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Review Case Reports
[Positron emission tomographic evaluation for frontal hypertrophic cranial pachymeningitis using 11C-methyl-L-methionine].
- M Takahashi, T Sasajima, K Mineura, Y Itoh, M Kowada, K Iwaya, J Hatazawa, T Ogawa, T Okudera, M Murakami, and K Uemura.
- Neurosurgical Service, Akita University Hospital.
- No Shinkei Geka. 1996 Mar 1; 24 (3): 287-93.
AbstractA case of frontal hypertrophic cranial pachymeningitis was presented with positron emission tomography (PET) using (11C-methyl)-L-methionine (11C-Met). A 55-year-old male developed right hemiparesis after generalized tonic convulsion one month prior to admission. MR images revealed patchy enhancement extending from the dura mater to the cerebral parenchyma surrounding high T2-weighted signal in the left frontal region. Left carotid angiogram showed atresia of the rostral superior sagittal sinus and obliteration of the cortical veins associated with compensatory venous channels coursing in the frontal deep white matter. PET demonstrated high 11C-Met uptake in the area corresponding to the enhancing lesion on the MR images. The ratio of lesion/normal cortex was 1.58 as an indicator of selective uptake in the lesion. The contralateral temporal gray matter was representative of a normal cortex. In contrast, 11C-Met did not accumulate in the frontal white matter where T2-weighted MR images showed abnormal high intensity lesion. This suggested that the frontal white matter lesion was derived from vasogenic edema due to venous infarction. The patient underwent an uneventful exploratory biopsy. The dura mater had proliferated to a thickness of 3.5mm and was tightly adherent to the left middle frontal gyrus. Microscopically, the thickened dura mater where the tracers had accumulated was composed of abundant collagenous fibers together with diffuse infiltration of inflammatory cells, including predominantly lymphocytes, plasma cells, and neutrocytes. The lymphocytes, which proved positive in both UCHL-1 and L26 staining, had no atypism. Histological findings corresponded to hypertrophic pachymeningitis. Met-PET clearly represented viable and infiltrative zones of inflammatory cells. The patient's neurological symptoms and signs gradually improved. Follow-up MR images three months after the surgery showed the enhancing lesion to be diminished and a marked regression of the vasogenic edema. Spatial determination of viable lesions permitting differentiation from biological inactive or vasogenic edema is an important guideline in selecting an appropriate surgical procedure in the diagnosis and treatment of hypertrophic cranial pachymeningitis. Met-PET would appear useful in delineating inflammatory lesions such as hypertrophic cranial pachymeningitis.
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