that they didn't begin there??? Plus they have quantitative findings from your MRIs? I am confused??? I think they should do something treatmentwise, but hang in there until these last rounds of tests are done. Then be assertive.
I do hope, however, and I do think that the NCV and the EMG helps convince the doctors of your condition and the need to begin acting more aggressively. Although it's the other more intense testing that usually helps Neurologists to build a case of MS. Also, nerve distress from the brain will not appear from an NCV or a EMG, so it's strange that they didn't begin there??? Plus they have quantitative findings from your MRIs? I am confused??? I think they should do something treatmentwise, but hang in there until these last rounds of tests are done. Then be assertive.
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