Röntgendiagnostik, Nuklearmedizin, Computertomographie, Sonographie,
DSA (Angiographie), Kernspintomographie
Speersort 8, D - 20095 Hamburg, Tel.: +49 40 - 33 09 15, +49 40
- 325 5520, Fax: +49 40 - 32 49 50
Dr. E.-U. Bieler, Radiologie und Nuklearmedizin
Dr. Rene Rückner, Radiologie
Dr. Rudolf Rieser, Radiologie
Dr. Andreas Keulers, Radiologie
Dr. Joachim Schubert, Diagnostische Radiologie
Datum: 9.9.97 / KEU*sch
Klinik/Fragestellung
Opticusneuritis
Kernspintomographie (MRT) des Neurocraniums vom 9.9.97
Sequenzen:
Axial, TSE-intermediär - /T2
Coronal, TIR - T2
Sagittal, dark fluid T2
Axial, TSE - T1 nach Gadolinium i.v. (magnetic transfer)
Zum Vergleich liegen Vorbilder vom 26.8.97 vor.
Ein Herd hochfrontal rindennah im Marklager rechts hat eindeutig an
Größe zugenommen und mißt heute etwa 1.8 cm und zeigt
nach Gadolinium i.v. ein kräftiges ringförmiges Enhancement.
Auch weitere Herde, teils periventrikulär, teils rindennah, sind Kontrastmittlel-aufnehmend
abgebildet. Der Hirnstamm selber unauffällig. Die sagittale Dark-fluid-T2-Sequenz
zeigt einen unauffälligen Balken, die Balkenstrahlung allerdings mit
oben erwähnten signalreichen Herden und den übrigen teils rindennah
gelegenen Signalerhöhungen. Auch im Kleinhirn sind punktförmige
Signalerhöhungen im Mark sichtbar. Des weiteren der N. opticus links
in der TIR-T2-Sequenz signalangehoben. Rechts dagegen signalarm.
Beurteilung:
- Im Vergleich zur Voruntersuchung
sind die Herdläsionen im Hirnparenchym partiell größenprogredient, dies gilt v.a. für den Herd rechts frontal,
- auf Grund der Bildmorphe unverändert zur Voruntersuchung am ehesten entzündlicher disseminierter ZNS-Prozeß,
wobei die klassischen Kriterien einer Encephalitis disseminata bei fehlendem Balkenbefall nicht voll erfüllt sind, wobei diese allerdings in allererster Linie ursächlich in Erwägung gezogen werden muß.
- Unverändert akute Neuritis nervi optici links.
- Des weiteren entzündlich verändert
die Siebbeinzellen und die Kiefernhöhlen beidseitig.
The Presbyterian Hospital
in the City of New York
at
Columbia Presbyterian Medical Center
Department of Radiology
Images reviewed, report edited and signed by
A. John Silver, MD.
January 22, 1998, 10:34
Date: January 20, 1998
Location: Milstein Hospital
Ord. Dr.: Liegner, Kenneth, 8 Barnard Road, Armonk, N.Y. 10504
Exam: MBMR Brain with and without Contrast
Clinical Information: Lyme Disease
Description:
Multiple T1 sagittal and axial pre and post contrast, proton density and
T2 weighted axial, proton density and T2 weighted coronal and post-contrast
T1 coronal images of the brain were obtained.
Findings:
Comparison with a previous outside study dated September 9, 1997:
Again noted are multiple periventricular white matter and inferior margianl
corpus callosal lesions that show increased signal on T2-weighted images.
Post contrast, many of theses lesions are seen to enhance, the largest
of which is in the right frontal subcortical white matter which is ring
enhancing. The present study shows marked improvement of the enhancement
pattern with only slight focal enhancement in a single lesion in the right
parietal lobe.
There are multiple rounded foci of increased T2 signal in the bilateral
frontoparietal white matter as well as the periventricular white matter
in the right temporal region. One of these foci in the right parietal lobe
demonstrates possible slight focal enhancement. No significant mass effect
is noted.
There is no evidence of cortical infarction, intracranial hemorrhage.
No obstructive hydrocephalus or midline shift or herniation is noted.
Mucosal thickening is noted within the bilateral maxillary sinuses and
sphenoid sinuses consistent with sinusitis.
Impression:
-
Multiple bilateral frontoparietal and right temporal white matter foci
of abnormal signal with questionable enhancement in the right parietal
region. These lesions are of uncertain etiology and may represent possible
granulomatous disease including Lyme Disease. Multiple infarcts secondary
to etiology like vasculitis are less likely. However, since several of
these lesions are possibly corpus callosal lesions,
multiple sclerosis demyelinating plaques cannot be ruled out.
-
Maxillary and shenoid sinusitis.
The Presbyterian Hospital
in the City of New York
at
Columbia Presbyterian Medical Center
Department of Radiology
Images reviewed, report edited and signed by
A. John Silver, MD.
September 28, 1998, 9:13
Date: September 28, 1998
Location: Milstein Hospital
Ord. Dr.: Liegner, Kenneth, 8 Barnard Road, Armonk, N.Y. 10504
Exam: MBMR Brain with and without Contrast
Clinical Information: Lyme Disease
Description:
MRI of the brain was performed utilizing sagittal T1, axial T1, prton density,
T2 and post gadolinium, axial, coronal, and sagital T1-weighted sequences.
Comparison was made with prior MRI dated January 20, 1998. The previously
noted frontal perietal white matter lesions appear unchanged as compared
to the prior study dated Jan. 20, 1998. The findings are as in the prior
impression.
Impression:
No significant change in the frontal parietal white matter lesions as compared
to prior study suggests static lesions.
Oral comment given:
-
Questionable enhancements seen in January didn't show up this time.
-
Lesions are static, might have been there for years.
-
No effect of antibiotics seen. Seems to be static inflammation.
-
No brain stem involvement.
-
Blood brain barrier is intact, not affected by inflammation.
-
Whatever inflammation there was associated with Lyme, it seems to be not
progressing.
-
Other reasons for static inflammation: you don't want to know these (one
of them being MS).
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Version: 9. April 2002.